THE UNIVERSITY OF NATURAL MEDICINE HIGH FRUCTOSE CORN SYRUP AND CHILDHOOOD OBESITY IN THE UNITED STATES: AN INVESTIGATION OF A CAUSAL RELATIONSHIP DISSERTATION SUBMITTED TO THE FACULTY OF THE DEPARTMENT OF NATURAL HEALTH SCIENCES IN CANDIDACY FOR THE DEGREE OF DOCTOR OF PHILOSOPHY BY ANITA DEHLINGER DELPRETE ALBUQUERQUE, NM SEPTEMBER 2011
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THE UNIVERSITY OF NATURAL MEDICINE
HIGH FRUCTOSE CORN SYRUP AND CHILDHOOOD OBESITY IN THE UNITED
STATES: AN INVESTIGATION OF A CAUSAL RELATIONSHIP
DISSERTATION SUBMITTED TO
THE FACULTY OF THE DEPARTMENT OF NATURAL HEALTH SCIENCES
IN CANDIDACY FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY
BY
ANITA DEHLINGER DELPRETE
ALBUQUERQUE, NM
SEPTEMBER 2011
High Fructose Corn Syrup and Childhood Obesity p. 2
Chapter 3 High Fructose Corn Syrup Discovery, Use & Prevalence 63 Consumption Trends 70 Metabolism and Adiposity 78 Economic Benefits 96 Genetically Modified Foods (GMO/GE) 98
Chapter 4 Other Contributing Factors
Portion size & Increased Caloric Intake 106 Physical Activity 109 Television, Computer & Video Games 111 Family Mealtime 114 Fast Food and Fat Consumption 115 Soda Consumption 117 Genetics 119
Conclusion 121
Appendix 128 End Notes 129
Bibliography 135
High Fructose Corn Syrup and Childhood Obesity p. 5
Introduction
There is a global epidemic occurring and it is threatening to be one of the most
costly epidemics the world has experienced…obesity. Ten years ago the World Health
Organization (WHO) declared this epidemic to be “the biggest unrecognized public
health problem in the world”1 and sadly it has expanded since that declaration. The
health risk factors associated with obesity and excess adiposity have catapulted obesity
and overweight to one of the top health risk factors in the United States. According to the
Mayo Clinic (2011), these include are heart disease, stroke, cancer, type 2 diabetes,
chronic respiratory diseases, and accidents.2 Of these top health threats, six have been
directly associated with obesity and excessive adiposity which is precisely why health
professionals (adult and pediatric) are growing more concerned.
Current projections estimate that by 2030 half of all Americans will be obese, not
overweight but obese!3 This epidemic has traversed socio-economic, ethnic, racial,
gender, geographic and age boundaries and demarcations. While some groups or
classification of individuals may have a slightly higher preponderance of occurrence, no
population has escaped unscathed by this health crisis. According to the most recent
estimates of the Centers for Disease Control and Prevention (2011), 17% of all children
and adolescents in the United States are obese. Unfortunately, the CDC estimate does not
include those children who are overweight and/or borderline obese thus omitting a
significant population who may be at risk of developing the same health risks as those
who are classified “obese”. Some estimates report that an additional 25% of U.S.
children and adolescents are overweight.4 Thus cumulatively, these estimates suggest
that, at minimum, 42% of all U.S. children and adolescents are overweight or obese. The
High Fructose Corn Syrup and Childhood Obesity p. 6
predominant questions for researchers is 1) what is/are causing these alarming rates of
overweight and obesity and 2) what can be done to stop and/or reverse these trends?
The impetus for deriving an answer to these pertinent questions is based in part
to averting future medical crises. Adverse health conditions that once only effected the
adult population are now manifesting in children and adolescents. Cardiovascular
disease, hypertension, high blood pressure, hyperlipidemia, type 2 diabetes, insulin
resistance, and sleep apnea, conditions that were once reserved to the “adult” population,
are becoming more prevalent among our youth. Increased prevalence of medical
conditions translates into increased medical cost and economic burden, especially for
those receiving government-funded medical care (Medicaid and Medicare). In 2000, the
economical cost associated with obesity in the United States was estimated to be $117
billion dollars.5
Interestingly, the surge of high fructose corn syrup (HFCS) consumption in the
United States parallels the child and adolescent overweight/obesity rates trajectory
spawning the investigation of a causal relationship between HFCS consumption and
obesity. Because of the prevalence of HFCS in beverages, soft drinks in particular,
several studies have investigated the role of carbonated beverages and obesity. However,
what has not been investigated is the cumulative dietary intake of HFCS consumed via
beverages (carbonated and non-carbonated juices) and food in relation to adiposity.
Similarly, certain aspects of HFCS and its metabolic processes, as well as glucose,
fructose and sucrose metabolism, have been investigated however, the sum total of all the
experimental “parts” (i.e. findings) have not been cumulatively analyzed. Because
HFCS contains fructose as well as glucose, several studies have researched metabolic and
High Fructose Corn Syrup and Childhood Obesity p. 7
blood profile differences and/or similarities between the various sweeteners.6 Other
research has specifically investigated effects of HFCS consumption on weight gain and
fat mass7. Some studies have looked at HFCS consumption and satiety8 while others
have investigated effects on insulin, leptin and ghrelin levels.9 There has been research
on the efficacy of genetically modified foods as well.10 The relevance of this latter
research is that the vast majority of HFCS is derived from GMO/GE corn. Additionally,
HFCS has been shown to contain trace amounts of mercury11raising concerns as studies
have revealed toxic effects of mercury ingestion on the liver12 (the primary organ for
carbohydrate and fat metabolism), kidneys and brain tissue.
While seemingly unrelated, each experiment, each research investigation
provides information about a specific aspect of HFCS, but in order to determine the true
relationship between HFCS and obesity a critical analysis of all the information is
necessary. This research investigates the causal relationship between HFCS consumption
and excess adiposity and obesity among U.S. children and adolescents.
High Fructose Corn Syrup and Childhood Obesity p. 8
CHAPT. 1- Obesity in the United States
ADIPOSITY DETERMINATION
In traditional “medical” terms, obesity is defined simply as an excess of body
fat,13 however, what defines “excessive” remains somewhat nebulous and often
subjective. Some contend that obesity falls into the classification of a non-communicable
disease (NCD)14 while others contend that obesity itself is not a “disease” but rather the
result of metabolic processes from which subsequent diseases may develop as a result of
being obese.15 The World Health Organization (WHO) includes harmful health
ramifications in their definition of obesity stating that obesity is “the condition of having
abnormal or excessive body fat accumulation that may impair health.”16 Some of these
deleterious health impairments will be discussed in detail later in this chapter. For
adults, excess adiposity is traditionally measured via a height-weight index known as the
Body Mass Index (BMI) [also known as the Quételet index named after creator and
statistician Lambert Adolphe Jacques Quételet] which is a ratio of weight in kilograms to
the square of height in meters, BMI= !"#$!! (!")!!"#!! ! !
; when converting BMI into pounds and
inches this calculation becomes !"#$!! !" ! !"#!!"#!! !" !
.17 In the United States, an adult with a
BMI ≥ 25 (but < 30) is classified as “overweight”, a BMI ≥ 30 (but < 40) is “obese” and a
relatively new term of “super obese” applies to those with a BMI >40.18 However, in
their 2000 Report of Consultation regarding obesity, WHO further delineated levels of
obesity into three categories or sub-classifications: BMI 30-34.9 as Obese Class I, BMI
35-39.9 as Obese Class II and BMI ≥ 40 as Obese Class III.19 It should be noted that the
BMI index is not an exact measurement of adiposity, nor the only way to estimate or
High Fructose Corn Syrup and Childhood Obesity p. 9
determine adiposity, but rather an agreed upon universal guideline of appropriate height-
weight ratio and approximation of general adiposity.
One criticism of the BMI is that it generally has a low sensitivity and high
specificity in detecting excess adiposity.20 In clinical testing, sensitivity refers to the true
positive rate, that is, it reliably identifies all the individuals with a specific condition. For
example, if 100 people are tested for condition X and all 100 people actually have
condition X, but the test only identified 75 as having condition X then the test would
have a sensitivity of 75%. For 15 people the test showed a false negative; these
individuals thought that they were fine when in fact they had condition X. A test with a
low sensitivity is unreliable because is will fail to identify individuals who actually have
specific conditions. Conversely, specificity of a test refers to the number of false
positives. For example, if 100 people are screened for disease Y and only 75 actually
have that disease but all 100 test positive, the test has a low specificity rate. A test with a
low specificity is unreliable because it will give false positives. In this scenario, fifteen
people think they have disease Y when in fact they do not. Ideally, a test will have a high
sensitivity rate as well as a high specificity so as to accurately identify those individuals,
and only those individuals, with a specific condition.
Muscle tissue weighs more than adipose tissue (i.e. fat) therefore, it is possible
for a professional athlete with a low body fat percentage to score a high BMI based on
density of the muscle and smaller stature. A “real life” example of a specificity error
would be that a 5’6” male athlete weighing 173lbs., with a 29” waist and a true body fat
percentage of 10% would register a BMI of 28 thus falling into the upper end of the
“overweight” classification. Clearly, this individual is not overweight, yet because of his
High Fructose Corn Syrup and Childhood Obesity p. 10
muscle density he falls into almost borderline “obese” category. Conversely, a sensitivity
error with respect to BMI would be a 5’9” female weighing 135 lbs. with a 36” waist who
registers a “normal” BMI of 20 yet has a true body fat percentage of 35%. Sole reliance
on the BMI index would indicate she is well within “normal” (which is often perceived as
“healthy”) limits. However, an elevated body fat percentage of 35% coupled with the
location of the excess adipose tissue, primarily the abdomen, potentially places her at risk
for developing adverse health conditions. Some researchers have coined the term
“metabolically obese but normal weight (MONW)”21 to classify individuals meeting this
criteria. While prevalence ranges between 5%-45% depending upon specific criteria and
BMI cut off, individuals who fall into this classification exhibit higher abdominal and
2000 (NHANES) and 1999-2002 (NHANES). They defined overweight as having a BMI
of ≥ 25 and obesity as a BMI ≥ 30. At the time of NHES I (1960-1962); 49.5 % of men
High Fructose Corn Syrup and Childhood Obesity p. 17
were overweight while 40.2% of women were overweight thus combined, 44.8% of men
and women over the age of 20 years were overweight. Those numbers increased slightly
by the NHANES II (1976-1980) to 52.9% for men and 42.0% for women for a
cumulative total of 47.4% for men and women. The most significant increases occurred
between the NHANES II (1976-1980) to the NHANES III (1988-1994), and the
NHANES III (1988-1994) to the NHANES (1999-2000) with an 8.6% increase and 8.5%
increase respectively. [Fig.1]
Similar trends were found in the obesity category. The NHES I (1960-1962) data
reveal 13.3% of adults were obese; 10.7% of men were obese and 15.7% of women were
obese. Collectively (men and women), there was a slight increase to 14.6% by the
NHANES I (1971-1974), and another slight increase to 15.1% by the NHANES II (1976-
1980). However, there was a substantial increase to 23.3% (an 8.5% increase) by the
0.0%
10.0%
20.0%
30.0%
40.0%
50.0%
60.0%
70.0%
80.0%
NHES I 1960-‐1962
NHANES I 1971-‐1974
NHANES II 1976-‐1980
NHANES III 1988-‐1994
NHANES 1999-‐2000
NHANES 1999-‐2002
U.S. Adult Overweight Rates 1960-‐2002
Men
Women
Combined
Fig 1. U.S. Adult Overweight rates 1960-‐2002. Data Source: Wang and Beydoun (2007) National Health Examination Survey (NHES I) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, NHANES 1999-‐2002. Graphic created by author.
High Fructose Corn Syrup and Childhood Obesity p. 18
NHANES III (1988-1994) and another significant (7.6%) increase to 30.9% by the
NHANES (1999-2000). By 2000, 30% of all adults were not merely overweight but
obese. Interestingly, women across all surveys had a higher percentage in the obesity
category (BMI ≥ 30) than men, whereas men had a higher percentage in the overweight
category (BMI ≥ 25) category than women. [Fig.2]
What was not analyzed and should be looked at in further studies is the
breakdown of these BMI ranges. For example, of the NHES I 13.3% obesity rates, were
the majority of individuals hovering around the 31-32 range or were they in the 40-45
range? Has the degree of adiposity increased as well as the prevalence? Similarly, is
there a greater prevalence of extreme or morbid obesity now than twenty, thirty or forty
years ago? Recently, morbid obesity has been added as a subcategory of obesity, this
refers to a BMI ≥ 40 and/or the individual is 100 pounds overweight. Unfortunately this
will be difficult to ascertain, as BMI specificity was not a category of the NHANES
0.0%
5.0%
10.0%
15.0%
20.0%
25.0%
30.0%
35.0%
40.0%
NHES I 1960-‐1962
NHANES I 1971-‐1974
NHANES II 1976-‐1980
NHANES III 1988-‐1994
NHANES 1999-‐2000
NHANES 1999-‐2002
Adult Obesity Rates 1960-‐2002
Men
Women
Combined
Fig 2. U.S. Adult Obesity rates 1960-‐2002. Data Source: Wang and Beydoun (2007) National Health Examination Survey (NHES I) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, NHANES 1999-‐2002. Graphic created by author.
High Fructose Corn Syrup and Childhood Obesity p. 19
surveys.
The health implications of this global epidemic are alarming. Dr. Catherine
LeGalès Camus, WHO Assistant Director-General of Non-communicable Disease and
Mental Health, warns, “The sheer magnitude of the overweight and obesity problem is
staggering. The rapid increase of overweight and obesity in many low and middle
income countries foretells an overwhelming chronic disease burden in these countries in
the next 10 to 20 years, if action is not taken now.”47 Currently, WHO estimates that
over 2.6 million people die each year as a result of being overweight and/or obese.48
Sadly, this epidemic does not exclude some of the most vulnerable and least self-
sufficient…our children.
