Stable weight depends on an even balance between energy intake from food and energy expenditure. Energy expenditure occurs during the day in three ways:
· As energy expended during rest (basal metabolism)
· As energy used to metabolize food (thermogenesis)
· As energy expended during physical activity
Basal metabolism accounts for about two-thirds of expended energy, which is generally used to maintain body temperature and muscle contractions in the heart and intestine.
Thermogenesis accounts for about 10% of expended energy.
When a person's consumes more calories than energy that is used, the body stores the extra calories in fat cells. Fat cells function as energy reservoirs. They enlarge or contract depending on how people use energy. If people do not balance energy input and output by eating right and exercising, fat can builds up. This can lead to weight gain.
· As energy expended during rest (basal metabolism)
· As energy used to metabolize food (thermogenesis)
· As energy expended during physical activity
Basal metabolism accounts for about two-thirds of expended energy, which is generally used to maintain body temperature and muscle contractions in the heart and intestine.
Thermogenesis accounts for about 10% of expended energy.
When a person's consumes more calories than energy that is used, the body stores the extra calories in fat cells. Fat cells function as energy reservoirs. They enlarge or contract depending on how people use energy. If people do not balance energy input and output by eating right and exercising, fat can builds up. This can lead to weight gain.
When energy input is equal to energy output, there is no expansion of fat cells (lipocytes) to accommodate excess. It is only when more calories are taken in than used that the extra fat is stored in the lipocytes and the person begins to accumulate fat.
What is Obesity?
People who are obese have an abnormally high and unhealthy proportion of body fat. To measure obesity, researchers commonly use a formula based on weight and height known as the body mass index (BMI). BMI is the ratio of weight (in kilograms) to height (in meters) squared. BMI provides a more accurate measure of obesity or being overweight than does weight alone.
Measurement of Obesity
Obesity is determined by measuring body fat, not just body weight. People might be over the weight limit for normal standards, but if they are very muscular with low body fat, they are not obese. Others might be normal or underweight, but still have excessive body fat. The following measurements and factors are used to determine whether or not a person is overweight to a degree that threatens their health:
· Body mass index (BMI) (a measure of body fat)
· Waist circumference
· Waist-hip ratio
· Anthropometry (skin fold measurement)
· The presence or absence of other disease risk factors (e.g., smoking, high blood pressure, unhealthy cholesterol levels, diabetes, relatives with heart disease)
A person's disease risk factors plus BMI may be the most important components in determining health risks with weight.
What is Obesity?
People who are obese have an abnormally high and unhealthy proportion of body fat. To measure obesity, researchers commonly use a formula based on weight and height known as the body mass index (BMI). BMI is the ratio of weight (in kilograms) to height (in meters) squared. BMI provides a more accurate measure of obesity or being overweight than does weight alone.
Measurement of Obesity
Obesity is determined by measuring body fat, not just body weight. People might be over the weight limit for normal standards, but if they are very muscular with low body fat, they are not obese. Others might be normal or underweight, but still have excessive body fat. The following measurements and factors are used to determine whether or not a person is overweight to a degree that threatens their health:
· Body mass index (BMI) (a measure of body fat)
· Waist circumference
· Waist-hip ratio
· Anthropometry (skin fold measurement)
· The presence or absence of other disease risk factors (e.g., smoking, high blood pressure, unhealthy cholesterol levels, diabetes, relatives with heart disease)
A person's disease risk factors plus BMI may be the most important components in determining health risks with weight.
Body-Mass Index/ BMI
The body-mass index, a measure of adiposity, has been categorized as follows: 18.5 to 24.9, 25.0 to 29.9, 30.0 to 34.9, 35.0 to 39.9, and 40.0 or more. These categories correspond to those proposed by the World Health Organization6 for “normal range,” “grade 1 overweight,” (25.0 to 29.9) “grade 2 overweight” (30.0 to 39.9), and “grade 3 overweight,” (40.0 or more). For many analyses, especially for cancers in specific sites and among participants who had never smoked, the upper categories of body-mass index were combined, because of the small numbers. In oncology, for analyses and discussion, it is customary to we refer to the range of 25.0 to 29.9 as corresponding to “overweight” and to values of 30.0 or more as corresponding to “obesity.”
