Robert Karp, MD

SUNY-Downstate Medical Center

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PRE-TEST

Q1. The most likely explanation for the obesity found among many Native Americans in the Southwest United States is

a. Being starved for several generations creates an increased survival value for newly appearing protective genetic patterns that promote efficiency in energy metabolism

b. Being starved for several generation leads to a natural selection of preexisting protective genetic patterns that promote efficiency in energy metabolism.

c. Both

d. Neither

Q2. Which child is most "at-risk" for obesity? The one who:

a. Lives in a family with income at below the poverty level

b. Lives in a family with income between one and three times the poverty level at the poverty level

c. Lives in a family with income at 3 times the poverty level

d. All are at equal risk

Q3. True or False: Answering often or sometimes to the question below increases the risk for obesity in childhood,

"I worry whether my food will run out before I get money to buy more."

Often true [_]

Some times true [_]

Never true [_]

Q4. Explain your answer in about 50 words

Q5. Appropriate interventions to prevent obesity include:

A. Encourage better parental shopping and food preparation.

B. Reduce dependence on fatty food

C. Introduce fruits and vegetables into the diet

D. Encourage use of food stamps

E. Encourage physical activity

F. Discourage of excessive time spent by children watching television.

G. In the case of families living in rural areas, encourage participation by children in activities of gardening, canning, and freezing vegetables.

H. All of the above

OBJECTIVES

After completing this module residents will be able to:

1. Describe the adaptation to semi-starvation that formed the evolution of protector genes and pathways.

2 List the metabolic control mechanisms on food intake that when maladaptive give way to morbid obesity

3. Identify the social, environmental, and economic phenomena that increase risk for obesity.

4. Describe interventions available to pediatricians addressing the phenomena listed above.

FACILITATOR PREPARATION

1. Fernandez JR, Allison DB. Understanding racial differences in obesity and Metabolic Syndrome. Nutrition Reviews. 2003;61:316-319.

2. Ravussin E, Bogardus C. Energy balance and weight regulation: genetics versus environment. Br J Nutr. 2000;83 Suppl 1:S17-20.

4. Hofferth SL, Curtin S. Food programs and obesity among US children. http://www.gwu.edu/~labor/papers/hofferth.pdf.

5. Drewnowski A, Spector S. Poverty and Obesity: The Role of Energy Density and Energy Costs. Am J Clin Nutrition 2004

6. Karp RJ. (1999 and 2005) Malnutrition among children in the United States: The impact of Poverty. (in) Modern Nutrition in Health and Disease, 9th edition. Shils ME, Olson JA, Shike M, and Ross AC (eds) Williams & Wilkins, Baltimore MD, 1999., Pp 1089-1001 and 2005,10th edition Pp 861-875.

7. Dietz W. (1999 and 2005) Childhood obesity (in) Shils, ME, JA Olson, M Shike, and AC Ross.(eds) Modern nutrition in Health and Disease, 9th edition. Williams and Wilkins, Baltimore, MD. pp 1071-1080 and 10th edition 2005 Pp979-990.

8. Karp RJ, Cheng C, and Meyers AF. The appearance of discretionary income: Influence on the prevalence of under- and overnutrition to the International Journal of Health Inequities.-- http://www.equityhealthj.com/content/4/1/10

9. Case study by Joanne Hurley in Greenwood MRC et al. (1993) Obesity in disadvantaged children (in) Karp RJ (ed) Malnourished Children in the United States: Caught in the cycle of poverty Springer Publishing Co of New York. Pp 115-29. This is attached as an appendix 1

INTRODUCTION

Neither genetics nor environment, alone, determine weight gain and obesity in childhood. Even in the United States today, a society where children’s energy intake and expenditures are out-of-balance, the outcome is not predetermined. Rather, obesity is an end-point for a complex interacting set of phenomena including food selection, physical activity, metabolism, endocrine control, and genetics. Teasing apart genetic from environmental precursors to obesity is an impossible task as these domains are inherently linked. Semi-starvation and physical labor are the natural state of humankind. Thus, the survival of the species requires both metabolic and cultural adaptation to periodic caloric deprivation. Endemic poverty among children of all backgrounds may be as an important to their obesity as heredity, race/ethnicity, or culture, per se. Low birth weight sets a trigger for obesity later in life. Exposure to intermittent abundance of food?, lack of exercise, and a compelling sense of deprivation later in life fire the gun. Food insecurity in itself, almost universal for poor families trying to survive without support for food or rent, leads to metabolic and cultural responses to deprivation and obesity. As such, socioeconomic as well as metabolic adaptations play an initiating role in the origins of obesity.