PEDIATRIC OBESITY TRENDS & HEALTH IMPACTS
In 2010, an appalling WHO estimate stated that over 42 million children under
the age of five were overweight; of these, 35 million were children living in developing
nations.49 What used to be an isolated condition affecting the affluent, obesity has
traversed economic boundaries and proliferated the homes of the middle-class as well as
the poor and economically disadvantaged. Sharron Dalton, Associate Professor in the
Department of Nutrition, Food Studies and Public Health at New York University states,
“The forces of globalization have put these relatively cheap foods and drinks- high in
calories, low in nutrients-within reach of almost anyone, anywhere, giving childhood
obesity a foothold in even the poorest countries.”50 Dalton boldly contends that,
“childhood obesity is arguably the most pervasive and serious threat to children’s health
today.”51
High Fructose Corn Syrup and Childhood Obesity p. 20
Obesity is associated with many significant health problems plaguing both adult
and pediatric populations. Sadly, what were once considered “adult” diseases and
disorders are becoming increasingly prevalent among children and adolescent
populations. Obesity-related cardiovascular conditions now affecting children and
adolescents include cardiovascular disease (CVD),52 hypertension,53
hypercholesterolemia, and dyslipidemia.54 A study that has provided a wealth of
knowledge and clinical insight into cardiovascular disease and children is the Bogalusa
Heart Study.
Sponsored by the National Heart, Lung, and Blood Institute (NHLBI), the
Bogalusa Heart Study (1972-2002) was and is the longest biracial study of children
investigating the early natural history and etiology of cardiovascular disease and
hypertension.55 Conducted by Tulane University School of Medicine, the study consisted
of all children and young adults, approximately 22,000 subjects, residing in the town of
Bogalusa Louisiana.56 Data surveys were conducted in 1973-74, 1976-77, 1978-79, 1981-
82, 1988-89 and 1988-2991 and consisted of anthropometric data (height, weight, length
of body segments and body segment masses), health history, hemoglobin, blood pressure,
serum lipids and lipoprotein levels, skinfold thickness, heat rate, salt intake, smoking,
alcohol use and dieting habits.57 Two parallel cohorts of children ages 7 to 9 years old
were identified, one in 1973 and the other in 1984, and reexamined throughout the
duration of the study into adulthood. The study clearly revealed that the etiology for
CVD, hypertension, and atherosclerosis begins in childhood. Freedman et al. (2004)
were specifically interested in data from the Bogalusa Heart Study surrounding the
relationship between BMI, skinfold measurements and adult adiposity. Analysis
High Fructose Corn Syrup and Childhood Obesity p. 21
confirmed their presumptions that child BMI and triceps skinfold measurements are
positively associated with adiposity later in life. They also found skinfold measurement
to have a slightly stronger association with adult adiposity than did BMI, nevertheless
they concluded that both were reliant predictors of adiposity into adulthood.58
In addition to cardiovascular health risks, conditions such as non-insulin-
dependent diabetes mellitus (NIDDM or type 2 diabetes mellitus), insulin resistance and
hyperinsulinemia are also prevalent among overweight and obese children. Endocrine
system health is also adversely affected, reproductive health (menstrual irregularities),59
mental health (depression, oppositional defiant disorder),60 musculoskeletal health61 and
sleep and respiratory health (sleep apnea, asthma)62 are other areas adversely affected by
excessive adiposity.
Since 1980, the number of overweight adolescents has tripled.63 Today, one in
three American children are overweight or at risk of becoming overweight and/or obese,
that is one third of the adolescent population. Dr. Cynthia Ogden and Margaret Carroll
(2010) analyzed the National Health Examination Surveys (NHES) and National Health
and Nutrition Examination Surveys (NHANES) with respect to pediatric and adolescent
obesity. Their findings were similar to those of Wang and Beydoun. Based on expert
committee recommendations and the 2000 CDC BMI-for-age-growth charts, Ogden and
Carroll’s obesity cutoff criteria were individuals who were ≥ 95th percentile of the sex-
specific BMI-growth charts.64 Their analysis of the NHES II (1963-1965) & III (1966-
1970) and NHANES I (1971-1974), NHANES II (1976-1980), NHANES III (1988-1994)
and NHANES 1999-2000, 2001-2002, 2003-2004, 2005-2006 and 2007-2008 concluded
that for children 2- 5 years of age obesity more than doubled between 1976-1980 and
High Fructose Corn Syrup and Childhood Obesity p. 22
Fig 3b. Obesity rates among U.S. Children and adolescents. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-‐11) III (ages 12-‐17) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, 2001-‐2001, 2003-‐2004, 2005-‐2006, 2007-‐2008. Graphic created by author.
2007-2008 increasing from 5.0% to 10.4% respectively. Similarly, among children 6-11
years of age the rate tripled from 6.5% (1976-1980) to 19.6% (2007-2009). For
adolescents aged 12-19, the percentage of those that were obese tripled as well, from
5.0% (1976-1980) to 18.1% (2007-2008).65 [Fig. 3a & 3b]
Fig 3a. Obesity rates among U.S. Children and adolescents. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-‐11) III (ages 12-‐17) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, 2001-‐2001, 2003-‐2004, 2005-‐2006, 2007-‐2008. Graphic created by author.
Prevalence of Obesity among U.S. Children 2-‐19 years
Total (2-‐19 yrs.)
0.0
5.0
10.0
15.0
20.0
25.0
Percen
tage th
at are Obe
se
Prevalence of Obesity among U.S. Children
Total (2-‐19 yrs.)
2-‐5 yrs.
6-‐11 yrs.
12-‐19 yrs.
High Fructose Corn Syrup and Childhood Obesity p. 23
They also discovered significant ethnic and gender disparities. In NHANES III
(1988-1994), there was not a significant difference between Mexican-American and non-
Hispanic White boys, 14.1% and 11.6% respectively (although some would argue
regarding health conditions 3% is significant enough). However, by NHANES 2007-
2008 those rates has increased to 26.8% and 16.7% respectively; Mexican-American
boys had a 61% greater prevalence of obesity than non-Hispanic White boys. While not
highlighted in their analysis, the data also showed a significant increase in the prevalence
of obesity in non-Hispanic Black boys. In 1998-1994, non-Hispanic Black boys had the
lowest prevalence of obesity at 10.7% (compared to non-Hispanic White boys at 11.6 and
Mexican-American boys at 14.1%). However, by NHANES 2007-2008, while still
trailing behind Mexican-American boys (26.8%), non-Hispanic Black boys (19.8%) had
surpassed non-Hispanic White (16.7%) boys by three percentage points. [FIG. 4]
Among adolescent girls, the trend between Mexican-American girls and non-
Hispanic Black girls was reversed. In NHANES III (1988-1994), the prevalence of
obesity among adolescent girls was 8.9% among non-Hispanic White girls, 16.3% among
non-Hispanic Black girls, and 13.4% among Mexican-American girls. By NHANES
2007-2008, those rates had increased to 14.5%, 29.2% and 17.4% respectively. [FIG. 5]
The prevalence of obesity among non-Hispanic Black girls increased an alarming 80%
between 1988-1994 and 2007-2008. While there was an overall lower prevalence of
obesity among non-Hispanic White boys and girls, Mexican-American boys and non-
Hispanic Black girls had the highest prevalence of obesity among all ethnicities.
Between these two reporting periods, non-Hispanic White boys and Mexican-American
girls had the lowest percentage point increase, 5.1 and 4.0 respectively; non-Hispanic
High Fructose Corn Syrup and Childhood Obesity p. 24
Black girls and Mexican-American boys had the highest percentage point increase of
12.9 and 12.7 respectively. [FIG 6] Given cultural and ethnic differences this data is
fascinating as it is usually presumed/assumed that trends occur within ethnicities
collectively. For example, Asians typically have smaller frames than Samoans. The
significant discrepancies of obesity prevalence between genders of the same ethnicity
warrants future research.
Fig 4. Percentage of obesity in U.S. boys between 1988-‐1994 and 2007-‐2008 categorized by ethnicity. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-‐11) III (ages 12-‐17) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, 2001-‐2001, 2003-‐2004, 2005-‐2006, 2007-‐2008. Graphic created by author.
0
5
10
15
20
25
30
non-‐Hispanic White boys
non-‐Hispanic Black boys
Mexican American boys
Prevalen
ce of o
besity
Prevalence of Obesity in U.S. boys 1988-‐1994 and 2007-‐2008
1988-‐1994
2007-‐2008
High Fructose Corn Syrup and Childhood Obesity p. 25
0
2
4
6
8
10
12
14
non-‐Hispanic white non-‐Hispanic black Mexican American
Percen
tage points
Percentage Point increase of obesity prevalence between 1988-‐1994 and 2007-‐2008
Boys
Girls
It is estimated that one third of obese preschool children and half of obese
school-age children will become obese adults66 putting them at risk for developing
serious and sometimes fatal health conditions such as: asthma, cardiovascular disease
0 5 10 15 20 25 30 35
non-‐Hispanic White girls
non-‐Hispanic Black girls
Mexican American girls
Percen
tage of o
besity
Prevalence of Obesity in U.S. girls 1988-‐1994 and 2007-‐2008
1988-‐1994
2007-‐2008
Fig 6. Percentage of increase of obesity in U.S. Children and adolescents between 1988-‐1994 and 2007-‐2008 categorized by ethnicity. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-‐11) III (ages 12-‐17) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, 2001-‐2001, 2003-‐2004, 2005-‐2006, 2007-‐2008. Graphic created by author.
Fig 5. Percentage of obesity in U.S. girls between 1988-‐1994 and 2007-‐2008 categorized by ethnicity. Data Source: Ogden et al. (2010) National Health Examination Surveys II (ages 6-‐11) III (ages 12-‐17) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, 2001-‐2001, 2003-‐2004, 2005-‐2006, 2007-‐2008. Graphic created by author.
High Fructose Corn Syrup and Childhood Obesity p. 26
(CVD), hyperlipidemia, high cholesterol, hypertension/high blood pressure, high
cholesterol, stroke, type 2 diabetes (NIDDM), musculoskeletal disorders such as
pizza and salad dressing.146 HFCS-42 was introduced into the U.S. market in 1967 for
use in foods (i.e. baked goods) as the sweetness was not enough to trump the flavor of the
High Fructose Corn Syrup and Childhood Obesity p. 70
food itself. The sweeter HFCS-55 followed ten years later in 1977, replacing sugar (cane
and beet sugar) and becoming the predominant sweetener used in beverages.147 By 2000,
HFCS-55 constituted 61% of all HFCS produced. There are several reasons HFCS has
replaced sugar in the food and beverage manufacturing industry: 1) HFCS is cheaper than
sucrose- 32 cents per pound versus 52 cents per pound, 2) HFCS is a liquid and therefore
easier to transport and use in beverages, 3) HFCS (both 42 and 55) is sweeter than
sucrose, 4) HFCS has a higher solubility than sucrose and 5) HFCS is acidic, containing
preservative properties and therefore maintains a longer shelf life under certain
conditions.148
CONSUMPTION TRENDS
In their analysis of consumption, prices and expenditures in the United States,
Judith Putnam and Jane Allshouse (1999) analyzed per capita consumption of major food
commodities in the United States over a twenty-seven year period, 1970-1997. Between
1982 and 1997, per capita consumption of sugar, primarily sucrose (been and cane sugar)
and HFCS, increased 34 pounds (roughly 28%) to a record average of 154 pounds per
annum, per person. That equates to 53 teaspoons of sugar per person, per day. A
teaspoon of table sugar yields 16 calories thus and additional 53 teaspoons of sugar a day
equates to an additional 848 calories a day. This is approximately half of the daily
caloric requirements of most adults [based upon 1500 kcal/day for women and 2000
kcal/day for men149].
Putnam and Allshouse discovered that not only was there a significant increase in
total sugar consumption, but also in types of sugar consumed. In 1970, sucrose was the
primary sugar sweetener used in the food and beverage industry yielding 83% of the
High Fructose Corn Syrup and Childhood Obesity p. 71
market share for calorie consumption, however, by 1997 that percentage had plummeted
to 43%. Conversely, HFCS’s total share of use and consumption rose from 16% (1970)
to 56% (1997) [Figure 5]. Not surprisingly, per person-per pound consumption of
sucrose and HFCS follow the same trajectory. In 1970, annual per capita use of sucrose
was 102 lbs., by 1997 that number had decreased to 60 lbs. per person. However,
individual consumption of HFCS per annum skyrocketed from 0.5 lbs. in 1970 to 62.4
lbs. per person in 1997 [Figure 6]
83%
43%
16%
56%
0%
20%
40%
60%
80%
100%
1970 1997
Percentage of Sucrose and HFCS used as primary caloric sweetener in the U.S.
Sucrose HFCS
Figure 5. The percentage of Sucrose and HFCS as primary caloric sweetener in the U.S. Resource: Putnam and Allshouse, 1999: Data Source from UDSA Economic Research Service. Statistical Bulletin No. 965. Graphic created by author.
High Fructose Corn Syrup and Childhood Obesity p. 72
Further analysis of the USDA Economic Research Service (ERS) data tables (tables
30, 51 & 52) reveal interesting trends, especially when cross-referenced with obesity
trends. Sucrose (table sugar) consumption experienced its sharpest decline between 1970
and 1986 decreasing from 72.5 lbs./yr. to 42.8 lbs./yr. respectively. Conversely, HFCS
experienced its sharpest rise in consumption within that same period from 0.4 lb./yr. to
32.3 lbs./yr. After 1986, HFCS consumption increased steadily until peaking at 44.2
lbs./yr. in 2002 while sucrose consumption rose only fractionally. [FIG 7] In 2003,
consumption for both sucrose and HFCS was at 43.4 lbs., however, from that point
forward sucrose consumption increased slightly while HFCS consumption decreased.
Since the majority of HFCS (61%) is earmarked for beverages, some suggest that the
increased availability of bottled water and diet drinks explains the HFCS consumption
decrease. Hodan Wells and Jean Buzby (2008), from the USDA Economic Research
Service (ERS), report that between 2000 and 2005 bottled water consumption increased
from 16.7 gallons per person to 25.4 gallons. In addition, consumption of diet beverages
102
60
0.5
62.4
0
20
40
60
80
100
120
1970 1997
Use of Sucrose and HFCS per pound per person
Sucrose HFCS
Figure 6 Use of Sucrose and HFCS per pound per person. Resource: Putnam and Allshouse, 1999: Data Source from UDSA Economic Research Service. Statistical Bulletin No. 965,. Graphic created by author.
High Fructose Corn Syrup and Childhood Obesity p. 73
increased 16 percent during that same time.150
United States Department of Agriculture (USDA) economists Stephen Haley, Jane
Reed, Biing-Hwan Lin and Annetta Cook (2005) analyzed the distribution of sweetener
consumption in the U.S. by demographic and product characteristics between 1994 and
1996. Data analyzed consisted of food intake surveys conducted by the USDA
Agricultural Research Service (ARS) which tracks household and individual food
consumption in the United States. Total data sample consisted of 20,862 individuals:
15,303 adults in the 1994-1996 Continuing Survey of Food Intakes by Individuals
(CSFII) and 5,559 children birth to nine years of age in the child-oriented 1998 CSFII.
