what doctors don tell you ageing well · 16 male pattern baldness 19 chronic back pain 22 stroke...

WWW.WDDTY.COM

WDDTYWHAT DOCTORS DON’T TELL YOU

Common conditions

2 Preventing cataracts 4 AMD: it’s inflammation not age6 Thyroid problems: never say forever8 Hearing loss11 Parkinson’s disease13 Osteoporosis: the brain–bone connection16 Male pattern baldness19 Chronic back pain22 Stroke

Women’s health

24 Beating the change27 Herbal helpers for women over 5029 Hair loss31 Saving face34 Varicose veins

Dangerous drugs

37 Medicine and the elderly41 The damaged brain46 HRT: the latest cancer risk47 Statins: the big ‘cure-all’ unmasked48 Building brittle bones

Ageing wellWhat you need to knowabout getting older – Part One

2 WDDTY Ageing well

Common conditions

Cataracts—cloudy, opaque pat-ches in the lens of the eye—areoften considered an inevitable

part of growing old, like becomingwrinkly and going grey. However,recent evidence suggests that commonprescription drugs, rather than old age,may be responsible for a significantproportion of cases.

Two studies published just a fewmonths apart have revealed that takingcertain antidepressants or hormonereplacement therapy (HRT)—drugsused by millions of people worldwide—can dramatically increase the risk ofcataracts.

The antidepressant study—the firstmajor investigation into such apossible link—analyzed data fromnearly 19,000 elderly cataract patientsand around 190,000 controls. It foundthat those currently taking selectiveserotonin reuptake inhibitors (SSRIs),the most widely prescribed anti-depressants in many countries, were 15per cent more likely to have cataracts.In the US alone, this means that22,000 cataract cases may be due toSSRI use.

The association was especiallystrong for Paxil (paroxetine), Effexor(venlafaxine) and Luvox (fluvoxamine).Paxil increased cataract risk by 23 percent, Effexor by 33 per cent and Luvoxby a whopping 39 per cent. Happily, thehigher risk was linked only to currentdrug use (Ophthalmology, 2010; 117:

1251–5). Although more research is needed

to confirm the link, previous animalstudies have suggested a plausibleexplanation for the increased risk ofcataracts among SSRI users.

“The eye’s lens has serotoninreceptors, and animal studies haveshown that serotonin can make thelens opaque and lead to cataractformation,” said study author DrMahyar Etminan. “If our findings are

confirmed in future studies, doctorsand patients should consider cataractrisk when prescribing some SSRIs forseniors,” he added.

The other study linking cata-racts toprescription drug use was an eight-yearinvestigation of more than 30,000postmenopausal Swedish women,which found that those using or whohad used HRT had significantly higherrates of cataract removal than thosewho had never used HRT. Indeed,cataract removal risk was increased by14 per cent in women who had everused HRT and by 18 per cent in currentHRT users—and the longer a womanused HRT, the higher was her risk.

Alcohol consumption also appearedto increase harmful HRT effects.Current HRT users who also reportedhaving more than one alcoholic drinkper day had a 42-per-cent greater riskof having to undergo cataract removalcompared with women who usedneither HRT nor alcohol (Ophthalmology,

2010; 117: 424–30).As a plausible mechanism for how

HRT could cause cataracts, it may bethat HRT increases levels of C-reactiveprotein, high levels of which have beenassociated with cataracts in otherstudies. As lead author Dr BirgittaLindblad said, “If future studiesconfirm the associations we found,increased risk for cataract removalshould be added to the list of potentialnegative HRT outcomes.”

These new findings suggest that, inmany cases, cataracts could beprevented by avoiding certain drugs.But it’s not only SSRIs and HRT thathave been linked to cataracts. Otherstudies have found significantlyincreased risks with statins (BMJ, 2010;

340: c2197), oral and inhaled cortico-steroids (Ophthalmology, 2009; 116: 652–7),antidiabetes drugs (Ophthalmology, 2001;

108: 1670–4) and some sun-sensitizingmedications, such as the painkillingnon-steroidal anti-inflammatory drug(NSAID) naproxen (Arch Ophthalmol, 2010;

128: 959–63).

The importance of dietOn the other hand, researchers are alsofinding that a healthy diet can offerpowerful protection against cataracts.

Scientists from the University ofWisconsin’s Department of Ophth-almology and Visual Sciences foundthat women who ate foods rich invitamins and minerals were less likelyto develop nuclear cataracts—thoseforming in the centre of the lens—themost common type of cataract.

The study involved over 1800women, aged between 55 and 86 years,who took part in the Carotenoids inAge-Related Eye Disease Study(CAREDS). The daily diets of thesewomen were assessed according totheir responses to a food-frequencyquestionnaire (the 1995 HealthyEating Index, HEI), while the presenceof nuclear cataracts was determinedfour to seven years later. Thesewomen’s diets were also assessed to seehow closely they reflected the 1990dietary guidelines for Americans.

A high HEI score was the strongestmodifiable predictor of a lowprevalence of nuclear cataracts. Whatcontributed to the higher healthy dietscores were intakes at or above therecommended levels for vegetables,fruits, grains, milk and meat (or beans,fish or eggs), and below-recommendedlevels of fat, saturated fat, cholesteroland salt. Women with the highest HEIscores were found to have a 37-per-centlower risk of developing cataracts thanthose with the lowest scores.

“These data add to the body ofevidence suggesting that eating foodsrich in a variety of vitamins andminerals may contribute to postponingthe occurrence of the most common

New evidence suggeststhat popular prescriptiondrugs could be causingcataracts—the leadingcause of blindnessworldwide

Preventing cataracts

WDDTY Ageing well 3

type of cataract in the United States,”the researchers concluded (Arch

Ophthalmol, 2010; 128: 738–49).There’s also evidence to suggest

that specific nutrients might beespecially helpful for warding offcataracts. In an earlier study by thesame team of researchers from theUniversityof Wisconsin, women withhigh dietary intakes of lutein andzeaxanthin—found in dark green leafyvegetables, as well as in kiwi fruit,grapes, corn and egg yolk—had a 23-per-cent reduced prevalence of nuclearcataracts. Those with the highestintakes of these nutrients were 32-per-cent less likely to have nuclearcataracts compared with those whohad the lowest intakes.

The researchers also commentedthat lutein and zeaxanthin, both ofwhich accumulate in the lens of theeye, are known to protect againstphotodamage (caused by ultravioletradiation), which predisposes tocataracts (Arch Ophthalmol, 2008; 126:

354–64). A number of other nutrients, mostly

antioxidants, also appear to beimportant for cataract prevention. A10-year study of more than 2400 olderadults in Sydney, Australia, found thathigher intakes of vitamin C (from bothfood and supplements) or thecombined intake of multipleantioxidants (vitamins C and E, beta-

carotene and zinc) significantlyreduced cataract risk (Am J Clin Nutr, 2008;

87: 1899–905).Oxidative stress is thought to play a

significant role in cataract formation,so it makes sense that antioxidants—which mop up free radicals thatdamage proteins and fibre cells in thelens—can be protective. Indeed, astudy in North India showed thathaving higher levels of antioxidants inthe blood—including vitamin C, alpha-/beta-carotene, zeaxanthin, lutein andlycopene—led to a significantly lowerlikelihood of having cataracts (Invest

Ophthalmol Vis Sci, 2008; 49: 3328–35).

Reducing the riskBesides avoiding certain drugs andeating a healthy, antioxidant-rich diet,there are a number of other ways toreduce your risk of cataracts.u Stop smoking. Smokers are more

likely to have cataracts, so kickingthe habit may help to save your sight(Arch Ophthalmol, 1997; 115: 1296–303).It’s thought that the cadmium incigarettes accumulates in the lensand causes damage. Also, cigarettesmoke is rich in free radicals, amongother things, so it could also be thatsmoking depletes levels ofprotective antioxidants (Br J

Ophthalmol, 1998; 82: 186–8).u Lose weight. Researchers at

Harvard University found that

people with a body mass index(BMI) of 30 kg/m2 or more(obesity) increased their risk ofcataract by at least a thirdcompared with a BMI of 23 kg/ m2

(overweight) or less (normal) (Int J

Obes Relat Metab Disord, 2002; 26:

1588–95).u Drink in moderation. The 10-year

Blue Mountains Eye Study inAustralia (described above) foundthat people who drank more thantwo standard alcoholic drinks perday or were total abstainers weresignificantly more likely to undergocataract surgery compared withmoderate drinkers. Indeed, in thisstudy, a moderate consumption ofalcohol—one or two drinks a day—was associated with a 50-per-cent lower incidence ofcataract surgery (Am J Ophthalmol,

2010; 150: 434–40).u Exercise. A recent study has

reported that vigorous exercise canprotect against cataracts. Theresearchers found that men who ran64 km/week or more had a 35-per-cent lower risk of developingcataracts compared with men whoran less than 16 km/week.

Using these men’s performancesin 10-km races, which provide agood measure of overall andcardiorespiratory fitness, it was alsofound that the fittest men had onlyhalf the cataract risk of those whowere the least fit (Invest Ophthalmol Vis

Sci, 2009; 50: 95–100).u Minimize heavy-metal exposure.

Long-term, low-level exposure totoxic metals—and lead, inparticular—results in theiraccumulation in the lens. Such abuildup increases the oxidativeburden of the lens, thus leading tocataracts (JAMA, 2004; 292: 2750–4).

u Sport those sunglasses. WhenJapanese researchers reviewedstudies carried out in Japan as wellas in Iceland, Australia andSingapore, they found that thoseexposed to the highest levels ofsunlight (ultraviolet light) also hadthe highest incidences of cataracts(Invest Ophthalmol Vis Sci, 2003; 44:

4210–4).Joanna Evans

For more information on cataracts,consult the WDDTY Good Sight Guide.

u Bilberry is rich in anthocyanosides, potent antioxidants with a particular affinityfor the eyes. In a report of 50 patients with senile cataracts, a combination ofbilberry (180 mg twice daily)—standardized to 25-per-cent anthocyanosides—and vitaminE (100 mg twice daily) for four months stopped the progression of cataracts in96 per cent of the treated patients compared with 76 per cent of the controlgroup (Altern Med Rev, 2001; 6: 141–66).

u Vitamin E was also tested on its own in a randomized controlled trial (RCT)of 50 patients with senile cataracts (100 mg twice daily for 30 days). Compared with a placebo, there was asignificantly smaller increase in the size of cortical cataracts (those in the outerrim of the lens) in the vitamin E group (Ann Nutr Metab, 1999; 43: 286–9).

u N-acetylcarnosine-containing eye drops called Can-C have shownpotential in the treatment of cataracts.An RCT of 49 patients reported that,after six months of twice-daily Can-C use, 90 per cent of the NAC-treated eyesimproved in visual acuity and 89 per cent improved in glare sensitivity.Theoverall visual outcome in the control group showed significant worsening aftertwo years. It should be noted, however, that this study was conducted by thecompany—Innovative Vision Products (IVP)—that helped to develop the eyedrops (Drugs R D, 2002; 3: 87–103).

Promising natural treatments

4 WDDTY Ageing well

AMD: it’s inflammation, not ageThe latest findings suggest that macular degenerationmay not be ‘age-related’, but due to mineral imbalancesand inflammatory disease

Failing eyesight has become soclosely associated with old agethat the condition has become

known as AMD, or ‘age-related maculardegeneration’. Around 15 millionAmericans and four million Britonssuffer from the problem—where thesharpness of our central visiondeteriorates—and health experts nowfear that AMD will take on epidemicproportions once the baby-boomersreach their 60s and 70s.

AMD comes in two forms—‘wet’ and‘dry’. The dry type is by far the morecommon. This type occurs whenphotoreceptors in the central part ofthe eye, or ‘macula’, deteriorate anddie. In contrast, the wet variety iscaused by abnormal blood-vesselgrowth, which can lead to blood andprotein leakages, irreversible and rapidvision loss, and even blindness. Also,the dry form can worsen and becomewet.

Because medicine has associatedAMD with the ageing process, it hasn’tlooked much beyond that for othercauses of the condition. This view hasalso influenced its treatment. Medicinecontends that it has nothing to offerthe sufferer who has dry AMD, and hasonly recently begun to offer regularinjections of anti-angiogenic drugsdesigned to reverse blood-vessel growthin those with the wet form. However,it’s a controversial—and painful—treatment, and only one of the drugs—Lucentis (ranibizumab)—is approvedin the US for wet AMD treatment.

However, doctors are now starting torecommend something called ‘photo-dynamic therapy’ (PDT), using thelight-activated drug Visudyne (verte-porfin), for some forms of wet AMD.The drug is injected into the patient’sarm and, after a short wait, a laserbeam is shone into the patient’s eyes toactivate the drug, which is supposed toseal up abnormal blood vessels anddestroy any that are leaking. However,

PDT has proved to be less effective thanLucentis injections in a study of 423AMD patients over a two-year period(Ophthalmology, 2009; 116: 57–65.e5).

Possible causes of AMDWhile macular degeneration primarilyaffects older people, there’s littleevidence to suggest that ageing is, onits own, the major cause of such failingeyesight. AMD affects 10 per cent ofpeople aged up to 74 years and, despiteits name, increases to only around athird of those between 75 and 85 yearsof age (www.agingeye.net/maculardegen/

maculardegeninformation.php).Medicine believes that one of its

causes could be exposure over theyears to direct sunlight and, especially,to blue-spectrum light. Doctors oftenadvise older people to wear sunglassesin direct sunlight to lessen their risk ofdeveloping AMD. This advice, however,may have been based on a series ofanimal studies that did not properlyreplicate the human experience. In aseries of laboratory tests, researchersshone intense ultraviolet light intoanimals’ eyes, which were held openmechanically. Aside from the fact thatthese studies amounted to extremeanimal cruelty, the tests also failed totake account of the blinking reflex and the way that we humans have ofavoiding looking directly at the sun.

This idea has also been supported by a Cambridge, UK, study of 446 AMD sufferers that found that directsunlight is not a cause (Br J Ophthal-

mology, 2006; 90: 29–32), whereas otherstudies suggest that, in fact, sunlight isimportant for good health. Blue light,in particular, helps the body to releasemelatonin, which protects the heartand the eyes by keeping blood pressurelevels low (J Clin Endocrinol Metab, 2003; 88:

4502–5).Another commonly held belief—

that alcohol can cause AMD—may alsobe mistaken. A major study involving

4439 people living in Beijing and inrural areas of China could find noconnection between wine- and beer-drinking, and AMD (Ophthalamology, 2009;

August 25, published online ahead of print).Instead, there’s growing evidence to

suggest that AMD is more likely to bethe result of a mineral imbalance thatis cumulative and so becomes moreapparent as we get older. Low levels ofzinc and copper are commonly foundin people with AMD, as one studydiscovered when it analyzed the healthprofiles of 44 subjects with thecondition. On average, the subjects’zinc and copper levels were 24-per-cent lower than those of the healthycontrols. The researchers, from theMayo Clinic in Rochester, Minnesota,also pointed out that, as shown byother studies where supplements wereable to slow the progress of AMD, thereappears to be a direct causal linkbetween zinc and copper levels, andfailing eyesight (Am J Ophthalmol, 2009;

147: 276–82.e1). On the other hand, iron tends to

cluster in the retina, and may also playa role in a broad range of oculardiseases, including AMD (along withglaucoma, cataract and conditionscausing intraocular haemorrhage)because of iron-induced ocularoxidative damage (Prog Retin Eye Res,

2007; 26: 649–73).Furthermore, too much lead can

cause AMD. One study of 25 AMD

Common conditions

WDDTY Ageing well 5

patients discovered that they all hadretinal lead levels that were up to 75per cent higher than those found inpeople with healthy eyes (Am J

Ophthalmol, 2009; September 4, published

online ahead of print).A diet that’s high in processed foods

can also lead to AMD. A survey of more than 4000 people, carried out byresearchers at Tufts University inBoston, MA, concluded that up to 20per cent of all cases of AMD could havebeen avoided by a diet lower inprocessed foods such as white bread,cakes and biscuits (Am J Clin Nutr, 2007; 86:

180–8).What’s more, new breakthrough

research suggests that AMD could bean inflammatory disease brought aboutby a polymorphism (variation) in thecomplement factor H (CFH) gene.Researchers from the US National EyeInstitute (NEI) and the NationalCancer Institute (NCI) reckon that thegene variation could be responsible forhalf of all cases of AMD. Indeed, peoplewho carry the polymorphism are nearlysix times more likely to develop thecondition (Science, 2005; 308: 385–9).

Possible treatmentsIf AMD is an inflammatory disease,then high-dose supplements could bean effective therapy. Vitamin B12supplements have been successfullyused to reduce the symptoms of otherinflammatory conditions such asbursitis (Lininger SW Jr et al., The Natural

Pharmacy: Complete Home Reference to Natural

Medicine. New York, NY: Three Rivers Press,

1999), and vitamin C, at high doses, hasbeen proven to have anti-inflammatoryproperties (Exp Eye Res, 1986; 42: 211–18).Vitamin E may be especially useful as it is able to suppress the symptoms ofinflammation in specific parts of thebody (J Vitaminol, 1972; 18: 204–9).

Copper and zinc are both stronganti-inflammatories, and AMD sufferersare usually deficient in both. Inflam-mation requires a higher copper intake

Age-related macular degeneration (AMD) has features in common withheart disease, and the many ways of maintaining a healthy cardiovascularsystem appear to also apply to eye health.u Eat an organic, unprocessed diet that’s low in fats, and high in fruit

and vegetables—especially lutein-rich varieties such as kale andspinach

u Supplement with zinc and copper every day, and take amounts thatare higher than the recommended daily allowance (RDA)

u Drink a glass of red wine a day (Am J Ophthalmol, 1995; 120: 190–6) as, inone study, those who drank one glass a day reduced their risk of AMDby 20 per cent compared with those who either drank beer or spirits, orwere teetotalers (Lancet, 1995; 351: 117)

u Don’t smokeu Supplement with antioxidants A, C and Eu Eat plenty of tomatoes, as they are rich in lycopene, which helps ward

off AMD (Arch Ophthalmol, 1995; 113: 1518–23)u Take vitamins B6 and B12 together with folic acid, as they can

reduce your AMD risk (Arch Intern Med, 2009; 169: 335–41)u Taking the antioxidant zeaxanthin can reduce your chances of

developing AMD. Besides supplements, it’s also found in foods such asmangoes, papaya, oranges, peaches, green beans, broccoli, sweetpotatoes and honeydew melon (Am J Clin Nutr, 1995; 62 [6 Suppl]:

1448S–61S). In addition, the density of the macular pigment can beimproved just by adding corn and spinach to the diet (Invest Ophthalmol

Vis Sci, 1997; 38: 1795–801).

Preventing AMD

to maintain levels of enzymes that arevital to the body’s anti-inflammatoryprocesses, at least in animal studies(Agents Actions, 1985; 16: 504–13). Inaddition, findings in animal (rat)studies showed that zinc is animportant healing agent during inflam-mation (Int J Tissue React, 1981; 3: 73–6). Inclinical studies, zinc was able to help70 per cent of men suffering fromprostate problems (Bush IM et al., ‘Zinc and

the Prostate’, presentation at the annual meeting

of the American Medical Association, Chicago,

1974). Supplemental zinc, copper andmanganese also reduced the risk ofrheumatoid arthritis in more than29,000 women aged 55–69 years andfollowed for 18 years (Am J Epidemiol,

2003; 157: 345–54).High-dose supplements of zinc and

copper, and of vitamins A, C and E—

the usual antioxidants—prevented theprogression of AMD in one study. Theresearchers, from the Age-Related EyeDisease Study Group in New Zealand,also found that most people are takinglevels of vitamins that are too low to beeffective. Yet, at the correct dosages,any combination of multivitamins andindividual supplements can preventAMD from worsening (N Z Med J, 2009;

122: 32–8).Lutein/zeaxanthin, the carotenoid

antioxidants found in dark-green leafyvegetables such as spinach and kale,are both highly effective in slowing the progress of AMD. This finding wasmade when these vegetables wereadded to the diets of 4519 studyparticipants, aged 60–80 years (Arch

Ophthalmol, 2007; 125: 1225–32).Bryan Hubbard

6 WDDTY Ageing well

Thyroid problems: never say forever

from these hormones failing to reachthe body’s tissues.

Doctors have just two ways ofdiagnosing a thyroid problem: theycan either look for symptoms, orconduct a blood test. However, bothmethods can be highly unreliable.Typical symptoms of hypothyroidisminclude tiredness, feeling the cold,dry skin, depression and weight gain,but these features can also be causedby a range of other health problems.Indeed, thyroid disease often mimicsother, more serious, problems.Symptoms of Graves’ disease, whichcan be caused by hyperthyroidism,are almost identical to many of thephysiological changes that occurduring pregnancy, making thediagnosis almost impossible inexpectant mothers (Endocr Pract, 2009;

Oct 15: 1–36; Epub ahead of print).A more reliable diagnostic test is

to carry out a standard blood testthat measures thyroid-stimulatinghormone (TSH) levels. But this canalso produce false-positive results,especially if the patient has anotherhealth problem. If a second bloodtest were to be carried out after thetrue illness has been cleared up, TSHlevels would probably show up asnormal. Unfortunately, second testsare rarely ordered, and the patientwill often already have started anunnecessary course of hormonedrugs, which can have serious side-effects.

CausesDoctors also tend to get it wrongwhen it comes to understanding thecauses of thyroid disease. Thestandard view is that thyroidproblems are either the result ofpeople living longer or because of agenetic inheritance. It used to becaused by iodine deficiency but, atleast in the West, so much of our foodthese days has been enriched withiodine that this cause has all butbeen eliminated. If anything, we arenow in danger of consuming toomuch iodine, especially through

iodine-enriched salt, which can leadto iodine-induced thyrotoxicosis, orhyperthyroidism (BMJ, 1976; 1: 372–5).

So, having eliminated iodinedeficiency as a cause, medicinebelieves that the other two causes—ageing and genetics—are beyond thepatient’s control, and that only anoutside agent such as a drug—levothyroxine for hypothyroidism anda beta-blocker for hyperthyroidism—is able to normalize the patient’shormone levels. In fact, levothyroxineis just as likely to cause an excess ofthyroid hormones (Lancet, 1991; 337:

171–2). But the above-mentioned two

causes certainly don’t account formost cases of thyroid disorders.Indeed, the growing evidencesuggests that hypothyroidism andhyperthyroidism are more oftencaused by environmental factors andby diet—including, paradoxically,consuming too much iodized salt,which was originally enriched tocombat thyroid dysfunction.

Other causes that doctors appearto overlook include:u food allergies. People with

multiple food allergies, such ascoeliac disease, are much morelikely to develop thyroid problems(J Pediatr, 2009; 155: 51–5).

u selenium deficiency. The thyroidgland has some of the highestconcentrations of selenium in the

Doctors tell us thatthyroid problems happenas we get older and thatwe have to live with them,but neither claim is true

Medicine just doesn’t seem tobe able to get it right when itcomes to thyroid problems,

and especially hypothyroidism, whenwe become sluggish and overweightbecause of an underactive thyroidgland.

Hypothyroidism is by far the morecommon of the two thyroid prob-lems—the other is hyperthyroidism,when the body goes into overdrive—and just 10 years ago, it wasconsidered one of the greatundiagnosed diseases. But nowadays,doctors are accused of having acomplete knee-jerk reaction, and areseeing thyroid problems where noneexist and giving people hormonedrugs unnecessarily.

“This is potentially an enormousproblem, given that one in fourpeople have their thyroid functionchecked,” says Jayne Franklyn,president of the British ThyroidAssociation (BMJ, 2009; 338: b725).

As a result, patients who arewrongly being given a hormone drugsuch as levothyroxine could besuffering from serious effects due toan excess of thyroid hormones.Worse, the misdiagnosis could alsobe masking more serious conditionssuch as depression.

Thyroid diagnosisThe thyroid, an endocrine glandfound at the base of the neck, playsan essential role in the body’sfunctioning and metabolism. Itcontrols the rate at which the bodyburns energy and makes proteins byreleasing the hormones T4 (thyrox-ine) and T3 (triiodothyronine). Thethyroid may be producing either toolittle of these hormones (hypothy-roidism) or too much (hyperthyroid-ism). Hypothyroidism can also result

Common conditions

WDDTY Ageing well 7

Alternatives to drugsIf your thyroid function needs to be stabilized, there are plenty of provenalternatives to drugs that may do the job just as well—and without theserious side-effects.u Bauhinia purpurea. A bark extract of this flowering plant can

significantly improve blood T3 and T4 levels, although the only dataapparently comes from laboratory mice. In the same study, a rootextract of Withania somnifera (Ashwagandha) was also tested, butonly could only enhance T4 levels (J Ethnopharmacol, 1999; 67: 233–9).

u Zinc. A deficiency of this mineral can not only cause hypothyroidism,but supplementing with zinc may also reverse the condition (Int J

Dermatol, 1976; 15: 757–61).u Bladderwrack (Fucus vesiculosus). If your thyroid problems are

related to iodine insufficiency, this seaweed is one way of increasingyour iodine intake (Food Add Contam, 1987; 5: 103–9).

u Neuro Emotional TechniqueTM (NET). This mind–body technique canhelp to normalize thyroid dysfunction. In one study of twohypothyroid patients, NET was successful in raising their TSH and T4levels back to normal (Complement Ther Clin Pract, 2009; 15: 67–71).

u Armour® Thyroid replacement therapy. This desiccated thyroidextract is derived from pigs and is an alternative to a synthetichormone replacement drug. One study found this extract to be moreeffective for hypothyroidism than a drug (N Engl J Med, 1999; 340: 424–9).

body, so any deficiency in thisessential trace element can lead tothyroid disease (Best Pract Res Clin

Endocrinol Metab, 2009; 23: 815–27).u pollutants. Common environ-

mental pollutants such as per-chlorate, thiocyanate and nitratesuppress iodine absorption andhave been found to cause thyroiddisease in both animal and humanstudies (Toxicol Ind Health, 1998; 14:

121–58; Best Pract Res Clin Endocrinol

Metab, 2009; 23: 801–13).u cancer treatment. The healthy

functioning of the thyroid can beaffected by radiotherapy given forcancer (Am J Clin Oncol, 2009; 32:

150–3).u diabetes, especially type 1, can

cause thyroid problems (Turk J

Pediatr, 2009; 51: 183–6).u preeclampsia, a common com-

plication of pregnancy, can affectthyroid functioning later in life(BMJ, 2009; 339: b4336).

u fluoride. This chemical in ourwater supply can interfere with thenatural absorption of iodine (Klin

Wochenschr, 1984; 62: 564–9).u iodine excess. This element is

considered to be essential forhealthy thyroid functioning, buttoo much can lead to hyperthy-roidism (J Endocrinol Invest, 1994; 17:

23–7). Avoiding iodine-enrichedsalt may not be enough, as iodineis also used in cough expectorants,antiseptics, and certain drugs andimaging contrast media (Z Kardiol,

2001; 90: 751–9).u prescription drugs. Even drugs

that don’t contain iodine cancause thyroid problems. Theseinclude lithium, given for bipolardisorder (manic depression),which often causes an underactivethyroid (N Engl J Med, 1995; 333:

1688–94), as does the heart drugamiodarone (BMJ, 1996; 313: 539–44).

u emotional problems. The thyroid

is especially vulnerable toemotional traumas such asbereavement and divorce (Acta

Endocrinol, 1993; 128: 293–6).