Waist Circumference and Waist-Hip Ratio
The extent of abdominal fat can also be used in assessing risk of disease. Some studies suggest that:
· Women whose waistlines are over 31.5 inches and men whose waists measure over 37 inches should watch their weight.
· A waist size greater than 35 inches in women and 40 inches in men is associated with a higher risk for heart disease, diabetes, and impaired functioning.
Evidence strongly suggests that more body fat around the abdomen and hips (the apple-shape) is a more consistent predictor of heart problems and health risks than BMI.
The distribution of fat can be evaluated by dividing waist size by hip size. For example, a woman with a 30-inch waist and 40-inch hip circumference would have a ratio of 0.75; one with a 41-inch waist and 39-inch hips would have a ratio of 1.05. The lower the ratio the better. The risk of heart disease rises sharply for women with ratios above 0.8 and for men with ratios above 1.0.
Anthropometry
Anthropometry is the measurement of skin fold thickness in different areas, particularly around the triceps, shoulder blades, and hips. This measurement is useful in determining how much weight is due to muscle or fat.
Obesity and Cancer
Link between cancer and obesity appears paradoxical as cancer is classically seen as illness producing anorexia and massive weight loss. To measure obesity, researchers commonly use a formula based on weight and height known as the body mass index (BMI). According to WHO approximately 1.6 billion of the world’s adult are overweight and over 400 million are obese. Cancers of the endometrium, kidney, gallbladder, breast, colon and adenocarcinoma of the esophagus have been linked to obesity. Obesity and physical inactivity may account for 25 to 30 percent of several major cancers. Those with a body-mass index of at least 40 had death rates from all cancers combined that were 52 percent higher (for men) and 62 percent higher (for women) than the rates in men and women of normal weight. On the basis of associations observed in some studies, it has been estimated that current patterns of overweight and obesity could account for 14 percent of all deaths from cancer in men and 20 percent of those in women. Women with large abdominal fat (apple shaped) have high risk of breast cancer than those having ‘pear’ shaped distribution. Data on link between obesity & cancers of the pancreas, prostate, liver, cervix, ovary and on hematopoietic cancers are scarce or inconsistent. Obesity and physical inactivity may account from 25-30% of several major cancers. For grade-III obesity, relative risk for dying by cancer is 1.70 for breast cancer, 1.63 for esophageal cancer, 1.94 for gastric cancer, 1.84 for colon cancer, 1.70 for renal cancer, 4.52 for liver cancer, 1.76 for gall bladder cancer, 1.49 for pancreatic cancer and 1.34 for prostate cancer.
Introduction
According to WHO 1.6 billion of the world’s adult were overweight in 2005 and over 400 million were obese. By 2015 the numbers are expected to nearly double.1,2 A recent study from United States reports 14% of deaths from cancer in men and 20% deaths in women were due to overweight and obesity.1 Obesity is not just a problem of west but it is a global phenomenon. According to WHO, figures for obesity in America are 35% for women and 20% for men, in China it is over 20% for both men and women. Even desperately poor countries like Nigeria and Uganda are struggling with the problem of obesity. There is substantial evidence that adipose tissue particularly visceral adipose tissue is a metabolically active endocrine organ. This leads to the release of insulin – like growth factors that are linked to increased cancer risk.3 The mechanism of this link may not be clear at present but there is enough evidence to say that link exists. As the prevalence of obesity is increasing worldwide, we can expect proportional increase in cancer cases. This will not only add to the high cost of cancer treatment but also add to human suffering as well.
Although we have known for some time that excess weight is also an important factor in death from cancer,4 our knowledge of the magnitude of the relation, both for all cancers and for cancers at individual sites, and the public health effect of excess weight in terms of total mortality from cancer is limited. The biological mechanism that explains how obesity worsens risk of cancer may be different for different cancers. The exact mechanisms by which obesity induces or promotes tumor genesis vary by cancer site. However, possible mechanisms include alterations in sex hormones and insulin. Insulin resistance is been associated with cancers of colon and rectum, breast and pancreas. Whatever may be the causes, the obesity still is seen as life style disease and by that definition it is largely preventable. It may be an oversimplified view as many people believe that obesity is genetic (there is evidence for that). It is right time to educate people and emphasize the need for life style changes to keep the weight in check.5 Life style choices that can check weight will not only help in preventing cancer but also help in preventing other diseases such as heart diseases, diabetes and many nervous and mental disorders.
