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Healing with FreshmanMedical School Physiology(How the Body is designed to Work)

Jerry Tennant, MDTennant Institute for Integrative Medicine

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Tennant Institute for Integrative Medicine5601 N. MacArthur Blvd.

Suite 200Irving, TX 75038

972-580-1156jtennant@tennantinstitute.com

© Copyright 2005All Rights Reserved

This book is written for those with chronic disease and those wishing to avoid chronicdisease. There are those who just want instructions on what to do to get well and don’treally care why or how it works. This first section is written for those.

Others want to know all the details about what they are doing and why. The second partof the book is written for those. If you don’t want/need to know the why and how, youcan skip the second part of the book.

Another use for the second part of the book is information for those who think you arecrazy for doing something other than “traditional medicine”. That includes friends,spouses, relatives, and some of your doctors.

The things that we recommend are primary from freshman medical school physiology.For the benefit of your doctors, we have included a bibliography at the back of thisbooklet with the medical references about the things we are recommending.

When we doctors go to medical school, we are taught basic physiology the first year.That teaches us how the body normally works. The second year we are taught what goeswrong with the body. The third and fourth years, we are taught to forget most of the firsttwo years and memorize symptom complexes as “diseases”. We are then taught whichdrugs cover up the symptoms of those diseases. When that doesn’t work, we are taughtto attempt to remove the offending part.

After we get into practice, control of the patient is taken from the doctor by the insurancecompanies. When a doctor makes a diagnosis, he/she must select a code number forwhatever diagnosis is made. That code number activates what are called “standards ofpractice”. That means that a computer programmed by an insurance company is now incontrol of your medical care. It tells the doctor what drugs must be prescribed andwhether you can have surgery. It tells the doctor when you can be hospitalized and howmany days you can stay there. Unless your doctor can justify another diagnosis code,you are controlled by the first one.

Most HMO’s and PPO’s also set standards for doctors as far as when you can see aspecialist and how many patients must be seen by the doctor daily. I know a family

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practice doctor that is required to see 60 patients/day or lose his job. Under suchcircumstances, there is little time to talk to patients about the basics of diet and otherthings needed to stay well. There is no time to do anything but quickly write you anotherprescription and get you out the door.

We do not accept any insurance. With that policy, the insurance companies cannotdictate the length of time we spend figuring out what is wrong with you. Neither do theydictate what we can do to attempt to make you well.

What we do is basic freshman medical school physiology plus oriental medicinecombined with modern electronics. There is nothing strange or unusual about what wedo except that oriental medicine is not recognized by the FDA and insurance companiesand thus is not commonly used or understood.

Our clinic and doctor(s) do not replace your personal physician(s). We are simplyconsultants in Integrative Medicine doing things that your doctor may not have time todo. We are not your primary physician, and you must look to your primary physicianas your basic and final advisor for medical care. You must consult with your primaryphysician for emergencies. We do not treat emergencies.

The Basics

The key to making chronic disease better is making a single cell work. If you give thebody the things a single cell needs to work, the body often has the power to heal all of thecells of the body. That means you get well!

A cell is made up of a cell membrane and the inside called the cytoplasm. The cellmembrane is made of fats. It controls the cell and is consider the “brain” of the cell.That means you must have the proper fats to make those membranes. About 20% of yourbody is this fat, so if you weigh 200 pounds, you need 40 pounds of perfect fat to behealthy. Since cells replace themselves on an average of about 8 weeks, you would needto absorb about five pounds of fat per week to stay healthy!

The cytoplasm of the cell is made up of proteins. There are eight proteins that the bodycan’t make (ten in children). Thus they are called essential proteins. You must eatenough protein to fill this need.

To be used, proteins and fats need vitamins and minerals. To date, I have never seen apatient with a chronic disease that is not mineral deficient, and most are vitamin deficientas well.

Cells need the following to be healthy:

1. Water with voltage (alkaline water)2. Fats to make cell membranes

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3. Proteins to make the cytoplasm (the “machinery”) inside cells.4. Vitamins to allow the body to make the fats and proteins work.5. Minerals to make the fats and proteins work and as On-Off switches and keep

your pH in the operating range.6. Oxygen7. Sunshine8. Voltage is the same as pH. The body must have voltage to function (the same as

saying you must have an alkaline pH). The body normally runs at pH of 7.2which is the same as -22 mV.

We will be giving you these things as a part of getting you well.

The next important thing to recognize is the importance of your liver/gallbladder. Thegallbladder is a storage tank for the bile made by the liver. It often becomes filled withsludge and doesn’t function normally. This sludge becomes a breeding ground for allsorts of infections. They produce poisons called “neurotoxins” that make you sick.However, you need your gallbladder because the liver can’t make bile fast enough toallow you to absorb the fat you need to keep healthy. The key is to clean it---not toremove it. (If you have already had it removed, you will need to take bile supplementsthe rest of your life).

The liver is in charge of:

1. Processing your digested food so that it can be used by the body to make newcells and to keep things working.

2. Getting the toxic things out of your body.3. Controlling the immune system so you can keep infections under control.

If your liver is sick, you lose these processeschronic disease.

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http://images.google.com/imgres?imgurl=http://www.bnaiyer.com/health/liver-3.jpg&imgrefurl=http://www.bnaiyer.com/health/liver-2.html&h=324&w=277&sz=24&tbnid=PShU2hJ6LYwJ:&tbnh=114&tbnw=97&hl=en&start=5&prev=/images%3Fq%3Dliver%2Bcells%26svnum%3D10%26hl%3Den%26lr%3D%26sa%3DG

The liver contains 35,000 square meters (about thesurface of seven football fields) of membrane surfaceused to accomplish these things. These membranesare made of fat. If you don’t eat enough fat of theproper kind or if you eat fats that have beenprocessed so they are similar to plastic, thesemembranes don’t work correctly. (These “plasticfats” are called “partially hydrogenated” fats andCanola Oil.)

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When the liver gets clogged up with debris because the membranes are made of plastic, ittries to wash itself with cholesterol. A high cholesterol means your liver is trying toclean itself---much like you would try to clean the filter from your air conditioner. If youinterfere with that process with drugs and continue to give your body only plastic fats torepair itself, you are doomed to chronic diseases of all types.

Once the liver cleans itself and repairs itself, the rest of the body can begin to heal. Theliver will begin to supply the nutrients needed, begin to remove toxic chemicals(pesticides, pharmaceuticals, etc.) and turn on the immune system to get rid of infections.Thus our initial efforts will be to clean up and repair your liver/gall bladder. It normallytakes eight to sixteen weeks for the liver to replace itself with all new cells.

Remember that the leading cause of death in the U.S. is reactions to pharmaceuticals.Just listen to the drug advertisements on TV and you will realize that all drugs have sideeffects. You should have the goal of getting off your drugs. However, do not do thatwithout guidance. Stopping drugs suddenly often causes the body to have a bad reaction.The primary exception is anti-cholesterol drugs. You should stop them immediately.They are all liver toxic and prevent the liver from cleaning itself. Your cholesterol levelwill go to normal as we clean the liver and give it the fat it needs to repair itself.

To be healthy, you must stop eating anything that says, “Partially hydrogenated” orCanola Oil. You will have to stop eating fried foods and cheese in restaurants becausethese almost always are made of partially hydrogenated oils. In addition, you must stopusing all forms of artificial sweeteners such as aspartame, Splenda, saccharine, xylitoland others ending in “–ol”. All of these are severe neurotoxins that the body doesn’tknow how to get rid of. Stop MSG as it is also a neurotoxin. Stop smoking. Stop eatingsoy. Stop drinking coffee, tea, and alcohol.

Eat lots of raw milk, butter and eggs. If they make you nauseated, that means your liverisn’t making enough bile to absorb them. You will need to take ox bile and digestive

http://www.abdn.ac.uk/emunit/emunit/temcells/images/liver.jpg http://www.greenhouse.gov.au/lgmodules/wep/hvac/training/components/images/filter.jpg

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enzymes with each meal until your liver can make bile on its own. You will be able toeat fats without trouble when we get your liver working again.

Eat things that don’t have the toxins listed above. Try to vary your diet, with 1/3 protein,1/3 fat, and 1/3 carbohydrates with the carbs from fruits and vegetables.

So that’s the summary. You will be given specific instructions inthe office according to your findings.

If You Want To Know The Details, Read The Following:

So you are sick and tired of being sick and tired. This workbook will be your guide togetting well.

Let’s assume that you have bought an old house that hasn’t been lived in for severalyears. However, you love that old house and want to return it to its former glory. Youdream of living in that wonderful house and all the fun you will have in it.

Well----your body is that house.

Now we have to start the process of returning it to normal. It won’t happen overnight,and there are no miracle pills to make it normal. In fact, medications are simply paint. Ifyou paint over a board eaten by termites, you may not see the holes in the board forawhile, but they are still there and the rotting goes on. Medications cover up thesymptoms, but the degeneration in your body continues. If you have arthritis and youtake medication, the degeneration in your joints continues. You just don’t feel the painwhile the joints continue to rot.

So now you own the old house. What must be done before you can move in? First youwill want to restore the utilities. You will need water, sewage, and electricity.

So let’s get started on those:

WATER

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The body is about 70-80% water. Thus it is the basis of who youare and how healthy you are. Unfortunately, you have probablybeen lead to believe that drinking things containing water is thesame as drinking water-----not so. When things are put into waterto make them into some other drink, it changes how the water reactsin the body. If you take good water from a well or anuncontaminated stream, it will be alkaline (finding good wateranywhere in the world is getting harder because of chemicalcontaminations). That means it contains electrons available foryour body to use in its metabolism. However, if you put chlorineand/or fluoride in it, it becomes acidic. Anything that is acidic is an

electron stealer. Anything that is alkaline is an electron donor. Drinking acidic watersteals electrons from your cells and damages them. Drinking water that has been madeinto carbonated beverages is drinking acid that is so concentrated, you can use it to cleanthe grease off your engine or clean out your toilet! Can that possibly be good for you?

Your cells are composed of water, but it is also what your body uses to wash the inside ofyour body to clean away the garbage that gets into the body. Would you wash your carwith coffee? Then consider washing the inside of your body with coffee or tea or sodas.

In addition, zinc is one of the most important elements in the body. Without zinc, youcan’t make stomach acid. Without stomach acid, you can’t digest your food. Withoutnutrition, the body can’t repair itself. In addition, without zinc, you can’t makeneurochemicals like serotonin, dopamine, norepinephrine and epinephrine.

Zinc is blocked by alcohol, coffee, and tea. (Alcohol also blocks selenium.) Trying toget your fluids by drinking these substances will almost guarantee that you will becomedepressed. Is it any wonder so much of our population is depressed?

Many think it is healthy to drink distilled water; it is not. Distilled water pulls mineralsout of your cells and into the water. You can kill yourself drinking distilled water. Forexample, if you put one drop of distilled water inside an eye, the cornea immediatelybecomes opaque and the cells inside the eye are killed as the minerals are pulled out ofthem.

Another problem is bottled water. Bottled water is almost always city water that has beenput through a filter. It is perhaps cleaner than city water, but it is still acidic and containsmany other chemicals. Many cities have tap water that has toxic levels of copper.Copper is also a zinc antagonist.

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If you look on the bottom of bottled water you buy most places, you will see a trianglethat contains the number one. That number relates to the kind of plastic used tomanufacture the bottle. A number one usually relates to a clear plastic that is not totallypolymerized. If you leave such a bottle in the sun, the polymers from the bottle will enterthe water and poison it. You probably have noticed that bottled water left in the suntastes like plastic. What most of us didn’t realize is that that plastic acts like estrogen inour bodies causing hormonal imbalances and blocking zinc.

Estrogen Unopposed by Progesterone blocks zinc, magnesium and vitamin B6 andleads to:

1. Increases in heart attacks and strokes,2. Aging,3. Anxiety,4. Allergies,5. Asthma,6. Breast cancer,7. Cervical cancer,8. Cold hands and feet,9. Decreased sex drive,10. Dry eyes,11. Endometriosis,12. Fat gain around hips,13. Fatigue,14. Fibrocystic breasts,15. Foggy thinking16. Gall bladder disease,17. Hair loss,18. Headaches,19. Hypoglycemia,20. Increased blood clotting21. Autoimmune disorders.

You should drink your water from a bottle made of glass or from a plastic bottle with atleast a number two in the triangle. Most sports water bottles have a number seven in thetriangle.

Perhaps the best water system is the one invented by Viktor Schauberger in Switzerland.It attaches to the main entering your home and provides good water for the entire house.It costs about $2,000 plus installation. Ask us for detail if you want to get one of thesesystems.

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For those who can’t afford the Shaubergersystem, I recommend the system developedby Nikken. Their explanation of how thesystem works may not be totally accurate,but I have personally tested the pH, Redoxpotential, rH2, and conductivity of tap waterbefore and after it has gone through theNikken system. The water coming out ofthe system is much better than that going in.The cost of the system is about $300-$400and you can make gallons and gallons ofwater before having to replace the filters. Itis much cheaper than buying bottled water.Put it in your sports bottle (number two orgreater in the triangle on the bottom) if youneed to be away from home.

My recommendation is that you avoiddrinking anything but water. If you mustdrink something else, know that it is toxic toyour system and be prepared for theconsequences.

When people are sick, they often have decreased minerals in their body. Drinking waterdilutes the minerals even more reduction in the voltage feel worse. The answer isto restore the minerals and voltage and that allows you to drink the necessary amount ofwater.

Sometimes I see doctors tell their patients to drink less water because some lab testshows they have too little of something in their blood such as sodium. If you dehydratethe patient, the lab test will come back to normal but the patient feels worse. Let’sassume you have two glasses of tea each containing eight ounces. One is very dark andthe other is very light. If I put the light colored one out in the sun and let some of thewater evaporate, soon both glasses of tea will be the same color. If I ran a lab test onboth glasses, the test might show a “normal” amount of tea in each. However, theremight not be enough volume left in the dehydrated glass to do much with. If we do thatto patients, we cause their blood pressure to be too low or the inside of the cells tobecome too thick to function. We must correct lab results by looking at total bodywater, intracellular water, and extracellular water. Then we know if the patient has toomuch or too little water or too much or too little “stuff” in the water. One can tell that

using a device called the Biological ImpedanceAnalysis device.

How much water to drink is always a question.The only sure way to know is to measure with theBIA device shown above. However, a good ruleof thumb is to drink water every time you feelhungry. If you still feel hungry a few minutes

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after drinking, then eat. The sense of hunger is often the signal the body really wantsmore water.

So in our old house analogy, you will begin by washing out the debris inside and outsideyour house.

Minerals

Minerals play an important role in the body. If you think about the battery in your car,you know that if you put distilled water in it, it won’t hold a charge. So it is with yourbody. In addition, mineral acts as On-Off switches in the body. This is particularly trueof calcium and magnesium. For example, to contract a muscle, calcium is necessary. Torelax the muscle, magnesium is necessary. Calcium turns things on and magnesium turnsthings off. If you run out of one of them, you get stuck in either on or off.

Minerals and vitamins are also important in manufacturing of things you need. Anexample is neurochemicals. To make serotonin from the protein L-tryptophan, you musthave:

1. Folate2. Calcium3. Iron4. Vitamin B35. Zinc6. Vitamin B67. Magnesium8. Vitamin C

To make dopamine and norepinephrine from the amino acid L-phenylalanine, oneneeds the following:

1. Folate2. Iron3. Zinc4. Magnesium5. Copper6. Vitamin B37. Vitamin B68. Vitamin C

If you don’t have calcium, magnesium zinc, iron, copper, and the necessary vitamins, youcan’t make serotonin. If you don’t have serotonin, you will become depressed.

The other problem is that the minerals need to be balanced. If you simply take a lot ofthe above minerals, you may be so out of balance that things don’t work correctly.

The easiest way to tell if you need a particular mineral is totaste that mineral in solution. You will need to purchasethis mineral testing/treatment kit. Ten minerals aredropped onto your tongue. If it tastes like water or sweet,

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you are deficient in it. If it tastes metallic or bitter, you don’t need it. Place the ones thatdon’t taste really bad in your morning juice. Recheck every week until each mineraldeficiency is corrected. When one of the minerals starts tasting really bad, you don’tneed it anymore.

Recheck your mineral level at least once every 3-4 months. Because our soils are sodepleted of minerals, you will need to replace them periodically.

Some of the most commonly consumed water substitutes are coffee, tea, and alcohol. Allthree block zinc and alcohol blocks selenium. Look at the symptoms caused by adeficiency of these minerals:Alcohol intolerance Zinc (30)Asthma Zinc (30)Belching Zinc (30)Bloating Zinc (30)Boils Zinc (30)Brittle nails Zinc (30)Bronchitis Zinc (30)Colds Zinc (30)Conjunctivitis Zinc (30)Delayed healing Zinc (30)Depression Zinc (30)Dermatitis Zinc (30)Disrupted sleep Zinc (30)Dry skin Zinc (30)Ear infections Zinc (30)Early graying hair Zinc (30)Eczema Zinc (30)Fidgeting Zinc (30)Frequent sore throats Zinc (30)Gastric-esophageal reflux disease (GERD) Zinc (30)Gastroenteritis Zinc (30)Hair Loss Zinc (30)Hay fever Zinc (30)Hyperactivity Zinc (30)Increased cholesterol Zinc (30)Infertility Zinc (30)Itchy skin Zinc (30)Joint pain Zinc (30)Joint stiffness Zinc (30)Loss of libido Zinc (30)Low blood sugar (hypoglycemic) Zinc (30)Low white blood cell count Zinc (30)Lung infections Zinc (30)Missed periods Zinc (30)Moodiness Zinc (30)

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Pimples Zinc (30)Pneumonia Zinc (30)Poor coping with stress Zinc (30)Poor memory Zinc (30)Pre-dinner tantrums Zinc (30)Prolonged infections Zinc (30)Psoriasis Zinc (30)Runny nose Zinc (30)Sinusitis Zinc (30)Stomach ulcers Zinc (30)Stretch marks Zinc (30)Temper outbursts Zinc (30)Thrush (mouth fungus) Zinc (30)Tinea (athlete's foot) Zinc (30)Warts Zinc (30)Arthritis Selenium (34)Asthma Selenium (34)Autoimmune diseases Selenium (34)Cancer Selenium (34)Cardiomyopathy Selenium (34)Depression Selenium (34)Diabetes Selenium (34)Heart disease Selenium (34)Hypothyroid Selenium (34)Increased cholesterol Selenium (34)Increased infections Selenium (34)

Note: zinc has an atomic number of 30 and selenium 34.

Drinking coffee, tea, and/or alcohol make you susceptible to the misery of all ofthese things = everything from athlete’s foot to cancer! Now doesn’t drinking watermake more sense?

It is also important to remember that taking antacids or drugs that block stomach acidproduction causes you to be deficient in zinc. This makes you susceptible to all of theabove things noted with zinc deficiency.

pH and Calcium

pH stands for “Potential Hydrogen”. It is a way of talking about the amount of acid andbase in our bodies. It is also a way of talking about the amount of voltage in our body.

pH is measured on a log rhythmic scale where 0 is the most acidic and 14 is the mostalkaline. Seven (7) is considered neutral.

Water (H2O) ionizes into hydrogen (H+) and hydroxyl (OH-) ions. When these

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ions are in equal proportions, the pH is a neutral 7. When there are more H+ ionsthan OH- ions then the water is said to be "acid". If OH- ions outnumber the H+ions then the water is said to be "alkaline". The pH scale goes from 0 to 14 and islogarithmic, which means that each step is ten times the previous. In otherwords, a pH of 4.5 is 10 times more acid than 5.5, 100 times more acid than 6.5and 1,000 times more acid than 7.5.

pH is also a measure of voltage. A pH of 0 is the same as +400 mVolts. A pH of 14 isthe same as -400 mVolts. Cells normally operate at about pH of 7.2 or -22 mVolts.

Chronic disease and pain are almost always associated with an acidic pH which is thesame as saying that chronic disease and pain are almost always associated with a loss ofvoltage. Health is associated with the presence of voltage which is the same as saying thathealthy people have an alkaline pH.

In the body, being able to hold a charge of voltage is associated with minerals in generaland calcium in particular.

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When you begin your day, you “turn on the body machinery”. This creates a byproductof carbonic acid. This acid must be eliminated from the body or the body loses its charge(becomes acidic). This is accomplished partly by having the carbonic acid dissociate intocarbon dioxide and water. The carbon dioxide is breathed out through the lungs.However, one cannot breathe fast enough to get rid of all the necessary carbon dioxide,so some of it is removed by combining with ammonia from the liver and intestine to formurea nitrogen. That is eliminated through the kidneys.

Daytime is a time of running the “machinery” and creating acids. Nighttime is a time ofreplacing worn out cells and eliminating the acids you created through the day that youdidn’t get rid of through the day.

Measurement of the salivary pH gives you a good indication of how the cellular pH. Youcan think of it as how much voltage is stored in your cellular batteries. It should never belower than 6.5.

Measurement of the urinary pH gives you an indication of how much acid is beingdumped out by the kidneys. It should also be about 6.5 after you get rid of your firstmorning urine. (The first morning urine represents the acid you got rid of during thenight). However, if your daytime urine pH is less than 6.5, you are dumping more acidbecause your tissue has become too acidic.

To be accurate, your salivary pH must be tested either the first thing when you wake upbefore you drink any water or two hours after a meal. Test it with pH strips. Here is thecolor code that tells you your pH:

Sometimes it is difficult to decide which color is the correct one on the strip. If you wantto have a more accurate way to measure pH, meters are available for about $100.

IF YOUR URINE OR YOUR SALIVARY pH FALLS BELOW 6.5, YOU NEEDMORE CALCIUM. However, you can’t just take any calcium. Calcium citrate isacidic. If you take it, you will make yourself more acidic. Calcium carbonate is alkalinewith a pH of about 10. It will cause your system to become more alkaline. A goodsource of calcium carbonate is from coral. In addition to the calcium, you get traceminerals as well.

Coral calcium is about 1/5 calcium carbonate. For example, 565 mg of coral calciumwould contain about 110 mg of calcium carbonate.

A guide for the amount to take is:

pH Coral calcium Calcium carbonate

<6.0 7700 mg (fourteen capsules/day) 110 mg x 14 = 1540 mg

6.0-6.5 5500 mg (ten capsules/day) 110 mg x 10 = 1100 mg.

7.0-7.5 3300 mg (six capsules/day) 110 mg x 6 = 660 mg.

>7.5 None None

Note that this recommendation has you taking some calcium even if your pH is above6.5. This is advantageous if you are dealing with serious illness because microorganismscan’t grow in an alkaline pH. Cancer cells have trouble growing with alkaline pH aswell.

A salivary pH of 6.5 suggests a cellular pH of 7.2. Thus one has to adjust the cellular pHnumbers by about 0.7.

The normal human cell has a lot of molecular oxygen and a slightly alkaline pH. Thecancer cell has an acid pH and lack of oxygen. Cancer cells cannot survive in an oxygenrich environment. At a pH slightly above 7.4 (salivary pH 6.7) cancer cells becomedormant and at pH 8.5 (salivary pH 7.8) cancer cells will die while healthy cells willlive. Again, the higher the pH reading, the more alkaline and oxygen rich the fluid is.Cancer and all diseases hate oxygen / pH balance.http://home.bluegrass.net/~jclark/coral_calcium.htm

Thus it is sometimes advantageous to push the pH above 6.5 if you are trying toovercome a chronic illness.

Neurochemicals and Plankton

There are two basic theories of how to get people with chronic disease well and keepthem that way. One is that we must find a drug that will substitute for a broken “gear” inthe body or to repair the “gears” mechanically (surgery). The other is the give the bodythe things it needs to manufacture new cells and let it heal itself.

For those wishing to support the latter theory, it has beendifficult to determine what is actually needed to make newcells. People are always saying things like they have a newherb from Africa or a fruit from China that will magically healeverything. Such findings are often useful for some but notpredictable for most. My feeling has always been thatHeavenly Father would not design a body that requires unusualpotions from far-away places to make us healthy.

My practice is one of Integrative Medicine where we see

There are very fewproducts thatprovide all or evenmost of the rawmaterials to makenew cells andsustain the existingones. The problemis that we need ALLof them at the sametime for things to

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work.

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primarily people who have been sick for years and who “have tried it all”. I personallysuffered from viral encephalitis and a bleeding disorder that kept me incapacitated forseven years. What I have come to appreciate is that one must provide the raw materialsfor the body to make new cells. If one does that, even severely and chronically illpatients can heal. So what are those raw materials?:

1. Water: The body is about 75% water. It needs to be clean water that isalkaline (contains voltage).

2. Fat: Every cell membrane in the body is made of two layers of fats calledphospholipids.

3. Proteins: Every cell in the body contains “machinery” made up ofproteins that do the work of the cell.

4. Carbohydrates: Needed primarily to provide vitamins and minerals.A. Vitamins: To use the fats and proteins, cells need vitamins.B. Minerals: To use the fats and proteins, cells need minerals.

Minerals are also used by the body as “On-Off” switches.5 Voltage: Voltage is stored in the cell membrane of every cell to give cells

the energy to work.

There are very few products that provide all or even most of the raw materials to make new cellsand sustain the existing ones. The problem is that we need ALL of themat the same time for things to work. For example, one needs a proteincalled tryptophan to make the brain chemical called serotonin. However,it takes eight vitamins and minerals for this to work. If you are missingone of them, e.g., zinc, you can’t make serotonin. You may get a few ofthe things you need to be healthy from a product you are taking thismonth and a few from the product you take next month but neither worksbecause you didn’t get them all at the same time!

libac(r(t

InevfuswsothIton

B

Bincaco

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ItIfbyo

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You may get a few ofthe things you need tobe healthy from aproduct you are takingthis month and a fewfrom the product youtake next month butneither works becauseyou didn’t get them all

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at the same time! One of those rare products that contains almost everything you need forfe (and the rebuilding of a healthy life) is phytoplankton. It contains the ten amino acids that theody cannot make and must be consumed in our diet (essential amino acids). The essential fattyids are also present (Omega 3 and Omega 6). Vitamins A (beta-carotene), B1 (thiamine), B2iboflavin), B3 (niacin), B5 (pantothenic acid), B6 (pyridoxine), B12 (cobalamin), C, and Docopherol) and major and trace minerals are all present in phytoplankton.

short, it contains almost everything one needs to sustain life. Therefore, it contains almosterything one needs to restore health by providing the raw materials to make new cells thatnction normally. This is particularly true if one stops putting toxic materials such as artificialeeteners and Trans fats (partially hydrogenated fats) into our body. It is exciting to findmething that seems to contain most of the things necessary to get well and stay well. It is likelyat phytoplankton will change the way we think about health.

have also found that one can replace neurochemicals with phytoplankton even when the liver iso sick to allow the person to take products with just the amino acids and vitamins/minerals

ecessary to make them.

lood Pressure

lood pressure is related to water. Any fluid system needs---fluids! Having a normal pressureside your vascular system is key to feeling well. The upper number of your blood pressure islled “systolic”. It is a measure of the highest pressure in your system. It is the result of the heartntracting and pushing blood into the vessels.

he second number is called “diastolic” pressure. It is a measure of the lowest pressure in thestem and is the pressure present when the heart is between beats and is refilling itself with bloodr the next pulse. It is the most important number because a persistently high pressure can

amage the vessels. It should be between 80-90.

is often said that blood pressure cannot be too low unless you have symptoms. That is not true.the blood pressure is too low, you will not have enough pressure to get enough blood to your

rain and you will have symptoms of chronic fatigue. When the diastolic pressure is below 80,u will often have symptoms.

lood pressure is much like tire pressure for your car. “Cold” pressure is the pressure in your tireshen the car has not been moving. It is the minimum operating pressure to make your tires work

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correctly. When the tire starts rolling, the heat created increases the pressure in the tires and iscalled the “hot” pressure. It is the maximum pressure experienced by the tires. If that is too high,it will damage the tire walls. Think of systolic blood pressure as “hot” pressure and diastolic bloodpressure as “cold” pressure. Your tires are designed to operate within these ranges. Too high ortoo low means the tires will not function correctly. So it is with blood pressure.

A major recommendation from the National Institutes of Health was published in May, 2003. TheNational High Blood Pressure Education Program is coordinated by the National Heart, Lung,and Blood Institute (NHLBI) at the National Institutes of Health. Copies of the JNC 7 Report areavailable on the NHLBI Web site at http://www.nhlbi.nih.gov or from the NHLBI HealthInformation Center, P.O. Box 30105, Bethesda, MD 20824-0105; Phone: 301-592-8573 or 240-629-3255 (TTY); Fax: 301-592-8563.

Published Abstract: The purpose of the Seventh Report of the Joint Evaluation, and Treatment ofHigh Blood Pressure (JNC 7) is to provide an evidence-based approach to the prevention andmanagement of hypertension. The key messages of this report are these:

In those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is amore important cardiovascular disease (CVD) risk factor than diastolic BP

Beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg

Those who are normotensive at 55 years of age will have a 90% lifetime risk of developinghypertension

Prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg)require health-promoting lifestyle modifications to prevent the progressive rise in bloodpressure and CVD.

For uncomplicated hypertension, thiazide diuretic should be used in drug treatment formost, either alone or combined with drugs from other classes.

This report delineates specific high-risk conditions that are compelling indications for theuse of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors,angiotensin-receptor blockers, beta-blockers, calcium channel blockers.)

Two or more antihypertensive medications will be required to achieve goal BP (<140/90mm hg, or <130/80 mm hg) for patients with diabetes and chronic kidney disease.

For patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of whichusually will be a thiazide diuretic,should be considered.

Regardless of therapy or care,hypertension will be controlled only ifpatients are motivated to stay on theirtreatment plan..

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“Because of the new data on lifetime risk of hypertension and the impressive increase in the risk ofcardiovascular complications associated with levels of BP previously considered to be normal, theJNC 7 report has introduced a new classification that includes the term “prehypertension” forthose with BPs ranging from 120–139 mmHg systolic and/or 80–89 mmHg diastolic. This newdesignation is intended to identify those individuals in whom early intervention by adoption ofhealthy lifestyles could reduce BP, decrease the rate of progression of BP to hypertensive levelswith age, or prevent hypertension entirely.

Cumulative incidence of cardiovascular events in women (panel A) and men (panel B) withouthypertension, according to blood pressure category at the base-line examination. Vertical barsindicate 95 percent confidence intervals. Optimal BP is defined here as a systolic pressure of <120mmHg and a diastolic pressure of <80 mmHg. Normal BP is a systolic pressure of 120–129mmHg or a diastolic pressure of 80–84 mmHg. High-normal BP is a systolic pressure of 130–139mmHg or a diastolic pressure of 85–89 mmHg. If the systolic and diastolic pressure readings for asubject were in different

categories, the higher of the two categories was used.”

The recommendations from the Committee on Prevention and Treatment of High Blood Pressureare:

Treat to a BP of <140/90 unless you have diabetes or chronic kidney disease. In that case,treat to <130/80.

For those with BP from 120/80 to 140/90, start behavior modifications for dietarychoices, exercise, stop smoking, etc.

For those over 140/90 (or diabetics or kidney disease with >130/80), start with a diazidediuretic as first choice medication.

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Add additional medications as needed to reach goal BP.

Since most physicians have to see so many patients per day, it has been my experience that manyskip step one of behavior modification and often start drug therapy in all patients whose bloodpressure is >120/80. Also, they often choose drugs other than diuretics as the beginningmedication. It has been my experience that many people with diastolic pressures <80 will havemental fog and/or dizziness because there isn’t enough pressure to get adequate blood to the brain.Several of my family members have been treated this way. When they report the symptoms totheir physicians, they are told to keep taking the medications. This is the common practice ofphysicians treating lab results and not the patient. If a patient can’t work because you havelowered their blood pressure too low, you haven’t really served the patient.

I find that most patients will have a normal blood pressure in 4-6 months after starting the programof restoring voltage and nutrition.

One of the principle causes of too low blood pressure is dehydration. If you don’t have enoughfluid in the system, you can’t create enough pressure. Another cause is mineral deficiency,particularly sodium and magnesium. Low blood pressure can be a symptom of a deficiency ofVitamin B5 = pantothenic acid. It can also be due to adrenal insufficiency. If your bloodpressure drops instead of increasing as you stand up, that is a sign that your adrenals are notworking correctly. Unstable blood pressure is often due to a lack of magnesium and/or VitaminB1 = thiamine.

Sewage

As we clean up our old house now and in the future we will wash out the debris and need afunctional sewage system to get rid of the toxic and waste materials. One of the most importantsystems in the body is the large intestine. We will start our cleanup by flushing out the largeintestine to remove the debris that has accumulated there. We will give you the instructions in theoffice.

