By Robert H. Lustig, MD

ABSTRACT Fructose consumption (as both high fructose corn syrup and sucrose) has increased coincidentally with the

worldwide epidemics of obesity and metabolic syndrome.

Fructose is a primary contributor to human disease as it

is metabolized in the liver differently to glucose, and is

more akin to that of ethanol. When consumed in large

amounts, fructose promotes the same dose-dependent

toxic effects as ethanol, promoting hypertension, hepatic

and skeletal muscle insulin resistance, dyslipidemia and

fatty liver disease. Also similar to ethanol, through direct

stimulation of the central nervous system “hedonic

pathway” and indirect stimulation of the “starvation pathway,”

fructose induces alterations in central nervous system

energy signaling that lead to a vicious cycle of excessive

consumption, with resultant morbidity and mortality.

Fructose from any source should be regarded as

“alcohol without the buzz.” Obesity prevention

and treatment is ineffective in the

face of the current “fructose glut”

in our food supply. We must learn

from our experiences with ethanol

and nicotine that regulation of

the food industry, along with individual

and societal education,

will be necessary to combat this

fructose epidemic.

INTRODUCTION

As America’s (and the world’s)

collective girth continues to increase,

we ponder the answer to our

dilemma: Who or what are to blame

for the obesity epidemic? That depends

upon who you ask. The Institute of Medicine says

it is an interaction between genetics and environment.

Well, our genetics have not changed in 30 years but our

environment sure has, and in particular, our diet. The distribution

curve for Body Mass Index (BMI) shows that all

segments of the population are increasing in weight (1),

so whatever is happening is clearly pervasive and insidious.

Even developing countries that have adopted a Western

diet for convenience and expense have paid for it by

manifesting the same obesity prevalence, co-morbidity

profi les and mortality (2).

SECULAR TRENDS IN FRUCTOSE

CONSUMPTION

One of the striking features of the modern Western diet

is its reliance on refi ned carbohydrate as the predominant

energy source. Due to the “low-fat” admonition by

the United States Department of Agriculture (USDA),

American Medical Association and American Heart Association

(AHA) in the early 1980’s, the percentage of fat

in the Western diet has reduced from 40% to 30% over

the past 25 years; which has resulted in the percentage of

carbohydrate rising from 40% to 55%; coinciding with

the obesity epidemic. Of this, a sizeable and

ever-increasing portion of the diet is attributable

to monosaccharides and disaccharides

used to sweeten foods

and drinks. Furthermore, in response

to the market for lower

fat fare, food companies have

chosen to substitute disaccharides

to maintain palatability of

processed foods. Until recently

the most commonly used sugar

in the U.S. diet was disaccharide

sucrose (e.g. cane or beet

sugar) which is composed of 50%

fructose and 50% glucose. However,

in North America and many other

countries, due to its abundance, sweetness,

and low price, high-fructose corn syrup

(HFCS) which contains between 42% and 55% of the

monosaccharide fructose, has overtaken sucrose as the

most ubiquitous caloric sweetener. These factors have led

to an inexorable rise in fructose consumption. Prior to

1900, Americans consumed approximately 15 gm/day of

fructose, mainly through fruits and vegetables. Prior to

World War II this amount had increased to 24 gm/day. By

THE BARIATRICIAN • 11

1977 fructose intake was 37 gm/day; by 1994 55 gm/day;

and currently Vos et al. estimates that adolescents average

72.8 gm/day (3). Thus current fructose consumption

has incrementally increased 5-fold compared to a century

ago. Disappearance data over the past 25 years from Economic

Research Service (ERS) of the USDA also supports

this secular trend. The ERS documents partial substitution

for sucrose by HFCS; however annual per capita

total caloric sweetener usage has increased from 73 to 95

lbs in that interval. Although soda has received most of

the attention (4, 5), high fruit juice intake (sucrose) is also

associated with childhood obesity, especially by lower income

families (6), although it is not captured in the ERS.

Thus, after adjustment for juice intake, per capita consumption

of mono- and disaccharides is at approximately

113 lbs/yr or 1/3 lb/day for all Americans.

HOW WE GOT HERE: POLITICAL,

ECONOMIC, AND MEDICAL DRIVERS

OF FRUCTOSE CONSUMPTION

The reader is referred to The Omnivore’s Dilemma (7)

for a complete discussion of the political and economic

factors that led to the secular trend in fructose consumption.

In brief, the 1966 industrialization of the discovery

of the glucose oxidase process to convert glucose to fructose

(8), combined with a directed policy by the

USDA in the 1970’s to reduce the price of food

by advancing growth and production of corn as

a dietary staple, provided the political and economic

impetus for this trend. In addition, during

this decade the medical establishment focused

on dietary reduction of coronary heart disease.

Two competing schools of thought dominated

this discussion. John Yudkin, a British physiologist

and nutritionist, championed the anti-sugar

movement. His work “Pure, White, and Deadly”

(9) espoused the primary role of sugar in human

disease. Conversely, the anti-saturated fat

movement was spearheaded by Minnesota epidemiologist

Ancel Keys. His work, the Seven

Countries: study (10), was one of the fi rst multivariate

linear regression analyses. A review

of this document (P. 262) notes: “The fact that

the incidence of coronary heart disease was signifi

cantly correlated with the average percentage

of calories from sucrose in the diets is explained

by the intercorrelation of sucrose with saturated

fat. Partial correlation analysis demonstrates that

with saturated fat constant there was no signifi -

cant correlation between dietary sucrose and the incidence

of coronary heart disease” (10). However, Keys neglected

to perform the converse analysis demonstrating that the

effect of saturated fat on cardiovascular disease (CVD)

was independent of sucrose. In other words, sucrose and

saturated fat co-migrated; it is impossible to tease out the

relative contributions of sucrose vs. saturated fat on CVD

from this study.

Furthermore, the medical establishment based their

low-fat recommendations on the goal of LDL reduction;

however, several studies have since demonstrated little to

no effect of low-fat diets on weight gain or CVD events

(11, 12). However, we now know that there are two LDL’s.

The large buoyant or Type A LDL is driven by dietary fat,

but is neutral from a cardiovascular standpoint. The small

dense or Type B LDL, which is driven by carbohydrate

and fructose (13), is the species associated with CVD (14).

Conversely, we have ample evidence that triglyceride

(TG) is a major risk factor for CVD (15) and that fructose

consumption is a primary contributor to TG accumulation

(16, 17). A recent analysis has led the AHA Nutrition

Committee to publish a policy statement on the negative

role of sugars in the pathogenesis of CVD (18).

Figure 1: Effects of introduction of corn sweeteners (HFCS) to

the American diet in 1975 on: a) the U.S. Producer Price Index

for sugar; b) the U.S. and international (London) price of

sugar; and c) the U.S. retail price of sugar and on HFCS. Data

document stabilization or lowering of sugar prices.

12 • THE BARIATRICIAN

HIGH FRUCTOSE CORN SYRUP (HFCS)

VS. SUCROSE

Although many consumer activist groups have specifi -

cally vilifi ed HFCS as the cause of obesity and CVD, scientifi

c studies of acute satiety vs. energy intake support

the notion that HFCS is not metabolically different from

sucrose (19-27). This has led to a vociferous campaign by

the Corn Refi ners Association to infl uence the debate on

fructose consumption by equating HFCS with sucrose,

suggesting that it is no different, “natural,” and it is safe

(see www.sweetsurprise.com). Indeed, the distinction between

HFCS and sucrose is not metabolic (as they are

essentially equivalent), but rather economic. The introduction

of HFCS to the Western diet in 1975 resulted in

stability of the U.S. Producer Price Index for sugar, and

sizeable reductions in the U.S. and international price of

sugar (Fig. 1). HFCS on average costs about one third

that of sucrose. This, along with changes in the Farm Bill

and food policy, promoted the addition of fructose to our

collective diets; not just in soft drinks and juice, but in

salad dressing, condiments, baked goods and virtually

every processed food, which raised our total consumption

5-fold in the last 100 years. Below, it becomes clear that it

is not the specifi c vehicle (sucrose vs. HFCS) that makes

it unsafe, but rather the total dose of fructose.

