fructose and metabolic syndrome: is there a link? no ... · fructose and metabolic syndrome: is...

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Fructose and metabolic syndrome: Fructose and metabolic syndrome: Is there a link?Is there a link?

Baptist Health South Florida, Feb. 6, 2014

Robert H. Lustig, M.D., M.S.L.Robert H. Lustig, M.D., M.S.L.Division of Endocrinology, Department of PediatricsDivision of Endocrinology, Department of Pediatrics

Institute for Health Policy StudiesInstitute for Health Policy StudiesUniversity of California, San FranciscoUniversity of California, San Francisco

Adjunct FacultyAdjunct FacultyUC Hastings College of the LawUC Hastings College of the Law

• No disclosures

PastPast

2001

Currently there are 30% more obese than undernourished people worldwide

(World Health Organization)

371 million diabetics in 2012(5% of the world‘s population)

(International Diabetes Federation)

PresentPresent

Experts predict:

165 million Americans will be obese by 2030(4 part obesity series in Lancet, 8/26/11)

42% of Americans will be obese by 2030 (Finkelstein et al. Am J Prev Med epub 5/7/12)

100 million Americans will have diabetes by 2050(CDC Division of Diabetes Translation, 2011)

MedicareMedicare will will bebe brokebroke byby 20262026

FutureFuture

Obesity is the problem Obesity is the problem (?)

2

Obesity is the problem (?)Obesity is the problem (?) Obesity is the problem (?)Obesity is the problem (?)

Basu et al. PLoS One 8:e58783, 2013

Obesity is the problem (?)Obesity is the problem (?)

• Obesity is increasing worldwide by 1% per year

• Diabetes is increasing worldwide by 4% per year

““ExclusiveExclusive”” view of obesity and view of obesity and metabolic dysfunctionmetabolic dysfunction

Obese (30%)

Normal weight (70%)

240 million adults in U.S.

72 million

168 million

Obese (30%)

Obese and sick

(80% of 30%)

Normal weight (70%)


72 million

168 million

Total: 57 million sick

““ExclusiveExclusive”” view of obesity and view of obesity and metabolic dysfunctionmetabolic dysfunction

Obese (30%)

Normal weight (70%)


72 million

168 million

““InclusiveInclusive”” view of obesity and view of obesity and metabolic dysfunctionmetabolic dysfunction

3

Obese (30%)

Normal weight (70%)


Normal weight,

Metabolic dysfunction

(40% of 70%)

Obese and sick

(80% of 30%)

57 million 67 million

Total: 124 million sick

72 million

168 million

““InclusiveInclusive”” view of obesity and view of obesity and metabolic dysfunctionmetabolic dysfunction

Relation between Relation between visceral and subcutaneous obesity:visceral and subcutaneous obesity:(thin on the outside, fat on the inside)(thin on the outside, fat on the inside)

Thomas et al. Obesity doi: 10.1038/oby.2011.142, 2011

Obesity is not the problemObesity is not the problem Obesity is not the problemObesity is not the problem

Metabolic Syndrome: where all the money goesMetabolic Syndrome: where all the money goes(75% of all healthcare dollars)(75% of all healthcare dollars)

Obesity is not the problemObesity is not the problem

Metabolic Syndrome: where all the money goesMetabolic Syndrome: where all the money goes(75% of all healthcare dollars)(75% of all healthcare dollars)

DiabetesDiabetesHypertensionHypertension

Lipid abnormalitiesLipid abnormalitiesCardiovascular diseaseCardiovascular disease

NonNon--alcoholic fatty liver diseasealcoholic fatty liver diseasePolycystic ovarian diseasePolycystic ovarian disease

CancerCancerDementiaDementia

Metabolic syndrome is difficult to define in adults Metabolic syndrome is difficult to define in adults

• WHO 1998 • AACE 2003

• EGIR 1998 • IDF 2005

• NCEP/ATPIII 2001 • AHA 2005

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Metabolic syndrome is difficult to define in adults Metabolic syndrome is difficult to define in adults