Over the course of primate evolution, control mechanisms on excessive food intake, which precede morbid obesity, have been far out weighed by those that protect against protein-energy malnutrition. Several generations of famine are sufficient to increase the predominance of weight sustaining genes. There are, however, specific social and environmental phenomena that increase risk for obesity in the general population. For example, urban parents cannot allow their children outside to play when there are inadequate or unsafe playgrounds. Play itself may be limited in homes where television and other screen-watching times are excessive. Schools cutting back on time for physical education, permitting sugar beverage sales, or providing lunches geared to prevent undernutrition all contribute to the overnutrition of children.

Of the socioeconomic precursors to obesity, none may be stronger than the food culture maintained by families at the edge of poverty. [see Karp, et al, 2005] The truly deprived are not obese rather the highest prevalence of obesity is among children living with incomes between one and three times the poverty level. Food insecurity plays an important role in this increased risk. At present, responses to the obesity epidemic have focused on education of families to risks and benefits of food and activity. The next level will include intervention in the metabolism of highest risk children with a drug therapy that enhances a sense of satiety while providing adequate nutrition.

For the general public, broad social and environmental changes are clearly necessary. Pediatricians and other health professionals have roles to play in giving families guidance, advocating repair of an “obesogenic” society, and, at times, recommending pharmacologic or surgical intervention for the most affected children.

Public support for the poor, including supplemental food programs, have substantial impact on nutrition in pregnancy and limit weight gain for older children and adults. Unfortunately, these resources are being limited in a society promoting self-sufficiency as a cure-all for the ills of the poor.

A CASE STUDY

Anna, a Pima tribe Native American, is now a 4-year old child. She weighed 7 lb 8oz (3.4kg) at birth and was 19 in. (48, cm) long, placing her at about the 50th percentile for weight and length. Her mother was not diabetic before or during the pregnancy. She participated in the Women, Infants and Children (WIC) feeding program. By the time Anna was 3 months old, however, she had reached the 90th percentile for both weight and length, and by six months of age, the 95th percentile. Anna remained at these levels until this visit. (see appendix 1)

She is in a pre-school group at the Later Day Saints Mission School on the Gila River reservation in Arizona. She is 41.5 inches (1.05 m) tall (85th %ile for age and sex) She weighs 46 lbs (20.9 kg-- >95th %ile), and her BMI is 19.0 kg/m2 which is > 95th %ile for age and sex. Eighty five percent of the girls in Anna’s pre-school group are above the 95th %ile in Body Mass Index. Anna’s story is typical of many of her nursery mates.

Q1 How might semi-starvation in the Pima tribal groups informed the evolution of protector genes and pathways that increase the risk for obesity in childhood?

A1 Neel coined the term ““thrifty gene”” to suggest that inherited metabolic changes likely to increase storage of body fat enhances one’s chance for survival during periods of starvation or debilitating disease. Thus, nutritional deprivation in a community’s past may also contribute to genetic susceptibility to obesity of present populations. During the ““Middle Passage,”” when newly enslaved Africans were brought to the Americas –– circa 1660 to 1810 –– men and women were bound in boats for several weeks during which many starved to death. Patterns of pre-adolescent truncal obesity developing in early adolescence among many African Americans may be a result of the thrifty gene that enabled survival of ancestors during this Middle Passage. As shown by Weyer and colleagues, extreme selection effects among African Americans have resulted in decreased resting metabolic rates and mean body temperatures

With respect to Anna, substantial data relating to truncal obesity and energy deprivation in recent memory has been collected for Native American tribal groups living in southwestern Arizona. These groups of Native Americans are said to have passed through a ““genetic hourglass”” where those who are more effective at storing body fat, maintaining high levels of blood sugar, and conserving energy have a greater survival value.

