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.

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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.

The Role of Antioxidants in
the Endurance Athlete

David B. Phillips, M.D.

Much has been talked about in the sports and science
community about the adverse affects of prolonged and
strenuous exercise as it relates to the production of
free radicals in an athlete’s body. What are these by-
products of aerobic exercise and why are they
damaging to the human body? More importantly, what
role do antioxidants play in neutralizing these damaging
molecules and what can we as athletes do to facilitate
this protective process?

An Apple a Day

The ‘Radical’ Concept
Free radicals are highly reactive species produced
during various molecular processes in the human body.
While environmental factors such as pollution, radiation
and cigarette smoke can spawn free radicals, in this
article we will focus on those free radicals produced
during endurance exercise.

Free radicals are atoms or groups of atoms with an odd
or unpaired number of elections and can be formed
when oxygen interacts with certain molecules. Once
formed, these reactive radicals can start a chain
reaction, similar to a domino effect. In other words,
these compounds attack the nearest stable molecule,
“stealing” its electrons in order to gain stability. When
the “attacked” molecule loses its electron, it becomes
a free radical itself, beginning a chain reaction. Once
the process is started it can cascade, resulting in the
disruption of a living cell. Free radical damage not only
contributes to accelerated aging, it also causes
damage to immune cells. It’s not uncommon for
endurance athletes such as triathletes or marathoners
to have a higher incidence of colds and upper
respiratory infections after competition and intense
training. Free radical damage to cellular DNA plays a
significant role in the evolution of certain cancers,
heart disease and neurological disorders such as
Alzheimer’s disease.

Exercise and Oxidative Damage
Endurance exercise can increase oxygen utilization
from 10 to 20 times over the resting state and up to 100
to 200 times in working muscles. This greatly
increases the generation of free radicals via oxidative
metabolism in skeletal mitochondria. Fortunately, the
body has an elaborate antioxidant defense system that
utilizes dietary intake of antioxidant vitamins and
minerals as well as our body’s own enzyme systems to
decrease concentrations of the most harmful oxidants
in tissues. Regular endurance training has been shown
to enhance our internal antioxidant defense system,
these changes of which occur slowly over time and
appear to parallel other adaptations to exercise. When
free radical production exceeds the ability of
antioxidant enzymes and nutritionally obtained
antioxidants to neutralize them, oxidative stress
results. So, what can we as endurance athletes do to
minimize the damage caused by the inevitable overflow
of free radicals during training and competition?

Fruits and Vegetables:
The Power of the Pyramid!
A recent change in dietary intake of fruits and
vegetables by the USDA has placed a greater emphasis
on increasing our daily consumption from the previous
5-7 servings a day to 7-9 servings and up to 13 servings
or more for endurance athletes! Vitamins C, E, and beta
carotene are the primary vitamin antioxidants.
Previous research looking into the effects of
supplementing our diets with these isolated nutrients
has yielded equivocal results. Once thought to be
beneficial to cardiac health, isolated vitamin E
supplementation has now been questioned. Beta
carotene supplements have been shown to increase
lung cancer in smokers as well as contribute to
thickening of the lining of arteries.

Recent studies now point to the synergistic role of
numerous antioxidants obtained from the consumption
of whole foods such as fruits and vegetables.
Therefore, a diet rich in naturally occurring antioxidants
appears to outweigh the risks inherent to
supplementing one’s diet with isolated laboratory made
supplements. Furthermore, various key trace minerals
such as zinc, selenium and manganese found in
naturally occurring foods are needed for the proper
functioning of various endogenous antioxidant enzymes.

Training Right, Eating Right:
Final Thoughts
The endurance athlete faces a challenge of balancing
daily aerobic exercise with preventative measures that
minimize the damaging affects of oxidative stress.
Clearly, fruits and vegetables rich in antioxidants are
vital to this balance. Many of us may find it difficult to
consume the recommended amounts of fruits and
vegetables to achieve this balance. For those who are
unable to take in enough daily produce, cryoevaporated
fruits and vegetables in capsule form, such as Juice
Plus+, make it possible to supplement what we are not
able to consume when we visit the salad bar.
Antioxidant supplementation helps to bridge the gap
between what we eat on a daily basis (what we know
we should be eating!) and the optimal amount of
phytonutrients needed to combat the damaging effects
of oxidative stress.

As endurance athletes, it is important to be aware of
not only the benefits of aerobic exercise but the
potentially negative aspects training and racing can
have on our bodies and long term health. Finding a
healthy balance between training and proper nutrition
will go a long way in promoting longevity in any
endurance athletic activity.

(Dr. Phillips recently completed the 2005 Ironman World
Championships in Kona; he is a USAT All-American and
the 2004 USAT National Long Course Masters
Champion; he was ranked #1 USAT Southeast Masters
Division 2004 and was also an All-American swimmer at
Harvard University.)