It’s not foreverA common belief in medicine is thata thyroid problem is forever. As aresult, thyroid patients will probablyhave to take a drug to maintainnormal hormone levels for the rest oftheir lives. In a few rare cases, thismay indeed be necessary, but theevidence suggests that it’s muchmore likely that thyroid problemswax and wane, assuming that thepatient even had the problem in thefirst place.

Sadly, medicine isn’t geared up forsuch an eventuality, and often won’teven take a second, confirmatoryTSH blood test a few months later,when the real cause of the imbalance

may have gone away, and hormonelevels may have normalized.

It’s also more likely that the causeof the thyroid problem is within thecontrol of the patient, and a littledetective work can often uncover thetrue culprit, which then can besorted out. Often, for example, theproblem is caused by environmentalpollutants, especially fluoride, andthese can be reduced or removed byusing air and water filters. Certainly,thyroid problems can worsen astoxins build up in the body, whichmay lead doctors to believe that theyare the direct result of ageing.

But one thing’s for sure: thyroidproblems are usually not ‘just one ofthose things’. In many cases, theycan be either avoided or reversed—and without the use of powerfulpharmaceuticals.

Bryan Hubbard

8 WDDTY Ageing well

Most of us assume that hearingloss is a normal and inevitablepart of ageing—and that’s a

viewpoint that appears to be wellsupported by the facts. In the US,hearing loss ranks as the third mostcommon chronic condition in theelderly, while UK figures show thatmore than half the population of those aged over 60 have some degreeof impaired hearing. There’s even amedical term—presbycusis—to des-cribe this gradual form of hearing loss.

However, emerging evidence nowindicates that the problem may havemore to do with lifestyle than simplygrowing old. Studies show that anumber of environmental factors,including noise pollution, diet,chemical exposures and evenprescription drugs, can contribute tohearing loss. Crucially, the evidencesuggests that hearing loss may well bea preventable condition.

Noise pollutionRepeated exposure to loud noise is oneof the most common causes of hearingloss. When noise is too loud—ingeneral, this means above 85 decibels(dB), the level of noise made by heavycity traffic—prolonged exposure candestroy the sensitive hair cells in theinner ear. These hair cells move assound waves travel through the earstructures, and the movement isconverted to nerve impulses that areinterpreted by the brain as sound.

A single loud noise, such as agunshot blast, can permanently harmthese inner-ear structures—althoughyears of exposure to less intensesounds, such as loud music, can alsocause irreversible damage (Pediatrics,

2001; 108: 40–3). As well as impairedhearing, such exposure to loud noisecan lead to tinnitus (persistent ringingin the ear), hyperacusis (extremeoversensitivity to sound) and other

hearing disorders (Int J Audiol, 2003; 42:

279–88). Traditionally, noise-induced hearing

loss (NIHL) has been considered adisease of adults who worked in noisyoccupations or used firearms. How-ever, there’s growing concern thatchildren and young adults are nowdeveloping the condition as a result of overexposure to amplified music,especially through the use of personalmusic devices such as MP3 players.

As a recent article in the BritishMedical Journal pointed out, “Thedevices increasingly use earphonesthat insert into the ear canal whichproduce higher sound levels in the earthan ‘over-the-ear earphones’ used atthe same volume. These sound levelscan exceed 120 decibels, similar inintensity to a jet engine” (BMJ, 2010;

340: c1261). Indeed, several small,controlled studies have found thatpersonal music players are associatedwith poorer hearing function inadolescents and young adults (Noise

Health, 2009; 11: 132–40; J Otolaryngol Head

Neck Surg, 2008; 37: 718–24). Although more research is needed

to clarify the role of personal musicplayers in hearing loss, in themeantime, the advice is simple: turndown the volume and take regularbreaks from using them. As a rule ofthumb, if the music is uncomfortablefor you to listen to, or if you can’t hear

any external sounds when you’ve gotyour headphones on, then the volumeis too loud.

In addition, it should be borne inmind that the higher the volume of the sound, the shorter the time youshould be listening to it. University ofColorado researchers have placed asafe listening limit of 4.6 hours per day on an iPod played at 70-per-cent of its volume if you’re using stock iPodearphones. However, this duration fallsprecipitously to just five minutes if thevolume is cranked up to maximum(www.colorado.edu/news/releases/2006/346.

html).Other ways to reduce the chances

of developing NIHL include:u wearing hearing protectors, such

as earplugs or earmuffs, when youknow you’re going to be arounddangerously loud noise. Lawn-mowers, power tools, rock concertsand motorcycles, for example, canall cause permanent damage tohearing if you don’t wear earprotection;

u turning the volume down on yourstereo, television and car radio.Also, avoid buying noisy toys,appliances or tools when there arequieter alternatives, and don’t useseveral noisy machines at the sametime. What’s more, don’t try todrown out unwanted noise withother sounds: for example, don'tturn up the volume on your carradio or headset to drown out trafficnoise, or turn up the televisionvolume while vacuuming;

u using sound-absorbing materialsto reduce noise at home and atwork. Rubber mats can be placedunder noisy kitchen appliances,computer printers and typewritersto cut down on noise. Curtains andcarpeting also help to reduceindoor noise, and double-glazedwindows can reduce the amount ofoutside noise that can penetrateinto the home or workplace;

u having your hearing checkedregularly, especially if you arefrequently exposed to loud noise ateither work or play.

NutritionBesides noise, what we eat can alsohave an impact on our hearing. Highfat and cholesterol consumption canlead to high blood-cholesterol levels

Hearing lossMost hearing loss is simplyseen as an inevitableconsequence of growingold. Yet, the evidencesuggests that it can beprevented.

Common conditions

WDDTY Ageing well 9

and the production of free radicals.This, in turn, can lead to impairedhearing by reducing the flow of oxygenand nutrients to the inner ear. Indeed,a study conducted in Taiwan—thelargest of its kind—found that thosewho had high levels of triglycerides (aform of fats made by the body) in theirblood had a significantly greater risk ofdeveloping NIHL (Otolaryngol Head Neck

Surg, 2007; 137: 603–6). Similarly, researchers in Turkey

reported that people with NIHL werehighly likely to have hyperlipidaemia—an excess of cholesterol and fatty acidsin the blood. The team also found that a low-cholesterol diet helped toimprove hearing, and alleviatedtinnitus in these patients (Int Tinnitus J,

2007; 13: 143–9).On the other hand, certain fats

may have an important role to play inprotecting our hearing. A studyrecently published in the AmericanJournal of Clinical Nutrition found thatconsumption of omega-3 fatty acids—in particular, the long-chain varietyfound in fish oil—reduced the risk ofage-related hearing loss. Participantswho consumed two or more servings of fish per week had a 42-per-centlower risk of developing presbycusiscompared with those who ate less than one serving a week. In addition,in those who already have hearing loss,fish consumption appears to prevent it from getting worse (Am J Clin Nutr,

2010; 92: 416–21).However, much of the research on

nutrition and hearing loss has focusedon antioxidants. Emerging evidenceshows that free-radical formation inthe inner ear plays a key role in thedevelopment of NIHL. Antioxidants,which mop up free radicals, maytherefore be an effective intervention.

Animal studies (so the results maynot necessarily apply to humans) havedemonstrated that a variety of dietaryantioxidants, including vitamins A, Cand E, can reduce NIHL when givenprior to noise exposure. A combinationof high-dose vitamin A (2.1 mg/kg),vitamin C (71.4 mg/kg) and vitamin E(26 mg/kg) plus magnesium (343mg/kg) can prevent NIHL when takenone hour prior to noise exposure andcontinued once a day for five dayssubsequently (Free Radic Biol Med, 2007; 42:

1454–63). It appears that the vitaminswork in synergy to reduce both free-

Usually, a hearing aid is the only ‘treatment’ for age-related hearing loss, butthere’s now evidence to suggest that certain herbs and supplements may beable to restore hearing loss.u Antioxidants are among the most promising therapies for hearing loss. In

one study, alpha-lipoic acid (60 mg/ day), vitamin C (600 mg/day) and thedrug rebamipide (300 mg/day), an amino-acid derivative that scavengesdamaging free radicals, were given orally for at least 8 weeks to 46 elderly patients with hearing loss. At the end of thetreatment, hearing levels were significantly improved at all frequenciestested (Acta Otolaryngol, 2009; 129: 36–44).

Another study—a placebo-controlled trial this time—demonstrated thatsupplementing with both vitamins E (600 mg/day) and C (1200 mg/day)can be beneficial for sudden-onset sensorineural hearing loss (nerve deafness) (Acta

Otolaryngol, 2008; 128: 116–21).u Ginkgo biloba may be useful for hearing loss, according to several

studies. In one, the herb was better than the conventional combined drugtreatment when tested in 52 patients with acquired sensorineural hearingloss (Indian J Otolaryngol Head Neck Surg, 2000; 52: 212–9).

Although an optimal dose has yet to be established, in general, studieshave used 30–200 mg daily, with the higher doses tending to providebetter results.

u Correcting nutritional deficiencies may help to restore hearing in somecases. Indeed, one study reported that zinc supplementation in patientswho were marginally zinc-deficient improved tinnitus and sensorineuralhearing loss in about one-third of elderly adults (Am J Otol, 1989; 10: 156–60).

Can hearing loss be treated?

radical formation and inner-ear hair-cell damage, while the magnesiumpreserves blood flow to the inner ear,as this is also affected by loud noise.

Remarkably, antioxidants deliveredas late as three days after noiseexposure were still found to bebeneficial (Neuroscience, 2005; 134:

633–42)—although, again, these animaltest results may not necessarily applyto humans.

Nevertheless, there is evidence tosupport the use of magnesium forhuman hearing. In a two-month,double-blind, placebo-controlled studyof 300 Israeli military recruits, dailysupplementation with 167 mg ofmagnesium significantly helped toprotect their hearing against noise-induced damage (Am J Otolaryngol, 1994;

15: 26–32). Another Israeli study of 20young men found similar results (Clin

Otolaryngol Allied Sci, 2004; 29: 635–41). Other nutrients that may be

involved in ear health are folate andvitamin B12. A recent study foundthat, among men aged 60 years orover, those with the highest folateintakes had the lowest risk of hearingloss (Otolaryngol Head Neck Surg, 2010; 142:

231–6). In an earlier study, which looked at

a group of army personnel exposed tomilitary noise, vitamin B12 deficiencywas commonly found among thosewith NIHL and/or chronic tinnitus.Interestingly, 12 patients who hadvitamin B12 replacement therapy sawtheir symptoms improve (Am J

Otolaryngol, 1993; 14: 94–9).

Drugs and other toxinsA staggering range of drugs areassociated with hearing loss—frompainkillers to oral contraceptives. Arecent study has revealed that theregular use of aspirin, acetaminophen(paracetamol) and non-steroidal anti-inflammatory drugs (NSAIDs) cansignificantly increase the risk ofhearing loss in men (Am J Med, 2010;

123: 231–7). Antibiotics, especially aminoglyco-

sides such as amikacin, gentamicinand tobramycin, chemotherapy drugs,hormone replacement therapy (HRT),antimalarials and loop diuretics havealso all been shown to have ototoxic(ear-damaging) effects (Braz J Otorhino-

laryngol, 2006; 72: 836–44; Hear Res, 2009; 252:

10 WDDTY Ageing well

29–36).Apart from medication, a number

of other agents have also been linkedto hearing loss, including pesticides,toluene, styrene, ethylbenzene, carbondisulphide, lead and mercury (Braz J

Otorhinolaryngol, 2006; 72: 836–44). Smoking also appears to damage

hearing—possibly by affecting theantioxidative mechanisms of the bodyor reducing the blood circulation tothe hearing system. Indeed, a study ofpeople working in noisy environmentsfound that long-term smokers weremore likely to develop permanent

hearing loss than non-smokers (Clin

Otolarygol, 2005; 30: 517–20). Another found that smokers had a

69-per-cent increased risk of hearingloss compared with non-smokers, andeven non-smokers living with smokerswere more likely to suffer hearing loss,too (JAMA, 1998; 279: 1715–9). Indeed,infants exposed to cigarette smoke hada fivefold greater incidence of hearingloss than unexposed infants (Ir Med J,

1992; 85: 111–2).

A sound solutionSo far, the evidence suggests that

hearing loss is not something thatshould simply be accepted as aninevitable part of ageing. It is acondition that can be prevented bypaying attention to what we eat, to ournoise exposure and to the toxins thatsurround us on a regular basis.

Ultimately, if you follow a healthy,balanced diet that includes plenty ofantioxidants and good fats, and focuson turning the volume down in yourlife, you should be well on the way toensuring the sweet sounds of goodhearing for years to come.

Joanna Evans

Common conditions

WDDTY Ageing well 11

Clean up your diet andlifestyle to avoid thisdebilitating disease

Parkinson’s disease

Parkinson’s disease (PD) is adebilitating neurologicaldisorder thought to affect

one or two people in every 1000.It’s named after Dr JamesParkinson, the Scottish physicianwho first described it as the‘shaking palsy’ in an 1817 essay.

Although it’s been around forsome time, modern medicine isstill baffled by the condition. Thesymptoms—including tremors,muscle rigidity and slowedmovements—can so closelyresemble a number of otherdisorders that PD is, in fact,notoriously difficult to diagnose.

Indeed, a recent study hasreported that at least one in 20Parkinson’s cases is a misdiagnosis(Mov Disord, 2009; 24: 2379–85). Thismeans that over 6000 people in theUK could be taking dangerous anti-Parkinson’s drugs unnecessarily.Alarmingly, many of these drugscan even cause the symptomsthey’re meant to treat—such asconfusion and involuntarymovements—and such side-effectsare not always reversible (Am Fam

Physician, 2007; 75: 1045–8).

Possible causesMedicine is also confused as towhat exactly causes PD. Thesymptoms are thought to arisefrom a lack of the chemicalmessenger dopamine in the brain,which happens when the specificbrain cells that produce it die or become impaired. However,researchers still don’t know whattriggers such a chain of events inthe first place.

Also, recent evidence suggeststhat ageing is less important thanhas been previously believed(Environ Health Perspect, 2005; 113:

1234–8). Indeed, what’s emerging isthat environmental factorsthroughout life—such as what weeat, where we live and what we dofor a living—are crucial pieces of

2006; 5: 13; Epidemiology, 2006; 17:

8–13). There’s also considerableanimal and laboratory evidenceto back this up. In fact, even lowlevels of PCB exposure—as seenin the general population—mayhave the potential to disruptnormal dopamine functioning inthe brain, which couldeventually lead to PD (Toxicol Sci,

2006; 92: 490–9).u Heavy metals. One study found

that those with the highestlifetime lead exposures are twiceas likely to have PD as those withthe lowest exposures (Environ Health

Perspect, 2006; 114: 1872–6). Othermetals, including aluminium,mercury, copper, manganese andiron, may also be risk factors(Neuroepidemiol-ogy, 1999; 18: 303–8).

u Dairy. Harvard researchers foundthat high intakes of dairy foodsnearly doubled the risk of PD inmen (Ann Neurol, 2002; 52: 793–801),and there’s a slightly increasedrisk in women, too (Am J Epidemiol,

2007; 165: 998–1006).u Fruit. Researchers at the

University of Hawaii found aconnection between high intakesof fruit and fruit juice, and PD inmiddle-aged men. Those who atemore than three servings a dayhad a 70-per-cent higher risk,while those eating only one ormore servings a day increased

the puzzle. So far, it appears that exposures

to particular toxins or foods canincrease the risk of PD.u Pesticides. Numerous animal

and human studies linkpesticides to PD. People livingwithin 500 metres of landsprayed with pesticides have a75-per-cent increased chance ofdeveloping the disease. Inaddition, those exposed toagricultural pesticides as a childor young adult have an evengreater risk (Am J Epidemiol, 2009;

169: 919–26). Household pesticide use is

also associated with PD. USresearchers reported that usinginsecticides and herbicides inyour home or garden can doubleyour risk of developing thedisease (Lancet, 2000; 335: 1701;

h t t p : / / n e w s . b b c . c o . u k / 2 / h i /

health/738020.stm).u Polychlorinated biphenyls

(PCBs). These man-madeorganic compounds, formerlywidely used in electrical andhydraulic equipment, werelinked to PD in two USoccupational studies, whichfound that female workersexposed to PCBs were aroundtwo to three times more likely todie with PD compared with thegeneral population (Environ Health,


Although there’s no cure for Parkinson’s disease (PD), itssymptoms and quality of life can be improved; however,only attempt the following under medical supervision.u Diet. The standard therapy for PD is levodopa, or L-

dopa, but its effectiveness can vary throughout the day.These fluctuations can be reduced when almost all ofthe day’s protein is eaten in the evening meal(Neurology, 1989; 39: 552–6). In one trial of 43 patients, 70per cent were successfully using such a proteinredistribution diet after more than a year (Arch Neurol,

1992; 49: 149–51). u Supplements. These appear to be beneficial for PD.

v Coenzyme Q10. PD patients have reduced levelsof this antioxidant in their blood and brain (Neurosci

Lett, 2008; 447: 17–9). In those with early PD, 1200 mg/day of CoQ10 for 16 months significantly slowed thecourse of the disease compared with a placebo(Arch Neurol, 2002; 59: 1541–50).v B vitamins. It’s been observed that those whohave a high intake of vitamin B6 have a lower risk of PD (Neurology, 2006; 67: 315–8). B6 supplements,therefore, may be useful for those in the early stagesof the disease (although this vitamin should not betaken by people who have heart conditions).v Vitamins C and E. In patients with early PD, highdoses of these antioxidants (750 mg of ascorbateand 800 IU of alpha-tocopherol, four times a day)delayed the need for L-dopa by an average ofaround 2.5 years (Ann Neurol, 1992; 32 Suppl: S128–32).v Amino acids. In one small trial, three weeks oftreatment with the amino acid L-methionineimproved rigidity, tremor and other symptoms inpreviously untreated PD patients. “Therapeuticeffects were similar to those observed with L-dopatreatment,” the researchers said (Rev Neurol [Paris],

1982; 138: 297–303). Other possibly helpful aminoacids are L-tryptophan (in conjunction with L-dopa)and L-tyrosine (Int J Neurosci, 1989; 45: 215–9; C R Acad

Sci III, 1989; 309: 43–7).u Herbs. An herbal remedy, called HP-200, containing an

extract of the tropical legume Mucuna pruriens, wasfound to considerably reduce PD symptoms, with onlymild, mainly gastrointestinal, side-effects (J Altern

Complement Med, 1995; 1: 249–55).

More recently, Mucuna was tested against thestandard PD drugs L-dopa and carbidopa by the UK’sInstitute of Neurology. Patients were randomly givensingle doses of either 15 g or 30 g of Mucuna for oneweek, then single doses of 200 mg and 50 mg ofstandard L-dopa and carbidopa, respectively, the nextweek. The trial was randomized, so no one knew whowas taking what. Mucuna worked faster and hadlonger-lasting benefits than the standard drugtreatment—with far fewer side-effects (J Neurol Neurosurg

Psychiatry, 2004; 75: 1672–7). u Acupuncture. A US study found that two sessions a

week for an average of around six weeks led toimprovements in tremor, walking, handwriting,slowness, pain, sleep, depression and anxiety in 85 percent of the study participants. What’s more, there wereno adverse effects from the treatment (Mov Disord, 2002;

17: 799–802). u Magnetic therapy. Repetitive transcranial magnetic

stimulation (rTMS), a non-invasive technique thatstimulates neurons in the brain, is showing promise forPD. A recent meta-analysis, which combined theresults of 10 randomized trials in PD patients, reporteda significant improvement in motor function with high-frequency rTMS treatment (Mov Disord, 2009; 24: 357–63).

u Exercise. Physical activity appears to be beneficial forPD patients by improving their physical performanceand activities of daily living (Clin J Sport Med, 2006; 16:

422–5). In particular, it can help with balance, therebypotentially reducing the risk of falls (J Neurol Phys Ther,

2009; 33: 14–26).u The Alexander Technique. This form of physical re-

education of the body can help PD patients bothphysically and mentally, according to one study.Patients who were given lessons in the technique weresignificantly less depressed, and reported greaterimprovement in their disability, compared with thosenot given any such lessons (Clin Rehabil, 2002; 16:

695–708).u Detox. As toxins such as pesticides and heavy metals

are thought to be involved in the development of PD,encouraging their removal from the body may behelpful. See our special report in WDDTY vol 20 no 10(page 15) for what works for detoxification.

Alternative and complementary therapies

their risk by 55 per cent. Theresearchers noted that it isunlikely that fruit itself is theproblem but, rather, the increasedexposure to plant-borne toxins,pesticides or herbicides (Present-

ation at the American Academy of

Neurology Annual Meeting in Honolulu,

2003).

Preventing Parkinson’sThese data suggest that lifestyle

changes, such as choosing organicfruit, limiting dairy, and avoidingpesticides and other toxicchemicals, may help to prevent PD.Also, drinking tea (CNS Neurosci Ther,

2008; 14: 352–65), taking regularexercise (Mov Disord, 2008; 23: 69–74)and maintaining a healthy weight(Neurology, 2006; 67: 1955–9) all appearto reduce PD risk.

Interestingly, experts nowreckon that genes alone are

responsible for less than 10 percent of PD cases—and even then,the environment may play a part(Environ Health Perspect, 2009; 117:

117–21). It’s likely thatenvironmental factors, such as dietand pesticide exposure, interactwith genes to bring about thedisease, suggesting that, withmore research, the vast majority ofcases may be preventable.

Joanna Evans

Common conditions


Osteoporosis:the brain–bone connectionNew research has revealedan intriguing link betweenosteoporosis anddepression

Osteoporosis, a leading causeof bone fractures, is the mostwidespread degenerative

disease in the West, affecting aroundthree million people in the UK and10 million in the US. Women aremost at risk, with one in six Westernwomen expected to suffer a hipfracture at some point in their lives.

Our genes, age, diet and lifestyleare all known to have an influence onour bone health. Now, it appears thatour mental health may also have a

significant part to play. Indeed, intriguing new research

has found that depression, acondition that afflicts more than 120million people worldwide, could bean important risk factor forosteoporosis—and especially inwomen.

The brain–bone linkTwo recent meta-analyses—poolingthe results of several previousstudies—have found a clearconnection between depression andlow bone mineral density (BMD), anindicator of osteoporosis andfracture risk. The latest, aninternational study carried out byscientists at the Hebrew University

of Jerusalem, assessed data from 23research projects in eightcountries, comparing bone densityin 2327 people suffering fromdepression with that of 21,141 non-depressed individuals.

The researchers found that thedepressed had substantially lowerBMD than the non-depressed, andthat depression was also associatedwith markedly greater activity ofosteoclasts, the cells that breakdown bone.

What’s more, the connectionbetween depression and bone losswas particularly strong inpremenopausal women with clinicaldepression diagnosed by apsychiatrist.