Relationship between Obesity and Cancer?
In 2001, it was concluded that cancers of the colon, breast (postmenopausal), endometrium (the lining of the uterus), kidney, and esophagus are associated with obesity. Some studies have also reported links between obesity and cancers of the gallbladder, ovaries, and pancreas.7 Obesity and physical inactivity may account for 25 to 30 percent of several major cancers—colon, breast (postmenopausal), endometrial, renal and cancer of the esophagus.7
In 2002, about 41,000 new cases of cancer in the United States were estimated to be due to obesity. This means that about 3.2 percent of all new cancers are linked to obesity.1,8,9 The contribution of excess body weight to the total burden of mortality from cancer depends on two factors: the relative risk of death due to cancer among overweight or obese persons as compared with persons of normal weight and the prevalence of overweight and obesity in a given population. The very high prevalence of obesity in the United States explains why small elevations in mortality due to cancer translate into substantial fractions of mortality due to cancer that are related to overweight or obesity. Calle et al. point out how much cancer-related mortality could be reduced among nonsmokers if body weight were adequately controlled. It is intriguing that the positive association between excess body weight and mortality due to cancer is not limited to a few forms of cancer indeed, positive associations represent the rule rather than the exception. The biologic mechanisms that are regularly invoked to explain the association between overweight or obesity and cancer concern steroid hormones, insulin, the insulin-like growth factor system, and mechanical processes such as the contribution of abdominal obesity to gastresophageal reflux and esophageal adenocarcinoma.1, 10
In both men and women, body-mass index was also significantly associated with higher rates of death due to cancer of the esophagus, colon and rectum, liver, gallbladder, pancreas, and kidney; the same was true for death due to non-Hodgkin’s lymphoma and multiple myeloma. Significant trends of increasing risk with higher body-mass-index values were observed for death from cancers of the stomach and prostate in men and for death from cancers of the breast, uterus, cervix, and ovary in women. Previous studies have consistently shown associations between adiposity and increased risk of cancers of the endometrium, kidney, gallbladder (in women), breast (in postmenopausal women), and colon (particularly in men).11-15 Adenocarcinoma of the esophagus has been linked to obesity. 14,16,17 Data on cancers of the pancreas, prostate, liver, cervix, ovary and on hematopoietic cancers are scarce or inconsistent.11-14, 18-21 The lack of consistency may be attributable to the limited number of studies, the limited range and variable categorization of overweight and obesity among studies, bias introduced by reverse causality with respect to smoking related cancers, and possibly real differences between the effects of overweight and obesity on the incidence of cancer and on the rates of death from some cancers.22,23 Experts have concluded that the chief causes of obesity are a sedentary lifestyle and overconsumption of high-calorie food.7,24, 25
In the last 50 years there are marked changes in dietary and work habits. People eat too much and do too little exercise. There is reduction in physical activity and more people have sedentary life styles. Since the beginning of the 20th century, obesity is being linked to diabetes, hypertension and myocardial infarction. In late 1940’s French researcher divided obesity into android type – predominant abdominal obesity particularly seen in males and described it is ‘apple’ shaped whereas gynoid type – with distribution of fat to the hips is characteristic of females and described as ‘pear’ shaped.5 But it took quite some time when in 1980’s abdominal fat was implicated as risk factor for IHD, diabetes and stroke. The distribution of fat is important risk determinant of breast cancer. Women with large abdominal fat (apple shaped) have high risk of breast cancer than those having ‘pear’ shaped distribution.24, 26, 27
Obesity has been studied extensively as risk factor for various cancers. According to American Institute of Cancer Research (AICR), obesity increases likelihood of developing breast, colon, endometrial, esophageal, renal and prostate cancers by 25-33%.
Abdominal fat has a sensitive system for releasing free fatty acids which are transported directly via the portal vein into the liver where it produces 3 important effects as insulin clearance, Glucogenesis and VLDL synthesis which leads to hyperinsulinaemia, hyperglycemia and hyperlipidaemia respectively. Free Fatty Acids (FFA) are synthesized in liver into VLDL predominantly triglycerides. Insulin resistance in liver cells increases glucose products to cause high blood glucose. Hyperinsulinaemia resultant from insulin resistance worsens as insulin level increase further as Liver’s ability to break the hormone decreases.