FIGURE 1. Genetic Hourglass

TEACHING CAPTION:

A free living and prosperous community carries panoply of genetic potentials for energy conservation. A generation or more of persistent famine permitted only those with “thrifty genes” to pass through the narrow place of the “genetic hourglass.” The population now has a plethora of famine protective genes leading to obesity with food abundance and limited activity. Those without the “thrifty genes” were less likely to survive.

In these populations, food is now abundant. Lifestyles, which once demanded physical endurance and strength for livelihood and survival are replaced with ones with far less need for physical labor. As a result, among the Pima Native American tribal groups in the United States, obesity begins in early childhood. According to Knowler et al., in the early 1990’’s, the Pima Indians had the highest reported rate of obesity in the United States. In a cohort of Pima Indians living in Arizona, Ravussin et al. determined that 54% of men and 37% of women exhibited non-insulin- dependent diabetes mellitus (NIDDM). Researchers then compared their studies of Pima Indians with those of other Pima Indians living in Mexico.

By contrast, Mexican Pimas who live under harsher conditions that demand much more physical labor, do not demonstrate the high levels of obesity and diabetes of the Pima in the United States. This suggests that genetic factors contribute substantially to the risk for obesity. Environmental factors such as past poverty, deprivation and a sedentary lifestyle add to that risk.

All this will help you advise Anna’s mother. You remind her of the obesity present all around her. It is not necessary. It is not healthy. It is not necessary to feed Anna all the time. This provide parents a chance to incorperate the information. Usually they understand and will voice a concern about obesity even as they feed highly caloric foods. It takes longer to transform action than to change behavior!

Q2. List the metabolic control mechanisms on food intake that when maladaptive precede morbid obesity.

A2. The discovery of leptin provided the first physiologic link between the environment, peripheral energy storage and the CNS but that the entire system is highly complex involving neuropeptides, cytokines, gut peptides and more. See Part III Section 4 for a more complete discussion of the pathophysiology of obesity in childhood.

TABLE 1 The weight control mechanisms as now understood

1. Begins with the secretion of leptin by fat cells.

2. Leptin is received by leptin specific receptors in the brain stem.

3. Neuro-peptide YY is then released triggering secretion of DOPA and other neuro-activity stimulants.

4. Satiety follows.

Leptin is a hormone secreted by fat cells when they are full. Secretion falls when fat cell size is reduced. The presence of leptin produces satiety. It is also associated with emotional calm and well-being. By contrast, a reduction in leptin is associated with all of the psychological characteristics of starvation: lethargy, anxiety and irritability. There is a food preoccupation and over consumption when food is available is highly probable.

Figure 2A
shows a 4 x 4 square. This square represents the fat storage of an overweight child. Assume that the fat cells of an obese person at steady state are of uniform size equal to those of a lean person.

Figure 2B

TEACHING CAPTION: Note that the leptin secretion is at a high but steady level. Obese people have a higher set point because of insulin resistance (see PII Section 4). It takes more leptin to signal satiety.

Figure 3A
shows a 3x3 square representing the fat storage of a normal weight child. This individual has 9 normal size fat cells

Figure 3B

TEACHING CAPTION: Note that the leptin level is at a low but steady level.

Figure 4A
shows what happens to the fat cells of the overweight child when she reduces to the size of the normal weight child. There are still 16 fat cells, but they have reduced in size

Figure 4B

TEACHING CAPTION: Note that the secretion of leptin is greatly reduced when the overweight child or adult reduces to the weight of a lean child.

There are two pathologic states associated with failure of production of leptin (the OB/OB rat with pure obesity) and the lack if leptin receptor (the DB/DB rat where the obesity is associated with insulin resistance and diabetes mellitus.) These animal models are similar to gene control in the Pima and other Native American tribal groups where child obesity and diabetes are common.

Q3 What social and environmental phenomenon increase risk for obesity.

A3. As noted in Ms Hurley’s Case study – See reference 9.