A variety of drugs can prevent and treat osteoporosis,but they all come with a raft of undesirable side-effects.Bisphosphonates, for instance, stop bone breakdown,but are linked with severe bone pain, oesophagealcancer, heart-rhythm irregularities and osteonecrosis ofthe jaw (ONJ), where bone tissue fails to heal after evenminor trauma, such as tooth extraction (Curr Opin

Rheumatol, 2009; 21: 363–8). Happily, a combination ofvitamins and minerals such as strontium and magnesiumoffer an alternative.u Calcium is important for bone health although, says

Annemarie Colbin, too much emphasis is placed onthis mineral alone. Indeed, there’s evidence that toomuch calcium can even increase the risk of brokenbones (Am J Epidemiol, 1997; 145: 926–34). Healthy bonesrequire many nutrients—magnesium, phosphorus,boron, copper, manganese and zinc, plus vitamins C,D, K, B6 and folic acid—all working together. We alsoneed sufficient amounts of protein for healthycollagen, and healthy fats for vitamin D uptake andprotection against bone-destroying free radicals (formore information on calcium, see WDDTY vol 20 no 3).

u Vitamin D is essential for strong bones and calciumabsorption, and not having enough D has been linkedto osteoporosis and low bone mineral density (BMD)in women aged over 50 (Joint Bone Spine, 2008; 75:

567–72). You can get D from food (fish, liver, eggs), butthe best source is the sun. Just 15 minutes ofsunshine on your skin every day should produce allthe vitamin D you need. In winter, you may need totake supplements. Studies show a 30-per-cent

decrease in non-spinal fractures among seniorstaking 800 IU/day of vitamin D (Ann Med, 2005; 37:

278–85).u Vitamin K is not just important for blood-clotting, but

also plays a major role in bone metabolism. In a three-year study of nearly 200 women aged 50–60 years,those taking vitamin K1 (phylloquinone; 1 mg/day)with a mineral+vitamin D supplement lost less bonethan those taking a placebo or the mineral+vitamin D alone (Calcif Tissue Int, 2003; 73: 21–6). Vitamin K2 (mena-tetrenone; 45 mg/day) boosted BMD and reducedspinal fractures in osteoporosis sufferers almost aseffectively as etidronate, but without the side-effects of the bisphosphonate (J Orthop Sci, 2001; 6: 487–92).However, due to its blood-coagulating properties,vitamin K should never be taken with warfarin.

Good food sources of vitamin K include leafy greenvegetables and fermented products such as natto.

u Strontium appears to have the dual effect ofincreasing bone formation while decreasing bonebreakdown (Bone, 2008; 42: 129–38). In a three-yearstudy of 1649 postmenopausal women withosteoporosis, 2 g/day of oral strontium ranelate (aprescription drug) increased BMD and reducedfracture risk by more than 40 per cent vs a placebo (N

Engl J Med, 2004; 350: 459–68). However, side-effects included diarrhoea, nausea

and even memory loss with long-term treatment(Drugs, 2010; 70: 733–59). Natural sources of strontiuminclude wholegrains, parsley, fish, Brazil nuts andlettuce.

Bone-building alternatives


The scientists concluded that“all individuals psychiatricallydiagnosed with major depressionare at risk for developingosteoporosis, with depressed youngwomen showing the highest risk”(Biol Psychiatry, 2009; 66: 423–32).

The other meta-analysis came tomuch the same conclusion. Onreviewing data from more than10,000 people from 14 separatestudies, US researchers from theMayo Clinic in Arizona reportedthat depression was associatedwith a significant decrease in BMDof the spine and hip, especially indepressed women and in those withclinical depression. “Depressionshould be considered as animportant risk factor forosteoporosis,” the researchersconcluded (Osteoporos Int, 2009; 20:

1309–20).So, is depression the cause of

the bone loss or does some otherfactor explain this novel link?

According to one study, it maynot be depression per se that’s theproblem, but the drugs used totreat it. In 5000 people aged 50 years and over, Canadianresearchers found that those regularly taking theantidepressants known as‘selective serotonin-reuptakeinhibitors’, or SSRIs, had a twofoldincreased risk of bone fractures.SSRI use was also dose-dependently associated withgreater odds of falling, and lowerBMD of the hip and spine (Arch Intern

Med, 2007; 167: 188–94). A review ofthe scientific literature reached asimilar conclusion (Eur Neuro-

psychopharmacol, 2009; 19: 683–92).Nevertheless, there’s also

evidence that depression itselfcould be causing bone loss. HebrewUniversity of Jerusalemresearchers have found thatdepression sets off the sympatheticnervous system—connecting thebrain to the internal organs andskeleton—which is primarilyaroused by stress. Its activationcauses secretion within the bone of‘noradrenaline’ (‘norepinephrine’),which has a detrimental effect onbone-building cells. The Israeliresearchers were able to show thatchronic treatment with a drug that

blocked noradrenaline in the bonealso blocked the effects ofdepression on bone (Proc Natl Acad

Sci USA, 2006; 103: 16876–81; Ann NY Acad

Sci, 2010; 1192: 170–5).Although more studies are

needed in this field—dubbed‘neuro-psycho-osteology ’—somescientists are already calling fordepression to be officiallyrecognized as a risk factor forosteoporosis. Indeed, the findingssuggest that dealing withdepression may be an importantmeans of keeping bones strong andpreventing fractures (see WDDTY vol 18 no 12, orwww.wddty.com/how-you-beat -depression, for more informationon how to treat depressionnaturally).

Other risk factorsBesides depression, other factorscan increase the risk ofosteoporosis. Some, such as beingfemale, getting older and having afamily history of the condition,can’t be changed. But there areother things we can do somethingabout.u Sedentary lifestyle. People whospend a lot of time sitting are morelikely to develop osteoporosis. AsMarilyn Glenville explains in TheNatural Health Bible for Women(Duncan Baird, 2010), bonestrength depends on supply anddemand. “If you demand lots fromit, it will supply the bone density toaccommodate your demands; if you make few demands on it, yourbone density will reduceproportionately.”

Studies show that regularweight-bearing exercise isimportant for building andmaintaining bone strength. Low-impact activities such as walkingand gentle aerobics can preventbone loss, while high-impactexercise like running and weight-training can increase bone density(Postgrad Med J, 2003; 79: 320–3).Football is a helpful activity. A 14-week study of women, aged 20–47years, who played football twice aweek showed significantlyincreased bone density in theshins. Surprisingly, similar femalerunners who trained for the same

amount of time didn’t see suchdramatic effects (Scand J Med Sci

Sports, 2010; Mar 4; Epub ahead of print).For the less mobile, whole-body

vibration training (WBVT), whichinvolves standing, sitting or lyingon a vibrating platform tostimulate muscle contractions, is agood option. Postmenopausalwomen having WBVT three times aweek for six months saw significantincreases in hip BMD, as well as instrength and balance (J Bone Miner

Res, 2004; 19: 352–9). WBVT alsoprevented bone loss in the spineand femur (thigh bone) comparedwith a placebo (J Bone Miner Res, 2004;

19: 343–51).If you already have osteoporosis,

exercise that improves balance andcoordination, such as Tai Chi orstep aerobics, can help to preventfalls and fractures (BMC Geriatr, 2006;

6: 6). u Acidic diet. While some foodssupply us with essential bone-building nutrients such as calcium,others can be detrimental to bonehealth. Says Annemarie Colbin,author of The Whole-Food Guide toStrong Bones: A Holistic Approach(Oakland, CA: New HarbingerPublications, 2009), watch out foracid-forming foods—such as meatand sugar—as excess intakes draincalcium and other minerals fromthe bones. Studies in mice showthat acidosis—a tilt towards anacidic blood pH—encourages boneloss and inhibits bone formation(Curr Opin Nephrol Hypertens, 2004; 13:

423–36). This may explain why olderwomen who eat chocolate (high insugar) every day have less bonedensity and strength (Am J Clin Nutr,

2008; 87: 175–80), and why certaindrinks are linked to osteoporosis(see below).

The best diet for better bonesincludes acid-forming andalkalizing foods such as leafy greenvegetables (kale, collard andmustard greens, watercress,arugula), roots (carrots, turnips,parsnips, radishes), broccoli andsquash (for more information, seeWDDTY vol 19 no 12).u Coffee and alcohol. Caffeineincreases urinary loss of calciumand magnesium (J Nutr, 1993; 123:

1611–4), and four or more cups of

Common conditions


coffee a day is linked to a higherrisk of fractures, particularly inwomen with low calcium intakes(Osteoporos Int, 2006; 17: 1055–64). Incontrast, tea appears to be bone-protective (Am J Clin Nutr, 2007; 86:

1243–7), as it contains otherhealthful ingredients such asflavonoids.

Heavy alcohol consumption isalso implicated in osteoporosis(Alcohol Clin Exp Res, 2010; Feb 24; Epub

ahead of print), but a moderateconsumption (1–2 drinks/day) maybe beneficial to bone in men and inpostmenopausal women (Am J Clin

Nutr, 2009; 89: 1188–96).u Smoking. Cigarettes are aknown risk factor for low BMD andosteoporosis (J Cross Cult Gerontol,

2005; 20: 109–25). Smoking morethan a pack a day is associated witha 60-per-cent greater risk ofosteoporosis (Bone, 2010; Mar 31;

Epublication ahead of print). Also,

Japanese researchers havediscovered changes such as fewermarrow cells and osteoblasts(bone-making cells) in the bonesof smoke-exposed rats. Althoughthese findings may not apply tohumans, they suggest that evenpassive smoking may adverselyaffect bones (Orthopedics, 2010; 33:

90–5).u Changes in weight. Studies haveshown that those who havesuccessfully lost weight also hadgreater bone loss compared withthose who didn’t lose weight (J Clin

Endocrinol Metab, 2007; 92: 3809–15). So,if you’re on a weight-loss diet, besure to increase your physicalactivity (preferably with high-impact exercise) and ensure thatyour intake of bone-buildingnutrients is adequate (see box,page 13).u Certain medications. Long-term use of corticosteroid

medications such as prednisoneand cortisone can lead toosteoporosis (Presse Med, 2006; 35:

1571–7). Other drugs that have been

linked to brittle bones includearomatase inhibitors, used to treatbreast cancer (Bratisl Lek Listy, 2010;

111: 27–32), and acid-blockingproton pump inhibitors (Curr

Gastroenterol Rep, 2010; Apr 24;

Epublication ahead of print).

Prevention is the keyUltimately, as osteoporosis is a‘silent’ condition—it’s usuallyasymptomatic until a bone fractureoccurs—understanding what causesit is our best weapon against it.Indeed, research suggests thatmaking simple changes to our dietand lifestyle now can have a bigimpact on our bones for years tocome.

Joanna Evans


‘Miracle’ drug cures forhair loss come at a price,but natural remedies likevitamin E may workwonders

Medical experts have recentlywarned that a top-selling anti-baldness drug can cause

serious sex-related side-effects and,yet, there’s no adequate warning onthe label.

Finasteride, sold in the UK and USas Propecia, is used to treat andro-genetic alopecia (AGA) in men—or‘male pattern baldness’. It inhibits 5-alpha-reductase, an enzyme thatconverts testosterone into anothermale hormone, ‘dihydrotestosterone’(DHT), a key cause of hair loss.

Clinical trials show that finasteridecan halt hair loss in up to 90 per centof users, and can even lead to hairregrowth in roughly half of them (Eur J

Dermatol, 2002; 12: 38–49). But doctors inthe US and in Ireland claim that thedrug can cause impotence and othersex-related side-effects, and are callingfor more detailed information to beincluded in the packaging.

Drugs manufacturer Merck, whichmakes Propecia, acknowledges on itswebsite that certain sex-related side-effects, such as a reduced desire forsex, difficulty in achieving an erectionand a decrease in semen, can occurwith the drug, although the companysays that less than 2 per cent of menexperience such side-effects. They alsosay that, according to their research,these side-effects will go away oncethe drug is stopped.

However, there are reports of thesesex-related side-effects continuing wellafter men have stopped the treatment.A recent BBC Radio 1 news reportfeatured the case of 26-year-old James,who stopped taking the drug afternoticing a loss of libido. He expectedthe problem to go away, but thingsonly got worse. “After about threeweeks . . . I more or less becamecompletely impotent,” he said.

James was then put on testosteronetherapy, a lifelong commitment. Sadly,that didn’t work, so he has now beenoffered a penile implant.

Male pattern baldness

“Every day, I wish I could turn backthe clock,” said James. “It did workwell for my hair, but the cost isridiculous—losing my sex life.”

Merck claims that such cases areextremely rare and could be caused by something other than finasteride.However, a recent study of the drugnoted that “[p]rolonged adverseeffects on sexual function such aserectile dysfunction and diminishedlibido are reported by a subset of men,raising the possibility of a causalrelationship” (J Sex Med, 2010 Dec 22;

Epub ahead of print).Also, a safety investigation by the

Swedish Medical Products Agency hasadvised that Propecia may result inirreversible sexual dysfunction. TheAgency’s updated safety informationlists difficulty in obtaining an erectionthat persists indefinitely, even afterstopping the drug, as a possible side-effect. A public assessment report in2009 by the UK’s Medical and Health-care Products Regulatory Agency(MHRA) also noted persistent erectiledysfunction after stopping treatmentwith Propecia as a possible undesirableeffect.

Other side-effects associated withfinasteride include allergic reactionssuch as rash, itching and hives,swelling of the lips and face; breasttenderness and enlargement; andtesticular pain. Finasteride has evenbeen linked to depression and malebreast cancer (J Cosmet Dermatol, 2010; 9:

331–2; Drug Safety Update, 2009; 3: 3).

Other hair-loss treatmentsAnother drug used to treat AGA isminoxidil (Rogaine/Regaine), a topic-al treatment that has to be applied at least twice a day for four monthsbefore any results are seen. However,in addition to possible allergic skinreactions, there’s also the risk ofsystemic effects due to absorption ofthe drug through the scalp. Suchreactions include blurred vision, chestpain, very low blood pressure, fast orirregular heartbeat, headache andweight gain (WDDTY vol 16 no 3).

Fortunately, there is a growing num-ber of promising non-pharmaceuticaloptions for dealing with baldness.

Saw palmetto (Serenoa repens) caninhibit 5-alpha-reductase levels by 32per cent with no effect on testosteronein men. Extracts of the plant have alsodemonstrated an antagonistic effecton testosterone receptors. Both theseactions—together with its impressivesafety profile—make saw palmetto auseful and safe herbal hair-loss remedy(Cutis, 2004; 73: 107–14).

In 2002, US researchers tested theefficacy of saw palmetto for mild-to-moderate male pattern baldness in adouble-blind, placebo-controlled study.Altogether, 26 men were given, twicedaily, either a softgel containing 200mg of saw palmetto extract with 50 mgof beta-sitosterol, a plant sterol foundin saw palmetto, or a placebo. Theresult was that 60 per cent of thosetaking the active softgel rated theirhair growth as improved compared

Common conditions


with only 10 per cent of those takingthe placebo (J Altern Complement Med,

2002; 8: 143–52). Beta-sitosterol and sawpalmetto are both components used inthe commercial hair-loss productHairGenesis (www.hairgenesis.com).

Other herbs may also be beneficialwhen applied topically. When the 7.5-per-cent herbal hair cream HairPrime(www.hairprime.com) was tested in 24 men with moderate-to-severe AGA, after 40 weeks, the hair countsof those using HairPrime increased by 77 per cent compared with 3 per centin the placebo group. But it didn’twork for everyone; nearly one-third ofusers saw only a modest response (J

Dermatol Treat, 1996; 7: 159–62). The exact formula of this herbal

hair cream is a proprietary secret.However, the European Handbook ofDermatological Treatment by A.D.Katsambas and T.M. Lotti (Springer,2003) states that the product includesextracts of fennel, buckwheat, mint,chamomile, Thuja and hibiscus in awater-based cream.

Green tea shows promise as a hair-loss remedy. One Korean review notedthat the polyphenol epigallocatechin-3-gallate (EGCG) in green tea mightbe able to prevent or treat AGA byinhibiting 5-alpha-reductase activity.They reported the results of test-tubestudies showing that EGCG canstimulate the growth of human hair(Phytomedicine, 2007; 14: 551–5). However,much more research is needed beforeany recommendations can be made.

Vitamin E, a potent antioxidant,may also have a role to play in treatingmale pattern baldness. A study byMalaysia-based company Carotech,presented at the Vitafoods Interna-tional Conference in Geneva in 2009,revealed that a patented tocotrienol (a form of vitamin E) complex mightincrease hair growth in people withAGA by 42 per cent.

The eight-month, randomizedplacebo-controlled trial gave 28 volun-teers with AGA either the tocotrienolcomplex (total tocotrienol, 100 mg)or a placebo (a softgel capsule with600 mg of soybean oil). Hair coverage,measured by counting the number ofhairs in a preselected 2 x 2-cm area,was significantly increased by anaverage of 41.8 per cent with toco-trienol, eight of whom had more than50-per-cent new hair growth. The

Hair transplantation has come a long way, and the latest techniques areable to achieve very natural-looking results. One such technique is called‘follicular unit extraction’ (FUE). This is a sutureless method of hairrestoration in which hair follicles are extracted from the back of headunder local anaesthesia—using special tools called ‘micropunches’—andimplanted in the bald areas. This is an extremely labour-intensive method,however, which means it’s the most expensive type of hair transplantprocedure (J Cutan Aesthet Surg, 2010; 3: 76–81). A typical session can set youback around £7000, and you may require multiple sessions. Although themore traditional hair-transplant techniques are cheaper, you could still endup spending up to £10,000 in total—depending on the extent of your hairloss.

Besides the hefty pricetag, the other drawback with hair transplantationis that it’s not risk-free. Common side-effects include pain, swelling andscabbing, while more unusual problems include bleeding and infection.

Yet another aspect to consider is that some techniques can leaveobvious scarring where the donor hair has been removed.

Finally, even when the surgical procedure goes perfectly and noscarring is visible, hair transplantation is not a cure for baldness. Thismeans that you may well continue to lose hair around the grafts.

What about hair transplants?

placebo group, on the other hand, sawno significant improvement in haircoverage, and only one volunteershowed a more than 20-per-centincrease in hair count (www.carotech.net/

index/news/219.html). These results, how-ever, have yet to be officially published.

Other antioxidants such as beta-carotene, lycopene, lutein, zeaxanthin,zinc and vitamin C may also help hairloss. As oxidative stress could beplaying a role in AGA, antioxidants—known to scavenge free radicals—mayhelp (J Cutan Aesthet Surg, 2010; 3: 82–6).

Zinc may be especially useful, as it’san essential cofactor for a number ofenzymes and is also involved inimportant functional activities in thehair follicle (Ann Dermatol, 2009; 21: 142–6).Zinc can also reduce 5-alpha-reductaseactivity in rat prostate tissue, althoughsuch animal results may not apply tohumans (Andrologia, 1993; 25: 369–75).Although clinical studies in AGApatients are lacking, one study in menwith alopecia areata (patchy hair loss)reported that zinc supplementationhad positive therapeutic effects in nineof the 15 patients studied (Ann Dermatol,

2009; 21: 142–6). Aromatherapy may be worth a try,

according to the evidence so far. In arandomized controlled trial of 86patients with alopecia areata, half ofthem massaged their scalp daily with

essential oils (thyme, rosemary,lavender, and cedarwood in a mixtureof carrier oils), while the other halfmassaged their scalp with only carrieroils, also daily. The researchers foundthat 44 per cent of the essential-oilgroup showed improvement comparedwith only 15 per cent of the controlgroup (Arch Dermatol, 1998; 134: 1349–52).

Another trial, this time in men andwomen with male pattern baldnessand lasting 26 weeks, showed thatessential oils used in combination withpulsed electromagnetic field therapy(PEMF; a technology more commonlyused for healing bone fractures) cansignificantly reduce hair loss andimprove hair counts compared with aplacebo in more than half of cases (Adv Ther, 2003; 20: 220–9).

Low-level light therapy (LLLT) hasrecently been approved by the US Foodand Drug Administration (FDA) forthe treatment of hair loss (South Med

J, 2010; 103: 917–21). This form of non-invasive therapy uses low-energy laserbeams to stimulate hair growth.

Previously, this sort of treatmentwas only available at hair-loss clinics,but the technology has now beenadapted for home use. The HairMaxLaserComb is one such home-usedevice, and has recently been tested in a randomized, sham-device-control-led, double-blind trial of 110 men with


male pattern baldness. Compared with the group using the

sham device, the men who used theHairMax LaserComb saw significantimprovements in hair density andoverall hair growth (Clin Drug Investig,

2009; 29: 283–92). However, one downside of this hair-

loss treatment is that the device isexpensive, costing between £290 and£460, depending on which model youchoose (see www.hairmax.com formore information).

Lifestyle changes may have somebenefit for hair loss. According to onereport, fried foods and red meat shouldbe avoided to reduce the over-allactivity of the oil- and sebum-producing glands, which are the sitesof 5-alpha-reductase activity, as hyper-active glands can lead to higher levelsof conversion to the DHT that causesmale pattern baldness.

The report also recommends avoid-ing sugary foods such as chocolates,sweets and cakes, as well as foods thatcontain artificial flavourings, additivesand preservatives. On the other hand,sprouts, green leafy vegetables, pulsesand nuts, along with plenty of waterevery day, can provide the nutrientsrequired for healthy, glowing hair (J

Cutan Aesthet Surg, 2010; 3: 82–6). Smoking is another lifestyle habit

to avoid, as nicotine is known toreduce blood flow to the hair folliclesand can also lead to the buildup ofdamaging free radicals in hair roots.One study found a strong connectionbetween smoking and the incidence of male pattern baldness in men (Arch

Dermatol, 2007; 143: 1401–6).Stem cells are now being studied

as a future cure for baldness. When ateam of researchers compared baldand hairy patches in scalp samples

from men with AGA, they discoveredthat, although both bald and hairypatches had similar numbers of stemcells, most of the cells in the baldpatches had failed to develop to thenext stage. Stem cells that hadmatured into so-called ‘progenitorcells’ were 10 to 100 times moreabundant in the hairy patches than inthe bald ones, thus suggesting thatthey are essential for new hair growth.

Currently, the research team—fromthe University of Pennsylvania Schoolof Medicine in Philadelphia—is tryingto work out why some stem cellsbecome dormant while others remainactive, in the hope of developing a new hair-loss treatment. Preliminarystudies in mice had suggested thatstem-cell transplants might be able toregenerate hair growth (J Clin Invest, 2011

Jan 4, pii: 44478; Epub ahead of print).Joanna Evans

Common conditions


More than 80 per cent of us willsuffer from disabling low backpain (LBP) at some point in

our lives. Although most of us willrecover within a few months, some willgo on to develop chronic LBP—painthat persists for three months orlonger. In most cases, it’s not possibleto identify a specific cause of the pain,and the treatment usually involvescourse after course of dangerous drugs(BMC Musculoskelet Disord, 2010; 11: 163).

Happily, there’s a vast array ofcomplementary and alternativetherapies now available for chronicLBP, many of which are supported bygood evidence of success (see box,page 20). But perhaps the best way totackle LBP is to prevent it frombecoming a problem in the first place.

Preventing back pain According to the latest evidence, thereare a number of ways you can reduceyour risk of LBP.u Stay active. Lower levels of physical

activity are linked to LBP (Aust J

Physiother, 2009; 55: 53–8), while regularexercise appears to prevent thecondition (Joint Bone Spine, 2008; 75:

533–9). This makes sense as havingstrong, flexible muscles areessential for a healthy back.

However, overly strenuous orexcessive exercise can be bad forthe back (Pain, 2009; 143: 21–5), so besure to choose the right form ofactivity for you.

According to Wisconsin-basedspine expert Dr Peter Ullrich, anideal back workout includes acombination of stretching, streng-thening and low-impact aerobicconditioning.

u Watch your weight. Being over-weight places an additional burdenon the spine and strain on the backmuscles. In one study of more than60,000 men and women, a highbody mass index (BMI) wassignificantly associated with an

Chronic back painThere is now a multitudeof effective drug-freealternative treatments forthis common, oftendisabling, condition

increased prevalence of LBP,particularly in women (Spine [Phila Pa

1976], 2010; 35: 764–8). u Stop smoking. Cigarette-smoking

appears to be linked to LBP,according to several studies. In arecent meta-analysis that pooledthe results of 40 separate studies,current smokers were 80-per-centmore likely to suffer from chronicLBP and also had more than twicethe risk of disabling LBP (Am J Med,

2010; 123: 87.e7–35). More worrying, exposure to

secondhand smoke duringchildhood can increase the risk ofdeveloping back problems later inlife. Researchers have postulatedthat this might be because tobaccosmoke has detrimental effects onthe developing spine (Eur J Public

Health, 2004; 14: 296–300). u Get enough sunshine. Mounting

research suggests that a lack ofvitamin D, produced naturally bythe body in response to sunlight,could be contributing to chronicmusculoskeletal pain, includingLBP (BMJ, 2005; 331: 109).

In one study of patients withchronic, non-specific (no obviouscause) LBP attending spinal andinternal medicine clinics in SaudiArabia for six years, 83 per centwere found to have abnormally lowlevels of vitamin D. After supple-menting with the vitamin, however,symptomatic clinical improvementwas seen in all those who had low

initial concentrations of the vitamin(Spine [Phila Pa 1976], 2003; 28: 177–9).

According to Dr Stewart Leavitt,a member of the AmericanAcademy of Pain Management andeditor-in-chief of the online journalPain Treatment Topics, vitamin Ddeficiency can cause musculoskele-tal pain by causing hypocalcae-mia—abnormally low levels ofcirculating calcium—which “sets inmotion a cascade of biochemicalreactions negatively affecting bonemetabolism and health”. One ofthese reactions is increased para-thyroid hormone (PTH), causing aspongy bone matrix to form. Thisleads to fluid absorption, resultingin an expansive pressure that trig-gers the abundant pain fibres in thetissues overlying the bones.

This suggests that anyone whohas non-specific LBP should betested for vitamin D deficiency.

u Manage stress. Psychological fac-tors such as stress and depressionare also thought to play a role inLBP. In one UK study that followed4500 adults (aged 18 to 75 years)for 12 months, the likelihood ofhaving a new episode of LBP wasgreater among those who scored inthe upper-third of a questionnairefor psychological distress (Spine

[Phila Pa 1976], 1995; 20: 2731–7). Inanother study, psychological dis-tress was a better predictor of backpain than the standard diagnostictechniques (Spine [Phila Pa 1976], 2004;

29: 1112–7). Psychological factors arealso implicated in the transitionfrom acute to chronic LBP (Spine

[Phila Pa 1976], 2002; 27: E109–20). u Avoid poor posture. In particular,

sitting in a chair for long periods of time creates imbalances in themusculoskeletal system that canincrease the risk of pain and injury.According to one study, workerswho sit for more than half a day inawkward postures are significantlymore likely to suffer from LBP (Eur

Spine J, 2007; 16: 283–98). (See WDDTYvol 20 no 3 for tips on keeping ahealthy back while sitting.)

