Promote Health Through Diet and Exercise


Return to the tutorial menu.

The Obesity Problem

At the beginning of the 21st century, for the first time in human history, more of the earth's population suffers from too much food, rather than from lack of food. This has resulted in an increasing number of persons who are obese. This is a problem even amongst children. Half of persons in the U.S. are overweight enough to be defined as obese. This number increased by 50% in the last decade of the 20th century. There are a multitude of health complications from obesity. (National Task Force, 2000)

How does obesity occur? The formula is simple:

Food eaten – Exercise = Weight Gained

Another way of explaining the situation:

Delicious, Calorie Dense Food + Sedentary Lifestyle = Obesity

Most people live in a food toxic environment and are bombarded by cues to buy and eat food throughout the day. In addition, stress drives overeating. (Bose et al, 2009)

Stress + Abundant Food = Obesity

One's beliefs about food and diet affect the BMI. People who implicate insufficient exercise as a cause for obesity tend to consume more food and have a higher BMI than people who believe obesity is caused by a poor diet. (McFerran and Mukopadhyay, 2013)

There is ordinarily a modest amount of calories burned to maintain normal body metabolic processes. In general, for a normal healthy adult to maintain body weight with just activities of daily living, caloric intake must be limited to 10 calories (kcal) per pound (22 calories per kg). Thus, a 150 lb (68 kg) person needs about 1500 calories (kcal) per day to avoid gaining weight. Exercise can increase caloric use, and exercise has a "carryover effect" to increase metabolism and burn more calories after exercise. Of course, growing children require more calories. (Willett et al, 1999)

Exercise can burn calories (average for a standard 70 kg person) as follows:

Activity (moderate)kcal/minute
chewing gum 0.2
walking 3
cycling 4
dancing 5
ice skating 6
swimming 6
jogging10
shoveling15



Health Promotion

Here's a concept: eat one less...do one more. Over time, reduce intake and increase activity.

Eat one less: helping per meal, meal per week, snack per day, etc.

Do one more: day with exercise, hour of exercise, repetition of activity, etc.

Here's another concept, especially for kids: go outside.

Why stare at pixels jumping around the screen of an electronic device when there are creative and rewarding activities to be accomplished with physical activity. Get a life.


Let's Move

Just brisk walking for 20 minutes a day can have major benefits. A good aerobic exercise with cardiovascular benefit is to climb 10 flights of stairs once a day. Increase by one flight per week to achieve the goal.

Young adults can generally eat more and not gain weight, but metabolism tends to slow in the mid-30's (and middle-aged people become more inactive), so that is when many adults begin to gradually gain weight. One pound (0.45 kg) of fat has 3500 kcal. An excess intake of only 0.3% of calories eaten translates into a 20 pound (9.1 kg) weight gain over the age range of 25 to 55 years. The average weight gain in young adults averages 0.2 to 0.8 kg per year.

The body mass index (BMI, defined below) may be related to multiple genetic factors in 30 to 40% of persons, and this may in part determine the fat distribution. Single gene defects that produce a defined disease marked by obesity, such as the Prader-Willi syndrome, are extremely rare. (Rosenbaum et al, 1997)

Food intake is regulated via neural circuits located in the hypothalamus. A hormone produced in adipocytes (fat cells) known as leptin has the function of informing the hypothalamus about the state of fat stores. Leptin inhibits food intake and increases energy expenditure via an interaction with specific leptin receptors located in the hypothalamus. Differences in leptin levels may explain differences in BMI. (Baskin et al, 1999)

Social factors play a major role in weight gain. Situations during life in which weight gain is more likely to occur include: adolescence, pregnancy, mid-life in women, and following marriage in men. Persons who emigrate to a more urbanized culture tend to gain weight. Behavioral or environmental changes in life, such as smoking cessation, are associated with weight gain. Weight gained during holiday periods and festivals is more than at other times of the year and tends not to be lost. (Yanovski et al, 2000) The chance of becoming obese increases by 57% if one has a friend who becomes obese in a given interval. Among pairs of adult siblings, if one sibling becomes obese, the chance that the other becomes obese increases by 40%. If one spouse becomes obese, the likelihood that the other spouse becomes obese increases by 37%. (Christakis and Fowler, 2007)




What are the Risks?