For the purpose of their analysis, sweetener consumption was divided into several
categories: 1) sugar (defined as refined cane and beet sugar), 2) corn sweetener (defined
as corn syrup and HFCS), 3) others (inclusive of honey, maple syrup, maple sugar,
sorghum syrup and molasses) and 4) total sweeteners (all categories combined).151 With
respect to socio-economic status of sweetener consumption, their findings are a bit
surprising. CSFII household income brackets were based on Federal poverty guidelines:
0.0 10.0 20.0 30.0 40.0 50.0 60.0 70.0 80.0
Poun
ds per person
Sucrose (Table Sugar) vs. HFCS ConsumpPon
Sucrose lb/yr
HFCS lb/yr
Fig 7. Sucrose (Table Sugar) and HFCS Consumption 1970-‐2010. Data Source: USDA ERS Briefing Room: Sugar and Sweeteners: Data Tables 51 (2011). Graphic created by author.
High Fructose Corn Syrup and Childhood Obesity p. 74
“low income” was defined as 130% or less of the poverty level, “middle income” was
131-350% of the poverty level and 350% and over the poverty level defined “high
income”. Low-income households had the lowest per pound, per capita consumption of
sweeteners totaling 99 lbs./year; 42.7 lbs. of sugar, 54.2 lbs. corn sweetener and 2.1 lbs.
other. Middle-income households had the highest per capita consumption at 105.8
lbs./year; 47.8 lbs. of sugar, 57.5 lbs. of corn sweetener and 0.5 lb. other. High-income
households were a hair behind middle-income households with a total sweetener
consumption of 102.1 lbs./year; 46.7 lbs. of sugar, 54.5 lbs. of corn sweetener and 0.9
other. According to their estimates, low-income household sugar consumption was 8.0%
less than the national average. In addition, they conclude that refined sugar consumption
(cane and beet) is more positively correlated with increasing levels of income than corn
sweetener (HFCS) consumption.152 That is to say that low income households consumed
more HFCS than refined [cane and beet] sugar. Not altogether surprising given the
relative cheapness of prepackaged, fast foods and “junk” foods. In the U.S. food and
beverage industry, the least expensive foods are unfortunately most often the highest in
sugar (specifically HFCS) and fat and lowest in nutrients. Their assertion would seem to
support the contention suggesting lower socio-economic households consume cheap,
manufactured foods due to their inability to pay for the more costly fresh fruits,
vegetables and whole grains.
Among Hispanic, non-Hispanic Black and non-Hispanic White ethnicities, non-
Hispanic Black individuals had the highest per capita consumption of sweeteners
consuming 45.0 lbs. of sugar, 58.2 lbs. of corn sweeteners and 3.1 lbs. other for a total
consumption of 106.3 lbs./year. Hispanic individuals had the lowest consumption of
High Fructose Corn Syrup and Childhood Obesity p. 75
sweeteners overall but the biggest differentiation between sugar and corn sweetener
consumption. Their total consumption was 94.1 lbs./year comprised of 38.2 lbs. of sugar,
55.5 lbs. of corn sweetener and 0.4 lb. of other. Non-Hispanic White individuals had the
second highest total consumption of sweeteners at 105.4 lbs./year. They had the highest
consumption of sugar at 48.6 lbs./year followed by 56.1 lbs. of corn sweetener and 0.7
other.
With respect to age variances, age categories were designated as follows: 2-11
years, 12-19 years, 20-39 years, 40-59 years and ≥ 60 years. Between genders, males
consumed more sweeteners in all categories. Average male consumption was 119.8 lbs.
of sweetener categorized into 51.8 lbs. of sugar, 66.4 lbs. of corn sweetener and 1.6 lbs.
of other. Average female consumption was a total of 86.9 lbs. of sweetener broken down
into 41.2 lbs. of sugar, 45.3 lbs. of corn sweetener and 0.4 lb. of other. What is
interesting about this data (although not terribly surprising) is that in both gender
categories, the highest total sweetener consumption occurred in individuals ages 12-19
years old. Furthermore, 12-19 year old males and females had the highest consumption
of corn sweetener among all age categories 58% for males and 57% for females. Males
(12-19 yrs.) consumed 159.8 lbs. of sweetener per year (40 lbs. more than the combined
average of all ages 2-60 and over); 65.7 lbs. of sugar, 93.0 lbs. of corn sweetener and 1.0
lb. other. Similarly, females (12-19 yrs.) consumed a total of 114.2 lbs. of sweetener;
49.5 lbs. of sugar, 64.6 lbs. of corn sweetener and 0.2 lb. other. [FIG 8]
High Fructose Corn Syrup and Childhood Obesity p. 76
With this level of consumption it is of no surprise that obesity and overweight rates have
increased dramatically among children and adolescents. A pertinent question arising out
of this data is: is it the increase in cumulative sugar consumption that is responsible for
the significant increase in child (and adult) adiposity or is it the type of sugar consumed
that is the decisive variable? At first glance, common sense would say certainly, more
sugar consumed = more calories = more fat, but sometimes things are not always as they
appear at face value.
When comparing the U.S. consumption rates of HFCS (USDA ERS 2011)
alongside the obesity rates of U.S. children and adolescents (Ogden et al. 2010) the
growth curves have striking similarities. [Fig 9] The period between 1972 and 1988
marks the most significant increase for both HFCS consumption and obesity rates. In
1972, the annual consumption of HFCS was 0.8 lb. per person and by 1988 that number
catapulted to 34.9 lb. per person. Similarly, the percentage of U.S. children 2-19 years of
age who were obese in 1972 was 5.0%, by 1988 that number had doubled to 10.0%.
Fig 8. U.S Sweetener consumption for adults and children per pound per person. Data Source: USDA ERS –Haley et al. 2005 Graphic created by author.
0 10 20 30 40 50 60 70 80 90 100
Males-‐ all ages
Males 12-‐19 yrs.
Females-‐ all ages
Females 12-‐19 yrs.
Poun
ds Per Person
Sweetener ConsumpPon among U.S. Adults (1994-‐1996) and children 12-‐19 years (1998)
Sugar (cane & beet)
Corn Sweetener (HFCS & corn syrup)
High Fructose Corn Syrup and Childhood Obesity p. 77
After 1988, both HFCS consumption and obesity rates continued to increase. HFCS
consumption peaked in 1999 with an annual per capita consumption of 45.4 lbs. and then
began a slow descent; currently the annual per capita rate of consumption is 35.1 lbs. per
person.153 Obesity rates, however, continued to climb until peaking in 2003, at which
point 17.1% of children and adolescents 2-19 yrs. old were obese. What is most alarming
about the obesity rates is that these numbers do not include children who were
overweight, only children who were categorized as obese. As mentioned earlier in the
discussion of BMI, and individual can be one or two pounds away from a label (or
diagnosis) of “obese” yet are still extremely overweight and at risk for severe health
complications.
This continued increase in obesity rates despite a decrease in HFCS consumption is not
necessarily surprising because the consumption of HFCS was still extremely high.
Obesity rates peaked in 2003 at 17.1% and at that time per capita HFCS consumption had
only decreased 2 lbs. down to 43.4 lbs. (from its peak at 45.4 lbs. in 1999). The data
0.0
5.0
10.0
15.0
20.0
25.0
30.0
35.0
40.0
45.0
50.0
1972 1978 1988 1999 2001 2003 2007
U.S. HFCS ConsumpPon and Child Obesity Rates
HFCS consumpgon per lb/per person
Percentage of children 2-‐19 yrs. Obese
Fig 9. U.S. HFCS Consumption 1970-‐2010 and U.S. Child and Adolescent obesity rates 1972-‐2007). Data Sources: USDA ERS Briefing Room: Sugar and Sweeteners: Data Tables (2011) and Ogden et al. (2010) National Health Examination Surveys II (ages 6-‐11) III (ages 12-‐17) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, 2001-‐2001, 2003-‐2004, 2005-‐2006, 2007-‐2008. Graphic created by author.
High Fructose Corn Syrup and Childhood Obesity p. 78
from 1972 to 1999 appears to be a “slam dunk” for the HFCS-obesity correlation theory,
however data from 1999 to 2003 appears to negate that supposition. What must be taken
into account is the compound interest effect with respect to physiological processes. As
discussed in chapter 2, metabolic processes involved in glucose and fructose are very
complex. If a child was overweight (not obese thus not registering in the data) in 2001
and maintained (but did not increase) a high refined carbohydrate diet (one common
among fast food and prepackaged foods), it is quite possible that physiologically by 2003
all of his/her glycogen stores were saturated resulting in all calories not immediately
utilized being converted directly into triglycerides and stored as additional fat. In this
scenario, if a child reduced soda consumption (which contains HFCS) from three a day to
one a day, while that would be a significant reduction in HFCS consumption,
physiologically that may still be too much sugar for his/her body to utilize. What is
surprising about the data is the consumption pattern of sucrose and HFCS between 2003-
2007 compared to obesity rates. According to the data tables (table 51), sucrose
consumption began to increase during this period while HFCS consumption and obesity
rates both decreased. Some experts contend that HFCS is not responsible for the
[alarming] rise in obesity rates, claiming that the metabolic processes between sucrose,
glucose, fructose and high fructose corn syrup are not significantly different.154
METABOLISM AND ADIPOSITY
Several studies have looked at differences between glucose and fructose
consumption and their relationship with metabolic processes. 155 However, the majority of
studies investigate and measure the differences between sugars consumed via liquid
High Fructose Corn Syrup and Childhood Obesity p. 79
only156 and do not take into account differentiation of sugars present in food. For
example, in one experiment [that included food] the breakfast consisted of a bagel and
cream cheese.157 While a registered dietician designed the meal, what is not known (or
perhaps what is not stated in the reports) is whether or not the bagel contained any
additional sugars such as HFCS or sucrose. Hypothetically, if a bagel contained 2 g. of
HFCS and test subjects were given a liquid beverage containing 10 g. of sucrose then
total sugar consumption for that meal would be 12 g. with a breakdown of 2 g. of HFCS
and 10 g. of sucrose. Conversely, if the subjects were given a beverage containing 10 g.
of HFCS then while the total sugar consumption would be a constant 12 g., the
differentiation would be 12 g. of HFCS and 0 g. sucrose. Over time this could result in
significant metabolic differences. Nevertheless, the research performed thus far has shed
some light on metabolic differences and/or similarities between the various sugars, and
spawned further questions.
In a comparison study of dietary fructose and glucose on circulating insulin, leptin
and ghrelin levels, Dr. Karen Teff of the University of Pennsylvania School of Medicine
and her colleagues (2004) discovered that dietary fructose reduces circulating insulin and
leptin but increases ghrelin and triglycerides.158 Their subjects were twelve normal
weight women ages 19-33 each with a BMI within “normal” ranges. Experimental
testing consisted of two 48-hour periods a month apart. For one two day period, the
subjects were only allowed to consume meals whose simple-sugar carbohydrates were
derived from fructose (HFr), namely in the form of a fructose-sweetened beverage; an
additional liter of water was consumed throughout the day. Conversely, during the
second 48-hour period, meals consisted of simple-sugar carbohydrates derived from
High Fructose Corn Syrup and Childhood Obesity p. 80
glucose (HGl) in the form of a glucose-sweetened beverage; an additional liter of water
was consumed throughout the day. The research team administered each meal and each
sweetened beverage consumed. Blood samples were taken thirty minutes after each meal
as well as at other hourly intervals throughout the day for the purpose of analyzing the
following plasma concentrations: glucose, insulin, leptin, ghrelin, GIP (gastric inhibitory
polypeptide, an endocrine hormone now believed to induce insulin secretion and also
effect fatty acid metabolism through stimulation of lipoprotein lipase159), GLP-1
(glucagon-like peptide-1, a hormone that induces insulin secretion while suppressing
glucagon secretion and also appears to restore the glucose sensitivity of pancreatic β-
cells160), triglycerides (TG) and free fatty acids (FFA). As anticipated by the team,
plasma glucose levels were lower after HFr meals compared to HGl meals. There was a
significant decrease of 65% (± 5%) in insulin levels after HFr meals compared with HGl
meals; in addition, insulin secretion continued to be blunted throughout the day by
approximately 49% (± 5%) during the days of HFr consumption. There was a slight
difference between HGl meals and HFr meals with respect to plasma leptin levels. As
with insulin there was a significant difference in ghrelin levels. On the HGl days, plasma
ghrelin decreased by 30-35% after each meal; conversely, the suppression of ghrelin after
HFr meals was deemed “not significant”. Interestingly, it was what occurred during the
duration of the day (i.e. non-meal times) that caught researchers attention. During the
evening and early morning hours (i.e. fasting state; 11:00pm-3:00am), on HGl days,
ghrelin concentrations did not increase above baseline however, on HFr days, plasma
ghrelin levels were elevated above baseline. GIP levels were similar in the fasting state
(i.e. 11:00pm-3:00am) for both HGl and HFr days. However, GIP concentrations
High Fructose Corn Syrup and Childhood Obesity p. 81
increased more rapidly after HGl meals (within 30 minutes of consumption) than HFr
meals (within 60 minutes of consumption). In addition, overall plasma GIP levels
remained higher throughout the day on HGl days than on HFr days. While there was not
much differentiation between peak levels of GLP-1 after HGl meals versus HFr meals,
the GLP-1 levels remained elevated for a longer period of time (120 minutes) after HFr
meals than HGl meals. Plasma TG (triglyceride) levels increased (i.e. spiked) more
rapidly 4-5 hours after a HFr breakfast than after a HGl breakfast, in addition the TG
peak was higher with the HFr meal than the HGl meal. Plasma TG levels also remained
elevated throughout the 24 hour period on the HFr days whereas TG levels decreased
after peaks and remained below baseline levels during the night on HGl days. During the
morning prior to breakfast (9:00 am), plasma TG levels were markedly higher (approx.