REFERENCES

“Antioxidants: What are They and What Role Do
They Play in Physical Activity and Health?”
Priscilla M. Clarkson, Ph.D.
“The Role of Antioxidant Vitamins and Enzymes in
the Prevention of Exercise-induced Muscle
Damage,” Sports Medicine, 1996; 21: 213-38
“Antioxidants: Role of Supplementation to Prevent
Exercise-induced Oxidative Stress,” Medicine and
Science in Sports and Exercise, 25(2): 232-236,
1993, Feb.
“Oxidative Stress in Endurance Athletes,”
Triathlete Magazine, 256: 74-76, 2005, August.
(Excellent in-depth review of specific nutritional
antioxidants.)

Deciding what to eat for dinner can be mind-bending. How do we keep track of the ever-evolving recommendations for what to put on, and leave off, the plate? Red meat might cause cancer! But don’t replace it with tofu—soy concoctions might be carcinogenic, too! Don’t even try to figure out where carbs stand this week. And the verdict on coffee, chocolate, and alcohol changes faster than you can order a mocha martini.

Vitamins—with their promise to bridge the gap between the nutrients our bodies need and those they get—have always seemed reassuringly simple: Just pop a multivitamin and let your body soak in those extra nutrients. But not any longer. During the past few years, study after study has raised doubts about what, if any, good vitamins actually do a body. They could even pose some real medical risks.

Half of all American adults take some sort of nutritional supplement. But research on a wide variety of patient populations and medical conditions has failed to find much evidence that multivitamins, the most commonly used of the lot, prevent major chronic diseases in healthy people. The most recent knock came this spring, when a study of more than 160,000 post-menopausal women, published in the Archives of Internal Medicine, found that the all-in-one pills did not prevent cancer, heart attacks, or strokes and did not reduce overall mortality.

Individual vitamins and minerals haven’t fared much better under scientific scrutiny, with research debunking some of the reputed benefits of vitamin B6, calcium, niacin, and others. In 2006, the National Institutes of Health convened an independent panel of experts to evaluate the evidence that vitamins could prevent chronic disease. The scientists ultimately issued a report stating that studies “do not provide strong evidence for beneficial health-related effects of supplements taken singly, in pairs, or in combinations.”

The news on antioxidants, the darlings of the vitamin menagerie, is even more troubling. These compounds, which include vitamins A, C, and E, selenium, beta carotene, and folate, fight free radicals, unstable compounds thought to damage cells and contribute to aging. But not only do antioxidant supplements fail to protect against heart disease, stroke, and cancer; they actually increase the risk of death, according to a 2007 analysis of research on more than 232,000 people, published in the Journal of the American Medical Association, as well as otherstudies.

Exactly why they might increase mortality is unclear, but doctors at prominent research institutions—including New York’s Memorial Sloan-Kettering Cancer Center and Seattle’s Fred Hutchinson Cancer Research Center—have highlighted some unsettling connections between supplemental antioxidants and an increased risk of a variety of cancers. Popping certain kinds of antioxidant pills can feed latent cancers growing in the body, for instance, and reduce the effectiveness of chemotherapy. These observations make a certain intuitive sense, since vitamins and minerals play an important role in the replication of healthy cells—why shouldn’t they be doing the same for cancerous cells? (Feeding mice a diet poor in antioxidants, on the other hand, can actually help shrink their brain tumors.) Scientists are also beginning to suspect that the body may actually need free radicals—which help kill cancer cells, ensure optimal immune function, and regulate blood sugar, among other things—so we shouldn’t necessarily be mopping them all up.

The list of worrisome findings goes on, but it doesn’t seem to have put a dent in the $25 billion supplement industry. Sales are not only robust but rising in the United States. Doctors still recommend multivitamins as part of basic preventative care. Despite the demonstrated risk, as many as 80 percent of cancer survivors swallow a daily dose, according to a study published in the Journal of Clinical Oncology in 2008.

Vitamins have a powerful psychological hold over us. As precautionary health measures go, supplements are easy. Compare the two seconds required to swallow a pill with the constant vigilance necessary to exercise and eat right.And the fact that vitamins are available without a prescription makes them seem safe—even though it probably makes them less so, since they’re not regulated by the FDA as drugs, and manufacturers are not required to prove that they’re effective at treating disease.*

But the risk-benefit calculus has changed. We know more about the risks, and it’s clear that there’s also less potential benefit. During the early 20^th century, diseases like scurvy and rickets were common until researchers began to isolate compounds in food—which became known as vitamins—that could altogether cure these ailments. It must have been remarkable to see devastating diseases alleviated with common foodstuffs.

During an era when many people legitimately had nutritional deficiencies, placing your bets on a multi might have been reasonable. But today, of course, actual deficiencies are much less common. Our salt, milk, flour, juice, cereal, and more are all fortified with extra nutrients, and a 2009 study published in the Archives of Pediatrics and Adolescent Medicine suggests that most of the kids who end up taking vitamins in the United States today don’t actually need them.