CORRELATION OF FRUCTOSE CONSUMPTION

WITH DISEASE

Numerous reviews have indirectly implicated fructose

consumption in the current epidemics of obesity and

Type 2 Diabetes Mellitus (T2DM) (28-30). Correlative

studies in humans link soft drink consumption with energy

overconsumption, body weight, poor nutrition (31)

and T2DM (32). Similarly, juice consumption also correlates

with risk for T2DM (33), suggesting that excessive

fructose consumption is playing a role in the epidemics

of insulin resistance, obesity, hypertension, dyslipidemia,

and T2DM in humans (28, 34-38). Collectively, this constellation

of fi ndings is referred to as the Metabolic Syndrome

(MetS). Conversely, early short-term prospective

studies limiting soft drink ingestion in children have met

with some success in stabilization of weight and CVD

parameters (39, 40).

MECHANISMS OF FRUCTOSE

TOXICITY

Although others have already pointed out the unique

metabolic effects of fructose (28-30, 34, 36, 38), this review

was written to outline the unique, pernicious, and

dose-dependent toxic effects of fructose in the pathogenesis

of both metabolic disease and excessive consumption.

Fructose is similar in its metabolism to a more familiar

toxin, ethanol. Therefore, it is necessary to delineate the

hepatic outcomes of metabolism of glucose and ethanol

fi rst. In each case, we will follow a 120 kcal oral bolus of

each carbohydrate.

Hepatic Glucose Metabolism

Glucose is the body’s preferred carbohydrate substrate

for energy metabolism. Each cell in the body can utilize

glucose for energy. Upon ingestion of 120 kcal of glucose

(e.g. two slices of white bread) (Fig. 2a), 24 kcal

(20%) enter the liver; the remaining 96 kcal (80%) of the

glucose bolus are utilized by other organs (41). Plasma

glucose levels rise, insulin is released by the pancreas

which binds to its receptor on the liver, generating two

metabolic signals (42). The fi rst is the phosphorylation of

the forkhead protein Foxo1; which reduces the expression

of the enzymes of gluconeogenesis (GNG), to keep blood

sugar levels from rising (43). The second is an increase

in the expression of the transcription factor Akt, which

causes the majority of G6P (about 20 kcal) to be deposited

as the non-toxic storage carbohydrate glycogen. Only a

small amount of G6P is broken down by the Embden-

Meyerhoff glycolytic pathway to pyruvate (approx 4 kcal).

Pyruvate enters the mitochondria where it is converted

to acetyl-CoA, which then participates in the Krebs tricarboxylic

acid (TCA) cycle, which generates adenosine

triphosphate (ATP), the chemical storage form of energy,

and carbon dioxide. Any pyruvate not metabolized in the

Figure 2: Hepatic metabolism of 120 kcal carbohydrate:

a) glucose; b) ethanol; and c) sucrose (fructose).

Similarities in hepatic metabolism between

ethanol and fructose are highlighted.

THE BARIATRICIAN • 13

mitochondrial TCA cycle exits back into the cytoplasm

as citrate through the “citrate shuttle” (44). This small

amount of citrate (perhaps 0.5 kcal) can serve as substrate

for the process of de novo lipogenesis, which turns excess

citrate into free fatty acids (FFA). These can then be

packaged with apolipoprotein B (apoB) to form very low

density lipoproteins (VLDL; measured in the triglyceride

fraction), which are transported out of the liver, and can

serve as a substrate for atherogenesis or obesity. Thus,

in response to a 120 kcal glucose bolus, only a tiny fraction

(less than 1 kcal) contributes to adverse metabolic

outcomes.

Hepatic Ethanol Metabolism

Ethanol is a naturally occurring carbohydrate, but is

also recognized as both an acute central nervous system

(CNS) toxin and chronic hepatotoxin, due to its unique

dose-dependent hepatic metabolism (Fig. 2b). Upon ingestion

of 120 kcal of ethanol (e.g. 1.5 oz. of 80 Proof

hard spirits), approximately 10% (12 kcal) is metabolized

within the stomach and intestine as a fi rst-pass effect, and

10% is metabolized by the brain and other organs (41).

Thus approximately 96 calories reach the hepatocyte (4

times more than with glucose). Ethanol enters the liver

and is converted by alcohol dehydrogenase 1B to form the

toxic substrate acetaldehyde, which in high dosage can

promote free radical formation and toxic damage. Acetaldehyde

is then quickly metabolized by the enzyme aldehyde

dehydrogenase 2 to acetic acid, which can then enter

the mitochondrial TCA cycle (as per glucose, above); but

now, a large amount of excess citrate is formed (perhaps

70 kcal), which exits into the cytosol and then participates

in synthesis of fatty acids through de novo lipogenesis.

Thus, the metabolism of an ethanol bolus is likely

to cause the liver to increase FFA and VLDL production,

and contribute to dyslipidemia. Intrahepatic lipid and

ethanol are both able to induce the transcription of the

enzyme c-jun N-terminal kinase-1 (JNK-1) (45). This enzyme

is the bridge between hepatic energy metabolism

and infl ammation; and once induced, begins the infl ammatory

cascade (46). As part of its infl ammatory action,

JNK-1 activation induces serine phosphorylation of insulin

receptor substrate-1 (IRS-1) in the liver (47), leading

to hepatic insulin resistance, hepatic triglyceride accumulation

in lipid droplets, with resultant infl ammation (48);

eventually leading to alcoholic steatohepatitis, and ultimately

to cirrhosis. Lastly, FFA can exit the liver, which

can contribute to skeletal muscle insulin resistance. The

VLDL produced (perhaps 30 kcal) can be transported to

the adipocyte to serve as a substrate for obesity, or participate

in atherogenic plaque formation. Thus, in response

to a 120 kcal ethanol bolus, a large fraction (perhaps 40

kcal) can contribute to disease.

Hepatic Fructose Metabolism and the MetS

The liver is the only organ possessing the Glut5 fructose

transporter and is solely responsible for fructose metabolism

(49). Upon ingestion of 120 kcal of sucrose (e.g.

8 oz. of orange juice; composed of 60 kcal glucose and 60

kcal fructose) (Fig. 2c), the entire 60 kcal fructose bolus

reaches the liver, along with 20% of the glucose bolus

(12 kcal), for a total of 72 kcal; in other words, the liver

must handle triple the substrate as it did for glucose alone

Figure 2: Hepatic metabolism of 120 kcal carbohydrate:

a) glucose; b) ethanol; and c) sucrose (fructose).

Similarities in hepatic metabolism between

ethanol and fructose are highlighted.

Figure 2: Hepatic metabolism of 120 kcal carbohydrate:

a) glucose; b) ethanol; and c) sucrose (fructose).

Similarities in hepatic metabolism between

ethanol and fructose are highlighted.