Poor lifting technique can alsobe the cause of back pain. Youshould always push, rather thanpull, when you need to move heavyobjects and, if you have to lift, letyour legs do the work by holding the


u Exercise. Not just good for preventing back pain,exercise can treat it, too. One review concluded thatexercise can reduce pain and improve physical functionin chronic or recurrent LBP (Joint Bone Spine, 2008; 75:

533–9). The most effective strategy appears to be anindividually designed exercise programme that includesstretching and strengthening, and is carried out underlimited supervision—for example, home-based exerciseswith regular follow-ups by a therapist (Ann Intern Med, 2005;

142: 776–85). However, group exercise can also help,especially if you join a class that focuses on the mind aswell as the body.v Yoga. A two-year study showed that an Iyengar yogaclass twice a week can improve functional disability, painintensity and depression in adults with chronic LBP, andalso allowed the use of less pain medication (Spine [Phila

Pa 1976], 2009; 34: 2066–76).v Pilates Method. Increasingly used to treat chronic LBP,this form of exercise can be effective for reducing painand improving general physical function (J Bodyw Mov Ther,

2008; 12: 364–70).v Qigong. The main posture used in this form ofexercise is similar to the posture recommended byhealthcare professionals dealing with back pain (Wien Med

Wochenschr, 2004; 154: 564–7). Also, when used as anadjunct to drug treatment, this meditative form ofmovement and breathing techniques can successfullyrelieve chronic pain (Am J Chin Med, 2010; 38: 695–703).

u Acupuncture. In one major review, acupuncture wasfound to be superior to the usual care for treating chronicLBP, thereby justifying the recent recognition of this traditional Chinese medicine technique as atherapeutic option for LBP by the UK’s National Institutefor Health and Clinical Excellence (NICE) (Ann R Coll Surg

Engl, 2010 Jun 7; Epub ahead of print). u Massage. Several studies suggest that therapeutic

massage is useful against chronic LBP, especially whencombined with exercise and patients’ self-care education(Spine [Phila Pa 1976], 2009; 34: 1669–84). In one trial, thebenefits of massage were still evident 9–10 months afterthe therapy had ended (Trials, 2009; 10: 96).

u Alexander Technique. This discipline, whichemphasizes the self-perception of body movement, wasfound to be more effective than conventional care ormassage as a treatment for chronic or recurrent backpain. What’s more, just six lessons followed byprescribed exercises were nearly as successful as 24lessons of Alexander Technique on its own (Br J Sports

Med, 2008; 42: 965–8).u Spinal manipulation. Performed by chiropractors as

well as some osteopaths and physical therapists, spinalmanipulation was recently pitted against back school(consisting of group exercise and education) andindividual physiotherapy (exercise, passive mobilizationand soft-tissue therapy) for the treatment of chronicLBP. The results showed that spinal manipulationprovided better short- and long-term functionalimprovements, and more pain relief, than either back

school or individual physiotherapy (Clin Rehabil, 2010; 24:

26–36).u Biofeedback. This mind–body technique was found to

be more effective than behavioural therapy orconservative medical treatment for sufferers of chronicback pain. The researchers also reported thatbiofeedback was the only method to significantlyreduce pain over the two-year follow-up (J Consult Clin

Psychol, 1993; 61: 653–8).u Hypnotherapy. Numerous studies show that hypnosis

is an effective treatment for a range of chronic painconditions. In a small preliminary study to assess itssuccess in chronic LBP, a brief, four-sessionstandardized self-hypnosis protocol, combined withpsychoeducation, dramatically reduced pain intensityand pain interference (Int J Clin Exp Hypn, 2010; 58: 53–68).

u Supplements. In addition to a balanced diet, a numberof supplements may be useful for beating back pain.v Vitamin D could be the key to curing LBP if you aredeficient in this nutrient (see main story). In a study of 360 patients with chronic LBP, vitamin D easedsymptoms in virtually all those with the most severe Ddeficiency (Spine [Phila Pa 1976], 2003; 28: 177–9). Althoughsunshine is our best source of this vitamin, most of usdon't get enough of it that way. Pain expert StewartLeavitt recommends (with the supervision of a qualifiedpractitioner) a daily supplement of 2000 IU of vitamin D3(cholecalciferol), along with a daily multivitamin that includes calcium and 400–800 IU of vitamin D. Bepatient, as it may take up to nine months to experiencethe maximum effects of this regimen.v B-complex vitamins may also help. A combination of vitamins B1, B6 and B12, taken twice a day at 50 mg, 50 mg and 1 mg, respectively, together with thepopular non-steroidal anti-inflammatory drug (NSAID)diclofenac (50 mg twice daily), was better at relievingback pain than the NSAID alone (Curr Med Res Opin, 2009;

25: 2589–99).v Proteolytic enzymes, such as trypsin and serra-peptase, may be useful as they are known to have anti-inflammatory properties (Indian J Pharm Sci, 2008; 70:

114–7).u Herbs. The following may help to relieve back pain.

v Capsaicin, found in all hot peppers, can ease manytypes of chronic pain when applied regularly to the skin.In one study, a capsaicin plaster was significantly betterthan a placebo in patients with chronic back pain(Arzneimittelforschung, 2001; 51: 896–903).v Devil's claw (Harpagophytum procumbens) iseffective for LBP when the daily dose provides at least50 mg of the active ingredient harpagoside. One trialfound it to be just as effective as the NSAID rofecoxib(Spine [Phila Pa 1976], 2007; 32: 82–92).v White willow bark (Salix alba) is chemically related toaspirin and appears to provide short-term relief of LBP.Studies used daily doses standardized to 120 mg or240 mg of salicin, which has anti-inflammatory actions(Spine [Phila Pa 1976], 2007; 32: 82–92).

Drug-free treatments for back pain

Common conditions


load close to your body, keepingyour back straight and bending onlyat the knees. Avoid lifting andtwisting simultaneously.

u Treat childhood back pain.Contrary to popular belief, non-specific LBP is a serious problemamong children and teenagers.Indeed, a review of the relevantstudies suggests that rates are

almost as high as in adults (Ugeskr

Laeger, 2002; 164: 755–8). There are also clear correlations

between experiencing LBP as achild/adolescent and suffering fromLBP—especially chronic LBP—as anadult (Arch Pediatr Adolesc Med, 2009;

163: 65–71). It is vital, therefore, thatthe condition, when it arises, bedealt with promptly.

The possible causes of childhoodLBP include intensive sportsactivities and carrying a too-heavybackpack, as well as the factorsmentioned above (Rev Chir Orthop

Reparatrice Appar Mot, 2004; 90: 207–14).For backpack safety tips, seehttp://orthoinfo.aaos.org/topic.cfm?topic= A00043.

Joanna Evans


Stroke

Stroke is a dreaded disorder thataffects some 150,000 people inthe UK each year. It occurs

when blood circulation to the brainfails due to either blockage (ischae-mic stroke) or bleeding (haem-orrhagic stroke), causing brain cellsto die, with symptoms such asparalysis, speech difficulties andvision problems.

According to the Stroke Associa-tion, around 1000 people aged under30 suffer a stroke every year. Often,it’s secondary to other health issuessuch as diabetes and heartconditions. The good news is thatthere are a number of ways to reducethe risk.

Stroke preventionFor years, millions of peopleworldwide, including the ‘worriedwell’, have been taking aspirin toprotect against heart attack andstroke. Yet, the latest evidence is thatthis ‘wonder drug’ may be doingmore harm than good. Not only canaspirin cause serious and fatalgastrointestinal injury and bleeding(Drug Ther Bull, 2009; 47: 122–5), but itcan also increase stroke risk,especially in the over-75s. Over thepast 25 years, the number of strokesassociated with such blood-thinnershas increased sevenfold (Lancet Neurol,

2007; 6: 487–93).Happily, there are safer ways to cut

your risk of suffering a stroke.u Eat plenty of fruit and

vegetables. Having more than therecommended five servings of fruitand veg per day (one serving =half a cup) can reduce the risk ofstroke by 26 per cent (Lancet, 2006;

367: 320–6).u Take regular exercise. Inactivity

can almost double your risk ofstroke (Am J Epidemiol, 1996; 143:

860–9), while vigorous exerciseearly in life protects against laterstroke, despite other risk factorssuch as social class, smoking,alcohol intake, family history,hypertension and diet. Continuedvigorous exercise later in lifereduces the risk even further. Ofmore than 11,000 men, aged 58years on average, those whoexercised moderately (one hour ofbrisk walking, five days a week)had a 46-per-cent lower stroke riskthan those who exercised little ornot at all (Stroke, 1998; 29: 2049–54).

u Maintain a healthy weight.Obesity is a risk factor for stroke,and also contributes to other riskssuch as high blood pressure,diabetes, high cholesterol andobstructive sleep apnoea (wherethe sufferer stops breathingtemporarily throughout thenight). As well as keeping an eyeon your BMI (body mass index), itis also worth watching yourwaistline, as this has beenindependently linked to stroke(Arch Intern Med, 2007; 167: 1420–7;

Stroke, 2003; 34: 1586–92).u Limit alcohol. Moderate alcohol

consumption—no more than twodrinks per day—can protectagainst ischaemic stroke, whileheavy drinking has the oppositeeffect (JAMA, 1999; 281: 53–60).

u Eat more wholegrains. Comparedwith eating no wholegrains,women who ate more than onewholegrain food a day reducedtheir stroke risk by around 35 percent (JAMA, 2000; 284: 1534–40).

u Increase your intake of ‘good’fats. Fish, rich in omega-3 fattyacids, can prevent stroke (Prev Med,

1999; 28: 520–9; JAMA, 2002; 288: 3130–6)but, if you’re worried aboutmercury, just eat a few walnuts aday. These, along with flaxseed,soybean and canola oils, are anexcellent source of essentialomega-6 alpha-linolenic acid(ALA), high blood levels of whichreduced stroke risk even in men athigh risk of cardiovascular disease(Stroke, 1995; 26: 778–82).

u Take supplements. B vitamins canhelp to reduce homocysteine,which has been linked to stroke(Stroke, 2002; 33: 2351–6).

Supplementing with even lowlevels of B vitamins (1 mg of folicacid (B9), 10 mg of B6 and 400mcg of B12) significantly loweredhomocysteine levels within sixweeks (Am J Clin Nutr, 1993; 57: 47–53). In another study, folic acidreduced the risk of stroke by 18per cent (Lancet, 2007; 369: 1876–82),while combining beta-carotene,selenium, vitamins E and A, andzinc reduced stroke deaths by 29per cent (Ann Intern Med, 2006; 145:

372–85). u Try herbs. Garlic and Ginkgo

biloba are powerful blood-thinners(Arzneim Forsch, 1993; 43: 119–22;

Haemostasis, 1989; 19: 219–23), andginger can also help: 5 g/day ofraw ginger for just one week led toa 37-per-cent drop in the blood-clotting agent thromboxane(Prostaglandins Leukot Essent Fatty Acids,

1989; 35: 183–5). u De-stress. Stress is a major

contributor to hypertensivedisease and stroke. Qi gong, anancient Chinese form of exercisethat emphasizes a tranquil mind,relaxed body and smoothbreathing, lowers blood pressure(Zhongguo Zhong Xi Yi Jie He Za Zhi,

1993; 13: 413–4, 388–9) and slashesstroke risk. In one long-termstudy, only 19 per cent of thosewho regularly practised Qi gongdied of stroke compared with 42per cent of the controls (J Tradit

Chin Med, 1986; 6: 235–8). Meditationalso appears to be beneficial(Stroke, 2000; 31: 568–73).

u Keep your gums healthy. Thosewith severe gum disease have atwo-fold higher risk of stroke (Arch

Intern Med, 2000; 160: 2749–55).u Get enough sunshine. Vitamin D

Anyone can suffer astroke—not just theelderly. But some little-known health tips, likekeeping your gumshealthy, can help slashyour risk

Common conditions


u Music therapy. Listening to music for a few hours every day can boostcognitive and emotional recovery in the early stages following a stroke. Finnishresearchers compared the recovery of 60 stroke patients who listened daily toeither music of their choice, audio books or nothing at all (controls) for twomonths. At this time, all patients also received the standard medical care andrehabilitation. The results showed that the recovery of verbal memory andfocused attention (ability to control and perform mental operations, and resolveconflicts) improved significantly more with music than with audio books andnothing at all. The music-listeners also felt less depressed and confused thanthe control group, and these differences were still evident six months later (Brain, 2008; 131: 866–76).

u Guided imagery, or visualization. Now used as part of stroke rehabilitation,this appears to be especially effective for helping patients to relearn their motorskills and how to perform everyday tasks (Brain Inj, 2004; 18: 1163–72; Stroke, 2006;

37: 1941–52).u Transcranial magnetic stimulation (TMS). This non-invasive brain-stimulation

technique appears to promote functional recovery in stroke patients. In arandomized controlled trial of 52 stroke patients who received either TMS orsham (control) brain stimulation in addition to the usual therapy, the TMS groupshowed greater improvement, as assessed by three disability scales (Neurology,

2005; 65: 466–8).u Vitamin E. Research in mice has revealed that a form of vitamin E called

‘tocotrienol’, found in supplements, may be able to prevent brain cells fromdying after a stroke. Tocotrienol appears to block the activity of a brain-damaging enzyme that is produced following a stroke—even when taken atvery low levels (J Neurochem, 2010; 112: 1249–60). These results, however, may notnecessarily apply to humans.

u Biofeedback—getting back information on bodily functioning to learn how toactively control these functions—has been applied to many aspects of strokerehabilitation, but the results are mixed. A review of 13 trials, involving only 269 patients, found no treatment benefits with electromyographic biofeedback(Cochrane Database Syst Rev, 2007; 2: CD004585). Nevertheless, researchers haveconcluded that “biofeedback in general can have a very positive impact” byboosting patients’ self-confidence (Top Stroke Rehabil, 2007; 14: 59–66).

u Traditional Chinese medicine. A preparation of 14 herbal and plant extractsknown as Danqi Jiaonang, or NeuroAid, taken as capsules, is currently beingstudied as a therapy for stroke. In a recent clinical trial, although the results did not reach statistical significance, the NeuroAid-treated post-stroke patientsshowed improvement over controls after 4 weeks of treatment (Cerebrovasc Dis,

2009; 28: 514–21); a longer and larger multicentre study of the remedy is currentlyongoing (Int J Stroke, 2009; 4: 54–60).

u Acupuncture is another traditional Chinese technique that’s proving useful.The method known as ‘Jin three-needle therapy’ appears to be especiallyeffective at improving cognitive function and in helping post-stroke patients toget along in their day-to-day life (Zhongguo Zhen Jiu, 2009; 29: 689–94).

Promising post-stroke therapiesdeficiency may play a role in heartdisease and stroke (Curr Vasc Pharma-

col, 2009; 7: 414–22). Exposing yourskin to sunlight for 10–15 minutes a day (with no sunscreen) is thebest way to get your dose ofvitamin D (BMJ, 2003; 327: 1228–9).Alternatively, supplementing with600–1000 IU of vitamin D3 (thenatural form) is a good idea forthose who don’t get much sun.

u Look after your lungs. The healthof your lungs appears to be a goodindicator of the risk of stroke(Stroke, 2009; 40: 1986–90). In fact,smoking, passive smoking andoutdoor air pollution have all beenlinked to stroke (Tob Induc Dis, 2004;

2: 7; Stroke, 2003; 34: 2776–80). Inaddition to not smoking, there area number of ways to protect yourlungs from harmful pollutants:v install ionizers in your homeand car, as they emit negativelycharged particles—or ‘negativeions’—into the air; these attach topollutants, causing them to ‘dropout’ of the atmosphere;v take antioxidants, such asvitamins A, C and E, whichscavenge free radicals; andv keep tabs on the levels ofpollution in your area bycontacting your local air-qualitymonitoring service. (Readers inthe UK can visit the UK NationalAir Quality Archive atwww.airquality. co.uk, while thosein the US can check out the USEnvironmental Protection Agencywebsite at www.airnow.gov.) Whenlevels are high, don’t exercise orexert yourself outdoors, as thefaster you breathe, the morepollution you will then draw intoyour lungs.

Joanna Evans


Women’s health

Beating the changeWe now know that therisks of HRT far outweighthe benefits, so whatalternatives are there tohelp women through themenopause?

Now that hormone replace-ment therapy (HRT) has beenlargely discredited, millions

of women embarking on themenopause are turning to alter-native medicine to manage theirsymptoms. In fact, only 10–25 percent of women experiencing meno-pausal symptoms seek treatmentfrom a traditional healthcareprovider, according to a recentreport, and many of them aredissatisfied with the conventionalmedical recommendations (J Womens

Health [Larchmt], 2005; 14: 634–49).However, finding a safe and

effective alternative treatment is no easy task. One of the favourites is so-called ‘natural’ progesterone,championed by the late Dr JohnLee. But, as WDDTY reported in2006, it is far from natural. Thereare even some concerns that itmight cause cancer, just like HRT(see WDDTY vol 17 no 2). Similarconcerns have been raised about soyand isoflavone supplements (seeWDDTY vol 16 no 8), which are alsoamong the more popular alternativeremedies for menopause. So what’sa girl to do?

Happily, research shows thatthere are a number of simple, safesteps you can take to help make thetransition into menopause a smoothone. u Exercise regularly. Growing

evidence suggests that beingphysically active is one of the bestthings you can do to keepmenopausal symptoms undercontrol. A recent study of 336menopausal women found thatthose who were the mostphysically active had less severesymptoms and generally feltbetter than their less-activecounterparts (Climacteric, 2010; 13:

355–61).

In another study, 36 post-menopausal women were splitinto two groups: an aerobic-exercise group and a resistance-exercise group. Both groupsexercised three times a week foreight weeks under the super-vision of a physiotherapist. At theend of the study, both types ofexercise were found to havepositive effects on the symptomsof menopause, although aerobicexercise had a slightly greaterimpact. In addition, both exercisegroups saw improvements in theirpsychological health, depressionand quality of life (Obstet Gynecol

Int, 2010; 2010. pii: 274261).Regular exercise can also

reduce the risk of postmeno-pausal breast cancer, osteo-porosis and cardiovasculardisease—an important considera-tion, as the risk of developingthese diseases increases after themenopause (Arch Intern Med, 2010;

170: 1758–64; Aust J Public Health, 1993;

17: 23–6). Aim for at least 30minutes of moderate-intensityphysical activity on most days.

u Boost your intake of omega-3fats. A new study has found thatomega-3 fatty-acid supplementscan help fight depression and hot flushes in women goingthrough the menopause. Thestudy involved 20 women withmajor depressive disorder given 2 g/day of eicosapentaenoic acid(EPA) and docosahexaenoic acid

(DHA) for eight weeks. Theresults showed that 70 per cent of the women saw a reduction ofat least 50 per cent in theirMontgomery–Asberg DepressionRating Scale (MADRS) scores.Moreover, hot flushes decreasedin both number and severity(Menopause, 2010 Oct 27; Epub ahead

of print).In addition, like exercise,

omega-3 supplements can alsohelp to prevent postmenopausalosteoporosis, breast cancer andheart disease (Obstet Gynecol Surv,

2004; 59: 722–30).u Take vitamin E. A randomized

controlled trial found that dailydoses of vitamin E (400 IU)significantly reduced the frequen-cy and severity of hot flushes inpostmenopausal women (Gynecol

Obstet Invest, 2007; 64: 204–70).Previous research carried outmore than 50 years ago alsosuggests that vitamin E may helpmood swings and vaginal dryness(NY State Med; 1952; 52: 1289).

u Consider aromatherapy. Thisform of treatment uses essentialoils extracted from the flowers,leaves, fruit, bark and roots ofmedicinal plants. Aromatherapy

Officially, you’re not in the menopause until it’s been a whole year sinceyour last menstrual period. However, the signs and symptoms ofmenopause may well appear long before that. These include:

u hot flushesu night sweatsu irritabilityu mood swingsu depressionu insomniau impaired memory or concentrationu loss of libidou vaginal drynessu increased abdominal fat.

Signs of menopause


massage works on the nervoussystem through the senses ofboth smell and touch.

In a small study carried out in Japan, 15 women with meno-pausal symptoms were examinedby a gynaecologist beforereceiving a 30-minute aroma-therapy session, involving aconsultation, massage and home-massage guidance. After onemonth of at-home care and asecond aromatherapy session, allreported significant improve-ments in their symptoms (J Altern

Complement Med, 2005; 11: 491–4). Intriguingly, another study

discovered that aromatherapymassage, with an additional focuson the abdomen, can reduceabdominal fat and improve bodyimage in post-menopausal women(Taehan Kanho Hakhoe Chi, 2007; 37:

603–12).u Take up yoga. A systematic

review of 18 clinical trials fromsix countries found that yoga-based and certain other mind–body therapies can be beneficialby alleviating a range ofmenopausal symptoms. Eight outof nine studies of yoga, tai chiand meditation-based prog-rammes reported improvement inoverall menopausal andvasomotor symptoms (such as hotflushes and night sweats); six ofseven trials using yoga-basedprogrammes indicated impr-ovement in mood and sleep, andfour studies reported reducedmusculoskeletal pain.

Results from the other trialssuggest that breath-control-basedand other relaxation therapiesare also promising for relievingmenopausal symptoms (Maturitas,

2010; 66: 135–49).u Consider acupuncture. One

small Swiss study showed thatacupuncture was able to signif-icantly reduce vasomotor symp-toms and physical disturbances inmenopausal women. What’smore, the effects were stillevident three months after thelast session (J Altern Complement

Med, 2001; 7: 651–8). More recently, a randomized

controlled trial of 175 womenreported that acupuncture, in

addition to the usual care, wasassociated with marked clinicalimprovement in hot flushes andother menopause-related symp-toms (Menopause, 2010; 17: 269–80).

u Try the herbal supplementFemal. This “unique blend ofpollen extracts from sevenorganically cultivated flowersgrown in . . . Sweden” alsocontains vitamin E. In one Danishstudy, 54 menopausal womenwere randomly given either twoFemal tablets each morning, ortwo identical placebo tablets, forthree months. The results showedthat 65 per cent of the Femalgroup enjoyed a reduction in hotflushes compared with 38 percent in the placebo group.

On looking at 15 other meno-pausal “quality-of-life” symptoms,Femal again came out on top(Climacteric, 2005; 8: 162–70).

Femal is available from Bootsand independent chemists.

u Lose weight. If you’re overweightor obese, losing weight can helpto keep hot flushes under control,according to a recent study.University of California at SanFrancisco researchers studied338 overweight or obese womenand found that those whofollowed an intensive weight-lossprogramme showed greaterimprovements in bothersome hotflushes compared with thosefollowing a structured health-education programme (controls)(Arch Intern Med, 2010; 170: 1161–7).

u Stop smoking. The results of onestudy suggest that women whosuffer from hot flushes are morelikely to be smokers (J Womens

Health, 1998; 7: 1149–55). Anotherstudy found that women takingHRT for relief of menopausalsymptoms were more likely to becurrent smokers.

“This relation between HRTuse and smoking could resultfrom an anti-oestrogen effect ofsmoking, intensifying meno-pausal symptoms,” said research-ers (J Epidemiol Community Health,

1987; 41: 26–9).u Investigate allergies. According

to Dr Ellen Grant, author of TheBitter Pill and Sexual Chemistry,hot flushes could be due to an

allergic reaction to commonfoods or chemicals. In her studyof 60 migraine sufferers, a varietyof foods and drinks, includingwheat, eggs, sugar, tea andcoffee, commonly caused vascularreactions such as flushing,headaches, and pulse or bloodpressure increases. The mostcommon chemical allergens werecigarette smoke and domestic gas(Lancet, 1979; 313: 966–9; WDDTY vol 17

no 2). So, if you suffer from hotflushes, keep a diary to try topinpoint any possible triggers.

u Consider black cohosh. Thisherb has a long history of tradi-tional use for a variety of ‘femalecomplaints’, including menstrualproblems and childbirth. Scien-tific studies have found it to be asafe and effective remedy for anumber of menopausal symp-toms, but mainly hot flushes andmood swings. Indeed, Germany’sgovernmental regulatory agencyCommission E has approved theuse of 40 mg/day of black cohosh(sold as Remifemin) for sixmonths for the relief of suchsymptoms.

Although early studiessuggested that the herb hasoestrogenic effects, more recentevidence shows that black cohoshdoes not have an oestrogenicmechanism of action but,instead, acts on serotonin rec-eptors to relieve menopausalsymptoms (J Womens Health

[Larchmt], 2005; 14: 634–49). Nevertheless, there have been

concerns (from animal studies,which may not apply to humans)as to its potential to increase thespread breast cancer, so it’sgenerally not recommended forpatients or women with a familyhistory of the disease (Cancer Res,

2008; 68: 8377–83). If you do wish to try black

cohosh, it’s best to do so onlyunder the supervision of a regis-tered naturopath or medicalherbalist.

u Give Ginkgo a go. Several studiesshow that Ginkgo biloba can helpto boost memory and concentra-tion, which can suffer during themenopause. One study found that120 mg/day for just one week


Women’s health

significantly improved memoryand attention compared with aplacebo in postmenopausalwomen (Pharmacol Biochem Behav,

2003; 75: 711–20). When combined with other

herbs, Ginkgo may also boost thelibido. A herbal formulation(Herbal vX) of Ginkgo and Muirapuama was tested in 202 healthypre- and postmenopausal womencomplaining of low sex drive.After one month of treatment,statistically significant improve-ment was found in frequency ofsexual desire, sexual intercourseand sexual fantasies, as well as insatisfaction with sex life in gen-eral, intensity of sexual desires,excitement of fantasies, ability toreach orgasm and intensity oforgasm (Adv Ther, 2000; 17: 255–62).