For some reason, people seem to fear this simple process. Very few people find it uncomfortableor distressing. It just means you need to be at home for a few hours.

Probiotics

The word “probiotic” refers to bacteria that normally live in our intestines and help with digestion.They are an important part of the digestive process and need to be replaced if they are diminishedin numbers by the use of antibiotics.

In addition to digestion, they are believed to assist with:

Competition against harmful micro-organisms including Candida, preventing colonizationof pathogens through the production of inhibitory substances including acids and hydrogen

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peroxide and natural antibiotics; Enhancement of digestion of lactose (milk sugar); Immune enhancement, including enhanced macrophage activity; Reduction in the levels of and deactivation of potential cancer causing chemicals,

particularly in the colon and direct anti-tumor activity of certain strains; Reduction in liver toxicity; Enhancement of peristalsis, digestion, regularity and re-absorption of nutrients, In infants,

promotion of healthy digestive tract colonization; Enhancement and balance of estrogen levels, prevention of osteoporosis through increased

calcium uptake; Protection against food poisoning, travelers' diarrhea, allergies, skin problems; Enhancement of vitamin status (B, K), digestion of proteins, fats, carbohydrates.

Electricity

Now that you have the water and sewage working in your old house, you need electricity. So it iswith our body. When two hydrogen atoms join with an oxygen atom to form water, the first thingthey do is exchange electrons. When electrons move from one place to another, that is called anelectric current. All of the chemical reactions in the body depend upon voltage (movement ofelectrons). Every cell has its own battery pack---the cell membrane---that stores voltage andprovides it to the cell as needed to keep it working.

Take a voltmeter that reads in millivolts. Place one electrode on your right temple and one on yourleft temple. It will read voltage.

In your house, there is a circuit breaker box that goes to the various circuits throughout the house.Different appliances and switches are on each circuit. When one of those quits working, you canmeasure the circuit to see what is happening with the voltage in that circuit.

Our bodies work much the same way. We have twelve paired circuits on which our organs areattached. These circuits provide voltage to our organs and move the voltage from place to place.These circuits are known as acupuncture meridians. By measuring the voltage or impedance(resistance to flow of electrons) in each circuit, we can determine if each organ has enough voltageto work correctly. We use a device called Meridian Energy Analysis Device (MEAD) to takethese measurements. If we find a circuit that isn’t working, we use various electronic devices toplace voltage into that circuit and recharge the cells.Note: The FDA has not yet approved these devices for this purpose nor considered these

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statements.In this chart, we look at the total body voltage and then at the voltage in each circuit. Normal iswhen all of the bars are between the top and bottom red lines.

One of the devices we use to restore voltage to the body is the TennantBiomodulator™. We may also use a variety of low-level lasers, infra-red, andother devices that can carry voltage into the body.

COOKING OILS

This is one of the most important parts of getting well. If you don’t stop puttingTrans Fats (“Plastic Fats”) into your body, you will never get well! Please payparticular attention to this section.

The summary of this section is as follows: Food suppliers recognized that the major loss of profitswas from spoilage. In order to stop spoilage and increase their profits, they did two things.

1. They added chemicals to the food to keep it from spoiling. These chemicals not onlypreserve food, they preserve the person who eats them.

2. They began to cook the fats in the food. Cooking fats at 350-380 degrees for 5-6 hourschanges the fats into something that is one carbon atom away from plastic. You can tell ifthis is what you are eating if the label says, “Partially Hydrogenated-----“. These partially

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hydrogenated fats are called “Trans Fats”.

When a cell in your body is worn out, it makes a new one. It looks around to see what buildingmaterials you have provided to make a new cell. If all you have given your body is plastic fat, itmakes a new cell out of plastic. Remember that the cell membrane that surrounds every cell ismade of fat. If you make that out of plastic, the cell doesn’t work very well. It is like wrapping allyour cells in cellophane.

The cell sends a message to your brain that it’s hungry. Your body sends the cell some glucoseand insulin. However, the glucose can’t get through the “cellophane” and the cell keepscomplaining that it’s hungry. The body keeps sending more insulin and glucose. Much of it getsput into fat cells. Your cells keep complaining that they are hungry. Your brain keeps you eatingto try to solve the hunger, but not much gets through the cellophane to the cells. Soon you areobese and your pancreas is worn out from making so much insulin. With all that glucose in yourblood stream, you are diagnosed with Type II diabetes. Drugs lower the levels of sugar in yourblood, but your cells are still coping with being made of plastic. Soon they began to wear out andyou get symptoms of worn out cells = heart attacks, strokes, liver failure, kidney failure, blindness,chronic fatigue, etc.

Most restaurants use plastic fats for frying food. If you eat out, you must stop eating fried food orchoose a restaurant that doesn’t use plastic fats. Most cheese is made from plastic fats. Thuscheeseburgers and French fries are major sources of plastic fats. Fast food isn’t dangerous becauseit’s fast---it is dangerous because it’s plastic.

The point you must understand is that if you insist on feeding your body plastic fats, you will neverget well! However, if you give your body good fat and the other things it needs, your body willbuild a new you that is vibrant and healthy!

Cells need the following to work:

1. Water with voltage (alkaline water)2. Fats to make cell membranes3. Proteins to make the cytoplasm (the “machinery”) inside cells.4. Vitamins to allow the body to make the fats and proteins work.5. Minerals to make the fats and proteins work and as On-Off switches and keep your pH in

the operating range.6. Oxygen7. Sunshine8. Voltage is the same as pH. The body must have voltage to function (the same as saying a

normal body has an alkaline pH). The body normally runs at a pH of 7.2 inside cells whichis the same as -22 mV.

There is a lot of confusion about the type of fat to eat. Many people are becoming toxic from toomuch Omega-3 fats (from fish oil, etc.). Your cell membranes are like your home. They need tobe strong enough to be substantial but have doorways and windows to let things in and out. If youbuild your house out of concrete blocks with no windows or doors, it will be strong but won’t work

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because you can’t get in or out. If you build it with mostly doors and windows, the next storm willtake it down.

In cells, saturated fats are strong and unsaturated fats are porous. You need saturated fat (animalfat for example) to make strong cells and unsaturated fats (fish oils for example) for doors andwindows. The ratio needs to be 4/1 meaning that you need to eat four times as much saturated fatas unsaturated fats = four times as many bricks as doors and windows.

Saturated fats have gotten a bad reputation because plastic fats are saturated. There is a differencebetween plastic fats and normal saturated fats.

The following discussion is for those who don’t understand this problem and insist that eating fatis harmful. Remember that your body should contain about 20% fat since all of your cellmembranes and most of your nervous system is fat. That means you need to give your body 24pounds of good fat to replace the fat in your system if you weigh 120 pounds. If you weigh 200pounds, you will need to give your body 40 pounds of good fat to get healthy!

Remember the following:

There is no proven connection between cholesterol and heart disease. In fact, those dyingfrom heart attacks generally have the lowest cholesterol levels and often have low “badcholesterol (LDL) levels.

Eating good fat doesn’t affect your cholesterol or make you obese. The liver makes asmuch or as little cholesterol as it wants.

Eating plastic fat (Trans fats) makes you obese and produces a liver and other cells thatcannot function.

The liver uses cholesterol to clean itself. A high cholesterol means your liver filtrationsystem is dirty and filled with toxic materials. (Why would you want to interfere with theliver’s ability to clean itself by taking cholesterol-lowering drugs?)

A very low cholesterol means the liver is too sick to clean itself and you will suffer majorillness or death soon.

To get well, you will need to eat at least 20% of your body weight in good fat. If youweigh 200 pounds, you will need to eat at least 40 pounds of good fat to get well! Seventy-five percent of that needs to be saturated fat like animal fat and twenty-five percent needsto be polyunsaturated fat like fish oil.

Eating lots of butter and eggs (a stick of butter and 6-12 eggs per day) will help you getwell much faster.

If eating fat makes you nauseated, it means your liver is too sick to use it. We will have totreat your liver so it can restore itself before you can get well.

The following is reproduced with permission from Sally Fallon with Pat Connolly and Mary G. Enig, Ph.D.Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats. ProMotionPublishing. 800-231-1776, and Sally Fallon. "Why butter is good for you (health aspects of dietary fat)." (CoverStory), Consumers' Research magazine. 03-01- Vol.79 (1996) pp 10(6). COPYRIGHT 1996 Consumers' Research Inc.

Why Butter is Good for You (health aspects of dietary fat)

Sally Fallon, et al

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Politically correct nutrition is based on the assumption that we should reduce our intake of fats,particularly saturated fats from animal sources. Fats from animal sources contain cholesterol,presented as the villain of the civilized diet.

Yet the textbooks tell us that fats from animal and vegetable sources provide a concentratedsource of energy in the diet; they also provide the building blocks for cell membranes, forhormones, and for prostaglandins (substances that mediate important chemical processes in thebody). In addition, they act as carriers for the important fat-soluble vitamins A, D, E, and K.Dietary fats are needed for conversion of carotene to vitamin A and for a host of otherprocesses.

The theory—and it is only a theory—that there is a direct relationship between the amount ofsaturated fat in the diet and the incidence of coronary heart disease, as well as certain types ofcancer, was proposed by a researcher named Ancel Keys in the late 1950s. Numerous subsequentstudies have questioned his data and conclusions. Nevertheless, Keys' articles received far morepublicity than those contradicting him. The vegetable oil industry and food processing industries,the main beneficiaries of the saturated fat/heart disease connection, began promoting and fundingfurther research designed to support Keys' theories.

The most well-known advocate of the low fat diet was Dr. Nathan Pritikin. Actually, Pritikinadvocated eliminating sugar, white flour, and all processed foods from the diet and recommendedthe use of fresh raw foods, whole grains, and a strenuous exercise program; but it was the low fataspects of his regimen that received the most attention in the media. Adherents found that they lostweight and that their blood cholesterol levels and blood pressures declined.

The success of the Pritikin diet was probably due to a number of factors having nothing to do witha reduction in dietary fat—weight loss alone, for example, will precipitate a reduction in bloodcholesterol levels—but Pritikin soon found that the fat-free diet presented many problems, not theleast of which was the fact that people just could not stay on it. Those who possessed enough willpower to stay fat-free for any length of time developed a variety of health problems including lowenergy, difficulty in concentration, depression, weight gain, and signs of mineral deficiencies.

After problems with the no-fat regimen became apparent, Pritikin introduced a small amount of fatfrom vegetable sources into his diet—something like 10 percent of the total caloric intake. Todaythe "diet dictocrats"—essentially the public health establishment, including primarily the largehealth charities and the federal government—advise us to limit fats to 25-30 percent of the caloricintake (12-15 percent of the diet by weight). A careful reckoning of daily fat intake, and avoidanceof animal fats, is presented as the key to perfect health.

The experts assure us the theory that animal fat consumption causes coronary heart disease isbacked by abundant evidence. Most people would be surprised to learn that there is, in fact, very

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little evidence to support the contention that a diet low in cholesterol and saturated fat actuallyreduces death from heart disease or in any way increases one's life span. Consider the following:

Before 1920, coronary heart disease was rare in America, so rare that when a young internistnamed Paul Dudley White introduced the German electrocardiograph to his colleagues atHarvard University, they advised him to concentrate on a more profitable branch of medicine.The new machine revealed the presence of arterial blockages, thus permitting early diagnosis ofcoronary heart disease; but in those days clogged arteries were a medical rarity, and White had tosearch for patients who could benefit from his new technology. During the next forty years,however, the incidence of coronary heart disease rose dramatically, so much so that by the mid-'50s, heart disease was the leading cause of death among Americans. Today, heart disease causes40 percent of all U.S. deaths.

If, as we have been told, heart disease results from consumption of saturated fats, one wouldexpect to find a corresponding increase in animal fat in the American diet. Actually the reverse istrue. During the sixty-year period from 1910 to 1970, the proportion of traditional animal fat in theAmerican diet declined from 83 to 62 percent, and butter consumption plummeted from eighteenpounds per person per year to four pounds. During the past eighty years, dietary cholesterol intakehas increased only one percent. During the same period the percentage of dietary vegetable fat inthe form of margarine, shortening, and refined oils increased about 400 percent, and theconsumption of sugar and processed foods increased about 60 percent.

The Framingham Heart Study is often cited as proof of the cholesterol/animal fat theory. Thisstudy began in 1948 and involved about 6,000 people from the town of Framingham,Massachusetts. Two groups were compared at five-year intervals— those who consumed littlecholesterol and saturated fat and those who consumed large amounts. Today, after 40 years, thecurrent director of this study admits: "In Framingham, Mass., the more saturated fat one ate, themore cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. . . .[W]e found that the people who ate the most cholesterol, ate the most saturated fat, and ate themost calories weighed the least and were the most physically active." The study did show thatthose who weighed more and had higher blood cholesterol levels were more at risk for futurecoronary heart disease; but weight gain and cholesterol levels had an inverse correlation with fatand cholesterol intake in the diet.

The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which cost150 million dollars, is the study most often cited by the experts to justify the low fat diet. Actually,dietary cholesterol and saturated fat were not tested in this study as all subjects were already on alow-cholesterol, low-saturated fat diet. Instead, the study tested the effects of a cholesterollowering drug. Statistical analysis of the results indicated a 24 percent reduction in the rate ofcoronary heart disease in the group taking drugs compared with the placebo group; however, non-heart disease deaths in the drug group increased—deaths from cancer, stroke, violence, andsuicide. Even the claim that a diet low in saturated fat and cholesterol reduced heart disease is

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suspect. Independent researchers who tabulated the results of this study found no significantstatistical difference in the coronary heart disease death rate between the two groups. However,both the popular press and medical journals touted the LRC-CPPT survey as the long-sought proofthat animal fats are the cause of heart disease, America's number one killer.

Mother's milk contains a higher proportion of cholesterol than almost any other food. It alsocontains over 50 percent of its calories as fat, much of it saturated fat. Both cholesterol andsaturated fat are essential for growth in babies and children, especially in development of the brain.(Yet, the American Heart Association is now recommending a low-cholesterol, low fat diet forchildren.) Most commercial formulas are low in saturated fats and some are almost completelydevoid of cholesterol. A recent study linked a low fat diet with failure to thrive in children.

As a final example, consider the French. The French diet is loaded with saturated fats in the formof butter, eggs, cheese, cream, liver, meats, and rich pates. Yet the French have a lower rate ofcoronary heart disease than many other western countries. In the United States, 315 of every100,000 middle-aged men die of heart attacks each year; in France the rate is 145 per 100,000. Inthe Gascony region, where goose and duck liver form a staple of the diet, this rate is a remarkablylow: 80 per 100,000. This phenomenon has recently gained international attention and has beendubbed the paradox francais.

Clearly, something is wrong with the theories we read in the popular press (and used to bolstersales of low fat concoctions and cholesterol-free foods). The notion that saturated fats per secause heart disease as well as cancer is not only not facile, it is just plain wrong. But it is truethat some fats are bad for us. In order to understand which ones, we must know something aboutthe chemistry of fats.

Fat Chemistry. Most fat in our bodies and in the food we eat is in the form of triglycerides, thatis, three fatty acid chains attached to a glycerol molecule. Elevated triglycerides in the blood havebeen positively linked to proneness to heart disease but these triglycerides do not come directlyfrom dietary fats; they are made in the liver from any excess sugars that have not been completelyburned. The source of these excess sugars is any food containing carbohydrates, but particularlyrefined sugar and processed carbohydrates.

In simple terms, fatty acids are chains of carbon atoms with hydrogen linkages. A fatty acid iscalled saturated when all available carbon bonds are occupied by a hydrogen atom.Monounsaturated fatty acids have one pair of carbon atoms double bonded to each other andtherefore lack two hydrogen atoms. The monounsaturated fatty acid most commonly found in ourfood is oleic acid, the main component of olive oil. Polyunsaturated fatty acids have two or morepairs of carbon double bonds and therefore lack four or more hydrogen atoms. The twopolyunsaturated fatty acids found most frequently in our foods are double unsaturated linoleic acidwith two double carbon bonds (also called omega-6) and triple unsaturated linolenic acid withthree double bonds (also called omega-3).

All fats and oils, whether of vegetable or animal origin, are some combination of saturated fatty

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acids, monounsaturated fatty acids (oleic acid), and the polyunsaturates linoleic and linolenic acid.In general, animal fats such as butter, lard, and tallow contain about 50 percent saturated fat andare solid at room temperature. Vegetable fats from northern climates contain a preponderance ofpolyunsaturated fatty acids and are liquid at room temperature. But vegetable oils from the tropicsare highly saturated. Coconut oil, for example, is 92 percent saturated. These fats are liquid in thetropics, but hard as butter in northern climes. Highly saturated tropical oils such as coconut andpalm oil are not harmful, as the popular press would lead us to believe. These fats and oils havenourished healthy populations, free of heart disease, for millennia. Vegetable oils are moresaturated in hot climates because the increased saturation helps maintain stiffness in plant leaves.Olive oil with its preponderance of oleic acid is the product of a temperate climate. It is liquid atwarm temperatures but hardens when refrigerated.

Researchers classify fatty acids not only according to their degree of saturation but also by theirlength.

1. Short-chain fatty acids have four to six carbon atoms (butter and coconut)

2. Medium-length fatty acids have eight to twelve (butter and coconut)

3. Long-chain fatty acids have 14 to 18 carbon atoms (beef fat)

4. Very-long-chain fatty acids have 20 to 24 carbon atoms (fish oils, organs)

Saturated fats vary in length from short to long. Butter and coconut oil contain a large portion ofshort- and medium-chain fatty acids, while stearic acid, the main component of beef fat, is a long-chain fatty acid with 18 carbons. Oleic acid, linoleic acid, and linolenic acid also have 18 carbons.Very-long-chain fatty acids, such as those found in fish oils and organ tissues, tend to be highlyunsaturated, with four, five, and even six double bonds.

Short- and medium-chain fatty acids have several interesting properties.

1. Longer chain fatty acids are absorbed by the lymph system and must be acted on by bilesalts.

2. Short-chain fatty acids (butter and coconut) are absorbed directly through the portal vein tothe liver. As they do not need to be acted upon by the bile salts, these short-chain fattyacids supply quick energy.

In general, the body uses the longer chain fatty acids, including the longer chain saturated fattyacids, to construct membranes and vital hormone-like substances, to create electric potentials, andto move electric currents.

It is the longer chain fatty acids that are stored in the adipose tissue, particularly oleic and linoleicacid. Thus butter and coconut oil, which contain a significant portion of short- and medium-chainfatty acids, do not contribute to weight gain as much as olive and vegetable oil. The short- and

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medium-chain fatty acids also have antimicrobial and antifungal properties in the intestinal tract;they have anti-tumor properties and help strengthen the immune system, while an excess ofpolyunsaturated fatty acids stimulate tumor growth.

Summary: (JLT)1. Short-chain fatty acids have four to six carbon atoms (butter and coconut)

a. Do not contribute to weight gain as much as olive and vegetable oil

b. Have antimicrobial and antifungal properties in the intestinal tract

c. Have anti-tumor properties and help strengthen the immune system,

2. Medium-length fatty acids have eight to twelve (butter and coconut)

a. Do not contribute to weight gain as much as olive and vegetable oil

b. Have antimicrobial and antifungal properties in the intestinal tract

c. Have anti-tumor properties and help strengthen the immune system,

3. Long-chain fatty acids have 14 to 18 carbon atoms (beef fat)

a. Absorbed by the lymph system and must be acted on by bile salts

b. Used to construct membranes and vital hormone-like substances, to create electricpotentials, and to move electric currents

c. Stored in the adipose tissue, particularly oleic and linoleic acid

4. Very-long-chain fatty acids have 20 to 24 carbon atoms (fish oils, organs)a. Absorbed by the lymph system and must be acted on by bile saltsb. Used to construct membranes and vital hormone-like substances, to create electric

potentials, and to move electric currentsc. Stored in the adipose tissue, particularly oleic and linoleic acid; an excess of

polyunsaturated fatty acids stimulate tumor growth.

Too Many Polyunsaturates. Unsaturated omega-3 and omega-6 fatty acids are called essentialfatty acids, or EFAs, because the body cannot manufacture them, at least not in the form in whichthey occur. Researchers vary in their estimates of the amount of polyunsaturated fatty acids neededin the diet, giving figures as low as 0.5 percent and as high as 15 percent, but recent scientificevidence supports the lower range and has led knowledgeable researchers to recommend limitingour intake of polyunsaturates to 4 percent of the caloric total, in approximate proportions of 1.5percent omega-3 fatty acid and 2.5 percent omega-6. (More recently, Yehuda et al have proventhat the proper ratio is 4:1 of omega-6 to omega-3 of the lower order linoleic and linolenic acids.JLT). What we find in the American diet is a high intake of polyunsaturates—something like 10 to30 percent of the total caloric intake. Worse, most of these polyunsaturates are in the form of

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omega-6 linoleic acid, with very little of vital omega-3 linolenic acid. Recent research has revealedthat too much omega-6 in the diet can interfere with the enzymes that produce longer chain, highlysaturated fatty acids, which are the precursors of important prostaglandins. These are localizedtissue hormones that direct many processes in the cells. When the production of prostaglandins iscompromised by excess omega-6 in the diet, coupled with too little omega-3, serious problemsresult including inflammation, hypertension, irritation of the digestive tract, depressed immunefunction, sterility, cell proliferation, cancer, and weight gain. Other studies indicate that excessiveunsaturated fatty acids in the diet of infants can interfere with brain development and with learningand behavior.

In contrast, dietary saturated fats (e.g., coconut, palm, beef, butter, eggs) contribute to optimalutilization of essential fatty acids. Thus, although not called essential, saturated fats areabsolutely necessary in the diet, not only for the role they play in enhancing EFA utilization, insupplying quick energy, and in their immune system enhancing characteristics, but also becauseof the important vitamins they carry.

A Serious Problem. A serious problem with the polyunsaturate family, and particularly omega-3(fish, flax, hemp), is its instability. With their double carbon bonds, these fatty acids tend topolymerize, that is, bond with each other and bond with other molecules. They are also more easilyrendered rancid when subjected to heat, oxygen, and moisture as in cooking and processing.Rancid oils are characterized by free radicals in the double bond, that is, single atoms or clusterswith an unpaired electron in an outer orbit. These compounds are extremely reactive chemically.They have been characterized as "marauders" in the body, for they attack cell walls and red bloodcells and cause damage in DNA/RNA strands, thus triggering mutations in tissue, blood vessels,and skin. Free radical damage to the skin causes wrinkles and premature aging; free radicaldamage to the tissues and organs sets the stage for tumors. Is it any wonder that tests and studieshave repeatedly shown a high correlation between cancer and the consumption of polyunsaturates?New evidence links exposure to free radicals with premature aging, with autoimmune diseasessuch as arthritis, and to Parkinson's disease, Lou Gehrig's disease, Alzheimer's, and cataracts.

(Note that recent work shows that many sources of omega-3 like cod liver oil are severelycontaminated with chemical toxins in the ocean. It is critical to only buy and use molecularly-distilled omega-3 oils that have removed these carcinogens. Most health food stores do not sellthese as it takes 100 pounds of cod livers to produce 10 pounds of toxin-free oil = more expensive.Use only molecularly-distilled omega-3 supplements. JLT)

It is important to understand that of all substances ingested by the body, it is polyunsaturated oilsthat are most easily rendered dangerous by food processing, especially unstable omega-3 linolenicacid. Consider the following processes inflicted upon naturally occurring fats before they appearon our tables:

Extraction. Oils naturally occurring in fruits, nuts, and seeds must first be extracted. In the olddays this extraction was achieved by a slow-moving stone press. But oils processed in largefactories are obtained by crushing the oil-bearing seeds and heating them to 230 degreesFahrenheit. The oil is then squeezed out at pressures from 10 to 20 tons per inch, therebygenerating more heat. During this process the oils are exposed to damaging light and oxygen.

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High-temperature processing causes the weak carbon bonds of the unsaturated fatty acids,especially triple unsaturated linolenic acid, to break apart, thereby creating dangerous free radicals.In addition, antioxidants including fat soluble vitamin E, which protect the body from the ravagesof free radicals, are neutralized or destroyed by high temperatures and pressures. (There is a safemodern technique for extraction that drills into the seeds and extracts the oil and its precious cargoof antioxidants under low temperatures, with minimal exposure to light and oxygen. Theseunrefined oils will remain fresh for a long time if stored in the refrigerator in dark bottles. Extravirgin olive oil is produced by crushing olives between stone or steel rollers. This process is agentle one that preserves the integrity of the fatty acids and the numerous natural preservatives inolive oil. If the olive oil is packaged in an opaque container, it will retain its freshness and preciousstore of antioxidants many months.)

Hydrogenation. This is the process that turns polyunsaturates (margarine and shortening)normally liquid at room temperature, into a fat that is solid at room temperature. To produce them,manufacturers begin with the cheapest oil (soy, corn, or cottonseed) already rancid from theextraction process. These oils are then mixed with tiny metal particles—usually nickel oxide.Nickel oxide is very toxic when absorbed and is impossible to eliminate totally from margarine.(Nickel is a severe neurotoxin. JLT) The oil with its nickel catalyst is then subjected to hydrogengas in a high-pressure, high-temperature reactor. Next, soap-like emulsifiers and starch aresqueezed into the mixture to give it a better consistency. The oil is yet again subjected to hightemperature when it is steam cleaned. This removes its horrible odor. Margarine's natural color, anunappetizing grey, is removed by bleach. Coal tar dyes and strong flavors must then be added tomake it resemble butter. Finally the mixture is compressed and packaged in blocks or tubs, readyto be spread on your toast. (and make “plastic cell membranes” JLT)

Forget Margarine. Margarine and other partially hydrogenated oils are even worse for you thanthe highly refined vegetable oils from which they are made because of chemical changes thatoccur during the hydrogenation process. Under high temperatures, the nickel catalyst causes thehydrogen atoms to change position on the fatty acid chain. Before hydrogenation, two hydrogenatoms occur together on the chain, causing the chain to bend slightly and creating an electroncloud at the site of the double bond. This is called the "cis" formation, the configuration mostcommonly found in nature. With hydrogenation, one hydrogen atom is moved to the other side sothat the molecule straightens. This is called the "trans" formation, rarely found in nature.

These man-made trans-fats are toxins to the body, but unfortunately your digestive system doesnot recognize them as such. Instead of being eliminated, the trans-fats are incorporated into thebody's cell membranes as if they were cis-fats; your cells actually become hydrogenated. Once inplace, trans-fatty acids with their misplaced hydrogen atom wreak havoc in cell metabolism.These altered fats actually block the utilization of essential fatty acids, causing many deleteriouseffects ranging from sexual dysfunction, increased blood cholesterol, and paralysis of the immunesystem.

In the 1940s, researchers found a strong correlation between cancer and the consumption offat, but the fats used were hydrogenated fats, not naturally saturated fats. (Until recently,the confusion between hydrogenated fats and naturally saturated fats has persisted not onlyin the popular press, but in scientific data bases, resulting in much error in study results.)

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Consumption of hydrogenated fats is associated with a host of other serious diseases, not onlycancer but also atherosclerosis, diabetes, obesity, immune system dysfunction, low birthweight babies and birth defects, sterility, difficulty in lactation, and problems with bones andtendons. Yet, hydrogenated fats continue to be promoted as health foods. Margarine'spopularity represents a triumph of advertising over common sense. Your best defense is toavoid it like the plague.

Go Butter.

The media's constant attack on saturated fats is extremely suspect. Claims that butter causeschronic high cholesterol values have not been substantiated by research, although somestudies show that butter consumption causes a small temporary rise. (Other studies haveshown that stearic acid, the main component of beef fat, actually lowers cholesterol.)Margarine, on the other hand, provokes chronic high levels of protective cholesterol and hasbeen linked to both heart disease and cancer. Butter has received so much adversepropaganda that we have lost sight of the fact that it has long been a valuable component ofmany traditional diets containing the following vital nutrients:

Fat-Soluble Vitamins

These include vitamins A (retinol), D, and E, as well as all their naturally-occurring constituentsneeded to obtain maximum effect. Butter is America's best source of these essential vitamins. Infact, vitamin A from butter is more easily absorbed and utilized than from other sources. (Thesefat-soluble vitamins are relatively stable and survive the pasteurization process.) These vitaminsact as catalysts to mineral absorption. Without them, we are not able to utilize properly theminerals we ingest, no matter how abundant they may be in our diets.

The only good source of fat-soluble vitamins in the American diet, one sure to be eaten, isbutterfat. Butter added to vegetables and spread on bread, and cream added to soups and saucesensures proper assimilation of the minerals and water-soluble vitamins in vegetables, grains, andmeat.

Arachidonic Acid

This is a polyunsaturate containing four double carbon bonds and is found in small amounts inanimal fats, but not in vegetable fats. Arachidonic acid is a precursor to important prostaglandinsand other vital substances. (Arachidonic acid makes up 17% of cell membranes and there is novegetable source for it = total vegans cannot have normal cells. JLT)

Short- and Medium-Chain Fatty Acids

Butter contains about 15 percent short-and medium-chain fatty acids. This type of saturated fat, asmentioned, is absorbed directly from the small intestine to the liver, where it is converted toenergy. These fatty acids also have antimicrobial, anti-tumor, and immune system supportiveproperties, especially 12-carbon lauric acid, a medium-chain fatty acid not found in other animal

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fats. Highly protective lauric (coconut and palm oil) should be called a conditionally essential fattyacid because it is one saturated fat that the body does not make itself. We must obtain it from oneof two dietary sources: butter or tropical oils. Propionic acid and butyric acid, very-short-chainfatty acids, are all but unique to butter. These have antifungal properties as well as anti-tumoreffects.

Omega-6 and Omega-3 Polyunsaturates

These occur in butter in small but equal amounts. This balance between linoleic and linolenicacid prevents the kind of problems associated with over-consumption associated with omega-6(or omega-3 JLT) fatty acids.

Conjugated Linoleic Acid

Butterfat also contains a form of rearranged linoleic acid called CLA that has strong anticancerproperties.

Lecithin

Lecithin is a natural component of butter. It is known to assist in the proper assimilationand metabolization of cholesterol and other fat constituents.

Cholesterol

Mother's milk is high in cholesterol because it is essential for growth and development.Cholesterol is also needed to produce a variety of steroids that protect against cancer, heartdisease, and mental illness.

Glycosphingolipids

This special category of fat protects against gastrointestinal infections, especially in the very youngand the elderly. For this reason, children who drink skim milk have diarrhea at rates three to fivetimes greater than children who drink whole milk.

Trace Minerals

Many trace minerals are incorporated into the fat globule membrane of butterfat, includingmanganese, zinc, chromium, and iodine. In mountainous areas far from the sea, iodine in butterprotects against goiter and other thyroid problems. Butter is extremely rich in selenium, a vitalantioxidant, containing more per gram than herring or wheat germ.

In summary, our choice of fats and oils is one of extreme importance. Most people, especiallyinfants and growing children, benefit from more fat in the diet rather than less. But the fats we eat

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must be chosen with care. Avoid all processed foods containing partially hydrogenated fats andpolyunsaturated oils. Instead use extra virgin olive oil and unrefined flaxseed oil in salad dressings.Acquaint yourself with the merits of coconut oil for baking. And finally, use good old-fashionedbutter, not margarine, with the happy assurance that it is a wholesome—indeed, an essential—food for you and your whole family.

COPYRIGHT 1996 Consumers' Research Inc. "Why Butter Is Good For You (HealthAspects of Dietary Fat)." (Reproduced here with permission of Ms. Fallon; JLT)

Common Name Foods Nomenclature Type Effect on membraneCaprylic 8:00 Saturated (SFA) RigidityCapric Coconut 10:00 Saturated (SFA) RigidityLauric Coconut, palm 10:00 Saturated (SFA) RigidityMyristic Coconut, palm 12:00 Saturated (SFA) RigidityPalmitic Palm, beef, mutton, butter, cocoa, lard, eggs 16:00 Saturated (SFA) RigidityStearic Cocoa, beef, mutton, eggs, palm, lard 18:00 Saturated (SFA) RigidityOleic (Omega-9) Safflower (high oleic), olive, canola, sesame, rice, butter, corn 18:1, ώ-9 PUFA FluidLinoleic (LA) (Omega-6) Safflower, Sunflower, soy, oat, peanut, lard, corn 18:2, ώ-6 PUFA FluidGamma-linolenic (GLA) (Omega-6) Borage, primrose, black currant, hemp 18:3, ώ-6 PUFA FluidAlpha-linolenic (ALA) (Omega-3) Flax, canola, soy, hemp 18:3, ώ-3 PUFA FluidArachiodonic (AA) (Omega-6) Eggs, butter, beef, mutton, shellfish 20:4, ώ-6 HUFA FluidEicosapentaenoic (EPA) (Omega-3) Fish oil, cold water fish 20:5, ώ-3 HUFA FluidDocosahexaenoic (DHA) (Omega-3) Fish oil, cold water fish 22:6, ώ-3 HUFA Fluid

PUFA = 2-3 double bondsHUFA = >3 double bonds

Polyunsaturated fats (PUFA) are extremely vulnerable to damage from heat, so they are notsuitable for high-temperature cooking. These oils are best used in salad dressings, sauces, and dips.To add flavor to grains and stir-fry dishes, sprinkle the cooked food with flaxseed oil just beforeserving.