14 • THE BARIATRICIAN

(50). The fructose is immediately converted to fructose-1-

phosphate (F1P) by the enzyme fructokinase (51), depleting

the hepatocyte of intracellular phosphate. This leads

to activation of the enzyme adenosine monophosphate

(AMP) deaminase-1, which converts the adenosine phosphate

breakdown products into the cellular waste product

uric acid (52, 53). Buildup of urate in the circulation inhibits

endothelial nitric oxide synthase (eNOS), resulting

in decreased nitric oxide (NO) and contributing to hypertension

(54-56). Almost the entire F1P load (50 kcal) is

metabolized directly to pyruvate, entering the mitochondrial

TCA cycle; again, excess citrate (perhaps 40 kcal)

will be exported to the cytosol, to participate in de

novo lipogenesis, with resultant dyslipidemia from

FFA and VLDL formation. Alternatively, a proportion

(10 kcal) of early glycolytic intermediaries

will recombine to form fructose-1,6-bisphosphate,

which then also combines with glyceraldehyde to

form xylulose-5-phosphate (X5P) (57, 58), which

activates carbohydrate response element binding

protein (ChREBP), also stimulating de novo lipogenesis

and contributing to fructose-induced dyslipidemia

(13, 17, 59-62). FFA export from the liver

leads to uptake into skeletal muscle, resulting in

skeletal muscle insulin resistance (63, 64). Some of

the FFA will precipitate in the hepatocyte, leading

to lipid droplet accumulation (65). Intrahepatic lipid

and FIP are both able to induce the transcription of

JNK-1 (45), which induces serine phosphorylation

of insulin receptor substrate-1 (IRS-1) in the liver

(47), thereby preventing normal insulin-stimulated

tyrosine phosphorylation of IRS-1, and promoting hepatic

insulin resistance. This will prevent Foxo1 from becoming

phosphorylated; Foxo1 enters the nucleus and gluconeogenesis

ensues, raising blood sugar and furthering the

hyperinsulinemia (43). Thus, in response to a 120 kcal

sucrose bolus, a large fraction (perhaps 40 kcal) can contribute

to disease.

Comparison of Hepatic Metabolic Detriments of Fructose

vs. Ethanol

As the brain does not possess the Glut5 transporter,

fructose does not lead to the acute CNS toxic effects like

those of ethanol. However, its hepatic metabolic profi le

strongly resembles that of ethanol. Table 1 demonstrates

the hepatic burden of a can of beer vs. a can of soda. Both

contain 150 kcal per 12 oz. can. The fi rst pass effect of

ethanol in the stomach and intestine removes 10% of the

ethanol. In the case of beer (3.6% ethanol and 6.6% other

carbohydrate (e.g. maltose, which is a glucose disaccharide),

this amounts to 92 calories reaching the liver, while

for soda this amounts to 90 calories reaching the liver.

Thus, hepatic metabolism of either fructose or ethanol results

in the majority of energy substrate being converted

to lipid, without any insulin regulation or ability to be

diverted to non-toxic intermediaries such as glycogen.

Intrahepatic lipid generation promotes infl ammation and

insulin resistance (66). Indeed, the hepatic metabolic

strain of beer and soda are congruous; such that beer or

sugar sweetened beverage consumption similarly led to

visceral adiposity, insulin resistance, and the metabolic

syndrome.

FRUCTOSE EFFECTS ON THE CNS LEAD

TO EXCESSIVE CONSUMPTION

The limbic structures central to the hedonic pathway

that motivates the “reward” of food intake are the ventral

tegmental area (VTA) and nucleus accumbens (NA). The

NA is also referred to as the “pleasure center” of the brain

(67) and is the seat of goal-oriented behavior. This is also

the brain area responsive to nicotine, morphine, cannabinoids,

amphetamine, nicotine, and ethanol (68). Food intake

is a result of activation of the reward pathway; for

example, administration of morphine to the NA increases

food intake in a dose-dependent fashion (69). Dopamine

neurotransmission from the VTA to the NA mediate the

reward properties of food (70). Leptin and insulin receptors

are co-localized in VTA neurons (71), and both

hormones have been implicated in modulating rewarding

responses to food and other pleasurable stimuli. Leptin

decreases VTA-NA activity, and extinguishes reward for

food (72, 73).

Soda (12 oz can) Beer (12 oz can)

Calories 150 150

Percent Carbohydrate 10.5% (sucrose) 3.6% (alcohol)

5.3% (other

carbs)

Calories From:

Fructose 75 (4.1 kcal/gm)

Alcohol 90 (7 kcal/gm)

Other carbs 75 (glucose) 60 (maltose)

1st pass stomachintestine

metabolism

Calories Reaching

Liver

90 92

Table 1: Similarities between soda and beer with respect

to hepatic handling

THE BARIATRICIAN • 15

However, increasing the palatability of food by addition

of fructose undermines normal satiety signals, and

as a result increases total caloric consumption both in

direct and indirect ways. Direct effects of fructose include

motivation of food intake independent of energy

need (74-79). Indeed, in animal models, sugar consumption

can lead to dependence (80). There are four indirect

effects of fructose on excessive food consumption. First,

fructose does not stimulate a leptin rise, thus contributing

acutely to a diminished sense of satiety (81). Secondly,

fructose induces hypertriglyceridemia, which reduces

leptin transport across the blood-brain barrier (82). The

third is chronic hyperinsulinemia, which interferes with

leptin signal transduction at the second messenger level

(83). By reducing leptin’s ability to extinguish hunger at

the hypothalamus, and likely leptin’s ability to extinguish

the dopamine reward signal at the NA (84, 85), chronic

hyperinsulinemia fosters a sense of starvation and need

for reward, leading to increased caloric intake (86). Lastly,

fructose has been shown to decrease the production in

hypothalamic neurons of malonyl-CoA, which may help

promote a sense of energy inadequacy (87). Together with

promoting hepatic and muscle insulin resistance, fructose

ingestion may alter the hedonic response to food to drive

excessive energy intake, setting up a positive feedback

cycle of hepatic and CNS dysfunction, leading to persistent

overconsumption. Whether this CNS “vicious cycle”

is tantamount to true addiction or merely psychological

dependence is not yet clear. What is clear is that obesity,

depression, and sugar craving and consumption are linked

epidemiologically and mechanistically (88).

SUMMARY

The hepatic metabolic pathways outlined above demonstrate

that fructose is a dose-dependent chronic hepatotoxin.

Fructose is capable of promoting hepatic and

skeletal muscle insulin resistance, hyperinsulinemia,

dyslipidemia, hepatic lipid deposition, and infl ammation;

similar to the dose-dependent toxic effects of ethanol.

Furthermore, the central pathways outlined above demonstrate

that fructose is capable of promoting hypothalamic

leptin resistance and activation of the reward pathway, resulting

in an abnormal drive to continuous consumption,

also similar to ethanol. Indeed, fructose may be described

as “alcohol without the ‘buzz’”.

The metabolic and central similarities between fructose

and ethanol are striking. Other stimulators of the nucleus

accumbens have led to disease and societal deterioration,

and thus have required education, regulation, and in some

instances, interdiction. America attempted ethanol interdiction

(prohibition) in the 1930’s, but was unsuccessful; it

will be even harder to restrict fructose consumption. Furthermore,

the Food and Drug Administration has given

fructose GRAS (generally regarded as safe) status, thus

declining to regulate its use. While many obesity programs

counsel voluntary reductions in personal fructose

consumption, recidivism is frequent; thus, a major effort

in public health education seems daunting. Nonetheless,

we have made signifi cant progress with ethanol reduction,

mostly through regulation. Soda taxes have recently

been proposed both in New York and California, and legislation

for the removal of soft drinks from schools has

been enacted in several states. However, until Yudkin’s

prophecies of 1972 are taken seriously and the public is

made aware of the specifi c dangers of the fructose fraction

of our current Western diet, our current vicious cycle

of consumption and disease will continue.

