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.

So what’s the big blasphemy, you ask?  Here it is:

Until you are eating right, you have no business exercising.

The free radical damage created when you exercise is so great that, unless you are consuming a huge variety of anti-oxidant rich and nutrient dense food, the net loss to your health is greater than any gain you receive from exercise. That’s right… I’m saying that there are people out there who have no business doing anything more strenuous than taking a leisurely walk outdoors in order to get a bit of fresh air and sunshine. But before you decide that this is your get-out-of-jail-free card with regards to exercise, we should talk about what it actually means to “eat right,” what you can do to get yourself there quickly, and what I mean by exercise.

Typically, when a person decides that they are ready to take their health seriously, one of the first things they’re taught is to begin to exercise. There’s all sorts of logic to this, as the benefits of exercise are manifold and dramatic (more on that, and how to reap its benefits, later), but it’s actually not the first thing that a person should do when they set out to get healthy.

For many people, adding exercise to their lives is easier than dramatically changing the way that they eat. And we have been taught that if you exercise enough, you can eat just about anything and stay healthy. If you exercise enough, you may be able to keep the scale weight stable, but that’s a far cry from being healthy and, in fact, you may become unhealthier in certain ways if you exercise vigorously but don’t eat the right food.

The very nature of exercise is to break down tissue in the body. The body responds by building stronger tissue, which is how muscles increase in size, and why you’re able to lift greater amounts of weight, or run further distances, over time. One problem with this, however, is that in addition to building stronger muscles, the body also builds protein carbonyls, which are oxidized protein from free radical damage. Free radical damage is something that the body is equipped to deal with if it is getting adequate nutrition, and if it isn’t exposed to any pollution, chemical or environmental toxins, or physical or emotional stress of any kind. That is to say, if you lived in a pristine environment, where the air, soil, and food were always fresh and unspoiled, with no chemical pollutants, and if you were always happy and stress free, your body could combat free radical production, provided that you ate a whole-food, plant-based diet, rich in a wide spectrum of fruits, vegetables, and grains, and that you avoided all preservatives, sugars, and additional fats. I don’t know about you, but I certainly don’t live in that world. I’d like to someday, but for now I have to accept that the air, water, and soil are polluted. I also have to accept that I become stressed at times, and it turns out that mental stress is a huge contributor to free radical production.

Additionally I enjoy exercise, which creates a huge amount of free radicals. Given that I can only partially control the environment I live in, I have to rely on the food that I eat to combat the free radical production in my body. The challenge is that although a diet rich in plant-based, whole foods is necessary to repair free radical damage, it’s not sufficient. It’s just not enough given the world that we live in, the stressful lives that we lead, and the extra damage created by exercise. Eating our fruits and vegetables is vital, but it’s not enough. This is when supplementation with an anti-oxidant rich, whole-food based product is essential. Juice Plus+® is one such product, and while there are others on the market, none of them can boast the more than fifteen different, double-blind, placebo controlled, randomized clinical trials that have been conducted on Juice Plus+®.

Three of these studies were specific to exercise, and executed by top exercise physiologists (Bloomer, 2006; Lamprecht M. O., 2007; Lamprecht M. O., 2009). And two of these studies were conducted on the elite military Cobra forces in Austria during a 28 week intense training period. Amongst the markers of health measured, they noticed that the Juice Plus+® group had produced much less protein carbonyls and had fewer illness days. And the harder they trained, the more they benefited from the whole food nutrition available in Juice Plus+®. This is significant because what every athlete wants is fewer illness days and quicker recovery time between trainings, which would be accomplished by reducing the amount of free radical damage in the body as a result of exercise.

Until you’re getting your phytochemical needs met through whole-food supplementation and/or from your whole-food, plant-based diet, I recommend that you avoid strenuous exercise. Instead, take a 10 – 20 minute walk at a relaxed pace. Allow yourself to use the time to focus on your breathing, to enjoy the fresh air, and to rejuvenate, rather than focusing on building muscle or endurance. Another option is to take a yoga class that focuses on restorative poses, and save the power yoga until you’ve got your nutrition handled.

Sources:
Bloomer, R. G. (2006). Oxidative Stress Response to Aerobic Exercise: Comparison of Antioxidant Supplements. Medicine & Science in Sports and Exercise, 38 (6), 1098-1105.

Lamprecht, M. O. (2009). Protein Modification Responds to Exercise Intensity and Antioxidant Supplementation. Medicine & Science in Sports & Medicine, 155-163.

Lamprecht, M. O. (2007, December). Several Indicators of Oxidative Stress, Immunity, and Illness Improved in Trained Men Consuming an Encapsulated Juice Powder Concentrate for 28 Weeks. The Journal of Nutrition, 2737-2741.