35%) on HFr days than on HGl days. Plasma FFA levels were similar for both HFr days
and HGl days and they concluded that the differences were not statistically significant
and would not be expected to influence insulin sensitivity. Their results indicate that
consumption of HFr meals and beverages results in lower circulating plasma leptin and
insulin concentrations and higher ghrelin and triglyceride levels than consumption of HGl
meals and beverages. [Ghrelin is a hormone produced by the oxyntic glands of the
stomach that stimulates hunger161 as well as protects against chronic stress induced
depression, anxiety162 and enhances cognition163. Like glucagon is the counterpart of
insulin, ghrelin is considered to be the counterpart of leptin, in fact, ghrelin rivals NPY
for potency in stimulating appetite.164] Teff et al. surmise that because insulin, leptin and
ghrelin are participants with the central nervous system (CNS) regarding long-term
regulation of energy, prolonged consumption of diets high in fructose could lead to
High Fructose Corn Syrup and Childhood Obesity p. 82
weight gain and obesity. In addition, due to the elevated plasma TG levels upon
consumption of fructose, chronic consumption of fructose could also contribute to CVD
and atherogenesis.165
In a short-term study investigating endocrine and metabolic profiles after
consumption of different sugars, Stanhope et al. (2008) examined differences between
HFCS and sucrose when compared to glucose and fructose consumption. The format was
a somewhat similar to Teff et al. however the duration was shorter (24 hours versus 48
hours) and the participants were a mixed gender sample of 18 men and 16 women. Like
Teff et al.’s study, subjects were given prepared meals with an accompanying beverage
that was sweetened with either HFCS, sucrose, fructose or glucose. Their analysis
centered on the differences and/or similarities in blood profiles for the 24-hour testing
period. They reported no significant differences between HFCS and sucrose in plasma
glucose, leptin, ghrelin, TG or FFA concentrations.166 Insulin was slightly “but
significantly” increased with sucrose consumption versus HFCS consumption, however
the team deemed this increase to be age related as there was no reported significant
increase in subjects > 35 years old but only in subjects < 35 years old. While they
reported that plasma profiles during sucrose and HFCS consumption “were not different”,
their data tables state that plasma TG level during HFCS consumption was 1,043.5 mg/dL
whereas levels were 738.7 mg/dL during sucrose consumption, that’s 304.8 mg/dL
difference which may not be statistically “significant” but is certainly relevant, especially
over prolonged accumulation. Melanson et al. (2007) also report no significant
differences in blood glucose, insulin, leptin levels or appetite upon consumption of HFCS
or sucrose.167 However, this too was a short-term (48 hour) study and the team concluded
High Fructose Corn Syrup and Childhood Obesity p. 83
that further research was needed to see if similar results would occur in a longer study.
Studies like these are often the foundation for those who contend that HFCS is
metabolically equivalent to sucrose and that it is the recipient of unwarranted criticism and
“bad press”. However, obesity is not result of short-term consumption but rather long-
term over indulgence therefore, emphasis within the scientific community should be on
long-term studies.
Overall, there are very few studies isolating metabolic differences and/or
similarities between HFCS and sucrose. A major contention of HFCS supporters such as
White et al. (2010) is that HFCS is compositionally similar to sucrose (more so than to
straight fructose or straight glucose) and that the majority of studies examine the
metabolic differences between glucose and fructose168 rather than between HFCS and
sucrose.169 This is a valid contention. In fact, research investigating metabolic
differences and/or similarities between sucrose and HFCS is extremely limited and long-
term studies are almost non-existent. The majority of research designs have been
conducted within a 24-48 hour testing period which might be sufficient for analysis of
short-term effects on blood and metabolic profiles, but certainly is not sufficient to
project any potential (or probable) long-term effects or adverse health ramifications.
One of the few long-term studies with human subjects conducted thus far was by a team
of researchers from the Department of Nutrition at The University of California- Davis
who observed the effects of fructose consumption on blood lipid profiles during a ten-
week period. Swarbrick et al. (2008) concluded that long-term consumption of diets high
in fructose could potentially increase the risk of developing CVD.170 While their
conclusion sounds robust, their sample consisted of seven overweight and/or obese, post-
High Fructose Corn Syrup and Childhood Obesity p. 84
menopausal women and thus is neither a substantial nor representative sample for
conclusions to necessarily be projected onto the general public. However, as with other
studies investigating the effects of fructose consumption, their results clearly indicate that
and again, obesity rates doubled. Another significant period occurs between 2003 and
High Fructose Corn Syrup and Childhood Obesity p. 92
2007. In 2003, child obesity rates peaked at 17.1% but by 2007 those rates had decreased
to 15.5%. During this time total sugar consumption decreased from 86.8 lbs. (2003) to
83.7 lbs. (2007) similarly, HFCS consumption decreased from 43.4 lbs. to 40.1 lbs. but
sucrose consumption increased negligibly from 43.4 lbs. to 43.6 lbs. At first glance this
appears to confirm the contention that it is the quantity of sugar consumed that is the
smoking gun with respect to adiposity and not the quality (type) of sugar ingested.
However, you will recall from the previous section that studies have shown that there are
metabolic differences between different sugars, even between HFCS and sucrose.
Certainly, the quantity of any food substance ingested plays a role in overall weight as
well as lean muscle tissue to adipose tissue ratio. However once cannot dismiss the type
of substance either, 300 calories in a chicken breast is not metabolically equivalent 300
calories of chocolate cake or 300 calories of carrots.
If there is no significant metabolic difference [with respect to adiposity] between
sucrose and HFCS, then one would expect to find obesity rates consuming sucrose to be
similar to obesity rates consuming HFCS however, the data does not reveal that.
Between 1978 and 1988 sucrose consumption decreased (65.1 lb. to 44.2 lbs.
respectively) but obesity rates increased (5.5% to 10.0% respectively). During this same
time period HFCS consumption experienced its greatest surge from 7.7 lbs. to 34.9 lbs.
Opposition would contend that the rise in obesity during 1978-1988, despite the decrease
of sucrose consumption, was directly attributed to an overall increase in total sugar
consumption but that theory does not explain the period between 2003 and 2007. Again,
between 2003 and 2007 sucrose consumption increased but HFCS consumption and
adolescent obesity rates both decreased. [Fig 10]
High Fructose Corn Syrup and Childhood Obesity p. 93
Another weakness of the “cumulative sugar consumption” hypothesis is the time
period between 1999 and 2003. During this time, obesity rates steadily increased from
13.9 % (1999) to 17.1% (2003) yet total sugar consumption decreased from 92.6 lbs. to
86.8 lbs. In addition, both sucrose and HFCS consumption decreased from 45.4 lbs. and
47.2 lbs. (1999) to 43.4 lbs. and 43.4 lbs. (2003) suggesting there were other variables
that were also influential factors.
An admitted weakness of utilizing the USDA Data Tables for analysis of sucrose
consumption, HFCS consumption and child obesity rates is that while the obesity rates
are specific to children and adolescents, the sugar and HFCS consumption data is
cumulative of the U.S. population which means adults are included in that data sample. It
is highly improbable that a three or five year-old child consumed 78.2 lbs. of sugar
(sucrose) in 1972 or 45.4 lbs. of HFCS in 1999. However, it is also just as unlikely that
Fig 10. U.S. HFCS and Sucrose Consumption 1970-‐2010 and U.S. Child and Adolescent obesity rates 1972-‐2007). Data Sources: USDA ERS Briefing Room: Sugar and Sweeteners: Data Tables (2011) and Ogden et al. (2010) National Health Examination Surveys II (ages 6-‐11) III (ages 12-‐17) and National Health and Nutrition Surveys (NHANES) I-‐III and NHANES 1999-‐2000, 2001-‐2001, 2003-‐2004, 2005-‐2006, 2007-‐2008. Graphic created by author.
0.0
10.0
20.0
30.0
40.0
50.0
60.0
70.0
80.0
1972 1978 1988 1999 2001 2003 2007
U.S. Sucrose ConsumpPon, HFCS ConsumpPon and Child Obesity Rates
HFCS consumpgon per lb./per person
Percentage of children 2-‐19 yrs. Obese
Sucrose consumpgon lb./person
High Fructose Corn Syrup and Childhood Obesity p. 94
the same three or five year old child purchased and prepared the food he/she ate.
Obviously, the parents/caretakers are responsible for ensuring that their child eats. It
stands to reason that if the parent/caretaker is consuming large quantities sugar-laden
foods that those same foods are being fed to their children. Nevertheless, the data does
suggest a correlation between consumption of HFCS and increased adiposity among
children and adolescents.
Daily per capita total carbohydrate consumption rose 27% from 386 grams (1970)
to 491 grams (1994). Putnam and Allshouse attribute this increase to the increased use of
grains and sweeteners, as carbohydrates from sugars also increased 21% during the same
period (from 152 grams to 184 grams.). Between 1977-1994, consumption of grain
products such as pizza and lasagna (pasta) increased 115%; snack foods such as pretzels,
popcorn, crackers, and corn chips rose 200%; and consumption of “ready to eat” cereals
increased 60%. It should be noted that most all of these popular grain products often
contain added sugar in the form of HFCS (HFCS-42 specifically). However, while
overall consumption of grain products increased, they assert that whole grain
consumption remained below the ADA recommended daily allowance.
Overall caloric intake increased 500 calories (15%) between 1970 and 1994.
Again, at the risk of being repetitive, all calories are not metabolically and
physiologically the same. While they may contain [and release] the same kcal energy
unit, the other physiological responses outside of ATP production can vary. The same
500 kcal from protein such as a chicken breast will not yield the same physiological
response in the body as 500 kcal of sugar. Protein consumption remained consistent at
eleven percent (11%) of total calories consumed but what is of great interest are their
High Fructose Corn Syrup and Childhood Obesity p. 95
findings that while the proportion of calories yielded from carbohydrates increased (47%
to 51%), the proportion of calories derived from fats decreased (42% to 38%). This data
is contrary to those who hypothesize that obesity is not related to the increase of sugar
intake but rather an increase in overall dietary fat consumption.192 Dr. Walter C. Willett
(1998) of the Department of Nutrition, Harvard School of Public Health and professor of
medicine at Harvard Medical School, expressed concerns regarding the low-fat diet craze
in the 1990s, specifically that substituting carbohydrates for dietary fat consumption
could induce serious metabolic abnormalities [such as hyperlipidemia and
hypertricglceridemia] within a sedentary population that also exhibited a prevalence of
insulin resistance.
In an ecological study of dietary fat intake and its relationship to [excess] adiposity,
Dr. Willett concluded that dietary fat was not the “primary cause” of obesity. For
example, at the time of the study approximately 60% of South Africans were overweight
yet less than 22% of their caloric intake was from dietary fats, he found similar findings
in Saudi Arabia. He concluded that “compensatory mechanisms” within the body occur
such that in the long-term, fat consumption within the rate of 18-40% appears to have a
minimal effect on overall adiposity.193 Subsequently, limiting or removing it from one’s
diet, contrary to popular hypotheses of that time, did not result in shedding of unwanted
pounds (fat). However, some studies have contradicted Dr. Willett’s conclusion.
Gazzaniga and Burns (1993) examined the relationship between diet composition and
body fatness in preadolescent children (9-11 yrs.) and discovered that dietary fat
consumption, specifically saturated fats, were significantly correlated to body fat
percentage (BF%). In obese subjects, a greater portion of caloric intake was derived from
High Fructose Corn Syrup and Childhood Obesity p. 96
dietary fats and significantly less in carbohydrates than in non-obese subjects.
Additionally, obese children expended more energy per day than did non-obese children.
Gazzaniga and Burns surmised this increased energy expenditure resulted from the
additional body weight that was being carried; in short, it requires more energy to move a
larger mass. They concluded that a diet higher in fat and lower in carbohydrates may
contribute to obesity in preadolescent children. A significant limitation of this study is
that data was extrapolated from a 24-hour recall survey completed by the parents so
human error is a factor. Additionally, their data reveals that obese subjects consumed
more calories overall than did the non-obese subjects (9384 kcal versus 7056 kcal
respectively194) , another variable that could be a contributor to their adiposity.
Putnam and Allshouse also discovered that types of fats consumed changed as well
as the percentage/proportion of the overall caloric constitution. In 1970, animal fat
comprised 35% of dietary fat consumption while other fats and oils (primarily vegetable
oils) comprised 43%. By 1994, animal fat had decreased to 25% of all fat consumption
and other fats and oils rose to 52%. The increase in “other fats and oils” category was
most likely due to a significant increase in consumption of fast foods, snack-foods, salad
dressings and other foods laden with hydrogenated vegetable oils. For salad dressings
and cooking oils alone per capita consumption almost doubled between 1970 and 1997
from 15 to 29 pounds per person per year. 195
ECONOMIC BENEFITS
Some contend that the increase in sugar consumption and hydrogenated oil
consumption is inversely proportional to the decrease in price of crop/raw material for
manufacturers, specifically corn, soybean and wheat. The Institute for Agriculture and
High Fructose Corn Syrup and Childhood Obesity p. 97
Trade Policy (IATP) asserts (2006):
“The problem with the extensive use of these cheap commodities in food
products is that they fall into the very dietary categories that have been
linked to obesity: added sugars and fats. U.S. farm policies driving
down the price of these commodities make added sugars and fats some
of the cheapest food substances to produce. High fructose corn syrup
and hydrogenated vegetable oils- products that did not even exist a few
generations ago but now are hard to avoid- have proliferated thanks to
artificially cheap corn and soybeans. Whether by intention or not,
current farm policy has directed food industry investment into producing
low-cost, processed foods high in added fats and sugars.”196
An example of this influence is Kraft Brand’s recent switch from cane sugar
(sucrose) to HFCS in their popular children’s juice line Capri Sun. Due to the economic
cost of sugar (cane and beet) they have now converted to using HFCS to sweeten these
beverages. While they contend that the change was made “to help better manage costs
for consumers in today’s difficult economic environment”197there is no doubt they are
preserving the welfare of their own profit margin as well. Government support for
producing grain, corn and soybean (the latter two commonly referred to as oilseed crops)
takes many forms: money invested in universities and corporations for specific crop
research, direct subsidy payments to farmers to produce specific crops (to offset the
low/set crop prices), as well as agreements for future crop exports.198 These subsidies
indirectly affect the cattle/livestock industry as well since the majority of U.S. livestock
are grain-fed instead of a healthier and more natural grass-fed. The IATP contends that
by keeping crop prices for feed grains so low, the U.S. farm policy has created an unfair
market advantage favoring large, industrialized livestock production over “diversified
sustainable” (i.e. mixed crop and livestock) livestock production. Sadly, produce crops
High Fructose Corn Syrup and Childhood Obesity p. 98
(i.e. fruits and vegetables) on the other hand receive far less government support.