And even more difficult to define in children And even more difficult to define in children

• WHO 1998 • AACE 2003

• EGIR 1998 • IDF 2005

• NCEP/ATPIII 2001 • AHA 2005

Circulation 119:628, 2009

Because each of these definitions sought to define theBecause each of these definitions sought to define the

metabolic syndrome phenomenologically, with cutoffs metabolic syndrome phenomenologically, with cutoffs

Because each of these definitions sought to define theBecause each of these definitions sought to define the

metabolic syndrome phenomenologically, with cutoffs metabolic syndrome phenomenologically, with cutoffs

It is easier to define the metabolic syndrome mecha nisticallyIt is easier to define the metabolic syndrome mecha nistically

WhereWhere’’s the insulin resistance?s the insulin resistance?

Cytokines

The standard model of insulin resistanceThe standard model of insulin resistance

Familial Partial Lipodystrophy: Dunningan or Type 2Familial Partial Lipodystrophy: Dunningan or Type 2

•X-linked or autosomal dominant•Absence of limb fat

�Easily visible veins�Defined musculature

•Normal or excess facial fat •Cushingoid facies (moon facies)•Dorsocervical fat pad•Acanthosis nigricans•Metabolic Syndrome

Peters et al. Nature Genet 18:292, 1998

• Fat mass

• Leptin• Adiponectin• Inflam. Cytokines• Metabolic Syndrome

Comparison between lipodystrophy and obesityComparison between lipodystrophy and obesity

Asterholm et al. Drug Disc Today Dis Models 4:17, 2007

LD obesity

±++

5

• Fat mass

• Leptin• Adiponectin• Inflam. Cytokines• Metabolic Syndrome

Comparison between lipodystrophy and obesityComparison between lipodystrophy and obesity

Asterholm et al. Drug Disc Today Dis Models 4:17, 2007

LD obesity

±++

So the metabolic syndrome can arise from too much, or too little fatSo the metabolic syndrome can arise from too much, or too little fati.e. iti.e. it’’s not the fat that countss not the fat that counts

Obesity Lipodystrophy

InsulinResistance

Chehab, Endocrinol 149:925, 2008

Obesity and lipodystrophy share insulin resistanceObesity and lipodystrophy share insulin resistance

Relation between obesity, T2DM, and Metabolic Syndr omeRelation between obesity, T2DM, and Metabolic Syndr ome

Steinberger et al. Circulation 119:628, 2009

REFRAMING THE DEBATEREFRAMING THE DEBATE


Obesity doesnObesity doesn’’t CAUSE metabolic syndromet CAUSE metabolic syndrome

Obesity is a MARKER for metabolic syndromeObesity is a MARKER for metabolic syndrome


Obesity doesnObesity doesn’’t CAUSE metabolic syndromet CAUSE metabolic syndrome

Obesity is a MARKER for metabolic syndromeObesity is a MARKER for metabolic syndrome

OBESITY IS A OBESITY IS A ““RED HERRINGRED HERRING””EVERYONE IS AT RISK OF METABOLIC SYNDROMEEVERYONE IS AT RISK OF METABOLIC SYNDROME

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Obesity isnObesity isn’’t enough!t enough!

Insulin resistance isnInsulin resistance isn’’t enough!t enough!

What kind of obesity?What kind of obesity?

What kind of insulin resistance? What kind of insulin resistance?

In which tissue?In which tissue?

Are all insulin pathways affected?Are all insulin pathways affected?