For high temperature cooking, use extra virgin olive oil or organic coconut butter.

In July 2002, the National Academy of Sciences’ Institute of Medicine, which advises thegovernment on health policy, made official what many researchers have argued for years: Trans fatworsens blood-cholesterol levels and almost surely increases the risk of heart disease. The instituteconcluded that people should consume as little Trans fat as possible.

That report has helped push the government and the food industry to start taking aggressive stepsto address this long-neglected threat to public health. The Food and Drug Administration (FDA)could be close to finalizing a rule that would require trans-fat labeling on packaged foods. Canadainstituted such a requirement early this year as part of its mandatory nutrition-labeling system.Labeling not only will help consumers cut back on trans, it will also be "a profound disincentivefor manufacturers" to use partially hydrogenated oils, says Marion Nestle, Ph.D., professor andchair of New York University’s department of nutrition and food studies, and author of "FoodPolitics: How the Food Industry Influences Nutrition and Health."

To figure the amount of Trans-Fatty Acid in packaged food by using the new U.S. labels

Find the amount of "Total Fat" on the label.

Find the amounts of "Saturated Fat", "Polyunsaturated Fat" and "Monosaturated Fat".(These are found on the label, listed directly under "Total Fat" and slightly indented. If one

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or the other is not listed, that particular food does not contain it.)

Add theses three together. If there are only two listed, add them together or use oneamount if only one is listed.

Subtract the total amount of #3 from the amount of #1.

The answer is the amount of Trans-fatty Acid in that product.

Frito-Lay has said that it would eliminate Trans fat from Cheetos, Doritos, and Tostitos chips.Even the fast-food industry, which generally does not have to label its foods, is starting to cutback: McDonald’s has said that in late spring of this year, its French fries would have 48 percentless trans fat--a significant improvement, though the fries will apparently still have a fair amountof trans and saturated fat.

Jason's Deli has eliminated partially hydrogenated oils from every food item at all of its 137restaurants nationwide and all 1.6 million box lunches provided to schools annually.http://www.bantransfats.com/

Trans fats are one carbon atom away from being plastic. This “near-plastic” fat ends up in yourcell membranes. Thus when you eat Trans fats, you become mostly plastic! Is it any wonder whyyour cells don’t work well and you don’t feel good when your cells are made of “near-plastic”?

http://www.consumerreports.org/main/detailv2.jsp?CONTENT%3C%3Ecnt_id=300681&FOLDER%3C%3Efolder_id=162689

http://www.bantransfats.com/images/cigs.gif

Here is a summary of a few facts regarding Canola Oil: It is genetically engineered rapeseed. Canada paid the FDA the sum of $50 million to have rape seed registered and recognized

as "safe". (Source: Young Again and others)

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Rapeseed is lubricating oil used by small industry. It has never been meant for humanconsumption.

It is derived from the mustard family and is considered a toxic and poisonous weed, whichwhen processed, becomes rancid very quickly.

It has been shown to cause lung cancer It is very inexpensive to grow and harvest. Insects won't eat it. Some typical and possible side effects include loss of vision, disruption of the central

nervous system, respiratory illness, anemia, constipation, increased incidence of heartdisease and cancer, low birth weights in infants and irritability.

Here is a review article about Canola Oil (rapeseed oil) and its toxic effects from a SwedishMedical Journal:

Physiopathological effects of rapeseed oil: a review.

Borg K

Acta Med Scand Suppl (1975) 585:5-13 ISSN: 0365-463X

Rapeseed oil has a growth retarding effect in animals. Some investigators claim that the highcontent of erucic acid in rapeseed oil alone causes this effect, while others consider the low ratiosaturated/monounsaturated fatty acids in rapeseed oil to be a contributory factor. Normallyerucic acid is not found or occurs in traces in body fat, but when the diet contains rapeseed oilerucic acid is found in depot fat, organ fat and milk fat. Erucic acid is metabolized in vivo to oleicacid. The effects of rapeseed oil on reproduction and adrenals, testes, ovaries, liver, spleen,kidneys, blood, heart and skeletal muscles have been investigated. Fatty infiltration in the heartmuscle cells has been observed in the species investigated. In long-term experiments in rats erucicacid produces fibrosis of the myocardium. Erucic acid lowers the respiratory capacity of the heartmitochondria. The reduction of respiratory capacity is roughly proportional to the content oferucic acid in the diet, and diminishes on continued administration of erucic acid. The lifespan ofrats is the same on corn oil, soybean oil, coconut oil, whale oil and rapeseed oil diet. Rats fed adiet with erucic acid or other docosenoic acids showed a lowered tolerance to cold stress (+4degrees C). In Sweden erucic acid constituted 3-4% of the average intake of calories up to 1970compared with about 0.4% at present.

Generally rapeseed has a cumulative effect, taking almost 10 years before symptoms beginto manifest. It has a tendency to inhibit proper metabolism of foods and prohibits normalenzyme function. Canola is a Trans Fatty Acid, which has shown to have a direct link tocancer. These Trans Fatty acids are labeled as hydrogenated or partially hydrogenated oils.Avoid all of them!

According to John Thomas' book, Young Again, 12 years ago in England and Europe, rapeseed was fed to cows, pigs and sheep that later went blind and began attacking people.There were no further attacks after the rape seed was eliminated from their diet.

Source: David Dancu, N.D. http://www.karinya.com/canola.htm

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MilkOne of the few total foods capable of supporting life is raw milk. However, when milk is heated topasteurize it, the proteins are destroyed. When it is homogenized, it is blown through nozzles tobreak the long fat chains into short broken pieces of fat. Thus pasteurized, homogenized milk is nolonger milk but instead contains toxic proteins and fat particles.

Most people who think they are “lactose intolerant” are really just sensitive to the toxic brew wecall milk that is available in grocery stores.

The state of Maryland was considering prohibiting people who own cows from drinking their ownmilk or from forming cooperatives so people who buy a portion of a cow could consume raw milk.This rebuttal letter written by Sally Fallon puts it all into perspective. I reproduce it here with herpermission.

RESPONSE TO LETTER FROM TED ELKINS, DEPUTY DIRECTOR,OFFICE OF FOOD PROTECTION AND CONSUMER HEALTH SERVICES,

MARYLAND DEPARTMENT OF HEALTH AND MENTAL HYGIENE

The following are comments and clarifications to a letter from Ted Elkins, Deputy Director, Office of FoodProtection and Consumer Health Services, sent to citizens who submitted comments to oppose the Noticeof Proposed Action to amend Regulation .06 under COMAR 10.15.06.Production, Processing,Transportation, Storage and Distribution of Milk.

Mr. Elkin ’s statements are in green; our rebuttals are in black.

To summarize, Mr. Elkin has made a series of statements unsupported by references and scientific studies.He has ignored many relevant findings concerning the safety and health benefits of raw milk and theincreasing evidence of disease caused by pasteurized milk. He has not reported on evidence of bias inreports on alleged problems with raw milk and has withheld discussion of the numerous incidents of food-borne illness in many commonly consumed foods, thus perpetuating the double standard that uninformedhealth officials have applied to raw milk. The citizens of Maryland deserve accurate information, notunsubstantiated boilerplate allegations.

“The State of Maryland and other federal and state health agencies have documented a long history of therisks to human health associated with the consumption of raw milk. Clinical and epidemiological studiesfrom the Food and Drug Administration (FDA), state health agencies, and others have established a directcausal link between gastrointestinal disease and the consumption of raw milk.”

While several incidents of food-borne illness in recent years have been attributed to the consumption of rawmilk, no positive correlation in these cases was established and government reports on these cases showstrong evidence of bias. For example, in 1983, a reported outbreak of Campylobacter in raw milk led to thepassage of anti-raw milk legislation in the state of Georgia. However, extensive testing failed to findCampylobacter or any other pathogens in any milk products from the dairy. All safety measures had beenfollowed faithfully. In spite of this lack of evidence, the author of the official report concluded: “The onlymeans available to ensure the public’s health would be proper pasteurization before consumption.”

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(American Journal of Epidemiology, 1983 Vol 114, No 4). Ironically, just 4 years later, a massive outbreak ofover 16,000 culture-confirmed cases of antimicrobial-resistant Salmonella typhimurium was traced topasteurized milk from one dairy in Georgia (JAMA 1987 Dec 11 ;258(22):3269-74). Yet health officials stillallow the sale of pasteurized milk in Georgia.

Another example concerns a November 2001 outbreak of Campylobacter in Wisconsin, which local healthofficials and the Centers for Disease Control blamed on raw milk from a cow-share program in SawyerCounty. According to an official report, posted on the CDC website, 70-75 persons became ill fromCampylobacter infection during the 12 weeks following November 10, 2001. However, independentinvestigators determined that the number of afflicted was over 800. Only 24 of 385 cow-share ownersbecame ill. Most had consumed hamburger at a local restaurant. There was no illness in the remaining 361cow-share owners and most of those who became ill did not consume raw milk. Health workers at localhospitals showed a clear evidence of bias by testing only those who said they had consumed raw milk;others who reported in sick but had not drunk raw milk were sent home without investigation. Mostimportantly, independent lab tests found no Campylobacter in the raw milk (www.realmilk.com). Thisoutbreak is one that health officials almost always emphasize when arguing against the consumption of rawmilk; yet the evidence of the case points to the fact that raw milk was not the cause of the outbreak.

“The microbial flora of raw milk may include human pathogens present on the cow's udder and teats.”

Standard sanitary procedures can completely eliminate the presence of human pathogens in human milk.Organic Pastures Dairy in California produces raw milk for retail sales. The dairy and the state haveconducted routinely tests for several years and have never found a human pathogen in the raw milk theyproduce (www.organicpastures.com).

The intrinsic safety of raw milk stands in sharp contrast to the dangers inherent in other foods. For example,a 1978 survey found Salmonella in many “health food” products, including soy flour, soy protein powder andsoy milk powder. The authors of the report concluded that “The occurrence of this pathogen in three typesof soybean products should warrant further investigation of soybean derivatives as potentially significantsources of Salmonella (Applied and Environmental Microbiology, Mar 1979, pp 559-566).

While raw milk often gets the blame for food-borne illnesses, Campylobacter is best known forcontaminating meats. For example, a study carried out during 1999-2000 found that 70.7 percent ofchicken and 14.5 percent of turkey samples from Washington, DC grocery stores was infected withCampylobacter. (Zhao C, et al. Applied and Environmental Microbiology, 2001:67(12):5431-5436).Maryland law does not require pasteurization of chicken and turkey, which is highly likely to contain humanpathogens, yet has taken steps to deny access to raw milk, which seldom if ever contains humanpathogens.

If the goal of the state of Maryland is to eliminate our exposure to human pathogens, perhaps healthdepartment officials should take steps to ban the use of coins and cookware. E. Coli has been shown tosurvive on coins for 7-11 days at room temperature; Salmonella enteritidis can survive 1-9 days on pennies,nickels, dimes and quarters; and Salmonella enteritidis can also survive on glass and Teflon for up to 17days (Jiang and Doyle. Journal of Food Protection 1999;62(7):805-7).

The truth is that humans are exposed to pathogens on a daily basis—on surfaces, in our water and in thefood we eat. To single out raw milk as a source of pathogens shows extreme bias against the only food thatis intrinsically safe and that furthermore contains many components that support our immunity topathogens.

“Further, the intrinsic properties of milk, including its pH and nutrient content, make it an excellent medium forthe survival and growth of pathogenic bacteria.”

This statement reveals the complete ignorance of over 40 years of science indicating that raw milk does notsupport the survival and growth of pathogenic bacteria. Milk contains numerous components that fight againstpathogens and strengthen the immune system. These include:

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Lactoperoxidase, an enzyme that uses small amounts of H2O2 and free radicals to seek out anddestroy bad bacteria. It is found in all mammalian secretions, such breast milk, tears and saliva.Lactoperoxidase levels are much higher in the milk of animals than humans. For example,lactoperoxidase levels are 10 times higher in goat milk than in human breast milk. So effective islactoperoxidase in fighting pathogens that other countries are looking into using lactoperoxidaseinstead of pasteurization to ensure safety of commercial milk (British Journal of Nutrition (2000), 84,Suppl. 1. S19-S25; Indian Journal Exp Biology Vol. 36, August 1998, pp 808-810; 1991 J Dairy Sci74:783-787; Life Sciences, Vol 66, No 23, pp 2433-2439, 2000)

Lactoferrin, an enzyme that steals iron away from pathogens and carries it through the gut wallinto the blood stream and also stimulates the immune system. Lactoferrin also ensures completeassimilation of iron by the infant.

Polysaccharides, special sugars that encourage the growth of good bacteria in the gut; protectthe gut wall

Medium-Chain Fatty Acids, special types of fats that disrupt cell walls of bad bacteria; levels areso high in goat milk that the test for the presence of antibiotics had to be changed.

Enzymes that disrupt bacterial cell walls.

Antibodies that bind to foreign microbes and prevent them from migrating outside the gut; initiateimmune response (British Journal of Nutrition (2000) 84. Suppl. 1, S3-S10, S11-S17).

White blood cells that produce antibodies against specific bacteria, producing immunity for life inthe infant.

B-lymphocytes, compounds that kill foreign bacteria and call in other parts of the immunesystem

Macrophages, components that engulf foreign proteins and bacteria

Neutrophils, which kill infected cells; mobilize other parts of the immune system

T-lymphocytes, components that multiply if bad bacteria are present, while producing immune-strengthening compounds.

Lysosyme, which kills bad bacteria by digesting their cell walls.

Hormones & growth factors, which stimulate the maturation of gut cells thereby preventing“leaky” gut.

Mucins, which adhere to bad bacteria and viruses, preventing those organisms from attaching tothe mucosa and causing disease.

Oligosaccharides, special types of sugars which protect other protective components from beingdestroyed by stomach acids and enzymes; they bind to bacteria and prevent them from attaching tothe gut lining and have other functions just being discovered.

B12 binding protein, a component that reduces the levels of vitamin B12 in the colon, whichharmful bacteria need for growth. This compound also ensures complete assimilation of B12 bythe infant.

Bifidus factor is a complex of good bacteria which promotes growth of Lactobacillum bifidis, ahelpful bacteria in baby’s gut, which helps crowd out dangerous germs

Fibronectin, which increases antimicrobial activity of macrophages and helps to repair damaged

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tissues (J Pediatr 1994 Feb; 124(2): 193-8; Curr Med Chem 1999 Feb;6(2): 117-27).

Most of these components are completely inactivated by pasteurization (Scientific American, December1995; The Lancet, Nov 17, 1984), making pasteurized milk highly susceptible to contamination. Mr. Elkin’sstatement, that “the intrinsic properties of milk, including its pH and nutrient content, make it an excellentmedium for the survival and growth of pathogenic bacteria,” applies only to pasteurized milk, not to raw milk.

It is of interest to note that until recently, the medical profession claimed that breast milk was sterile.Research conducted over the last 20 years indicates that breast milk contains pathogens, often at veryhigh levels. It is actually beneficial for breast milk to contain pathogens because the bioactive componentsin milk program the baby to have immunity for life to any pathogens with which he comes in contact (J ApplMicrobiol. 2003;95(3):471 -8; Neonatal Netw. 2000 Oct; 19(7)21-5; J Hosp Infec. 2004 Oct;58(2): 146-50; JNutr. 2005 May; 135(5): 1286-8; Curr Med Chem. 1999 Feb;6(2): 117-27; Adv Exp Med Biol. 2004;554: 145-54; Scientific American, December 1995; Lancet. 1984 Nov 1 7;2(841 2): 111-3; Lancet. 1984 Nov17;2(8412):111-3; Cent Afr J Med. 2000 Sep;46(9):247-51; Eur J Pediatr. 2000 Nov; 159(11 ):793-7; J DairySci 1991 ;74:783-787).

Maryland health officials do not require breastfeeding mothers to pasteurize their milk before giving it totheir babies; yet these same officials discourage mothers who are unable to breastfeed from giving theirinfants the most appropriate and immune-building substitute—raw milk from another mammal such as acow or goat.

A 1994 study found that premature infants fed raw human milk had lower rates of infection compared tothose fed pasteurized human milk (Lancet November 17, 1984). In fact, pasteurization of human milk forbabies carries considerable risk. A recent outbreak of Pseudomonas aeruginosa in a neonatal intensivecare unit caused by a contaminated milk bank pasteurizer resulted in 31 cases of infection and 4 deaths(Arch Dis Child Fetal Neonatal Ed 2003 Sep;88(5):F434-5).

The intrinsic safety of raw milk has been proven in several published reports showing that raw milk passesthe “challenge test.” That is, when pathogenic bacteria are introduced to raw milk, their numbers rapidlydecline; subsequent testing reveals no pathogens even though they were introduced in large numbers. Forexample, Lactoperoxidase in raw milk has been shown to kill added fungal and bacterial agents (LifeScience 2000 66(25):2433-9; Indian Journal of Experimental Biology 1998;36:808-1 1).

In a challenge test, raw goat milk killed Campylobacter jejuni (Hygiene (London) 1985 Feb;94(1):31-44).

When Campyloba cter was added to raw milk at 4 degrees C at levels of 13,000,000 per ml, levels wereless than 10 per ml nine days later (Doyle, et al. Applied and Environmental Microbiology, 1982;44(5):1154-58). The anti-microbial properties of raw milk are even more active when milk is not refrigerated.Researchers found that bovine strains of Campylobacter were decreased by 100 cells per ml and poultrystrains decreased by 10,000 cells per ml in 48 hours in raw milk at room temperature (37 degrees C) (DikerKS. Mikrobiyol Bul 1987 Jul;21(3):200-5).

Most recently, the University of California conducted challenge tests on Organic Pastures raw milk inCalifornia, finding that pathogens added to raw milk disappeared completely within 36 hours(www.organicpastures.com).

“On August 10, 1987, FDA published 21 CFR Part 1240.61, a final regulation mandating thepasteurization of all milk and milk products in final package form for direct human consumption. Thisregulation addresses milk shipped in interstate commerce and became effective September 9, 1987. Inthe Federal Register notification for the final rule to 21 CFR Part 1240.61, FDA made a number of findingsincluding the following: ‘Raw milk, no matter how carefully produced, may be unsafe.’ ”

This statement may be part of the official record but it contradicts other statements published by the USgovernment. A study carried out over 19 years and posted on the Centers for Disease Control website givesthe incidence of food-borne illness from raw milk at 1.9 cases per 100,000 people, 1973-1992 (AmericanJournal Public Health Aug 1998, Vol 88., No 8). This report cites many incidents reputed to be caused by

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raw milk but not necessarily proven; the actual rate of illness caused by raw milk, on a per-consumer basis,may in fact be much lower.

Based on the same CDC website, the incidence of food-borne illness from all foods including pasteurizedmilk during the period 1993-1997 is 4.7 cases per 100,000 people (US Census Bureau 1997 populationestimate 267,783,607). Based on CDC website, the incidence of reported food-borne illness from otherfoods (not including milk) is 6.4 cases per 100,000 people, per year from 1993-1997. Therefore, theincidence of food-borne illness from consuming raw milk is at least 2.5 times lower than the incidence offood-borne illness from consuming pasteurized milk; and at least 3.5 times lower than the incidence offood-borne illness from consuming other foods.

Thus the statement published in the FDA register is false; raw milk is safer than any other food in the foodsupply. If a food is to be taken out of the food supply because it “may be unsafe,” then we would havenothing left to eat. Raw salads, fruits, vegetables, shellfish, eggs and meat, plus pasteurized milk, soyproducts, baby formula and mayonnaise have all caused proven outbreaks of illness. Yet these foodsremain in the food supply, putting the citizens of Maryland at continued risk.

According to our government, food-borne diseases cause approximately 76 million illnesses, 325,000hospitalizations and 5,000 deaths per year; the most common source of these infections is fruits,vegetables and salads. For example, in 1997, there were 1104 reported cases of food-borne illness fromsalads and 719 from fruits and vegetables while only 23 from milk, mostly pasteurized milk (MMWR Vol45, No SS-5).

"It has not been shown to be feasible to perform routine bacteriological tests on the raw milk itself todetermine the presence or absence of all pathogens and thereby ensure that it is free of infectiousorganisms."

This statement would not hold up in a court of law. Today it is completely feasible to perform routinebacteriological tests on raw milk; these can be performed at the farm and are very inexpensive. There iseven a test for E. coli O157:H7 that can be carried out on the farm and costs only $8 per test. It isshameful that health officials of the state of Maryland are unfamiliar with these tests.

“Opportunities for the introduction and persistence of Salmonella on dairy premises are numerous andvaried, and technology does not exist to eliminate Salmonella infection from dairy herds or to preclude re-introduction of Salmonella organisms. Moreover recent studies show that cattle can carry and shed S.dublin organisms for many years and demonstrated that S. dublin organisms cannot be routinely detected incows that are 'mammary gland' shedders.”

This statement applies only to large confinement herds. It has proven completely possible to eliminatepathogens from dairy premises when cows are raised on pasture and reasonable sanitary protocols arefollowed. Over several years of testing, not a single human pathogen has been found on the premises ofOrganic Pastures dairy in California, not in the manure and not in the milk (www.organicpastures.com).

“During this rulemaking process, the American Academy of Pediatrics and numerous other organizationssubmitted comments in support of the proposed regulation. In deciding upon mandatory pasteurization,FDA determined that pasteurization was the only means to assure the destruction of pathogenicmicroorganisms that might be present.”

This statement is completely false. Pasteurization does not ensure the destruction of pathogenicmicroorganisms in milk. A study published in 2002 found evidence of Mycobacterium paratuberculosis inmany samples of pasteurized cow’s milk (Appl Environ Microbiol 2002 May;68(5):2428-35). M.paratuberculosis has been associated with Crohn’s disease.

Other studies indicate that B. Cereus spores, botulism spores and protozoan parasites survivepasteurization (Elliott Ryser. Public Health Concerns. In: Marth E, Stelle J, eds. Applied DairyMicrobiology, New York, Marcel Dekker, 2001).

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Furthermore, the US government has documented numerous outbreaks of food-borne illness frompasteurized milk. These include:

1945—1,492 cases for the year in the US 1945—1 outbreak, 300 cases in Phoenix, Arizona. 1945—Several outbreaks, 468 cases of gastroenteritis, 9 deaths, in Great Bend, Kansas 1976—Outbreak of Yersinia enterocolitica in 36 children, 16 of whom had appendectomies,

due to pasteurized chocolate milk 1978—1 outbreak, 68 cases in Arizona 1982—over 17,000 cases of Yersinia enterocolitica in Memphis, TN 1982—172 cases, with over 100 hospitalized from a three-Southern-state area. 1983—1 outbreak, 49 cases of Listeriosis in Massachusetts 1984—August, 1 outbreak S. typhimurium, approximately 200 cases, at one plant in Melrose

Park, IL 1984—November, 1 outbreak S. typhimurium, at same plant in Melrose Park, IL 1985—March, 1 outbreak, 16,284 confirmed cases, at same plant in Melrose Park, IL 1985—197,000 cases of antimicrobial-resistant Salmonella infections from one dairy in

California 1985—1,500+ cases, Salmonella culture confirmed, in Northern Illinois 1987—Massive outbreak of over 16,000 culture-confirmed cases of antimicrobial-resistant

Salmonella typhimurium traced to pasteurized milk in Georgia 1993—2 outbreaks statewide, 28 cases Salmonella infection 1994—3 outbreaks, 105 cases, E. Coli & Listeria in California 1993-1994—outbreak of Salmonella enteritidis in over 200 due to pasteurized ice cream in

Minnesota, South Dakota and Wisconsin 1995—1 outbreak, 3 cases in California 1995—outbreak of Yersinia enterocolitica in 10 children, 3 hospitalized due to post-

pasteurization contamination 1996—2 outbreaks Campylobactor and Salmonella, 48 cases in California 1997—2 outbreaks, 28 cases Salmonella in California

The fact that Mr. Elkins does not present the full story, by enumerating the many outbreaks of food-borneillness in pasteurized milk, provides clear evidence of bias on the part of a Maryland health official.

“This decision was science-based, involving epidemiological evidence. FDA and the Centers for DiseaseControl and Prevention (CDC) in Atlanta have documented illnesses associated with the consumption ofraw milk, including ‘certified raw milk’ and have stated that the risks of consuming raw milk far outweigh anybenefits.”

It is obvious that this decision was not science-based and that it contradicts the epidemiological evidenceprovided by our government agencies.

“Based on research, which has failed to demonstrate a significant difference between the nutritional value ofpasteurized and unpasteurized milk, the FDA and CDC reiterate that the health risks associated with rawmilk consumption far outweigh the benefits.”

Mr. Elkins seems to be unaware of numerous studies showing the benefits of raw milk over pasteurized. Forexample, studies carried out during 1935-1940 at Randleigh Farm, a research facility in upstate New York,found that rats fed raw milk had better growth and denser bones than those fed pasteurized milk. The ratson pasteurized milk developed hairless patches due to vitamin B6 deficiency and on autopsy showed poorintegrity of internal organs (Annals of Randleigh Farm).

These studies confirm the findings of Francis Pottenger who noted that the organs of cats fed raw milk werein excellent condition, with creamy yellow subcutaneous tissue of high vascularity. The heart size of raw-milk fed cats was moderate, the liver in good condition, the intestines firm and the uterus well supported. Bycontrast the internal organs of pasteurized-milk fed cats were inferior, with slight fatty atrophy of the liver,

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inferior condition of the heart, lack of intestinal tone and moderate distention of the uterus. The skin of thepasteurized-milk fed cats had a purplish discoloration due to congestion and the fur was of poor quality(Pottenger’s Cats, Price-Pottenger Nutrition Foundation).During 1930-31, Dr. Ernest Scott and Professor Lowell Erf of Ohio State University carried out rat studiesthat compared the effects of a diet of whole raw milk with one of whole pasteurized milk. Rats fed wholeraw milk had good growth, sleek coats and clear eyes. The rats had excellent dispositions and enjoyedbeing petted. By contrast, rats fed whole pasteurized milk had rough coats, slow growth, anemic, and loss ofvitality and weight. They were very irritable, often showing a tendency to bite when handled (JerseyBulletin 1931 50:210-21 1;224-226, 237).

Studies of guinea pigs carried out by Dr. Rosalind Wulzen and Paul N. Harris, Department of Zoology,Oregon State College are particularly revealing. Animals fed whole raw milk had excellent growth and noabnormalities. By contrast, those fed pasteurized milk had poor growth, muscle stiffness, emaciation andweakness and death within one year. Autopsy revealed atrophied muscles streaked with calcification andcalcium deposits under the skin, in the joints, the heart and other organs (American Journal of PathologyVol XX VI, Jul-Nov 1950 pp 595-615).

As for pasteurized milk, many recent studies document the association of pasteurized milk with diabetes(Br J Nutr 2006 Mar;95(3):603-8;Diabetes 2000 Jun;49(6):91 2-7), frequent ear infections (J Pediatr Rio J2006 mar-Apr;82(2):87-96; Rev Alerg Mex 2001 Sep-Oct;48(5):141-4; Acta Paediatr 2000 Oct;89(10):1174-80; Acta Otolaryngol 1999;1 19(8):867-73) and asthma (Ann Allergy Asthma Immunol 2002 Dec;89(6Suppl 1):33-7; J Allergy Clin Immunol 2001 Nov; 108(5):720-5; West J Nurs Res 1996 Dec;18(6):643-54;Pediatr Pulmonol Suppl 1995;1 1:59-60). Of interest is a 2002 study showing that “farm milk,” that is rawmilk, had a protective effect against this debilitating and even lift-threatening condition (Lancet 2002 Feb 16;359(9306):623-4).

The scientific literature contains many case histories of recovery from these conditions by eliminatingpasteurized milk from the diet. Meanwhile, reports of recovery from these and other conditions byconsuming raw milk are accumulating. The growing numbers of Maryland consumers—especially growingchildren—who cannot tolerate pasteurized milk deserve to have a choice for raw milk.

“Numerous documented outbreaks of milk borne disease involving Salmonella and Campylobacterinfections have been directly linked to the consumption of raw milk in the past twenty years. Since theearly 1980's, cases of raw milk-associated campylobacteriosis have been reported in the states ofArizona, California, Colorado, Georgia, Kansas, Maine, Montana, New Mexico, Oregon, andPennsylvania. An outbreak of salmonellosis, involving 50 cases was confirmed in Ohio in 2002. Recentcases of E. coli O1 57:H7, Listeria monocytogenes and Yersinia enterocolitica infections have also beenattributed to raw milk consumption.”

It would be helpful if Mr. Elkins would provide references so that they could be evaluated for legitimacy andbias. Given the double standard applied to raw milk, it is likely that many of these cases were merelyreported, not proven. The 2002 Ohio outbreak that he cites was a case in which health officialsdemonstrated clear evidence of bias. According to the CDC report, “The source for contamination was notdetermined; however, the findings suggest that contamination of milk might have occurred during themilking, bottling or capping process.” There were many possible of vectors of illness on the dairy besidesraw milk—besides providing raw milk, the dairy also operated a petting zoo. There have been severalincidences of illness contracted by children visiting a petting zoo, cases that have nothing to do with rawmilk. Based on this one incident, in which raw milk was not proven the culprit, the dairy, which had been inbusiness for decades without incident, caved in to health department pressure and stopped the sale of rawmilk.

“State health and agricultural agencies utilize the U.S. Public Health Service/FDA Pasteurized MilkOrdinance (PMO) as the basis for the regulation of Grade ‘A’ milk production and processing. The PMO hasbeen sanctioned by the National Conference on Interstate Milk Shipments (NCIMS) and provides anational standard of uniform measures that is applied to Grade ‘A’ dairy farms and milk processingfacilities to assure safe milk and milk products. Section 9 of the PMO specifies that only Grade ‘A’pasteurized milk be sold to the consumer.”

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This issue is a red herring. The individual states do not need to follow the PMO. The PMO is achoice, not an obligation. California, the top milk-producing state, does not follow the PMO butcreated its own regulations. Furthermore, the state can accept the PMO but have exceptions incertain areas, as does Colorado. In any event, PMO regulations do not prohibit consumers fromdrinking raw milk. It must be stressed that neither the federal government nor the individualstates prohibit the consumption of raw milk. Such laws would be inherently unconstitutional,depriving citizens the right to liberty and property without due process of law.

“In summary, since raw milk may contain infective doses of human pathogens, its consumptionincreases the risk of a variety of illnesses. Even when milk is produced and handled undersanitary conditions, the only proven, reliable method of reducing the level of human pathogens inmilk and milk products to safe levels is pasteurization. The FDA has strongly advised against theconsumption of raw milk. As the State agency responsible for health of the citizens of Maryland,the Department of Health and Mental Hygiene cannot, in good conscience, condone orencourage the sale of raw milk.”

As we have demonstrated in this letter, raw milk does not contain “infective doses of humanpathogens” and its consumption does not “increase the risk of a variety of illnesses.”Pasteurization does not guarantee a safe product and the risk of contracting food-borne illnessfrom raw milk is lower that the risk of contracting food-borne illness from pasteurized milk. Thestatements made in writing by Mr. Elkins would not hold up in a court of law and are an insult toMaryland consumers.

But in any event, Maryland consumers are not asking for legalization of the sale of raw milk, butonly confirmation of the right to drink the raw milk from their own cows, which is a public policy ofthe state of Maryland. Maryland consumers are not asking the Department of Health and MentalHygiene to condone or encourage the sale of raw milk, but merely insisting that the state ofMaryland support the rights of its citizens to enter into contractual agreements guaranteed byMaryland law (title 16, Section 401), which recognizes the right of an owner of dairy livestock tocontract with another for the boarding and care of that livestock. MDHMH is interfering in areaswhere it has no jurisdiction whatsoever and is overstepping the bounds of its regulatory authority.

Sally Fallon, PresidentThe Weston A. PriceFoundation May 23,2006

Phosphatidylcholine

DESCRIPTIONPhosphatidylcholine is a phospholipid that is a major constituent of cell membranes.