According to the IATP, it is this lack of support that creates a riskier economic
environment for produce farmers. Although fresh produce carries a higher price point,
the lack of support for growing these crops “makes growing vegetables a much riskier
proposition”.199
GENETICALLY MODIFIED FOODS (GMO/GE)
One of the largest areas of research today, estimated at $40 to $100 billion
dollars,200 is biotechnology and genetic engineering specifically, genetically modified
organisms (GMO, GM or genetically engineered, GE) crops. In an effort to increase crop
production and ultimately profitability, scientists have genetically modified crops to be
resistant to pesticides, fungi, bacteria and insects. To genetically modify a crop, scientists
splice together one or more genes into the crop’s genome using viral promoters,
transcription terminators, reporter genes and antibiotic resistant marker genes.201
Bacterium, fungi, and viruses are used as catalysts to graft in the desired gene product to
the host. The problem is that despite the industry driven propaganda, little scientific
research exists regarding the safety and efficacy of these GM products. Dr. Arpad
Pusztai and his colleague, Dr. Stanley W.B. Ewen, from the Rowett Research Institute
(RRI) in Scotland secured a multi-million dollar grant to investigate the impact, if any, on
genetically modified potatoes on animal and human health.202Once a staunch supporter of
GMO, his findings not only changed his stance but also eventually resulted in his
indefinite suspension at the institute and termination of research funding. After working
for RRI for 36 years and publishing almost 300 papers and nine books, Dr. Pusztai was
“removed from service, his research papers were seized, and his data confiscated”203 in
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retaliation for comments made during a 1998 interview regarding his findings on the
effects of GM foods relative to their safety. Prior to splicing with the genetic marker
(gene product), Pusztai and Ewen first isolated the gene product (i.e. protein) lectin from
the snowdrop plant to determine its toxicity and/or effect on absorption of a normal diet
within the intestinal tract. Even at high doses, adding lectin by itself (administered via an
eyedropper) to normal (i.e. non-GM) food did not exhibit any adverse effects; the rats
were not harmed. However, this was not the case for rats fed GM “pest resistant”
potatoes spliced with lectin and the Cauliflower Mosaic Virus (CaMv). The rats fed GM
potatoes where the lectin had been added genetically via splicing suffered damaged
organs, intestinal tract and immune system.204 They concluded that the splicing process
somehow “destabilized the potato genome”205and those elements which made the potato
resistant to insects (i.e. substances that were toxic to the insect) were also making the
potato toxic. Furthermore, they discovered that the splicing process itself was
unpredictable. Their results revealed that genetic differences can occur between sibling
batches of GM foods despite being derived from the same root-stock and subjected to
indistinguishable conditions. It was assumed that these offspring batches would contain
an identical genetic composition however, Pusztai and Ewen’s nearly three year
experiment proved contrariwise. The GM batches were not the same. When discussing
the strains of GM spliced potatoes Dr. Pusztai recounts,
“We had two successful lines, both coming from the same genetic
transformation of the parent line at the same time. They were going
through the same laboratory tests and were growing in the fields for two
years down in the South of England. And when we looked at the two lines,
we found that against our expectations they were different. They were
different compositionally. For example, one of the lines contained exactly
High Fructose Corn Syrup and Childhood Obesity p. 100
the same amount of protein as the parent line but the other line, even
though it was as successful in protecting the plant against aphids
nematodes, it contained 20 percent less protein. Now this was a totally
unpredictable effect.”206
This unpredictability was most troublesome to the scientists and they realized that more
research was needed before deeming GE products as safe for human consumption, “We
don’t eat a lot of these things in GM foods that are now being sold. So it should be in our
interest to get it properly tested.”207 Mae-Wan Ho et al. (2000) reported that post-Pusztai
research has discovered that the CaMv promoter is susceptible to horizontal transfer (i.e.
it participates and potentially instigates unintended rearrangement of genetic coding) and
recombination hot spots (areas where the DNA break and then repair)208 thus contributing
to significant instability within the line. In addition, it has the potential for insertion
mutagenesis, insertion carcinogenesis and reactivation of dormant viruses or to create
new viruses in species it is transferred to.209 Dr. Ho, a geneticist, and her colleagues
recommend that “all transgenic crops containing CaMv 35S or similar promoters which
are recombinogenic should be immediately withdrawn from commercial production or
open field trials. All products derived from such crops containing transgenic DNA
should also be immediately withdrawn from sale and from use for human consumption
and animal feed.”210 Not surprisingly, this recommendation has met its share of criticism.
In many countries, lack of sufficient research regarding the safety and efficacy of
genetically modified foods has resulted in stringent restrictions and even moratoriums on
production. The United Kingdom (UK) has placed a moratorium on all GE foods
pending research on the environmental and human health effects. In 1997, Austria
banned the use of Bt corn. In 1999, Greece banned seven GE crops (including corn),
High Fructose Corn Syrup and Childhood Obesity p. 101
Italy banned GE corn and oil byproducts and Brazil banned the cultivation of GE soybean
and are now exporting GE-free soybeans. Germany banned the cultivation of GE corn
in 2000. Norway banned all GE foods and food manufacturers in Switzerland have
banned all GE ingredients. Japan has mandated testing on potential health risks of GE
foods and its two largest breweries have banned the use of all U.S. GE/GMO corn.211
Sadly, the U.S. is nowhere to be found in the list. Why? The answer is as disturbing as
Pusztai and Ewen’s results.
FDA APPROVAL
In 1992, in response to numerous inquiries regarding the safety and regulatory
oversight of foods produced through genetic modification such as recombinant DNA
techniques (i.e. gene splicing and cell fusion), the U.S. Food and Drug Administration
(FDA) issued a policy statement essentially deeming genetically modified foods to be
“functionally and physiologically equivalent” to normal, non-modified foods and
therefore fall under the GRAS (generally recognized as safe) purview as per sections
201(s) and 409 of the 1958 Federal Food, Drug and Cosmetic (FD&C) Act.212 According
to 201(s) of this Act, “any substance that is intentionally added to food is a food additive,
that is subject to premarket review and approval by FDA, unless the substance is
generally recognized, among qualified experts, as having been adequately shown to be
safe under the conditions of its intended use.”213 (italics added) Substances (foods, food
additives, chemicals etc.) that are recognized as GRAS do not require a formal premarket
review by the FDA. Instead, the process is voluntary. Manufacturers are encouraged,
although not mandated, to seek the FDA for guidance and “consultation”. Again, this
process is not mandated and somewhat akin to telling a ten year old child it would be nice
High Fructose Corn Syrup and Childhood Obesity p. 102
if they cleaned their room before watching TV but did not require them to. The GRAS
label is a very broad and somewhat nebulous term, particularly when applied to
genetically modified foods. According to the FDA, foods that are derived from new plant
varieties, despite how they are derived, “are not routinely subjected to scientific tests for
safety”.214 It is the “how” that is becoming a point of contention for many scientists,
consumers and regulating authorities. Proponents (from both private corporations as well
as government agencies) of genetic engineering contend that modifying the genetic code
of a food, such as introducing a protein from another food or plant, does not change the
constitution of the item and thus the original properties of that food are still intact and
thus safe. Because the food as a whole was not altered it is considered safe as the FDA
“has not found it necessary to conduct, prior to marketing, routine safety reviews of
whole foods derived from plants.”215 In the example of Puzstai’s potatoes, 20% less
protein is not a constitutional change because it is still by definition a potato. To add
further confusion to the GMO/GE safety and efficacy debate is the FDA’s stance that
food is deemed “adulterated” (and thereby rendered harmful and unlawful) if it “bears or
contains an added poisonous or deleterious substance that may render the food injurious
to health.”216(italics added) By FDA standards, GMO/GE foods do not have “added”
substances requiring pre-market research and approval. Apparently, microorganisms,
viruses, bacterium etc. added to a food substance via DNA recombinant techniques is not
really “added”, so there appears to be somewhat of a tap dance over terminology and
definitions. Additionally, there remains no guidance on the process by which these
substances, harmful or not, are added. As seen in Pusztai’s and Ewen’s research, the
recombinant process itself was unpredictable. In addition, there are no long-term studies
High Fructose Corn Syrup and Childhood Obesity p. 103
to prove or disprove the safety of these new biotechnological processes, nor the safety of
the resulting food product. Even scientists within the FDA have expressed concerns
regarding product versus process. In response to the 1992 Statement of Policy, Dr. Linda
Kahl (FDA compliance officer) stated in a memorandum to the FDA Biotechnology
Coordinator, “the document is trying to force an ultimate conclusion that there is no
difference between foods modified by genetic engineering and foods modified by
traditional breeding practices. This is because of the mandate to regulate the product, not
the process.”217 In 2001, the FDA stated that they no longer felt the “voluntary
consultation process” for genetically modified foods was sufficient to ensure the safety of
foods into the U.S. commerce supply.218 However, to date no definitive actions or
regulations have been implemented and the process remains voluntary.
GMO/GE PROCESSING: WHY THE CONCERN
The relevance (and importance) of understanding GE/GMO crops with respect to
HFCS is that virtually all of the corn used to produce HFCS is GE/GMO corn. A
popular strain of GE/GMO corn used in the U.S. is Bt-corn. It is derived from the soil
bacterium Bacillus thuringiensis (Bt) which has a delta endotoxin that is toxic to
caterpillars, specifically during the larvae stage. Industry scientists claim that the Bt delta
endotoxin is selective, “generally not harming insects in other orders”219and because of
this selectivity they deem it safe for humans and other animals. However, Pusztai’s
research has shown, it is not necessarily the gene product used that is harmful but rather
the recombinant DNA splicing process itself. In an examination of the possible
toxicological effects of three GM corn varieties on mammalian and human health, French
researchers Joël Spiroux de Vendômois and his colleagues (2009) discovered toxic,
High Fructose Corn Syrup and Childhood Obesity p. 104
adverse reactions affecting the liver, kidneys as well as the heart, adrenal glands, and
spleen in subjects fed GMO grain.220 de Vendômois et al. performed a comparative
analysis of three popular commercialized GM corn specifically, NK 603, MON 810 and
MON 863 (all manufactured by the Monsanto Corporation). NK 603 (Monsanto’s
Roundup Ready® Corn line) was created to be resistant to the pesticide Roundup®,
whereas MON 810 and MON 863 both contain Bt endotoxins. The data analyzed were
the pre-approval research trails (one per GMO product) Monsanto submitted to the FDA
that, resulting from a lawsuit, were obtained and made public by Greenpeace attorneys in
Denmark and Germany (MON 810 and MON 863) as well as the Swedish Board of
Agriculture (NK 603).221 According to de Vendômois et al., the sample size for each
clinical trial consisted of 200 male and 200 female Sprague-Dawley rats for a total of 400
test subjects, yet only ten were randomly selected and measured at the 5th and 14th week
mark. They rightly conclude that this extremely minute sample size of ten rats measured
only twice in 14 weeks was (and is) “insufficient to ensure an acceptable degree of power
to the statistical analysis performed and submitted by Monsanto.” In addition, they
discovered that Monsanto’s statistical analysis ignored gender differences and skewed
actual results in favor of not detecting a substantial effect by approximately 70%.222
Utilizing Monsanto’s own data they performed sex-specific analysis via the Shapiro test,
Bartlett test, Welch method, Kruskal-Wallis rank sum test as well as an ANOVA per sex,
per variable for each GMO. Results were substantially different from that reported to the
FDA.223
Male rats fed NK 603 were more sensitive than the counterpart female rats and had
relatively higher liver weights (11% increase at the end of the trial) than the non-NK 603
High Fructose Corn Syrup and Childhood Obesity p. 105
group. These rats (male and female) also exhibited “statistically significant” urine ionic
disturbances and kidney deficiencies that suggested potential renal leakage. MON 863
rats also exhibited diminished renal function however, in the MON 863 group renal
disturbances were specifically attributed to increased creatinine levels the development of
“statistically significant” differences in serum glucose and triglyceride levels (up to 40%
increase and a physiological state “indicative of a pre-diabetic profile”), elevated
creatinine, elevated blood urea nitrogen levels, increased liver weight and increased body
weight overall (3.7%). Males on the other hand experienced a decrease (7%) in kidney
weight as well as a chronic nephropathy and an overall decrease in body weight (3.3%).
MON 810 rats (male and female) displayed significant disturbances within the liver as
well as elevated blood urea nitrogen, increased adrenal gland, kidney and spleen weights.
Just as Pusztai (and others) has espoused the necessity of further testing, de Vendômois et
al. conclude that because these GMO/GE substances are not naturally occurring and
subsequently have not been a staple within the human diet (not until the last 10-12 years),
it is essential that long-term studies be performed as “the consequences for those who
consume them, especially over long time periods are currently unknown.” 224 The United
Nation’s Food and Agriculture Organization (2000) acknowledged the lack of studies
regarding long-term effects from consumption of GMO foods and recommended
monitoring changes in nutrient levels in foods derived from GMO products as well as
assessment of the nutritional status of the consumer population.225
High Fructose Corn Syrup and Childhood Obesity p. 106
CHAPT. 4- Other Contributing Factors to Childhood Obesity
PORTION SIZE & INCREASE IN CALORIC INTAKE
Analysis of patterns and trends of U.S. food portion sizes reveals that portion size,
both inside and outside of the home, has increased substantially since the 1970s.226
Young and Nestle (2002), from the Department of Nutrition and Food Studies at NYU,
report that per capita caloric intake contained 500 more calories in 1996 than in 1977
(similar to findings of Putnam and Allshouse). In addition, 1996 portion sizes exceeded
both USDA and FDA standards; cookies exceeded USDA standards by 700%, pasta
exceeded by 480%, muffins by 333% and steaks and bagels trailed at 224% and 195%
respectively.227 In the 1950’s there was one size of french fries (which is now considered
“small”) offered by McDonald’s whereas now, there is small, medium, large and extra-
large (a.k.a. “supersized”). Interestingly, these increases are not unilateral across the
globe. In 1999, an extra-large soda at McDonald’s in Rome, London and Dublin was the
equivalent of a large in the U.S. Similarly, a large order of french fries in the U.K.
yielded 446 calories per serving versus 610 calories per serving for the same “size” in the
U.S.
Their data indicates that the upward trend towards larger portion sizes began in the
1970, increased sharply in the 1980s, and has continued the ascent into the 1990s.
Researchers Samara Nielsen and Barry Popkin from the University of North Carolina
(Chapel Hill) found similar trends as well. They analyzed 63,380 surveys from the
National Food Consumption Survey 1977 (NFCS77), Continuing Survey of Food Intake
for Individuals 1989 and 1996 (CFSII89 and CFSII96) collectively and concluded that
portion sizes served inside and outside of the home increased between 1977 and 1996.