“Anna's mother is a Pima Indian; her father is Hispanic. Anna was the first child born to her mother, who was 18 years of age. Psychosocial factors appear to contribute to Anna's weight gain. She eats to ease her pain of being abandoned by her mother, of being held back a grade in school, of being ridiculed by her peers, and of being cared for most of the time by her maternal grandparents. They feed and care for her, but show little emotional attachment to her. They expressed little if any interest in helping her with her problems at school in general or with her weight problem in particular.

“[Anna] eats breakfast with her grandparents before the bus takes her to school. She then eats another breakfast and lunch at school. After the bus brings her home in the afternoon, she often snacks on soda pop and chips while she watches television. Extra meals and snacks of around 250 to 285 calories have been a major contributor to her dramatic weight gain over a brief period. Small increases in caloric intake on a consistent basis can have a significant effect on body weight over time.

“Anna typifies the emotional poverty of being left alone and being fed as a means of social control, that is, "keeping her out of trouble." She experienced periods of special stress, such as those times when she was sent back to her mother who had abandoned her, or when she was having difficulties at school; these contributed to her pattern of behavior. Food became her immediate source of gratification and solace.” One of the foods that provide most solace is “fry-bread.” This is a patty flour and water fried in lard. (See Appendix 2)

Q4 What are the economic factors affecting the likelihood of obesity?

A4 See Part 2 – Social; and Economic influences on nutritional status and Reference 8 http://www.equityhealthj.com/content/4/1/10.

For families living well below the poverty level, increasing income does increase discretionary spending. Any money received is used to pay the cost of necessities - food, rent, heat, and the expenses of getting to work such as clothes, day-care, and transportation. Nothing is left to improve nutritional quality of the diet or, at lowest income, provide sufficient caloric intake. The governing principle is called the “Engel’s phenomenon.’ As the cost for food and other necessities increase or income falls food selection narrows to those items containing most energy at lowest cost. Essential nutrients disappear from the diet and micronutrient deficiency follows.

FIGURE 6. Engel Curve

TEACHING CAPTION: Poorer workers’ increased earnings do not generate discretionary income until the total of income from earnings plus supplementation reaches poverty level. Past poverty level discretionary income appears until, at about three times poverty level income, all new money earned is available for discretionary spending.-- not necessarily food, housing or other essential needs. [See Karp RJ. The problem of changing Food Habits -1; in Malnourished Children in the United States.]

Only recently have the principles of the Engels’ phenomenon been applied to the onset of obesity. There is a paradoxical association between poverty and obesity in childhood. As shown by Hofferth and Curtin with data from Panel Study of Income Dynamics Child Development Supplement of 1999, leanness is the rule (a 12% incidence of obesity) for families living below poverty level. Twenty two percent of children living in families with incomes from one to three times poverty level are likely to be obese. Past three times poverty income, the incidence among children diminishes to the 12 % level again. An important difference, however, is that impoverishment increases the risk for micronutrient deficiency. [1,22]

The ratio of change in food expenditures to change in income is called the marginal propensity to spend on food. In developing countries, the marginal propensity to spend on food is high for the poor and low for the affluent. Similarly, in the United States, the last dollar earned by a poor family will represent obligate spending with some part going for food. For the affluent, expenditures for food change little with increased or decreased income. Rather, increased income provides an opportunity for a choice, as new income is available entirely for discretionary spending. This “income of opportunity” is not available to the poor.

Thus, the appearance of discretionary income will have a profound effect on risk for malnutrition. It is a marker for the opportunity to be "plump and healthy.” Low cost, high-energy foods are readily available and even desirable for families at-risk for food insecurity. Once sufficient income is obtained, concern for the cost of necessities recedes, and neither under nor over nutrition is likely. The opportunity to be "plump and healthy" can be rejected.

As shown in the figure below, the movement of subpopulations through economic levels does not go directly from undernutrition to optimal nutrition. Unless steps are taken to assure affordable foods, rising incomes are likely to be associated with obesity, imbalance and persistent specific nutrient deficiency.

Figure 7. The prevalence of obesity versus the appearance of discretionary income

TEACHING CAPTION: The movement from widespread poverty ("developing") to affluence ("developed") is likely to be accompanied by a middle phase where incomes rise, but the population does not feel secure. Without systems of support, the likelihood of overnutrition and nutrient imbalance will increase. [See Karp, Meyers, Cheng]

Q5 Aren’t there other factors in the diets of the poor that might increase the level of obesity? Must all of the obesity be related to the larger societal issue of poverty?