Part 2
What should athletes (and the rest of us) be eating?
Whether you’re a competitive athlete, a weekend warrior, or someone who exercises regularly for fitness and enjoyment, you’ve likely been told that when you exercise you need a great deal of protein. Even the most serious of athletes can thrive with just 8-10% of their total calories coming from protein, but more than 10% is not healthy for them or anyone else. The catastrophe that is the Standard American Diet is filled with processed foods and animal products, which are acid-producing foods. Over time this release of acid creates metabolic acidosis, which seems to create a muscle wasting response. In a study conducted at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston, researchers found that a diet rich in fruits and vegetables offsets the wasting of muscle tissue due to metabolic acidosis.
Generally when people think of acidic foods, citrus foods come to mind. In reality, foods should be considered alkaline or acidic based on the residues that are created in the body and excreted in the urine, rather than whether they are alkaline or acidic themselves. Thus the renal acid load (the acid load on the kidneys) can be measured through analysis of urine. What becomes clear is that fruits and vegetables are metabolized to alkaline residues and therefore prevent metabolic acidosis and muscle wasting. And they are the richest source of the phytonutrients that act as natural antioxidants and natural anti-inflammatory agents. These should be the staple of an athlete’s diet.
We’ve been taught that milk and cheese are healthy sources of calcium and protein, but their protein profile is so high that the body responds by leaching calcium bicarbonate from bones. This is the beginning of the osteoporosis spiral: the bones grow weaker, and then people feel that they need to consume more dairy in an effort to increase calcium intake. But the body can’t handle the protein load from the extra dairy, and the cycle of leaching and alkalinizing begins again. It’s not just dairy, however, that’s dangerous to eat. Any protein, whether it is from animal sources or from soy, creates acidosis when too much is consumed. And you’d be surprised by how little protein is actually “too much” protein.
The most protein that the average person will ever need to consume in their lives is when they are a baby. Babies need lots of protein and fat to support the tremendous growth of muscle, bone, and brain that occurs during the first two years of life. But here’s the kicker: this super diet that a baby needs should be comprised of approximately 6% protein! Breast milk, nature’s perfect food, is made up of 6% protein. That’s it. At no other time during a person’s life is there more need for protein than during infancy. So if Mother Nature designed breast milk to have 6% protein, then that is all we ever need in our diet to be healthy. However, it is hard for people, especially athletes, to shake the belief that they don’t need all that protein. That is because whenever you reduce your protein intake, it takes time for the body to adjust to the new diet and there is a period of detoxification that can make a person feel weak. There are other confounding factors that are beyond the scope of this article. However, the stakes are high and it is important to explore the long-term benefits of a more plant-based diet. With a variety of plants (whole grains, vegetables, fruits, legumes, beans, nuts and seeds) it is impossible to get less than 8% of total calories from protein. Plants are also a source of slow-releasing proteins which are more healthy than the quick hit of animal protein. Just as slow-releasing complex carbohydrates are more healthy than fast-releasing simple sugars, slow-releasing plant proteins are more beneficial than fast-releasing animal protein.
So how has it come to be that as a culture we consume so much protein? The diet industry, and its fascination with high-protein, low carbohydrate diets is partly to blame. But the diet industry and the doctors and nutritionists who are part of it were first duped by the food industry. It is the food industry that has driven our desire, and perceived need, for large amounts of protein in the diet.
Whey is a byproduct from the creation of cheese, and for centuries it’s simply been thrown away. But the dairy industry saw an opportunity to reuse this waste product, and protein supplements were born. Today, you can walk into any gym or health food store and find whey-based protein products that are marketed as healthy means of building muscle. Even worse than athletes believing that they need huge amounts of protein is that this myth has trickled down to the rest of society so that even sedentary people are making high protein shakes with whey (or soy) protein, convinced that more protein and fewer carbohydrates are the keys to weight loss and health. And people are giving their children high protein snacks, shakes, and bars, believing these to be healthy alternatives to junk food like cookies or candy bars. While junk food is never a good choice, young children certainly don’t need to be consuming these high protein meal replacement bars and drinks. Fruits, vegetables, and whole grains are what kids should be snacking on in order to build muscle and fuel their brains. It is quite useful, in fact, to think about the analogy of food as fuel when we discuss how athletes, and the rest of us, should eat.
For the human body, the “gasoline” that fuels are the macronutrients in our food: carbohydrates, proteins and fats. These macronutrients provide the calories and building blocks for the body. The most effective source for energy turns out to be complex carbohydrates as found in whole grains. For this reason, whole grains are essential to the diet of an athlete, and to anyone who is exercising regularly. Acceptable whole grain choices are: all types of rice, other than white rice; quinoa, which is naturally high in protein, and has a nice chewy texture and pleasant taste that works well in recipes where rice is usually called for; buckwheat; amaranth; spelt; steel-cut oats; and millet. Chickpeas are an excellent source of protein, and can build muscles just as well as meat can.
If macronutrients are the “gasoline” that fuels the human body, then the micronutrients found in plants are the “oil” that protect this delicate human machinery. Just as we need to regularly put new, clean oil in our cars, we regularly need to replenish the plants in our diets. Plants have so much to offer, and eating a rainbow variety (every color fruit and vegetable that you can find that’s grown locally and organically) will serve to keep you healthy – to keep your engine running smoothly. You want to eat fiber rich, anti-oxidant packed, nutrient dense leafy greens every day: kale, chard, bok choi, spinach, collard greens, dandelion greens, mustard greens, arugula, etc. They are excellent in a “Green Drink”, which is the fruit and vegetable breakfast smoothie that I drink every morning (see Green Drink recipe), but they’re great lightly sautéed in a bit of water, with a squeeze of lemon, or stir fried with garlic (again with water – there’s no need to use oil) and a heap of your other favorite vegetables, served over the whole grain of your choice. Greens aren’t just high in fiber and pretty in color. They truly are the “oil” that protects the various tissues in your body, all of which have unique needs. For example, too much exercise contributes to macular degeneration, but dark greens are high in luteins which can protect against macular degeneration. Luteins also may prevent clogging of the arteries, and are a powerful anti-inflammatory. And luteins are just one example of the manifold benefits that come from eating a wide range of fruits and vegetables.
The bottom line is that athletes need to be eating whole grains, fruits, and vegetables all day, every day, to keep their motors running. They also need to supplement with an anti-oxidant rich, whole-food based product like Juice Plus+®. Athletes literally cannot eat enough fruits and vegetables to get all of the nutrients they need to combat free-radical damage, so the right source of supplementation is key for them.