Obesity is measured most accurately by calculating the body mass index, or BMI. The BMI is calculated as follows:

 Body Mass Index = weight in kg / height in meters2

An ideal body mass index (BMI) is in the range of 20 to 24 and anything above or below that range will increase certain risks for morbidity and mortality. In general, a BMI >28 increases the risk for morbidity. Using a definition of obesity as a BMI of 30 or more, a third the U.S. population qualifies as obese, while half are defined as overweight defined by a BMI >24. (Note: this tutorial's author's BMI is 22.)

The risk for mortality is greater in persons who are overweight. In a study of persons who were overweight at the age of 50 years, mortality was 20 to 40 percent higher than that among participants who had a BMI of 23.5 to 24.9 at that age. The mortality risk among obese subjects was two to at least three times that of participants with a BMI of 23.5 to 24.9. (Adams et al, 2006)

However, the distribution of fat has importance in determination of risk. A central distribution of fat, as is more typical of men, carries a higher risk for morbidity. A more peripheral distribution, as in hips and thighs in women, carries a lesser risk. The risk can be determined by measuring waist circumference and by calculating a waist-to-hip circumference ratio. In general, a waist:hip circumference ratio >0.9 for men and >1.0 for women carries an increased risk for morbidity. (Pischon et al, 2008)

Another risk is the time of onset of obesity. Obesity in childhood increases the risk for morbidity, regardless of whether obesity persists into adulthood.

Risks for morbidity are increased as follows when the BMI is 26, versus 21:

SexDiabetes MellitusHypertensionCoronary Artery DiseaseCholelithiasis
Women42 - 31.52 - 3
Men82 - 322 - 3



Specific Health Risks with Obesity

There are some diseases that are seen with increased frequency in persons who are obese, including certain types of cancer, diabetes mellitus, coronary artery disease, stroke, hypertension, cardiomyopathy, non-alcoholic steatohepatitis, osteoarthritis, reproductive problems, sleep apnea, and gallbladder disease.

Cancer

The following cancers are seen with increased frequency in persons who are overweight:

A third to half of cases of endometrial carcinoma occur in women with a BMI >29. Breast cancer risk is increased with obesity only for women who are postmenopausal. Half of cases of breast carcinoma in postmenopausal women occur in association with a BMI of >29. Risks for cancers of the lung, colon/rectum, and breast are diminished with healthy lifesytle/dietary patterns. (National Task Force, 2000) (Mai et al, 2005)

For persons who are grossly overweight (BMI >40) the risks are greater, with death rates from all cancers for men more than 52% and for women more than 62% greater than in persons of normal weight. The range of cancer types is broad, including esophagus, colon, rectum, liver, gallbladder, pancreas, kidney, non-Hodgkin lymphoma, and multiple myeloma in both men and women. In, prostate and stomach cancers are more frequent with increasing BMI, while in women breast, uterus, cervix, and ovarian cancers are more frequent. (Calle et al, 2003)

Diabetes Mellitus

In the U.S. there are 15 to 16 million adults who have diabetes mellitus, or about 8% of the population 20 years or older in age. Of these, 90 to 95% are classified as diabetes mellitus type II (DM type II), the type associated with obesity. About 80 to 90% of persons with type II diabetes mellitus are obese. About two-thirds of persons with DM type II have a BMI of at least 27, and half of persons with DM type II have a BMI of at least 30. (National Task Force, 2000)

The prevalence of DM type II in the U.S. increased by 25% in the last decade of the 20th century.

Among persons with a BMI >30 who already have impaired glucose tolerance and are at risk for developing type II diabetes mellitus, adopting lifestyle changes that decrease weight, decrease consumption of saturated fats and sugar in the diet, and increasing exercise will reduce the risk for type II diabetes mellitus by over 50 to 60%.

A characteristic pathologic finding in the islets of Langerhans of the pancreas can be seen in association with type II diabetes mellitus. A major complication of diabetes mellitus results from the accelerated, advanced atherosclerosis.