The current burst of articles on metabolic syndrome shows the relevance of obesity in the contemporary society. It is the gift of modern western life style with its negative features of physical inactivity, excessive intake of energy and stress.
The International Agency for Research on Cancer (IARC) has concluded that there is sufficient evidence of a cancer-preventive effect of avoidance of weight gain for cancers of the colon, breast (in post menopausal women), endometrium, kidney (renal cell carcinoma), and esophagus (adenocarcinoma).14 Potential biologic mechanisms include increased levels of endogenous hormones (sex steroids, insulin, and insulin-like growth factor I) associated with overweight and obesity and the contribution of abdominal obesity to gastresophageal reflux and esophageal adenocarcinoma.14 Moderate relative risks (less than 2.0) associated with overweight and obesity both for colon cancer and for breast cancer in postmenopausal women have been documented consistently.11 Much higher relative risks have been observed for uterine cancer (2 to 10) and kidney cancer (1.5 to 4), and the increased risk of kidney cancer associated with excess weight is higher in women than in men in majority studies.11, 28, 29 Increases by a factor of two to three in the risk of adenocarcinoma of the esophagus in association with high body-mass index have been reported16, 17, and the magnitude of this association has been found by other investigators to be greater in nonsmokers.16
Conclusion
International experts in the field of nutrition, cancer biology and public health are working on this link between life style and cancer and have come out with health recommendations for prevention of cancer. Their recommendations need to be incorporated in management plans and advising people how they can reduce their own cancer risk.91 It may take time to establish the exact link between obesity and cancer but the time has come to start talking to patients about the link between life style and cancer prevention through healthy weight, healthy eating habits and increasing physical activity.
An apple a day keeps the doctor away, but if you remain in a pear, you can avoid either of them.
References
1. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. New England Journal of Medicine. 2003; 348(17):1625–38.
2. The Tribune, Thursday 4th October 2007.
3. Martin G Healthy eating V Cancer GMC Today. 2007, 6, 6-7.
4. Lew EA, Garfinkel L. Variations in mortality by weight among 750,000 men and women. J Chronic Dis 1979; 32 : 563-76.
5. Berne C, Bjorntrop P. The Metabolic Syndrome. In: ArnetzBB, Ekman R,editors. Stress in health and disease. Weinheim:WILEY-VCH Verlag GmbH&Co.KGaA;2006.p317-332.
6. Thun MJ, Calle EE, Namboodiri MM. Risk factors for fatal colon cancer in a large prospective study. J Natl Cancer Inst.
7. Vainio H, Bianchini F. IARC handbooks of cancer prevention. Volume 6: Weight control and physical activity. Lyon, France: IARC Press, 2002.
8. Polednak AP. Trends in incidence rates for obesity-associated cancers in the U.S. Cancer Detection and Prevention 2003; 27(6):415–421.
9. McLaughlin JK, Blot WJ, Devesa SS, Fraumeni JF Jr. Renal cancer. In: Schottenfeld D, Fraumeni JF. Cancer epidemiology and prevention. 2nd ed. New York: Oxford University Press. 1996: 1142-55.
10. Obesity and Mortality from Cancer N Engl J Med.2008; 348; 17.
11. World Cancer Research Fund. Food, nutrition and the prevention of cancer: a global perspective. Washington, D.C.: American Institute for Cancer Research. 1997:371-3.
12. Carroll K. Obesity as a risk factor for certain types of cancer. Lipids 1998; 33:1055-9.
13. Bergstrom A, Pisani P, Tenet V, Wolk A, Adami H-O. Overweight as an avoidable cause of cancer in Europe. Int J Cancer. 2001; 91:421-30.
14. IARC handbooks of cancer prevention. Vol. 6. Weight control and physical activity. Lyons, France: International Agency for Research on Cancer, 2002.
15. Peto J. Cancer epidemiology in the last century and the next decade. Nature. 2001; 411: 390-5.
16. Chow W-H, Blot WJ, Vaughan TL. Body mass index and risk of adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst. 1998; 90: 150-5.