However, as the trial was uncon-trolled, we don’t know to whatextent the results are down to the‘placebo effect’.

In one double-blind, placebo-controlled trial, the supplementArginMax (from www.arginmax.com and www.virilityhealth.co.uk), which contains Ginkgo, plusL-arginine, ginseng, damiana,multivitamins and minerals, wastested in just over 100 women,aged 22–73 years, who reported alack of sexual desire.

In those going through themenopause, the supplementincreased the frequency of inter-course, satisfaction with thesexual relationship and vaginaldryness.

In postmenopausal women,half reported increased sexual

desire compared with only 8 percent with the placebo. Moreover,the formulation has been shownto exhibit no oestrogenic activity(J Sex Marital Ther, 2006; 32: 369–78).

u Eat healthily. Keeping to abalanced diet that includes avariety of fruit and vegetables canprotect against bone loss, cancerand premature death (Am J Clin

Nutr, 2000; 71: 142–51; Cancer Epidemiol

Biomarkers Prev, 2004; 13: 1485–94;

JAMA, 2000; 283: 2109–15). The nutrients that are

especially important formenopausal women are calcium,vitamins D, C and the Bs, andpotassium, zinc, copper andmagnesium. Aim to get thesefrom your diet, and supplementwhen necessary.

Joanna Evans


Herbal helpers for women over 50Here are some of thehelpful herbs that womencan take as they gothrough the menopauseand after

Awomen grow older and reachthe menopause and beyond,the inevitable changes that

occur in their bodies due to ageand hormones may require lifestylechanges, including a new look atnutritional requirements. Thefollowing herbs have all beenproven to help.

Black cohosh (Actaea racemosa)This is good for menopausalsymptoms, but needs aprescription from a registerednaturopath or medical herbalist(McKenna DJ et al. Botanical Medicines:

The Desk Reference for Major Herbal

Supplements, 2nd edn. London, Oxford &

NY: The Haworth Press, 2002: 41–3). Theherb can also help withpostoperative functional deficitsfollowing ovariectomy or a fullhysterectomy.

Contraindications: Pregnancy;lactation; oestrogen-dependenttumours, including some breastcancers due to its potentialoestrogenic actions; and salicylatehypersensitivity, as this is asalicylate-containing plant.

Drug interactions: Hormonereplacement therapy (HRT), as thisherb may lead to oestrogen excess.

In studies using a fluid extractof this herb, up to 890 mg/day hasbeen given—with no toxic effects(Brinker F. Herb Contraindications & Drug

Interactions, 3rd edn. Sandy, OR: Eclectic

Medical Publications, 2001: 40–1; also

www.eclecticherb. com/emp), althoughthe usual dose of an ethanolicextract is only 8 mg/day.

Evening primrose oil (EPO) Postmenopausal women oftensuffer from dry skin (eczema-like),hair loss, breast pain and poorwound-healing due to depleted

oestrogen. However, EPO(Oenothera biennis) can help toreverse these conditions (McKenna

op.cit., 327–35).Contraindications: Epilepsy; and

mania. Drug interactions: Phe-

nothiazines: induces seizures andhallucinations; tamoxifen: speedsup clinical response; cyclosporine:less kidney damage; andanticoagulants: may enhanceblood-thinning effects.

The highest dose generallyrecommended is 0.1 mL/kg/day, sosomeone weighing 55 kg (8.5stone) should take 5.5 mL/day (Brinker op. cit., 92–3; see also

www.eclecticherb.com/emp).

Garlic (Allium sativum)It is well established that garliclowers blood pressure, bloodglucose, blood lipids and chol-esterol, but it also prevents bloodclots, and is mildly antibiotic,antifungal, anticancer, anti-oxidant, immunomodulatory andliver-protective (McKenna op. cit., pp

375–96).Contraindications: Gastritis;

early pregnancy; hypothyroidism;and oesophageal reflux.

Drug interactions: Warfarin or other blood-thinners: because it enhances anticoagulation;indomethacin; dypiridamole;paracetamol/ acetaminophen: itmay prevent liver toxicity; andinsulin (as it lowers blood glucose,insulin doses may need adjusting).

A dose of 4 g/day of fresh garlic,or 8 mg of essential oil of garlic assupport therapy, is typicallyprescribed to reduce blood lipids,and to prevent age-dependentvascular changes (Brinker, op. cit., pp

99–101).

Ginkgo biloba (maidenhair tree)Ginkgo helps to prevent memoryloss, loss of mental alertness,dementia, stroke, free-radicaldamage in traumatic brain injury

and Alzheimer’s (Arch Phys Med

Rehabil, 2000; 81: 668–78).Contraindications: Bleeding

disorders, especially those withreduced blood-clotting, so it maycontribute to haemorrhage if usedfor a lengthy period prior tosurgery.

Drug interactions: Aspirin (whenused chronically to prevent bloodclots), anticoagulants, heparin,other non-steroidal anti-inflammatory drugs (NSAIDs),ticlopidine, thiazide, trazodone,cyclosporine and papaverine; itmay enhance meclofenoxate, usedto treat senile dementia andAlzheimer’s, and the effects ofmonoamine oxidase inhibitors(MAOIs), a class of antidepressantdrugs.

In a study of 33 women takingan average dose of 209 mg/day,Ginkgo leaf extract counteractedthe sexual dysfunction associatedwith antidepressants, mostly SSRIs(selective serotonin reuptakeinhibitors), but also phenelzine(an MAOI), vivactil (protriptyline,a tricyclic), and venlafaxine,nefazodone and bupropion( s e r o t o n i n – n o r e p i n e p h r i n ereuptake inhibitors, SNRIs) .

It is also thought that Ginkgomay reduce the efficacy ofanticonvulsants such ascarbamazepine (Brinker op. cit., pp

103–7).Ginkgo is usually given as a total

daily dose of 120–240 mg of thestandardized extract [containingat least 24-per-cent ginkgo flavone


Women’s health

glycosides and 6-per-cent terpenelactones (ginkgolides andbilobalides)] for at least eightweeks to treat chronic conditions,and a review of its benefits istypically carried out before it is taken for more than threemonths.

Arnica montana (wolfsbane)Never use Arnica internally unless it’sdispensed in a homeopathic potency,as it has toxic effects on the liver andkidneys. It can also causegastrointestinal irritation if takenundiluted (Brinker F. Herb Contraindications

& Drug Interactions, 3rd edn. Sandy, OR:

Eclectic Medical Publications, 2001: 31–2; see

also www.eclecticherb. com/emp). TheArnica tablets sold over-the-counter(OTC) at many pharmacies comefrom manufacturing pharmacies suchas Nelsons or Weleda, and haveundergone processes to have suchtoxicity removed, so they can safely betaken as advised by the packaging,without the guidance of a homeopath.There should be no side-effects orcontraindications.

Arnica tablets can reduce bruisesand contusions, as can suitablydiluted Arnica creams [Schilcher H,

Kammerer S. Leitfaden Phytotherapie, 3 aufl

(Guide to Phytotherapy, 3rd edn). Munich, Jena:

Urban & Fischer Verlag, 2010: 30–2]. Indeed,virtually every cosmetic and plasticsurgeon in London’s Harley Streetrecommends taking Arnica beforeand after surgery by their middle-agedpatients to minimize the severebruising that is inevitable after suchsurgery.

Hawthorn (Crataegusoxyacantha)With the reduced oestrogen inpostmenopausal women comes anincreased risk of heart problems.Women aged over 50 then suddenlyrun the same risks of atherosclerosis,hypertension and congestive heartfailure as do men.

However, hawthorn has proved tohave numerous beneficial actions onthe heart and cardiovascular system.It can regulate heart rhythm throughits anti-arrhythmia actions, and dilatethe coronary arteries, therebyreducing the chances of heart attack.It can also increase the blood supplyto the heart. Furthermore, hawthorncan lower systolic pressure (the firstnumber in a blood pressure reading),which is especially beneficial in peopleover 50, who have the highest risk ofisolated systolic hypertension (ISH). Ifleft untreated, ISH can lead to heartdisease, stroke and dementia. Theherb also improves low bloodpressure, which can lead to dangeroussudden fainting episodes (McKenna DJ et

al. Botanical Medicines: The Desk Reference for

Major Herbal Supplements, 2nd edn. London,

Oxford & NY: The Haworth Press, 2002:

659–70). However, those taking beta-blockers for blood pressure shouldknow that hawthorn may cause aslight rise in diastolic blood pressure(the second number in a bloodpressure reading).

Hawthorn used with garlic powderprotects the heart, liver and pancreasagainst damage from isoprenaline, abronchodilator known to have apowerful stimulant effect on theheart and cardiovascular system.Taken with adenylic acid, the herbenhances the action of digoxin,prescribed for cardiac and coronaryinsufficiencies. When used as analcoholic extract (4:1 ratio), itinhibits the arterial contractionsinduced by phenylephrine (Brinker, op.

cit., pp 118).

St John’s wort (Hypericum perforatum)This herb has been in continuousrecorded use as a natural medicinesince the days before Hippocrates (ca.460–ca. 370 BC).

Although best known nowadays forits antidepressant effects, it’s alsoknown to promote wound-healing,

and can inhibit protein kinase C,which has the beneficial effect ofpreventing the usual diabetic vascularcomplications of nephropathy,retinopathy and neuropathy. Inaddition, St John’s wort has antiviralactivity, coronary vasodilatory effects,painkilling (analgesic) and liver-protective effects, and can helpagainst sleep disturbances by boostingmelatonin synthesis (McKenna, op. cit., pp

923–71).However, this herb should not be

used in pregnancy, prior to sunexposure or solarium therapy, orultraviolet light therapy, or in thosewith endogenous (genetic)depression—especially in those caseswith psychotic symptoms or highsuicidal risk.

St John’s wort can haveinteractions with nefazodone,sertraline, trazodone, fluoxetine,paroxetine, indinavir, warfarin,phenoprocoumon, reserpine, proteaseinhibitors, theophylline (requires a250-per-cent increase in the daily doseof St John’s wort to maintaineffectiveness), monoamine oxidaseinhibitors (MAOIs), midazolam andnaloxone, as well as with photo-sensitizers (causing light sensitivity)such as piroxicam and tetracycline.Prior to surgery, it may interactadversely with anaesthetics (so theanaesthetist should always beinformed when St John’s wort hasbeen taken) (Brinker, op. cit., pp 178–84).

For mild-to-moderate depression,therapeutic doses of the herb extractare 300–900 mg/day, and up to 1800mg/day for more severely depressedpatients. The extract should bestandardized at 0.3-per-centhypericin.

Harald Gaier

Harald Gaier is a registered naturopath,osteopath, homeopath and herbalist, andpractises at The Allergy and NutritionClinic, 22 Harley Street, London (e-mail:[email protected]).


Hair lossAs oestrogen levels fallduring the menopause,you may have increasinglyregular bad-hair days.Here’s how to keep yourlocks full and healthy.

Massage your scalp, using the technique below, for a few minutes every day,twice a day. You can also use this technique when you want to massageessential oils into your scalp (see box, page 30).1. Using your fingertips, make small circular movements all along your

hairline, beginning in the middle of the forehead, then working down thesides, around the ears and over to the back.

2. Using the tips of the thumbs and fingers of both hands, pinch your scalp allover your head—but be careful not to pull too hard at your hair as you dothis. Make the movements quick and fluid. Your scalp should tingle whenyou’ve finished.

3. Make your hands into claws and place your fingertips at your hairline onyour forehead (palms over your head). Use your fingertips to ‘comb’ yourwhole scalp from front to back.

4. Finally, beginning at the centre of your head, work outwards and around,using your fingertips to make small circular movements that gentlymanipulate the scalp. Use a firm pressure, and do this over the whole ofyour head.

Four-step scalp massage

Hair problems of every varietyare more common during themenopause, and can worsen

postmenopausally. Although thechange may be imperceptible toothers, when running your handsthrough your hair, you may find thatit feels thinner all over. Alternatively,your hair may look noticeablythinner at the front. Othermenopausal hair problems includedullness, dryness, split ends, poorhair growth and dandruff. You mayeven find that your body hair,including pubic hair, is thinner orcompletely gone, while some womenwill find unwanted hair growing onthe face.

Causes of hair changesAs you go through the menopause,levels of oestrogen in your body fall,such that your body ‘believes’ that ithas more male hormones (such asthe androgen testosterone) incirculation. What has happened isthat counter-balancing oestrogen isno longer present. As androgensdominate your system, you mayexperience masculine symptomssuch as male-pattern bald-ness, acneand increased facial hair (particularlyon the upper lip).

You may even be genetically pre-disposed to hair loss. In ‘androgenicalopecia’, a tendency towards hor-monal imbalance is inherited, andshows up particularly in later life.According to research, up to 13 percent of women have this sort of hairloss prior to the menopause. Afterthe menopause, the condition is evenmore common, with one studyshowing that as much as 75 per centof women over the age of 65 areaffected.

If you notice a lot of hair on yourpillow in the morning or your hair-dresser mentions that your hairseems thinner, you should see adoctor for a check-up. Although itmight simply be related to the

menopause, other medicalconditions can result in hair loss,including anaemia (low iron) andthyroid problems. Stress, too, cancause hair loss—at any age.

Conventional treatments If you’ve entered the menopause andyour hair is thinning, your doctor islikely to offer one of these options: u Hormone replacement therapy

(HRT). Most women find thethought of going bald terrifying.Some have told me that they’veconsidered taking HRT just to stophair loss in its tracks. However,although HRT raises your levels ofoestrogen, it doesn’t always solvethe hair-loss problem and,ironically, one of the listed side-effects of HRT itself is hair loss.Unfortunately, there’s no way topredict how your body will responduntil you try it.

u Minoxidil. First developed for highblood pressure, this vasodilatorcan also thicken the hair. It’staken as either a pill or as a lotionapplied directly to the hair andscalp. As with any drug, there are

side-effects, the most commonone of which is an itchy scalp.Other side-effects include acne,headache, very low blood pressure,irregular heartbeat, chest painand blurred vision. Mostimportant, however, is that thismedication does not address thecause of the problem, so as soon asyou stop using it, your hair losswill resume.

u Spironolactone. This syntheticcorticosteroid has mild diureticproperties, and acts by interferingwith the binding of malehormones in the hair follicles toprevent hair loss. However, it hasbeen linked with an increased riskof stomach bleeding, as well asrashes, irregular periods anddrowsiness.

Your diet I think of hair as a barometer ofoverall health (along with the skinand nails). If you consider a cat ordog, when such an animal is unwell,its glossy, sleek fur coat becomesdull, limp, lifeless and thin. Thisoffers a clue as to how you might beable to slow the deterioration of yourhair—namely, by looking after yourentire state of health by eating well, and making sure to have yourfull quota of essential vitamins andminerals.

As well as making the choice toeat healthy foods, make sure you eatregularly throughout the day, includingmid-morning and mid-afternoon


Women’s health

u Homeopathy. See a homeopath for a constitutional remedy or try thefollowing, taking a 30 C potency of the appropriate remedy, twice daily: v Nat Mur (Natrum Muriaticum) is the ideal remedy if your hair falls out whenit’s brushed, combed or even touched v Phos (Phosphorus) is suitable if you have bald spots and your hair comesout in clumps v Sepia is the one to use when your hair loss is accompanied by fatigue andchronic headaches.

u Acupuncture. In traditional Chinese medicine, hair loss (and prematuregreying) is linked to a deficiency in the kidney meridian. You may wish to seean acupuncturist to have the relevant meridians stimulated to promote hairgrowth.

u Aromatherapy. Massaging essential oils into your scalp can increase thecirculation to your head while reducing stress. Certain oils are beneficial tohair health. Rosemary essential oil is thought to stimulate hair follicles. Dilute3–6 drops in 3 tsp of a carrier oil such as jojoba or grapeseed, and massagethe blend into your scalp. Clove oil (at the same dilution), which containseugenol, is known to stimulate hair growth, and cedar of Lebanon oil canalso help. Do this two to three times per week, using the four-step technique(see box, page 29). If you can bear to, leave the diluted essential oil in yourhair overnight and wash it out in the morning. (Wear a shower cap to protectyour bed linen.)

Other natural treatmentssnacks, and don’t skip meals. Thiswill help to keep your blood-sugarlevels in balance and, in turn, controlyour hormone levels by helping toprevent an excess of the malehormone testosterone in yoursystem. u Protein. Your hair follicles need

good-quality protein in differentforms in order to grow, so stock upon pulses, nuts, seeds and fish. Inthe body, protein is broken downinto its constituent parts, which arecalled ‘amino acids’. The mostimportant of these for preventinghair loss are arginine, cysteine,lysine and tyrosine, all of which arefound in protein-rich foods.

u Essential fats. If you have dry hairthat breaks easily and lacks shine,you may lack the necessary levels ofessential fatty acids. Boost yourintake by eating plenty of oily fish(such as salmon, tuna and sardines),nuts and seeds.

u Biotin. Egg yolk, brown rice, lentils,oats, soybeans, sunflower seeds,walnuts and green peas are rich inbiotin. This important B vitaminhelps to metabolize essential fats,and is crucial for healthy hair, as well as for the overall health of yourskin and nails.

u Iron. Eat plenty of iron-rich foodssuch as dark-green vegetables, andstock up on vitamin-C-rich foods,too, which will help your body tobetter absorb iron.

Supplements u B-complex vitamins (containing 25

mg of each B vitamin) should betaken daily, and are essential for yournervous system so, if your hair loss isstress-related, supplementing withthis will help.

u Vitamin C with bioflavonoids (500mg twice daily as magnesium ascor-bate) will help in the manufacture ofcollagen, which holds hair tissuetogether, thus preventing splitting.Vitamin C also aids iron absorption.

u Vitamin E (600 IU daily) is thoughtto help reduce testosterone levels inwomen.

u Zinc (50 mg daily, as zinc citrate)helps the oil glands on hair folliclesto prevent shedding, whereas a zincdeficiency can weaken hair, causingit to break, while preventing it fromgrowing back at its normal rate.

Self-helpu Be gentle with your hair. Use a

soft brush and avoid blow-drying,curling or straightening your hairas much as possible. If you mustuse hair straighteners or curlingtongs, then make sure to use aheat-resistant hair protector spray,too, made from natural products(together with a natural shampooand conditioner). To preventbreakages, comb your haircarefully when wet, making sure totease out tangles rather thanpulling.

u Avoid stress. Stress can worsenhair loss, so endeavour to keepyour stress levels to a minimum.Find a relaxation routine that suitsyou, be it meditation, visualizationor a breathing exercise. Make sureyou spend at least part of eachday—even if it’s only 30 minutes—doing something you enjoy foryourself, such as reading a book orlistening to your favourite music.

Marilyn Glenville Adapted from The Natural HealthBible for Women by Marilyn Glenville,London: Duncan Baird Publishers,2010. Dr Glenville is a nutritionaltherapist, psychologist, author andbroadcaster specializing in femalehormone problems.

u Omega-3 fatty acids (1000 mg offish oil daily, containing 700 mg EPAand 500 mg DHA) should be takenfor three months (or take linseed/flaxseed oil if you’re a vegetarian).

Herbsu Horsetail (Equisetum arvense). The

outer skin of the stems of this herbcontains large amounts of silica, achemical compound that improvesthe formation of connective tissue inthe body and, so, improving thehealth of the hair (and skin andnails, too). Take 300 mg in capsuleform, twice daily.

u Siberian ginseng (Eleutherococcussenticosus). If stress is contributingto your hair loss, this will help tosupport your adrenal glands. Take 1 tsp of tincture in a little water, or250–300 mg in capsule form, twicedaily.

u Herbal hair rinse. Make your ownrosemary hair rinse by steeping 30 g(1 oz) of rosemary leaves and stemsin 570 mL (1 pint) of water for 20minutes. Wash and rinse your hair asyou would normally, then do a finalrinse using your rosemary ‘tea’. Dothis every time you wash your hair, asrosemary is believed to encouragehair growth from follicles. For extrashine, add a cup of nettle tea.


Saving faceResearch shows that youcan keep wrinkles at baywithout resorting to botoxor surgery

u Coenzyme Q10. Topical application of this antioxidant not only protectsagainst sun damage, but also appears to improve the appearance ofwrinkles. A clinical trial showed that the use of a 1-per-cent CoQ10 creamfor five months significantly reduced wrinkles, as rated by a dermatologist(Biofactors, 2008; 32: 237–43).

u Vitamin C. In one placebo-controlled trial, a topically applied creamcontaining 5-per-cent vitamin C led to a “clinically apparent improvement”of sun-damaged skin after six months. In particular, deep furrows and skinelasticity were improved (Exp Dermatol, 2003; 12: 237–44).

u Niacinamide. According to clinical testing, applying 5-per-centniacinamide (vitamin B3) in a moisturizer to the face can improve varioussigns of ageing, including hyperpigmentation, fine lines and wrinkles,redness/ blotchiness, yellowing (sallowness) and elasticity (Int J Cosmet Sci,

2004; 26: 231–8; Dermatol Surg, 2005; 31: 860–5). u Alpha-lipoic acid (ALA). In a trial of 33 women, aged 40–75 years, each

treated half her face with a cream containing 5-per-cent ALA, and the otherhalf of her face with a placebo cream, twice daily for 12 weeks.

The results showed significant improvement in the signs of photoageingon the ALA-treated side of the face. Specifically, laser profilometry—whichmeasures the surface of the skin with extreme accuracy—revealed anaverage decrease in skin roughness of 51 per cent compared with 41 percent on the placebo-treated side (Br J Dermatol, 2003; 149: 841–9).

Natural wrinkle fighters

Skin changes such as wrinkles andsagging are among the mostvisible signs of ageing. To an

extent, such changes are an inevitablepart of growing old—the result of‘intrinsic’ (internal) factors beyond our control that include genes andchanges in hormone levels over time.

However, research shows that thevast majority of skin ageing is due to‘extrinsic’ (external) factors, such assun exposure, smoking, poor nutrition,environmental pollution and stress.These are factors that we can dosomething about and, ultimately, ourunderstanding of them is the key tokeeping our skin young- and healthy-looking for longer.

Sun exposureAlthough sunlight is undoubtedly goodfor us, when it comes to our skin,overexposure to the sun is its number-one enemy. Ultraviolet (UV) radiationfrom the sun is by far the mostimportant factor in skin ageing,especially its premature ageing. In fact, ‘photoageing’, as it’s known, isestimated to account for up to 90 percent of all visible skin-ageing (Int J

Cosmet Sci, 2008; 30: 87–95). Both ultraviolet A (UVA) and B

(UVB) radiation are responsible, butUVA penetrates more deeply into theskin and, thus, is able to damage both the epidermis—the outermost layer,made up of skin cells, pigment andproteins—and the dermis—the nextlayer in, made up of collagen andelastin fibres (Acta Dermatovenerol Alp

Panonica Adriat, 2008; 17: 47–54). The tell-tale signs of photoageing

include wrinkles, sagging, dry or roughskin, age spots, spider veins and actinickeratoses—thickened wart-like, rough,reddish-brown to blackish patches ofskin (Coll Antropol, 2008; 32 Suppl 2: 177–80).Most at risk are those of us who live insunny climates, spend a lot of timeoutdoors and have fair skin (Arch

Dermatol, 2002; 138: 1462–70).The most obvious plan of action is

to protect the skin with a sunscreen.Indeed, UV filters are now found innumerous everyday cosmetic productssuch as makeup, moisturizers andhand creams. However, several sun-screen chemicals are linked to adverseeffects, such as hormone disruptionand allergic reactions (see WDDTY vol19 no 3).

A safer option is to use productsthat contain physical filters, such aszinc oxide and titanium dioxide, ratherthat chemical filters. These agents arecapable of reflecting both UVA andUVB rays and, as they don’t penetrateinto the skin, they are unlikely to havetoxic/allergic effects (Acta Dermatovenerol

Alp Panonica Adriat, 2008; 17: 47–54).Even better, look for products that

contain antioxidants such as vitaminsC and E, and coenzyme Q10, as thesenatural free-radical fighters play animportant role in protecting the skinagainst UV-induced damage (Curr Probl

Dermatol, 2001; 29: 157–64). One 16-weekstudy found that twice-daily applicationof a cream containing antioxidantsprovided protection against UVB-induced oxidative stress in theepidermis, a crucial factor in skinageing (Photodermatol Photoimmunol Photo-

med, 1999; 15: 115–9). Another revealedthat the topical application ofcoenzyme Q10 was effective againstUVA-induced oxidative stress in the


Women’s health

skin, concluding that “CoQ10 has theefficacy to prevent many of thedetrimental effects of photoaging”(Biofactors, 1999; 9: 371–8).

Antioxidants taken internally mayalso be beneficial. Taking supplements,or including plenty of antioxidant-rich foods in your diet, can bolster theskin’s natural defences againstsunlight (see below).

Other ways to protect yourselfagainst the sun include avoidingexposure between 11am and 3pm,when the sun’s rays are strongest, andwearing protective clothing, such as awide-brimmed hat and long sleeves,when you’re outdoors during the day.Also, be sure to avoid indoor tanningdevices, which are another source ofUV radiation.