And those of us who aren’t athletes, and who like to bike, swim, run, or do yoga for general fitness and enjoyment, should be eating the same exact stuff: a whole-food, plant-based diet with tons of leafy greens, and fruits and vegetables in every color of the rainbow, along with a whole-food based supplement like Juice Plus+®. Your kids can eat this way, too!

Part 3
The first article in my series on exercise focused on the nutritional needs of people who exercise. Contrary to current recommendations on exercise, weight loss, and diet, I urge people to avoid any strenuous physical activities unless the resulting increase in free radical damage, or exercise-induced oxidative stress, is being offset by consuming plenty of antioxidants from whole foods.

But let’s say you are balancing exercise-induced oxidative stress with enough fruit and vegetable nutrition in your diet: you’re eating a wide variety of organic vegetables, fruits, and whole grains, and you’re supplementing with a product like Juice Plus. What’s next? What’s the best way to exercise?

In terms of weight training, most personal trainers and exercise manuals would have you focus on the large and visible muscle groups in your arms, legs, chest, butt, and abdomen. Building these muscles will give you peripheral strength and may help you look good, but they won’t provide much in the way of deep strength and true health. The most important muscles to build and train are the ones that you can’t see, but you can feel, which are referred to as core muscles. Core strength is the most important aspect of a healthy physique, and focusing on these critical muscles will not only give you strength and stamina, over time it will help you to tone and highlight the muscles that we all want to show off in our arms, legs, bellies, and butts. But you have to do the deep, inner work first. As with a building or a sculpture, you’ve got to build from the inside out; when the foundation is strong, the upper floors and extremities are strengthened as well.

Gravity takes a huge toll on the spine, and the only thing that can offset this is core strength. Even though I eat well and am very physically active, my spine still has problems and is compressed. Most people are in the same boat as I am, or a boat that’s even less sea-worthy. If you don’t believe me, go get an x-ray: if you’re over 40, you have discs that are starting to degenerate, which can be very serious.

Rule #1 when it comes to exercise and moving your body is: learn how to walk straight. If you can support your weight and hold yourself up using core strength, your spine will thank you, and many aspects of health will be positively affected.

Another mistake that fitness trainers and do-it-yourself-exercisers make is that instead of focusing on core strength and posture, they focus on cardiovascular fitness. Cardiovascular activity is excellent for someone who is eating well, and there are great benefits to huffing and puffing while exercising (especially outdoors), but most people don’t do enough strength training. While most of us desire a six-pack, there are more important muscles to strengthen and build than the rectus abdominal muscles that you can see. It may look good, but won’t actually contribute to your health and longevity. What you really want to focus on and engage are the big transverse abdominal muscles that start under the ribcage and go all the way down your abdomen. I think it’s valuable for anyone interested in exercise to get an anatomy book and learn about the small muscles that hold up the spine, as well as all of the other muscle groups in the body.
Pilates and yoga classes are excellent places to learn about core muscles and to begin to work on deep muscle strength. As a certified yoga instructor I’m often asked about Bikram, or “hot” yoga. I don’t generally recommend hot yoga because I believe that the body needs a great deal of airflow, ideally found outside. In an over-heated room, it’s easy to overstretch and injure yourself without knowing it. Instead, I prefer to do yoga in a comfortably warm room, so that the body heats from the inside out, rather than jacking up the temperature in a room and making you feel hot on the outside before your muscles are actually warmed up.
Finally, it’s important to remember that it’s hard to have that six-pack, or those slim, toned arms, if you don’t eat right. A plant-based, whole-food diet will get you there faster than traditional stomach crunches or bicep curls. Animal products contribute to that beer-gut that most men dread, and cutting them out is the first place to start when attempting to exercise and gain health.