Phosphatidylcholine is also known as 1, 2-diacyl-: ussn: ue-glycero-3-phosphocholine,PtdCho and lecithin. It is represented by the following chemical

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structure:

Phosphatidylcholine

The term lecithin itself has different meanings when used in chemistry and biochemistrythan when used commercially. Chemically, lecithin is phosphatidylcholine.Commercially, it refers to a natural mixture of neutral and polar lipids.Phosphatidylcholine, which is a polar lipid, is present in commercial lecithin inconcentrations of 20 to 90%. Most of the commercial lecithin products contain about20% phosphatidylcholine.

Lecithins containing phosphatidylcholine are produced from vegetable, animal andmicrobial sources, but mainly from vegetable sources. Soybean, sunflower and rapeseedare the major plant sources of commercial lecithin. Soybean is the most common source.Plant lecithins are considered to be GRAS (generally regarded as safe). Egg yolk lecithinis not a major source of lecithin in nutritional supplements. Eggs themselves naturallycontain from 68 to 72% phosphatidylcholine, while soya contains from 20 to 22%phosphatidylcholine.

The fatty acid makeup of phosphatidylcholine from plant and animal sources differs.Saturated fatty acids, such as palmitic and stearic, make up 19 to 24% of soya lecithin;the monounsaturated oleic acid contributes 9 to 11%; linoleic acid provides 56 to 60%;and alpha-linolenic acid makes up 6 to 9%. In egg yolk lecithin, the saturated fatty acids,palmitic and stearic, make up 41 to 46% of egg lecithin, oleic acid 35 to 38%, linoleicacid 15 to 18% and alpha-linolenic 0 to 1%. Soya lecithin is clearly richer inpolyunsaturated fatty acids than egg lecithin. Unsaturated fatty acids are mainly bound tothe second or middle carbon of glycerol.

Choline comprises about 15% of the weight of phosphatidylcholine. (See monograph onCholine.)

ACTIONS AND PHARMACOLOGY

ACTIONS

Phosphatidylcholine may have hepatoprotective activity.

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Phosphatidylcholine is important for normal cellular membrane composition and repair.Phosphatidylcholine is also the major delivery form of the essential nutrient choline.Choline itself is a precursor in the synthesis of the neurotransmitter acetylcholine, themethyl donor betaine and phospholipids, including phosphatidylcholine andsphingomyelin among others. Phosphatidylcholine is involved in the hepatic export ofvery-low-density lipoproteins.

MECHANISM OF ACTION

Phosphatidylcholine's role in the maintenance of cell-membrane integrity is vital toall of the basic biological processes. These are: information flow that occurs within cellsfrom DNA to RNA to proteins; the formation of cellular energy and intracellularcommunication or signal transduction. Phosphatidylcholine, particularlyphosphatidylcholine rich in polyunsaturated fatty acids, has a marked fluidizing effect oncellular membranes. Decreased cell-membrane fluidization and breakdown of cell-membrane integrity, as well as impairment of cell-membrane repair mechanisms, areassociated with a number of disorders, including liver disease, neurological diseases,various cancers and cell death.

PHARMACOKINETICS

Phosphatidylcholine is absorbed into the mucosal cells of the small intestine, mainly inthe duodenum and upper jejunum, following some digestion by the pancreatic enzymephospholipase, producing lysophosphatidylcholine (lysolecithin). Reacylation oflysolecithin takes place in the intestinal mucosal cells, reforming phosphatidylcholine,which is then transported by the lymphatics in the form of chylomicrons to the blood.Phosphatidylcholine is transported in the blood in various lipoprotein particles, includingvery-low-density lipoproteins (VLDL), low-density lipoproteins (LDL) and high-densitylipoproteins (HDL); it is then distributed to the various tissues of the body. Somephosphatidylcholine is incorporated into cell membranes.

Phosphatidylcholine is also metabolized to choline, fatty acids and glycerol. The fattyacids and glycerol either get oxidized to produce energy or become involved inlipogenesis. Choline is a precursor of acetylcholine. Serum choline levels peak between 2to 6 hours after oral intake.

INDICATIONS AND USAGE

Phosphatidylcholine may be indicated to help restore liver function in a number ofdisorders, including alcoholic fibrosis, and possibly viral hepatitis. It may also beindicated for the treatment of some manic conditions. There is some evidence thatPhosphatidylcholine may be useful in the management of Alzheimer's disease and someother cognitive disorders. A possible future role in cancer therapy is also suggested byrecent research. It may also be indicated in some with tardive dyskinesia. (Recent studiesby Kane and Kane have found it critical in most chronic diseases including Lou Gehrig’sdisease, Alzheimer’s, Lyme disease, autism, etc. JLT)

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RESEARCH SUMMARY

Clinical studies have demonstrated that choline is essential for normal liver function.Phosphatidylcholine is a better delivery form and is also more tolerable than choline. But,in addition, research has shown that phosphatidylcholine, independent of its cholinecontent, has striking hepatoprotective effects. In two animal studies using baboons feddiets high in alcohol, some supplemented with a soy-derived polyunsaturated lecithin(60% phosphatidylcholine) and some unsupplemented, both fibrosis and cirrhosis werelargely prevented in the phosphatidylcholine group. Most of the unsupplemented animalsin these studies, which continued for up to eight years, developed fibrosis or cirrhosis.

Because these researchers had previously found that choline, equal in amounts containedin the phosphatidylcholine-rich lecithin they subsequently used, had no comparableprotective effects on the liver, they concluded that the polyunsaturated phospholipidsthemselves may have been responsible for the benefits observed.

In vitro studies have shown that these phospholipids increase hepatic collagenase activityand may thus help prevent fibrosis and cirrhosis by encouraging collagen breakdown.Several other mechanisms under investigation may also contribute.

Others have reported similarly encouraging results in animal models. Clearly, humantrials are warranted.

In addition, phosphatidylcholine has demonstrated other protective effects in non-alcoholic liver disorders, including protection against various other toxic substances. Itsbenefits in viral hepatitis were reported some years ago by several different researchgroups in Europe and elsewhere. In one of these studies, individuals suffering fromhepatitis type A and B were given 1.8 grams of phosphatidylcholine daily. Comparedwith unsupplemented controls, the phosphatidylcholine group enjoyed quicker recoveries,fewer relapses and quicker normalization of liver function tests.

Researchers in Great Britain treated chronic active hepatitis C patients with 3 grams dailyof phosphatidylcholine in double-blind fashion. The phosphatidylcholine patients hadsignificantly reduced symptoms, compared with controls. All histological evidence of thedisease disappeared in some cases. These researchers, like others, have hypothesized thatphosphatidylcholine's possible antiviral effects are related to the supplement's apparentability to increase cellular membrane fluidity and repair the membranes of liver cells.

Phosphatidylcholine may help some with tardive dyskinesia, a neurological disordercharacterized by defective cholinergic nerve activity. Both supplemental choline andphosphatidylcholine were found to reduce the muscular hyperactivity of this disorder byabout 50% in some studies. However, one significant trial did not see a beneficial effect.

There is some very preliminary evidence that phosphatidylcholine may help controlmanic symptoms in some.

There has been hope, for some time, that phosphatidylcholine would demonstrate clear-cut benefits in cognitive disorders, such as age-related memory loss and Alzheimer's

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disease. There are a few reports that supplemental choline can improve short-termmemory skills and enhance the memories of those who are initial poor learners.

Those with Alzheimer's disease have a diminished ability to synthesize and/or utilize theneurotransmitter acetylcholine, particularly in those areas of the brain related to memory,thus the hope that supplemental choline/phosphatidylcholine might be of benefit. A fewstudies have suggested some small benefit in memory restoration, but most have not.Research continues.

Recently it has been suggested that phosphatidylcholine might eventually have sometherapeutic role in some cancers. There is no evidence of this to date, but animal studiesindicate that deficiencies in choline and phosphatidylcholine may disrupt cell membranesignal transduction in ways that could lead to various cancers. There is ample evidencethat liver cancer is promoted in various animals by choline-deficient diets, and it has beenshown that excess choline can protect against liver cancer in a mouse model.

Phosphatidylcholine has been used to lower serum cholesterol levels, based on thepremise that lecithin cholesterol acyltransferase (LCAT) activity has an important role inthe removal of cholesterol from tissues. A few studies have shown reduction in serumcholesterol with phosphatidylcholine intake. The results were quite modest, and moststudies have not shown any significant cholesterol-lowering activity.

CONTRAINDICATIONS, PRECAUTIONS, ADVERSE REACTIONS

CONTRAINDICATIONS

There are no reported or known contraindications of phosphatidylcholinesupplementation.

PRECAUTIONS

Those with malabsorption problems may develop diarrhea or steatorrhea when usingphosphatidylcholine supplements. Those with the antiphospholipid-antibody syndromeshould exercise caution in the use of phosphatidylcholine supplements.

ADVERSE REACTIONS

No major side effects have been reported. Mild side effects have been noted occasionallysuch as nausea, diarrhea and increased salivation in some. This holds for all forms ofphosphatidylcholine.

INTERACTIONS

There are no known interactions.

OVERDOSAGE

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There are no reports of overdosage.

DOSAGE AND ADMINISTRATION

There are several forms of phosphatidylcholine supplements. Typical commercial lecithinsupplements contain 20 to 30% phosphatidylcholine. Softgel capsules containing 55%and 90% phosphatidylcholine are available. Liquid concentrates containing 3 grams ofphosphatidylcholine per 5 milliliters (one teaspoon) are also available.

Recommended doses range from 3 to 9 grams of phosphatidylcholine daily in divideddoses.

LITERATURE

Atoba MA, Ayoola EA, Ogunseyinde O. Effects of essential phospholipid choline on thecourse of acute hepatitis-B infection. Trop Gastroenterol. 1985; 6:96-9.

Buko V, Lukivskaya O, Nikitin V, et al. Hepatic and pancreatic effects ofpolyenoylphosphatidylcholine in rats with alloxan-induced diabetes. Cell Biochem Funct.1996; 14:131-137.

Canty DJ, Zeisel SH. Lecithin and choline in human health and disease. Nutr Rev. 1994;52:327-339.

Cohen BM, Lipinski JF, Altesman RI. Lecithin in the treatment of mania: double-blind,placebo-controlled trials. Am J Psychiatry. 1982; 139:1162-1164.

Gelenberg AJ, Dorer DJ, Wojcik JD, et al. A crossover study of lecithin treatment oftardive dyskinesia. J Clin Psychiatry. 1990; 51:149-153.

Growdon JH, Gelenberg AJ, Doller J, et al. Lecithin can suppress tardive dyskinesia. NEngl J Med. 1978; 298:1029-1030.

Hanin I, Ansell GB, eds. Lecithin. Technological, Biological and Therapeutic Aspects.New York and London: Plenum Press; 1987.

Hirsch MJ, Growdon JH, Wurtman RJ. Relations between dietary choline or lecithinintake, serum choline levels, and various metabolic indices. Metabolism. 1978; 27:953-960.

Jackson IV, Nuttall EA, Ibe IO, Perez-Cruet J. Treatment of tardive dyskinesia withlecithin. Am J Psychiatry. 1979; 136:1458-1460.

Jenkins PJ, Portmann BP, Eddleston AL, Williams R. Use of polyunsaturatedphosphatidylcholine in HBsAg negative chronic active hepatitis: results of prospectivedouble-blind controlled trial. Liver. 1982; 2:7-81.

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Kosina F, Budka K, Kolouch Z, et al. Essential cholinephospholipids in the treatment ofvirus hepatitis. Cas Lek Cesk. 1981; 120:957-960.

Lieber CS, Leo MA, Aleynik SI, et al. Alcohol Clin Exp Res. 1997; 21:375-379.

Lieber CS, De Carl LM, Mak KM, et al. Attenuation of alcohol-induced hepatic fibrosisby polyunsaturated lecithin. Hepatol. 1990; 12:1390-1398.

Little A, Levy R, Chuaqui-Kidd P, Hand D. A double-blind, placebo-controlled trial ofhigh-dose lecithin in Alzheimer's disease. J Neur Neurosurg Psych. 1985; 48:736-742.

Visco G. Polyunsaturated phosphatidylcholine in association with vitamin B complex inthe treatment of acute viral hepatitis B. results of a randomized double-blind clinicalstudy. Clin Ter. 1985; 114:183-188.

Wurtman RJ, Hefti F, Melamed E. Precursor control of neurotransmitter synthesis.Pharmac Rev. 1981; 32:315-335.

Wurtman RJ, Hirsch MJ, Growdon JH. Lecithin consumption raises serum-free-cholinelevels. Lancet. 1977; 2(8028):68-69.

TOXINS

Now that we have the utilities turned on, we are ready to start cleaning. Over time,several undesirable things are likely to be present. There are likely to be bacteria, fungus,roaches, spiders, ants, mice, termites, etc. present. These things must be removed for usto live happily in our remodeled home.

We live in a toxic society. We have been in the process of poisoning ourselves to deathfor years. We have been lead to believe that scientists know everything and that thegovernment agencies would not allow companies to do anything that will harm us. Therecent episodes of Vioxx, Bextra, NutraSweet and many others show us that isn’t true.We used DDT as a pesticide for years until finally it killed most of our eagles bypoisoning the fish they eat. Now we have a new syndrome where harmless amoebae inour lakes and rivers have turned into meat-eating pathogens that cause chronic fatiguebecause the apple, orange, and tobacco farmers are using pesticides that kill the algae thatthe amoebae used for a food supply. When aspartame (NutraSweet) was first tested, itwas given to seven monkeys. One died and five had seizures. When given to mice, over40% developed brain tumors. Still the government now allows it to be put into most ofour food. MSG causes monkey to have holes in their brains. However, the governmentallows it to be put into children’s vitamins, seasonings, crackers, potato chips, etc. Youcannot depend on the government to protect you from things that aren’t healthy.

One of the unsuspected problems with these various toxins is that the body becomesADDICTED to them. Food manufactures know this. That is why they put knownneurotoxins like aspartame and MSG in their products. You become addicted. Thatmakes you want to use more of their product and have trouble when you try to stop using

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it. It is not likely that many of us would think about being addicted to Diet-sodas or cornchips!

Because stopping addictions is difficult and uncomfortable, you will find giving up thesetoxic things difficult. Therefore I recommend you eliminate these toxic things one at atime. Check them off the list each time you can go for a couple of weeks without cravingeach item or being tempted to eat them when others are doing so.

Here is the list. Think of these things as spiders, rodents, termites and other things youdon’t want in your house:

1. All forms of tobacco.2. All artificial sweeteners. That includes aspartame (NutraSweet, Equal), Splenda,

Saccharine, sorbitol, mannitol, etc. Use Stevia if you must have a sweetener. Gothrough your pantry and throw out anything that contains any artificialsweeteners.

3. Mono Sodium Glutamate (MSG). Go through your pantry and throw out anythingthat contains MSG. Don’t forget to look at vitamins, spices, etc.

4. Trans Fats. Look for “hydrogenated” or “partially hydrogenated” oil or “CanolaOil” on the label. Try not to eat in restaurants that use Trans fats. Use real butterinstead of margarine.

5. Drink raw whole milk instead of 2% or skim milk. You should know thatheating milk to pasteurize it changes its proteins to toxic ones. Homogenization isaccomplished by forcing the milk through nozzles under pressure. That fracturesthe fats into abnormal small chains that are water soluble. These are often toxic.That is why so many people have trouble with milk products. Unfortunately, onlyCalifornia allows raw milk to be sold, so you will have to have it shipped to youunless you own an interest in your own cow. In many states you can join a clubso you can get raw milk that isn’t pasteurized or homogenized.

6. Sugar. Processed sugar has been separated from the minerals that make it lessharmful. In addition, it causes the release of an enzyme that destroys cells(phospholipase A2, PLA2)

7. Toothpaste. Just read the label on any major brand toothpaste or mouthwash.You'll see they are loaded with dangerous toxins and chemicals such as sodiumfluoride, triclosan, FD&C Blue Dye #1 and 2, sodium lauryl sulfate, and hydratedsilica. All of these common ingredients have been found to be harmful to humans.That is why your toothpaste tube has a poison warning on it! Instead, use 2/3baking soda and 1/3 sea salt. http://www.oramd.com/hiddendangers.htm If you don’t like thebaking soda, use essential oils, e.g., Shine.

8. Aluminum. You will find it in white flour and Extra-dry antiperspirants. Stopusing aluminum cookware, aluminum foil, and drinking from aluminum cans.

9. Copper. Copper toxicity is a problem from exhaust fumes, tap water (copperpipes), pesticides, etc. Copper blocks zinc, a critical element in over 350metabolic processes.

10. Antiperspirants that contain aluminum, polyethylene glycol, or propylene glycol.Ethylene glycol and propylene glycol are clear liquids used in antifreeze anddeicing solutions. Exposure to large amounts of ethylene glycol can damage the

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kidneys, heart, and nervous system. Use a deodorant instead of an antiperspirant.An example is Roll.

11. Coffee. Even decaffeinated coffee blocks zincdepression.12. Tea. Same as coffee.13. Alcohol. Same as coffee.

Deodorants vs. Antiperspirants

Most people think that antiperspirants and deodorants are the same thing, but they aren’t.Antiperspirants work by clogging, closing, or blocking the pores with powerfulastringents such as aluminum salts so that they can’t release sweat. (Note that aluminumcan accumulate in the brain.) Deodorants work by neutralizing the smell of the sweat andby antiseptic action against bacteria. Deodorants are preferable because they don’tinterfere with sweating, a natural cooling and detoxifying process.

Baking Soda Simple Solution

Baking soda works wonders because it neutralizes the odor of sweat. Just sprinkle a lightcovering of baking soda onto a damp washcloth. Pat on. Don’t rinse. This tip—just usingbaking soda—has saved me on many occasions, especially when traveling.

Basic Deodorant Powder

1/2 cup baking soda1/2 cup cornstarcha few drops essential oils such as lavender or cinnamon

Place the ingredients in a glass jar. Shake to blend. Sprinkle a light covering of thepowder on a damp washcloth. Pat on. Don’t rinse.

Basic Liquid Deodorant

1/4 cup each witch hazel extract, aloe vera gel, and mineral water1 teaspoon vegetable glycerina few drops antibacterial essential oils such as lavender (optional)

Combine the ingredients in a spray bottle. Shake to blend.Makes 3/4 cupShelf Life: Indefinite

http://www.care2.com/channels/solutions/consumer_guides/114

If you don’t want to make your own deodorant, use ROLL Natural Organic QuenchScented Deodorant and ROCK by Forever Green.

As your liver gets sicker, the immune system becomes weaker. There are always over1,000 types of pathogenic organisms in your body just waiting to eat you when youimmune system fails. These infectious organisms feed on carbohydrates and must have

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an acidic medium (voltage deficient). Thus if your liver is so sick you get nauseatedwhen you eat fat, you will need to avoid feeding these infections by avoidingcarbohydrates until you can get your liver/immune system working again.

If you are so sick you are disabled, you will need to avoid other possible sources ofincreased toxins that you body will not be able to manage. In addition you will need toavoid carbohydrates (increase destruction of cells). The Intense Detoxification Dietincludes the following and must be followed for two months if you are disabled by yourillness. If you eat in restaurants, eat ½ the amount of these items you might otherwiseeat:

REMOVE THESE FROM THE DIET IF YOU ARE DISABLED BY YOUR ILLNESSAND/OR YOU GET NAUSEATED WHEN YOU EAT FAT:

1. No grains2. No pasta3. No starchy vegetables (potato, carrot, parsnip, beet, radish, peas, corn)4. No fruit or fruit juice5. No beans6. No corn syrup, dextrose, sucrose, honey, sugar, maltodextrin.7. No fast foods8. No carbonated drinks9. No artificial sweeteners.10. No hydrogenated oils.11. No MSG12. No Canola oil or mayonnaise13. No peanuts or peanut butter14. No mustard. Mustard seeds contain goitrogens, naturally occurring substances in

certain foods that can interfere with the functioning of the thyroid gland.Individuals with already existing and untreated thyroid problems may want toavoid mustard seeds for this reason. Cooking may help to inactivate thegoitrogenic compounds found in food. However, it is not clear from the researchexactly what percent of goitrogenic compounds get inactivated by cooking, orexactly how much risk is involved with the consumption of mustard seeds byindividuals with pre-existing and untreated thyroid problems.http://www.whfoods.com/genpage.php?tname=foodspice&dbid=106

15. No spinach. Spinach contains oxalic acid. Oxalic acid is corrosive to tissue.When ingested, oxalic acid removes calcium from the blood. Kidney damage canbe expected as the calcium is removed from the blood in the form of calciumoxalate. The calcium oxalate then obstructs the kidney tubules. Persons with pre-existing skin disorders or eye problems, or impaired kidney or respiratoryfunction may be more susceptible to the effects of the substance.

16. No cashews. See corn.17.Absolutely No Corn (Aflatoxicosis is poisoning that results from ingestion of

aflatoxins in contaminated food or feed. The aflatoxins are a group of structurallyrelated toxic compounds produced by certain strains of the fungi Aspergillusflavus and A. parasiticus. Aflatoxins produce acute necrosis, cirrhosis, andcarcinoma of the liver in a number of animal species; no animal species isresistant to the acute toxic effects of aflatoxins; hence it is logical to assume that

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humans may be similarly affected. In the United States, aflatoxins have beenidentified in corn and corn products, peanuts and peanut products, cottonseed,milk, and tree nuts such as Brazil nuts, pecans, pistachio nuts, and walnuts. Othergrains and nuts are susceptible but less prone to contamination.http://www.cfsan.fda.gov/~mow/chap41.html

18.Cleaning Up the Pests

In our house analogy, it is likely that the rats have built a nest in our old home. Therewill be spider webs, ants, mice, crickets, termites etc. These pests will damage ourhome and steal our food if we don’t get rid of them. So it is with our body. Heavymetals in our tissues and biotoxins (chemicals that damage our cells) will haveconcentrated in our liver and gall bladder because those organs try to remove thesepests from our body---often unsuccessfully. Most of these toxic things are fat-soluble (dissolved in the fat of our bodies). This is particularly true of our cellmembranes and our brain, endocrine glands and liver. Since they are fat-soluble, they tend to get stored and concentrated in our liver and gall bladder.Bacteria, viruses and fungi then tend to grow in our gall bladder and produce moretoxins. In this manner, our liver and gall bladder become a “rat’s nest” that must becleaned out for us to start feeling better.

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GALL BLADDER

There are many misconceptions about the gall bladder. Note the following facts:

1. The gall bladder is a very important organ---not something to be disposedof if it annoys you. The same symptoms of pain, bloating and heartburnoccur in 50-100% after you have had your gall bladder removed as before.More than 500,000 North Americans have their gall bladder removedevery year.

2. The liver makes 1 ½ quarts of bile per day to digest fats. Since the livercan’t make bile fast enough to digest a fatty meal, the gall bladder isnecessary to store bile. Without the gall bladder, you can’t do a good jobof digesting fats. Since every cell membrane in the body is made of fat, ifyou can’t digest the fats, you can’t repair your cells (heal) without help.

3. Forty percent of Americans have abdominal pain, bloating, loose stools,and symptoms often thought to be from the stomach (heartburn due to gaspushing stomach acid into esophagus), fever and chills, nausea andvomiting, and yellowing of the skin----all due to gall bladder malfunction.

4. The most likely people to make gallstones are Fair complexion, Female,Fat, Fertile (previous pregnancies), and over Forty (the Five F’s).

5. Gall stones are more common in people who eat a low fat diet, obesity,take oral contraceptives, take calcium, estrogen, antibiotics, and non-steroidal anti-inflammatory drugs.

To help clean the gall bladder, you will take:

1. Taurine is an amino acid needed to make bile. You will need to take 1000mg. /day. In studies, 100% of those taurine-deficient developed gallstones. Inthose given taurine supplements, the formation of gallstones dropped to zero.

2. Vitamin C: Take 2000 mg. /day.

You should plan on taking vitamin C long term.

If you have had your gallbladder removed, you will need to take Bile Salts (Ox Bile) 500mg. each time you eat. You can use Digestabs = contain bile and digestive enzymes.

You will be given an appointment for us to begin the process of cleaning yourgallbladder. Attempting to do it on your own using herbal remedies, lemonade, etc. willoften give you significant pain.

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LIVER CLEANUP:

The liver, the largest solid organ, is the body’s detoxification center and a vast center formetabolic activity including:

1.Lipid/carbohydrate/protein metabolism2.Blood synthesis3.Bilirubin metabolism4.Urea cycle5.Ammonia detoxification6.Biliary processes7.Bile and cholesterol synthesis8.Oxidative energy metabolism9.Hormone metabolism10. Immune function (Kupffer cells)11. Clearance of drugs (pharmaceuticals)12. Processing of nutrients, toxins, and bile acids from the intestine.

The liver’s detoxification processes has three distinct phases. The purpose is to changefat-soluble toxins into water-soluble products that can be excreted from the body.Conversion of cholesterol into bile is a primary process in the elimination of wastes.Thus a high cholesterol is a symptom of the liver attempting to clear toxins from the bodyand should not be interrupted with anti-cholesterol drug therapy:

Phase I: polarity is increased by a process called oxidation or hydroxylation usingenzymes called PP450 oxidases. It requires oxygen as toxins are burned or oxidized.Elevation of very long chained fatty acids is indicative of interruption of Phase I.

Phase II: toxins are made more water-soluble using oxidation, reduction, hydrolysis,dehalogenation, methylation, sulfation, glucuronidation, peptide conjugation, acetylation,and glutathione conjugation.

Phase III: toxins ported from cells for removal via gallbladder and kidneys.

When detoxification is occurring, nitrogen may be retained involving albumin, uric acid,BUN or Creatinine. Ammonia levels rise due to impaired ability to convert ammoniainto urea. Oral butyrate therapy addresses both control of nitrogen in states of increasedblood ammonia and interruption of abnormal lipid metabolism. It also clears what arecalled “renegade fats” from the liver.

To accomplish this cleanup, you will be given instructions in our office:

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REBUILDING

BEFORE

With our old house, now that we have the water,large intestine, Biomodulator therapy) and haveliver cleanse), we are ready to start rebuilding ourotten boards and replacing broken windows, los

The “brain” of every cell is the cell membrane.environment, communicate with other cells, alloto exit the cell, store voltage for the needs of themade primarily of fatty acids called phospholipifat-soluble, they are stored in the cell membranefunction of the cell.

If you eat Trans Fats (nearly plastic), your cellsplastic. You must stop eating them and then conof your cells with membranes that work. Cells nSome cells replace themselves every 48 hours anevery eight months. Thus it will take up to eigh

Phosphatidylcholine (PC): This is the most abmembrane and protects the liver’s 33,000 squareliver against damage from alcohol, pharmaceuticdue to viral, bacterial and fungal infections (Liebintravenously but can also be given orally. If youse both IV and oral until you are better and thenor at least functional. Generally speaking, disabinjections of PC. They are usually given daily fotolerate oral fats. The liver cells are completelyis replaced every six weeks. Nerve cells take mo

From Extreme Home Makeover

AFTER

sewage, electricity on (pure water,cleaned up the pests (gall bladder andr old house. We start removingt shingles, etc.

Cell membranes interact with thew nutrients to enter the cell and wastecell, etc. Every cell membrane is

ds. Since most toxins in the body ares. These toxins interfere with the

function as if they were made ofsume good fats so you can replace allormally die and replace themselves.d some cells only replace themselves

t months to rebuild yourself.

undant phospholipid (fat) of the cellmeters of membrane. It protects theals, pollutants, drugs and infectionser). PC is most effective when givenu are disabled, you may choose to

continue with oral until you are wellled people will require 5-40 IVr at least a week and until you canreplaced every two months. The skinnths to be replaced. The capsules are

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taken for 6-12 months.

Heavy Metals

Many people have accumulated heavy metals like mercury (silver fillings, seafood),lead (paint, gasoline), cadmium (auto exhaust, zinc-depleted soil), etc. These metalsalso accumulate in cell membranes and short-out the systems. One molecule ofmercury can inhibit 2000 molecules of zinc! The way to determine if you have heavymetal poisoning is with a hair test since only 1-5% remains in the blood and the rest isin your tissue. If you have heavy metals in your system, we can give you a liquid thatcontain both phosphatidylcholine and EDTA, a material that will slowly release themetals from the cells. This is called DetoxMax Plus. We also use a light (CollinsLight) that provides missing electrons to help the metals release from the cells and aninfrared sauna to help release the metals from the cells.

Proteins

An essential amino acid for an organism is an amino acid that cannot be synthesized bythe organism from other available resources, and therefore must be supplied as part of itsdiet.

Eight amino acids are generally regarded as essential for humans: tryptophan, lysine,methionine, phenylalanine (or tyrosine), threonine, valine, leucine, isoleucine. Twoothers, histidine and arginine are essential only in children. http://en.wikipedia.org/wiki/Essential_amino_acid

Two of the essential amino acids, lysine and tryptophan, are poorly represented in mostplant proteins. Thus strict vegetarians should ensure that their diet contains sufficientamounts of these two amino acids. Without tryptophan, you will become severelydepressed. The symptoms of lysine deficiency include anemia, enzyme disorders, lack ofenergy, hair loss, bloodshot eyes, weight loss and retarded growth as well as reproductiveproblems, poor appetite and poor concentration.

EGGS

Eggs are one of nature's most nutritious foods. One large egg contains only 70 caloriesand an incredible amount of nutrition. An egg is one of the few foods that containeverything necessary for life. The other is plankton.

Lutein and zeaxanthin are important for maintaining good vision. Studies have shownthat these antioxidants help prevent age-related macular degeneration-the leading causeof blindness in people over 65, and help decrease the risk of cataracts. According to theAmerican Heart Association, lutein also protects against the progress of early heartdisease. A great source of these is Wolf Berries.

Recognized as an essential nutrient, choline has been shown to play a strong role in braindevelopment and function. One egg provides half your daily requirement of choline.

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Protein is essential for building and repairing body tissue. Muscles, organs, skin, hair aswell as antibodies, enzymes, and hormones are all made from protein.

Protein is composed of 20 different amino acids. There are 8 essential amino acids thatthe body cannot make, and so they must come from foods. Eggs are one of the few foodsconsidered to be a complete protein because they provide all eight essential amino acids.You should eat 2-4 eggs per day.

Some worry about cholesterol. As noted above, the liver makes cholesterol when it istrying to clean itself of toxins. Thus the relationship of heart disease to cholesterol issimply the presence of toxins that cause inflammation. It is well known thatmeasurements of inflammation (like C-reactive Protein) is much more related to heartattacks and strokes than cholesterol.

Ansel Keyes who first proposed that there might be a relationship between cholesteroland heart disease has often said that there is no relationship between what you eat andyour blood cholesterol levels unless you are a rabbit or a rat. If you eat a diet that has nocholesterol in it, your blood cholesterol won’t change 5%. If you eat buckets ofcholesterol, your blood cholesterol won’t change 5%. Thus the idea that you shouldavoid eating eggs, whole raw milk, fatty meats, etc. is pure nonsense and was proposedprimarily to sell cholesterol-lowering drugs. Restricting these fat sources in children isparticularly harmful since their brain (mostly fat) is developing and needs enormousamounts of fat to develop normally.

Seventeen percent (17%) of the normal cell membrane is a fat called Arachidonic acid.The primary source of that is eggs. If you don’t eat eggs, it is hard to make good cellmembranes = you will be sick because you don’t have normal cells. There is novegetarian source of Arachidonic acid, so it is very difficult for total vegetarians to behealthy.

Remember that eating good fats doesn’t make you fat! It makes you healthy. EatingTrans fats (almost plastic) makes you fat because “plastic” cell membranes won’t reactcorrectly to insulin. In an effort to get glucose into your plastic cells, the body makesmore and more insulin (we call that insulin-resistant). Insulin locks fat inside of fat cells

and it cannot be used as long as insulin ispresent. Thus eating more and more Trans fatsmakes us obese and diabetic because our cellsare “plastic”. Thus-----eat eggs along withother fats to get the proteins and fats you needto make neurochemicals and good cells.

You want free-range eggs, not eggs fromchickens not allowed to move and fed 24 hoursa day until they can no longer produce.

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Juicing for Those Who are Disabled

If you are disabled (for example, you get nauseated when you eat fat), you need to juicevegetables. There are several reasons for this:

1. You need the nutrients available in their natural form in vegetables.2. The water available from inside the vegetables is perfect for getting inside your

cells.3. When you digest vegetables in their whole form, you have to spend energy

(voltage) to digest the fiber. Fiber is good for scraping debris from your intestine,but you don’t have the extra energy it requires to move it along your intestine. Wehave already cleaned out your intestine, so you don’t need the fiber while we aregetting you feeling better, but you do need the nutrition in the vegetables.