Metabolic Syndrome

The global epidemic of obesity and diabetes mellitus has led to a marked increase in the number of persons worldwide with metabolic syndrome. Both type 2 diabetes mellitus and metabolic syndrome share common features, and patients may be defined as having one or both. Metabolic syndrome, also known as syndrome X, or the insulin resistance syndrome, is defined as follows (Eckel et al, 2010):

Diabetes or impaired fasting glycaemia or impaired glucose tolerance or insulin resistance, plus 2 or more of the following:
  • Obesity: BMI > 30 or waist-to-hip ratio > 0.9 (male) or > 0.85 (female)

  • Dyslipidemia: triglycerides = or > 150 mg/dL or HDL cholesterol < 35 (male) or < 39 (female) mg/dL

  • Hypertension: blood pressure > 140/90 mm Hg

  • Microalbuminuria: albumin excretion > 20 mg/min

Patients with both type 2 diabetes and the metabolic syndrome are at increased risk for cardiovascular complications from both arerial and arteriolar disease. They should be treated to keep the Hgb A1C under 7% (Tuomilehto et al, 2001).

Therapeutic goals and recommendations include:
  • Lose 10% of body weight over the first year through lifestyle modifications with diet and exercise, thereafter continue weight loss or maintain weight.

  • Institute a regular program of physical activity that includes 30 to 60 minutes of moderate-intensity exercise daily.

  • Reduce intake of saturated fats, trans fats, and cholesterol.

  • Stop smoking

Coronary Artery Disease

Persons with diabetes mellitus are at increased risk for accelerated and advanced atherosclerosis that increases the risk for coronary artery disease that can lead to myocardial ischemia and myocardial infarction. However, even obese persons who do not have hyperglycemia can have an increased risk for coronary atherosclerosis. Obese persons have a >50% risk for a total serum cholesterol >250 mg/dL. In contrast, a study of middle-aged women revealed that those who did not smoke, were not overweight, maintained a healthy diet, and exercised at least moderately for a half hour each day had an incidence of coronary events 80% lower than the rest of the population. (Stampfer et al, 2000)

Atherosclerosis is potentially reversible. Adoption of major lifestyle changes including diet and exercise in middle aged adults can lead to lowering of LDL cholesterol levels by 37% in just one year and reduce the amount of coronary arterial stenosis. (Ornish et al, 1998)

Hypertension and Stroke

Persons who are obese tend to have an increased blood pressure. Hypertension that is untreated can increase the risk for heart failure, kidney failure, and stroke.

The rate of ischemic cerebrovascular disease is 75% higher in women with a BMI >27 and 137% higher in women with a BMI >32, compared to women with a BMI of 21 or less. Though not included in this study, risks for men are increased as well. (National Task Force, 2000)

The prevalence of cardiovascular diseases and their complications increases as the amount of dietary sodium increases. It is estimated that if adults from 40 to 85 years of age in the U.S. were to decrease sodium intake by just 9.5%, there would be 1 million fewer deaths and $32 billion saved in health care costs over their lifetime. (Smith-Spangler et al, 2010)

Cardiomyopathy

Some obese patients who have little or no coronary artery disease and do not have a history of hypertension may still develop heart failure. In these patients, the heart is globally enlarged, similar to a dilated cardiomyopathy. If such persons lose weight, the heart diminishes in size. This obesity cardiomyopathy may be related to blood volume expansion or other factors. (Dela Cruz and Matthay, 2009)

Non-alcoholic Fatty Liver Disease (NAFL)

NAFL is being recognized more frequently. Dietary patterns play a role in the development of steatosis (fatty change) in the liver. Obesity increases the risk for alterations in hepatocyte function that lead to accumulation of lipid in hepatocytes and hepatomegaly. NAFL reduces the metabolic function of the liver. NAFL can proceed to non-alcoholic steatohepatitis (NASH), to liver failure, and even cirrhosis, with an increased risk for development of hepatocellular carcinoma. (Choudhury and Sanyal, 2004)

Osteoarthritis

Increased weight will increase the stress on weight-bearing joints, particularly lower extremities, leading to osteoarthritis. A BMI of 30 or more markedly increases the risk for osteoarthritis of the knees. Interestingly, obese persons are less likely to have osteoporosis, but osteoarthritis more than makes up for this.