Intrahepatic fat explains metabolic perturbation Intrahepatic fat explains metabolic perturbation better than visceral fatbetter than visceral fat

Fabbrini et al. Proc Natl Acad Sci 106:15430, 2009

HepaticInsulin

SensitivityIndex

InsulinStimulated

GlucoseDisposal

Rate

InsulinStimulatedPalmitate

SuppressionRate

VLDLSecretion

Rate

ContributionOf Free

Fatty AcidsTo VLDL

Insulin Receptor Knockouts (IRKO)Insulin Receptor Knockouts (IRKO)Kahn Lab, Kahn Lab, JoslinJoslin 19981998--presentpresent

Obesity, Metabolic SyndromeLiver (LIRKO)Brain (NIRKO)

Protected from ObesityMuscle (MIRKO)White Adipose Tissue (FIRKO)Brown Adipose Tissue (BATIRKO)β-cell (βIRKO)Vascular Smooth Muscle (VSMCIRKO)Glomerular Podocyte (PODIRKO)

Biddinger and Kahn, Ann Rev Physiol 68:123, 2006 Brown and Goldstein, Cell Metab 7:95, 2008

Insulin has two effects on the liverInsulin has two effects on the liver

Result: ObesityHyperglycemia, hyperinsulinemia, DMLow TG, VLDLNormal BPNOT Metabolic Syndrome

Result: ObesityHyperglycemia, hyperinsulinemia, DMHigh TG, VLDLLow BPMetabolic Syndrome

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In order to explain Metabolic Syndrome:

• We are looking for a ubiquitous factor that– promotes obesity (preferably visceral)– promotes hypertension– induces selective hepatic insulin resistance

• blocks Foxo1 to promote gluconeogenesis(hyperglycemia, hyperinsulinemia, and diabetes)

• stimulates de novo lipogenesis(dyslipidemia, atherosclerosis)

U.N. General AssemblyU.N. General AssemblySept 20, 2011Sept 20, 2011

• Non-communicable disease is now a bigger problemthan acute infectious diseases worldwide

• Plan to target, tobacco, alcohol, and diet

U.N. General AssemblyU.N. General AssemblySept 20, 2011Sept 20, 2011

• Non-communicable disease is now a bigger problemthan acute infectious diseases worldwide

• Plan to target, tobacco, alcohol, and diet

• But exactly what about diet?Total calories?Fat?Red meat?Dairy?Carbohydrate?

The FictionThe Fiction“Beating obesity will take action by all of us, based on onesimple common sense fact: All calories count, no matter wherethey come from, including Coca-Cola and everything else wit hcalories…”

-The Coca Cola Company, “Coming Together”, 2013

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• Some Calories Cause Disease More than Others

• Different Calories are Metabolized Differently

• A Calorie is Not A Calorie

The ScienceThe ScienceHigh Fructose Corn Syrup is 42High Fructose Corn Syrup is 42--55% Fructose;55% Fructose;

Sucrose is 50% FructoseSucrose is 50% Fructose

GlucoseGlucose FructoseFructose

SucroseSucrose

Ventura et al. Obesity 19:868, 2011

Actual fructose content in soft drinksActual fructose content in soft drinks

55%

150150

125

100

75

50

25

0

Grams per day

U.S. Commerce Service 1822-1910, combined with Economic Research Service, USDA 1910-2010

150150

125

100

75

50

25

0

Grams per day


Growth ofSugar Industry

StabilizationHFCS +Sugar for Fat

WWII

150150

125

100

75

50

25

0

Grams per day



StabilizationHFCS +Sugar for Fat

WWII

Theoreticalthreshold based on EtOH

AHA threshold for CVD

9

150150

125

100

75

50

25

0

Grams per day



Stabilization

WWII

Emergence of CVD as health issue 1931

HFCS +Sugar for Fat



150150

125

100

75

50

25

0

Grams per day



Stabilization

WWII

Emergence of CVD as health issue 1931

HFCS +Sugar for Fat

Emergence of Adolescent T2DM as health issue 1988



Global consumption of sugar/sugarcropsGlobal consumption of sugar/sugarcropsCalories per day, 2007Calories per day, 2007

Data from Food and Agriculture Organization, World Health Organization, 2007 Mozaffarian et al. N Engl J Med 364:2392, 2011

Foods that cause weight gainFoods that cause weight gain

Mozaffarian et al. N Engl J Med 364:2392, 2011


Mozaffarian et al. N Engl J Med 364:2392, 2011


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Loweringsugar

Raisingsugar

Effects of sugar on obesity (metaEffects of sugar on obesity (meta--analysis)analysis)