ACKNOWLEDGMENTS

The author would like to thank Jean-Marc Schwarz,

Ph.D., for his insight and assistance in vetting all the carbohydrate

pathways and biochemistry elaborated in this

article, and Andrea Garber, Ph.D., R.D., Kristine Madsen,

M.D., Patrika Tsai, M.D., M.P.H., Michele Mietus-

Snyder, M.D., and Jung Sub Lim, M.D., Ph.D. for useful

discussions and clinical excellence. ?

About the Author

Robert H. Lustig, MD is Professor of Pediatrics in the

Division of Endocrinology at University of California,

San Francisco. He is a neuroendocrinologist, with specifi

c interests in the central regulation of energy balance.

He is interested in the interactions between leptin

and insulin and how these two hormones are perturbed

to drive weight gain. He is a member of the Endocrine

Society Obesity Task Force and other advisory groups.

References

1. Hill JO, Wyatt HR, Reed GW, Peters JC 2003 Obesity

and the environment: where do we go from here? Science

299:853-855.

2. Ebbeling CB, Pawlak DB, Ludwig DS 2002 Childhood

obesity: public-health crisis, common sense cure. The Lancet

360:473-482.

3. Vos MB, Kimmons JE, Gillespie C, Welsh J, Blanck HM

2008 Dietary fructose consumption among US children and

adults: the Third National Health and Nutrition Examination

Survey. Medscape J. Med. 10:160.

4. Ludwig DS, Peterson KE, Gortmaker SL 2001 Relation

between consumption of sugar-sweetened drinks and childhood

obesity: a prospective,observational analysis. The

16 • THE BARIATRICIAN

Lancet 357:505-508.

5. Warner ML, Harley K, Bradman A, Vargas G, Eskenazi B

2006 Soda consumption and overweight status of 2-year-old

Mexican-American children in California. Obesity 14:1966-

1974.

6. Faith MS, Dennison BA, Edmunds LS, Stratton HH 2006

Fruit juice intake predicts increased adiposity gain in children

from low-income families: weight status-by-environment

interaction. Pediatrics 118:2066-2075.

7. Pollan M 2006 The Omnivore’s Dilemma. Penguin, New

York.

8. Marshall RO, Kooi ER 1957 Enzymatic conversion of Dglucose

to D-fructose. Science 125:648-649.

9. Yudkin JS 1972 Pure, white, and deadly. Viking Penguin,

New York.

10. Keys A 1980 Seven countries: a multivariate analysis of

death and coronary heart disease. Harvard University Press,

Cambridge.

11. Howard BV, Manson JE, Stefanick ML, Beresford SA,

Frank G, Jones B, Rodabough RJ, Snetselaar L, Thomson C,

Tinker L, Vitolins M, Prentice R 2006 Low-fat dietary pattern

and weight change over 7 years: the Women’s Health Initiative

Dietary Modifi cation Trial. JAMA 295:39-49.

12. Howard BV, Van Horn L, Hsia J, Manson JE, Stefanick

ML, Wassertheil-Smoller S, Kuller LH, LaCroix AZ, Langer

RD, Lasser NL, Lewis CE, Limacher MC, Margolis KL,

Mysiw WJ, Ockene JK, Parker LM, Perri MG, Phillips L,

Prentice RL, Robbins J, Rossouw JE, Sarto GE, Schatz IJ,

Snetselaar LG, Stevens VJ, Tinker LF, Trevisan M, Vitolins

MZ, Anderson GL, Assaf AR, Bassford T, Beresford SA, Black

HR, Brunner RL, Brzyski RG, Caan B, Chlebowski RT, Gass

M, Granek I, Greenland P, Hays J, Heber D, Heiss G, Hendrix

SL, Hubbell FA, Johnson KC, Kotchen JM 2006 Lowfat

dietary pattern and risk of cardiovascular disease: the

Women’s Health Initiative Randomized Controlled Dietary

Modifi cation Trial. JAMA 295:655-666.

13. Aeberli I, Zimmermann MB, Molinari L, Lehmann R,

l’Allemand D, Spinas GA, Berneis K 2007 Fructose intake

is a predictor of LDL particle size in overweight schoolchildren.

Am. J. Clin. Nutr. 86:1174-1178.

14. Krauss RM 2001 Atherogenic lipoprotein phenotype and

diet-gene interactions. J. Nutr. 131:340S-343S.

15. Austin MA, Hokanson JE, Edwards KL 1998 Hypertriglyceridemia

as a cardiovascular risk factor. Am. J. Cardiol.

81:7B-12B.

16. Fried SK, Rao SP 2003 Sugars, hypetriglyceridemia, and

cardiovascular disease. Am. J. Clin. Nutr. 78:873S-880S.

17. Teff KL, Elliott SS, Tschop M, Kieffer TJ, Rader D, Heiman

M, Townsend RR, N.L. K, D’Alessio D, Havel PJ 2004

Dietary fructose reduces circulating insulin and leptin, attenuates

postprandial suppression of ghrelin, and increases

triglycerides in women. J. Clin. Endocrinol. Metab. 89:2963-

2972.

18. Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre

M, Lustig RH, Sacks F, Steffen L, Wylie-Rosett J (in press)

Effects of sugars on cardiovascular disease and cardiovascular

disease risk factors. Circulation.

19. Soenen S, Westerterp-Plantenga MS 2007 No differences

in satiety or energy intake after high-fructose corn syrup,

sucrose, or milk preloads. Am. J. Clin. Nutr. 86:1586-1894.

20. Anderson GH 2007 Much ado about high-fructose corn

syrup in beverages: the meat of the matter. Am. J. Clin. Nutr.

86:1577-1578.

21. Bray GA 2007 How bad is fructose? Am. J. Clin. Nutr.

86:895-896.

22. Bowen J, Noakes M, Clifton PM 2007 Appetite hormones

and energy intake in obese men after consumption of fructose,

glucose, and whey beverages. Int. J. Obes. 31:1696-

1703.

23. Melanson KJ, Angelopoulos TJ, Nguyen V, Zukley L,

Lowndes J, Rippe JM 2008 High-fructose corn syrup, energy

intake, and appetite regulation Am. J. Clin. Nutr. 88:1738S-

1744S.

24. Stanhope KL, Havel PJ 2008 Endocrine and metabolic

effects of consuming beverages sweetened with fructose, glucose,

sucrose, or high-fructose corn syrup. Am. J. Clin. Nutr.

88:1733S-1737S.

25. Duffey KJ, Popkin BM 2008 High-fructose corn syrup: is

this what’s for dinner? . Am. J. Clin. Nutr. 88:1722S-1732S.

26. White JS 2008 Straight talk about high-fructose corn syrup:

what it is and what it ain’t Am. J. Clin. Nutr. 88:1716S-

1721S.

27. Fulgoni V 2008 High-fructose corn syrup: everything

you wanted to know, but were afraid to ask Am. J. Clin. Nutr.

88:1715S.

28. Le KA, Tappy L 2006 Metabolic effects of fructose. Curr.

Opin. Nutr. Metab. Care 9:469-475.

29. Rutledge AC, Adeli K 2007 Fructose and the metabolic

syndrome: pathophysiology and molecular mechanisms.

Nutr. Rev. 65:S13-S23.

30. Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI,

Kang DH, Gersch MS, Benner S, Sanchez-Lozada LG 2007

Potential role of sugar (fructose) in the epidemic of hypertension,

obesity and the metabolic syndrome, diabetes, kidney

disease, and cardiovascular disease. Am. J. Clin. Nutr.

86:899-906.

31. Vartanian LR, Schwartz MB, Brownell KD 2007 Effects

of soft drink consumption on nutrition and health: a systematic

review and meta-analysis. Am. J. Public Health 97:667-

675.