4. Most toxins in vegetables stick to the fiber. Getting rid of the fiber means yourfragile liver doesn’t have to deal with more toxins right now.

5. If you need fiber to keep you from having your stools too loose, we will supplythat with FiberNet. It has the added benefit of soaking up the toxins that yourbody is getting rid of.

Juicing is not chopping. Juicing means that you squeeze the juice from the vegetables sothat the juice is collected and the fiber (pulp) is removed. You cannot do this with amachine with a spinning blade. That chops the vegetables into little pieces that includethe fiber (pulp). Get a real juicer-squeezer if you don’t have one. The Omega is a highlyrated brand.

Another major issue is heating. Heat destroys many of the nutrients in your food. Blade-based blenders heat up the food. It is okay to put your juice from the juicer into a blenderto mix in the items mentioned below like nuts, protein powder, etc, but run it at very lowspeed so that heat is not a problem.

How much do I need? You will need one pound of raw vegetables per 50 pounds of bodyweight per day. Thus if you are a 200 pound man, you will need to juice four pounds ofvegetables per day. You can consume this as a meal or divide it up throughout the day.

NOTE: If you are taking anticoagulants, the Vitamin K in the vegetables maythicken your blood. Monitor your INR (coagulation test) weekly until you are sureit is okay. You may need to alter your medication dose when you start juicing andwhen you stop juicing.

Now that you're ready for the benefits of vegetable juice, you need to know what to juice.I recommend starting out with these vegetables, as they are the easiest to digest:

Celery

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Fennel (anise) Cucumbers

These aren't as beneficial as the more nutritionally intense dark green vegetables. Onceyou get used to these, you can start adding the more nutritionally valuable, but lesspalatable, vegetables into your juice.

Vegetables to avoid include carrots and beets. Most people who juice usually usecarrots. The reason they taste so good is that they are full of sugar. I would definitelyavoid all vegetables that grow underground to avoid an increase in your insulin levels.

If you are healthy, you can add about one pound of carrots or beets per week. I do believethat the deep, intense colors of these foods provide additional benefits for many that arejust not available in the green vegetables listed above.

Step 2: When you've acclimatized yourself to juicing, you can start adding thesevegetables:

Red leaf lettuce Green Leaf lettuce Romaine lettuce Endive Escarole Spinach

Step 3: After you're used to these, then go to the next step:

Cabbage Chinese Cabbage Bok Choy

An interesting side note: Cabbage juice is one of the most healing nutrients for ulcerrepair as it is a huge source of vitamin U. (Vitamin U is not a vitamin. Vitamins are essentialnutrients that cannot be synthesized (either at all or in sufficient quantities) by a given organism andtherefore must be taken with food for the organism's continued good health. The term "vitamin U" wascoined because the compound is very effective in the medical treatment of gastric ulcers. It is found in rawcabbage leaves and other green vegetables.)http://www.althealth.co.uk/services/info/supplements/vitamin_u.php

Step 4: When you're ready, move on to adding herbs to your juicing. Herbs also makewonderful combinations, and there are two that work exceptionally well:

Parsley Cilantro

You need to be cautious with cilantro, as many cannot tolerate it well. If you are new tojuicing, hold off. These are more challenging vegetables to consume, but they are highlybeneficial.

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Step 5: The last step: Only use one or two of these leaves, as they are very bitter:

Kale Collard Greens Dandelion Greens Mustard Greens (bitter)

When purchasing collard greens, find a store that sells the leaves still attached to the mainstalk. If they are cut off, the vegetable rapidly loses many of its valuable nutrients.

One important note: I prefer to juice my vegetables at room temperature.

Lesson 4: Make your juice a balanced meal.

Balance your juice with protein and fat. Vegetable juice does not have much protein orfat, so it's very important for you to include these fat and protein sources with your meal.

Use eggs. Eggs will add a significant amount of beneficial fats and protein to yourmeal. An egg has about 8 grams of protein, so you can add two to four eggs permeal. I suggest that you add the whole eggs, raw, into the vegetable pulp (not thejuicer). The reason I advocate this is because once you heat the eggs, many oftheir nutrients become damaged. If you are concerned about salmonella, purchaseorganic eggs; it's unlikely you'll have any problems. Additionally, if you are notsensitive to milk, you can add some raw milk cheese, as it will improve the flavor.

There is a potential problem with using the entire raw egg if you are pregnant.Biotin deficiency, a common concern in pregnancy, could be made worse byconsuming whole raw eggs.

Incorporate seeds. Raw seeds, freshly ground and alternated regularly, areanother great addition to the pulp. The simplest way to grind the seeds is to use aninexpensive coffee grinder. The seeds are full of protein and essential fatty acidsthat bring a juice into balance beautifully. I recommend pumpkin and flax seeds.

Use chlorella. Chlorella is an incredibly powerful nutrient from the sea and is aform of algae. It can be helpful for mercury detoxification as it binds verystrongly to mercury to eliminate it from the body. The normal dose is oneteaspoon in the juice. However, about 30 percent of people cannot tolerate thechlorella, so if it makes you nauseous you should definitely avoid it.

o Is a useful source of chlorophyll.o Adds magnesium and protein.o Binds to heavy metals and pesticides.

If you have high iron or vitamin D levels you will want to avoid chlorella thoughas it is loaded with both of these nutrients.

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Consider a protein powder. While protein powders are convenient, I believethem to be far inferior to whole food choices like eggs or chlorella. Glutamine isan amino acid and the majority of our skeletal muscle is made of it. You canobtain glutamine powder and add one teaspoon into your drink for a veryeffective healing addition. You can also use protein powders. Some people areconcerned about my milk avoidance suggestion and taking whey protein.Although whey protein is from milk, most people tolerate it quite well as themajor protein in milk that causes an allergy is casein. I would strongly adviseagainst the use of soy protein powders. I recommend THUNDER from ForeverGreen. (JLT)

Add some garlic. Don't worry; this won't give you "dragon breath." I like to addone to two cloves of garlic in my juice, as it incorporates the incredible healingpotential of fresh garlic. I strongly advise you to do this regularly to balance outyour bowel flora. The ideal dose is just below the social threshold where peoplestart to notice that you have eaten garlic. One large clove, two medium cloves orthree small cloves is the recommended dose.

Add oil. You can add the BodyBio oil to your juice mixture if you prefer to take itthis way. (JLT)

Lesson 5: Make your juice taste great.

If you would like to make your juice taste a bit more palatable, especially in thebeginning, you can add these elements:

Coconut: This is one of my favorites! You can purchase the whole coconut or useshredded coconut. It adds a delightful flavor and is an excellent source of fat tobalance the meal. Coconut has medium chain triglycerides, which have manyhealth benefits.

Cranberries: You can also add some cranberries if you enjoy them. Researchershave discovered that cranberries have five times the antioxidant content ofbroccoli, which means they may protect against cancer, stroke and heart disease.In addition, they are chock full of phytonutrients and help many women avoidurinary tract infections. Limit the cranberries to about 4 ounces per pint of juice.

Lemons: You can also add half a lemon (leaving much of the white rind on). Ifyou are a protein metabolic type you will not want to use lemons as they will pushyour pH in the wrong direction.

Fresh ginger: This is an excellent addition if you can tolerate it. It gives yourjuice a little "kick"

24 carat Chocolate: Dark chocolate has more antioxidants than any other foodtested with perhaps the exception of Wolf Berries (Lycium barbarum). Thischocolate from Forever Green does not contain wax, fillers, caffeine, and otheritems that give chocolate a bad reputation. You can add it to your drink. It isalready in THUNDER protein powder. (JLT)

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Wolf berries: Wolfberry contains 19 types of amino acids and 21 traceminerals. It has more beta-carotene than carrots and nearly as much Vitamin C asoranges and protein as bee pollen.

Lesson 6: Drink your vegetable juice right away, or store it very carefully.

Juicing is a time-consuming process, so you'll probably be thinking to yourself, "I wonderif I can juice first thing and then drink it later?" This isn't a great idea. Vegetable juice isvery perishable so it's best to drink all of your juice immediately. However, if you'recareful you can store it for up to 24 hours with only moderate nutritional decline. To storeyour juice:

1. Put your juice in a glass jar with an airtight lid and fill it to the very top. There shouldbe a minimum amount of air in the jar as the oxygen in air (air is about 20 percentoxygen) will "oxidize" and damage the juice.

2. Wrap the jar with aluminum foil to block out all light. Light damages the juice.

3. Store it in the refrigerator until about 30 minutes prior to drinking, as vegetable juiceshould be consumed at room temperature.

Most people juice in the morning, but if that does not work out well for your scheduleplease feel the freedom to choose whatever meal works out best for your lifestyle.

Lesson 7: Clean your juicer properly.

We all know that if a juicer takes longer than 10 minutes to clean, we'll find excuses notto do it. I find that using an old toothbrush works well to clean any metal grater. For theOmega 8003, the whole process takes about 5 minutes. Whatever you do, you need toclean your juicer immediately after you juice to prevent any remnants fromcontaminating the juicer with mold growth.

Warning: Don't follow the juicing recommendations that come with the juicer, as theymost often emphasize carrot and fruit combinations.

http://www.mercola.com/nutritionplan/juicing.htm#

Vitamin B12

According to John V. Dommisse, MD, an expert in vitamin B12 (cyanocobalamin)deficiency and therapy, the psychiatric conditions most associated with vitamin B12deficiency include toxic brain syndrome, paranoia, violence and depression. There is awell documented association between B12 deficiency and dementia. In an article entitled"Subtle Vitamin B12 Deficiency in Psychiatry: A Largely Unnoticed But DevastatingRelationship?" published in Medical Hypotheses, 2 Domisse expresses the opinion thatmost cases of so-called "Alzheimer's dementia" ("idiopathic dementia") are actually casesof B12 deficiency. According to Domisse, B12 deficiency can cause depression and even,

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in certain cases, bipolar-1 disorder (manic-depressive illness) and, more commonly,bipolar-2 disorder (cyclothymic personality).

Says Domisse: "The third most common psychiatric manifestation of this deficiency isviolent behavior, yet how often is this deficiency ever sought or treated in criminal casesof violent behavior? I have witnessed numerous cases of rage attacks, temper outbursts,domestic violence, etc., where the violence ceased after the patient's B12 deficiency wasdiagnosed and properly treated."

The fourth and last major psychiatric effect of this deficiency is paranoid ideation andeven paranoid psychosis (but not schizophrenia).

Fatigue is another symptom of vitamin B12 deficiency but the medical community hasbeen slow to recognize the connection. "Even after major articles, like that ofLindenbaum in the New England Journal of Medicine in 1988," says Domisse, "fatigue isstill not recognized as a prominent feature of B12 deficiency syndrome. Peripheralneuropathy is another non-psychiatric condition that can result from this and other Bvitamin deficiencies. However, by the time the deficiency is recognized (serum levelbelow 200 pg/ml), just as in the case of the dementia, the neuropathy may well havebecome irreversible. Then the treating physician will say, 'See, B12 treatment does notreverse dementia (or neuropathy)!'"

A major point by this author is that the range used to establish serum vitamin B12deficiency in conventional medicine (less than 200 to 400 pg/ml) is far too low. Whenperipheral neuropathy occurs in this range, it is often permanent. The author suggests that1,000 to 2,000 pg/ml may be the optimal range. The hydroxy- and methyl- forms ofvitamin B12 are generally recommended. Cyanocobalamin at high doses has never beenshown to be toxic. Oral doses of 1,000 to 5,000 ug daily have been used in cases ofpernicious anemia to maintain these patients' vitamin B12 levels. Oral doses of 1,000 to2,500 ug after both breakfast and supper seem the best way to maintain very high levelsof serum vitamin B12 .

Any child with violent tendencies, especially when accompanied by fatigue andneuropathy, should be tested for vitamin B12 deficiency. An acute condition can betreated with oral supplements or vitamin B12 injections. In the long term, the bestprotection is a diet rich in animal foods.

http://www.westonaprice.org/children/childviolence.html

Symptoms of B12 deficiency include:

Anemia B12Brown spots over joints B12Bursitis B12Dementia B12Depression B12Diarrhea B12Dizziness B12

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Irritability B12Mood swings B12Nausea B12Negative thinking B12Pale smooth tongue B12Paranoia B12Poor Memory B12Psychosis B12Restlessness B12Schizophrenia B12Sore tongue B12Temper outbursts B12Tingling B12Violence B12Weakness B12

Replacing Your Cells = A Completely New You

The process of rebuilding a new and healthy you is based in the fact that your body isconstantly replacing itself. You get new retinal elements every two days. You get anentirely new skin every six weeks. You get a new liver every eight weeks. It takesmonths to get new nerve cells. As each new cell is built, the process looks for the properbuilding materials. If all it finds is “plastic” Trans fats, it uses them to build the new cellmembranes. Remember the cell membrane is the “brain” of the cell and determineswhether that is a healthy or sick cell. That membrane is almost completely fat. The“manufacturing” part of the cell is the cytoplasm. It is almost entirely protein.

We have to supply your body with good fats and good proteins so it can make good newcells. If you keep doing what you are doing as far as nutrition is concerned, you willkeep making the same quality of cells you have been making. If you are sick, thatobviously isn’t very good. DOING MORE OF WHAT ISN’T WORKING DOESN’TMAKE IT WORK BETTER.

If your digestion is working well enough to absorb good fats and proteins, you will beable to make good new cells. We have started by cleaning up your digestion organs andproviding the voltage to get things working again. Now we are going to give you the fatsyou need to start making good cells. You will be given a list of things to provide yourbody with the materials you need to start rebuilding.

One issue is whether your digestive system is working well enough to get the fats fromyour mouth to your cells so they can make new ones. One can give them intravenouslyso that we know the fats will get to the cells that are making new ones. In addition, wecan give glutathione, a material that helps the cells use antioxidants to clean up toxicthings called free radicals.

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Experience shows that getting the digestive system working well enough to absorb fats isdifficult because it needs to make new cells so it can work. If the digestive system can’tfunction well enough to supply the fats needed to rebuild itself, we will have to give thefats intravenously until it can rebuild.

If the digestive system is working, we can give the necessary fats orally.

Remember that fats and proteins require vitamins and minerals to work, so replacingthem is also important.

We will help you decide if you need intravenous therapy for awhile or if oral will work.In either case, you will need two months of intensive work to build you a new liver andthen several months to finish building the new you from top to bottom.

As you can see, there is no magic bullet to cure you in a flash. The only way for you tobe healthy is to build a new body with good materials. I can’t control what you put intoyour mouth----thus the result you will experience is mostly determined by your choices.Those of us in our clinic will guide you, but only you can heal yourself.

We look forward to watching for the new you as you rebuild yourself into renewedhealth.

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BIBLIOGRAPHYAbbott, B.C., Hill, A.V., and Howarth, J. V. (1958). The positive and negative heat production associated with a si ngle impulse. Proc. Roy. Soc.B. 148: 149-187.Aggeli, A., Bell, M., Boden, N., Keen, ]. N., Knowles, P. P., McLeish, T. C. B., Pitkeathly, M., and Radford, S. E. (1997). Responsive gels formedby the spontaneous self-assembly of peptides into polymeric beta-sheet tapes. Nature 386: 259-262.Alberts, B., Bray, D., -Lewis, ]., Raff, M., Roberts, K., and Watson, ]. D. (1994). Molecular Biology of the Cell, Third edition, Garland, N. Y.Alberts, B., Bray, D., Lewis, ]., Raff, M., Roberts, K., and Watson, ]. D. (1989). Molecular Biology of the Cell, Second edition, Garland, N. Y.Alberts, B., Bray, D., Lewis, )., Raff, M., Roberts, K., and Watson, ]. D. (1983). Molecular Biology of the Cell, First edition, Garland, N. Y.Albin, G., Horbett, T. A., and Ratner, B. D. (1985). Glucose sensitive membranes for controlled delivery of insulin: insulin transport studies. /.Contr. Rel. 2: 153-164.Albrecht-Buehler, G. (1980). Autonomous movements of cytoplas -mic fragments. Proc. Nat'1. Acad. Sci. 77(11): 6139-6643.Albrecht-Buehler, G. (1985). Is the cytoplasm intelligent too? Cell Motil. and Cytoskd. 6: 1 -21.Albrecht-Buehler, G. (1998). Altered drug resisrance of microrubules in cells exposed to infrared light pulses: Are microrubules the "nerves" ofcells? Cell Motil. and Cytoskel. 40:183-192.Albrecht-Buehler, G., and Bushnell, A. (1982). Reversible compres sion of the cytoplasm. Exf. Cell Res. 140:173-189.Alien, R. D., Cooledge, ]. W., and Hall, P. ]. (1960). Streaming in cytoplasm dissociated from the giant amoeba, chaos chaos. Nature 187: 896-899.Almdal, 1C, Dyre, ]., Hvidt, S., and Kramer, O. (1993). Towards a phenomenological definition of the term'gel.' Polym. Gels and Ntwks. 1: 5-17.Alonso, A., Nunez-Fernandez, M., Beltramo, D. M., Casale, C. H., and Barra, H. S. (1998). Na, K-ATPase was found to be the membranecomponent responsible for the hydrophobic behavior of the brain membrane tubulin. Biochem. Biophys. Res. Commun. 253: 824-827.Anisimova, V. I., Deryagin, B. V., Ershova, I. G., Lychnikov, Y. I., Simonova, V. K., and Churaev, N. V. (1967). Preperation of structuarallymodified water in quartz capillaries. Russ. J. Phys. Chem. 41: 1282-1284.Annaka, M., andTanaka, T. (1992). Multiple phases of polymer gels. Nature 355: 430-432.Asakura, A., Taniguchi, M., and Oosawa, F. (1963). Mechano-chemi-cal behavior of F-actin. /. Mol. Biol. 7: 55- 63.Ault, ]. G., Demarco, A. J., Salmon, E. D., and Rieder, C. L. (1991). Studies on the ejection properties of asters: astral microtubule turnoverinfluences the osciliatoty behavior and positioning of mono -oriented chromosomes. /. Cell Sci. 99:701-710.BBartels, E. M., and Elliott, G. F. (1985). Donnan potentials from the A- and I-bands of glycerinated and chemically skinned muscles, relaxed andin rigor. Biophys. J.48: 61-76.Bausch, A. R., Mbller, A., and Sackmann, E. (1999). Measurement of local viscoelasticity and forces in living cells by magnetic tweezers. Biophys.J. 76: 573-579.Beall, P. T. (1980). Water-macromelecular interactions during the cell cycle. Nuclear-cytolasmic Interactions in the Cell Cycle, ed. G. Whitson,Acad. Press, NY.Beall, P. T., Brinkiey, B. R., Chang, D. C., and Hazlewood, C. R (1982). Microtubule complexes correlated with growth rate and wa ter protonrelaxation times in human breastcancer cells. Cancer Res, 42: 4124-4130.Bernal, J. D. (1961). Origin of life on the shores of the ocean. Oceanography, ed. M. Sears. AAAS. 67:95-118.Berridge, M. J. (1994). The biology and medicine of calcium signaling. Mol. Cell. Endicrinol. 98: 119-124.Bi, G.-Q., Alderton, ]. M., and Steinhardt, R. A. (1995). Calcium-regulated exocytosis is required for cell membrane resealing. /. Cell Biol. 131:1747-1758.Bingley, M. S. (1966). Furthet investigations into membrane potentials in amoebae. Exf. Cell Res. 43: 1-12.Block, S. M. (1996). Fifty ways to love your lever: myosin motors. Cell 87: 151-157.Bloodgood, R. A.(1977). Motility occurring in association with the surface of the Chlamydomonas flagellum. /. Cell BioL 75: 983-989.Bloodgood, R. A. (1978). Unidirectional motility occurring in association with the axopodial membrane of Echinosphaerium nucleophilum.CellBiol. Int. Rep. 2: 171-176.Bloodgood, R. A., Leffler, E. M., and Bojczuk, A. T. (1979). Reversible inhibition of Chlamydomonas flagellar surface motility. / CellBiol. 82: 664-674.Blyakhman, R, Shklyat, T., and Pollack, G. H. (1999). Quantal length changes in single contracting sarcomeres. /. Muscle Res. Cell Mitol.20: 529-538.Boyle, P. J., and Conway, E. J. (1941). Potassium accumulation in muscle and associated changes. /. Physiol. 100: 1-63.Brandt , P. W., Diamond, M. S., and Schachat, F. H. (1984). The thin filament of vertebrate skeletal muscle co-operatively activates as aunit. /. Mo 1. Biol. 180: 379-384.Bratton, C. B., Hopkins, A. L., and Weinberg, J. W. (1965). Nuclear magnetic resonance studies of living muscle. Science 147: 738- 739.Bray, D. (1992). Cell Movements, Garland, NY.Brooks, S. C. (1940). The intake of radioactive isotopes by living cells. Cold Spring Harbor Symp. Quant. Biol. 8: 171-180.Brummer, S. B., Bradspies, J. I., Entine, G., Leung, C., and Lingertat, H. (1972). Polywater, an organic contaminant. / Phys. Chem. 76:457-458.Bungenberg de Jong, H. (1932). Die Koazervation und ihre Bedeutung fiir die Biologic. Protoplasma 15: 110-173.Buxbaum, R. E., Dennerll, T, Weiss, S., and Heidemann, S. R. (1987). F-actin and microtubule suspensions as indeterminate fluids. Sci-ence235: 1511-1514.CCameron, I. E. (1988) . Ult ra s t ruc tu ra l observations on the transectioned end of ftog skeletal muscles. Physiol. Chem. Phys. Med.NMR. 20:221-225.Cameron, E E. , Kanal, K. M., Keener, C. R., and Ftillerton, G. D. (1997). A mechanistic view of the non- ideal osmotic and motionalbehavior of intracellular water. Cell Biol. Int'l. 21(2): 99-1 13.Cameron, I. E. Cook, K. R., Edwards, D., Fullerton, G. D., Schatten, G., Schatten, H., Zimmerman, A. M., and Zimmerman, S. (1987)./. Cell. Physiol. 133: 14-24.Cameron, I. E., Cook, K. R., Edwards, D., Fullerton, G.D., Schatten, G., Schatten, H., Zimmerman, A. M., and Zimmerman, S. (1997).Cell cycle changes in watet p ropert ies in sea utchin eggs. J. Cell Physiol. 133(1): 99-113.

Cameron, E E.,Fullerton, G. D., and Smith, N. K. R. (1988). Influence of cytomatrix proteins on water and on ions in cells.ScanningMicroscop. 2(1): 275-288.

69

Cameton, E E., Hardman, W. E., Fullerton, G. D., Miseta, A., Koszegi, T, Eudany, A., and Kellermayer, M. (1996). Maintenance of ions,proteins and water in lens fiber cells before and after treatment with non-ionic detergents. Cell Bio. Int. 20(2): 127-137.Canny, M. J. (1998). Transporting water in plants. Am. ]. Sci. 86: 152-159.Carmeliet, E. (1992). A fuzzy subsarcolemmal space for intracellular Na in cardiac cells? Cardiovasc. Res. 26: 433-442.Casademont, J., Carpenter, S., and Karpati, G. (1988). Vacuolation of muscle fibers near sarcolemmal breaks represents T tubule dilatat ionsecondaty to enhanced sodium pump activity. /. Neuropath. Exp. Neural. 47: 618-628.Challice, C. E. (1965). Studies on the microstructute of the heart. /. Roy. Microsc. Soc. 85: 1-21.Chanutin, A. and Hermann, E. (1969). The interaction of organic and inorganic phosphates with hemoglobin. Arch. Biochem. Biophys. 131:180-184.Chaudhury, M. K., and Whitesides, G. M. (1992). How to make watet run uphill. Nature 256:1539- 1541.Chen, W. T. (1981). Mechanism of retraction of the trailing edge during fibroblast movement. /. CellBiol. 90(1): 187-200.Cheng, Y.-P. (1971). The ultrastructute of the rat sino -arrial node. Acta. Anat. Nippon. 46: 339-358.Choi, D. W. (1988). Glutamate neuortoxicity and diseases of the nervous system. Neuron 1:623-34.Chou, K. C. (1992). Energy-optimized structure of antifreeze pro tein and its binding mechanism. /. Mol. Biol. 223: 509-517.Clarke, M. S. F., Caldwell, R. W., Miyake, K., and McNeil, P. E. (1995). Contraction-induced cell wounding and release of fibroblastgrowth factor in heart . Circ. Res. 76: 927-934.Clegg, J. S. (1982). Interrelationships between water and cell metabolism in Attemia cysts. IX. Evidence for organization of soluble cj-toplasmic enzymes. Cold Spring Harbor Symp. Quant. Biol. 46(Pt. 1): 23-37.Clegg, J. S. (1 984). Intracellular water and the cytomatrix: some methods of study and cutrent views. /. CellBiol. 99: 167s-171s.Clegg, J. S. (1988). On the internal environment of animal cells. Microcompartmentation, CRC Press, Boca Raton.Clegg, J. S., and Drost-Hansen, W. (1991). On the biochemistry andcell physiology of water. Biochem. and Mol. Biol. of Fishes, Vol. 1, ed. Hochachka, and Mommsen, Elsevier, N. Y.Clegg, J. S., and Jackson, S. A. (1988). Glycolysis in permeabilized L-929 cells. Biochem.]. 255:335 -344.Cohn,W. E., and Cohn, E. T. (1939). Permeability of red corpuscles of the dog to sodium ion. Proc. Soc. Exf. Biol. 41: 445-449.Collins, E. W., Jr. and Edwards, C. (1971). Role of Donnan equilibrium in the testing potentials in glycerol-extracted muscle. Am. J.Physiol. 22(4): 1130-1133.Collins, K. D. (1995). Sticky ions in biological systems. Proc. Nat'1.Acad. Sci. 92: 5553 -5557.Cooke, R. (1997). Actomyosin interaction in striated muscle. Physiol.Rev. 77(3): 671-697.Cope, F. W. (1969). Nuclear magnetic resonance evidence using D,,0 for structured water in muscle and brain. Biophys. J. 9: 303-319.Curran, M. J., and Brodwick, M. S. (1991). Ionic control of the size of the vesicle matrix of beige mouse mast cells. /. Gen. Physiol. 98:771-790.Cussler, E. E., Stokar, M. R., and Varberg, J. E. (1984). Gels as size selective exttaction solvents. AIChE Journal 30(4): 578-582.DDamadian, R. (1971). Tumor detection by nuclear magnetic resonance. Science 171: 1151-1153.Dayhoff, J., Hameroff, S., Lahoz- Beltra, R., and Swenberg, C. E. (1994). Cytoskeletal involvement in neuronal learning: a review. Eur.Biophys. J. 23: 79-93.Dean, R.(1941). Theories of electrolyte equilibrium in muscle. Biol. Symp. 3: 331-348.deBeer, E. L, Sontrop, A., Kellermayer, M. S. Z., and Pollack, G. H. (1998). Actin-filament motion in the in vitro motility assay isperiodic. CellMotil. and Cytoskel. 38: 341-350.DeDuve, C. (1995). Vital Dust, Basic Books Press, New York.Delay, M. J., Ishide, N., Jacobson, R. C., Pollack, G. H., and Tirosh, R. (1981). Stepwise sarcomere shortening: Analysis by high-speedcinemicrography. Science 213: 1523-1525.Dempster, J. A., Van Hoek, A. N., and Van Os, C. H. (1992). The quest for water channels. NIPS 7: 172-176.Derjaguin, B. V. (1966). Effects of lyophilic sutfaces on the properties of boundary liquid films. Disc. Frad. Soc. 42: 109-119.DeVries, A. L. (1982). Fish glycopeptide and peptide antifreezes: then interaction with ice and water. Biophysics of Water, ed. F. Franks,and S. Mathias, Wiley Interscience, N. Y.Discher, E. E., Mohandas, N., and Evans, E. A. (1994). Molecular maps of red cell deformation: hidden elasticity and in situ connectiv ity.Science 266: 1032-1035.Dos Remedies, C. G., and Moens, P. D. (1995). Actin and the acto-myosin intetface: a review. Biochim. Biophys. Acta. 1228(2-3): 99-124.Doyle, D. A., Cabral, J. M., Pfuetzner, R. A., Kuo, A., Gulbis, J. M., Cohen, S. E., Chait, B. T, and MacKinnon, R. (1998). Structute ofthepotassium channel: molecular basis of K conduction and selectivity. Science 280: 69-77.Draper, M. H., and Weidmann, S. (1951). Cardiac resting and action potentials recorded with an inttacellulat electrode. /. Physiol. 115:74-94.Drummond, D. R., Peckham, M., Sparrow, J., and White, D. C. (1990). Alteration in kinetics caused by mutations in actin. Nature348:440-442.Dujardin, F. (1835). Stir les pretendus estomacs des animalcules infusoires et sur une sustance appelee satcode. part 2 of "Recherchesur les organismes inferieur." Ann. De Sci. Natur, part. Zool. 2d Ser., 4.Dusek, K. and Pattetson, D. (1968). A transition in swollen polymer networks induced by intramolecular condensation. /. Polymer Sci. A-26: 1209-1216.Edelmann, L. (1978). Vizualization and x-ray microanalysis of po tassium tracers in freeze-dried and plastic embedded frog muscle.Microsc. Acta. Suppl. 2: 166-174.Edelmann, E. (1980). Preferential localized uptake of K and Cs over Na in the A -band of freeze-dried embedded muscle section: de -tection by x-ray microanalysis and laser microprobe mass analysis. Physiol. Chem. Phys. 12(6): 509-514.Edelmann, E. (1983). Electron probe x-ray microanalysis of K, Rb, Cs, and Ti in cryosections of striated muscle. Physiol. Chem. Phys.Med. NMR. 15(4): 337-344.Edelmann, E. (1988). The cell waterproblem posed by election microscopic studies of ion binding in muscle. Scanning Microsc. 2(2):851-865.Ehrenpries, S.(1967). Discussion on P. G. Waser: Receptor localization by autoradiographic techniques. Ann. N. Y. Acad. Sci. (Discussion).144: 754(1).Endo, (1972). Length dependence of activation of skinned muscle fibers by calcium. Symp. on Quant. Biol. Cold Spring Harbor, N.Y.Endo, S., Sakai, H., and Matsumoto, G. (1979). Microtubules in squid giant axon. Cell Struct. Funct. 4: 285-293.Ernst, E. (1970). Bound water in physics and biology. Acta Biochim et Biophys. Acad. Sci. Hung. 5(1): 57-69.

70

Fenn, W. O. (1953). Introduction to a symposium on the metabolism of potassium. Lancet 73: 163-166.Fenn, W. O., and Cobb, D. M. (1934). The potassium equilibrium in muscle. /. Gen. Physiol. 17:629-656.Fernandez, J. M., Villalon, M., and Verdugo, P. (1991). Reversible condensation of mast cell secretory products in vitro. Biophys. J. 59:1022-1027.Fischer, M. H., and Moore, G. (1907). On the swelling of fibrin. Am. J. Physiol. 20: 330-342.Fisher, H. F. (1964). A limiting law relating the size and shape of protein molecules to their composition. Proc. Natl. Acad. Sci. USA.51: 1285-1291.Fisher, I. R., Gamble, R. A., and Middlehurst, J. (1981). The Kelvin equation and the condensation of water. Nature 290: 575-576.Fishman, H. M., Tewari, K. P., and Stein, P. G. (1990). Injury-induced vesiculation and membrane redistribution in squid giant axon.Biochim. Biophys. Acta. 1023: 421-435.Fleischer, S.,Fleischer, B., and Stoeckenius, W. (1965). The struc-tute of whole and fragmented mitochondria after lipid depletion. Fed.Proc. 24: 296-298.Fletcher, N. H. (1970). Chemical Physics of he, Cambridge, London.Frank, H. S. and Wen, W. Y. (1957). Structural aspects of ion-solvent interaction in aqueous solutions: a suggested pictrue of waterstructure. Discuss. Faraday Soc. 24: 133-140.Frommet, M. A., and Lancet, D. (1972) Freezing and non-freezing water in cellulose acetate membranes. /. Appl. Polymer Sci. 16: 1295-1303.Fushime, K., and Verkman, A. S. (1991). Low viscosity in the aqueous domain of cell cytoplasm measured by picosecond polarizationmicrofluorimetry. /. Cell Biol. 112:719- 725.Gabriel, C., Sheppard, R. J., and Grant, E. H. (1983). Dielectric properties of ocular tissues at 37 degrees C. Phys. Med. Biol. 28(1): 43-49.Garamvolgyi, N. (1959). Kontraktion isolierter Muskelfibtillen. Acta. Physiol. Acad. Sci. Hung. 16: 139-146.