A5. “Yes, but…” There are cluster effects of poverty that are indirectly related to the lack of income. For example, poverty creates stress and stress itself, has an impact on hypothalamic-pituitary axis function. While data are limited in humans, primate studies such as those by Rosenblum show substantial truncal obesity with a food insecurity-like model call “variable foraging.” Wise food selection and use of home prepared meals are associated with better micronutrient status but not with reducing obesity levels. Education is essential so that families choose the best (meaning rich in micronutrients rather than energy) foods. A low-glycemic index diet would not be more expensive than one with high glycemic diet.

One must do the best one can do with individuals through counseling

Q6. What can a pediatrician do? Aren’t these issues beyond the capacity of a physician working one-to-one with patients? Can you make recommendations?

A6. Begin with an open discussion by residents of the options.

Anna’s story shows genetics interacting with environment to produce obesity. This is occurring among many poorer populations in epidemic proportions. Families living at or just above the poverty level in the United States have easy access to an ample supply of energy rich, nutrient diminished foods. Only those poor children living in families well below the poverty level are unaffected by the obesity epidemic. Interventions should attempt an integration of social and economic support.

Two interacting sets of interventions are available to health professionals. These are, first, addressing the impact of income poverty on food selection and second, providing support for use of affordable, healthful foods.

The particularly economic intervention begins with an assessment for food insecurity. The first three questions of the USDA/Cornell Radimer food insecurity surveys are used in our work to determine which children are “at-risk.”

TABLE 2. Is this child “at-risk” for food insecurity?

Please tell me whether the following statements are true of you:

A. I worry whether my food will run out before I get money to buy more.

Often true [_]; Sometimes true [_]; Never true [_]

B. I worry about whether the food I can afford to buy for my family will be enough.

Often true [_]; Sometimes true [_]; Never true [_]

Question C is only for people who give a positive answer to A or B.

C. The food I buy just doesn’t last, and I don’t have money to get more.

Often true [_]; Sometimes true [_]; Never true [_]

TEACHING CAPTION: These questions are adapted from the CDC and Cornell/Radimer Food Insecurity Questionnaires. They are highly sensitive and likely to capture all children affected by food insecurity or hunger.

Supplemental programs (WIC and Food Stamps) are particularly effective in preventing food insecurity and maintaining high quality diets. These improve nutritional status in two ways. First, the foods given have a high nutritional value. Second, families spend the same dollar amount to meet less energy needs. Thus, the nutrient value of the foods purchased by a poor family increases to that of "non-poor" essentially reversing the Engel’s phenomenon. Supplemental food programs have shown substantial impact on nutrition in pregnancy and limit weight gain for older children and adults.

With respect to the social variables affecting poor children, socially determined overeating is likely to occur within a common set of circumstances where across-generational influences are working. Often grandmothers are involved. Although we have no direct data on the matter, we can speculate what the grandmothers bring to the situation; memories of familial histories that influence feeding practices. These may take the form of "Eat when food is plentiful against the time when it mar not be so." Thus, cultural influences are important factors. Interventions must be appropriately structured to help the parents, grandparents, and children understand the potential long-term sequella of obesity and the benefits of weight control. For example, long-established familial preferences, particularly in African-American families, for high-fat, fried foods will be contradictory to advice given by health professionals that a low-fat diet should be considered. The best approach may be an attempt to achieve a few well-defined interventions in patterns related to acquisition and preparation of food. It is important to remember that a modification of dietary patterns, including modest reduction in food intake, in combination with enhanced physical activity will modulate adiposity in growing children, more so than in adults.

Severe food restriction, however, is almost never warranted as it may lead to negative impacts on linear growth. Some behavioral objectives appropriate for a disadvantaged population could include the following suggestions for diet change in low-income families.