Te Morenga et al. BMJ 345:e7492, 2013

Obesity is not the problemObesity is not the problem

Metabolic syndrome is the problemMetabolic syndrome is the problem

Fructose is not glucoseFructose is not glucose

• Fructose is 7 times more likely than glucoseto form Advanced Glycation End-Products (AGE’s)

• Fructose does not suppress ghrelin

• Acute fructose does not stimulate insulin (or leptin)

• Hepatic fructose metabolism is different

• Chronic fructose exposure promotes the metabolic syndrome

Elliot et al. Am J Clin Nutr, 2002Elliot et al. Am J Clin Nutr, 2002Bray et al. Am J Clin Nutr, 2004Bray et al. Am J Clin Nutr, 2004Teff et al. J Clin Endocrinol Metab, 2004Teff et al. J Clin Endocrinol Metab, 2004Gaby, Alt Med Rev, 2005Gaby, Alt Med Rev, 2005

Le and Tappy, Curr Opin Clin Nutr Metab Care, 2006Le and Tappy, Curr Opin Clin Nutr Metab Care, 2006Wei et al. J Nutr Biochem, 2006Wei et al. J Nutr Biochem, 2006Johnson et al. Am J Clin Nutr 2007Johnson et al. Am J Clin Nutr 2007Rutledge and Adeli, Nutr Rev, 2007Rutledge and Adeli, Nutr Rev, 2007Brown et al. Int. J. Obes, 2008Brown et al. Int. J. Obes, 2008

A different model of insulin resistanceA different model of insulin resistance

Cytokines

Fructose

Fatty liver

Sensitivity

Hepatic insulin resistance

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A different model of insulin resistanceA different model of insulin resistance

Cytokines

Fructose

Fatty liver

Sensitivity

Hepatic insulin resistance

The second problem The second problem

The browning reaction or Maillard reaction The browning reaction or Maillard reaction or nonor non--enzymatic glycationenzymatic glycation

Instead of roasting 1 hour at 375 degreesInstead of roasting 1 hour at 375 degreeswe slow cook at 98.6 degrees for 75 yearswe slow cook at 98.6 degrees for 75 years

Aging and costal cartilage Aging and costal cartilage

Courtesy Dr Baynes

Figueroa-Romero et al. Rev Endo Metab Dis 9:301, 2008

Generation of reactive oxygen species by carbohydra te Generation of reactive oxygen species by carbohydra te

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The furan ring of fructose is more unstable,so at equilibrium, fructose exists in the linear fo rm

Lim et al. Nat Rev Gastro Hepatol 7:251, 2010

Glucose

Fructose

Days of in vitro glycation

Flu

ores

cenc

e

600

400

200

0

Ahmed and Furth, Clin Chem 38:1301, 1992

Fructose and glycationin vitro

0 8 16 24

Rates of reactivity

Rate Carbonyl (/mM/hr) %

Glucose 0.6 0.002

Galactose 2.8 0.02

Fructose 4.5 0.7

Bunn and Higgins, Science 213:222, 1981

NonNon--enzymatic glycation: fructose >> glucoseenzymatic glycation: fructose >> glucose

Hepatocyte death Hepatocyte death in vitro in vitro upon fructose exposure upon fructose exposure (after generation of H(after generation of H 22OO22))

Treatment ED 50

Fructose 1.5 ± 0.13 M

Glucose >1.5 M

Glycoaldehyde 20 ± 2 mM

Glyoxal 5 ± 0.5 mM

Lee et al. Chemico-biological Interactions 178:332, 2009

Hepatocyte death Hepatocyte death in vitro in vitro upon fructose exposure upon fructose exposure (after generation of H(after generation of H 22OO22))

Treatment ED 50 ED50 (with H 2O2)