Dietary factorsNutrition is one of the most importantfactors involved in skin health and itscondition. If the skin is not sufficientlynourished, it won’t be able to defenditself against external insults, such asthe sun’s rays, that contribute to thesigns of ageing (Dermatoendocrinol, 2009;

1: 271–4).Indeed, an international study

conducted in 2001 confirmed that thefoods we eat can have a significantimpact on the state of our skin (J Am

Coll Nutr, 2001; 20: 71–80). Researchers atMelbourne’s Monash University studied453 people living in Australia, Greeceand Sweden to determine whether ornot food and nutrient intakes wererelated to wrinkling of the skin in sun-exposed areas.

What they discovered was that ahigh intake of vegetables, legumes andolive oil appeared to be protectiveagainst developing wrinkles, while ahigh intake of meat, dairy and butterhad the opposite effect. In particular,full-fat milk (rather than skimmedmilk, cheese and yoghurt), red meat(especially processed meat), potatoes,soft drinks/cordials and cakes/pastrieswere all associated with extensive skin-wrinkling. Protective foods includedleafy green vegetables, broad beans,lima beans, nuts, olives, driedfruit/prunes, cherries, grapes, applesand tea.

According to the researchers, theseprotective foods may have contributedto less skin-wrinkling because of theirhigh contents of antioxidant vitamins

Of the countless creams on the market claiming to erase wrinkles and stopsagging, few have undergone rigorous scientific trials to prove theireffectiveness. One exception is No 7 Protect & Perfect Intense Beauty Serum,made by Boots, which was tested last year in a double-blind, randomizedcontrolled trial. After one year, the researchers found “significant clinicalimprovement in facial wrinkles”, which they believed was due to the increasedproduction of fibrillin-1 in the skin, a protein that promotes skin elasticity. Bearin mind, however, that the study was funded by Boots (Br J Dermatol, 2009; 161:

419–26).Nevertheless, for those who might be looking for a more natural solution

(the Boots serum contains a raft of harsh chemicals), your best bet is to lookfor products with high levels of antioxidants such as vitamin C and E, and co-enzyme Q10.

Weleda’s new Pomegranate Firming Face Serum, for example, containsantioxidant-rich pomegranate juice and, according to the website,dermatological tests have shown that, after 28 days of use, the depth ofwrinkles was reduced by 29 per cent while skin moisture levels increased by39 per cent (www.weleda.co.uk).

Hope in a jar?

and phytochemicals. Indeed, previousstudies found that certain antioxidantsand plant ingredients can protect theskin against UV radiation when takenas supplements, so high intakes ofthese nutrients would tend to lead toless wrinkling at sun-exposed sites. The antioxidant vitamins C and E, thecarotenoids beta-carotene and lyco-pene, and the proanthocyanidins, agroup of flavonoids found in grapeseeds and other plant sources, are justsome of the nutrients that appear tohave photoprotective effects (seeWDDTY vol 19 no 3).

The Monash researchers also notedthat sugar and sugar products cancontribute to poor skin health throughthe ‘glycosylation of proteins’—when asugar molecule attaches itself to aprotein molecule—in the skin. This, inturn, can contribute to skin-wrinklingand photoageing, and might explainwhy foods such as soft drinks andcakes/pastries are associated withmore wrinkling of the skin (J Am Coll

Nutr, 2001; 20: 71–80).A more recent study also reported

a link between diet and skin-ageing.Using data from the first NationalHealth and Nutrition ExaminationSurvey, UK researchers examined theassociations between nutrient intakesand ‘skin-ageing appearance’ in morethan 4000 American women aged40–74 years. They found that havinghigher dietary intakes of vitamin C(from orange juice, citrus fruits, fruit

juices and tomatoes) and linoleic acid(found in oils such as rapeseed andsoybean oils, and in foods such as greenleafy vegetables and nuts), and lowerintakes of fats and carbohydrates, wereassociated with better skin-ageingappearances.

In fact, higher vitamin C intakeswere associated with fewer wrinklesand less senile dryness (dry skin as aresult of ageing); higher linoleic-acidintakes were associated with less of alikelihood of senile dryness andthinning skin; and higher fat andcarbohydrate intakes were linked witha more wrinkled and thinning skin.These associations were independentof age, race, education, sunlightexposure, income, menopausal status,body mass index, supplement use,physical activity and energy intake (Am

J Clin Nutr, 2007; 86: 1225–31).In general, the evidence suggests

that including plenty of antioxidant-rich fruit and vegetables in your diet isone of the best things you can do tosave your skin.

Smoking and pollutionCigarette-smoking is another impor-tant causal factor in skin ageing; so, if you need yet another reason to quitthe habit, think of your skin. Smokingincreases the quantities of matrixmetalloproteinases (MMPs)—enzymesthat break down the collagen, elastinfibres and connective tissue in the skin(J Dermatol Sci, 2007; 48: 169–75). These


enzymes also cause oxidative stress,which impairs collagen production (J

Investig Dermatol Symp Proc, 2009; 14: 53–5).The result of this double whammy isskin that’s old before it’s time. Indeed,studies show that the longer youcontinue to smoke, the older you’lllook (Plast Reconstr Surg, 2009; 123:

1321–31).Fortunately, just stopping smoking

can have a rejuvenating effect on theskin. In a study of 64 women who tookpart in a nine-month stop-smokingprogramme, the results suggested thatkicking the habit can dramaticallyreduce the biological age of your skin.

The women’s skin was assessedbefore and after the programme interms of lines, pigmentation, elasticity,brightness and texture to establish its biological age. At the end of theprogramme, an average reduction ofabout 13 years in the biological age ofthe women’s skin was found whereas,at the beginning of the study, their skinhad an average biological age of nineyears older than their actual,chronological age (Skinmed, 2010; 8:

23–9). These results suggest thatstopping smoking is an important wayto prevent and even reverse the signs of

skin-ageing. Besides tobacco smoke, the air

pollution from road traffic and othersources can also have a negativeimpact on the skin.

A recent German study of 400elderly women found that air-pollutionexposure was significantly linked toextrinsic signs of skin ageing and, inparticular, pigment spots. An increasedexposure to soot and particles fromtraffic was associated with 20-per-centmore pigment spots on the foreheadand cheeks. Back-ground particlepollution that was not directlyattributable to traffic was alsopositively associated with pigmentspots on the face (J Invest Dermatol, 2010

Jul 22; Epub ahead of print).While it’s impossible to completely

avoid air pollution, increasingantioxidant intake can boost the skin’snatural defences. Also, keep tabs onthe air pollution in your area bycontacting your local air-qualitymonitoring service (in the UK: www.airquality.co.uk/index.php; in the US:www.epa.gov/oar/airpolldata.html).When pollution levels are high, avoidspending a lot of time outdoors ifpossible. For further advice on how to

minimize your exposure to airpollution, see WDDTY vol 18 no 5.

Other face-saving factorsClearly, wrinkles, sagging and the othersigns of skin ageing are not simply theinevitable consequence of getting old.The sun, tobacco smoke and outdoorair pollution can all have a negativeimpact on our skin, and what we eatcan determine how well our skinresponds to these insults.

In addition, severe physical andpsychological stress can both taketheir toll on the appearance of yourskin (Acta Dermatovenerol Alp Panonica

Adriat, 2008; 17: 47–54), so consider stressmanagement techniques such asmeditation and yoga as part of youranti-ageing regime.

Also, it may help to get into thehabit of sleeping on your back ratherthan on your side, as years of restingyour face on the pillow in the same wayevery night can lead to wrinkles knownas ‘sleep lines’ (Scand J Plast Reconstr Surg

Hand Surg, 2004; 38: 244–7).Finally, don’t forget to drink plenty

of water to keep your skin hydrated andsmooth-looking.

Joanna Evans

can be effective forsmaller varicose veins,but the risk of neovascularizationremains high. There are alsoconcerns over the development ofdeep vein thrombosis (DVT), visual

may simply develop elsewhere inthe legs (BMJ, 2006; 333: 287–92).Other possible complicationsinclude bleeding, bruising,infection, scarring and nervedamage. There is alsoevidence that suggests thatsurgery for varicose veinsmight even increase the riskof thrombosis (blood clots)(BMJ, 1996; 312: 1158).

Two newer treatments areradiofrequency ablation andlaser treatment, which useheat to seal off varicoseveins. These less invasivetechniques appear to be atleast as effective assurgery, but with fewerrisks (J Vasc Surg, 2009; 49: 230–9).

Nevertheless, we still don’t knowhow safe and effective these treat-ments are in the long term.

Yet another option is sclero-therapy, in which chemicals areinjected into varicose veins tocause their walls to collapse. This


Women’s health

Varicose veinsVaricose veins affect nearlya third of us and rarely goaway on their own so,thankfully, there’s a rangeof herbs and supplementsthat can help

The following self-care methods may help to prevent varicose veins or, atleast, stop them from getting worse.u Exercise regularly to aid your circulation. Walking or anything that gets

the legs moving is ideal.u Reduce leg strain by avoiding prolonged standing and excessive

heavy lifting.u Elevate the legs. To improve leg circulation, take a few short breaks

daily to raise your legs to above the level of your heart by, for example,lying down with your legs propped up on three or four pillows.

u Don’t cross your legs when sitting, as this can slow the upward flowof blood back to the heart and increase pressure on the leg veins.

u Try massage and other therapies that increase circulation.u Watch your weight, as overweight and obesity are known to contribute

to the development of varicose veins (Am Fam Physician, 2008; 78: 1289–94).u Avoid high heels. Low-heeled shoes work the calf muscles more,

which is better for venous blood flow. u Avoid wearing tight clothing around your waist, legs and groin, as this

can reduce blood flow.u Consider your diet. Hard stools and constipation can lead to varicose

veins as straining increases pressure in the abdomen that, in turn,increases pressure on the lower legs. So, it’s important to consumegood amounts of water-soluble fibre and liquids. Foods that areespecially helpful for varicose veins include berries, cherries, grapes,buckwheat and onions.

Tips for prevention

Varicose veins are veins thathave become twisted andswollen because blood isn’t

flowing through them properly.They can develop anywhere in thebody, but the veins in the legs arethe most commonly affected, asthey have to move blood alongagainst gravity. Increased bloodpressure and hormonal changesduring pregnancy can also triggerthe problem, which helps to explainthe higher incidence of varicoseveins in women than in men(Cochrane Database Syst Rev, 2007; 1:

CD001066).For many sufferers, varicose

veins are simply a cosmeticconcern. Others, however, mayexperience aching, throbbing,itching or burning sensations,which usually worsen with pro-longed standing.

Rarely, varicose veins can lead to more serious problems such asinfection, leg ulcers and thrombo-sis (Am Fam Physician, 2008; 78:

1289–94).

Treating varicose veinsConventional treatment of varicoseveins includes a range of options—from compression stockings tosurgery and laser treatments.Compression stockings, whichsteadily squeeze the legs toimprove blood flow, are usually thefirst course of action, but studiesconclude that they are no moreeffective than simply resting(Cochrane Database Syst Rev, 2007; 1:

CD001066). Surgery, on the other hand, can

effectively get rid of these unsightlyveins and help to relieve symptoms.However, varicose veins maygradually recur through a processof ‘neovascularization’—regrowthand enlargement of veins—evenafter successful surgery, or they


Also known as ‘telangiectasias’ or ‘sunburst varicosities’, so-called spiderveins are a smaller, milder form of varicose veins. Although they areharmless and generally cause no pain or discomfort, many people hatethe way they look.

Sclerotherapy is the usual treatment for spider veins but, as alreadymentioned (see main text), it’s been associated with serious side-effectssuch as stroke and deep vein thrombosis (DVT). More commonly,sclerotherapy causes hyperpigmentation, or darkening of the skin, alongthe course of the treated vein. This side-effect is reported in up to 30 percent of patients treated for spider/varicose veins. In most cases, itdisappears within 6–24 months but, for some, the discoloration maypersist for five or more years (J Dermatol Surg Oncol, 1987; 13: 547–50).

Fortunately, the natural remedies and preventative tips for varicoseveins can benefit spider veins, too. In addition, vitamin K cream is claimedto be an effective natural treatment. Topical vitamin K was able to reducelaser-induced bruising and purpura (red/purple discolorations due tobleeding under the skin) (J Am Acad Dermatol, 2002; 47: 241–4; Dermatol Surg,

1999; 25: 942–4). However, WDDTY could find no published studies showingthat vitamin K can reduce or eliminate spider veins themselves.

Nevertheless, an unpublished study reported in WDDTY’s sisterpublication PROOF! (vol 4 no 3) tested the efficacy of a 5-per-centpharmaceutical-grade vitamin K product (Dermal-K) on 50 women. Amongthese women after six months, three saw significant reduction or completehealing of their spider veins within 8–14 days, 17 saw significant reductionor complete healing in 15–30 days, 26 achieved significant reductionwithin 31–46 days, two had a significant reduction within 47–120 days andtwo showed no effects at all. There was no improvement in 50 women whoused an aloe vera skin cream as a comparison.

So, vitamin K cream may be worth a try, but proceed with caution as thelong-term safety of this treatment remains unknown.

Another option is to mask spider veins with makeup. Indeed, there arelong-lasting (and some waterproof) body makeups specially formulated tocamouflage spider veins and other skin blemishes. In the UK, the BritishRed Cross runs a free treatment service at centres across the country,used by patients with birthmarks, burns, scars and spider veins (seewww.redcross.org.uk).

Spider veinsdisturbances and stroke (Am Fam

Physician, 2008; 78: 1289–94; J Neurol

Neurosurg Psychiatry, 2010; 81: 582–3). Happily, there are a number of

natural ways to treat varicose veins.

Natural remediesu Supplements. Among the most

useful supplements are thosethat contain flavonoids, some ofwhich have anti-inflammatoryeffects and can help tostrengthen the blood vessels.v Hydroxyethylrutoside (HR), atype of flavonoid derived fromrutin (found in buckwheat andasparagus), improved varicoseveins in a controlled trial ofpregnant women (Zentralbl Gynakol,

1995; 117: 190–7). Typically, the HRdose is 1000 mg/day, but itsefficacy may be increased bycombining the supplement withtopical HR gel, applied two tothree times a day (Angiology, 2008;

59 Suppl 1: 7S–13S).v Proanthocyanidins, flavonoidsfound naturally in apples, pinebark, grapeseed, bilberry andsome red wines, have also beensuccessfully used to treatvaricose veins. A single dose ofproanthocyanidins (150 mg)improved leg-vein function inpeople with widespread varicoseveins (Sem Hop, 1981; 57: 2009–13).v Daflon, a combination of theflavonoids diosmin and hesperi-din, has been shown to beeffective for chronic venousinsufficiency (CVI; pooling ofblood in the legs), a conditioncommonly associated withvaricose veins. According to onereview, its comprehensive modeof action on the veins, lymphaticvessels and microcirculationmakes it the treatment of choicenot only for the early stages ofCVI, but also for the more severestages, too (Angiology, 2001; 52 Suppl

1: S49–56).v Pycnogenol (maritime pine-bark extract) may be even moreeffective than Daflon, accordingto one study. Italian researchersfound that, after eight weeks,CVI patients taking 150 or 300mg/day of Pycnogenol improvedmore than those taking 1000mg/day of Daflon (Clin Appl Thromb

Hemost, 2006; 12: 205–12).u Herbs. Plant remedies are a

popular treatment for varicoseveins, and the following appearto be especially useful.v Horse chestnut (Aesculushippocastanum). Extracts fromthe seeds of this plant (HCSE)have traditionally been used totreat patients with CVI and toalleviate its associated symp-toms. Four clinical trials inpatients with CVI and one studyin patients with varicose veinsshowed that HCSE—taken eitheras an oral tincture or tablets (20mg or 50 mg), or applied as atopical gel—can reduce leg painand swelling as well as heavinessand itching (Adv Ther, 2006; 23:

179–90). For best results, take itas early in the condition aspossible (BMC Cardiovasc Disord,

2001; 1: 5; doi: 10.1186/1471-2261-1-5).v Gotu kola (Centella asiatica).This appears to have a beneficialeffect on the connective tissuesin varicose veins (Int J Clin

Pharmacol Res, 1990; 10: 229–33). In arandomized placebo-controlledtrial—the ‘gold standard’ ofscientific evaluation—a titratedextract of gotu kola (60 or 120mg/day) was effective forreducing leg swelling and legheaviness in patients with CVI(Angiology, 1987; 38: 46–50).v Butcher’s broom (Ruscusaculeatus). Taken orally, thisherb can improve venous tone


Women’s health

and poor circulation (Fortschr Med,

1989; 107: 52, 55–8). In a placebo-controlled trial of 148 womenwith CVI, those taking butcher’sbroom extract saw significantimprovements in leg swelling aswell as in heaviness, tension andtingling (Arzneimittelforschung, 2002; 52:

243–50). Dosage for capsulesstandardized for ruscogenins is7–11 mg, although some expertsrecommend higher dosages of16.5–33 mg of total ruscogeninsthree times a day (Altern Med Rev,

2001; 6: 608–12).v Witch hazel (Hamamelisvirginiana). This herb is famous forits astringent and anti-inflammatory properties (Altern Med

Rev, 2001; 6: 608–12), and, in the formof an ointment, it is recommendedby the German Commission E forvaricose veins.

Note, however, that theointment may need to be appliedthree or more times a day forseveral weeks before there is anynoticeable improvement.v Red vine leaf (Folia vitisviniferae) extract. A source offlavonoids, this herb was able toreduce calf swelling in patientswith CVI (Arzneimittelforschung, 2000;

50: 109–17). Another studyconcluded that red vine leaf extractshows “a fast onset of action and anexcellent efficacy” in the treatmentof CVI (Praxis [Bern 1994], 2006; 95:

187–90). The usual dose is 360–720mg/day.

u Hydrotherapy. The use of water totreat illness appears to work forvaricose veins. In a study of 61patients, three and a half weeks ofhydrotherapy reduced leg swellingand other symptoms of varicose

veins (Vasa, 1991; 20: 147–52). Inanother study, thermalhydromassage therapy was alsoeffective for patients with CVI(Minerva Cardioangiol, 2008; 56: 401–8).

u Reflexology. This form of footmassage reduced symptoms in astudy of 55 women with varicoseveins and leg swelling (Cochrane

Database Syst Rev, 2007; 1: CD001066).u Homeopathy. According to WDDTY

columnist Dr Harald Gaier, thereare several effective homeopathicremedies for varicose veins,including H. virginiana (witchhazel), Aristolochia clematis,Paeonia officinalis, Viburnum opulusand Ruta graveolens.

For best results, see a qualifiedhomeopath, who can prescribe aremedy based on your individualsymptoms.

Joanna Evans


Medicine and the elderly: Age shall not weary them—but drugs mightFor the elderly, the cure isvery likely worse than thedisease

Poets may exhort us not to growold, but they could have addedthe rider that, when we do, stay

away from the doctor for as long aspossible. Growing evidence suggeststhat aggressive interventions by doctorsare accelerating the decline in thegeneral health and mental capacities ofthe elderly, and may even be a directcontributor to their death.

The over-65s take one-third of allpharmaceuticals that are prescribed bydoctors every year, despite the fact thatthey represent just 13 per cent of thetotal population. On average, an elderlyperson is taking around six drugs at anygiven time (Johnston CB. UCSF Division of

Geriatrics Primary Care Lecture Series May 2001.

Geriatric Assessment in a Time Dependent

Practice: Practical Approaches for Primary Care

Practitioners).Polypharmacy—when more than one

drug is prescribed at a time—is an evenbigger problem in hospitals and carehomes, where the average patient isgiven at least seven different drugsevery day. In addition, powerfuldementia drugs are being prescribedfor most patients as a ‘chemical cosh’to keep them quiet, evidently mainly forthe convenience of the medical staff. Anofficial UK government review hasrevealed that the drugs are beinginappropriately prescribed in around 80 per cent of cases. In the UK alone,this works out to around 150,000people who are being given anti-psychotic drugs just to keep thempacified. Worse, the drugs are directlyresponsible for about 1800 deaths everyyear (http://news.bbc.co.uk/2/hi/8356423.stm).

This may perhaps explain why 11 percent of elderly patients, admitted tohospital for other medical conditions,will suffer a heart attack while they arethere. In addition, they are also twice as likely as a younger patient to die

within 30 days from such an attack.Researchers made the discovery whenthey examined the health records of7054 patients who were admitted tohospital as part of the US Veterans’Health Administration between 2003and 2004. Of those patients, 792—or11.2 per cent—suffered a heart attackwhile under hospital care (Arch Intern Med,

2006; 166: 1410–6).

Tick-box medicineMost patients are over 65 and, yet, theyrarely see a doctor who specializes ingeriatric medicine. This might bebecause, in almost every country exceptthe UK, there is a serious shortage ofgeriatricians. In Canada, for example,there are fewer than 200 qualifiedgeriatricians serving the entire country.In an attempt to attract more medicalgraduates into geriatric medicine, DrLaura Diachum, at the University ofWestern Ontario, has gone as far as todescribe the speciality as “totally sexy”(J Am Geriatr Soc, 2006; 54: 1453–62).

As a result of the lack of geriatricspecialists, an elderly patient isinvariably seen by a general practi-tioner, whose almost instinctivetendency will be to start reaching forthe prescription pad. Sadly, as discover-

ed by a doctoral thesis defended bySandra Pennbrant, at the SahlgrenskaAcademy in Sweden, elderly patientstend to become passive when faced bythe doctor and feel intimidated by thepractitioner’s power and, so, fail toparticipate in the consultation byalmost never challenging the decisionto start taking a drug or even askingany questions (http://gupea.ub.gu.se/dspace/

handle/2077/21198).Doctors routinely hand out

prescription drugs simply because thepatient is old, not because he or sheneeds them, says Michael Oliver, anemeritus professor of cardiology atEdinburgh University. This ‘tick-boxmedicine’, as he calls it, means thatelderly people are not only taking drugs they don’t need, but they are alsobeing exposed to side-effects that canseriously endanger their health.“Nowadays, few elderly people areallowed to enjoy being healthy,” he says(BMJ, 2009; 338: b873).

One example of this so-called tick-box medicine is bringing down levels of blood cholesterol, especially in theelderly. But this is, in fact, a failure tounderstand the changing metabolismof older patients, who appear to needhigher levels of cholesterol for their

Dangerous drugs


Dangerous drugs

Aside from avoiding drugs and medicine, there are three keys to a healthy lifeinto old age: diet; exercise; and an active social life.u Diet. Vitamin E—found in nuts, seeds, and corn and olive oil—is arguably

the single most important nutrient in determining whether or not we will livea long and healthy life. In a study of 698 men and women, aged over 65 andliving in Tuscany, Italy, those who had low levels of the vitamin in theircirculation suffered a decline in their physical capacity over a three-yearperiod compared with those who had higher levels of the vitamin. This wasalso the only vitamin that had a direct impact on the physical wellbeing ofthe study participants. Their levels of folate, vitamin D, iron and B vitaminsapparently made no difference to the physical decline. The researchersbelieve that vitamin E, which is an antioxidant, prevents damage to DNA,muscles and neurons (JAMA, 2008; 299: 308–15).

The Mediterranean diet, primarily consisting of fresh fruit, vegetables andolive oil, has been proven in countless studies to help maintain health intoolder age. One study, involving 1393 participants, discovered that the dietprotects against cognitive decline as we age. Those who stayed close to thediet nearly halved their chances of developing mild cognitive impairmentcompared with those who ate low amounts of fruits and vegetables (Arch

Neurol, 2009; 65: 216–25).u Exercise. Even moderate exercise, such as a brisk walk every day, can help

to keep you healthy into older age, and even elderly patients who alreadyhave conditions such as heart disease and arthritis can see improvement. Inheart patients aged 50 years and over, moderate exercise that leaves you alittle out of breath increased life expectancy by 3.7 years in men and 3.5years in women (Arch Intern Med, 2005; 165: 2355–60). Older people withosteoarthritis of the knee also noticed improvements in their knee pain andmobility after 18 months of brisk walking for 40 minutes, three times a week(JAMA, 1997; 277: 25–31). Overall, older people who take regular exercise havestronger hearts, better circulation, stronger bones, better balance, less pain,better sleep quality, sharper minds and a lower risk of developing mostcancers (Am Fam Physician, 2002; 65: 419–26).

u Social networks. An active social life, including volunteer work, attendingsports and social events, and visiting friends and relatives, is as important asexercise for helping older people to maintain good health. In a US study of906 retired people, it was found that physical decline was up to a third morerapid in those who were socially inactive, even when they took regularexercise (Arch Intern Med, 2009; 169: 1139–46). Curiosity and maintaining aninterest in the world also play important roles in determining how long—andhow well—we live. One study of 1118 men, with an average age of 70 years,found that having this attitude in life was the single most important factor indetermining longevity.

In ancillary analyses in 1035 older women (mean age: 69 years), curiosityappeared to be equally important in women as well (Psychol Aging, 1996; 11:

449–53).

Living a long and healthy lifegeneral wellbeing and, especially, tosupport mental acuity. One study thatinvolved 3572 men, aged 71–93 years,discovered that those who had thelowest cholesterol levels—from 2.09 to4.32 mmol/L (80.0 to 167.0 mg/dL)—were up to 40 per cent more likely todie than those whose cholesterol levelswere higher. Indeed, this study, whichmonitored the health of the partici-pants for 20 years, questioned whetherthere was any “scientific justificationfor lowering cholesterol to very lowconcentrations (below 4.65 mmol/L[179.8 mg/dL]) in elderly people”(Lancet, 2001; 358: 351–5).

Not only may higher cholesterollevels be health-giving in the elderly,but the cholesterol-lowering drugsthemselves may also be doing moreharm than good, according to a studyfrom the Yale University School ofMedicine. There, the researchers foundthat, while there was a marginal benefitfrom the drugs in reducing heartfatalities, they also found that thepatients were dying of other causes as a result of taking the drugs (JAMA, 1994;

272: 1335–40). Worse, most general practitioners

are unaware of the dangers of the drugs they are prescribing to theirelderly patients, despite the frequentdrug alerts and warnings they are sentby drug-monitoring agencies.