TABLE 3. Diet Changes Likely To Be Effective

a. Encourage better parental shopping and food preparation.

b. Reduce dependence on fatty food

c. Introduce fruits and vegetables into the diet

d. Encourage use of food stamps

e. Encourage physical activity

f. Discourage of excessive time spent by children watching television. In the case of families living in rural areas, encourage participation by children in activities of gardening, canning, and freezing vegetables

REFERENCES

1. Fernandez JR, Allison DB. Understanding racial differences in obesity and Metabolic Syndrome. Nutrition Reviews. 2003;61:316-319.

2. Ravussin E, Bogardus C. Energy balance and weight regulation: genetics versus environment. Br J Nutr. 2000;83 Suppl 1:S17-20.

3. Hofferth SL, Curtin S. Food programs and obesity among US children. http://www.gwu.edu/~labor/papers/hofferth.pdf.

4. Drewnowski A, Spector S. Poverty and Obesity: The Role of Energy Density and Energy Costs. Am J Clin Nutrition 2004

5. Karp RJ. (1999 and 2005) Malnutrition among children in the United States: The impact of Poverty. (in) Modern Nutrition in Health and Disease, 9th edition. Shils ME, Olson JA, Shike M, and Ross AC (eds) Williams & Wilkins, Baltimore MD, 1999., Pp 1089-1001 and 2005,10th edition Pp 861-875.

6. Dietz W. (1999 and 2005) Childhood obesity (in) Shils, ME, JA Olson, M Shike, and AC Ross.(eds) Modern nutrition in Health and Disease, 9th edition. Williams and Wilkins, Baltimore, MD. pp 1071-1080 and 10th edition 2005 Pp979-990.

7. Karp RJ, Cheng C, and Meyers AF. The appearance of discretionary income: Influence on the prevalence of under- and overnutrition to the International Journal of Health Inequities.-- http://www.equityhealthj.com/content/4/1/10

8. Case study by Joanne Hurley in Greenwood MRC et al. (1993) Obesity in disadvantaged children (in) Karp RJ (ed) Malnourished Children in the United States: Caught in the cycle of poverty Springer Publishing Co of New York. Pp 115-29.

See also:

Alaimo K, Olson J, Frongillo T. Low Family Income and Food Insecurity in Relation to Overweight in US Children. Archives of Pediatric and Adolescent Medicine. 2001;155:161-1167.

Kersey, M, Geppert J, Cutts, DB. Hunger and Health in Latino Children Born to Immigrant Families.

Klein HS. (1978) The Middle Passage. Princeton, NJ, Princeton University

Press.

Knowler WC, Pettitt DJ, Saad MF, Charles MA, Nelson RG, Howard BV, Bogardus C, Bennett PH: Obesity in the Pima Indians: its magnitude and relationship with diabetes. American Journal of Clinical Nutrition. 1991;53supp:1543S-1551S.

Olson C, Rauschenbach BS, Frongillo EA Jr, Kendall A Factors contributing to household food insecurity in a rural upstate New York county. Family Economics and Nutrition Review. 1997;10:2-17.

Gohil BJ, Rosenblum LA, Coplan JD, Kral JG. Hypothalamic-Pituitary

Adrenal Axis Function and the Metabolic Syndrome X of Obesity. CNS Spectrums 2001; 47:581-589.

Ludwig DS. Dietary glycemic index and obesity. J Nutrition. 2000;130supp:280S-283S

Warren J, Henry JK, Simonette. Low glycemic index breakfasts and reduced food intake in preadolescent children. Pediatrics 2003;112:e414-e419

Neel JV. Diabetes mellitus: a “thrifty geneotype” rendered detrimental by “progress”. American Journal of Human Genetics 1978;14:353-362.

Bouchard, C, Perusse L, LeBlanc C, Tremblay A, Theirault G: Inheritance of the amount and distribution of human body fat. International Journal of Obesity 1988;12:205-215.

Appendix 1(Anna — a Pima tribe Native American)

Joanne Hurley, HIS, RD (research dietitian at the Gila River reservation in Arizona)

Anna is 8 1/2 years old. She is 53 in. in height and weighs 150.5 lb. Fifty--six percent of the girls in Anna's second-grade class are above the 95th percentile in weight for height. Anna's story is thus typical of many of her schoolmates.