Garrigos, M., Morel, ]. E., and Garcia de la Torre, J. (1983). Rein vestigation of the shape and state of hydrationof the skeletal myosin stibfragment 1 monomer in solution. Biochem. 22: 4961-4969.

Gary-Bobo, C. M., and Lindenberg, A. B. (1969). The behavior of nonelectroytes in gelatin gels. /. Colloid andInterface Sci. 29(4): 702-709.Gershon, N. D., Porter, K. R., andTrus, B. L. (1985). The cytoplas-mic matrix: its volumes and surface area and the diffusion of mol-ecules through it. Proc. Natl Acad. Sci. USA. 82(15): 5030-5034.Ginzburg, B. Z., and Cohen, D. (1964). Calculation of internal hydrostatic pressure in gels from the distribution coefficients of non-electrolytes between gels and solutions. Trans. Faraday Soc. 60: 185-189.Glynn, I. M., and Karlish, S. J. D. (1975). The sodium pump. Ann. Rev. Physiol. 37:13-55.Gomez, A. M., Kerfant, B. G., and Vassort, G. (2000). Mictotubule disruption modulates Ca2 signaling in rat cardiac myocytes. Circ.Res.86: 30-36.Goodsell, D. S. (1991). Inside a living cell. Trends Biochem. Sci. 16(6): 206-210.Graham. T. (1833). TitlePhil. Mag. 2:175,269,351.Granick, S. (1991). Motions and telaxations of confined liquids. Science 253: 1374-1379.Granzier, H. L. M., Myers, J. A., and Pollack, G. H. (1987). Stepwise shortening of muscle fiber segments. /. Mus. Res. Cell Motil, 8: 242-251.HHagiwara, S., Chichibu, S., and Naka K. (1964). The effects of various ions on resting and spike potentials ofbarnacle muscle fibers. /. Gen.Physiol. 48: 163-179.Hardy, W. (1932). Problems of the boundary state. Phil. Trans. Roy. Soc. London Ser. A. 230: 1-37.Harrington, W. F. (1979). On the ot igin of the contractile fotce in skeletal muscle. Proc. Natl. Acad. Sci. 76(10): 5066-5070.Hatano, S. (1972). Conformational changes of plasmodium actin polymers formed in the presence of Mg . /. Mech. Cell Motil. 1: 75-80.Hatano, S., Totsuka, T., and Oosawa, F. (1967). Polymerization of plasmodium actin. Biochim. Biophys. Acta. 140: 109-122.Hatoti, K., Honda, H., and Matsuno, K. (1996a). ATP dependent fluctuations of single actin filaments in vitro. Biophys. Chem. 58: 267-272.Hatori, K., Honda, H., and Matsuno, K. (1996b). Communicative intetaction of myosins along an actin filament in the presence of ATP.Hatori, K., Honda, H., Shimada, K., and Matsuno, K. (1998). Propagation of a signal coordinating force generation along an actin filament inactomyosin complexes. Biophys. Chem. 75:81-85.Hazlewood, C. F. (1979). A view of the significance and understanding of the physical properties of cell-associated water. Cell-Associated Water, ed.W. Drost-Hansen, and J. S. Clegg, Acad. Press, N. Y.Hazlewood, C. E, Nichols, B. L, and Chamberlain, N. F. (1969). Evidence for the existance of a minimum of two phases of ordered water in askeletal muscle. Nature 222: 747-750.Hazlewood, C. P., Singer, D. B., and Beall, P. (1979). Electron microscope examination of common red cell ghosts: cytoplasmic con -tamination. Physiol. Chem. Phys. 11(2): 181-184.Heidorn, D. B. (1985). A Quasielectric Neutron Scattering Study of Water Diffusion in Frog Muscle, PhD Thesis, Rice University, Houston, TX.Heimburg, T., andBiltonen, R. L. (1996). A Monte Carlo simulation study of protein-induced heat capacity changes and lipid-inducedproteinclustering. Biophys. ]. 70: 84-96.Hennessey, E. S., Drummond, D. R., and Sparrow, J. C. (1993). Molecular genetics ofactin function. Biochem. ]. 282:657-671.Heppel, L. (1939). The electrolytes of muscle and liver in potassium-depleted tats. Amer. J. Physiol. 127:385-392.

Heppel, E. (1940). The diffusion of radioactive sodium into the muscles of potassium-depleted rats. Amer. J. Physiol. 128: 449-454.Hille, B. (1973). The permeability of the sodium channel to metal cations in myelinated nerve. /. Gen Physiol. 59: 637-658.Hille, B.(1984). Ionic Channels of Excitable Membranes, Sinauer, Sunderland, MA.Hille, B. (1992). Ionic Channels of Excitable Membranes, Second edition, Sinauer, Sunderland, MA.Hillman, H. (1994). New considerations about the structure of the membrane of the living animal cell. Physiol. Chem. and Med. NMR. 26:55-67Hirokawa, N. (1998). Kinesin and dynein superfamily proteins and the mechanismof organelle transport. Science279: 519 -524.Hodgkin, A. E, and Katz, B. (1949). The effect of sodium on the electrical conductivity of the giant axon of the squid. /. Physiol. 108:37-77.Hodgkin, A. E., and Horowicz, P. (1959a). Movements of Na and K insingle muscle fibres. /. Physiol. 145: 405-432.

71

Hodgkin, A. E., and Horowicz, P. (1959b). The influence of potas sium and chloride ions on the membrane potential of single muscle

Hoenger, A., and Milligan, R. A. (1997). Motor domains of kinesin and Ho/interact with microtubule protofilaments with the same bindinggeometry. /. Mol. Biol. 265(5): 553-564.Hoeve, C. A. J., Willis, Y. A., and Martin, D. J. (1963). Evidence for a phase transition in muscle contraction. Biochem. 2: 282-286.Hoffman, A. S. (1991). Conventional and environmentally-sensitive hydrogels for medical and industrial uses: a review paper. Polymer Gels268(5): 82-87.Holstein, T, and Tardent, P. (1984). An ultrahigh-speed analysis of exocytosis: nematocyst discharge. Science 223: 830-833.Horn, R. G., and Israelachvili, J. (1981). Direct measurement of structural forces between two surfaces in a nonpolar liquid. /. Chem. Phys.75(3): 1400-1411.Howard, J. (1997). Molecular motors: structural adaptations to cel lular functions. Nature 389: 561-567.Hubley, M. J., Rosanske, R. C., and Moerland, T. S. (1995). Diffusion coefficients, of ATP and creatine phosphate in isolated muscle: Pulsegradient P NMR. of small biological samples. NMR. in Biomed. 8: 72-78.Hutchings, B. E. (1969). Tetracycline transport in Staphylococcus Aureus H. Biochim. Biophys. Acta. 174:734-748.Huxley, A. P., and Niedergerke, R. (1954). Structural changes in muscle during contraction: Interference microscopy of living muscle fibres.Nature173: 971-973.Huxley, A. P., and Niedergerke, R. (1958). Measurement of the stria-tions of isolated muscle fibres with the interference microscope. /. Physiol.144: 403-425.Huxley, H. E.(1996). A personal view of muscle andmotility mechanisms. Ann. Rev. Physiol. 58: 1-19.Huxley, H. E., and Hanson, J. (1954). Changes in the cross stria-tions of muscle during contraction and stretch and their structuralinterpretation. Nature 173: 973-976.Hyman, A. A., and Karsenti, E. (1996). Morphogenetic properties of microtubules and mitotic s pindle assembly. Cell 84:401-410.IInoue, L, Kobatake, Y, and Tasaki, I. (1973). Excitability, instability, and phase-transition in squid axon membrane under internal per-fusion withdilute salt solutions.Biochem. Biophys. Acta. 307: 471-477.Inoue, S., and Salmon, E. D. (1995). Force generation by microtubule assembly/disassembly in mitosis andrelated movements. Mol. Biol. of Cell6:1619-1640.Irving, M., St.-C., Alien, T., Sabido-David, C., Craik, J. S., Brandmeler, B., Kendrick-Jones,J., Corrie, J. E. T., Trentham, D. R., andGoldman, Y. E.(1995). Tilting of the light-chain region of myo-sin during step length changes and active force generation in skeletal muscle.Nature 375: 688-691.Ishijima, A., Doi, T., Sakurada, K., and Yanagida, T. (1991). Sub-piconewton force fluctuations of actomyosin in vitro. Nature 352: 301-306.Israelachvili, J. N., and McGuiggan, P. M. (1988). Forces between surfaces in liquids. Science 241: 795-800.Israelachvili, J., and Wennerstrom, H. (1996). Role of hydration and water srructure inbiological and colloidal interactions. Nature 379:219-225.Ito, T., Suzuki, A., and Stossel, T. P.(1992). Regulation of water flow by actin-binding protein-induced actin gelation. Biophys.J.61: 1301-1305.JJacobs, W. P. (1994). Caulerpa. Set. Amer. 271(6): 100-106.Jhon, M. S., and Andrade, J. (1973). Water and hydrogels. /. Biomed. Mater. Res. 7:509-522.Jordan-Lloyd, D., and Shore, A. (1938). The Chemistry of Proteins, Second edition, J. A. Churchill, London.Joseph, N. R., Engel, M. B., and Catchpole, H. R. (1961). Distribu tion of sodium and potassium in certain cells and tissues. Nature 4794: 1175-1178.KKamitsubo, E. (1972). Motile protoplasmic fibrils in cells of the Characeae. Protoplasma 74: 53-70.Kamiya, N. (1970). Conrractile properties ofthe plasmodial strand. Proc. Jpn. Acad. 46:1026-1031.Kas, J., Strey, H., and Sackmann, E. (1994). Direct imaging of reptation for semi-flexible actin filaments. Nature 368: 226-229.Kasturi, S. R., Hazlewood, C. F., Yamanashi, W. S., and Dennis, L. W. (1987). The nature and origin of chemical shift for intracellular waternuclei inAnemia cysts. Biophys. J. 52: 249-256.Katayama, E. (1998). Quick-freezedeep-etch electron microscopy of the actin-heavy meromyosin complex during the in vitro motility assay. /.Mol. Biol. 278: 349-367.Katayama, E., and Nonomura, Y. (1979). Electron microscopic analysis of tropomyosin paracrystals. /. Biochem. 86: 1511-1522.Katchalsky, A., and Zwick, M. (1955). Mechanochemistry and ion exchange /. Polymer Sci. 16: 221-234.

Kellermayer, M. S. Z., and Pollack, G. H. (1996). Rescue of in vitro actin motility halted at high ionic strength by reduction of ATP tosubmicromolar levels.Biochim. Biophys. Acta.. 1277:107-114.Kellermayer, M., Ladany, A.,Jobsr, K., Szucs, G., Trombitas, K., and Hazlewood, C. F. (1986). Cocompartmentation of proteins and K within theliving cell. Proc. Natl. Acad. Sci. USA. 83(4): 1011-1015.Kellermayer, M., Ludany,A., Miseta, A., Koszegi,T.,Berta, G.,Bogner,P., Hazlewood, C. E, Cameron, I. L., and Wheatley, D. N. (1994). Releaseof potassium, lipids, and proteins from nonionic detergent treated chicken red blood cells. /. Cell. Physiol. 159: 197-204.Kim, E., Bobkova, E., Miller, C. J., Orlova, A., Hegyi, G., Egelman, E. H., Muhlrad, A., and Reisler, E. (1998). Intrastrand cross-linkedactinbetween Gin-41 and Cys-374. III. Inhibition of motion and force generation with myosin. Biochem. 37(51): 17801-17809.Riser, P. R, Wilson, G., and Needham, D.(1998). A synthetic mimic of the secretory granule for drug delivery. Nature 394: 459-462.Kitamura, K., Tokanaga, M., Iwane, A. H., and Yanagida, T. (1999). A single myosin head moves along an acin filament with regular steps of 5.3nanometers. Nature 397(6715): 129-134.Klenchin, V. A., Sukharev, S. L, Serov, S. M., Chernomordik, L. V., and Chizmadzhev, Yu. A. (1991). Electrically induced DNA uptake by cells is afast process involving DNAelectrophoresis. Biophys ]. 60: 804-811.Klinger, R. G., Zahn, D. P., Brox, D. H., and Frundes, H. E. (1971). Interaction of the hemoglobin with ions. Binding of ATP to humanhemoglobin under simulated in vitro conditions. Europ. J. Biochem. 18: 171-177.Kojima, H., Muto, E., Higuchi, H., and Yanagida, T. (1997). Mechanics of single kinesin molecules measured by optical trapping nanometry.Biophys. J. 73: 2012-2022Kolara, G. B. (1976). Water structure and ion binding: a role in cell physiology? Science 192: 1220-1222.Kolberg, R. (1994). A membrane flip for a bacterial ion channel. / NIHRes. 6: 35-36.Korn, E. D. (1966). Structure of biological membranes. Science 153:1491-1498.

72

Kraft, T., Messerli, M., Rothen-Rurishauser, B., Perriard, J.-C., Wallimann, T., and Brenner, B. (1995). Equilibration and exchange offluorescently labeled molecules in skinned skeletal muscle fibers visualized by confocal microscopy. Biophys.J. 69: 1246-1258.Krause, T. L., Fishman, H. M., Ballinger, M. L., and Bittner, G. D. (1984). Exrent and mechanism of sealing in transected giant axons of squid andearthworms. /. Neurosci. 14: 6638-6651.

Krauskopf, K. B. (1967). Introduction to Geochemistry, McGraw-Hill, Appendix III.Kull, F. J., Sablin, E. P., Lau, R.,Fletterick, R. J., and Vale, R. (1996). Crystal structure of the kinesin motor domain reveals a structuralsimilarity to myosin. Nature 380: 550-555.Kuroda, K. (1 964). Behavior of naked cytoplasmic drops isolated from plant cells. Primitive Motile Systems in Biology, ed. R. D. Alien, and N.Kamiya, Acad. Press, N. Y.Kushmerick, M. J., and Podolsky, R. J. (1969). Ionic mobility inmuscle cells.Science 166(910): 1297-1298.LLehninger, A. L. (1964). The Mitochondrion, Benjamin, Menlo Park, CA.Lev, A. A., Korchev, Y. E., Rostovtseva, T. K., Bashford, C. L., Edmonds, D. T., and Pasternak, C. A. (1993). Rapid switching of ioncurrent in narrow pores: implications for biological ion channels. Proc. Roy. Soc. Land. B. 252: 187-192.Lewis, A., Rousso, I., Khachatryan, E., Brodsky, L, Lieberman, K., and Sheves, M. (1996). Directly probing rapid membrane protein dynamicswith an atomic force microscopic: a study oflight -induced conformational alterations in bacteriorhodopsin. Biophys. J.70: 2380-2384.Ling, G. N. (1 992). A Revolution in the Physiology of the Living Cell. Krieger Pub. Co., Malabar, Fl.Ling, G. N. (1997). Debunking the alleged resurrection of the sodium pump hypothesis. Physiol. Chem. Phys. & Med NMR. 29: 123-198.Ling, G.N., and Ochsenfeld, M. M. (1973). Mobility of potassium ion in frog muscle cells, both living and dead. Science 181: 78-81.Ling, G. N., and Walton, C. L. (1976). What retains water in living cells? Science 191: 293-295.Ling, G. N., Kolebic, T, and Damadian, R. (1990). Low paramagnetic-ion content in cancer cells: its significance in cancel detection bymagnetic resonance imaging. Physiol. Chem. Phys. & Med. NMR. 22: 1-14.Ling, G. N., Niu, Z., and Ochsenfeld, M. (1993). Predictions of polarized multilayer theory of solute distribution confirmed from a study ofthe equilibrium distribution in frog muscle of twenty-one nonelectrolytes including fivecryoprotectants. Physiol. Chem. Phys. Med. NMR.25(3): 177-208.Ling, G. N., Walton, C., and Bersinger T. J. (1980). Reduced solubility of polymer-oriented warer for sodium salts, amino acids and othersolutes normally maintained at low levels in living cells. Physiol. Chem. Physics 12: 111-138.Lippincott, E. R., Cessac, G. L., Stromberg, R. R., and Grant, W. H. (1971). Polywater - a search for alternative explanations. J. Colloid InterfaceSci, 36: 443-460.Lippincott, E. R., Stromberg, R. R., Grant, W. H., and Cessac, G. (1969). Polywater. Vibrational spectra indicate unique stable polymericsttucture. Science 164: 1482-1487.Lopez-Beltran, E. A., Mate, M. J., and Cerdan, S. (1996). Dynamics and environment of mitochondrial watet as detected by H NMR. /. Biol.Chem. 271(18): 10648-10653.Lowey, S.,and Luck, S. M. (1969). Equi l ib r ium binding of andenosine diphosphate to myosin. Biochem. 8: 3195-3199.Luby-Phelps, K., Mujumdat, S., Majumdar, R. B., Ernst, L. A., Galbraith, W., and Waggoner, A. S. (1993). A novel fluorescenceratiometric method confirms the low solvent viscosity of the cytoplasm. Biophys. J. 65: 236-242.Luby-Phelps, K., Taylor, D. L., and Lanni, F. (1986). Probing the structure of cytoplasm. J. Cell. Biol. 102(6): 201 5-2022.Luck, W. A. P. (1976). Water in biological systems. Topics Current Chem. 64: 113-180.Ling, G. N. (1952). The role of phosphate in maintenance of the resting potential and selective ionic accumulation in frog muscle cells.Phosphorous Metabolism, 11: 749-795. ed. W. McElroy, and B. Glass, J. Hopkins Press, Baltimore.Ling, G. N. (1955). New hypothesis.for the mechanism of cellular resting potential. Fed. Proc. 14: 93-94.Ling, G. N. (1962). A Physical Theory of the Living State: the Association-Induction Hypothesis, Blaisdell Publ. Co., Waltham, MA.Ling, G. N. (1965). The physical state of water in living cell and model systems. Proc. N. Y. Acad. Set. 125: 401-417.Ling, G. N. (1973). How does ouabain control the levels of cell K and Na ? By interferencewith a Na pump or by allosteric control of K -Naadsorption on cytoplasm protein sites. Physiol. Chem. and Physics 5: 295-311.Ling, G. N. (1978). Maintenance of low sodium and highpotassium levels investing muscle cells. /. Physiol. 280: 105-123.Ling, G. N. (1984). In Search of the Physical Basts of Life, Plenum Publ. Co., New York.Ling, G. N. (1988). A physical theory of the living state: application to water and solute distribution. Scanning Microsc. 2(2): 899-913.MManiotis, A., and Schliwa, M. (1991). Microsurgical removal ofcen-trosomes blocks cell reproduction and centriole generation in BSC-1cells.Cell67: 495-504.Marsh, D. J., De Bruin, S. H., and Gratzer, W. B. (1977). An investigation of heavy meromyosin-ADP binding equilibria by proton releasemeasurements. Biochem.16: 1738-1742.Matsumoto, G. (1984). A proposed membrane model for generation of sodium currents in squid giant axons. /. Theor. Biol. 107: 649-666.Matsumoto, G., Ichikawa, I. M., Tasaki, A., Murofushi, H., and Sakai, H. (1984). Axonal microtubules neccessary for generation of sodium currentin squid axons: I. Pharmacological study on sodium current by microtubule proteins and 260 K protein. / Membr. Biol. 77: 77-91.Matsumoto, G., Kobayashi, T., and Sakai, H. (1979). Restoration of the excitibility of squid giant axon by tubulin tyrosine ligase and microtubuleproteins. /. Biochem.86:1155-1158.Matsumoto, G., Murofushi, H., Endo, S., and Sakai, H. (1982). Biological Functions of Microtubules and Related Structures, ed. H. Sakai., H. Mohri,and G. G. Borisy, Academic Press, Tokyo.Matsumoto, G., Murofushi, H., Endo.'S., Kobayashi, T., and Sakai, H. (1983). Structure and Function of Excitable Cells, ed. D. C. Chang, I.Tasaki, W. J. Adelman, and R. H. Leuchtag, Plenum Press, N. Y.Maughan, D., and Lord, C. (1988). Protein diffusivities in skinned frog skeletal muscle fibers. Molecular Mechanism of Muscle Contraction, ed. H.Sugi, and G. H. Pollack, Plenum Press, N.Y.Maughan, D., and Recchia, C. (1985). Diffusible sodium, potassium, magnesium, calcium, and phosphorous in frog skeletal muscle. J. Physiol368: 545-563.Mclntosh, J. R. (1973). The axostyle of Saccinobaculus. II. Motion of the microtubule bundle and a structural comparison of straight and bentaxostyles. J. Cell Biol. 56:324-339.McLachlan, A. D., and Karn, J. (1982). Periodic charge distributions in the myosin rod amino acid sequence match cross-bridge spacings inmuscle. Nature 299:226-231.McNeil, P. L, and Ito, S. (1990). Molecular traffic through plasma membrane disruptions of cells in vivo. ]. Cell Sci. 96: 549-556.McNeil, P. L., and Steinhardt, R. A. (1997). Loss, restoration, and maintenance of plasma membrane integrity. /. Cell Biol. 137(1): 1-4.

73

Meaves, H., and Vogel, W. (1973). Calcium inward currents in inter nally perfused giant axons. /. Physiol. (London) 235: 225-265.Mehta, A. D., Rock, R. S., Rief, M., Spudich, J. A., Mooseker, M. S., and Cheney, R. E. (1999). Myosin-V is a processive actin -based motor.Nature 400(6744): 590-593.Menetret, J. R, Hoffmann, W., Schroeder, R. R., Rapp, G., and Goody, R. S. (1991). Time-resolved cryo-electron microscopic study of thedissociation of actomyosin induced by photolysis of photolabile nucleotides. J. Mol. Biol. 219(2): 139-144.Mentre, P. (1995). L'Eau dans la Cellule: Une Interface Dynamique et Heterogene des Macromolecules, Masson, Paris.Mentre, P., and Debey, P. (1999). An unexpected effect of an oua-bain-sensitive ATPase activity on the amount of antigen-antibody complexesformed in situ. Cell and Mol. Biol. 45(6): 781-791.Metuzals, J., and Izzard, C. S. (1969). Spatial patterns of thread-like elements in the axoplasm of the giant nerve fiber of the squid (Loligo pealii L.)as disclosed by differential interference microscopy and by electron microscopy. /. Cell Biol. 43:456-479.Metuzals, J., and Tasaki, I. (1978). Subaxolemmal filamentous network in the giant nerve fiber of the squid (Loligo pealei L.) and its possible rolein excitability. /. Cell Biol. 78: 597-621.Miki, M., and Koyama, T. (1994). Domain motion in actin observed by fluorescence resonance energy transfer. Biochem. 33: 10171-10177.Miller, D. J. (1979). Are cardiac muscle cells 'skinned' by EGTA or EDTA? Nature 277: 142-143.Mimori, Y., and Miki-Nonumura, T. (1995). Extrusion of rotating microtubules on the dynein-track from a microtubule-dynein gamma-complex.Cell Motil. And Cytoskel.30:17-25.Miyagishima, Y. (1975). Catecholamine in the myocardium: a fluorecence histochemical study. Jpn. Circ. J. 39: 357-375.Miyano, M., and Osada, Y. (1991). Electroconductive organogel. 2. appearance and nature of current oscillation under electric field.Macromol. 24: 4755-4761.Mond, R., and Amson, K. (1928). Uber die lonenpermeabilitaet des quetgestreiften Muskels. Pfliiger's Arch. Ges. Physiol. 220: 69-81.Morel, J. E. (1991). The isometric force exerted per myosin head in a muscle fibre is 8 pN. Consequence on the validity of the ttaditionalconcepts of force generation. /. Theor. Biol. 151:285-288.Moriyama, Y, Yasuda, K., Ishiwata, S., andAsai, H. (1996). Ca (2+)-induced tension development in the stalks of glycerinated Vorticellaconvallaria. Cell Motil. and Cytoskel. 34(4): 271-278.Muto, E., and Yanagida, T. (1997). Cooperative binding of kinesin molecules to a microtubule in the presence of ATP. Biophys. J. 72: A62.NNanavati, C., and Fernandez, J. M. (1993). The secretory granule matrix: a fast-acting smart polymer. Science 259(5097): 963-965.Natori, R. (1975). The electric potential change of internal membrane during propagation of contraction in skinned fibre of toad skeletal muscle.Jpn. J. Physiol.25(1): 51-63.Naylor, G. R., Barrels, E. M., Bridgman, T. D., and Elliott, G. F. (1985). Donnan potentials in rabbit psoas muscle in rigor. Biophys. J. 48(1): 47-59.Naylor, W. G., and Merrillees, N. C. R. (1964). Some observations on the fine structure and metabolic activity of normal and glycerin -atedventricular muscle of toad. /. Cell Biol. 22:533-550.Negendank, W. (1982). Studies of ions and water in human lymphocytes. Biochim. Biophys. Acta. 694: 123-161.Neher, E., Sackmann, B., and Steinba'ch, J. H. (1978). The extracellular patch clamp: a method for resolving currents through individual openchannels in biological membranes.Pfliiger's Archiv. Ges. Physiol. 375: 219-228.Nickels, J. (1970). Localisation of a microelectrode tip in muscle cell: A light and electron microscopic study. Acta. Physiol. Scand. 80: 360-369.Nickels, J. (1971). A method for localisation of the muscle cell and the motor end plate after in vivo registrarion with a microelectrode. Pfliiger'sArchiv. Ges. Physiol. 330: 45-50.Nicklas, R. B. (1997). How cells get the right chromosomes. Science 275: 632-637.Noble, D., and Bett, G. (1993). Reconstructing the heart: a challenge for integrative physiology. Cardiova.se. Res: 27: 1701-1712..Noda, C., and Yugari, Y. (1973). Effect of catecholamines in restoring the beating of cultured rat heart cells treated with reserpine. Jpn. J.PharmacoL23(6): 839-846.OOdelblad, E., Bhar, B. N., and Lindstrom, G. (1956). Proton magnetic resonance of human red blood cells in heavy-water exchange experiments.Arch. Biochem. Biophys. 63: 221- 225.Ogata, M. (1996). Hydrodynamic ptoperties of water in myoplasm in resting and acrive states. Proc. Jpn. Acad. Set. B 72(6): 137-141.Okada, Y., and Hirokawa, N. (2000). Mechanism of the single-headed processivity: Diffusional anchoring between the K-loop of kinesin and the Cterminus of tubulin. PNAS. 97(2): 640-645.Okuzaki, H., and Osada, Y. (1994). Electro-driven chemomechanical polymer gel as an intelligent soft material. /. Biomater. Sci. Polymer Edn. 5:485-496.Oosawa, P., Fujime, S., Ishiwata, S., and Mihashi, K. (1972). Dy namic property of F-actin and thin filament. CSHSymposia on Quant. Biol.XXXVII: 277-285.Oparin, A. I. (1971). Routes for the otigin of the first forms of life. Sub-Cell Biochem. 1: 75-81.Oparin, A. I. (1964). The Chemical Origin of Life, ed. C. Thomas;Springfield, 111.Oplatka, A. (1996). The rise, decline, and fall of the swinging crossbridge dogma. Chemtntcts. Bioch. Mol. Biol. 6: 18-60.Oplatka, A. (1997). Critical review of the swinging crossbridge theoryand of the cardinal active role of water in muscle contiaction. Crit. Rev.Biochem. Mol. Biol. 32(4): 307-360.Oplatka, A. (1998). Do the bactetial flagellar motor and ATP syn-thase operate as water rurbines? Biochem. Biophys. Res. Commun. 249: 573-578.Osada, Y, and Gong, J.(1993). Stimuli-responsive polymer gels and their application to chemomechanical systems. Prog. Polym. Sci. 18: 187-226.Osada, Y, and Ross-Murphy, S. (1993). Intelligent gels. Sci. Amer.268: 82-86.Osterhout, W. J. V., and Hill, S. E., (1938). Calculations of bioelectric potentials. /. Gen. Physiol. 22: 139-146.Overbeek, J. Th. G. (1956). The Donnan equilibrium. Prog. Biophys Biophys Chem. 6: 58-84.Pashley, R. M., and Kitchener, J. A. (1979). Surface forces in adsorbed mmultilayers of water on quartz. /. Colloid and Interface Sci. 71: 491-500.Pauling, L.(1945). The adsorption of water by proteins. J. Am. Chem. Soc. 67: 555-557.Pauling, L.(1959a). A molecular theory of genetal anesthesia. Science134: 15-21.Pauling, L. (1959b).Hydrogen Bonding, ed. L. Hadzi, Pergamon Press, London.Peachey, L. D. (1965). The sarcoplasmic reticulum and transverse tubules of the frog's sartorius. /. Cell Biol. 25: 209- 231.Peters, R.(1984). Nucleo-cytoplasmic flux and intracellular mobility in single hepatocytes measuted by fluorescence microphotolysis. EMBOJ. 3:1831-1836.