32. Schulze MB, Manson JE, Ludwig DS, Colditz GA, Stampfer

MJ, Willett WC, Hu FB 2004 Sugar-sweetened beverages,

weight gain, and incidence of type 2 diabetes in young and

middle-aged women. JAMA 292:927-934.

33. Bazzano LA, Li TY, Joshipura KJ, Hu FB 2008 Intake

of fruit, vegetables, and fruit juices and risk of diabetes in

women. Diab. Care 31:1311-1317.

34. Havel PJ 2005 Dietary fructose: implications for dysTHE

BARIATRICIAN • 17

regulation of energy homeostasis and lipid/carbohydrate

metabolism. Nutr. Rev. 63:133-157.

35. Gross LS, Li S, Ford ES, Liu S 2004 Increased consumption

of refi ned carbohydrates and the epidemic of type 2 diabetes

in the United States: an ecologic assessment. Am. J.

Clin. Nutr. 79:774-779.

36. Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ 2002

Fructose, weight gain, and the insulin resistance syndrome.

Am. J. Clin. Nutr. 76:911-922.

37. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs

JB, D’Agostino RB, Gaziano JM, Vasan RS 2007 Soft drink consumption

and risk of developing cardiometabolic risk factors and

the metabolic syndrome in middle-aged adults in the community.

Circulation 116:480-488.

38. Brown CM, Dulloo AG, Montani JP 2008 Sugary drinks in the

pathogenesis of obesity and cardiovascular diseases. Int. J. Obes.

32:528-534.

39. James J, Thomas P, Cavan D, Kerr D 2004 Preventing childhood

obesity by reducing consumption of carbonated drinks:

cluster randomised controlled trial. BMJ 328:1237.

40. Ebbeling CB, Feldman HA, Osganian SK, Chomitz VR, Ellenbogen

SJ, Ludwig DS 2006 Effects of decreasing sugar-sweetened

beverage consumption on body weight in adolescents: a randomized,

controlled pilot study. Pediatrics 117:673-680.

41. Zakhari S 2006 Overview: how is alcohol metabolized by the

body? Alcohol Res. Health 29:245-254.

42. Brown MS, Goldstein JL 2008 Selective versus total insulin

resistance: a pathogenic paradox. Cell Metab. 7:95-96.

43. Qu S, Su D, Altomonte J, Kamagate A, He J, Perdomo G, Tse T,

Jiang Y, Dong HH 2007 PPAR? mediates the hypolipidemic action

of fi brates by antagonizing FoxO1. Am. J. Physiol. Endocrinol.

Metab. 292:E421-E434.

44. Scott CC, Heckman CA, Snyder F 1979 Regulation of ether

lipids and their precursors in relation to glycolysis in cultured

neoplastic cells. Biochim. Biophys. Acta 575:215-224.

45. Samuel VT, Liu ZX, Qu X, Elder BD, Bilz S, Befroy D, Romanelli

AJ, Shulman GI 2004 Mechanism of hepatic insulin resistance in

non-alcoholic fatty liver disease. J. Biol. Chem. 279:32345-32353.

46. Hirosumi J, Tuncman G, Chang L, GoÅNrgu?n CZ, Uysal KT,

Maeda K, Karin M, Hotamisligil GS 2002 A central role for JNK

in obesity and insulin resistance. Nature 420:333-336.

47. Tuncman G, Hirosumi J, Solinas G, Chang L, Karin M, G.S.

H 2006 Functional in vivo interactions between JNK1 and JNK2

isoforms in obesity and insulin resistance. Proc. Natl. Acad. Sci.

USA 103:10741-10746.

48. Onishi Y, Honda M, Ogihara T, Sakoda H, Anai M, Fujishiro

M, Ono H, Shojima N, Fukushima Y, Inukai K, Katagiri H, Kikuchi

M, Oka Y, Asano T 2003 Ethanol feeding induces insulin resistance

with enhanced PI 3-kinase activation. Biochem. Biophys.

Res. Comm. 303:788-794.

49. Douard V, Ferraris RP 2008 Regulation of the fructose transporter

Glut5 in health and disease. Am. J. Physiol. Endocrinol.

Metab. 295:E227-E237.

50. Dirlewanger M, Schneiter P, Jequier E, Tappy L 2000 Effects

of fructose on hepatic glucose metabolism in humans. Am. J.

Physiol. Endocrinol. Metab. 279:E907-E911.

51. Fiaschi E, Baggio B, Favaro S, Antonello A, Camerin E, Todesco

S, Borsatti A 1977 Fructose-induced hyperuricemia in essential

hypertension. Metabolism 26.

52. Gao XB, Qi L, Qiao N, Choi HK, Curhan G, Tucker KL, Ascherio

A 2007 Intake of added sugar and sugar-sweetended drink

and serum uric acid concentration in U.S. men and women. Hypertension

50:306-312.

53. Taylor EN, Curhan GC 2008 Fructose consumption and the

risk of kidney stones. Kidney Int. 73:489-496.

54. Savoca MR, Evans CD, Wilson ME, Harshfi eld GA, Ludwig

DA 2004 The association of caffeinated beverages with blood

pressure in adolescents. Arch. Ped. Adolesc. Med. 158:473-477.

55. Nakagawa T, Tuttle KR, Short R, Johnson RJ 2006 Hypothesis:

fructose-induced hyperuricemia as a causal mechanism for the

epidemic of the metabolic syndrome. Nat. Clin. Pract. Nephrology

1:80-86.

56. Nguyen S, Choi HK, Lustig RH, Hsu CY (in press) The association

of sugar sweetened beverage consumption with serum uric

acid and blood pressure in a nationally representative sample of

adolescents J. Pediatr.

57. Bonsignore A, Pontremoli S, Mangiarotti G, De Flora A, Mangiarotti

M 1962 A direct interconversion: D-fructose 6-phosphate

to sedoheptulose 7-phosphate and D-xylulose 5-phosphate catalyzed

by the enzymes transketolase and transaldolase. J. Biol.

Chem. 237:3597-3602.

58. Kabashima T, Kawaguchi T, Wadzinski BE, Uyeda K 2003 Xylulose

5-phosphate mediates glucose-induced lipogenesis by xylulose

5-phosphate-activated protein phosphatase in rat liver. Proc.

Natl. Acad. Sci. USA 100:5107-5112.

59. Faeh D, Minehira K, Schwarz JM, Periasami R, Seongsu P,

Tappy L 2005 Effect of fructose overfeeding and fi sh oil administration

on hepatic de novo lipogenesis and insulin sensitivity in

healthy men. Diabetes 54:1907-1913.

60. Lê KA, Faeh D, Stettler R, Ith M, Kreis R, Vermathen P, Boesch

C, Ravussin E, Tappy L 2006 A 4-wk high-fructose diet alters lipid

metabolism without affecting insulin sensitivity or ectopic lipids

in healthy humans. Am. J. Clin. Nutr. 84:1374-1379.

61. Hellerstein MK, Schwarz JM, Neese RA 1996 Regulation of

hepatic de novo lipogenesis in humans. Ann. Rev. Nutr. 16:523-

557.

62. Schwarz JM, Linfoot P, Dare D, Aghajanian K 2003 Hepatic

de novo lipogenesis in normoinsulinemic and hyperinsulinemic

subjects consuming high-fat, low-carbohydrate and low-fat, highcarbohydrate

isoenergetic diets. Am. J. Clin. Nutr. 77:43-50.

63. Montell E, Turini M, Marotta M, Roberts M, Noé V, Ciudad CJ,

Macé K, Gómez-Foix AM 2001 DAG accumulation from saturated

fatty acids desensitizes insulin stimulation of glucose uptake in

muscle cells. Am. J. Physiol. Endocrinol. Metab. 280:E229-E237.