Fructose 1.5 ± 0.13 M 12 ± 2 mM

Glucose >1.5 M 1.5 M

Glycoaldehyde 20 ± 2 mM 0.5 ± 0.1 mM

Glyoxal 5 ± 0.5 mM 0.02 ± 0.002 mM

Lee et al. Chemico-biological Interactions 178:332, 2009

Prevented by addition of:antioxidant vitamins (VitB 1, VitB 6, VitC)P450 inhibitorshydroxyl radical and carbonyl scavengers heavy metal chelators

The MethionineThe Methionine--Choline Deficient DietCholine Deficient Diet

Pickens et al. J Lipid Res 50:2072, 2009

Fastest animal model of NASH• sucrose necessary to provide the substrate for steatosis• methionine deficiency reduces glutathione, the hepatic hydroxyl radical scavenger

• choline deficiency reduces phosphatidyl choline, another mechanism of hepatic lipid export

Sucrose is necessary for NAFLD in theSucrose is necessary for NAFLD in theMethionineMethionine--Choline deficient dietCholine deficient diet


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TUNEL staining in the TUNEL staining in the MethionineMethionine--Choline deficient dietCholine deficient diet


Association of fructose consumption with Association of fructose consumption with severity of steatosis and fibrosisseverity of steatosis and fibrosis

Grade of Steatosis

p =0.06 p < 0.005

Stage of Fibrosis

p < 0.0007

Non NonOccasional OccasionalDaily Daily

Error bar = 95%CI

Abdelmalek et al. Hepatology 51:1961, 2010

10 Most Obese States

> 30% obese

10 Most Obese States 10 Laziest States

> 30% obese < 63% active



10 Most Unhappy States 10 Most Obese States 10 Laziest States


10 Most Unhappy States

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Adult Heart Disease Rate




Adult Heart Disease Rate

Figure 1. Adjusted Hazard Ratio of the Usual Percent of Calories from Added Sugar for CVD Mortality Among US Adults Aged >20 Years – NHANES Linked Mortality Files, 1988-2006

Histogram is the distribution of usual percent of calories from added sugar in population. Lines show the adjusted HRs from Cox models. Mid-value of quintile 1 (7.5%) was the reference standard. Model was adjusted for age, sex, race/ethnicity, educational attainment, smoking status, alcohol consumption, physical activity level, family history of CVD, antihypertensive medication use, health eating index score, body mass index, systolic blood pressure, total serum cholesterol and total calories. Solid line indicates point estimates ; dashed lines indicate 95% CIs. CVD indicates cardiovascular disease; HR, hazard ratio; NHANES, National Health and Nutrition Examination Survey.

Yang et al. JAMA Int. Med epub Nov 15, 2013

Hazard ratio for CV mortality based on percent calories as sugar

for US adult population, 1988-2006

Prevalence of diabetes, 2010

Romaguera-Bosch et al. Diabetologia 56:1520, 2013

SSBSSB’’s and BMIs and BMI--adjusted risk of diabetes in adjusted risk of diabetes in EPICEPIC--Interact (Europe)Interact (Europe)

An international longitudinal panel analysis of An international longitudinal panel analysis of diet and diabetesdiet and diabetes

Food and Agriculture Organization (FAO); FAOSTATFood Supply data in kcal/capita/day calculation: Food Supply= ∑Supply Elements - ∑Utilization Elements =

(Production + Import Quantity + Stock Variation – Export Quantity) - (Feed + Seed + Processing + Waste).

Only industrial waste factored in.

Extracted Food Supply data for 2000 and 2007:Total Calories Roots & Tubers, Pulses, Nuts, Vegetables Fruits-Excluding Wine MeatOils CerealsSugar, Sugarcrops & Sweeteners

International Diabetes Federation (IDF)2000 (1st ed) and 2007 (3rd ed)

The World Bank World Development Indicators Databas eGDP expressed in purchasing power parity in 2005 US dollars for

comparability among countries Basu et al. PLoS One, Feb 27, 2013

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Total 204 countries; complete data for 154 countrie s (50 not different)


Basu et al. PLoS One, Feb 27, 2013


Data monitoring and quality

Generalized estimating equations

Conservative fixed effects approach (Hausman test)

Hazard model to control for selection bias (Heckman selection model)

Longitudinal data to determine what preceded diabetes (Granger causality)

Period effects controlled for secular trends that may have occurred as a

result of changes diabetes detection capacity or importation policies.