74

Petka, W. A., Harden, J. L., McGrath, K. P, Wirtz, D., andTirrell, D. A. (1998). Reversible hydrogels from self-assembling artificial proteins. Science281: 389-392.Pfann, W. G. (1962). Zone melting. Science 135:1101-1109.Pfeffer, W. F. (1877).Osmotische Untersuchungen: Studien zur Zell -Mechanik, Engelmann, Leipzig.Pinto da Silva, P., and Branton, D. (1970). Membrane splitting in freeze-ethching. Covalently bound ferritin as a membrane marker. /. CellBiol.45: 598-605.Pissis, P., Anagnostopoulou-Konsta, A., and Apekis, L. (1987). A dielectric study of the state of water in plant stems. /. Exptl. Bat. 38(194):1528-1540.Plumb, R. C., and Bridgman, W. B. (1972). Ascent of sap in trees. Science 176: 1129-1131.Pollack, G. H. (1977). Cardiac pacemaking: an obligatoty tole of catecholamines? Science 196: 731-738.Pollack, G. H. (1983). The sliding filament / ctoss-bridge theory. Physiol. Rev. 63: 1049-1113.Pollack, G. H. (1990). Muscle dr Molecules-: Uncovering the Principles of Biological Motion, Ebnet and Sons, Seattle, WA.Pollack, G. H. (1996). Phase transitions and the molecular mechanism of contraction. Biophs. Chem. 59:315-328.Pollack, G. H., Iwazumi, T., ter Keurs, H. E. D. ]., and Shibata, E. F. (1977). Sarcomere shortening in striated muscle occurs in stepwise fashion.Nature 268: 757-759.Pollard, T. (1984).Actin-binding protein evolution. Nature 312(5993): 403.Porter, K. R., Beckerle, M., and McNivan, M. (1983). The cytoplas-mic matrix. Mod. Cell Biol. 2: 259-302.Prausnitz, M. R., Milano, C. D., Gimm, ]. A., Langer, R., and Weaver, ]. C. (1994). Quantitative study of molecular ttansport due toelectroporation: uptake of bovine serum albumin by erythrocyte ghosts. Biophys. J. 66(5): 1522-1530.Prochniewicz, E., Zhang, Q., Janmey, P. A., and Thomas, D. D. (1996). Cooperativity in F-actin: binding of gelsolin at the barbed endaffects structure and dynamics of the whole filament. /. Mol. Biol. 260(5): 756-766.Pruliere, G., and Dotizou, P. (1989). Sol-gel processing of actin to obtain homogeneous glasses at low temperartires. Biophys. Chem. 34: 311-315.Purcell, E. M. (1977). Life at low Reynolds number. Am. ]. Physics 45(1): 3-11.RRabenstein, D. L., Ludowyke, R., and Lagunoff, D. (1987). Proton nuclear magnetic resonance studies of mast cell histamine. BiochemRao, P. N., Hazlewood, C. R,and Beall, P. T. (1982). Cell cycle phase-specific changes in relaxation times and water content in HeLa cells. CellGrowth, ed. C. Nicolini, NATO Adv. Study Inst. Series, Ser. A38: 535-547.Rieder, C. L, and Salmon, E. D. (1994). Motile kinetochores and polar ejection forces dictate chtomosome position on rhe vertebrate mitoticspindle. /. CellBiol. 124(3): 223-233.Rief, M., Gautel, M., Oesterhelt, R, Fernandez, ]. M., and Gaub, H. E. (1997). Reversible unfolding of individual titin immunoglobin domainsby AFM. Science 276: 1109-1112.Robinson, G. W., and Cho, C. H. (1999). Role of hydration water in protein unfolding. Biophys.]. 77:3311-3318.Robinson, G. W., Zhu, S.-B., Singh, S., and Evans, M. W. (1996). Water in Biology, Chemistry, and Physics, World Scientific, London.Rorschach, H. E., Bearden, D. W., Hazlewood, C. E, Heidorn, D. B., and Nicklow, R. M. (1987). Quasi-elastic scattering studies of watetdiffusion. Scanning Microsc. 1(4): 2043-2049.Rorschach, H. E., Lin, C., and Hazlewood, C. F. (1991). Diffusion of water in biological rissues. Scanning. Microsc. Suppl. 5: S1-S10.Rozycka, M., Gonzalez-Serratos, H., and Goldman, W. (1993). Non-homogeneous Ca release in isolated frog skeletal muscle fibres. /. Mus. Res. CellMotil. 14: 527-532.Ruch, T. C., and Patton, H. D. (1965). Physiology and Biophysics, Saundets, Philadelphia.Sachs, F., and Qin, F. (1993). Gated, ion-selective channels observed with patch pipettes in the absence of membranes: novel properties ofagigaseal. Biophys. J. 65(3): 1101-1107.Sakahibara, H., Kojima, H., Sakai, Y., Katayama, E., and Oiwa, K. (1999). Inner-arm dynein c of Chlamydomonas flagella is a single-headedprocessive motor. Nature 400(6744): 586-590.Sato, H., Tasaki, L, Carbone, E., and Hallett, M. (1973). Changes in axon birefringence associated with excitation: implications for rhestructure of the axon membrane. /. Mechanochem. Cell Motil. 2:209-217.Sato, M., Wong, T. Z., Brown, T., and Alien, R. D. (1984). Rheo-logical properties of living cytoplasm: a preliminary investigation of squidaxoplasm (Loligo pealei). Cell Motil. 4:7-23.Sawahata, K., Gong, J. P., and Osada, Y. (1995). Soft and wet touch-sensing system made of hydrogel. Macromol. Rapid Commun. 16:713-716.Schliwa, M. (1986). The Cyto'skeleton: An Introductory Survey, Springer, N. Y.Schiiltze, M. (1861). Mailer's Arch, fur Anatomie und Physiologic und fur Wissenschaftliche Medicin, Berlin.Schiiltze, M. (1863). Das Protoplasma des Rhizopoden und der Pflanzenzellen. Bin Beitrag zur Theorie der Zelle, Leipzig.Schutt, C. E., and Lindberg, U. (1992). Actin as the generator of tension during muscle contraction. Proc. Natl. Acad. Sci. USA. 89(1):319-333.Schutt, C. E., and Lindberg, U. (1993). A new perspective on muscle contraction. FEES. 325: 59-62.Schutt, C. E., and Lindberg, U. (1998). Muscle contractions as a Markov process I: energetics of the process. Acta. Physiol. Scan. 163: 307-324.Schwann, T. (1839) . Mikroskopische Untersuchungen iiber die Ubereinstimmung in der Struktur und dem Wachstum der Thiere und Pfl/tnzen,Berlin.Schwister, K., and Deuticke, B. (1985). Formation and properties of aqueous leaks induced in human erythrocytes by electrical breakdown.Biochim. Biophys. Acta. 816: 332-348.Schwyter, D. H., Kron, S. J., Toyoshima, Y. Y., Spudich, J. A., and Reisler, E. (1990). Subtilisin cleavage of actin inhibits in vitro slidingmovement of actin filaments over myosin. /. Cell Biol. I l l : 465-470.Serpersu, E. H., Kinosita, K.,Jr. and Tsong, T. Y. (1985). Reversibleand irreversible modificationof erythrocyte membrane permeability byelectric field. Biochim. Biophys. Acta. 812: 779-785.Slatin, S. L., Qiu, X-Q, Jakes, K. S., and Finkelstein, A. (1994). Identification of a translocated protein segment in a voltage-dependent channel.Nature 371: 158-161.,Solomon, A. K. (1960). Red cell membrane structure and ion transport. /. Gen. Physiol. 43: 1-15.Somlyo, A. V., Gonzalez-Serratos, H. G., Shuman, H., McClellan, G., and Somlyo, A. P. (1981). Calcium release and ionic charges in thesarcoplasmic reticulum of tetanized muscle: an electron probe study. / Cell Biol. 90(3): 577-594.Spira, M. E., Benbassat, D., and Dormann, A. (1993). Resealing of the proximal and distal cut ends of transected axons: electrophsiologicaland ultrastructural analysis./ Neurobiol. 24: 300-316.Spudich, J. A. (1994). How molecular motors work. Nature 372: 515-518.

75

Spyropolous, C. S. (1961). Initiation and abolotion of electric response by thetmal and chemical means. Am. J. Physiol. 200: 203-208.Stebbings, H., and Hunt, C. (1982). The nature of the clear zone around microtubules.Cell and Tissue Res. 227:609-617.Stebbings, H., and Willison, J. H. M. (1973). Stucture of microtubules: a study of freeze-etched and negatively stained microtubules from theovaries of Notonecta. Z. Zellforsch u. Mikrosc. Anat. 138(3): 387-396.Stein, W. D. (1990). Channels, Carriers, and Pumps: An Introduction to Membrane Transport, Acad. Press, San Diego.Steinbach, B. (1940). Sodium and potassium in frog muscle. /. Biol. Chem. 133: 695-701.Steinberg, I. Z., Oplatka, A., and Katchalsky, A. (1966). Mecha-nochemical engines. Nature 210: 568-571.Stephenson, D. G., Wendt, I. R., and Forrest, Q. G. (1981). Non-uniform iondistributions and electricalpotentials in sarcoplasmic regions ofskeletal muscle fibres. Nature 289(5799): 690-692.Stillinger, F. A. (1980). Water revisited. Science 209:451-457.Sugitani, M, Kobayashi, T., and Tanaka, T. (1987). Polym. Preprints Jpn. 36: 2876-2878.Suzuki, M. (1994). A new concept of a hydrophobicity motor based on local hydrophobicity transition of functional polymer substrate formicro/nano machines.Polym. Gels and Ntwks. 2:279-287.Szasz, A., van Noon, D., Scheller, A., and Douwes, F. (1994). Water states in living systems. I. Structural aspects. Physiol. Chem, Phys. & d. NMR.26: 299-322.Szent-Gyorgyi, A. (1951). Chemistry of Muscular Contraction, Acad. Press, N. Y.Szent-Gyorgyi, A. (1960). Introduction to a Submolecular Biology, Acad. Press, N. Y., London.Szent-Gyorgyi, A. (1972). The Living State. With Observations on Cancer, Acad. Press, N. Y.Tabcharani, J. A., Jensen, T.J., Riordan, J.R., and Hanrahan, J.W. (1989). Bicarbonate permiability of the outwardly rectifying anion channel. /Memb. Biol. 112(2): 109-122.Tanaka, T.(1981). Gels. Sci. Amer. 244:110-113.Tanaka, T., Annaka, M., Franck, I., Ishii, K., Kokufuta, E., Suzuki,A., and Tokita, M. (1992). Phase transitions of gels.Mechanics of Swelling. NATO ASI Series Vol H 64, Springer-Verlag,Berlin.Tang, J., and Janmey, P. A. (1998). Twodistinct mechanisms ofactin bundle formation. Biol. Bull. 194: 406-408.Tang,}., and Janmey, P. A. (1996). Polyelectrolyte nature of F-actin and the mechanism of actin bundle formation. J. Biol. Chem.271(15): 8556-8563.Taniguchi, Y., and Horigome, S. (1975). The states of water in cellulose acetate membranes. /. Appl. Polymer Sci. 19: 2743-2748.Tasaki, I, Byrne, P. M., and Masumura, M. (1987). Detection of thermal responses of the retina by use of polyvinylidene fluoride multi layerdetector.Jpn. ]. Physiol. 37:609-619.Tasaki, I. (1988). A macromolecular approach to excitation phenomena: mechanical and thermal changes in nerve during excitation. Physiol.Chem. and Phys. and Med. NMR. 20: 251-268.Tasaki, I. (1982).Physiology and Electrochemistry of Nerve Fibers, Acad. Press, NY.Tasaki, I. (1998). Repetitive mechanical responses of the amphibian skin to adrenergic stimulation. Jpn. ]. Physiol. 48: 297-300.Tasaki, I. (1999a). Rapid structural changes in nerve fibers and cells associated with their excitation processes. Jpn. J. Physiol. 49(2): 125-138.Tasaki, I. (1999b). Evidence for phase transition in nerve fibers, cells and synapses. Ferroelectric 220: 305-316.Tasaki, I., and Hagiwara, S. (1957). Demonstration of two stable potential states in the squid giant axon under tetraethylammonium chloride. /.Gen. Physiol. 40: 859-885.Tasaki, I., and Byrne, P. M. (1992). Discontinuous volume transitions in ionic gels and their possible involvement in the nerve excitation process.Biopolymers 32: 1019-1023.Tasaki, I., and Byrne, P. M. (1994). Discontinuous'volume transitions induced by calcium-sodium ion exchange in anionic gels and theirneurobiological implications. Biopolymers 34: 209-215.Tasaki, I., and Iwasa, K. (1981). Temperature changes associated with nerve excitation: detection by using polyvinylidene fluoride film. Biochem.Biophys. Res. Commun.101: 172-176.Tasaki, I., Kusano, K., and Byrne, P. M. (1989). Rapid mechanical and thermal changes in the garfish olfactory nerve as sociated with apropagated impulse. Biophys.]. 55: 1033-1040.Tasaki, I., Singer, I., and Takenada, T. (1965). Effects of internal and external ionic environment on excitability of squid giant axon: A mac -romolecular appraoach. /. Gen. Physiol. 48: 1095-1123.Taylor, S. R., Shlevin, H. H., and Lopez, J. R. (1975). Calcium in excitation -contraction coupling of skeletal muscle. Biochem. Soc. Transact. 1:759-764.Terakawa, S., Nagano, M., and Watanabe, A. (1977). Intracellular divalent cations and plateau duration of squid giant axons treated withtetraethylammonium. Jpn. J. Physiol. 27: 785-800.Thomas, D. D. (1987). Spectroscopic probes of muscle cross-bridge rotation. Ann. Rev. Physiol. 49: 641-709.Tigyi, J., Kellermayer, M., and Hazlewood, C. F. (1991). The Physical Aspect of the Living Cell, Akad. Kiado, Budapest.Tirosh, R., and Oplatka, A. (1982). Active streaming against gravity in glass microcapillaries of solutions containing acto-heavy meromyo-sin andnative tropomyosin. _/. Biochem. 91: 1435-1440.Tokita, M., and Tanaka, T. (1991). Reversible decrease of gel-solvent friction. Science 253: 1121-1123.Toney, M. F., Howard, J. N., Richer, J., Borges, G. L., Gordon, J. G., Melroy, O. R., Wiesler, D. G., Yee, D., and Sorensen, L. B. (1994).Voltage-dependent ordering of water molecules at an electrode -electrolyte interface. Nature 368: 444-446.Trantham, E.G., Rorschach, H. E., Clegg, J. C., Hazlewood, C. F, Nicklow, R. M., and Wakabayashi, N. (1984). Diffusive properties of waterin Artemia cysts as determined from quasi-elastic neutron scattering spectra.Biophys. J. 45(5): 927-938.Trautwein, W., and Uchizono, K. (1963). Electron microscopic and electrophysiologic study of the pacemaker in the sino-atrial node of therabbit heart. Z. Zellforsch. 61: 96-109.Trentham, D. R., Eccleston, J. P., and Bagshaw, C. R. (1967). Kinetic Analysis of ATPase Mechanisms. Quart. Rev. Biophys. 9: 218-281.Trombitas, K., and Pollack, G. H. (1995). Visualization of the transverse cytoskeletal network in insect-flight muscle by scanning-electronmicroscopy. Cell Motil. and Cytoskel.32: 226-232.Trombitas, K., and Tigyi-Sebes, A. (1979). The continuity of thick filaments between sarcomeres in honey-bee flight muscle. Nature 281(5729):319-320.Trombitas, K., Baatsen, P., Schreuder, J., and Pollack, G. H. (1993). Contraction-induced movements of water in single fibres of frog skeletalmuscle. /. Mus. Res. Cell Motil. 14: 573-584.Troshin, A. (1948). Salt currents in the complex coascervate: gelatine and gum arabic. Izv. Akad Nauk SSSR ser biol. No 4: 180-185.

76

Troshin, A. (1966). Problems of Cell Permeability, Pergamon Press, Oxford.Troshin, A. S. (1956). Problems of Cell Permeability, English edition: Pergammon Press, Oxford, Translated by W. F. Widdas.Troyer, D. (1975). Possible involvement of the plasma membrane in saltatory particle movement in heliozoan axopods. Nature 254: 696-698.Tskhovrebova, L., Trinick, J., Sleep, J. A., and Simmons, R. M. (1997). Elasticity and unfolding of single molecules of the giant muscle protein titin.Nature 387:308-312.Tsukita, S., Tsukita, S., Kobayashi, T., and Matsumoto, G. (1986). Subaxolemmal cytoskeleton in squid giant axon. II. Morphologicalidentification of microtubule- and microfilament-asociated domains ofaxolerama. /. Cell Biol. 102: 1710-1725.Tuganowski, W., Krause, M., and Dorczak, K. (1973). The effect of dibutyryl 3'5' -cylic AMP on the cardiac pacemaker, arrested with re -serpineand alpha-methyl-tyrosine. Naunyn-Schmiedebergs Arch.Pharmakol. 280: 63-70.UUrry, D. W. (1993). Molecular Machines: How motion and other functions of living organisms can result from reversible chemical changes.Angewandte Chemie Intl. Ed. Engl. 32: 819-841.Uvnas, B., Aborg, C. H., Lyssarides, L., andThyberg, J. (1985). Cation exchanger property of isolated rat peritoneal mast cell granules. Acta.Physiol. Scand. Suppl. 125: 25-31.Uvnas, B., and Aborg, C. H. (1977). On the cation exchanger properties of rat mast cell granules and their storage of histamine. Acta. Physiol.Scand. 100: 309-314."VVale, R. D., and Toyoshima, Y. Y. (1988). Rotation and transition of microtubules in vitro induced by dyneins from Terahymena Cilia.. Cell 52: 459-469.Vale, R. D., Funatsu, T., Pierce, D. W., Romberg, L., Harada, Y, and Yanagida, T. (1996). Direct observation of single kinesin molecules movingalong microtubules. Nature 380: 451-453.Valentijn, K., Valentijn, J. A., and-'Jamieson, J. D. (1999). Role of actin in regulated exocytosis and compensatory membrane retrieval: insightsfrom an old acquaintance. Biochem. Biophys. Res. Commun, 266: 652-661.vanIterson, W. (1965). Symposium on the fine structure and replication of bacteria and their parts. Bact. Rev. 29: 299-325.Verdugo, P. (1990). Goblet cells secretion and mucogenesis. Ann.. Rev. Physiol. 52: 157-176.Verdugo, P., and Orellana, M. V. (1995). The secretory granule as a biomimetic model for drug delivery. Proc. Intern. Symp. Control Rel. Bioact.Mater.22: 25-33.Verdugo, P., Deyrup-Olsen, L, Martin, A. W, and Luchtel, D. L. (1992). Polymer gel-phase transition: the molecular mechanism of productrelease in mucin secretion?NATO ASI Series Vol. H64, Mechanics of Swelling, ed. T. K. Karalis, Springer, Berlin.Verdugo, P., Orellana, M. V, and Freitag, C. (1995). The secretory granule as a biomimetic model for drug delivery. Proc. Intern. Symp. ControlRel. Bioact. Mater. 22:25.Visscher, K., Schnitzer, M. J., and Block, S. M. (1999). Single kinesin molecules studied with a molecular force clamp. Nature 400(6740): 184-189.Vogler, E. A. (1998). Structure and reactivity of water at biomaterial surfaces. Adv. Colloid and Interface Sci. 74:69-117.Von Hippel, P. H., and Wong, K-Y. (1964). Neutral salts: the generality of the stability of macromolecular conformation. Science 145: 577-580.Von Zglinicki, T. (1988). Monovalent ions are spatially bound within the sarcomere. Gen. Physiol. Biophy. 7: 495-504.WWalczak, E. C., Mitchison, T. J., and Desai, A. (1996). XKCM1: a Xenopus kinesin-related protein that regulates microtubule dynamics duringmitotic spindle assembly. Cell 84: 37-47.Walker, M. and Trinick, J. (1986). Electron microscope study of the effect of temperature on the length of the tail of the myosin molecule. /.Mo 1. Biol.192: 661-667.Walker, R. A., Salmon, E. D., and Endow, S. A. (1990). The Droso-phila claret segregation protein is a minus-end directed motor molecule.Nature 347: 780-782.Walzthony, D., and Eppenberger, H. M. (1986). Melting of myosin rod as revealed by electron microscopy. II. Effects of temperature and pH onlength and stability of myosin rod and its fragments. Eur. J. Cell Biol. 41: 38-43.Walzthony, D., Eppenberger, H. M., and Walliman, T. (1986). Melting of myosin rod as revealed by electron microscopy. I. Effects of glyceroland anions on length and stability of myosin rod. Eur. J. Cell Bio. 41: 33-37.Wang, C., Stewart, R. J., and Kopecek, J. (1999). Hybrid hydrogels assembled from synthetic polymers and coiled-coil protein domains. Nature397: 417-420.Wang,N., Butler, J.P.,and Ingber, D.E.(1993). Mechanotransduction across the cell surface and through the cytosk-eleton. Science 260: 1124-1127.Warner, F. D., and Mitchell, D. R. (1981). Polarity of dynenin-mi-crotubule interactions in vitro: cross-bridging between parallel and anti-parallel microtubules. /. Cell Biol. 89:35-44.Washabaugh, M. W, and Collins, K. D. (1986). The systematic characterization by aqueous column chromatography of solutes which affect proteinstability. J. Biol. Chem. 261: 12477-12485.Watterson, J. G. (1991). The role of water in cell function. Biofizika. 36(1): 5-30.Watterson, J. G. (1997). The pressure pixel-unit of life? BioSytems 41: 141-152.Weisenberg, R. C., and Cianci, C. (1984). ATP-induced gelation-contraction of microtubules assembled in vitro. /. CellBiol. 99: 1527-1533.Weiss, R. M., Lazarra, R., and Hoffman, B. R (1967). Potentials measured from glycerinated cardiac muscle. Nature215: 1305-1307.Wells, A. L, Lin, A. W., Chen, L.-Q., Safer, D., Cain, S. M., Hasson, T., Carragher, B. O., Milligan, R. A., and Sweeney , H. L. (1999). MyosinVI is an actin-based motor that moves backwards. Nature 401: 505-508.Whittam, R. (1961). Active cation transport as a pace-maker of respiration. Nature 19: 603-604.Wiggins, P. M. (1990). Role of water in some biological processes. Microbiol. Rev. 54(4): 432-449.Wiggins, P. M., and van Ryn, R. T. (1990). Changes in ionic selectivity with changes in density of water in gels and cells. Biophys. J. 58: 585-596.Wohlfarth-Botterman, K. E. (1964). Diffetentiations of the ground cytoplasm and their significance for the generation of the motive force ofameboid movement. Primitive Motile Systems in Cell Biology, ed. R. D. Alien, and N. Kamiya, Acad. Press, N. Y.Wojcieszyn, J. W., Schlegel, R. A., Wu, E.-S., and Jacobson, K. A. (1981). Diffusion of injected mactomolecules within cytoplasm of livingcells. Proc. Nat'1. Acad. Sci. USA 78(7): 4407-4410.Woodbury, D. (1989). Pure lipid vesicles can induce channel-like conductances in planar bilayers. /. Memb. Biol. 109(2): 145-150.

77

Wordeman, L., and Mitchison, T. J. (1995). Identification and partial characterization of mitotic centromere- associated kinesin, a kinesin-related protain that associates with centromeres during mitosis. /. Cell Biol. 128: 95-104.XXie, T-D, Sun, L., and Tsong, T. Y. (1990). Studies of mechanisms of electric field-induced DNA transfection. Biophys. J. 58: 13-19.Xu, X.-H. N, and Yeung, E. S. (1998). Long-range electrostatic trapping of single-protein molecules at liquid-solid interface. Science 281:1650-1653.YYanagida, T., and Oosawa, R (1978). Polarized fluorescence from ep-silon-ADP incorporated into F-actin in a myosin-free single fiber: conformation ofF-actin and changes induced in it by heavy meromyosin. / Mol. Biol. 126: 507-524.Yanagida, T., Nakase, M., Nishiyama, K., and Oosawa, R (1984). Direct observation of motion of single F-actin filaments in the ptesence ofmyosin.Nature 307:58-60.Yang, P., Tameyasu, T,, and Pollack, G. H. (1998). Stepwise shortening in single sarcomeres of single myofibrils. Biophys. J. 74: 1473-1483.Yano, M., Yamada, T., and Shimizu, H. (1978). Studies of the chemo-mechanical conversion in artificially produced streamings. /. Biochem. 84: 277-283.Yano, M., Yamamoto, Y, and Shimizu, H. (1982). An actomyosin motor. Nature 299: 557-559.Yasunaga, H., and Ando, I. (1993). Effect of ctoss-linking on the molecular motion of water in polymer gel as studied by pulse H NMR and PGSRH NMR.Polym Gels and Ntwks 1: 267-274.Yasunaga, H., Kobayashi, M., Matsukawa, S., Kurosu, H., and Ando, I. (1997). Structures and dynamics of polymer gel systems viewed from NMR.spectroscopy.NMR. in Polymer Science, Acad. Press, London.Yawo, H., and Kuno, M.(1985). Calcium dependence of membrane sealing at the cut end of the cockroach giant axon. /. Neurosci. 5: 1626-1632.Yen, T. J., Li, G., Cshaar, B. T., Szilak, L, and Cleveland, D. W. (1992). CENP-E is a putative kinetochore motor that accumulates justbefore mitosis. Nature359: 536-539.Yoshizaki, K., Seo, Y, Nishikawa, H., and Morimoto, T. (1982). Application of pulsed-gradient 31P NMR on frog muscle to measure the diffusionrates of phosphorous compounds in cells. Biophys. J. 38: 209-211.Yuan, S., and Hoffman, A. S. (1995). Synthetic sulfonated microspheres as drug delivery carriers. Proc. Int ern. Symp. Control Rel. Bioact.Mater. 22: 26-27.Zimmermann, U., Zhu, ]. J., Meinzer, R C., Goldstein, G., Schneidet, H., Zimmermann, G., Benkert, R., Thurmer, F., Melcher, P., Webb, D., andHaase, A. (1994). High molecular weight organic compounds in the xylem sap of mangroves: implications for long -distance water transport. Bot.Acta. 107:218-22Yamada, T. (1998). H-NMR spectroscopy of the intracellular water of testing and rigor frog skeletal muscle. Mechanisms of Work Production andWork Absorption in Muscle, ed. H. Sugi, and G. H. Pollack,

CopperReferences:

1]AggettP.J.,Fairweather-Tait. AdaptationtoHighandLowCopper Intakes: ItsrelevancetoEstimatedSafe and adequatedailydietary intakes. Am J ClinNut.67:1061S -

63.1998

2]AllcroftR.&UvarovO. ParenteralAdministrationofCopperCompoundstoCattlewithSpecialReferenceto Copper Glycine (Copper Amino-acetate). Vet. Rec. 71:

797-810.1959

3] AminoffM.J.PharmacologicmanagementofParkinsonismandothermovementdisorders. In:Katzung,B.G. (editor),Basic &ClinicalPharmacology(sixth edition).

Prentice-Hall International, London.419-431,1995

4]ArnonD.I.&StoutP.R. TheEssentialityofCertainElementsinMinuteQuantityforPlants,withSpecialReference to Copper. Plant Phvsiol. 14:371-5,1939

5]BarberR.S. et al.FurtherStudies on AntibioticandCopper Supplements for FatteningPigs.Brit. J. Nutr.1170-79,1957

6]BaumslagN., etal. TracemetalContentofmaternalandneonatehair. ArchEnvironHealth.29,1974

7]BaxterJ.H.&WykJ.S.VanABoneDisorderAssociatedwithCopperDeficiency.Bull. JohnsHopk.Hosp.93:1 -23,1953

8]BennetsH.W., etal.StudiesonCopperDeficiencyinCattle: theFatalTermination(FallingDisease).Aust. VetJ. 18:50-63, 1942

9]BeshgetoorL.&HambridgeM.Clinicalconditionsalteringcoppermetabolisminhumans. AmJClinNutr.67:1017S-21S,1998

10]Boccuzzi G., etal.Protectiveeffectofdehydroepiandrosteroneagainst copper -induced lipidperoxidation in

Calves. Anim. Prod. 4: 303-7,1962

71] Nakakoshi T. Copper andhepatocellular carcinoma. Radiology (United States), Jan. 214(1) p304 -6,2000

72] Narasaka S. Studies in theBiochemistryof Copper.XX. Thyroidasa Factor in theRegulationof Blood

Copper Level. Jap. J. Med. Sci. 4: 33-36,1938

73] Neelakantan V. &Mehta B.V. Copper Status of Soils in Western India. Soil Sci. 91:251-6,1961

74] Nolan K.R. Copper toxicity syndrome. J Orthomol Psych. 12:270-282,1983

75] O'DellB.L.Biochemistryof Copper. TheMedicalClinics of North America 60. Saunders Press. 1960

76] OsieckiHenryTheNutrientBible.BioConcepts Publishing.1998

77]OwenC.A,Copperdeficiencyandtoxicity:Acquiredandinherited inplants,animalsandman.Park Ridge

NJNoyesPub. 1981

78

78] Pfeiffer C. Mental and ElementalNutrients. Keats NewCanaan. 1975

79] PirrieR.SerumCopperand itsRelationship toSerum Iron inPatientswith Neoplastic Disease. J Clin.Path.

5: 190-3, 1952

80] Polukhina1.N.&MasljanajaH.K. Influenceof Nitrogen andCopper on theAnatomicalStructureof Oat

StemsinRelationtotheResistanceofOatsonPeatSoils. (English translation), Izv.Timir.Sol.ShokhAkad.,

No.l, 205-8, 1961

81]PrattW.B. Elevatedhaircopperin idiopathicscoliosisandofnormalindividuals. ClinChem.24,1978

82] Ramaswamy M.S. Copper in Ceylon Teas. Tea Quart. 31:76-80,1960

83] ReavleyNicolaTheNewencyclopaedia ofVitamins.Minerals.SupplementsandHerbs.Bookman Press.

1998

84] Robertson H. A. &Broome A.W.J.Factors Influencing theBlood Copper Levelof Sheep: theEffect of

change in Basal Metabolic Activity. J.Sci. Fd. Agric. (Supp. Issue), 8, s. 82-s. 87,1957

85] Roelofsen H., Wolters H., Van Luyn M.J., et al.Copper-inducedapical trafficking ofATP7Bin polarized

hepatoma cells provides a mechanism for biliary copper excretion.Gastroenterology (United States), Sep.

119(3):782-93, 2000

86]SandsteadHH. Copper bioavailability and requirements.American Journal of Clinical Nutrition. 35:809-

814, 1982

87] SchultzeM.O. TheEffect of Deficiencies in Copper and Iron on theCytochromeOxidaseof Rat Tissues. J.

Biol. Chem. 129: 729-37,1939

88] Shore D., etal.CSF copper concentrations in chronic schizophrenia. American Journal of Psychiatry.

140:754-757, 1983

89] SidhuK. S., etal.Need to revise the national drinking water regulation for copper. RegulToxicol

Pharmacol. 22(1): 95-100,1995

90] SoliozM. et alCopper pumping ATPases: common concepts in bacteria and man. FEBS Lett. 346:44-7,

1994

91] Stine J.B., et al. Copper and Cheddar Flavour.Dairy World, Chicago. 32:10-14,1953 (Chemical

Abstracts, 48,900)

92] Sugimoto Y, et alCations inhibit specifically type1 5 alpha-reductase found in human skin.J Invest

Dermatol. 104(5): 775-778,1995

93] Takamiya K. Anti-tumour Activities of Copper Chelates. Nature. 185:190-1,1960

94]TimberlakeC.F. ComplexFormationbetweenCopperandsomeOrganicAcids.PhenolsandPhenolicAcids

Occurring in Fruit. J. Chem. Soc. 2795-8,1959

95] Tumlund et al.Copperabsorption, excretion and retention byyoungmen consuming lowdietarycopper

determined by using stable isotope 65Cu. AM J Clin Nut. 67: 1219-1225,1998

96] Van Campen D.R. Zinc interference with copper absorption in rats. Journal of Nutrition. 91:473,1967

97] Van den Berg G.J., et al.Dietary ascorbic acid lowers theconcentration of soluble copper in thesmall

intestinal lumen of rats. BrJNutr. 71(5): 701-707,1994

98] Van Koetsveld E.E.TheManganeseand Copper contents ofhairasan indication of the feedingcondition of

cattle regarding manganese and copper. Tijdschr. Dieregeneesk. 83:229,1958

99] Vir et al. Serum and hair concentrations of copper during pregnancy. Am J ClinNutr. 34:2382-2388,1981

Metals and Glucose ControlI] Abraham A. S., et al.The effects of chromium supplementation on serum glucose and lipids in patients with and wi thout non-insulin dependentdiabetes. Metabolism. 41:768-771,1992

79

2] Anderson R., et al.Beneficial effects of chromium for people with Type II Diabetes. Diabetes. 45(Suppl. 2): 124A/454,1996 , 3] Anderson R.A.,Roussel A-M, Zouari N., et al.Potential antioxidant effects of zinc and chromium supplement in people with type II diabetes mellitus. J Am Coll Nutr.20(3):212-218.20014] Anderson R. A., et al. Chromium supplementation of human subjects: Effects on glucose, insulin, and lipid variables. Metabolism. 32:894-899,19835] Anderson R. A., et al. Supplemental chromium effects on glucose, insulin, glucagon. and urinary chromium losses in subjects consuming low-chromiumdiets. American Journal of Clinical Nutrition. 54:909-916,19916] Anderson R. A., et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with ; type 2 diabetes.Diabetes. 46:1786-1791,19977] Anderson R. A. Nutritional factors influencing the glucose/insulin system: chromium. J Am Coll Nutr. 16(5):404-410,1997 ; 8] Baly P.. et al. Effect ofmanganese deficiency on insulin binding, glucose transport & metabolism in rat adipocytes. J Nutr. 120:1075-1079,19909] Boden G., et al.Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus.Metabolism. 45:1130-1135,199610] Boyd S. G., et al. Combined dietary chromium picolinate supplementation and an exercise program leads to a reduction of serum cholesterol and insulinin college-aged subjects. J Nutr Biochem. 9:471-475,1998II] Cam M. C., et al.Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes.Eur J Endocrinol. 141(5):546-554,199912]Chanetal. The role of copper, molybdenum selenium and zinc in nutrtion and health. Clin Lab Med. 18(4): 673-85,1998 13] Chauser A. Zinc.Insulin and Diabetes. J of American College ofNutrition 17(2): 109-115,199814] Cohen N., et al.Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin-dependent diabetesmellitus. Journal of Clinical Investigations. 95(6):2501-2509,199515] Combs G.F. and Combs S.B. The Role of Selenium in Nutrition. Academic Press, Inc., Orlando, USA, 1986 16] Corica F.. Allegra A.. Di Benedetto A., etal. Effects of oral magnesium supplementation on plasma lipid concentrations of patients with non-insulin-dependent diabetes mellitus. Magnes Res. 7:43-47,199417] Davies S.,etal.Age-related decreases in chromium levels in 51.665 hair, sweat, and serum samples from 40.872 patients -implications for theprevention of cardiovascular disease and type II diabetes mellitus. Metabolism. 46(5):469-473,1997 18] Evans G. W. The effect of chromium picolinateon insulin controlledparameters in humans. Int J Biosocial Medical Research. 11:163-180,198919] Evans G. W., et al. Chromium picolinate increases membrane fluidity and rate of insulin internalization. J Inorg Biochem.46(4):243-250,1992 :