64. Krssak M, Falk Petersen K, Dresner A, DiPietro L, Vogel SM,

Rothman DL, Roden M, Shulman GI 1999 Intramyocellular lipid

concentrations are correlated with insulin sensitivity in humans:

a 1H NMR spectroscopy study. Diabetologia 42:113-116.

65. Cave M, Deaciuc I, Mendez C, Song Z, Joshi-Barve S, Barve

S, McClain C 2007 Nonalcoholic fatty liver disease: predisposing

factors and the role of nutrition. J. Nutr. Biochem. 18:184-195.

66. Postic C, Girard J 2008 Contribution of de novo fatty acid

synthesis to hepatic steatosis and insulin resistance: lessons from

genetically engineered mice. J. Clin. Invest. 118:829-838.

67. Phillips PE, Walton ME, Jhou TC 2007 Calculating utility:

preclinical evidence for cost-benefi t analysis by mesolimbic dopamine.

Psychopharmacology 191:483-495.

68. Tupala E, Tiihonen J 2004 Dopamine and alcoholism: neurobiological

basis of ethanol abuse. Prog. Neuropsychopharmacol.

18 • THE BARIATRICIAN

Biol. Psychiatry 28:1221-1247.

69. Kelley AE, Bakshi VP, Haber SN, Steininger TL, Will MJ,

Zhang M 2002 Opioid modulation of taste hedonics within the

ventral striatum. Physiol. Behav. 76:365-377.

70. Carr KD, Tsimberg Y, Berman Y, Yamamoto N 2003 Evidence

of increased dopamine receptor signaling in food-restricted rats.

Neuroscience 119:1157-1167.

71. Figlewicz DP, Evans SB, Murphy J, Hoen M, Baskin DG 2003

Expression of receptors for insulin and leptin in the ventral tegmental

area/substantia nigra (VTA/SN) of the rat. Brain Res.

964:107-115.

72. Farooqi IS, Bullmore E, Keogh J, Guillard J, O’Rahiilly S,

Fletcher PC 2007 Leptin regulates striatal regions and human

eating behavior. Science epub Aug 9 2007/science.1144599.

73. Shalev U, Yap J, Shaham Y 2001 Leptin attenuates food

deprivation-induced relapse to heroin seeking. J. Neurosci.

21:RC129:121-125.

74. Erlanson-Albertsson C 2005 How palatable food disrupts appetite

regulation. Basic Clin. Pharmacol. Toxicol. 97:61-73.

75. Pelchat ML 2002 Of human bondage: food craving, obsession,

compulsion, and addiction. Physiol. Behav. 76:347-352.

76. Spangler R, Wittkowski KM, Goddard NL, Avena NM, Hoebel

BG, Leibowitz S, F. 2004 Opiate-like effects of sugar on gene expression

in reward areas of the rat brain. Mol. Brain Res. 124:134-

142.

77. Ackroff K, Sclafani A 2004 Fructose-conditioned fl avor preferences

in male and female rats: effects of sweet taste and sugar

concentration. Appetite 42:287-297.

78. Lenoir M, Serre F, Cantin L, Ahmed SH 2007 Intense sweetness

surpasses cocaine reward. PLoS ONE 2:e698.

79. Lindqvist A, Baelemans A, Erlanson-Albertsson C 2008 Effects

of sucrose, glucose and fructose on peripheral and central

appetite signals. Regul. Pept. 150:26-32.

80. Avena NM, Rada P, Hoebel BG 2008 Evidence for sugar addiction:

behavioral and neurochemical effects of intermittent, excessive

sugar intake. Neurosci. Biobehav. Rev. 32:20-39.

81. Adams SH, Stanhope RW, Cummings BP, Havel PJ 2008 Metabolic

and endocrine profi les in response to systemic infusion of

fructose and glucose in rhesus macaques. Endocrinol. 149:3002-

3008.

82. Shapiro A, Mu W, Rocal C, Cheng KY, Johnson RJ, Scarpace

PJ 2008 Fructose-induced leptin resistance exacerbates weight

gain in response to subsequent high fat feeding. Am. J. Physiol.

Integr. Comp. Physiol. 295:R1370-R1375.

83. Lustig RH 2006 Childhood obesity: behavioral aberration or

biochemical drive? Reinterpreting the First Law of Thermodynamics.

Nature Clin. Pract. Endo. Metab. 2:447-458.

84. Figlewicz DP 2003 Insulin, food intake, and reward. Seminars

in Clinical Neuropsychiatry 8:82-93.

85. Anderzhanova E, Covasa M, Hajnal A 2007 Altered basal and

stimulated accumbens dopamine release in obese OLETF rats as

a function of age and diabetic status. Am. J. Physiol. Regul. Integr.

Comp. Physiol. 293:R603-R611.

86. Han JC, Rutledge MS, Kozlosky M, Salaita CG, Gustafson

JK, Keil MF, Fleisch AF, Roberts MD, Ning C, Yanovski JA 2008

Insulin resistance, hyperinsulinemia, and energy intake in overweight

children. J Pediatr 152:612-617.

87. Cha SH, Wolfgang M, Tokutake Y, Chohnan S, Lane MD 2008

Differential effects of central fructose and glucose on hypothalamic

malonyl-CoA and food intake. Proc. Natl. Acad. Sci. USA

105:16871-16875.

88. Mietus-Snyder ML, Lustig RH 2008 Childhood obesity: adrift

in the “limbic triangle”. Ann. Rev. Med. 59:119-134.

About the Author (Patient Handout – page 38)

Dr. Harry Lefebre’s personal interest in weight control

began as an overweight child. He has nurtured his interest

throughout his entire medical career. He was a

Family Physician for 10 years and his medical practice

began focusing entirely on Bariatrics in 1985. Dr.

Lefebre is Board Certifi ed in Bariatrics and has been an

ASBP member since 1983.

Posted by: Dr. Mercola

1. Canned Tomatoes

The expert: Fredrick vom Saal, PhD, an endocrinologist at the University of Missouri who studies bisphenol-A

The resin linings of tin cans contain bisphenol-A, a synthetic estrogen that has been linked to ailments ranging from reproductive problems to heart disease, diabetes, and obesity. Acidity — a prominent characteristic of tomatoes — causes BPA to leach into your food.

2. Corn-Fed Beef

The expert: Joel Salatin, co-owner of Polyface Farms and author of books on sustainable farming

Cattle were designed to eat grass, not grains. But farmers today feed their animals corn and soybeans, which fatten up the animals faster for slaughter. A recent comprehensive study found that compared with corn-fed beef, grass-fed beef is higher in beta-carotene, vitamin E, omega-3s, conjugated linoleic acid (CLA), calcium, magnesium, and potassium.

3. Microwave Popcorn

The expert: Olga Naidenko, PhD, a senior scientist for the Environmental Working Group

Chemicals, including perfluorooctanoic acid (PFOA), in the lining of the bag, are part of a class of compounds that may be linked to infertility in humans. In animal testing, the chemicals cause liver, testicular, and pancreatic cancer. Studies show that microwaving causes the chemicals to vaporize — and migrate into your popcorn.

4. Nonorganic Potatoes

The expert: Jeffrey Moyer, chair of the National Organic Standards Board

Root vegetables absorb herbicides, pesticides, and fungicides that wind up in soil. In the case of potatoes they’re treated with fungicides during the growing season, then sprayed with herbicides to kill off the fibrous vines before harvesting. After they’re dug up, the potatoes are treated yet again to prevent them from sprouting.