High Fructose Corn Syrup and Childhood Obesity p. 107
Their findings regarding the increase of portion sizes within the home suggests that new
patterns of behavior have also occurred. In addition to the increased consumption of high
density, low nutrient foods (e.g. fast foods and prepared foods), families (children and
adults) are simply consuming more. Researchers Fisher et al. (2003) further contend that
larger portion sizes “may constitute an obesigenic environmental influence” for
preschoolers.228 They discovered preschoolers consumed more calories when given large-
portion lunches irrespective of their level of hunger. Furthermore, they observed that
when given the larger portioned meal, the average bite size was larger as well. The larger
bite size was not determined to be sex specific only meal size specific, that being the
average bite size was smaller during the normal, age appropriate sized meals. They also
observed that children who ate more when served the large portion also had greater
intakes even in the absence of hunger. This observation would suggest that consumption
was not solely biological (i.e. a physiological response to the hunger-satiety feedback
mechanism) but behavioral as well.
Adults are also prone to consuming larger portions,229 subsequently consuming
more calories, irrespective of hunger.230 In a study investigating the relationship between
the size of a pre-packaged snack and caloric intake, researchers Rolls et al. (2003)
discovered that additional caloric consumption was correlational to the size of the
packaged snack. On five separate days 60 adults (34 women and 26 men) were served a
package of potato chips as an afternoon snack, three hours prior to dinner. Snack sizes
varied each day: 28 g., 42 g., 85 g., 128 g., or 170 g. Researchers discovered that
subjects consumed the contents of the larger package (170 g.) just as readily as the
smaller package (28 g.) and that during dinner caloric intake was not modified to offset
High Fructose Corn Syrup and Childhood Obesity p. 108
the additional calories consumed at snack-time.231 Clearly, hunger and satiety are not the
only variables governing consumption.
Nielsen and Popkin suggest that growth in the food industry sector, variety of new
products, an increase in people eating out, aggressive marketing as well as price
competition among manufacturers are possible contributors for this increase. Today,
corporations spend between $10 to $15 billion dollars annually on child/youth-targeted
advertising including brand licensing, product placement, contests, promotions, in-school
marketing, video games, mobile marketing (cell phone, ipod® etc.) and social networking
sites (Facebook®, Twitter® etc.), compared to just $100 million in 1983. 232 Contrary to
what one might think, this demographic (children and adolescents) constitutes a large
segment of consumers, a $200 billion dollar segment according to some estimates, of
which the majority is spent on candy, snack food, soda and cereal.233 WHO contends
evidence suggests that “the heavy marketing of these foods and beverages” to young
children bears some responsibility in the prevalence of obesity among children.234
The increase of portion size has resulted in an increase of overall caloric
consumption.235 However, studies also suggest that it is not portion size alone that is
responsible for excessive caloric intake but a combination of large portions of high-
density foods.236 High-density (a.k.a. energy density) food refers to the amount of energy
in a given weight of food and is dependent upon water, protein, carbohydrate and fat
content.237 For example, a salad is considered “low-density” due to the high fiber, high
water and low fat and low calorie (kcal) content, as the name implies it is less dense.
Conversely, a cheeseburger or Snicker’s bar is high-density due to the high fat, high
sugar, low water and low fiber content. Compositionally, these latter foods are
High Fructose Corn Syrup and Childhood Obesity p. 109
comprised of high k/cal compounds resulting in an overall high(er) k/cal yield.
Obviously, a pound of lettuce and a pound of cheese are not caloric equivalents despite
registering the same weight on a scale. Consequently, consumption of these high-
density/high-energy foods results in a higher caloric intake.238 Sadly, data reveals that as
consumption of high-density foods has risen, consumption of high fiber fruits and
vegetables has declined.239 Pediatricians and nutrition experts are rightfully concerned
that this decline has resulted in insufficient levels of vital nutrients such as iron, folate,
calcium and vitamin A.240 The cumulative effect of years of insufficient nutrient intake
can result in significant adverse health conditions.
DECREASED PHYSICAL ACTIVITY, INCREASED TELEVISION & COMPUTER USAGE Physical Activity
With respect to excess adiposity and obesity, diet and exercise are
inextricably intertwined. When caloric consumption exceeds caloric expenditure the
body converts the excess energy (calories) into fat. Physical activity is a cornerstone
foundation for health and wellbeing of both adults and children. Physical activity
strengthens the immune system, increases bone density, improves mental health and self
esteem, reduces stress, increases energy and protects against diseases/conditions such as
CVD, hyperlipidemia, hypertension, insulin resistance, certain cancers (breast, pancreatic
and colon) and osteoporosis.241 In addition, physical activity helps maintain a healthy
body weight and can reduce excess adiposity.242 In a 12 month randomized trial of 201
overweight, sedentary women researchers (Jakicic, et al. 2003) discovered that both
moderate and vigorous levels of exercise yield weight loss (8% to 10% of body weight
respectively) and improved cardiovascular fitness.243 This benefit applies to children as
High Fructose Corn Syrup and Childhood Obesity p. 110
well. A 29.6- week study of 292 elementary school students in Songhkla, Thailand
suggests that a long-term school-based exercise program can prevent weight gain and
may facilitate a “remission” of obesity in children. 244
In 2003, the Youth Risk Surveillance Survey (YRSS) reported that 62.6% of
students (ninth through 12th grade) nationwide met the recommended standards of
physical activity (≥ 20 minutes of rigorous activity ≥ 3 days/week) and 24.7% met the
standards for moderate physical activity (≥ 20 minutes of rigorous activity ≥ 3
days/week). Only 11.5% of youth did not engage in any type of physical activity, sadly
that number doubled (23.1%) by the 2009 Youth Risk Surveillance Survey.245 By 2009,
18.4% of students participated in ≥ 60 minutes of rigorous physical activity ≥ 7
days/week and 37.0% participated in ≥ 60 minutes of rigorous physical activity ≥ 5
days/week. Standards and definitions of physical activity were modified between 2003
and 2009 thus making definitive conclusions between the two data samples difficult to
draw and allowing only for observational estimates. Nevertheless, in 2003 87.3% of
students engaged in rigorous and moderate physical activity (categories combined)
whereas 55.4% of students in 2009 engaged in rigorous physical activity (again,
categories combined). Again, it is impossible to make a direct and completely accurate
comparison between the two sets of data because of dissimilar variables.
First, there is a significant difference between 20 minutes of exercise ≥ 3 days a
week and ≥ 60 minutes of rigorous physical activity ≥ 7 days/week. If there are only
three categories of reported physical activity to chose from (7 days a week, 5 days a week
or no activity) as in the 2009 survey, hypothetically there could be a significant number
of students who participated in rigorous exercise two to three days a week or who
High Fructose Corn Syrup and Childhood Obesity p. 111
exercise daily but for only 30 minutes not 60 and therefore did not fall into any
recognized category. Second, the 2003 “insufficient moderate physical activity”
category was removed in the 2009 survey. What is not known is whether or not that was
combined with the “no rigorous physical activity during the week” category. The 2003
survey reported “moderate” and “insufficient” exercise whereas the 2009 survey only
reported “rigorous”. If the categories were combined it might explain the increase in “no
rigorous physical activity” in 2009 especially taking into consideration the increase in
participation of physical education class (PE). In 2003, 55.7% of students reported
attending ≥ 1 day of PE and 28.4% reported attending ≥ 5 days of PE. By 2009, those
numbers had increased to 56.4% and 33.3 % respectively. Albeit not statistically
significant, it is an increase and somewhat surprisingly, not a decrease.
Television, Computers and Video Games
The YRSS surveys also reported daily television and computer usage. In 2003,
28.4% of students reported watching ≥ 3 hours of television per day. That number
decreased slightly in 2009 to 32.8% however, reported computer usage was 24.9% ≥ 3
hours per day. The 2003 survey did not collect data regarding computer usage (again,
dissimilarities between the 2003 & 2009 survey data) therefore any conclusion is purely
speculative. Despite the inconsistencies in data collected the 2003 and 2009 Youth Risk
Surveillance Surveys, these reports provide an overview of national trends in the
adolescent population. Television and computer usage are both sedentary activities
requiring minimal energy expenditure. There are no studies on other sedentary activities
such as board games and reading as they relate to overweight and obesity. However,
prior to the “computer age” obesity and overweight was not as pervasive prompting
High Fructose Corn Syrup and Childhood Obesity p. 112
researchers to investigate a possible connection between the two.
As of 1999, video games accounted for over 30% of the toy market in the United
States with approximately 97% of teenagers (12-17) playing either on a computer,
console, portable (hand held) unit or via the internet.246 Dr. Jean-Philippe Chaput, from
the Department of Pediatrics at the University of Ottawa, and his colleagues (2011)
discovered that during one hour of playing video games, energy expenditure was
significantly higher however, ad libitum energy intake (i.e. consumption) was
significantly increased during the resting state post-playtime.247As with other studies
regarding television viewing,248Chaput et al. discovered that post-play consumption was
not associated with appetite or hunger. There is some mildly good news regarding video
games and that is the emergence of “active” video games. These are video games that
require users to move their body to elicit a desired response on the monitor and game
genres range from sports and races to dance and yoga. Dr. Elaine Biddiss and Jennifer
Irwin (2010) found that active video games can facilitate light to moderate physical
activity in some cases increasing energy expenditure 100% and elevating heart rate
20%.249 Maddison et al. also discovered that active video games have a positive
influence on BMI and body fat composition in overweight and obese children, namely
reducing both.250 While this activity may not compare to activity expended during
participation in real athletic events, it is certainly a move (no pun intended) in the right
direction.
There appears to be a direct relationship between hours of television watched and
adiposity.251 In analysis of the California Teen Longitudinal Survey of 1993 and 1996,
Kaur et al. found that children who watched television ≥ 2 hours a day were twice a likely
High Fructose Corn Syrup and Childhood Obesity p. 113
to be overweight in the 1996 follow up study than those who watched < 2 hours a day.252
Similarly, an earlier study by Dietz and Gortmaker (1985) found that every one hour of
television viewing resulted in a 2% increase in prevalence of obesity among 12-17 year
olds.253 Dr. Ross Anderson et al. (1998) from Johns Hopkins School of Medicine
investigated the correlation between television and BMI specifically. They discovered
that children who watched television ≥ 2 hours a day had higher BMIs and greater body
fat than children who watched < 2 hours a day.254 They also surmised that repeated
exposure to food commercials prompt children to increase consumption regardless of
hunger or lack thereof, ultimately resulting in weight gain. A recent study (2011) found
that children who engage in high levels of television viewing are more responsive to
advertising geared towards food than non-food (e.g. toys).255 Additionally, “high
viewing” children migrated towards high-density, high carbohydrate and high fat food
selections even after watching commercials marketing toys, whereas the “low viewing”
children did not. Temple et al. (2007) found that television watching increased the time
spent eating, the amount consumed and caloric intake.256 There also appears to be an
inverse relationship to television at mealtime and consumption of whole grains, fruits,
and vegetables. Children from families that have the television on during two or more
meals a day consume less grains, green and yellow vegetables, non-fried potatoes, beans
and nuts than children from families who do not watch television during mealtime.257
This intertwines with another proposed contributor to child obesity: the reduction (and for
some families cessation) of traditional “family meal time”.
High Fructose Corn Syrup and Childhood Obesity p. 114
REMOVAL OF TRADITIONAL FAMILY MEALTIME
Family mealtime has been positively associated with adolescents making healthy
food choices, diminished consumption of fried foods, diminished frequency of eating
disorders, increased family connectedness and improved adolescent mental health.258
Family dinners are positively correlated with children eating breakfast as well as higher
consumption of fruits, vegetables and whole grains.259 Consistent family mealtime is also
positively correlated with healthy child and adolescent body weight. Children and
adolescents who never report eating family meals are significantly more likely to become
overweight and/or obese.260Despite the benefits of family meals, sadly, the prevalence of
regular family mealtime appears to be diminishing.
In 1991, only 27% of adolescents (12-17 years old) ate dinner with their family
every day, 47% ate with them 4 to 6 days a week and 27% ate together 1-3 days a week.
261 The percentage of younger children (< 12 years old) who eat as a family every day is
slightly better at 41%-to 45% but still abysmally small especially given the role it appears
to have with proper nutrient intake. In a comparative study of 16,862 children (9-14
years old) who ate dinner as a family never/some days, most days or every day, Gillman
et al. (2000) observed that children who ate meals with their family daily consumed more
vegetables and fruits (twice as much) and less fried foods and soda.262 These youth also
had a higher intake of essential nutrients such as calcium, iron, vitamin C, folate and
fiber. Furthermore, they consumed less saturated fat, trans fat and high glycemic foods.
What is interesting about their data is that children who ate meals with their family daily
consumed more calories than those in the never/some category (9294.6 k/cal. and 8677.2
k/cal. respectively), however they had a lower BMI than those who ate never/some days.
High Fructose Corn Syrup and Childhood Obesity p. 115
Surprisingly, children who ate family meals daily had slightly less physical activity than
those who never or some times ate with the family. To summarize, children who ate
meals with family daily consumed more calories, more nutrients, and had less physical
activity than children who never or some times ate family meals, yet they had a lower
BMI. This suggests that what is consumed plays a key role in weight and adiposity in
children and adolescents.
FAST FOOD & FAT CONSUMPTION
Changes in fast food consumption patterns also play a role in obesity and share
similar trajectories. Contrary to most expectations, dietary fat consumption has
decreased among children and adolescents over the last 20 to 30 years.263 In an analysis
of food intake trends from 1965-1996, Cavadini et al. (2000) discovered a significant, and
somewhat surprising, dietary “shift” among U.S. adolescents (ages 11 to 18 years). In an
analysis of 12,498 Nationwide Food Nutrition Surveys (NFCS), researchers discovered
that total energy intake among adolescents decreased between 1965 and 1996 as did the
proportion of energy derived from fat. In 1965, the percentage of total energy (caloric)
intake derived from fat was 38.7%. This proportion decreased steadily until 1996 when it
accounted for only 32.7% of total intake. Similarly, the consumption of saturated fats
followed similar trends falling from 15% (1965) to 11.6% (1996). [Fig 11] According to
their analysis, there was a 17% decrease of overall energy intake during this 30 year
period which they acknowledge seems “counter intuitive” given the rise in adolescent
overweight and obesity.