Anna weighed 7 lb 81/2 oz at birth and was 191/2 in. long, placing her in the 50th percentile for weight for height. Her mother was not diabetic before or during the pregnancy. She participated in the Women, Infants, and Children (WIC) program, receiving food provided by the program. By the time Anna was 3 months old, she had reached the 90th percentile for weight for height, and by 6 months of age, the 95th percentile. She remained at this level until she reached the age of 21/2 when she began to gain weight rapidly.

Anna's mother is a Pima Indian; her father is Hispanic. Anna was the first child born to her mother, who was 18 years of age. Psychosocial factors appear to contribute to Anna's weight gain. She eats to ease her pain of being abandoned by her mother, of being held back a grade in school, of being ridiculed by her peers, and of being cared for most of the time by her maternal grandparents. They feed and care for her, but show little emotional attachment to her. They expressed little if any interest in helping her with her problems at school in general or with her weight problem in particular.

She eats breakfast with her grandparents before the bus takes her to school. She then eats another breakfast and lunch at school. After the bus brings her home in the afternoon, she often snacks on soda pop and chips while she watches television. Extra meals and snacks of around 250 to 285 calories have been a major contributor to her dramatic weight gain over a brief period. Small increases in caloric intake on a consistent basis can have a significant effect on body weight over time.

Anna typifies the emotional poverty of being left alone and being fed as a means of social control, that is, "keeping her out of trouble." She experienced periods of special stress, such as those times when she was sent back to her mother who had abandoned her, or when she was having difficulties at school; these contributed to her pattern of behavior. Food became her immediate source of gratification and solace.

In addition, the current food intake patterns of Anna's community contributed to her problem as well. A study recently completed by the Cleveland Clinic reveals that the community as a whole has a very high intake of fat in their diet. Many of the homemakers cook on hot plates or out of doors, and most of the cooking involves frying. Morbid obesity in very young children in this community is adding to the high number of non-insulin-dependent diabetics under the age of 18 in this population

Appendix 2

In the southwest United States it is assumed that fry-bread -- essentially kneaded flour and water fried in Crisco or lard -- is indigenous to Native Americans. It’s highly caloric, palatable and cheap (about 2cents/100 calories). This food is actually of recent origins beginning with the provision of surplus fat and flour distributed on the reservations. Fry bread is now ingrained as an essential part of Native American culture, and is one contributor to the epidemic of obesity, coronary heart disease, and Type 2 DM.

Sarah Quandt describes three interacting sources for food cultures. #1 is an interaction of availability, food costs, and social preconditions; #2 is a part of acting out the rituals of a social structure or class; and #3 (a modification of #2) considers subjective experiences as a significant modifier of how history shapes consumption. One can see all of the elements of these three theories reflected in the role that fry bread plays in the food culture of some Native American tribes. It is very inexpensive (one or two cents for 100 calories. It represents a unique characteristic of Native American life. The Bureau of Indian Affairs provided flour and lard as a surplus food. The homemakers turned this poverty bread into a tasty and sustaining food stuff endowing fry bread with symbolic power. Thus the cooking and consumption of fry bread is an example of how a people’s history shapes and sustains its food culture even when the economic necessity of fry bread consumption becomes unnecessary.

Annotated Answers

A1. The answer is C. The adaptation to malnutrition is classically Darwinian. In a hostile environment, characteristics already present in the gene pool will provide a selective advantage and spread through the population. With continued environmental pressure, newly appearing genetic material, not associated with potentially lethal characteristics and with the good fortune to survive, will alter the gene pool and spread.

A2. The answer is B. The poorest children in any society are likely to have protein-energy malnutrition and be growth retarded or wasted. At highest incomes (>3 times the poverty level in the United States, food supplies are secure and families can chose nutritious food. The "near poor" are most at risk.

A3 The answer is True. Explanation is below

A4. "Food insecurity represents begins with an apprehension for not having sufficient food to feed the family. At its first level, it's simply a concern, as expressed in the "Often/sometimes" answer. Actual changes in patterns for feeding self (the adult), or child, or actual hunger represent higher levels of food insecurity."

A5. The answer is H. The obesity epidemic will not be halted by any one single intervention. Rather, a multisytems response is required. Each intervention is necessary; none are sufficient.