5. Farmed Salmon

The expert: David Carpenter, MD, director of the Institute for Health and the Environment at the University at Albany

Nature didn’t intend for salmon to be crammed into pens and fed soy, poultry litter, and hydrolyzed chicken feathers. As a result, farmed salmon is lower in vitamin D and higher in contaminants, including carcinogens, PCBs, brominated flame retardants, and pesticides such as dioxin and DDT.

6. Milk Produced with Artificial Hormones

The expert: Rick North, project director of the Campaign for Safe Food at the Oregon Physicians for Social Responsibility

Milk producers treat their dairy cattle with recombinant bovine growth hormone (rBGH or rBST, as it is also known) to boost milk production. But rBGH also increases udder infections and even pus in the milk. It also leads to higher levels of a hormone called insulin-like growth factor in milk. In people, high levels of IGF-1 may contribute to breast, prostate, and colon cancers.

7. Conventional Apples

The expert: Mark Kastel, codirector of the Cornucopia Institute

If fall fruits held a “most doused in pesticides contest,” apples would win. And increasing numbers of studies are starting to link a higher body burden of pesticides with Parkinson’s disease.

Dr. Mercola’s Comments:

This is one of the best “foods to avoid” lists I’ve seen come out of the mainstream media. It is very rare when this happens, but I agree with every food on this list.The reality is that most food nowadays is far from pure. Pesticide residues have been detected in 50 percent to 95 percent of all commercially grown U.S. foods, and that is only one type of toxin.

Babies are actually born toxic due to the toxic load of their mothers, some of which comes from dietary contaminants and food additives. One study by the Environmental Working Group (EWG) found that blood samples from newborns contained an average of 287 toxins, including mercury, fire retardants, pesticides, and Teflon chemicals!

The list above is a great starting point to cleaning up your diet, but focusing on organically grown, biodynamic whole foods is really the key to success here.

I want to expand on some of the toxic foods mentioned above, as well as add a few more to the list, so you can significantly reduce your exposure to toxins in the foods you eat.

Why Fresh is Better Than Canned

Many leading brands of canned foods contain BPA — a toxic chemical linked to reproductive abnormalities, neurological effects, heightened risk of breast and prostate cancers, diabetes, heart disease and other serious health problems.

According to Consumer Reports’ testing, just a couple of servings of canned food can exceed the safety limits for daily BPA exposure for children.

The current US federal guidelines put the daily upper limit of “safe” exposure at 50 micrograms of BPA per kilogram of body weight. You should know, however, that even low-level exposure to BPA can be hazardous to your health, and Consumer Reports’ testing found that eating popular canned foods may expose you to excessive amounts of BPA:

• Del Monte Fresh Cut Green Beans had BPA levels ranging from 35.9 ppb to as much as 191 ppb
• Progresso Vegetable Soup had BPA levels ranging from 67 to 134 ppb
• Campbell’s Condensed Chicken Noodle Soup had BPA levels ranging from 54.5 to 102 ppb

So, ideally avoid canned foods entirely and stick to fresh fruits and vegetables, or switch over to brands that use glass containers instead.

Grass-Fed is the Healthy Choice for Beef

Grass-fed beef is vastly superior to grain-fed beef, and in fact it’s the clear beef of choice you should be eating. It is far more important to choose grass-fed than to choose organic, as most grass-fed beef are also organic

Not only is it raised in a more sustainable way for the environment and a more humane way for the animal, but it’s the superior choice for your health.

Grass-fed beef, for instance, is lower in fat than regular beef and, more importantly, contains higher amounts of conjugated linoleic acid (CLA), a fatty acid. Grass-fed animals have from three to five times more CLA than grain-fed animals.

CLA has been making headlines for its extreme health benefits, which include:

• Fighting cancer and diabetes
• Helping you lose weight
• Increasing your metabolic rate, a positive benefit for promoting normal thyroid function
• Helping you maintain normal cholesterol and triglyceride levels
• Enhancing your immune system

Keep in mind that grass-fed meat is almost always preferable to certified organic meat also because most organic beef is fed organic corn, which is what causes the myriad of health problems associated with eating beef. If you can find organic, grass-fed meat, that would be ideal.

What You Need to Know About Milk

I strongly recommend you avoid milk that has the added growth hormone rBGH.

Samuel Epstein, MD, a scientist at the University of Illinois School of Public Health, is one of the top experts on cancer prevention, and he has been speaking out against rBGH in milk, the so-called “crack for cows,” for years.

For starters, Dr. Epstein points out that rBGH milk is “supercharged with high levels of a natural growth factor (IGF-1), excess levels of which have been incriminated as major causes of breast, colon, and prostate cancers.”

But that’s not all.

“This milk is qualitatively and quantitatively different from natural milk,” states Dr. Epstein. “In addition to the issue of increased IGF-1 levels, these differences include:

• Contamination of milk by the GM hormone rBGH
• Contamination by pus and antibiotics resulting from the high incidence of mastitis in rBGH-injected cows
• Contamination with illegal antibiotics and drugs used to treat mastitis and other rBGH-induced disease
• Increased concentration of the thyroid hormone enzyme thyroxin-5′-monodeiodinase
• Increased concentration of long-chain and decreased concentration of short-chain fatty acids
• A reduction in levels of the milk protein casein.”

You very well may be drinking rBGH milk and not know it, as no labels are required. This is despite the fact that nearly every American wants it labeled, but the government, as usual, bowed to industry lobbyists and, amazingly, does not require this on the label.

However, as increasing numbers of people and dairies choose to avoid rBGH, you can find labels that say “rBGH-free” or a similar variation. Organic milk is also rBGH-free.

This is certainly preferable to milk that contains this dangerous hormone … but I still don’t recommend drinking any milk, organic or otherwise, that is pasteurized.

You can avoid both the risks of rBGH and pasteurization by only drinking raw milk that comes from a small farmer you know and trust. This is the only way to drink milk if you’re interested in protecting your health.

The Most Important Foods to Buy Organic

Most fruits and vegetables contain unacceptable and unsafe levels of pesticides, so it’s a wise choice to buy organic produce as often as you can.

However, if you need to pick and choose which foods to buy organic, the most important foods to buy organic are animal products — not produce. This is because animal foods, which are raised on pesticide-laced feed, tend to have higher concentrations of pesticides.

Non-organic meats have up to five times more pesticides than non-organic vegetables.

Non-organic butter can have up to 20 times as many pesticides as non-organic vegetables.

So when prioritizing your purchases, look for organic meats, eggs and dairy products before anything else.

There is one exception to this rule, and that is you may be better off choosing fresh local foods over organic foods. Often, locally grown foods are raised according to organic standards at a more affordable price.

Is Farmed Salmon the Only Seafood to Avoid?

Farmed salmon is among the worst seafood choices out there, as numerous studies show the salmon contain toxins and cancer-causing pollutants. Farmed salmon typically have at least 10 times more cancer-causing persistent organic pollutants than their wild counterparts.

That said, I do not agree that farmed salmon is the only fish you need to stay away from.

A recent study from the U.S. Geological Survey detected mercury in every fish sampled from nearly 300 U.S. streams. Among them, 27 percent contained mercury at levels that equaled or exceeded the U.S. EPA’s criterion for the protection of human health, and more than two-thirds exceeded mercury safety levels for fish-eating mammals like mink and otters.

Therefore, I do not recommend eating any fish — whether farm-raised or from an ocean, lake, river or stream — unless you have lab results in your hand that can attest to its purity.

There are still some safe areas out there, such as in certain pristine waters in Alaska, but it will take some searching on your end to seek them out. The ONLY safe fish I have discovered so far is Vital Choice wild red salmon, which remains the only source of fish I’ll eat.