High Fructose Corn Syrup and Childhood Obesity p. 116
While this study suggests dietary fats are not positively correlated with obesity it
could be that, as with sugars, it is the type of dietary fat that is most influential. As with
the rise of HFCS, the use of hydrogenated oils (a.k.a. trans fatty acids) in the food
industry surged during the 1980’s and 1990’s. Approximately 40% of all processed
foods in the United States contain trans fatty acids.264 According to some estimates,
hydrogenated oils comprised 4-7% of U.S. caloric fat content by 1990.265 While attractive
to the food industry because of its long shelf life duration and stability during high
temperature deep-frying,266 trans fatty acids have been associated with cardiovascular
disease, high cholesterol, systemic inflammation, insulin resistance, visceral adiposity,
and type 2 diabetes.267 Additionally, partially hydrogenated soybean oils have been
shown to increase blood glucose levels, insulin and LDL levels.268 In fact, the adverse
health affects associated with trans fatty acids led to the FDA requiring manufacturers to
list trans fat content on all food labels as of January 2006.269 While the labeling is
required and can certainly be found on national fast food restaurant chain websites, most
Fig. 11 Percentage of Total Energy Intake among U.S. Adolescents 1965 to 1996. Data Source: Nationwide Food Consumption Surveys (NFCS) Cavadini et al. 2000. Graphic created by author.
0
10
20
30
40
50
60
1965 1977 1989-‐91 1994-‐96
Percentage of Total Intake
Percentage of Total Energy Intake Among U.S. Adolescents 1965-‐1996
Total Fat
Saturated
Carbohydrate
High Fructose Corn Syrup and Childhood Obesity p. 117
foods consumed in fast food restaurants do not have food labels printed on the wrapper or
cardboard container.
St.-Onge et al. (2003) reports a significant increase in fast food consumption among
children and adolescents over the last 20 to 30 years. Between 1977 and 1989, fast food
consumption among adolescents 12-18 years old increased from 6.5% to 16.7%, and had
reached 19.3% by 1994.270 While overall fat consumption had decreased, studies indicate
that individuals (children and adults) who consume fast foods on a regular basis consume
more calories, more fat, more sugar and less fruits and vegetables than individuals who
do not eat fast food.271 Fast food is laden with added sugars and fats and thus combined
increase the energy content (calories) significantly. In a three-year study, Duffey et al.
(2007) concluded that fast food consumption has a positive association with BMI. The
greater the fast food consumption the higher the corresponding BMI.272
SODA CONSUMPTION
Not surprisingly, there has likewise been a dramatic increase in the consumption of
carbonated beverages during emergence of HFCS into the food and beverage market. In
1986, approximately 28 gallons of non-diet, carbonated beverages were consumed
annually per person, by 1997 that number grew to 41 gallons per person. The 2009
YSSR Surveys found that 29.2% of students drank ≥ 1 soda per day. The average soda
contains 30-40 g. of sugar (primarily from HFCS-55) averaging approximately 150
calories. At the minimum rate of one soda per day that is an additional 1050 k/cal.
(calories) per week and 54,600 k/cal. per year. Studies have associated sugar-sweetened
beverages with obesity in children.273 However, in a review of children’s beverage
High Fructose Corn Syrup and Childhood Obesity p. 118
consumption from 1987-1998, researchers Park et al. (2002) discovered that carbonated
beverage consumption actually decreased from 1987-88 to 1997-98 from 84% to 72%
respectively.274 In 2000, soda consumption accounted for one third of all added sugar
intake in the U.S. diet.275 In an investigation of the effects of HFCS sweetened soda on
body weight and food intake, Todoff and Alleva (2001) found that after three weeks of
HFCS consumption both male and female subjects gained weight (females significantly
and males to a lesser, but still measureable, extent).276 Other studies have concluded that
consumption of sugar-sweetened beverages is associated with increased BMI and obesity
in children and adolescents.277 However, a long-term study investigating beverage
consumption and BMI in children (Blum et al. 2005) had results researchers were not
anticipating.
Consumption of regular soda, diet soda, milk, 100% juice, or other sweetened
beverages (sports drinks, kool-ade etc.) in 166 children (grades 3rd-6th) over a two-year
period was examined. Researchers discovered that children who were overweight and/or
who had gained weight during the two-year period had a significantly higher
consumption of diet soda than normal weight subjects.278 In fact, diet soda was the only
beverage associated with increased BMI. Blum et al. concluded that the mechanism
behind the increased BMI and diet soda consumption remained unclear [positing that
perhaps the overweight subjects increased their consumption of diet soda in an attempt to
lose weight] and suggested that further longitudinal studies were needed. A common
question that arises when discussing the role of soft drinks and obesity/adiposity is
whether it is the beverage itself that is responsible for the purported weight gain or
whether it is the increase of total caloric consumption that is the real culprit? Again,
High Fructose Corn Syrup and Childhood Obesity p. 119
there is evidence on both sides. Some studies show a clear correlation between soft drink
consumption and adiposity279 while others show no correlation at all.280 Others suggest
that increase in overall caloric consumption is responsible and sugar-sweetened
beverages, specifically soft drinks, should not be singled out.281
ROLE OF GENETICS
To paraphrase Dr. Dean Ornish when asked about the role of genetics and obesity,
indeed overweight children frequently have parents who are also overweight but so are
the family dog and cat.282 Some researchers investigating monozygotic twins have
implied that body weight and composition are influenced by genetic factors283 while
others contend that genetic factors appear to influence and affect the body’s response to
external factors (i.e. environmental factors)284and that expression of a specific genotype
is dependent upon the environment.285 As seen in the discussion on leptin, genes and
genetic coding certainly participate in human physiology and metabolic processes,
however a genetic predisposition to a condition does not definitively guarantee an
expression of that condition. The environmental conditions must support, if not
catalyze, the emergence of that condition. For example, dry wood has a predisposition
to burn when ignited, dry wood soaked in gasoline has a greater predisposition to burn
when ignited but without the catalyst of fire, neither scenario will result in burning
wood. The environmental factor of fire must be present for the ignition to occur.
“Biological” and “environmental” have often been theoretical rivals. In psychology,
there are those who contend behavior is determined by environmental factors and those
who contend it is determined by innate biological factors. Similarly, the debate
continues regarding the origins of overweight and obesity and the truth most likely lies
High Fructose Corn Syrup and Childhood Obesity p. 120
somewhere in the middle. Children learn from and imitate their parents’ behavior. Just
as healthy eating patterns are established by parents286 so are unhealthy eating patterns.
Most children are overweight and obese because they consume the same foods that their
parents eat and employ the same behaviors that their parents employ. For example,
researchers at Harvard’s School of Medicine (Gilman et al. 2009) have found a
significant association between parental smoking and smoking initiation among
adolescents 12-17 years old.287 The reality is that in today’s society it is much easier
(and sadly encouraged) to cast blame for being overweight/obese on “genetics” than to
take responsibility for one’s own inability to exercise restraint and self-control.
High Fructose Corn Syrup and Childhood Obesity p. 121
CONCLUSION
The obesity epidemic in the United States is reaching critical mass (no pun
intended) and a solution must be found. If nothing is done to arrest this epidemic or at
the very least, slow down the rate of acceleration, the impending health and economic
costs could be cataclysmic. Obesity has been directly associated with a cornucopia of
adverse health conditions including, but not limited to, CVD, hyperlipidemia, cancer,
breathing impairments, sleep disorders, high blood pressure, insulin resistance, NIDDM
(type 2 diabetes) and psychological problems.288
There are additional tangential health concerns potentially associated with mercury
byproducts that have been detected in HFCS. Laboratory tests have clearly detected
trace, yet significant, amounts of mercury in HFCS produced in the United States. Aside
from hepatic and renal toxicity, mercury has been the center of much debate regarding a
possible association (and some would contend causal relationship) with birth defects and
learning disabilities such as Autism, Autism Spectrum Disorder (ASD) and Attention
Deficit Hyperactivity Disorder (ADHD).289 Dufault et al. (2009) found a striking
similarity between HFCS consumption rates and annual growth rates of ASD in
California. While no direct causal relationship was determined, they rightly concluded
that mercury contamination could be a contributing factor and that significant research is
needed in this area of neurodevelopment. In an analysis of blood mercury levels and
diagnosis of autism, Drs. Catherine DeSoto and Robert Hitlan (2007) found a
“statistically significant” relationship between blood mercury levels and the diagnosis of
ASD.290 In another prospective study of mercury toxicity and autism, Geier and Geier
High Fructose Corn Syrup and Childhood Obesity p. 122
(2007) found that over 50% of individuals diagnosed with ASD had mercury toxicity
biomarkers (specifically coproporphy, pentacarboyxyprophyrin and precoproporphyrin)
that were more than two standard deviations above the mean than their non-ASD
siblings.291 While there may not yet be a definitive causal relationship between HFCS
and learning disabilities such as ASD and ADHD, there is little evidence vindicating it
either. Clearly, this is an area of research that needs further investigation, especially in
light of potential en utero fetal toxicity.
The goal of this research was to determine whether or not high fructose corn syrup
(HFCS) is responsible, either in whole or in part, for the current obesity epidemic
plaguing children in the United States. To claim that HFCS is the sole contributor and/or
cause of child overweight and obesity would be synonymous with claiming cigarette
smoking is the only cause of lung cancer or driving while intoxicated is the only cause of
automobile accidents. However, is it just as erroneous to claim that cigarette smoking
does not contribute to lung cancer or that driving while intoxicated does not result in
automobile accidents, and the same applies for HFCS and obesity. While there are
several aggregate contributors to the overweight and obesity epidemic, such as decrease
in physical activity, increased use and prevalence of television, computers and electronic
media etc., increase in portion sizes and prevalence of prepared, packaged and “fast”
foods, research shows that HFCS is clearly a contributing factor and, in the eyes of this
author, one of the most significant ones.
There have been many studies investigating metabolic differences and/or
similarities between various sweeteners: glucose, fructose, sucrose and HFCS. However,
the majority are short-term studies often 24-48 hours in duration. While short-term
High Fructose Corn Syrup and Childhood Obesity p. 123
metabolic profile results are valuable, they are not applicable for determining long-term
physiological responses and metabolic profiles. They are woefully insufficient in
predicting long term adiposity as confirmed by Light et al.’s research. Results from this
eight-week study revealed a significant difference in adiposity between subjects that
consumed HFCS and those that consumed sucrose, glucose and fructose. Not only did
the HFCS subjects have an overall higher weight gain and greater abdominal fat increase,
their livers weighed significantly more than all the other subjects… even more than the
sucrose “equivalent” group. A healthy liver is essential for proper metabolism, fat
emulsification and energy production/storage. Light et al.’s study clearly shows that long
term HFCS consumption has an adverse affect on the liver and similar studies with
human subjects are desperately needed. However, champions of HFCS and industry
supporters have altogether ignored studies like Light et al. choosing rather to focus on
short-term blood profile results in defense of their pro-HFCS stance. If the liver is
overloaded or worse, damaged, normal metabolic processes will be impeded. Studies
have shown that mercury and recombinant DNA splicing both adversely affect the liver
(as well as other organs). Mercury is known to cause hepatotoxicity292 and trace, yet
cumulatively significant, amounts have been detected in HFCS. Add to this equation the
fact that the majority of HFCS is produced from genetically modified corn and GMO/GE
corn has toxic effects on the liver.293 In addition, like Light et al.’s rats fed HFCS, rats
fed GMO/GE corn experienced liver weight gain (11% in 14 weeks).294 When these three
aspects of HFCS are looked at collectively, the case against HFCS becomes even more
damaging.
The real question that many would prefer to remain the proverbial “white elephant”
High Fructose Corn Syrup and Childhood Obesity p. 124
is what do we do about it? As with many policy decisions, this will most likely be a
function of economics. To ban the use of HFCS in foods and beverages would have a
significant financial impact to food and beverage manufacturers, as profit margins would
shrink. This, of course, would be passed along to the consumer (as seen in the case with
Capri Sun) with most likely higher prices and smaller portions, the days of “super size
me” would come to an abrupt end (which is not altogether an adverse side effect). There
could also be a potential impact on commercial farmers. Although a large portion of corn
is used for grain-feed, a significant portion is used to make HFCS. It is unknown whether
or not other industries (biofuels for example) would absorb the utilization. If not, there
could be a potential surplus of corn especially given the more stringent regulations other
nations have regarding use of GE/GMO corn imported from the U.S.
There is of course, the separate matter of the use of GE/GMO corn and the
unknown, yet potential, adverse health ramifications to humans. Again, this will most
likely be a decision of economics rather than consumer health. Powerful corporations
such as Monsanto, ConAgra and Calgene, Inc. have invested tens of billions of dollars
into R & D and are not likely to let the return on their “investment” dissipate, and
certainly not without a lengthy and costly fight. Add to this equation other special
interest groups (the Corn Growers Association for example) and federal bureaucracies
(FDA, EPA and UDSA) and the removal of HFCS from the U.S. food supply becomes all
the more unlikely. Nevertheless, unlikely not does mean unnecessary. For years,
radium was touted as containing beneficial properties and curative powers and was a
common additive in products such as toothpaste, hair creams, salves and even food
items.295 However, it has since been discovered that this wonder compound is poisonous
High Fructose Corn Syrup and Childhood Obesity p. 125
and exposure, much less ingestion, results in serious and often deadly effects.
There is of course the issue of current and future economic costs of obesity-related
health issues. The economic impact of the treatment of obesity-related diseases and
disorders is astounding and one that, given the current economic climate, cannot be
sustained indefinitely. At some point the money will run out.
At this juncture, the most viable solution appears to be grassroots education for
both children and adults. It is not the role of government to mandate what individuals eat
or do not eat, but it is their role to provide accurate information particularly regarding
dangerous and/or toxic substances in our food supply. In the United States there are
many examples of consumer education changing consumer trends. While corporations
(such as biotech companies, pharmaceutical companies, food and beverage manufacturers
etc.) protectively guard their profits they know that at the end of the day the customer is
always right. If consumers don’t buy the product they change the product. In the 1980’s
when Coca- Cola changed their formula sales decreased so significantly that they had to
revert to the original formula. The growing “organic” movement is another example of
consumer driven manufacturing. Consumers are demanding that stores carry organic
products and what was once only found at health food stores and local farmer’s markets
is now widely accessible in superstores such as Target, Costco, Kroger and Walmart.
Even manufactures have changed what they provide due to consumer pressure and desire
to maintain their profit margin.
In addition to consumer education, the FDA should require manufacturers to list
the amount of HFCS contained in the food/beverage just as the 2006 ruling requires trans
fats to be listed. Currently, if a food/beverage contains HFCS it must be listed as an
High Fructose Corn Syrup and Childhood Obesity p. 126
ingredient but that does not give the consumer information as to how much is contained
in the food/beverage. There should also be careful consideration given to developing a
national database for analysis of food composition with respect to types of sugars and
types of fats. This would enable researchers to accurately analyze caloric and nutrient
trends.