In fact, researchers have discoveredthat around one in five elderly patientsis being given drugs that are dangerous,and could be the cause of debilitatingside-effects. In a study of 760,000elderly people taking a prescriptiondrug, it was revealed that 21 per centwere taking one or more drugs thatwere on the Beers list, a compilation ofall the prescription drugs that geriatricpatients, in particular, should avoid(Arch Intern Med, 2004; 164: 1621–5).

In another study, researchers foundthat 20 drugs had been identified asbeing too dangerous for use by theelderly and, yet, most of these patients(79.6 per cent) were being prescribedone of these drugs and 20.4 per centwere taking two or more, including thebeta-blocker propranolol, the anti-hypertensive agents methyldopa andreserpine, the painkiller dextropropoxy-phene and the anticoagulant dipyrid-amole (JAMA, 1994; 272: 292–6).

Many elderly people regularly take acommon NSAID (non-steroidal anti-

inflammatory drug) such as aspirin andibuprofen to help ease their aches andpains. Yet, according to a survey of 4099people aged 70 years and over, thesedrugs increase the risk of kidneydysfunction. Those who took an NSAIDat least once a day had the highestlevels of blood urea nitrogen and serumcreatinine, both of which are markers ofkidney problems (J Am Geriatr Soc, 1999; 47:

507–11).

Prescribed drugs may also beresponsible for dry eyes and dry mouth,assumed to be a natural consequence of growing old. However, common pain-killers such as aspirin could be respon-sible, according to a study of 2481patients aged 65–84 years. Antidepress-ants and antipsychotics may also be thecause of similar side-effects (Arch Intern

Med, 1999; 159: 1359–63).What’s more, doctors are more than


Mental decline isn’t an unavoidable consequence of ageing. There’s lots wecan do to stay sharp right up to the end.

People who exercise at least once a week, don’t smoke and maintain anactive social life are more likely to retain their cognitive abilities throughouttheir 70s and 80s, according to a study of 2500 participants aged 70–79.However, an eight-year follow-up showed major cognitive decline in 16 percent of this population, whereas 53 per cent displayed normal, age-relateddecline. Yet, the research team saw a unique profile of activity and socialengagement that appeared to have protective effects in around 30 per centof participants who displayed no cognitive decline whatsoever. A goodeducation, not smoking and a good level of literacy were found to beimportant factors, and those who carried out volunteer work and were notliving on their own also appeared to be less likely to suffer from cognitivedecline (Neurology, 2009; 72: 2029–35).

Maintaining an interest in intellectual pursuits, such as reading and doingcrossword puzzles, can also help to ward off dementia—and the more youdo, the better. The study participants who engaged in 11 intellectualactivities a week, such as reading every day and doing the crosswords fourtimes a week, delayed the onset of dementia by 1.29 years compared withthose who read or did the crosswords

Staying sharpready to prescribe ‘off-label’—handingout drugs for health problems for whichthey have been neither tested norlicensed to treat. The problem hasbecome so prevalent, and dangerous,that America’s drugs watchdog, theFood and Drug Administration (FDA),has warned doctors to stop usingatypical antipsychotic drugs to treatgeneral behavioural problems in elderlypatients. Indeed, agents such as olanza-pine, aripiprazole, risperidone andquetiapine are so dangerous that theydouble the risk of death—and they aresupposed to be prescribed only to thosewith schizophrenia (www.fda.gov/cder/drug/

advisory/antipsychotics.htm).

The four giantsIn 1965, when geriatric medicine wasstill in its infancy, Bernard Isaacs, aprofessor of geriatric medicine atBirmingham University in the UK, saidthe elderly were faced with four ‘giants’that would determine their health:immobility; instability; incontinence;and impaired intellect (Isaacs B. An

Introduction to Geriatrics. London: Ballière, Tindall

and Cassell, 1965). Every health concernin the elderly could be traced back toone of those four conditions, he said.However, neither Isaacs nor the otherpioneers of geriatric medicine couldhave foreseen that, in many olderpatients, these ‘giants’ would be causedby the very medicines that weresupposed to help them, and not by theageing process itself.u Immobility and instability. Around

30 per cent of all over-65s fall eachyear, and this proportion rises to halfof all those in hospital or in nursingcare, where multiple drugs are anessential part of their daily regimen.Also, 25 per cent of these patientsdie within six months of falling.While there may be a number ofreasons why an elderly person falls,prescription drugs are among thebiggest causes, responsible foraround 18 per cent of all cases(Johnston CB. UCSF Division of Geriatrics

Primary Care Lecture Series May 2001.

Geriatric Assessment in a Time Dependent

Practice: Practical Approaches for Primary

Care Practitioners).Tranquillizers and sedatives, such

as benzodiazepine, can increase therisk of a fall in an elderly patient bynearly threefold. Flurazepam andtriazolam (both of which are benzo-

diazepines) are the most dangerous,according to Canadian researchers,and the elderly patient was mostlikely to suffer a fall within the firsttwo weeks of starting such drugtherapy (Age Ageing, 1996; 25: 273–8).

In a separate small US study ayear later, the geriatric researchersin Durham, NC, found that benzo-diazepines acted directly on thecentral nervous system, and affectneuromuscular processing andbalance control, thereby causingfalls, disorientation and slowerresponses in the elderly (J Am Geriatr

Soc, 1997; 45: 435–40).Powerful antidepressants of the

class known as ‘SSRIs’ (selectiveserotonin-reuptake inhibitors) aswell as the older tricyclic drugs, canalso significantly increase the risk offalls in the elderly (N Engl J Med, 1998;

339: 875–82). As a consequence,elderly people taking an SSRI are 2.4times more likely to suffer hipfractures compared with those nottaking these drugs, researchers fromthe University of Toronto, Ontario,have found. However, the earliertypes of antidepressant are not muchsafer for elderly patients. In thisstudy, which involved 8239 patients,aged 66 years and over, who hadbeen treated in hospital for hipfractures, it was found that thosetaking a tricyclic antidepressantsuch as desipramine or nortriptyline

were 2.2 times more likely to sufferfrom hip fractures as a result of falls(Lancet, 1998; 351: 1303–7).

Insulin can also cause falls, and isamong the three drugs that are alsomost likely to cause an adversereaction in the elderly; the other twoare warfarin, a blood thinner, anddigoxin, a heart drug. The threedrugs alone accounted for 59,108 ofthe 177,504 cases of adverse drugreactions reported by US emergencyservices in 2004–2005. Insulin cancause sudden hypoglycaemia (lowblood sugar), which may result in aseizures or unconsciousness (Ann

Intern Med, 2007; 147: 755–65).In fact, most prescription and

over-the-counter drugs appear toincrease the risk of falling. In a meta-analysis of studies published from1996 to 2007, involving more than79,000 participants, aged over 60,who were taking some sort ofpharmaceutical, it was found thatmany drugs “significantly” raisedthe risk of falls. The biggest culpritsincluded sedatives, SSRIs, antihyper-tensives, diuretics, beta-blockers,and even NSAID painkillers such asaspirin and ibuprofen.

“Elderly people may be moresensitive to drugs’ effects and lesseffective at metabolizing medica-tions, leading to adverse eventswhich, in turn, lead to falls,” saidresearcher Carlo Marra, at the


Dangerous drugs

University of British Columbia inVancouver, Canada (Arch Intern Med,

2009; 169: 1952–60).u Incontinence. This is often viewed as

an unfortunate consequence ofageing, but this is not so. The USAgency for Health Care Policy andResearch reports that eight out of 10cases of incontinence can b eitherresolved or greatly improved bymedical interventions (Agency for

Health Care Policy and Research. Overview:

Urinary Incontinence in Adults, Clinical

Practice Guideline Update. Rockville, MD.

March 1996; www.ahrq.gov/clinic/uiovervw.

htm). The one exception is age-related prostate enlargement, whichcan cause urinary incontinence.

In fact, incontinence can arise for many reasons and in people of all ages, although one in 10 of thoseaged over 65, and three in 10 agedover 80, have some loss of bladdercontrol, and half of all elderlypatients in nursing homes haveincontinence. Many prescriptiondrugs cause temporary incontin-ence and, as the elderly take one-third of all drugs prescribed, it’s notunreasonable to conclude that theyare a primary cause of the condi-tion in the over-65s. Anticholinergicagents, which block the passage ofneural impulses, include drugs suchas antihistamines, antidepressants,opiates, antispasmodics and Parkin-son’s drugs, and can all lead toincontinence (Cochrane Database Syst

Rev, 2006; 4: CD003781), as can heartdrugs such as the calcium-channelblockers.

Diuretics, or ‘water pills’, increasethe body’s loss of fluid by promotingthe production of urine and, as aresult, can frequently cause acuteincontinence. They are among themost regularly prescribed drugsamong the elderly—and oftenunnecessarily so, as one study hasidentified (BMJ, 1994; 308: 511–3).

Alpha-adrenergic blockers, whichinclude drugs for hypertension (high

blood pressure) such as doxazosin(Cardura), prazosin (Minipress) andterazosin (Hytrin), can also causeincontinence (Drug Saf, 1994; 11: 12–20),as can the angiotensin-convertingenzyme (ACE) inhibitors such asbenazepril (Merck Manuals; www.merck.

com/mmhe/sec11/ch147/ch147a.html).u Impaired intellect. Around 22 per

cent of those aged 71 years and overhave some degree of cognitiveimpairment, which is often seen as a forerunner of dementia andAlzheimer’s disease (Ann Intern Med,

2008; 148: 427–34). However, research-ers at the Mayo Clinic reckon thatthis figure could be lower, with only12 per cent of individuals agedbetween 70 and 89 years displayingsuch symptoms, according to a studyfunded by the National Institute onAging (www.mayoclinic.org/news2006-rst/

3306.html). The Mayo researchers define

cognitive impairment as havingproblems with remembering words,or placing things in time and space,or finding it more difficult to makedecisions, or suffering from short-term memory loss. The problemdoubles in those aged between 80and 89, and it also appears to affectmore people who have received onlybasic levels of education.

However, although ageing is agenuine factor in cognitive decline,pharmaceuticals also play a role inaccelerating the problem. Scientistsfrom the University of Florida havedemonstrated that any drug that has anticholinergic (nerve-blocking)qualities can speed cognitive declinein the elderly patient. Although thisincludes drugs known to haveanticholinergic actions, such asthose used to treat an overactivebladder, many other drugs havesimilar effects, but have not beenlisted as such in the literature(Presentation at the American Academy of

Neurology 60th Annual Meeting, Chicago, IL,

Abstract S51.001, 17 April 2008).

Indeed, it appears that almostevery commonly prescribed or over-the-counter drug can producesymptoms that resemble dementiain the elderly. A pair of researchersfrom the Medical University of SouthCarolina have reported that manydrugs cause side-effects that includeconfusion and memory loss, twosigns of cognitive impairment. Inaddition, the problem can bemagnified when the patient is takingmore than one drug at the sametime (J R Soc Med, 2000; 93: 457–62).

PolypharmacyIt’s evident that the dangers to theelderly of taking any one drug are badenough, but it’s almost impossible tomeasure the negative impact of takingmany drugs at the same time, as mostelderly patients are doing.

Even young Hollywood celebrities,such as Heath Ledger and BrittanyMurphy, may have died as a result oftaking several pharmaceuticals at thesame time. As Dr Bruce Goldberger, aprofessor of toxicology at the Universityof Florida’s College of Medicine, said ofthe latter’s death, “Mixing a number ofthese drugs could have resulted in herdeath”.

Every drug is tested for its safety andefficacy on its own, but no one is testingthe lethal cocktails that can result fromtaking several powerful chemicalcompounds in combination.

Nevertheless, what is clear, aspharmacologists at the University ofWales College of Medicine, Cardiff, havepointed out, is that drugs—andespecially polypharmacy—may beresponsible for many of the commonhealth problems seen among theelderly, such as confusion, weakness,incontinence, depression and falls, all of which have been blamed on growingold (Drugs Aging, 1998; 12: 485–94).

Without drugs and medicine,perhaps getting older wouldn’t be suchan unhealthy rite of passage.

Bryan Hubbard


The damaged brain: How drugs cause dementiaNew evidence shows thatall forms of dementia maylargely be caused by mostof the drugs we take as weget older

We may be living longer andbetter than ever but, by thetime we reach our golden

years, the chances of us having anyawareness of it are rapidly fading.Dementia of all varieties, includingAlzheimer’s disease, is now epidemic,approaching an incidence similar tothat of the major killers: for instance,seven million Americans aged over 65are currently diagnosed with dementiacompared with 10 million of all ageswith cancer.

Furthermore, the incidence rates ofdementia are sharply on the increase.Predictions suggest that the disorderwill increase fourfold among the elderlywithin the next 40 years, and escalateacross all age groups.

Nevertheless, the raw statistics failto reveal the most insidious aspect of the disease—namely, that thechances that any one of us will sufferfrom dementia sharply increases withevery decade. According to one team ofresearchers, who tracked the incidenceof the disorder over time, after the ageof 60, your risk of developing dementiadoubles every five years. This meansthat, by the time you reach your mid-80s, you face a one-in-four risk ofhaving dementia and, by the time youreach 90, the odds increase to onechance in three (Alzheimer Dis Assoc Dis,

2003; 17: 63–7). One reason for the prevalence is

simply due to the ambiguous nature ofthe term. Virtually every form ofcognitive decline is now classified asdementia, including memory loss, andimpairment in planning, judgment,reasoning and ordinary thoughtprocesses.

However, modern medicine musttake the greatest blame for the mentaldecline seen among the elderly. Eventhough they represent only one-

seventh of the population, the over-65stake one-third of all prescriptiondrugs—and usually a cocktail of them.The average senior is taking six drugsat a time, many of which affect thebrain.

Evidence is emerging that a largecoterie of drugs given for otherconditions, such as high cholesterol,depression, inflammation, insomnia,anxiety, heart disease and arthritis—inshort, most of the drugs given to us aswe grow older—can all bring ondementia.

Many of these drugs cause actualdamage to the structure of the brain,including shrinking brain volume anddestroying the crucial fatty structuresof brain cells, thus leading to theabnormal accumulation of tissue invital brain structures.

Given the fact that some 90 per centof Americans from their mid-50sonwards are taking at least one drugregularly and nearly one-third aretaking five or more drugs, it may wellbe—as American psychiatrist Grace E.Jackson claims in her brilliant anddamning self-published study—thatdementia is, in many cases, a drug-induced disease (Jackson GE. Drug-Induced

Dementia. AuthorHouse, 2009). Of the 36million Americans who now takestatins, for instance, an estimated162,000 people could be severelycognitively impaired because of thesedrugs in the US alone.

The chicken or egg dilemmaAlthough used as an all-purpose catchphrase, dementia could be defined asany condition in which there is anobservable abnormality involvingneurons or glial cells. On the basis ofsuch a description, it could be said thatthere are four types of true dementia:u Lewy body dementia, in which

patients have movement disordersmuch like those seen in Parkinson’sdisease, with abnormal deposits of‘Lewy body’ proteins, named afterthe German neurologist who firstobserved them, throughout theneurons of the brain;

u vascular dementia, where thebrain’s blood supply has become cutoff or interrupted, usually as a resultof large or small strokes, causing thedeath of neurons;

u frontotemporal dementia, usuallydiagnosed in patients aged under65, where the frontal or temporallobes (including the hippocampus)of the brain shrink; and

u Alzheimer’s disease.According to Jackson, Alzheimer’svictims all share three specificabnormalities:u senile plaques, abnormal clumps of

amyloid and other sorts of proteinsthat form outside of cells in the graymatter of the brain;

u neurofibrillary tangles, abnormal,twisted bundles of fibres withinbrain neurons mostly made up oftau proteins that impair theformation of tubulin, a proteinnecessary for healthy connectivenerve tissue, the result of which is that messages in the brain aren’ttransmitted properly; and

u granulovacuolar degeneration(GVD), where neurons in the brainhave abnormal ‘holes’ (vacuoles),each of which contains a small,dense protein.

The problem is that researchers cannotagree on whether these characteristicfindings are the cause or the effect ofan abnormal process in the body. The


Dangerous drugs

Although medicine used to believe that the master conductor of brainactivity was the neurons, or nerve cells, that create and releaseneurotransmitters and electrical signals, this view has been revised by amore holistic view of the brain. This concept appreciates that the brainworks in its entirety through a web of activity between neurons and fourvarieties of glial cells. Glial cells, which surround the neurons, keep themin place, provide them with nutrients, and destroy and mop uppathogens. They also insulate one neuron from another and modulatethe transmission of signals. One major function of glial cells is to formmyelin—the insulating sheath that covers every tentacle of a nerve cell—which is largely made up of lipid (fatty) tissue.

Yeon-Kyun Shin, a professor of biophysics at Iowa State University,recently went on record to say that high cholesterol is vital for goodbrain function, and a lack of cholesterol impairs the brain’s thinkingability and memory.

“If you deprive the brain of cholesterol, then you directly affect themachinery that triggers the release of neurotransmitters.Neurotransmitters affect the data-processing and memory functions; inother words, how smart you are and how well you remember things,” hesaid (Proc Natl Acad Sci USA, 2009; 106: 5141–6).

Why the brain needs fats

evidence from studies of the effects ofaluminium and mercury on the brainsuggest that they are the result oftoxicity rather than being a true causeof dementia. In test-tube studies usinghuman brain cells, for instance, minutedoses of mercury produced changesidentical to those seen in Alzheimer’sdisease (J Neurochem, 2000; 74: 231–6).

In other, animal studies, professor ofmedical biochemistry Boyd Haley andcolleagues at the University ofKentucky fed rats aluminium, butobserved no changes in tubulin levels,whereas mercury-fed rats displayeddiminished tubulin levels similar tothose seen in typical Alzheimer’spatients. Furthermore, someresearchers suggest that the vacuolesseen in GVD are filled with toxicmaterials, such as aluminium, whichthe neuron has ‘fenced in’ to keep therest of the brain safe (Am J Pathol, 1999;

155: 1163–72).Research at the University of

Pittsburgh has discovered that a fat-binding agent known as ‘apolipo-protein D’ (or apoD in medico-speak) ispresent in the brain plaques seen inpatients with Alzheimer’s disease.

However, apoD is also found in otherkinds of pathology, and many animaland human studies have shown thatantipsychotic drugs induce theproduction of apoD. Furthermore,scientists have found this type of

lipoprotein in fat and brain cellsfollowing injury, which suggests that itplays a role in cell renewal and repair.

Nevertheless, the evidence ingeneral suggests that toxicity—a formof insult to the brain—rather thannatural cellular degeneration is thecause of dementia.

Antidepressants There is no doubt that certain drugscause damage to the structure of thebrain, thereby impairing its function.Among the chief offenders areantidepressants, which appear totarget the white matter of the brain.

The white matter is the part of thebrain that contains bundles of nervefibres covered with myelin, a white fattysubstance that forms an insu-latingsheath around each fibre. It is throughthese neural bundles that messages arepassed between different areas of graymatter, which is made up ofunmyelinated nerve cells, within thenervous system.

This means that the white matter israther like a telephone network,responsible for the rapid transmissionof nerve impulses and cell-to-cellcommunication.

One natural aspect of ageing islosing neural connections. Each of usbegins adulthood with some 176,000km of white matter, but we all shouldexpect to lose around 10 per cent of

these connections with every decade oflife.

However, antidepressants clearlyhasten this process. In 2008, a USstudy carried out by Duke UniversityMedical Center in Durham, NC,published the results of the 10-yearstudy, which examined the magneticresonance imaging (MRI) scans ofmore than 1800 patients performedover two periods of time—first, from1991 to 1994, and then, from 1997 to1999. The authors compared thefindings for the 163 patients who had begun taking antidepressantsbetween the first and second scanswith those for patients who were notusing any such drugs.

They found similar incidencesbetween the two groups of virtuallyevery condition looked at—diabetes,stroke, heart attacks, hypertension—save one. Those taking the anti-depressant drugs experienced more‘bright spots’ in the white matter onMRI. This sort of appearance on a scanis thought to indicate damage to bloodvessels, impaired blood flow,demyelination (degeneration of themyelin sheath of nerve cells),disintegration of the blood–brainbarrier and even damage to the nervecells in the gray matter of the brain(Stroke, 2008; 39: 857–62).

Indeed, those taking the drugssuffered a 36-per-cent incidence ofwhite-matter damage compared with27 per cent in those who had beendrug-free over the decade. In addition,all types of antidepressants —be theyold or new—hastened the decline.What’s more, although the worstoffenders were the old-style tricyclicantidepressants, adverse effects wereobserved with all of the newer types ofdrugs that inhibit the uptake ofserotonin. Overall, 60 per cent of thepatients who used either type ofantidepressants showed increaseddamage to white matter that was abovethe norm.

Antidepressants also appear toshrink the hippocampus, part of thelimbic system of the brain that isinvolved in long-term memory, spatialnavigation, learning and mood. Thereis solid scientific evidence that patientswho are chronic users ofantidepressants, particularly SSRIs(selective serotonin reuptakeinhibitors) such as Prozac (fluoxetine),


It is well known that patients taking statins lose coenzyme Q10 (CoQ10)in a dose-related manner. The drugs block production of bothcholesterol and CoQ10 by inhibiting the enzyme precursor of not onlycholesterol, but also that of CoQ10.

CoQ10 participates in chemical reactions, particularly those thatinvolve cellular energy production, and helps to make cell membranesmore resistant to oxygen damage. It is found abundantly in the heartmostly because of the huge energy requirements of cardiac cells.

In fact, studies have shown that a deficiency of CoQ10 is linked withheart failure and impaired heart function. Of 15 published studies in theliterature, nine have confirmed that statins can significantly lower CoQ10levels (Arzneim Forsch, 1999; 49: 324–9).

Critics of statins believe that the widespread use of these drugs hascaused an increase in ‘statin cardiomyopathy’, where the heart loses itsability to pump blood or heart rhythm is disturbed, leading to irregularheartbeats. Drug manufacturers tacitly acknowledge this effect byoffering several drug formulations that combine a statin with CoQ10.

But a less well-known problem with blocking CoQ10 is that itinterferes with cognitive performance, resulting in memory loss andmuddled thinking. In an elderly person, this sort of side-effect is almostinvariably passed off as age-related dementia, requiring yet another coterie of ‘wonder drugs’.

Other researchers have been discovering that statins also inhibit andcause mutations in mitrochondria cells, the energy power packs of thebody. Scientists now suspect that an array of neurodegenerativediseases are due to mutated or altered mitochondria.

The role of coenzyme Q10have smaller hippocampal structurescompared with controls.

In one fascinating study, thehippocampi of long-time depressedpatients who were taking long-termmedication were compared with thoseof two other patient groups: thosewho’d just been diagnosed with the illness and had not yet beguntaking any drugs; and a group of non-depressed controls. There was no difference in brain size betweenthe just-diagnosed depressed patientsand the controls, whereas the long-time medicated showed ahippocampus that was 12 per centsmaller, on average, than those of the others (Proc Natl Acad Sci USA, 2003;

100: 1387–92). The importance of this study is that

it demonstrates that it’s the drugsthemselves, and not the depression onits own, that causes the brain to shrink.

Autopsies of cavaders have alsorevealed brain damage in those who’dbeen long-term users of anti-depressants. In one Dutch study, ofpatients who’d been taking anti-depressants, 73 per cent showedevidence of brain cell death (apoptosis)compared with 33 per cent in patientsusing long-term steroids and 6 per centof their matched controls (Am J Pathol,

2001; 158: 453–68). In addition, epidemiological studies

have also shown a greater incidence ofdementia among populations usingantidepressants. Researchers inCopenhagen carried out a sweepingstudy, involving nearly a third of theentire Danish population, focused onpatients aged over 40 who’d takenantidepressants, even if just one singletime. The risk of developing dementiawas two to five times higher in thosewho’d used antidepressants comparedwith non-users (J Affect Disord, 2009: 117:

24–9). However, Jackson believes that this

population study may haveunderestimated the risk, as one-fifth ofthose using antidepressants diedduring the study follow-up period.

StatinsStatins, those ‘miracle’ cholesterol-lowering drugs, also appear to lead toprogressive cognitive decline. This isparticularly ironic, as medicine hasbeen under the illusion that cuttingdown on cholesterol in the elderly is

desirable particularly for the brain (seebox, page 42) and, consequently, thatstatins can keep Alzheimer’s at bay.

It is true that statins can cross the blood–brain barrier and altercholesterol metabolism in the brain,but this has no bearing on Alzheimer’sdisease. Earlier this year, HarvardUniversity researchers, in conjunctionwith a number of other centres in theUS, Germany and Spain, gave statinsfor 12 weeks to patients with mildAlzheimer’s disease or mild memoryloss.

During the course of this study, theyfound a “modest but significant”inhibition of brain cholesterolbiosynthesis. Nevertheless, althoughthe drugs lowered cholesterol in thebrain, this had no alleviating effects onAlzheimer’s disease whatsoever(Alzheimer Dis Assoc Disord, 2010 May 13

doi: 10.1097/WAD.0b013e3181d61fea).In fact, the lack of effectiveness

of statins as a treatment forAlzheimer’s disease was finally estab-lished last year, when two reviewersindependently analyzed two large-scalerandomized controlled trials, involvinga total of 26,340 patients as part of theHPS 2002 and PROSPER 2002 studies,

and reached an agreement afterdiscussing their results. Theirconclusion was that statins given latein life to individuals at risk of vasculardisease have no effect in preventingeither Alzheimer’s disease or dementia(Cochrane Database Syst Rev, 2009; 2:

CD003160).Indeed, far from helping memory

and cognitive function, statins cancause sudden and complete memoryloss.