Eating smaller fish, like anchovies and sardines, is also an option, as their small size makes them far less likely to be contaminated.

An important point to remember if you’re not eating fish is that your body still has a requirement for omega-3 fats. Fortunately, you can easily meet your omega-3 needs by taking a high-quality krill oil supplement, instead of risking your health by eating contaminated fish.

Another Food to Avoid: Unfermented Soy

This one did not make the above list, but it’s one I would definitely add.

Any soy that is unfermented — soy milk, tofu, soybean oil, soy burgers, and all the other processed soy products out there all belong to this category — is not a health food and in fact is not a food I would advise eating at all. This is true whether it is “organic” or not.

Soy infant formula is also on this list and is one of the absolute worst foods you can give your baby.

Unfermented soy products have been linked to everything from reproductive disorders and infertility to cancer and heart disease.

Further, unfermented soy contains isoflavones that are clearly associated with reduced thyroid function. Eating unfermented soy products is likely the single largest cause of hypothyroidism in women.

Another major problem with unfermented soy is that it contains natural toxins known as “antinutrients.” This includes a large quantity of inhibitors that deter your enzymes needed for protein digestion.

While a small amount of these antinutrients would likely not be a problem, the amount of soy that many Americans are now eating (and drinking in the form of soy milk) is quite significant.

The result of consuming too many of soy’s antinutrients is extensive gastric distress and chronic deficiencies in amino acid uptake, which can result in pancreatic impairment and cancer.

For more details on soy foods, including the fermented varieties that can actually be healthy, please read Why This Type of Soy is Better.

Guidelines for Healthy Food

Whatever food you’re looking to eat, whether imported organic or locally grown, from either your local supermarket or a farmer’s market, here are the signs of a high-quality, healthy food:

1. It’s grown without pesticides and chemical fertilizers (organic foods fit this description, but so do some non-organic foods)
2. It’s not genetically modified
3. It contains no added growth hormones, antibiotics, or other drugs
4. It does not contain artificial anything, nor any preservatives
5. It is fresh (if you have to choose between wilted organic produce or fresh conventional produce, the latter may be the better option)
6. It did not come from a factory farm
7. It is grown with the laws of nature in mind (meaning animals are fed their native diets, not a mix of grains and animal byproducts, and have free-range access to the outdoors)
8. It is grown in a sustainable way (using minimal amounts of water, protecting the soil from burnout, and turning animal wastes into natural fertilizers instead of environmental pollutants)

If the food meets these criteria, it is likely a good choice. Most often, the best place to find these foods is from a sustainable agricultural group in your area. You can also review my free nutrition plan to get started on a healthy eating program today.

Dr. Mercola is the founder of the world’s most visited natural health web site,Mercola.com. You can learn the hazardous side effects of OTC Remedies by getting a FREE copy of his latest special report The Dangers of Over the Counter Remedies by going to his Report Page.

consumption for Americans

December 2, 5:26 PMOregon Natural Health Examiner

The Center for Disease Control (CDC) has released the findings of their first study on how many fruits and vegetables Americans are eating within each state. The CDC’s focus on preventative health care rides on the coat tails of research these last few years that points to the overwhelming advantages of a fresh, balanced diet. The research summary for this report states, “Fruits and vegetables are important for optimal child growth, weight management, and chronic disease prevention.”
The research is accompanied by a nationwide program to improve the diets of Americans. This program is set to be released next month as the Healthy People 2010system. It includes sharing information and recipes for preparing fruits and vegetables as they arrive in season to stores and farmer’s markets. The CDC is incorporating the involvement of state officials, health professionals, employers, retail owners, farmers, school staff, and community members increase outreach and make this program a success.
Healthy People 2010 hopes to increase fruit consumption by Americans by 75% and vegetable consumption by 50%. Oregonians needed a little more improvement in their diets. Only 25 -29% of our state’s residents ate vegetables three or more times a day while 30 -34% ate fruit two or more times a day.
The CDC has a user friendly web site designed to encourage the average citizen to get more involved in their dietary choices. The site includes a short quiz to determine how many fruits and vegetables are needed daily for various body types, budget tips, recipes and a fruit and veggie of the month calendar. Clicking on the tab marked interactive tools brings the viewer to a program that analyzes the meal choices that the viewer enters with a simple drag and click of the mouse. Healthy People 2010 is cosponsored by the National Cancer Institute, USDA, FDA, American Cancer Society, and the National Council for Fruit and Vegetable Nutrition Coordinators.
Vintage PSA encourages children to eat fruit.

Dallas, TX 1/15/2009 08:36 PM GMT (TransWorldNews)

In the wake of the economic recession, businesses are becoming more efficient in reducing expenditures and maximizing investments. Employers are weathering the lean times by cutting back. One of the first cutbacks that most firms make relates to employee perks and benefits. For most companies, employee health care is one of their costliest items and is constantly under review. Often times, the only choice that companies can make in order to reduce this cost is to share the burden with their workers. However, employers are also investing in corporate wellness programs to offset higher medical costs that their employees may incur.

According to the 2008 Annual Employer Health Benefits Survey by the Kaiser Family Foundation/Health Research and Education Trust, health care costs for private and public employers and workers increased 119% and 117% respectively, during the period of 1999-2008. The following is a summary of the survey’s findings:

• Increases in the average single and family premiums
• Increases in the percentage of workers enrolled in high-deductible health plans with a savings option
• Increases in cost sharing (insurance deductible)
• Increases in wellness program offerings

In 2008, the average premium for workers with health insurance offer through their employer was $4,704 for single coverage and $12,680 for family coverage – a 5% increase from 2007.

To mitigate the costs, employers are moving towards consumer-driven medical plans. Statistics from this survey show that employees who are covered under their company’s plan with a deductible of at least $1,000 for single coverage increased from 10% to 18% in the past two years and, with small organizations, the rate of covered employees with a deductible of at least $1,000 has increased from 16% to 35%.

Wellness programs were offered to workers as part of their health benefits package in over two-thirds on the respondents surveyed. Over one-half of small companies and almost 90% of large companies offer one or more of the following to workers as a part their health benefits:

• Weight loss program
• Gym membership discounts or on-site exercise facilities
• Smoking cessation program
• Personal health coaching
• Classes in nutrition or healthy living
• Web-based resources for healthy living
• Wellness newsletter

Corporate health management has become pervasive in all industries due to the impact it has on reducing and/or controlling employer and employee medical costs and positively affecting the health of workers. A well planned and managed corporate wellness program can have the following effects for employers and employees:

• Decrease medical claims and savings for employer – With its wellness program, the Travelers Corporation claims a $3.40 return for every dollar invested in health promotion, yielding total corporate savings of $146 million in benefits costs.
• Decrease medical costs for employees – With lower health care claims, medical costs decreased 16% for City of Mesa (Arizona) employees who participated in the health promotion program.
  
  

• Decrease employee absenteeism – Du Pont saw that each dollar invested in workplace health promotion yielded $1.42 over two years in lower absenteeism costs.
  
  

• Increase productivity, healthier employees – Union Pacific Railroad employees who participated in the company-sponsored wellness program lowered their risk of high blood pressure by 45% and high cholesterol by 34%; 30% moved out of the at-risk range for weight problems and 21% stopped smoking.

Through the implementation of wellness, organizations and workers are seeing medical cost savings that are measurable and health benefits that are immeasurable.

For 2009 and beyond, the Employer Health Benefits Survey reports that approximately 40-45% of the firms surveyed predicted an increase in their employee’s health care premium contribution, deductible amounts for office visits, insurance cost sharing and/or prescription drugs costs.