Ironman Sports Medicine Conference Role of Sugar in Obesity and Chronic Disease

Ironman Sports Medicine Conference
Role of Sugar in Obesity and Chronic Disease
October 8, 2007
Kristine Clark, PhD, RD, FACSM

Outline

1. Introduction to the Problem
A. Obesity – sweeping the nation

Twenty years ago, the common perception was that sugar intake was associated
with several chronic diseases: Diabetes, coronary heart disease, obesity, and
hyperactivity in children. Sugar was also thought to be the sole cause of dental
caries. Recent advances in scientific knowledge, however, have shed some light
on the role of sugar in chronic diseases and dental caries. The evidence
indicates that sugar is not in itself associated with the aforementioned chronic
diseases and is not the sole offender in the development of dental caries.

B. Who is at risk?

Prevalence
The prevalence of overweight (Body Mass Index (BMI) of 25 or more) and
obesity (BMI of 30 or more) increased over the last decade across racial / ethnic
groups, as shown in Table 1.

Mexican American and black (non-Hispanic) adults in the U.S. are considerably
more overweight and obese than white (non-Hispanic) adults.

Increase in Overweight and Obesity Prevalence
Among U.S. Adults* by Racial / Ethnic Group
Overweight
Obesity

(BMI > 25)
(BMI > 30)
Prevalence (%)
Prevalence (%)

Racial / Ethnic
1988 to
1999 to
1988 to
Group
1994
2000
1994
1999 to 2000
Black
62.5
69.2
30.2
39.9
(non-Hispanic)
Mexican
67.4
73.4
28.4
34.4
American
White
52.6
62.3
21.2
28.7
(non-Hispanic)
Source: CDC, National Center for Health Statistics, National Health and Nutrition

---

Examination Survey. Flegal et. al. JAMA. 2002; 288:1723-7 and IJO. 1998;22:39-47.
*Ages 20 and older for 1999 to 2000 and ages 20 to 74 for 1988 to 1994.
The American Indian population also has high prevalence rates of overweight.
Among the highest rates reported (overweight defined as BMI of > 27.8 for men
and > 27.3 for women) are for American Indians in Arizona at 80 percent for
women and 67 percent for men, according to researchers of the Strong Heart
Study in 1995.
Gender: For women, the black (non-Hispanic) population has the highest
prevalence of overweight (78 percent) and obesity (50.8 percent).
For men, the Mexican American population has the highest prevalence of
overweight (74.4 percent) and obesity (29.4 percent).
Overweight, obesity and severe obesity (BMI of 40 or more) prevalence
increased for men and women in various racial / ethnic groups in the U.S. over
the last decade.

Increase in Overweight (BMI > 25) Prevalence Among
U.S. Adults (Ages 20 to 74) by Racial / Ethnic Group and Gender

Men
Women
Prevalence (%)
Prevalence (%)

0. Racial /
1988 to
1999 to
1988 to
Ethnic
1994
2000
1994
1999 to 2000
Group
Black (non-
58.2
60.1
68.5
78
Hispanic)
Mexican
69.4
74.4
69.6
71.8
American
White (non-
61.6
67.5
47.2
57.5
Hispanic)
Source: CDC, National Center for Health Statistics, National Health and Nutrition
Examination Survey. Health, United States (Table 70) 2002.

Increase in Obesity (BMI > 30) Prevalence Among
U.S. Adults (Ages 20 to 74) by Racial / Ethnic Group and Gender

Men
Women
Prevalence (%)
Prevalence (%)

Racial / Ethnic
1988 to
1999 to
1988 to
Group
1994
2000
1994
1999 to 2000
Black (non-
21.3
28.8
39.1
50.8
Hispanic)
Mexican
24.4
29.4
36.1
40.1
American
White (non-
20.7
27.7
23.3
30.6

---

Hispanic)
0. Source: CDC, National Center for Health Statistics, National Health and Nutrition
Examination Survey. Health, United States (Table 70) 2002.

Increase in Severe Obesity (BMI > 40) Prevalence Among
U.S. Adults (Ages 20 and older) by Racial / Ethnic Group and
Gender

Men
Women
Prevalence (%)
Prevalence (%)

Racial / Ethnic
1988 to
1999 to
1988 to
Group
1994
2000
1994
1999 to 2000
Black (non-
2.4
3.5
7.9
15.1
Hispanic)
Mexican
1.1
2.4
4.8
5.5
American
White (non-
1.8
3
3.4
4.9
Hispanic)
Source: CDC, National Center for Health Statistics, National Health and Nutrition
Examination Survey. Flegal et. al. JAMA 2002:288:1723-7.

Socioeconomic Status (SES)
Overweight affects African American women and men across all SES levels.
Minority women with low income appear to have the greatest likelihood of being
overweight.
Among Mexican American women, age 20 to 74, the rate of overweight is about
13 percent higher for women living below the poverty line versus above the
poverty line.