This evidence emerged when flightsurgeon Duane Graveline sufferedglobal amnesia when taking atorva-statin (Lipitor) for the first time. Whenhis family doctor Jay S. Cohen took uphis case with Pfizer, the drug’smanufacturer, he was sent clinicalevidence gathered before the drug’srelease showing that there were 4.5cases of severe cognitive disturbanceout of every 100 patients given thedrug.

This included cases of impaired,worsening or general lapses ofmemory, general forgetfulness andshort-term memory loss. Pfizer’s ownstudies had also discovered instancesin which patients had difficultyconcentrating, or suffered abnormally


Dangerous drugs

slow or difficulty in thinking, slowed ordecreased mental activity, impairedintellect or judgment and evenirrational thinking.

Graveline and Cohen then con-ducted an online literature search ofMedWatch, the US Food and DrugAssociation (FDA) database of reporteddrug side-effects, for reports of severecognitive impairment or seriousamnesia associated with Lipitor. Theyfound 662 such reports, including 399cases of amnesia and 236 cases ofmemory impairment. The investigatingpair also found that, over time, thecomplaints had become more frequent(Townsend Lett Docs, 2009; 311: 64–70).

MedWatch, which is thought to benotified of only 2.5 to 5 per cent of alldrug side-effects, therefore suffers fromvast underreporting, so the trueincidence of memory problems fromstatins is probably closer to 66,000 or more. In fact, Graveline and Cohenbelieve that virtually every patienttaking the drug suffers from cognitivedamage in one form or another thatmay be too mild to be initiallydetected. This is perhaps because allstatins lower levels of coenzyme Q10,known to be vital for brain function(see box, page 43).

Graveline and Cohen’s detectivework has also been vindicated by ameta-analysis carried out by DukeUniversity in Durham, NC, whichuncovered 60 patients with memoryloss attributable to statins. Half thepatients had noticed cognitive declinewithin just two months of starting thedrugs; of these, more than half foundthat their memory improved as soon asthey stopped taking the drugs.Furthermore, all of the four patientswho started taking the drugs againsuffered a recurrence of their memoryproblems.

As a further nail in the coffin, notone single experimental study couldfind any evidence to support anybenefit with statins in delayingcognitive decline (Pharmacotherapy, 2003;

23: 871–80).

Antipsychotic agentsAnother major culprit causingdementia is that broad class of drugscalled ‘antipsychotics’. The first so-called ‘neuroleptic’ medications weredeveloped in the 1950s to relievepatients suffering from hallucinations,

paranoid schizophrenia and otherpsychoses. Unfortunately, these drugsbrought with them unwantedextrapyramidal (brain motor system)side-effects such as tardive dyskinesia,characterized by muscle stiffness, tics,tremors and other awkwardmovements.

The arrival of clozapine (Clozaril)introduced the next generation ofneuroleptics—which also includesolanzapine (Zyprexa), quetiapine(Seroquel) and risperidone (Risper-dal)—that were dubbed ‘atypicalantipsychotics’ to distinguish themfrom their older and supposedly moredangerous cousins. These drugs aresupposed to suppress the psychotic andantisocial aspects of schizophreniawithout all the antipyramidal effects(World J Biol Psychiatry, 2000; 1: 204–14).

However, this newer generation ofdrugs comes with its own laundry list ofdangerous, even life-threatening, side-effects, including serious mentaldeterioration.

There is no doubt that the so-called‘antipsychotic drugs’ can cause orspeed up the development of dementia(J Neurol Neurosurg Psychiatry, 2007; 78:

233–9). This is ironic because thesedrugs are often given to sedate or calmpatients with dementia, whereas itappears that they are also speeding upand worsening the process of cognitivedecline.

Nevertheless, the most compellingevidence comes from autopsy studiesthat have compared patients usingantipsychotic drugs with those who didnot. In one study by the Wolfson Centrefor Age-Related Diseases at King’sCollege London, those who’d beengiven neuroleptics had a 30-per-centgreater density of amyloid plaques and65- to 367-per-cent moreneurofibrillary tangles than those whowere free of neuroleptic drugs (Int J

Geriatr Psychiatry, 2005; 20: 872–5). Moreover, in a similar US study, 102

patients with schizophrenia showedevidence on autopsy of brain

Besides the agents already mentioned (see main story), there ismounting evidence that you should also avoid the following types ofdrugs. u Stimulants, such as methylphenidate (Ritalin). A vast number of

animal studies show that all amphetamines cause parts of the brain toshrink, trigger degeneration of dopamine cells in the brain and reducethe survival of neurons in the hippocampus, among many othereffects (Jackson GE. Drug-Induced Dementia. AuthorHouse, 2009).

u Beta-blockers, calcium-channel blockers and ACE inhibitors, andother drugs that aggressively lower blood pressure. These antihyper-tensives can lower blood flow to the brain and produce all thehallmarks of Alzheimer’s disease (Drugs Aging, 1999; 15: 15–28).

u Antiarrhythmic drugs, given to correct abnormal heart rhythms, canalso cause dementia.

u Anticholinergic drugs, a giant category that includes drugs forgastro-intestinal problems such as diverticulitis and ulcerative colitis,respiratory ailments such as asthma and genitourinary disorders suchas cystitis or prostatitis, are associated with cognitive decline in theelderly (Presentation at the American Academy of Neurology 60th Anniversary

Annual Meeting in Chicago, IL, 17 April 2008).u Opioids, many of which can cause delirium (Drugs Aging, 1993; 3: 349–57;

Postgrad Med J, 2004; 80: 388–93). u Non-steroidal anti-inflammatory drugs (NSAIDs). Initially thought to

offer protection against Alzheimer’s, different types of these commonpainkillers can cause a variety of cognitive changes, ranging fromdelirium (indomethacin and sulindac) to disturbances in memory andconcentration (naproxen and ibuprofen) (Drugs Aging, 1999; 15: 15–28).

u Levodopa. This antiparkinsonian medication causes cognitivesymptoms in up to 60 per cent of users (Clin Geriatr Med, 1998; 14:

101–27).

Other drugs to avoid


deterioration that was suggestive ofAlzheimer’s or some other form ofdementia. The signs were present in 74per cent of those who’d been givenantipsychotic drugs, but in only 36 percent of those who’d died prior to theadvent of these drugs (Alzheimer Dis Assoc

Disord, 1994; 8: 211–27). In other words, taking anti-

psychotics more than doubled thepatients’ chances of developingdementia.

The worst combination of all istaking an antipsychotic together withan antidepressant, which appears toquadruple the speed at which thedisease develops (J Neurol Neurosurg

Psychiatry, 2007; 78: 233–9).What’s more, Alzheimer’s patients

who are given an antipsychotic—acommon practice, usually to sedatethem—have double the usual risk ofdeath. In a major study involvingvarious centres across the UK—the firstindependent study of its kind not paidfor by a drug company—less than halfthe patients (46 per cent) taking anantipsychotic were still alive at the two-year follow-up. After three years, only30 per cent of those takingantipsychotics were alive comparedwith 59 per cent taking a placebo(Lancet Neurol, 2009; 8: 151–7; doi:

10.1016/S1474-4422(08)70295-3).In another UK study that was

focused on care facilities in the NorthEast of England, the London-basedresearchers compared the efficacy ofthe antipsychotic quetiapine, thecholinesterase inhibitor rivastigmineand a placebo in calminginstitutionalized patients withdementia. Neither of the patients in theactive-treatment groups were anycalmer than those who were simplytaking sugar pills, although there wasone significant difference withquetiapine—it was associated withsignificantly greater cognitive decline(BMJ, 2005; 330: 874).

Antipsychotics also appear to shrinkthe volume of the frontal lobes of thebrain by 0.2 per cent per year,according to a University of Iowa study(Arch Gen Psychiatry, 2003; 60: 585–94).

Other studies have shown sizereductions in a variety of areas of thebrain with both older (haloperidol) and

newer (olanzapine) antipsychoticmedications (Arch Gen Psychiatry, 2003; 60:

585–94). What is coming to light is a clear

association between antipsychoticdrugs and cognitive decline. In apainstaking English survey, every caseof dementia recorded on a dementiaregister during 1993–1994 wasexamined. Researchers studied thepatients’ diagnoses and treatmentsfrom their various medical carers andinterviewed their next of kin, thenmatched these patients to a similargroup of elderly people living inSoutheast London.

Of the patients on the register, 13per cent had a past history ofpsychiatric treatment, and the use ofpsychiatric drugs was three to fourtimes higher among those who’d goneon to develop dementia (Age Ageing,

1998; 27: 181–8).

BenzodiazepinesIn addition to the major anti-psychotic drugs, benzodiazepinetranquillizers and sleeping pills arealso responsible for cognitive decline.One Argentinian study noted evidencethat sleeping pills, which are oftenhanded out without a prescription inthat country, led to severe memoryand cognitive impairment, anddelirium (Vertex, 2001; 12: 272–5).

Newer studies now show that thiseffect has to do with an effect ongangliosides in the brain. Thesemolecules, which contain fat andsugar, are present to a large extent inbrain lipids and on the surface ofevery neuron. They are essential forregulating cell growth, maintainingthe integrity of the material con-tained within cells, and responding toforeign invasion by toxins andbacteria. Without these gangliosides,we lose myelin and entire neurons,and may even die.

A series of studies by the Institutefor Medical Research in Belgrade,Yugoslavia, has demonstrated that, atleast in rats—so it may not apply tohumans—chronic doses of Valium(diazepam) led to the loss of 46 percent of gangliosides in the cerebellumwithin six months. After a short periodof total drug withdrawal, the rat brain

still had not fully recovered (Physiol Res,

1999; 48: 143–8). When the researchers repeated the

study in 2002, focusing especially onthe effects of the drug on variousregions of the brain, they foundsignificant reductions of gangliosides inthe hippocampus, cerebral cortex andcerebellum, as well as increases ofsimple gangliosides in other areas(Neurol Sci, 2002; 23: 69–74). These findingsare consistent with those of manyhuman neurological diseases, includingAlzheimer’s.

Indeed, in a 1993 British study,researchers took computed tomog-raphy (CT) brain scans of long-termbenzodiazepine users and comparedthem with those of drug-free controls.The scans revealed that the drug usershad a reduction of brain tissue in theirfrontal and occipital lobes, as well as inthe left caudate nucleus—areas thatare crucial for cognitive function(Psychiatry Res, 1993; 48: 135–44).

At present, in the US alone, sixmillion patients are being treated fordementia at a cost of $90 billion, orone-third of all Medicare bills. Thismeans that 1 per cent of the entiregross domestic product of the US isbeing spent on a mostly iatrogenic(doctor-induced) condition.

Medicine has reached the pointwhere it is chasing its own tail,attempting to mop up with yet moredrugs and treatments a vast and costlyproblem that it has itself caused in thefirst place.

Evidence is mounting that one of themajor toxic insults to the brain is themercury from amalgam fillings, but thiseffect may be eclipsed by the dangers we face from the modernmedical response to ageing.

Keeping bright and alert in old agerequires a few simple practices: regularexercise; eating an antioxidant-richwholefood diet along with good fats;minimizing toxic exposure to heavymetals; engaging in regular brainworkouts (crossword puzzles orreading); and staying connectedthrough a social network. However, nowthere is one more simple homily to addto the list: avoid as many prescriptiondrugs as you can.

Lynne McTaggart


Dangerous drugs

HRT: the latest cancer riskJust when it looks as if itcouldn’t get any worse forHRT, a new study showsthat it causes lung cancer

According to the US Women’s Health Initiative study, hormone therapyincreases your chances of developing the following diseases by thesepercentages:

u Coronary heart disease-related events, 29 per centu Stroke, 41 per centu Deep vein thrombosis, 200 per centu Blood clot in lungs, more than 200 per centu Invasive breast cancer, 24 per centu All cancers among previous users, 86 per centu Ovarian cancer, 38 per centu Lung cancer, 60 per cent.

The current risks of HRT

Anyone with shares in hormonereplacement therapy (HRT) is inthe doldrums. HRT was touted

as the modern-day equivalent of thefountain of youth—until 2002, whenthe US Women’s Health Initiative(WHI) study, one of the largest-everstudies of these drugs, discovered thatwomen taking HRT were more likely tohave breast cancer, ovarian cancer,stroke and heart disease.

And now, new evidence from theWHI data shows that the use of HRTduring the menopause increases lungcancer by 60 per cent after five years.

Dr Rowan Chlebowski, a medicaloncologist at Harbor-UCLA MedicalCenter in Los Angeles, CA, analyzedthe WHI statistics, and found a linkbetween prolonged HRT use and non-small cell (NSC) lung cancer.

Although most of the adversepublicity after the WHI study focusedon the breast cancer risk, this is thefirst time that a link between HRT andlung cancer has been identified. It alsohappens that NSC lung cancer is theleading cause of death in women.

The most vulnerable women weresmokers using HRT, who accounted forslightly more than half of all cases ofNSC lung cancer. In the WHI study, theresearchers found one extra death from this for every 100 womenusing Prempro, Wyeth’s combinationoestrogen–progestin HRT drug.

Ovarian cancer riskThis announcement, made at theannual meeting of the AmericanSociety of Clinical Oncology in May,coincided with the release of thefindings from a large-scale, long-termDanish study showing that women whotake HRT increase their risk of ovariancancer by 38 per cent (JAMA, 2009; 302:

298–305). The study, which included more than

900,000 women aged 50–79, foundthat the current use of hormonesaccounted for a 38-per-cent greaterchance of ovarian cancer. This

translates to one extra case every yearfor every 8300 women using HRT, or140 extra cases during the eight-yearfollow-up, accounting for 5 per cent ofall cases of the cancer.

The risk of having the disease werethe same regardless of how long thedrug was taken, which formulation wasused, how much oestrogen wasincluded in the mix and what sort ofdelivery method was chosen.

As ovarian cancer is difficult todetect and is often fatal, such a riskshould not be brushed aside, theCopenhagen researchers noted.

HRT to blameUp to now, medicine has tended toblame a familial ‘predisposition’—thatis, a family history of breast cancer andthe presence of certain predisposinggenes—on many incidences of breastcancer, particularly in women usingHRT. Nevertheless, the latest trawlthrough the WHI data shows that HRTshoulders much of the blame.

Epidemiologists from the Universityof Rochester Medical Center, in NewYork, followed-up the more than 16,000postmenopausal women given eitherHRT or a placebo during the five-yearWHI study, which was abruptlyabandoned when the health risksemerged. When they evaluated the 349women who’d developed breast cancer,they could find no link with a familyhistory.

The researchers concluded that afamily history and hormones have“independent and non-interactingeffects”—in other words, the cases ofcancer were most likely entirely causedby HRT (Epidemiology, 2009; 15 May: doi:

10.1097/EDE. 0b013e3181a71279).

Fewer cases after the factsFollowing the disclosures of the WHItrial, breast cancer rates fell by 13 percent among more affluent women inCalifornia, but only by 7 per cent inrural areas. When researchers from theNorthern California Cancer Centerinvestigated the discrepancy, theyfound that women in the more ruralareas had not heard about the linkbetween HRT and cancer, and so hadcontinued taking the drugs—whichwould again tend to point the finger atHRT (BMC Med, 2009; in press).

After the WHI results were reported,Wyeth’s products took a hammering,and their use declined by 50 per cent. Nevertheless, sales ofthe oestrogen-only drug Premarin andvarious cream formulations stillconstitute a business totalling up toone billion dollars per year.

Last month, the US Food and DrugAdministration added a final nail in theHRT coffin with a boxed warning forPrometrium, a progesterone drug,warning of the WHI’s results showingincreased risks of heart attack, stroke,invasive breast cancer, blood clots anddeep vein thrombosis, and a greater riskof dementia, among those takingcombined oestrogens and progesto-gens of any variety.

Lynne McTaggart


The big ‘cure-all’ unmaskedThe great all-purposepreventative forcholesterol has been foundto cause prostate cancer

If you must take a statin drug, take the smallest dose possible. Newevidence shows that even the minimum daily dose of 20 mg/day causespotentially fatal muscle pain and weakness—and may even lead tocomplete breakdown of muscle tissue (N Engl J Med, 2008; 359: 789–99).Higher doses or taking the drug with other drugs had a magnifying effect,causing a far higher incidence of myopathy than the official figures claim.The latest evidence shows that as much as 1.6 per cent of patients developmuscle weakness—that’s 128,000 patients in the US alone.

Take as little as possible

Statins, the gold standard ofcholesterol treatment, havebecome the liver tonic of themodern age. Doctors hand

them out for everything fromosteoporosis to senile dementia, asearly studies suggest that they mayhave preventative effects.

When early laboratory evidenceshowed that statins induce apoptosis(cell death) and reduce prostatecancer cell growth and spreading(Cancer Epidemiol Biomarkers Prev, 2008; 17:

88–94), medicine concluded that statinswere a potent cancer preventative (J

Natl Cancer Inst, 2006; 98: 1819–25). Earlystudies bolstered this view, offeringpreliminary evidence that long-termstatin use could prevent cancers of thebreast, prostate, blood and colon.

Studies of populations with prostatecancer found links between statins andthe prevention of more advanced formsof the disease (Curr Opin Urol, 2008; 18:

333–9). Doctors were particularlyenthusiastic when a case-control studyfound a cancer risk reduction of 20 percent with statins (J Clin Oncol, 2004; 22:

2388–94).Now, that reputation—that statins

are a powerful cancer preventative—has been sullied with the latest findingsthat statins may actually causeprostate cancer in overweight men.Researchers at the Fred HutchinsonCancer Research Center in Seattle,WA, discovered the link while studyingmore than 1000 cases of prostatecancer, diagnosed between2002–2005, compared with a similarnumber of age-matched controls.

Although there was no risk ofdeveloping the disease in normal-weight statin users, including thosewho had taken the drugs for more than10 years, overweight men— those witha body mass index of more than 30kg/m2—increased their risk by 1.5times over overweight non-users. Also,the risk increased to 1.8 times withstatin use for five or more years (Am J

Epidemiol, 2008; 168: 250–60).

But the Seattle evidence is only thelatest to challenge the myth of cancerprevention. A University of Athensreview of 19 epidemiological studiesfound no evidence of a protective effectwith statins and even suggested thatthe earlier evidence of lowered risk wasjust coincidental (Int J Cancer, 2008; 123:

899–904). More detailed analyses found a lower

incidence of advanced cancer, but noreduction in the risk of overall prostatecancer (Curr Opin Urol, 2008; 18: 333–9). Aneven larger meta-analysis of 35randomized controlled trials showed alink between the drug and developingcancer, depending on the patient’s age:the older the man, the more likely hewas to develop cancer (J Clin Oncol, 2006;

24: 4808–17). Another meta-analysis of prava-

statin in elderly patients confirmed anassociation between the drug and anincreased risk of cancer withincreasing age (CMAJ, 2007; 176: 649–54).

As for other forms of cancer, theDepartment of Pharmacology team atthe University of Athens School ofMedicine has systematically examinedand combined all the evidence of statinuse and cancer incidence. Their reviewof 14 studies found no evidence tosupport claims that statin use canprotect against malignancies of theblood, such as leukaemia (Br J Clin

Pharmacol, 2007; 64: 255–62). They also found no evidence that

statins can significantly reduce the riskof colorectal cancer, although theyconcluded that there might be someeffect with higher doses (J Clin Oncol,

2007; 25: 3462–8). The same methodologyalso found no evidence that statins canreduce the risk of either pancreatic orbreast cancers (Am J Gastroenterol, 2008;

103: 2646–51; J Clin Oncol, 2005; 23: 8606–12).Yet another research team, from the

Department of Epidemiology andSurvellance Research at the AmericanCancer Society, found that neithershort- or long-term (five years or more)use of the drug prevented colorectalcancer (J Natl Cancer Inst, 2006; 98: 69–72).

Similarly, a Boston University studyof more than 3600 patients inMassachusetts could also find noprotective effect other than a lower riskof stage IV (advanced, metastasizing)cancer among statin users, anassociation that the authors believerequires confirmation (J Natl Cancer Inst,

2007; 99: 32–40). The final blow was dealt by a

University of Connecticut School ofPharmacy meta-analyses of nearly90,000 participants involved in allstudies claiming a protective effectagainst all cancers. Again, the dataindicate that no type of cancer isaffected by statin use (JAMA, 2006; 295:

74–80).Aside from the damning evidence

against its role as a cancerpreventative, the latest evidence alsoshows that statins don’t preventfractures or type 2 diabetes either(Pharmacoepidemiol Drug Saf, 2007; 16:

627–40; Curr Med Res Opin, 2008; 24:

1359–62). This kicks away several plat-forms on which the drug’s reputationas a preventative treatment has beenbased.

Lynne McTaggart


Dangerous drugs

Building brittle bonesAtrial fibrillation is thelatest in a long line ofside-effects caused byFosamax and its relatives

The world’s most popular drugsfor osteoporosis cause heartproblems—and we’re only just

finding out 10 years after themanufacturers, who may have knownit all along.

A recent study with the tortuousacronym HORIZON (Health Out-comes and Reduced Incidence WithZoledronic Acid Once Yearly) foundthat postmenopausal women takingzoledronic acid (Acasta) by injectionjust once a year reported higher bonedensity, but also higher rates ofserious atrial fibrillation (AF), thanthose taking a placebo (N Engl J Med,

2007; 356: 1809–22). Acasta is a bis-phosphonate like Fosamax, whichreduces the turnover of bone.

That discovery was followed thisyear by a University of Washingtonstudy looking at the use of aledro-nate sodium (Fosamax) amongfemale patients at an integratedhealthcare delivery system between 1October 2001 and 31 December2004. When 719 women with con-firmed AF were compared with 966controls without AF, a significantlyhigher number of those with AF hadused alendronate. In fact, usingalendronate at any point in their livesnearly doubled their risk of AF. Theresearchers estimated that this classof drugs may cause up to 3 per centof the AF in postmenopausal womenwith osteoporosis (Arch Intern Med, 2008;

168: 826–31).But not all studies agree. A Danish

epidemiological study examined13,586 patients with AF and atrialflutter, and found that etidronate andalendronate were both used toalmost the same degree by those withand without AF. Their conclusion:“No evidence was found that use ofbisphosphonates increases the risk of atrial fibrillation and flutter” (BMJ,

2008; 336: 813–6).Nevertheless, according to some

law firms, the association betweenbisphosphonates and heart problems

emerged 10 years ago, when evi-dence of AF with Fosamax wasspotted on reviewing the evidence of a five-year study (1992–1997)called the Fracture InterventionTrial. Its findings showed a 50-per-cent higher risk of AF for thosetaking Fosamax compared withtaking a placebo (JAMA, 1998; 280:

2077–82). However, this is only the latest in

a litany of problems with what wasfirst touted to be the solution toosteoporosis and other bone diseasessuch as Paget’s disease of the bone.Fosamax and the other bisphos-phonates work by limiting thenormal tearing down of old bone,part of the dynamic process ofconstant renewal in bone growth.

Worse bone problemsIn the 12 years since its launch onthe world market, Fosamax and itsrelatives have been the target of anumber of lawsuits for causingosteonecrosis of the jaw, or ‘deadjaw’. This condition is characterizedby a permanent loss of blood tobone tissue.

This severe condition causesextreme pain, numbness, looseningof the teeth and exposure of bone in the oral cavity. When allowed to goundetected and untreated, thissituation can lead to death of bonetissue and even collapse of the bonewithin the jaw—a condition that isirreversible. In this case, the expos-ed bone can eventually lead toinfection and fracture, and mayrequire long-term antibiotic therapyor surgery to remove the dead anddying bone tissue.

In fact, Merck & Co, the manu-facturers of Fosamax, have even beenthe subject of a number of personal-injury lawsuits filed by women whohave developed osteonecrosis of thejaw while taking the drug.

Other side-effectsBefore these latest disclosures, thebiggest concern with this class ofdrugs was the potential for gastro-intestinal damage. Soon after thelaunch of Fosamax, patients com-

plained of stomach pain, heartburnand irritation of the oesophagus. Insevere instances, the drug causedfatal oesophageal perforation (Am J

Gastroenterol, 2001; 96: 3212–3). Patients were advised to take the

drug with a large glass of water whilestanding up—and had to remainstanding for at least half an hour toreduce the time that the drug is incontact with the lining of theoesophagus.

In addition to damaging theoesophagus, these drugs also causestomach ulcers—and permanently insome cases (Dig Dis Sci, 2002; 47: 1665–78;MedGenMed, 2002; 4: 3). They can alsocause severe hepatitis, skin ‘poison-ing’ and a painful inflammation ofthe eye known as ‘anterior uveitis’(Gastroenterol Clin Biol, 2002; 26: 179–80;Aten Prim, 2002; 29: 61–2; Invest Clin, 2002;

43: 49–52).The most astonishing aspect of

the osteoporosis drug saga is that,despite all of the serious and evenfatal side-effects, the drug companieshave been given license to use thesedrugs as a long-term preventative—before a woman has developed osteo-porosis. Also, doctors routinelysuggest that they be taken for adecade after the menopause (Dan Med

Bull, 2002; 49: 1–18), despite the lack ofany evidence that they do any good.

In fact, women who take the drugfor at least seven years suffer threetimes more fractures of the spine inthe last two years of taking the drugthan in the first three years. So,although the bones have greaterdensity, they are more brittle (J Clin

Endocrinol Metab, 2001; 86: 1835). Lynne McTaggart

what doctors don tell you ageing well · 16 male pattern baldness 19 chronic back pain 22 stroke...

Documents