If vitamins are useful for anything, it’s probably for tapping into our old friend the placebo effect. In a 2008 survey, 38 percent of doctors confessed to recommending vitamins because they believed the pills could promote health purely through the power of positive expectations. Consider a famous 1975 study designed to probe whether vitamin C supplements alleviated colds better than a placebo, an inert lactose tablet. It turned out that it didn’t matter much which pill the subjects were actually taking. What mattered was what they thought they were getting: Those who believed they were taking vitamin C had fewer and milder cases of the sniffles than those who believed they were just swallowing lactose. That would be reason enough to pop a supplement—there are worse things than deceiving yourself into better health—if it weren’t for the emerging evidence that the pills might be capable of causing real harm.

That’s not to say that vitamins aren’t important. Vitamins are critical to all sorts of bodily functions, and we have to get them through diet because our bodies can’t make them on their own. The Office of Dietary Supplements at the NIH recommends that we get certain levels of a variety of kinds of vitamins, and that recommendation is sound. But encouraging us to get a complete suite of vitamins is not the same as suggesting that we get them by popping a pill.

In fact, the reports littering the ODS site seem to converge upon the same point: There is some good news for supplements, but it’s extremely limited. The 2006 NIH panel, for instance, concluded that postmenopausal women should probably take calcium and vitamin D to safeguard their bones; that pregnant women should keep taking folate; and that adults with age-related macular degeneration, an eye disease, should take a combination of antioxidants and zinc. But beyond that, the panel’s strongest recommendation was that scientists conduct further research on the risks and benefits of vitamins. For every study that turns up disconcerting vitamin side effects, there seem to be two more that conclude that we simply don’t know enough yet about supplements to make evidence-based recommendations.

Until we do, we should stop treating supplements like health candy and more like prescription meds, to be used only when there’s a demonstrated need. Doctors should create individualized regimes, tailored to a particular patient’s deficiencies. As for the rest of us, we can put the pills back on the shelf and save our cash for one of those martinis.

Correction,Jan. 8, 2010: This article originally and incorrectly stated that vitamin supplements are not regulated at all by the FDA. (Return to the corrected sentence.)

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.

An important advantage to having plant-based foods as an abundant part of your daily diet appears to result from thephytochemicals they contain. As noted in the UF findings recently published in the Journal of Human Nutrition and Dietetics, these natural substances prevent oxidative stress– a process linked to being overweight and to the onset of diseases including heart disease and diabetes. Phytochemicals include lycopene from tomatoes, isoflavones from soy, beta carotene from carrots, anthocyanins from blueberries, allicin from garlic, and many more.

Without enough phytochemicals and antioxidants to counteract oxidative stress, damaging free radicals cause inflammation and other toxic problems in the body. In overweight people, excess fat tissue and certain enzymes that are more active also trigger the production of excessive free radicals, according to a media statement by the UF researchers.

The research team, headed by Heather K. Vincent, Ph.D., studied a group of 54 young adults divided into a normal weight and an overweight or obese group, analyzing their dietary patterns over several days. Surprisingly, the people in both groups took in about the same amount of calories. However, the overweight and obese young people were found to be eating fewer plant-based foods. That means those who were carrying around excess pounds were consuming fewer protective trace minerals and phytochemicals and consuming far more saturated fats.

In addition, those eating less plant-based foods were found to have higher levels of oxidative stress and inflammation in their bodies than their normal-weight counterparts. This is a crucial finding because oxidative stress and inflammation are processes clearly associated with the onset of obesity, heart disease, diabetes and joint disease.

“Diets low in plant-based foods affect health over the course of a long period of time,” Dr. Vincent explained in a statement to the press. “This is related to annual weight gain, inflammation and oxidative stress. Those are the onset processes of disease that debilitate people later in life.”

“People who are obese need more fruits, vegetables, legumes and wholesome unrefined grains,” she said. “In comparison to a normal-weight person, an obese person is always going to be behind the eight ball because there are so many adverse metabolic processes going on.”

In order to get enough protective phytochemicals daily, the UF researchers concluded that people should try to consume plant-based foods such as leafy greens, fruits, vegetables, nuts and legumes at the start of each meal. As a way to encourage people to get enough phytochemicals from meals and snacks, Dr. Vincent also called for use of aphytochemical index, which compares the number of calories consumed from plant-based, nutrient-rich foods with the overall number of calories taken in each day.

“Fill your plate with colorful, low-calorie, varied-texture foods derived from plants first. By slowly eating phytochemical-rich foods such as salads with olive oil or fresh-cut fruits before the actual meal, you will likely reduce the overall portion size, fat content and energy intake. In this way, you’re ensuring that you get the variety of protective, disease-fighting phytochemicals you need and controlling caloric intake,” said Vincent, an assistant professor in the UF Orthopaedics and Sports Medicine Institute, in the media statement.

Check out this great article:

http://www.NaturalNews.com/027616_degenerative_disease_phytochemicals.html

It’s really interesting!