Causes of Childhood Obesity
There are many factors that contribute to causing child and adolescent obesity -
some are modifiable and others are not.

Modifiable causes include:
Physical Activity - Lack of regular exercise.

Sedentary behavior - High frequency of television viewing, computer usage, and
similar behavior that takes up time that can be used for physical activity.

Socioeconomic Status - Low family incomes and non-working parents.

Eating Habits - Over-consumption of high-calorie foods. Some eating patterns
that have been associated with this behavior are eating when not hungry, eating
while watching TV or doing homework.

---

Environment - Some factors are over-exposure to advertising of foods that
promote high-calorie foods and lack of recreational facilities.

Non-changeable causes include:
Genetics - Greater risk of obesity has been found in children of obese and
overweight parents.

2. The American Diet: Linking obesity to sugar

Despite having been labeled as "empty calories," sugars are truly important
compounds from the perspective of the human organism. Humans have retained
the ability to synthesize all forms of carbohydrates the body needs from simple
sugars. This is not the case with the other dietary macronutrients, fats, and
proteins. Following ingestion, all digestible complex dietary carbohydrates are
broken down in the gut to simple sugars before they are absorbed into the body.
Because simple sugars are all identical chemically, the absorption process
cannot distinguish simple sugars resulting from the breakdown of complex
dietary carbohydrates from corresponding simple sugars occurring naturally in
the foods themselves or from corresponding simple sugars added to foods during
processing. Within the body, most dietary sugars are converted to glucose, a
major fuel used by all cells and the primary fuel required by brain tissue for
normal function. Low levels of glucose in the blood will impair the brain and
cause permanent mental impairment or worse--coma or death. The body can
store a limited amount of glucose as glycogen, which it can draw upon for less
than a day. After this, other sources such as proteins, from the breakdown of
body tissues, must be used to synthesize glucose for the cells (15).

The consumption of total sugars has increased significantly in the past 30 yr in
the U.S. with shifts in the sources of sweeteners. Before the late 70’s-early 80’s,
carbonated soft drinks were sweetened with sucrose, a 50% fructose containing
sugar. Currently the leading source of fructose in the U.S. diet is most likely
sucrose, given that USDA data indicate per capita consumption of this caloric
sweetener is higher than other caloric sweeteners. High fructose corn syrup,
however, is the principle sweetening agent in carbonated soft drinks and is 5%
higher in fructose than sucrose for beverage applications, but lower in fructose
(42% versus 50%) for other applications (breads, yogurts, etc). It has been
argued that increased consumption of fructose in the diet may be a contributing
factor to the dramatic increase in obesity in the U.S. and developing countries,
because fructose, unlike glucose, does not stimulate the production and
secretion of insulin from the pancreatic Beta cells.

A. Carbohydrate consumption data
1. Monosaccharides – glucose, fructose, galactose
2. Disaccharides – sucrose . lactose, maltose

---

3. Polysaccharides – starch, glycogen, fiber

B. Metabolic processes of carbohydrates

1. discuss differences in absorption and metabolism of sucrose,
glucose, and fructose

2. differences between high fructose corn syrup (HFCS) and
sucrose

There is no scientific evidence to suggest that high fructose corn
syrup is uniquely responsible for people becoming obese. Obesity
results from an imbalance of energy consumed vs energy
expended.

•Corn syrup: 100% glucose, is used as a thickening agent
•High fructose Corn Syrup: a sweetening agent made from 42% or
55% fructose and the rest from glucose
•Sucrose (table sugar): a sweetening agent made of 50% fructose,
50% glucose

3. Sugar and its association with chronic diseases

A. Diabetes: Research evidence shows the leading cause of diabetes is
obesity, advancing age, and heredity. All caloric sweeteners trigger an insulin
response in the body. In fact, table sugar, honey, and high fructose corn syrup
trigger about the same insulin release because they contain nearly equal
amounts of fructose and glucose.

The relationship between dietary carbohydrates and insulin resistance (a risk
factor for diabetes mellitus, ischemic heart disease, and hypertension) is not
clear based on available research (7). In two studies based on a large,
prospective study of U.S. women, sucrose and carbohydrate intake were not
associated with an increased risk of diabetes (6,27). However, based on the
same population, associations were found between a diet with high glycemic
load[2] (26) and high intake of refined grains (21) and the risk of diabetes. The
general consensus, based on epidemiological studies, is that sugar intake alone
is not associated with the development of diabetes mellitus. Sugars fed at levels
equivalent to those consumed by the U.S. population do not produce adverse
glycemic effects in non-diabetics (23). The effects of sugar intake on glucose
tolerance, insulin levels, and plasma lipids are confounded by other dietary
components. The American Diabetes Association has also acknowledged, in its
nutrition recommendations for people with diabetes, that there is no evidence
that refined sugars such as sucrose or high fructose corn syrup behave any
differently from other types of simple carbohydrates (1).