20] Fugii S., Takemura T., Wada M., et al. Magnesium levels in plasma, erythrocyte. and urine in patients with diabetes mellitus.HormMetabRes. 14:161-162,198221] Haglund et al. Evidence of a relationship between childhood onset type 1 diabetes and low groundwater concentration of zinc. Diabetes Care Aug.19:8 873-5,199622] Jing M.A., Folsom A.R., Melnick S.L., et al. Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes,insulin, and carotid arterial wall thickness: the ARIC study. J Clin Epidemiol. 48:927-940,1995 23]KellyG.S. Insulin resistance: lifestyle andnutritional interventions. Alternative Medicine Review. 5(2):109-132,2000 24] Leach R.M.Jr. Metabolism & Function of Manganese. Traceelements in Human Health & Disease. Vol.III. 25] Lee N. A., et al. Beneficial effect of chromium supplementation on serum triglyceride levels inNIDDM. Diabetes Care. 17(12):1449-1452,199426]Mather H. M., etal.Hypomagnesemia in diabetes. Clin Chem Acta. 95:235-242,197927] McNeillJ. Enhanced in vivo sensitivity of vanadyl-treated diabetic rats to insulin. Canadian Journal of Physiology and Pharmacology. 68(4):486-491,199628]MechegianiE.,etal. Zinc-dependent low thymic hormone level in type I diabetes. Diabetes. 12:932-937,1989 29]MertzW., etal. Present knowledgeof the role of chromium.Federation Proceedings. 33:2275-2280,1974 30]NakamuraT.,etal. Kinetics of zinc status in children with IDDM. DiabetesCare. 14:553-557,1991 31] Niewoener C. B.. et al. Role of zinc supplementation in type II diabetes mellitus. Am J Med. 63-68,1988 32] Paolisso G., et al.Improved insulin response and action by chronic magnesium administration in aged NIDDM subjects. Diabetes Care. 12(4):265-269,198933] Paolisso et al. Hypertension, diabetes and insulin resistance: the role of intracellular magnesium.Am J Hypertens. 10:3 346-55,199734] Pepato M. T., etal. Effect of oral vanadyl sulfate treatment on serum enzymes and lipids of streptozotocin-diabetic young rats. Mol Cell Biochem.198(1-2):157-161,199935]PidduckH.G.,et al.Hyperzincuria of diabetes mellitus and possible genetic implications of this observation. Diabetes.19:240-247,1970

36]PreussH.G.,etal.Chromium update: examining recent literature 1997-1998.Ciirr Opin Clin Nutr Metab Care. 1:509-512,199837]Poucheret P.. et al. Vanadium and diabetes. Mol Cell Biochem. 188(l-2):73-80,199838] Prout I.E., et al. Zinc Metabolism in Patients with Diabetes Mellitus. Metabolism. 9:109-17,196039] Pryor K. Nutritional approaches to optimal blood glucose and insulin levels: key factors in longevity and resistance to

80

diabetes and other degenerative diseases.Vitamin Research News. April 200040] Rabinowitz M. B., et al.Effects of chromium and yeast supplements on carbohydrate and lipid metabolism in diabetic men.Diabetes Care. 6(4):319-327,198343]RaoK.V.R., etal. Effect of zinc sulfate therapy on control and lipids in type I diabetes. JAPI. 35:52,198744]RaymanM.P. The importance of selenium to human health.Lancet. 356(9225): 233-241,200045]ReavenG. Role of insulin resistance in human disease. Diabetes. 37:1595-1607,199846] Resnick L. Magnesium in the pathophysiology and treatment of hypertension and diabetes mellitus: where are we in 1997?Am J Hypertension. 10:368-370,1997

47] Rubinstein A.H.Manganese-induced hypoglycemia. The Lancet. 2:1348-1351,196248] Rubenstein A.H.. et al. Hypoglycemia induced by manganese. Nature. 194:188-9,196249] SakuraiH., etal. Insulin-like effect of vanadyl ion on streptozotocin-induced diabetic rats. JEndocrinol. 126(3):451-459,199050] SeeligM.S..et al. Low Magnesium: A Common Denominator in Pathologic Process in Diabetes Mellitus. CardiovascularDisease and Eclampsia. Journal of the American College of Nutrition. October: 11(5): 608/Abstr39,199251] Sjogren A., etal. Oral administration of magnesium hydroxide to subjects with insulin-dependent diabetes mellitus.Magnesium. 121:16-20,198852] Sjogren A. et al. Magnesium, potassium and zinc deficiency in subjects with type II diabetes mellitus. Acta Med Scand.224(5):461-466,198853] Singh R.B., et al. Current zinc intake and risk of diabetes and coronary artery disease and factors associated with insulinresistance in rural and urban populations of North India. J Am Coll Nutr. 17:564-570,199854] Stapleton S.R. Selenium: an insulin-mimetic. Cell MolLife Sci. 57(13-14): 1874-1879,200055] Striffler J. S.,etal.Chromium improves insulin response to glucose in rats. Metabolism. 44:1314-1320,199556] Striffler J. S.,etal.Dietary chromium decreases insulin resistance in rats fed a high-fat, mineral-imbalanced diet.Metabolism. 47:396-400,199857] Striffler J.S., etal. Overproduction of insulin in the chromium-deficient rat. Metabolism. 48:1063-1068,199958] Toplack H., et al. Addition of chromium picolinate to a very low calorie diet improves the insulin-glucose ratio after weight

reduction. International Journal of Obesity. 19(2):s057,199559]UeharaS.,etal. Clinical significance of selenium level in chronic pancreatitis. J Clin Biochem Nutr. 5:201-207,198860] Wallace E. C.Diabetic epidemic. Energy Times. 9(4):24-28 199961] Watts D.L. The nutritional relationships of manganese. J. Orthomol. Med. 5(4):219-22,1990

Heavy Metal References:1] Abe T., et al.High hair and urinary mercury levels offish eaters in the nonpolluted environment of Papua New Guinea. ArcEnviron Health. 50:367-373,19952] Abraham J.E., SvareC.W. & Frank C. W. The effect of dental amalgam restorations on blood mercury levels.J Dent Res. 63:71-7319843] Alexander. The uptake of lead by children in differing environments. Environ Hlth Prospectus. 19744] Aller A. J. The clinical significance of beryllium. J Trace Elements and Electrolytes in Health and Dis. 4,1,19905] Altmann P., et al. Disturbance of cerebral function by aluminum in haemodialysis patients without overt aluminum toxicityLancet. Jul, 19896] Ames B.N. Dietary carcinogens and anticarcinogens. Science. 221:1256-1264,19837] Annest J.I., et al. Chronological trend in blood lead levels between 1976 and 1980. N.E.J.M. 308,23,19838] Anthony H., et al. Environmental Medicine in Practice. Southhamptom: BSAENM Publications. 204-208,19979] Aposhian H.V.DMSA and DMPS-water soluble antidotes for heavy metal poisoning. Ann Rev Pharmacol Toxicol. 23:193-215198310] Aschner M., et al. Interactions of methylmercury with rat primary astrocyte cultures: inhibition of rubidium and glutamatuptake and induction of swelling. Brain Res. 530:245-250,199011] Ashby J., et al. Studies on the genotoxicity of beryllium sulphate in vitro and in vivo. Mutation Res. 240,3,199012] Atchison W.D. & Hare M.F. Mechanisms of methylmercury-inducedneurotoxicity. FASEB J. 8:622-629,199413] Baaumslag N., et al. Trace metal content of maternal and neonate hair. Zinc, copper, iron and lead. ArchEnviron. Hlth. 29,19714] Baker E.L., etal. A nationwide survey of heavy metal absorption in children living near primary copper, lead and zinc smelter. AnJ Epidemiology. 206,4,197715] Bapu C., Rao P. & Sood P.P.Restoration of methylmercury inhibited adenosine triphosphatases during vitamin and monothio

81

therapy. J Environ Path Toxicol Oncol. 17:75-80,199816] Barregard L., Sallsten G. & JarvholmB. People with high mercury uptake from their own dental amalgam fillings. QccupEnvironMed. 52:124-128,199517] Barth G..ed. The Lewis and Clark Expedition. Selections from the Journals Arranged by Topic. New York: Bedford St. Martins158-162,199818] Batuman V.. et al. Contribution of lead to hypertension with renal impairment. N.E.J.M. 309.1.198319] Beattie J.H. & Peace H.S.The influence of a low-boron diet and boron supplementation on bone, major mineral and sex steroimetabolism in postmenopausal women. Brit J Nutr. 69,3,199320] Bhat R.K., et al.Trace elements in hair and environmental exposure. Sci Total Environ. 22(2): 169-178,198221] Bigazzi P.E.Lessons from animal models: the scope of mercury-induced autoimmunity. Clin Immunol Immunopathol. 65:81-!199222] Birchall J.D. & Chappell J.S. Aluminum, chemical physiology and Alzheimer's disease. Lancet. Oct. 198823] Blakley B.R., Sisodia C.S. & Mukkur T.K. The effect of methylmercury. tetraethyl lead, and sodium arsenite on the humoraimmunity response in mice.Toxicol Appl Pharmacol. 52:245-254,198024]BlumerW. & Reich T. Leaded gasoline-a cause of cancer. Environmental International. 3:456-471,198025] Bonhomme C.. et al. Mercury poisoning by vacuum-cleaner aerosol. Lancet. 347:115,199626] Boogaard P.J., et al. Effects of exposure to elemental mercury on nervous system and the kidneys in workers producing naturagas^Arch Environ Health. 5:108-115,199627] BoyceB.F., et al. Hypercalcaemic osteomalacia due to aluminum toxicity. Lancet. Nov, 198228] BoydN.D.. et al. Mercury from dental "silver" tooth fillings impairs sheep kidney function. Am J Phvsiol. 261 :R1010-R1014.19929] Capel I.D., etal. Assessment of zinc status by the zinc tolerance test in various groups of patients. Clin Biochem. 15(2):257-260198230] Cavalleri A. & Gobba F. Reversible color vision loss in occupational exposure to metallic mercury. Environ Res. 77:173-177,199831] Chang L.W. Neurotoxic effects of mercury. A review. Environ Res. 14:329-373,197732] Cheraskin E. & Ringsdorf W.M. The distribution of lead in human hair. J Of Med Assoc of Alabama. April, 197933] Cheraskin E. & Ringsdorf W.M. Prevalence of possible lead toxicity as determined by hair analysis. J Orthomol Psych. 8,2. AmJIndMed. 2,1,5-14,198134] Cianciola M.E., et al. Epidemiologic assessment of measures used to indicate low-level exposure to mercury vapor. J ToxicolEnviron Health. 52:19-33,199735] Cimino J.A. & Demopoulos H.B. Introduction: Determinants of cancer relevant to prevention, in the war on cancer. J EnvironPath. &Toxi.3:l-10,198036] Clarke N.E., Clarke C.N. & Mosher R.E. The "in vivo" disolution of metastatic calcium: An approach to athero-sclerosis. AmiMedSci. 229:142-149,195540] Coccini T., et al. Low-level exposure to methylmercury modifies muscarinic cholinergic.receptor binding characteristics in ratbrain and lymphocytes: physiologic implication and new opportunities in biological monitoring. Environ Health Perspect. 108:29 -33,200041] Collipp P.J., et al. Hair zinc levels in infants. Clin Pediatr. 22(7):512-513,198342] Cooper G.P. & Manalis R.S. Influence of heavy metals on synaptic transmission: a review. Neurotoxicology. 4:69-83,198343] Cornell C.R., Markesbery W.R. & Ehmann W.D. Imbalances of Irace elements related to oxidative damage in Alzheimer's diseasebrain. Neurotoxicology. 19:339-346,199844] Crapper-McLaughlin D.R. Aluminum loxicily in senile dementia: Implications for treatment. Read before the Fall Conference,American Academy of Medical Prevenlics, Las Vegas, NV, Nov 8,198145] Cranlon E.M.. el al. Standardization and interpretation of human hair for elemental concentrations. J Holistic Med. 4:10-20,198246] Crinnion W. J. Unpublished research. Healing Naturally. Kirkland, WA. 199947] David O., el al. Lead and hyperaclivity. behavioral response to chelalion: A pilol study. Am J Psychiatry. 133:1155-1158,197648] De Souza Queiroz M.L., et al. Abnormal antioxidanl system in erythrocytes of mercury exposed workers. Human & Exp Toxicol.17:225-230,199849] Del Maestro R.F. An approach to free radicals in medicine and biology. Acta Physiol Scand. 492(suppl):153-168,198050] Diamond G. & Zalups R.K. Understanding renal loxicity of heavy metals. Toxicol Pathol. 26:92-103.199851] Dieter M.P., et al. Immunological and biochemical responses in mice treated wilh mercuric chloride. Toxicol Appl Pharmacol.68:218-228,198352] Dirks M.J., el al. Mercury excretion and inlravenous ascorbic acid. ArchEnviron Health. 49:49-52,199453] Dix Y. Metabolism of polycyclic aromatic hydrocarbon derivatives to ultimate carcinogens during lipid peroxidation. Science.221:77,1983

82

54] Dormandy T.L. Free-radical reaction in biological systems. Ann R Coll Surg Engl. 62:188-194,198055] Dormandy T.L. Free-radical oxidation and antioxidants. Lancet. i:647-650,197856] Druel P., el al. Immune type glomerulonephrilis induced by HgC 12 in Brown-Norway rat. Ann Immunol (Inst Pasteur). 129C:777 -792,197857] Durham H.D., Minotti S. & Caporicci E. Sensitivity of platelel microlubles lo disassembly by methylmercury. J Toxicol EnviroHealth. 48:57-69, 199758] Ely J.T., et al. Urine mercury in micromercurialism: a bimodal distribution and its diagnostic implications. Unpublished.59] Ely D.L., el al. Aeromelric and hair trace metal conlenl in learning-disabled children. Environ Res. 25(2):325-339,198160] EmerickR.J. & Kayongo-Male H. Silicon facilitation of copper utilization in the rat J Nutr Biochem. 1,199061] Enestrom S. & Hultman P. Immune-mediate glomerular nephritis induced by mercuric chloride in mice. Experientia. 40:1234-1240,198463] Enestrom S. & Hullman P. Dose-response sludies in murine mercury-induced autoimniunity and immune-complex disease.ToxicolApplPharmacol.113:199-208,199264] Engqvisl A., Colmsjo A. & Skare I. Specialion of mercury excreted in feces from individuals wilh amalgam fillings. Arch EnvironHealth.53:205-213,199865] Erickson, el al. Tissue mineral levels in victims of Sudden Infanl Deallh Syndrome 1. Toxic melals - lead and cadmium. Fed Res.17,10,108366] Falconer M.M.. et al. The molecular basis of microtuble stability in neurons. Neurotoxicology. 15:109-122,199467] FiedlerN., el al. Neuropsychological and slress evaluation of residential mercury exposure. Enviro Heallh Perspect 107:343-347,199968] Florence T.M.. Lilley S.G. & Slauber J.L. Skin absorption of lead. Lancet Jul. 16,198869] Foli M.R., Hennigan C. & Errera J. A comparison of five toxic melals among rural and urban children. Environ Pollul Ser A EcolBiol.29:261-270,198270] Fukuda Y., et al.An analysis of subjective complainls in a populalion living in a methylmercury-polluted area. Environ Res.81:100-107,199971] GalsterW.A. Mercury in Alaskan Estimo mothers and infants. Environ Heallh Perspect 15:135-140,197672] Ganther H.E. Selenium: relation to decreased loxicity of methylmercury in diels conlaining luna. Science. 175:1122,197273] Ganlher H.E. Modification of methylmercury toxicily and melabolism by selenium and vilamin E: possible mechanisms.EnvironHeallh Perspect 25:71-76,197874] Garrell P.J., et al.Aluminum encephalopalhy: Clinical and immunological features. Quart J Med. 69,258, 198875] Gibson R.S. & Gage L. Changes in hair arsenic levels in breast and bottle fedinfanls during Ihe firsl year of infancy. Sci TolalEnviron.26:33-40,198276] Goldberg R.L., Kaplan S.R. & Fuller G.C.Effecl of heavy melals on human rheumatoid synovial cell proliferation and collagensynthesis. Biochem Pharmacol. 32:2763-2766,198377] Grandjean P., et al. Methylmercury neurotoxicily in Amazonian children downslream from gold mining.Environ Heallh Perspect107:587-591,199978] Grandjean P., el al. Relation of a seafood diet to mercury, selenium, arsenic and polychlorinated biphenyl and other organochlorineconcentrations in human milk. Environ Res. 71:29-38. 199579] Giaziano J.H., Lolacono N.J. & Meyer P. Dose-response sludy of oral 2.3-dimercaptosuccinic acid in children wilh elevatedblood lead concentrations. J Pediatr. 113:751-757,198880] Giaziano J.H. Role of 2.3-dimercaptosuccininc acid in the treatment of heavy metal poisoning. Med Toxicol. 1:155 -162,198681] Grazino J.H. & Blum C. Lead exposure from lead crystal. Lancet. 337,199182] Gunderson E.L. PDA Total Diet Study. April 1982-April 1986. Dietary intake of pesticides, selected elements and other chemicals.Distributed by: Association of Official Analytical Chemists. Arlington, VA.83] Hahn L.J., et al. Dental "silver" tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissueanalysis. FASEB J. 3:2641-2646.198984] Hahn L. J., et al. Whole body imaging of the distribution of mercury released from dental fillings into monkey tissue. FASEB J.4:3256-3260,199085] Halbach S., et al. Compartmental transfer of mercury released from amalgam. Hum Exp Toxicol. 16:667-672,199786] Halbach S., et al. Systemic transfer of mercury from amalgam fillings before and after cessation of emisson. Environ Res. 77:115-123,199887] Hansen J.C., Christensen L.B. & Tarp U. Hair lead concentration in children with minimal cerebral dysfunction. Danish Med Bull.27:259-262,198088] Harada M., et al. The present mercury contents of scalp hair and clinical symptoms in inhabitants of the Minamata area. Environ

83

Res. 77:160-164,199889] Harnly M., et al. Biological monitoring for mercury within a community with soil and fish contamination. Environ HealthPerspect. 105:424-429,199790] Harrison W., Yurachek J. & Benson C. The determination of trace elements in human hair by atom ic absorption spectroscopy.ClinChimActa.23(l):83-91,196991 ] Herrstrom P., et al. Dental amalgam, low-dose exposure to mercury, and urinary proteins in young Swedish men. Arch EnvironHealth. 50:103-110,199592] Hibberd A.R., Howard M.A. & Hunnisett A.G. Mercury from dental amalgam fillings: studies on oral chelating agents forassessing and reducing mercury burdens in humans. J Nutr Environ Med. 8:219-231.199893] Homma-Takeda S., et al. Selective induction of apoptosis of renal tubular cells caused by i norganic mercury in vivo. EnvironToxicol Pharmacol. 7:179-187,199994] Huel G., Boudene C. & Ibrabim M.A. Cadmium and lead content of maternal and newborn hair: Relationship to parity, birthweight and hypertension. Arch Environ Health.,35(5^):221-227.198195] Hunt C.D., Shuler T.R. & Mullen L.M'. Concentration of boron and other elements in human foods and personal-care products.J Am Diet Assoc. 91,5,199196] Hurry V.J. & Gibson R.S. The zinc, copper and manganese status of children with malabsorption syndromes and in -born errorsofmetabolism. Biol Trace Element Res. 4:157-173.198297] InSug O., et al. Mercuric compounds inhibit human monocyte function by reactive oxygen species, development of rmtochondrial jmembranepermeability transition and loss ofreductive reserve. Toxicology. 124;211-224,199798]JenkinsD.W.ToxicTraceMetals inMammalian HairandNails.USEnvironmentalProtection AgencypublicationNo. (EPA)-600/4-79-049.EnvironmentalMonitoringSystemsLaboratory.197999]JenkinsD.W.Biologicalmonitoringoftoxic tracemetalsVol.1.Biologicalmonitoringandsurveillance.EPA600/3-80-089,1980.ClinChem.36,3,1990100] Jones R.J. Thecontinuing hazard of lead in drinking water. Lancet. Sept 16,1989101] Kanematsu N., et al.Mutagenicityof cadmium,platinum and rhodium compounds in cultures mammalian cells. Gifu ShikaZasshi.17,2,1990102] KingN., et al. The effect of in ovo boron supplementation on bonemineralization of thevitamin D-deficient chicken embryo.BiolTraceElementRes.31,1,1991103] KisselK.P.Teens fall ill after taking,playing with mercury. The SeatleTimes: January15,1998104] Klevay L. Hairasabiopsymaterial-assessmentofcoppernutriture. Am JClinNutr. 23(8):1194-1202,1970105]KolataG.Newsuspect inbacterial resistance:amalgam.TheNewYork Times:April24,1993106] Kopito L., et al. Chronic plumbism in children. Diagnosed byhair analysis. J.A.M.A. 209,2,1969107]LangworthS.,BlinderC.G.&SundqvistK.G.Minoreffectsof lowexposuretoinorganicmercuryonthehumanimmunesystemScanJWorkEnvironHealth.19:405-413,1993108] Lebel J.,Mergler D. &LucotteM.Evidenceof earlynervoussystemdysfunction in Amazonian populations exposed to low-.levelsofmethylmercury.Neurotoxicology.17:157-167,1996109] LevineS.A. &Reinhardt J.H.Biochemical-pathologyinitiated byfree radicals, oxidant chemicalsand therapeuticdrugs in theetiology of chemicalhypersensitivitydisease. J OrthomolPsychiatr. 12(3):166-183,1983110] Lichtenberg H. Symptoms before and after proper amalagam removal in relation to serum-globulin reaction to metals. JorthomolecMed.11:195-204,1996112] Lieb J. &Hershman D. Isaac Newton:mercurypoisoningor manicdepression.Lancet.1479-1480,1983113]MagourS.,MaserH.&Grein H.Theeffect ofmercuryand methylmercuryon brainmicrosomalNa+,K+ ATPaseafterpartialdelipidisation with Lubrol.PharmacolToxicol.60:184-186,1987114]MaloneyS.R.. PhillipsC.A. &Mills A.Mercury in thehairofcrematoria workers.Lancet. 352:1602,1998115] Marlowe M.,etal. Increased lead burdens and trace mineral status in mentally retarted children. J SpecEduc. 16:87-99,1982116] Marlowe M., et al. Lead and mercury levels in emotionally disturbed children. J Orthomol Psychiatr. 12(4):260-267,1983117] Marlowe M. & Mood C. Hair aluminum concentration and nonadaptive classroom behavior. J of Advancement in Med. 1,3,1988118] Matte T.D., et al. Acute high-dose lead exposure from beverage contaminated by traditional Mexican pottery. Lancet. 344,8929,1994

119] Matthews A.D. Mercury content of commercially important fish of the Seychelles and hair mercury levels of a selected part ofthe population. Environ Res. 30:305-312.1983120] Medeiros D.M. & BorgmanR.F. Blood pressure in young adults as associated with dietary habits, body conformation and hairelement concentrations. NutrRes. 2:455-466.1982121] Medeiros D.M, Pellum L.K. & Brown B.J. The association of selected hair minerals and anthropometric factors with blood

84

pressure in a normotensive adult population. Nutr Research. 3:51-60,1983122] Medeiros D.M. & Pellum L.K.Elevation of cadmium, lead and zinc in the hair of adult black female hypertensives. Bull EnvironToxicol.32,1984123] Miettinen J.K. Absorption and elimination of dietary mercury (2+) ion and methylmercury in man. In: Miller MW, ClarksonT.W., eds. Mercury, Mercurials and Mercaptans. Proceedings 4th International Conference on Environmental Toxicology. New York:Plenum Press; 1973124] Miller O.M., Lund B.O. & Woods J.S.Reactivity of Hg(II) with superoxide: evidence for the catalytic dismutation of superoxidebv Hg<m J Biochem Toxicol. 6:293-298,1991125] Miura K., et al. The involvement of microtubular disruption in methylmercury-induced apoptosis in neuronal and nonneuronalcell lines. Toxicol Appl Phamacol. 160:279-288,1999126] Moser P.B., Krebs N.K. & Blyler E.Zinc hair concentrations and estimated zinc intakes of functionally delayed normal sizedand small-for-age children. Nutr Research. 2:585-590.1982127] Musa-Alzudbaidi L., et al. Hair selenium content during infancy and childhood. Eur J Pediatr. 139:295-296,1982128] Nakatsuru S., et al.Effect of mercurials on lymphocyte functions in vitro. Toxicology. 36:297-305,1985129] Narang A.P.S., et al. Arsenic levels in opium eaters in India. Trace Elements in Med. 4,4,1987130] Ngim C.H., et al.Chronic neurobehavioral effects of elemental mercury in dentists. Br J Indust Med. 49:782-790,1992131] Niculescu T., etal. Relationship between the lead concentration in hair and occupational exposure. Brit J Industrial Med. 40,67,1983132] Ninomiya T., et al. Expansion of methylmercury poisoning outside of Minamata: an epidemiological study on chronicmethylmercury poisoning outside Minamata. Environ Res. 70:47-50,1995133] Nolan K.R.Copper toxicity syndrome. J Orhtomol Psychiatr. 12(4):270-282,1983134] Nordlind K.Inhibition of lymphoid-cell DNA synthesis by metal allergens at various concentrations. Effect on short-timecultured non-adherent cell compared to non-separated cells. Int Arch Allergy Appl Immunol. 70:191-192,1983135] Nriagu J.O. Lead and Lead Poisoning in Antiquity. Wiley N.Y. 1983136] Orloff K.G.. et al. Human exposure to elemental mercury in a contaminated residential building. Arch Environ Health. 52:169-172.1997137] OrtegaH.G., et al. Neuroimmunological effects of exposure to methylmercury forms in the Sprague -Dawley rat. Activation ofthe hypothalamic-pituitary-adrenal axis and lymphocyte responsiveness. Toxicol Indust Health. 13:57 -66,1997138] Oskarsson A., et al. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillingsin lactating women. Arch Environ Health. 51:234-241,1996139] OudarP, Caillard L. & Fillon G. In vitro effects of organic and inorganic mercury on the serotonergic system. Pharmacol Toxicol.65:245-248,1989140] Patterson J.E., Weissberg B. & Dennison P.J. Mercury in human breath from dental amalgam. Bull Environ Contam Toxicol.34:459-468,1985141] Pearl D.P., et al. Intraneuronal aluminum accumulation in Amyotrophic Lateral Sclerosis and Parkinsonism -Dementia of Guam.Science. 217,1982142] Pendergrass J.C., et al. Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesionin Alzheimer's disease brain. Neurotoxicity. 18:315-324,1997143] Pendergrass J.C. & Haley B.E. Mercury-EDTA complex specifically blocks brain beta-tubulin-GTP interactions: similarity toobservations in Alzheimer's disease. In: Friberg L.T., Scrauzer G.N., eds. Status Quo and Perspectives of Amalgam and other DentalMaterials. Stuttgart: GeorgThieme Verlag.98-105,1995144] Peters H. A. Trace minerals, chelating agents and the por-phyrias. Fed Proc. 20(3)(Part II)(suppl 10):227-234.1961145] Peters H.A.. et al. Arsenic, chromium and copper poisoning from burning treated wood. N Engl J Med. 308(22): 1360-1361,1983146] Peters H.A.. et al. Seasonal arsenic exposure from burning treated wood. J.A.M.A. 11;25,18,2393-2396,1984147] Peto R.. et al. Can dietary beta-carotene materially reduce human cancer rates? Nature. 290:201.1981148] Rajanna B. & Hobson M. Influence of mercury on uptake of dopamine and norepinephrine by rat brain synaptosomes. ToxicolLett. 27:7-14,1985149] Rajanna B., et al. Effects of cadmium and mercury on Na+. K+ ATPases and the uptake of 3H-dopamine in rat brain synaptosomes.Arch Int Physiol Biochem. 98:291-296,1990150] Redhe O. & Pleva J. Recovery from Amyotrophic Lateral Sclerosis and from allergy after removal of dental amalgam filling. IntJ Risk Safety Med. 4:299-236,1994151] Rees E.L. Aluminum poisoning of papua New Guinea natives as shown by hair testing. J Orthomol Psychiatr. 12(4):312-313,1983152] Salonen J.T., et al. Intake of mercury from fish, lipid peroxidation. and the risk of myocardial infarction and coronary, cardiovascular.and any death in eastern Finnish men. Circulation. 91:645-655,1995

85

153] Schroeder H. A. & Perry H.M. Jr. Antihypertensive effects of metal binding agents. J Lab Clin Med. 45:416,1955154] Seven M.J. & Johnson L.A. (eds). Metal Binding in Medicine: Proceedings of a Symposium Sponsored by HahnemannMedical College and Hospital. Philadelphia. Philadelphia. J.B. LippincottCo., 1960155] Sharp D.S. & Smith A.H. Elevated blood pressure in treated hypertensives with low-level lead accumulation. Arch EnvironHlth. 44,1,1989156] Shenker B.J., Guo T.L. & Shapiro I.M. Low-level methylmercury exposure causes human T -Cells to undergo apoptosis:evidence of mitochondrial dysfunction. Enviro Res. 77:149-159.1998157] SiblerudR.L. The relationship between mercury from dental amalgam and mental health. Am J Psychotherapy. 43:575-587.1989158] Sitprija V., et al. Metabolic problems in northeastern Thailand: possible role of vanadium. Mineral and Electrolyte Metabol.19,1,1993159] Skerfving S. Mercury in women exposed to methylmercury through fish consumption, and in their newborn babies and breastmilk. Bull Environ Contam Toxicol. 41:475-482,1988160] Stopford W. & Goldwater L.J. Methylmercury in the environment: a review of current understanding. Environ Health Perspect.12:115-118,1975161] Stortebecker P. Mercury Poisoning from Dental Amalgam. A Hazard to Human Brain. Stockholm: Stortebecker Foundation forResearch. 24,1985162] Szylman P., et al. Potassium-wasting nephropathy in an outbreak of chronic organic mercurial intoxication. Am J Nephrol.15:514-520,1995163] Thatcher R.W., et al. Effects of low levels of cadmium and lead on cognitive functioning in children. Arch Environ Health,37(3):159-166,1982164] Thimaya S. & Ganapathy S.N. Selenium in human hair in relation to age, diet, pathological condition and serum levels. Sci TotalEnviron. 24:41-49,1982165] Thompson C.M., et al. Regional brain trace-element studies in Alzheimer's disease. Neurotoxicology. 9:1-8,1988166] Ting K.S.. et al. Chelate stability of sodium dimercaptosuccinate on the intoxication from many metals. Chinese Med J. 64:1072 -1075,1965167] Tollefson L. & Cordle F. Methylmercury in fish: a review of residue levels, fish consumption and regulatory action in the UnitedStates. Environ Health Perspect. 68:203-208,1986168] TrepkaM.J., et al. Factors affecting internal mercury burdens among East German children. Arch Environ Health. 52:134-138,1997169] Vanderhoff J.A., et al. Hair and plasma zinc levels following exclusion of biliopancreatic secretions from functioning gastrointestinaltract in humans. Dig Pis Sci. 28(41:300-305.1983170] Vimy M.J. & Lorsheider F.L. Intra-oral air mercury released from dental amalgams. J Dent Res. 64:1069-1071,1985171] Vimy M.F. & Lorsheider F.L. Serial measurements of intra-oral air mercury: estimation of daily dose from dental amalgams. JDentRes. 64:1072-1075,1985172] Walker P.R., LeBlanc J. & Sikorska M. Effects of aluminum and other cations on the structure of brain and liver chromatin.Biochem. 28,9,1989173] Watanabe C. & Satho H.Evaluation of our understanding of methylmercury as health threat. Environ Health Res. 104:367-378,1996174] Watts D.L. Prevalence of lead in environment threatens children. Hlth Freedom News. Oct, 1985175] Watts D.L. Implications of lead toxicity. TEI Newsletter. 1,2,1985176] Wedeen R.P., Mallik D.K. & Batuman V. Detection and treatment of occupational lead nephropathv. Arch Intern Med. 139:53-57,1979177] Welsh S.O. & Scares J.H. Jr. The protective effect of vitamin E and selenium against methylmercury toxicity in the Japanese quail. Nutr Rep Int.13;43,1976178] Westhoff D.D., et al. Arsenic intoxication as a cause of megaloblastic anemia. Blood. 75,45,2.241-246.179] Willett W.C.. et al. Prediagnostic serum selenium and risk of cancer. Lancet. 2(83431:130-134.1983180] Wilson R.L. Iron, zinc, free radicals and oxygen tissue disorders and cancer control, in Iron Metabolism.Ciba Foundn Symp 51 (new series). Amsterdam,Elsevier. 331-354,1977181] Yamanaka S., Tanaka H. & Nishimura M. Exposure of Japanese dental workers to mercury. Bull Tokyo Den Coll. 23:15-24,1982 182] Yokel R.A. Hair as anindicator of excessive aluminum exposure. Clin Chem. 28,4,1982183] Zalups R.K. & Cernichiari E.2.3-dimercapto- 1-propanesulfonic acid (DMPS) as a rescue agent for the nephropathy induced by mercuric chloride. TheToxicologist. 10:271(Abstractonly), 1990184] Zalups R.K. & Lash L.H. Interactions between glutathione and mercury in the kidney, liver and blood. In: Chang L.W., ed.Toxicology of Metals.BocaRaton: CRC Press. 145-163,1996185] Zheng W.. et al. Choroid plexus protects cerebrospinal fluid against toxic metals. FASEB J. 5:2188-2189.1991

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