Data monitoring and quality

Generalized estimating equations

Conservative fixed effects approach (Hausman test)

Hazard model to control for selection bias (Heckman selection model)

Longitudinal data to determine what preceded diabetes (Granger causality)

Period effects controlled for secular trends that may have occurred as a

result of changes diabetes detection capacity or importation policies.

Controlled for:

GDP per capita % population living in urban areas

Obesity % of population over age 65

physical inactivity




Diabetes prevalence rose from 5.5% to 7.0% for 204 countries 2000-2007



Diabetes prevalence rose from 5.5% to 7.0% for 204 countries 2000-2007

Sugar

Sugar+controls

Sugar+controls+period

Overall

Model # countries Effect (95% CI)




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Context

Only changes in sugar availability correlated with changes in diabetes prevalence

Every extra 150 calories increased diabetes prevalence by 0.1%

But if those 150 calories were a can of soda, diabetes prevalence

increased 11-fold, by 1.1%; p <0.001)

These data meet the criteria for Causal Medical Inference (Bradford Hill):

— dose — directionality

— duration — precedence

Controlled for many confounders; obesity exacerbated, but did not confound the effect

These data estimate that 25% of diabetes worldwide is explained by sugar


Limitations

Ecologic, not raw data analysis

Ecologic fallacy: inferences about individuals are based on aggregates

Could the sugar consumers and the diabetes be different people?

Food supply, not food consumption data (wastage, esp. in the U.S.?)

but wastage does not appear to be different based on different foods

And leaving the U.S. out of the analysis did not change the findings

Only one decade (but longitudinal time-series data, not 2 cross-sectional

points in time)

Not a complete dietary analysis

Different techniques used to screen for diabetes in different countries

Different diagnostic criteria for diabetes in different countries

Some countries used self-reported data; many diabetics are undiagnosed

Data includes both Type 1 and Type 2 diabetes



Foodstuffs and metabolic syndromeFoodstuffs and metabolic syndrome

•• TransfatsTransfats•• Branched chain amino acidsBranched chain amino acids•• EthanolEthanol•• FructoseFructose

•• Liver is the only site for energy metabolismLiver is the only site for energy metabolism•• Not insulin regulatedNot insulin regulated•• No glycogen popoff, mitochondria are overwhelmedNo glycogen popoff, mitochondria are overwhelmed

ROS

FRUCTOSE

ROS

ROS

Mitochondria

Peroxisome

ROS

UPR

Celldeath

FRUCTOSE

Acetyl-CoA

ROSATP

ROS

Cellular/metabolic

dysfunction

NH2

EndoplasmicReticulum

Acyl-CoA Lipiddroplet

pSer-IRS-1

PKCεεεε

JNK1

Insulin resistance

Fat deposition

Insulin Receptor

Toward a unifying hypothesis of metabolic syndromeToward a unifying hypothesis of metabolic syndrome

Bremer et al., Pediatrics 129:557. 2012

No drug targetNo drug target

•• Mitochondrial overload promotes lipogenesis, leading to Mitochondrial overload promotes lipogenesis, leading to hepatic insulin resistance, and metabolic syndromehepatic insulin resistance, and metabolic syndrome

•• Mitochondrial overload releases ROSMitochondrial overload releases ROS’’s, which lead to cell s, which lead to cell dysfunction, aging, and deathdysfunction, aging, and death

•• Only options are:Only options are:-- reduce substrate availability (diet)reduce substrate availability (diet)-- reduce hepatic flux (fiber)reduce hepatic flux (fiber)-- increase clearance (exercise)increase clearance (exercise)

Bremer et al., Pediatrics 129:557, 2012

Recognition at the Recognition at the American Heart AssociationAmerican Heart Association

Johnson et al. Circulation 120:1011, 2009

Recommends reduction in added sugar intake from 22 tsp/day to 9 tsp/day (males) and 6 tsp/day (females)

17

Philpott, Mother Jones 2012 (from Bureau of Labor Statistics)

How our food dollars have been reallocatedHow our food dollars have been reallocated

Question 1:Question 1:

Can our Can our ““toxic food environmenttoxic food environment”” be changed be changed

without government/societal intervention? without government/societal intervention?