---

B. Heart Disease
The Sugars Task Force of the U.S. Food and Drug Administration (29) presented
a comprehensive review of epidemiological, clinical, and animal studies dealing
with the relationship between sugar intake and heart disease or risk factors for
heart disease (14). The report concluded that at current levels of consumption,
sugar is not an adverse risk factor in heart disease. The same conclusion was
made by the National Research Council in its report on chronic disease risk (23).
There is no conclusive evidence that dietary sugar is an independent risk factor
for coronary artery disease in the general population. However,
hypertriglyceridemia[3] and central fat distribution,[4] consequences of abnormal
glucose tolerance and diabetes mellitus, are independent risk factors for
coronary heart disease (8). A 1996 randomized study of 32 hypertriglyceridemic
patients provided evidence that an "extrinsic sugar-free" diet significantly lowers
abnormally elevated plasma triglyceride levels (28). Evidence also suggests that
insulin resistance and compensatory hyperinsulinemia[5] have major roles in the
regulation of blood pressure in subjects predisposed to hypertension due to
hereditary or environmental factors, possibly mediated by activity of the
sympathetic nervous system. But there are multiple metabolic abnormalities
associated with hyperinsulinemia in hypertensive patients that increase the risk
of coronary heart disease (24).
4. Dietary Therapy
Despite popular belief that sugar causes obesity, a number of studies show an
inverse relationship between reported sugar consumption and degree of
overweight (10,11,20,25). An increase in the percentage of calories from sugar
is, by definition, associated with a decreased consumption of calories from fat.
Obesity is basically a consequence of higher energy intake than energy
expenditure, where excess calories are stored as fat (5). The type of calories
consumed is the subject of much study in obesity research. For instance, extra
calories consumed as sugar cause an appropriate compensatory increase in
carbohydrate oxidation (metabolism of carbohydrates for energy), whereas extra
calories consumed as fat do not (17). Simply stated, obesity results from energy
intake in excess of energy requirements. Many factors contribute to obesity, but
evidence does not single out dietary sugar as a cause (25).

A. Dietary therapy involves instruction on how to adjust a diet to reduce the
number of total calories eaten.

B. Reducing calories moderately is essential to achieve a slow but steady weight
loss, which is also important for maintenance of weight loss.

C Strategies of dietary therapy include
1. teaching about calorie content of different foods
2. food composition (fats, carbohydrates, and proteins)
3. reading nutrition labels
4.types of foods to buy

---

5. how to prepare foods
References:
(1.) American Diabetes Association. 1994. Nutrition recommendations and
principles for people with diabetes mellitus. Diabetes Care 17:519-522.
(2.) Anderson, G.H. 1997. Sugars and health; A review. Nutrition Research 17(9):
1485-1498.
(3.) Bornet, F.R., Billaux, M.S., and Messing, B. 1997. Glycaemic index concept
and metabolic diseases. International Journal of Biological Macromolecules 21
(1-2):207-219.
(4.) Bowman, S.A. 1999. Diets of individuals based on energy intakes from
added sugars. Family Economics and Nutrition Review 12(2):31-38.
(5.) Bray, G.A. 1996. Obesity. In Ekhard E. Aiegler and L.J. Filer, Jr. (Eds.),
Present Knowledge in Nutrition (7th ed.) (Chapter 2). International Life Sciences
Institute Press, Washington, DC.
(6.) Colditz, G.A., Manson, J.E., Stampfer, M.J., Rosner, B., Willett, W.C., and
Speizer, F.E. 1992. Diet and risk of clinical diabetes in women. American Journal
of Clinical Nutrition 55(5):1018-1023.
(7.) Daly, M.E., Vale, C., Walker, M., Alberti, K.G., and Mathers, J.C. 1997.
Dietary carbohydrates and insulin sensitivity: A review of the evidence and
clinical implications. American Journal of Clinical Nutrition 66(5): 1072-1085.
(8.) Eschwege, E., Balkau, B., and Fontbonne, A. 1994. The epidemiology of
coronary heart disease in glucose-intolerant and diabetic subjects. Journal of
International Medicine (Suppl)736:5-11.
(9.) Farris, R.P, Nicklas, T.A, Myers, L., and Berenson, G.S. 1998. Nutrient intake
and food group consumption of 10-year-olds by sugar intake level: The Bogalusa
Heart Study. Journal of the American College of Nutrition 17(6):579-85.
(10.) Gibney, M., Sigman-Grant, M., Stanton, J.L.J., and Keast, D.R. 1995.
Consumption of sugars [published erratum appears in American Journal of