Reproductive Problems

Women who are obese are more likely to have menstrual irregularities and ovulatory infertility, including the polycystic ovarian syndrome (PCOS). Women with PCOS typically have irregular bleeding, hirsutism, and/or infertility in association with chronic anovulation and androgen excess not attributable to another cause. PCOS is estimated to occur in 4% of women, but there is an increased prevalence with diabetes mellitus and obesity. Conversely, women with PCOS are more likely to have obesity and diabetes mellitus. PCOS is characterized by insulin resistance, hyperandrogenism, and abnormal gonadotropin release with inadequate follicle stimulating hormone release, leading to anovulation. Weight loss can aid in treatment of PCOS. (Guzick, 2004)

Obesity in women who are pregnant increases the likelihood for gestational diabetes that can affect the developing fetus. Maternal obesity increases the risk for macrosomia, stillbirth, and neural tube defects. The increased maternal risks include hypertension, pre-eclampsia, and hemorrhage. (Dixit and Girling, 2008)

Obstructive Sleep Apnea

Persons who are obese have a greater likelihood for obstructive sleep apnea (OSA), or periods of absent breathing while asleep. OSA is the major feature of obesity hypoventilation syndrome, which is defined by a body mass index of 30 or more along with sleep-disordered breathing and chronic daytime alveolar hypoventilation with PaCO2 of 45 mm Hg or more and PaO2 less than 70 mm Hg. Persons who snore while sleeping have a propensity to develop sleep apnea. The increased soft tissue in upper airways contributes to the problem. Sleep apnea is accompanied by decreased ventilation (hypoventilation) and pulmonary dysfunction. (Littleton and Mokhlesi, 2009)

Gallbladder Disease

Biliary tract lithiasis, manifested mainly by development of cholelithiasis (gallstones), is more likely to occur in persons who are obese. The gallstones are typically of the mixed type with cholesterol. Cholelithiasis can lead to cholecystitis and to pancreatitis.




What Can Be Done?

The best approach is prevention. Adopting a lifestyle that includes a healthy diet and exercise will prevent obesity from happening. Losing weight once it has been been gained is difficult, but worth trying for health benefits.

National Policy

What nation has experienced a marked reduction in coronary artery disease over the past 40 years? Finland. Mortality from ischemic heart disease remained high following World War II. The North Karelia Project began in 1972 as a community-based intervention to influence diet and other lifestyles needed to prevent coronary artery disease. This project was subsequently adopted nationally. Ischemic heart disease mortality in a working-age population declined by 73% in North Karelia and by 65% in the whole country from 1971 to 1995. The project utilizes low-cost intervention activities with widespread participation through community organizations as well as national policies. (Papadakis and Moroz, 2008)

In addition, interventions to reduce salt intake were undertaken in Finland (reduce salt content in food processing, label food product contents, and promote educational campaigns) with the result that the average systolic and diastolic blood pressure measures declined by more than 10 mm Hg over 30 years, with a 75 to 80% decrease in deaths from stroke and coronary artery disease. (Karppanen and Mervaala, 2006)

Diets

If you diet, your body adapts to the lower caloric intake and becomes more efficient at utilizing and storing as fat any calories taken in. Thus, if you go off the diet, you gain weight even faster than before. The best diet is the one you continue to follow. Legitimate weight loss programs incorporate lifestyle changes that have more longer-lasting effects. (Sacks et al, 2009)

Dieting is more frustrating for women. Since women average twice as much body fat as men, women will tend to gain weight twice as fast, or lose weight half as fast, as men. Thus, when husband and wife adopt a new diet to lose weight, the advantage is seen more quickly by the husband. The wife needs more encouragement and dedication. Consumption of foods recommended in current dietary guidelines is associated with decreased risk of mortality for both men and women. (Kant et al, 2009)

What about "low carbohydrate" diets? Like many popular myths, this diet does have a shred of reality behind it, based upon "specific dynamic action" (SDA) of foods, or the amount of calories required just to digest, absorb, and metabolize the food. More complex proteins and fats require more energy to process, up to 30% of calories in proteins and up to 10% in fats, while simple carbohydrates require only 5%. The average diet takes about 10%, and this is part of the basal metabolic rate. Thus, one could eat a just little more protein or fat and increase the total calories consumed, without weight gain. However, these differences in SDA are not marked. If total calories are reduced, particularly from carbohydrates, lipolysis and ketosis with acidosis occur. (Bravata et al, 2003) (Sacks et al, 2009)