Especially when there are potentially addictiveEspecially when there are potentially addictive

substances involved?substances involved?

Question 2:Question 2:

Can we afford to wait to enact public health measur esCan we afford to wait to enact public health measur es

when health care will be bankrupt due to when health care will be bankrupt due to

chronic metabolic disease?chronic metabolic disease? Nat Rev Gastroenterol Hepatol 7:251, 2010

J Am Diet Assoc 110:1305, 2010

Further readingFurther reading

Arterioscler Throm Vasc Biol 25:2451, 2005

Is fast food addictive?

Andrea K. Garber, Robert H. Lustig

Curr Drug Abuse Rev 4:146, 2011

Pediatric Annals 41:23, 2012


Arterioscler Throm Vasc Biol 25:2451, 2005

Andrew A. Bremer, M.D., Ph.D. a, Michele Mietus-Snyder, M.D. b, Robert H. Lustig, M.D. c*

Pediatrics 129:557, 2012

Nature 487:27, 2012

Advances in Nutrition 4:1, 2013

Annals NY Academy of Sciences, 1, 2013


18

PLoS One 8:e57873, 2013


Current Opinion Gastroenterology, 29:170, 2013

We have started a nonWe have started a non--profit to provide profit to provide

medical, nutritional and legal analysis and consult ationmedical, nutritional and legal analysis and consult ation

to promote personal and public health vs. Big Foodto promote personal and public health vs. Big Food

INSTITUTE FOR RESPONSIBLE NUTRITIONINSTITUTE FOR RESPONSIBLE NUTRITIONINSTITUTE FOR RESPONSIBLE NUTRITIONINSTITUTE FOR RESPONSIBLE NUTRITIONINSTITUTE FOR RESPONSIBLE NUTRITIONINSTITUTE FOR RESPONSIBLE NUTRITIONINSTITUTE FOR RESPONSIBLE NUTRITIONINSTITUTE FOR RESPONSIBLE NUTRITION

www.responsiblefoods.orgwww.responsiblefoods.orgwww.responsiblefoods.orgwww.responsiblefoods.orgwww.responsiblefoods.orgwww.responsiblefoods.orgwww.responsiblefoods.orgwww.responsiblefoods.org

Please let me know if you would like more informati on!Please let me know if you would like more informati on!

[email protected]@earthlink.net

UCSF Weight Assessment for Teen and Child Health (W ATCH)Andrea Garber, Ph.D., R.D.Kristine Madsen, M.D., M.P.H.Patrika Tsai, M.D., M.P.H.Stephanie Nguyen, M.D. M.A.S.Emily Perito, M.D.Jung Sub Lim, M.D., Ph.D.

UCSF Dept. of Epidemiology and BiostatisticsNancy Hills, M.S.

Touro University Dept. of BiochemistryJean-Marc Schwarz, Ph.D.

San Francisco General Hospital Depts. of Medicine a nd RadiologySanjay Basu, M.D., Ph.D.Susan Noworolski, Ph.D.Kathleen Mulligan, Ph.D.

UC Berkeley Dept. of Nutritional Sciences and Integ rative BiologyPat Crawford, R.D., Ph.D.Paula Yoffe, B.S.

Vanderbilt University Dept. of PediatricsAndrew Bremer, M.D., Ph.D.

Children’s National Medical CenterMichele Mietus-Snyder, M.D.

CollaboratorsCollaborators

fructose and metabolic syndrome: is there a link? no ... · fructose and metabolic syndrome: is...

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