---

Clinical Nutrition 1997 May;65(5): 1572-1574]. American Journal of Clinical
Nutrition 62(1 Suppl): 178S-193S.
(11.) Gibson, S. and Williams, S. 1999. Dental caries in pre-school children:
Associations with social class, toothbrushing habit and consumption of sugars
and sugar-containing foods. Further analysis of data from the National Diet and
Nutrition Survey of children aged 1.5-4.5 years. Caries Research 33(2):101-113.
(12.) Gibson, S.A. 1996. Are high-fat, high-sugar foods and diets conducive to
obesity? International Journal of Food Sciences and Nutrition 47(5):405-415.
(13.) Gibson, S.A. 1997. Non-milk extrinsic sugars in the diets of pre-school
children: Association with intakes of micronutrients, energy, fat and NSP. British
Journal of Nutrition 78(3):367-378.
(14.) Glinsmann, W.H., Iransquin, H., and Park, Y.K. 1986. Report from FDA's
Sugars Task Force: Evaluation of Health Aspects of Sugars Contained in
Carbohydrate Sweeteners. Journal of Nutrition 166(155):51-216.
(15.) Guyton and Hall. 1996. Textbook of Medical Physiology, 9th Edition. W.B.
Saunders, Philadelphia.
(16.) Harnack, L., Stang, J., and Story, M. 1999. Soft drink consumption among
US children and adolescents: Nutritional consequences. Journal of the American
Dietetic Association 99(4):436-441.
(17.) Horton, T.J., Drougas, H., Brachey, A., Reed, G.W., Peters, J.C., and Hill,
J.O. 1995. Fat and carbohydrate overfeeding in humans: Different effects on
energy storage. American Journal of Clinical Nutrition 62(t):19-29.
(18.) Kandelman, D. 1997. Sugar, alternative sweeteners and meal frequency in
relation to caries prevention: New perspectives. British Journal of Nutrition
77(Suppl 1):S121-S128.
(19.) Krummel, D.A., Seligson, F.H., and Guthrie, H.A. 1996. Hyperactivity: Is
candy causal? Critical Reviews in Food Science and Nutrition 36(1-2):31 47.

---

(20.) Linseisen, J., Gedrich, K., Karg, G., and Wolfram, G. 1998. Sucrose intake
in Germany. Zeitschrift fur Ehrnahrungswissenschaft 37(4):303-314.
(21.) Liu, S., Manson, J.E., Stampfer, M.J, Hu, F.B., Giovannucci, E., Colditz,
G.A., Hennekens, C.H., and Willett, W.C. 2000. A prospective study of whole-
grain intake and risk of type 2 diabetes mellitus in US women. American Journal
of Public Health 90(9):1409-1415.
(22.) Naismith, D.J., Nelson, M., Burley, V., and Gatenby, S.J. 1995. Does a
high-sugar diet promote overweight in children and lead to nutrient deficiencies?
Journal of Human Nutrition and Dietetics 8:249-254.
(23.) National Research Council, Committee on Diet and Health, Food and
Nutrition Board. 1989. Diet and Health: Implications for Reducing Chronic
Disease Risk. National Academy Press, Washington, DC.
(24.) Reaven, G.M., Lithell, H., and Landsberg, L. 1996. Hypertension and
associated metabolic abnormalities--the role of insulin resistance and the
sympathoadrenal system. New England Journal of Medicine 334(6):374-381.
(25.) Ruxton, C.H., Garceau, F.J., and Cottrell, R.C. 1999. Guidelines for sugar
consumption in Europe: Is a quantitative approach justified? European Journal of
Clinical Nutrition 53(7):503-513.
(26.) Salmeron, J., Manson, J.E., Stampfer, M.J., Colditz, G.A., Wing, A.L., and
Willett, W.C. 1997. Dietary fiber, glycemic load, and risk of non-insulin-dependent
diabetes mellitus in women [see comments]. JAMA 277(6):472-477.
(27.) Shimakawa, T., Herrera-Acena, M.G., Colditz, G.A., Manson, J.E.,
Stampfer, M.J., and Willett, W.C. 1993. Comparison of diets of diabetic and
nondiabetic women [published erratum appears in Diabetes Care 1994
Apr;17(4):349]. Diabetes Care 16(10):1356-1362.
(28.) Smith, J.B., Niven, B.E., and Mann, J.I. 1996. The effect of reduced
extrinsic sucrose intake on plasma triglyceride levels. European Journal of
Clinical Nutrition 50(8):498-504.

---

(29.) Sugars Task Force. 1986. Evaluation of Health Aspects of Sugars
Contained in Carbohydrate Sweeteners. Health and Human Services, Food and
Drug Administration. Washington, DC.
(30.) Wolraich, M.L., Wilson, D.B., and White, J.W. 1995. The effect of sugar on
behavior or cognition in children. A meta-analysis. JAMA 274(20): 1617-1621.

---