There clearly needs to be more specific, long-term studies regarding HFCS and
metabolic processes. As shown, the majority of the experiments to date are short term
(24 to 48 hours) and with small sample sizes. Additionally, large scale, independent
studies regarding GMO/GE foods and the effects of long-term ingestion are needed. The
current studies are scarce, insufficient and often industry driven. There is too little
information and too many unknowns (and what is known is extremely disturbing). With
respect to adiposity and obesity, more research should specifically examine the effect
GMO/GE foods have on the liver and hepatic enzymes as well as potential effects on
regulatory hormones such as insulin, leptin and ghrelin. The rats fed MON 863 who
exhibited a “pre-diabetic profile” are a clear example of why this needs further
examination as this could have significant implications for human health.
In short, there is no “smoking gun”, no magic bullet that the “blame” can be cast
upon. Multiple facets contribute to and fuel this epidemic. This means that each factor
must be carefully examined and dealt with accordingly. Those in the food and beverage
industry often shift the focus towards the lack of physical activity and we, as a society,
certainly need to look at ways to address this significant decline. Physical activity burns
calories. To maintain a healthy body weight, energy expenditure should mirror energy
consumption. However, that does not mean that we should ignore and fail to address
High Fructose Corn Syrup and Childhood Obesity p. 127
other contributing factors such as portion size, hydrogenated oils or, as this author
contends, the utilization of HFCS as the primary food and beverage sweetener.
High Fructose Corn Syrup and Childhood Obesity p. 128
APPENDIX Table 1. MMWR Youth Risk Behavior Surveillance Summaries-‐ United States 2003 and 2009
Participated in rigorous physical activity -‐ 5 days/week n/a 37.0% Participated in rigorous physical activity ≥ 3 days/week 62.6% n/a Participated in moderate physical activity ≥ 5 days/week 24.7% n/a Insufficient moderate physical activity -‐7 days/week 33.4% n/a No rigorous physical activity during the week 11.5% 23.1% P.E. Class Attendance
1 day a week or more 55.7% 56.4% 5 days a week or more 28.4% 33.3% Computer use ≥ 3 hours per day ** n/a 24.9% Television use ≥ 3 hours per day 38.2% 32.8% Dietary Behaviors
Soda Consumption-‐ drank ≥ 1 soda per day *** n/a 29.2% Milk Consumption-‐ drank ≥ 3 glasses of milk per day 17.0% 14.5% male 22.7% 19.8% female 11.2% 8.7% Ate vegetables ≥ 3 times a day n/a 13.8% Ate fruits and vegetables ≥ 5 times a day 22.0% 22.3% Obesity, Overweight and Weight Control
Obese
12.0% Overweight 13.5% 15.8% Described themselves as overweight 29.6% 27.7% Trying to lose weight 43.8% 44.4% Had exercised to lose weight and/or prevent weight gain 57.1% 61.5% Had restricted food consumption to lose weight and/or prevent weight gain 42.2% 39.5%
* The 2003 and 2009 Youth Risk Behavior Surveillance Surveys differ in data collected and reported for Physical Activity. In 2003, the three designated categories were: Sufficient Rigorous Physical Activity (e.g., running, swimming, soccer, cycling etc. for ≥20 minutes for ≥ 3 days/week), Sufficient Moderate Physical Activity (walking, skating, pushing lawnmower, mopping floors etc. for ≥30 minutes ≥5 days/week) and Insufficient Amount of Physical Activity. The 2009 survey designations: Physically active at least 60 minutes 7 days/week (activity that elevated heart rate and made them breath hard), Physically Active at least 60 minutes 5 days/week (activity that elevated heart rate and made them breath hard) and Did not participate in at least 60 minutes of activity on any day. ** Computer usage was not measured in the 2003 survey. *** Soda consumption was not measured in the 2003 survey.
High Fructose Corn Syrup and Childhood Obesity p. 129
End Notes 1 (World Health Organization (WHO), 2000) 2 (The Mayo Clinic, 2011) (The Mayo Clinic, 2011) 3 (UK Daily Mail, 2011) 4 (Dehghani, 2005) 5 (U.S. Department of Health & Human Services) 6 (Rodin, 1988) (Elliott, 2002) (Crapo, 1982) (Light, 2009) (Swarbrick, 2008) (Stanhope K. H., 2008) (Stanhope K. G., 2008) (Jurgens, 2005) 7 (Light, 2009) 8 (Soenen, 2007) (Monsivais, 2007) (Melanson K. A., 2008) 9 (Melanson K. Z., 2007) (Teff, 2004) 10 (Pusztai A. , 2001) (Pusztai D. A., 2000) (de Vendomois, 2009) (Ho M.-W. R., 2000) (Ho M.-W. R., 1999) 11 (Dufault R. L., 2009) (Dufault R. S., 2009) 12 (Wadaan, 2009) (Ung, 2010) (Donaldson, 1978) 13 (Krebs, 2007) 14 (World Health Organization (WHO), 2000) 15 (Dalton, 2004) 16 (World Health Organization, 2011) 17 (Whitney, 1998) 18 (Centers for Disease Control and Prevention, 2011) 19 (World Health Organization (WHO), 2000) 20 (Bedogni, 2003) (Reilly, 2000) (Lazarus, 1996) (Sarria, 2001) (Ellis, 1999) 21 (Conus, 2004) (Conus F. R.-L., 2007) 22 (Conus F. R.-L., 2007) (Conus F. A.-L.-O.-P.-L., 2004) 23 (Krebs, 2007) 24 (Ferreira, 2004) (Schouten, 2011) (Gosnell, 2007) (World Health Organization (WHO), 2000) 25 (Reilly, 2000) 26 (Savva SC, 2000) 27 (World Health Organization, 2011) 28 (Williams, 1997) (Goran M. G., 1999) (Sjostrom, 1992) (Goodpaster, 2000) (World Health Organization
(WHO), 2000) 29 (Maffeis, 2001) (Gower, 1999) (Larsson, 1984) (Freedman D. D., 2009) 30 (Krebs, 2007) 31 (Gower, 1999) (Addo, 2010) 32 (Krebs, 2007) 33 (Goran M. I., 1998) 34 (Goran M. I., 1998) 35 (Georgia State University Department of Kineseology and Health) 36 (Kuczmarski, 2000) (National Center for Health Statistics, 1977) 37 (Kuczmarski, 2000) 38 (National Center for Health Statistics, 1977) (Kuczmarski, 2000) 39 (Krebs, 2007) 40 (Himes J.H., 1994; Hedley A.A., 2004; Guo S.S., 2002; Gower, 1999; Maffeis, 2001; Savva SC, 2000;
St. Onge, 2003; Paeratakul S, 2003; Young, 2002; Bowman S. G., 2004) (Krebs, 2007) (Elliott, 2002) 41 (Krebs, 2007) 42 (Centers for Disease Control and Prevention, 2011) (Centers for Disease Control and Prevention, 2011) 43 (World Health Organization, 2005) 44 (Associated Press, 2011) 45 (UK Daily Mail, 2011) 46 (Wang Y. B., 2007) 47 (World Health Organization, 2005) 48 (World Health Organization, 2010) 49 (World Health Organization, 2010) 50 (Dalton, 2004)
High Fructose Corn Syrup and Childhood Obesity p. 130
51 (Dalton, 2004) 52 (Crowely, 2010) (Meyer, 2006) 53 (Chiolero, 2007) (Boyd, 2005) 54 (Gidding, 1995) 55 (U.S. National Institute of Health, 2006) 56 (Gidding, 1995) (Tulane University School of Medicine, 2011) 57 (U.S. National Institute of Health, 2006) 58 (Freedman D. K., 2005) 59 (Richards, 1985) 60 (Mustillo, 2003) (Woo, 2009) 61 (Dietz W. G., 1982) 62 (Carroll, 2007) (Goldsobel, 2008) (Belamarich, 2000) 63 (U.S. Department of Health & Human Services) 64 (Ogden, 2010) 65 (Ogden, 2010) 66 (Wang Y. B., 2007) 67 (Van Cleave, 2005) (U.S. Department of Health & Human Services) (U.S. National Library of Medicine
National Institutes of Health) (Wang G. D., 2002) (Miller, 2004) (Ogden C, 2010) (Krebs, 2007) (Langreth, 2009)
68 (Must A, 1992) 69 (Moss, 2011) 70 (Stettler N. S., 2005) 71 (Ekelund, 2006) (Stettler N. K., 2003) 72 (Whitaker R. P., 1998) 73 (Gordon-Larsen, 2010) 74 (World Health Organization (WHO), 2000) 75 (Centers for Disease Control and Prevention, 2011) (Colditz, 1992) 76 (Wolf A. C., 1994) 77 (Woo, 2009) 78 (Merriam-Webster, 2011) 79 (Tortora, 1993) 80 (Tortora, 1993) 81 (Guyton, 1991) 82 (Bray G. N., 2004) (Whitney, 1998) (Guyton, 1991) 83 (Bray G. N., 2004) 84 (Guyton, 1991) 85 (Tortora, 1993) (Whitney, 1998) (Parker, 2010) 86 (Tortora, 1993) (MedBio, 2011) (Heinz, 1968) 87 (Stanhope K. S., 2009) 88 (McDevitt, 2001) 89 (Schwartz, 1995) 90 (Stanhope K. S., 2009) 91 (Guyton, 1991) 92 (Saad, 1998) (Bray G. N., 2004) (Farooqi S. K., 2001) 93 (Tortora, 1993) 94 (Guyton, 1991) (Tortora, 1993) 95 (Gautron, 2011) 96 (Saad, 1998) 97 (Dickie, 1946) 98 (The Jackson Laboratory, 2011) 99 (The Jackson Laboratory, 2011) 100 (The Jackson Laboratory, 2011) 101 (The Jackson Laboratory, 2011) 102 (The Jackson Laboratory, 2011) 103 (Zhang, 1994)
High Fructose Corn Syrup and Childhood Obesity p. 131
1995) (Campfield, 1995) 105 (Campfield, 1995) 106 (Friedman, 2002) 107 (Howard Hughes Medical Institute, 2004) 108 (Millington, 2007) 109 (Perl, 2004) 110 (Liu L. K., 1998) 111 (Liu L. K., 1998) 112 (Medical Research Council, 2011) 113 (Farooqi I. J., 1999) 114 (Farooqui, 2002) 115 (Emilsson, 1997) 116 (Murray, 2003) (Tortora, 1993) 117 (Grundy, 1998) 118 (Elliott, 2002) 119 (Schwarzbein, 1999) 120 (Tortora, 1993) 121 (Murray, 2003) 122 (Bhosale, 1996) (Wikipedia, 2011) 123 (Bhosale, 1996) 124 (Bhosale, 1996) 125 (Marshall, 1957) 126 (Marshall, 1957) 127 (Takasaki, 1971) (Takasaki, 1972) (Takasaki, 1966) 128 (Takasaki, 1966) 129 (Takasaki, 1966) (Takasaki, Formation of Glucose Isomerase by Streptomyces sp., 1973) 130 (Takasaki, 1971) 131 (Lamot, 1983) (Bhosale, 1996) 132 (U.S. Department of Agriculture (USDA), 2011) 133 (Parker, 2010) 134 (Parker, 2010) 135 (Dufault R. L., 2009) 136 (Dufault R. L., 2009) 137 (Wadaan, 2009) 138 (Ung, 2010) 139 (Ung, 2010) 140 (Elmhurst College, 2011) (OUKosher, 2011) 141 (Bhosale, 1996) 142 (Parker, 2010) 143 (Schoonover, 2006) 144 (Haley S. R.-H., 2005) 145 (Bray G. N., 2004) 146 (Putnam, 1999) (Parker, 2010) 147 (U.S. Department of Agriculture (USDA), 2011) 148 (Schoonover, 2006) 149 (Whitney, 1998) 150 (Wells, 2008) 151 (Haley S. R.-H., 2005) 152 (Haley S. R.-H., 2005) 153 (U.S. Department of Agriculture (USDA), 2011) 154 (White J. , 2009) (White J. , 2010) 155 (Crapo, 1982) (Angelopoulos, 2009) (Swarbrick, 2008) (Stanhope K. G., 2008) (Stanhope K. H., 2008)
(Melanson K. A., 2008) (Petersen, 2001) (Jurgens, 2005) (Elliott, 2002) 156 (Stanhope K. G., 2008) (Stanhope K. H., 2008) (Light, 2009; Bowman S. G., 2004) (Rodin, 1988)
High Fructose Corn Syrup and Childhood Obesity p. 132
157 (Teff, 2004) 158 (Teff, 2004) 159 (WIkipedia, 2011) 160 (Wikipedia, 2011) 161 (Cummings, 2001) 162 (Lutter, 2008) 163 (Atcha, 2009) 164 (Cummings, 2001) 165 (Teff, 2004) 166 (Stanhope K. G., 2008) 167 (Melanson K. Z., 2007) 168 (Jurgens, 2005) (Elliott, 2002) (White J. 2008) (White J. F., 2010) 169 (White J., 2008) (White J., 2009) 170 (Swarbrick, 2008) 171 (Swarbrick, 2008) 172 (White J. F., 2010) 173 (White J. F., 2010) 174 (Council on Science and Public Health, 2008) 175 (Council on Science and Public Health, 2008) 176 (American Dietetic Association, 2004) 177 (American Dietetic Association, 2004) (Lineback, 2003) 178 (Lineback, 2003) 179 (Lineback, 2003) 180 (Kraft Brands, 2011) 181 (McDonalds, 2011) 182 (White J. , 2009) 183 (Melanson K. Z., 2007) 184 (Angelopoulos, 2009) 185 (White J. , 2009) 186 (White J. , 2010) 187 (Light, 2009) 188 (Light, 2009) 189 (American Diabetes Association, 2010) 190 (White J. F., 2010) 191 (U.S. Department of Agriculture (USDA), 2011) 192 (Bray G. P., 1998) (Lineback, 2003) 193 (Willett, Is dietray fat a major determinant of body fat?, 1998) (Willett, Dietary fat and obesity: and
unconvincing relation, 1998) 194 (Gazzinga, 1993) 195 (Putnam, 1999) 196 (Schoonover, 2006) 197 (Kraft Brands, 2011) 198 (Schoonover, 2006) 199 (Schoonover, 2006) 200 (Farrell, 1987) 201 (Pusztai A. , 2001) 202 (Cummins, 2000) 203 (Pusztai D. A., 2000) 204 (Cummins, 2000) (Pusztai D. A., 2000) 205 (Pusztai D. A., 2000) 206 (Pusztai D. A., 2000) 207 (Pusztai D. A., 2000) 208 (Ho M.-W. R., 2000) 209 (Ho M.-W. R., 1999) (Ho M.-W. R., 2000) 210 (Ho M.-W. R., 1999)
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