The "glycemic index" (GI) is a measure of the ability of foods to raise the blood sugar and stimulate insulin release via the the rate of carbohydrate absorption after a meal. Many factors together, including carbohydrate type, fiber, protein, fat, food form and method of preparation, determine the GI of a particular food. Low GI foods such as complex carbodydrates that take longer to digest are associated with decreased return of hunger and a lower blood glucose. Sugar, obviously, has a very high GI, while a salad would have a low GI.

Thus, the type of food eaten in a diet is not as important as just reducing overall intake. In fact, attendance at group meetings to reinforce weight loss strongly predicts longer term success in weight loss (0.2 kg per session attended). (Wadden et al, 2005)

Pharmacologic Therapies

Americans are enfatuated with "quick fixes", fads, and pill-popping, so a popular approach to weight loss is the infamous "diet pill". Weight tends to be gained with cessation of the drug use.

Sympathomimetic amines, principally amphetamines, have been used for this purpose, but they fall out of favor because of the potential for abuse.

Sibutramine is a serotonin - norepinephrine reuptake inhibitor that acts to alter brain centers that control hunger and satiation. Serotonin reuptake inhibitors act to increase serotonergic activity by stimulating serotonin in brain synapses. On the basis of the serotonin hypothesis of appetite control, this would be expected to reduce appetite. (Rosenbaum et al, 1997)

Orlistat is an inhibitor of pancreatic and gastric lipase when taken with meals, thus inhibiting the hydrolysis of triglycerides so that absorption of fats is reduced, by about 30% at the most. It does not appear to affect the absorption of other nutrients or drugs. It induces a mild state of malabsorbtion of fats and can be accompanied by diarrhea, bloating, and flatulence. It is most effective when combined with lifestyle changes for weight reduction. (Bray, 2008)

Rimonabant is a specific cannabinoid (CB1) receptor blocker shown to reduce food intake and body weight and to alter metabolic activity in adipose tissue. CB1 receptors are present in brain, liver, muscle, gastrointestinal tract, and adipose tissue. Stimulation of CB1 receptors in fat cells promotes lipogenesis and inhibits production of adiponectin. Adiponectin has antidiabetic and antiatherosclerotic properties. (Després et al, 2005)

Use of pharmacologic therapies in combination with lifestyle modifications (diet, exercise) is more successful than either pharmacologic therapy or lifestyle modification alone. (Wilding, 2007)

Surgical Therapies

Surgical therapies are drastic and may only be of value when other methods have failed and the BMI is greater than 40. Procedures that decrease nutrient absorption such as jejunoileal bypass have too many complications to be effective. Restrictive procedures limiting food intake include vertical banded gastroplasty (VBG) and Roux-en-Y gastric bypass (RYGB) and can be effective by promoting a feeling of satiety with smaller amounts of food. However, adoption of a liquid or semisolid diet can defeat the purpose of the surgery, or as one patient stated, 'If I could do what I am supposed to do following surgery, then I wouldn't have needed the surgery.' Some degree of malnutrition can occur but can be treated with dietary supplementation. Surgical complications may result in more severe forms of malnutrition. Liposuction is NOT weight reduction surgery; it is for body contouring. (Bult et al, 2008)




References

Adams KF, Schatzkin A, Harris TB, et al. Overweight, Obesity, and Mortality in a Large Prospective Cohort of Persons 50 to 71 Years Old. N Engl J Med. 2006;355:763-778.

Baskin DG, Figlewicz Lattemann D, Seeley RJ, Woods SC, Porte D Jr, Schwartz MW. Insulin and leptin: dual adiposity signals to the brain for the regulation of food intake and body weight. Brain Res. 1999;848:114-123.

Bose M, Oliván B, Laferrère B. Stress and obesity: the role of the hypothalamic-pituitary-adrenal axis in metabolic disease. Curr Opin Endocrinol Diabetes Obes. 2009;16:340-346.

Bravata DM, Sanders L, Huang J, et al. Efficacy and safety of low-carbohydrate diets: a systematic review. JAMA. 2003;289:1837-1850.

Bray GA. Medications for weight reduction. Endocrinol Metab Clin North Am. 2008;37:923-942.

Bult MJ, van Dalen T, Muller AF. Surgical treatment of obesity. Eur J Endocrinol. 2008;158:135-145.

Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.W. adults. N Engl J Med. 2003;348:1625-1638.

Christakis NA, Fowler JH. The Spread of Obesity in a Large Social Network over 32 Years. N Engl J Med. 2007;357:370-379.

Choudhury J, Sanyal AJ. Insulin resistance and the pathogenesis of nonalcoholic fatty liver disease. Clin Liver Dis. 2004;8:575-594.

Dela Cruz CS, Matthay RA. Role of obesity in cardiomyopathy and pulmonary hypertension. Clin Chest Med. 2009;30:509-523.

Després J-P, Golay A, Lars Sjöström A Effects of Rimonabant on Metabolic Risk Factors in Overweight Patients with Dyslipidemia. N Engl J Med. 2005;353:2121-2134.

Dixit A, Girling JC. Obesity and pregnancy. J Obstet Gynaecol. 2008;28:14-23.

Eckel RH, Aberti KGMM, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet. 2010;375:181-183.

Guzick DS. Polycystic ovary syndrome. Obstet Gynecol. 2004;103(1):181-193.

Kant AK, Leitzmann MF, Park Y, Hollenbeck A, Schatzkin A. Patterns of recommended dietary behaviors predict subsequent risk of mortality in a large cohort of men and women in the United States. J Nutr. 2009;139:1374-1380.

Karppanen H, Mervaala E. Sodium intake and hypertension. Prog Cardiovasc Dis. 2006;49:59-75.

Littleton SW, Mokhlesi B. The pickwickian syndrome-obesity hypoventilation syndrome. Clin Chest Med. 2009;30:467-478,

Mai V, Kant AK, Flood A, Lacey JV Jr, Schairer C, Schatzkin A. Diet quality and subsequent cancer incidence and mortality in a prospective cohort of women. Int J Epidemiol. 2005;34:54-60.

McFerran B, Mukhopadhyay A. Lay Theories of Obesity Predict Actual Body Mass. Psychol Sci. doi: June 5, 2013:10.1177/0956797612473121.

National Task Force on the Prevention and Treatment of Obesity. Overweight, obesity, and health risk. Arch Intern Med. 2000;160:898-904.

Ornish D, Scherwitz LW, Billings JH, et al. Intensive lifestyle changes for reversal of coronary heart disease. JAMA. 1998;280:2001-2007.

Papadakis S, Moroz I. Population-level interventions for coronary heart disease prevention: what have we learned since the North Karelia project? Curr Opin Cardiol. 2008;23:452-461.

Pischon T, Boeing H, Hoffmann K, et al. General and abdominal adiposity and risk of death in Europe. N Engl J Med. 2008;359:2105-2120.

Rosenbaum RL, Leibel JH. Medical progress: obesity. N Engl J Med. 1997;337:396-407.

Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med. 2009;360:859-873.

Smith-Spangler CM, Juusola JL, Enns EA, Owens DK, Garber AM. Population strategies to decrease sodium intake and the burden of cardiovascular disease. Ann Intern Med. 2010;152:481-487.

Stampfer MJ, Hu FB, Manson JE, Rimm EB, Willett WC. Primary prevention of coronary heart disease in women through diet and lifestyle. N Engl J Med. 2000;343:16-22.

Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343-1350.

Wadden TA, Berkowitz RI, Womble LG, et al. Randomized Trial of Lifestyle Modification and Pharmacotherapy for Obesity. N Engl J Med. 2005;353:2111-2120.

Wilding JP. Treatment strategies for obesity. Obes Rev. 2007;8 Suppl 1:137-144.

Willett WC, Dietz WH, Colditz GA. Primary care: guidelines for healthy weight. N Engl J Med. 1999;341:427-434.

Yanovski JA, Yanovski SZ, Kara N, et al. A prospective study of holiday weight gain. N Engl J Med. 2000;342:861-867.


Return to the tutorial menu.