17. Vaughan TL, Davis S, Kristal A, Thomas DB. Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev. 1995; 4: 85-92.
18. Lew EA, Garfinkel L. Variations in mortality by weight among 750,000 men and women. J Chronic Dis. 1979; 32: 563-76.
19. Michaud DS, Giovannucci E, Willett WC, Colditz G, Stampfer M, Fuchs C. Physical activity, obesity, height, and the risk of pancreatic cancer. JAMA. 2001; 286: 921-9.
20. Wolk A, Gridley G, Svensson M. A prospective study of obesity and cancer risk (Sweden). Cancer Causes Control. 2001; 12: 13-21.
21. Moller H, Mellemgaard A, Lindvig K, Olsen J. Obesity and cancer risk: a Danish record-linkage study. Eur J Cancer. 1994; 30: 344-50.
22. Calle EE, Terrell DD. Utility of the National Death Index for ascertainment of mortality among Cancer Prevention Study II participants. Am J Epidemiol. 1993; 137: 235-41.
23. Physical status: the use and interpretation of anthropometry: report of a WHO Expert Committee. World Health Organ. 1995; 854:1-452.
24. Friedenreich CM. Physical activity and cancer prevention: From observational to intervention research. Cancer Epidemiology, Biomarkers and Prevention.2001; 10(4): 287–301.
25. Kritchevsky D. Diet and cancer: What’s next? Journal of Nutrition. 2003; 133(11):3827–29.
26. Kaaks R, Van Noord PAH, Den Tonkelaar I. Breast cancer incidence in relation to height, weight and body-fat distribution in the Dutch “DOM” cohort. International Journal of Cancer. 1998; 76(5): 647–51.
27. Männistö S, Pietinen P, Pyy M. Body-size indicators and risk of breast cancer according to menopause and estrogen-receptor status. International Journal of Cancer. 1996; 68(1): 8–13.
28. Hill HA, Austin H. Nutrition and endometrial cancer. Cancer Causes Control. 1996; 7: 19-32.
29. Wolk A, Lindblad P, Adami H-O. Nutrition and renal cell cancer. Cancer Causes Control. 1996; 7: 5-18.
1. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. New England Journal of Medicine. 2003; 348(17):1625–38.
2. The Tribune, Thursday 4th October 2007.
3. Martin G Healthy eating V Cancer GMC Today. 2007, 6, 6-7.
4. Lew EA, Garfinkel L. Variations in mortality by weight among 750,000 men and women. J Chronic Dis 1979; 32 : 563-76.
5. Berne C, Bjorntrop P. The Metabolic Syndrome. In: ArnetzBB, Ekman R,editors. Stress in health and disease. Weinheim:WILEY-VCH Verlag GmbH&Co.KGaA;2006.p317-332.
6. Thun MJ, Calle EE, Namboodiri MM. Risk factors for fatal colon cancer in a large prospective study. J Natl Cancer Inst.
7. Vainio H, Bianchini F. IARC handbooks of cancer prevention. Volume 6: Weight control and physical activity. Lyon, France: IARC Press, 2002.
8. Polednak AP. Trends in incidence rates for obesity-associated cancers in the U.S. Cancer Detection and Prevention 2003; 27(6):415–421.
9. McLaughlin JK, Blot WJ, Devesa SS, Fraumeni JF Jr. Renal cancer. In: Schottenfeld D, Fraumeni JF. Cancer epidemiology and prevention. 2nd ed. New York: Oxford University Press. 1996: 1142-55.
10. Obesity and Mortality from Cancer N Engl J Med.2008; 348; 17.
11. World Cancer Research Fund. Food, nutrition and the prevention of cancer: a global perspective. Washington, D.C.: American Institute for Cancer Research. 1997:371-3.
12. Carroll K. Obesity as a risk factor for certain types of cancer. Lipids 1998; 33:1055-9.
13. Bergstrom A, Pisani P, Tenet V, Wolk A, Adami H-O. Overweight as an avoidable cause of cancer in Europe. Int J Cancer. 2001; 91:421-30.
14. IARC handbooks of cancer prevention. Vol. 6. Weight control and physical activity. Lyons, France: International Agency for Research on Cancer, 2002.
15. Peto J. Cancer epidemiology in the last century and the next decade. Nature. 2001; 411: 390-5.
16. Chow W-H, Blot WJ, Vaughan TL. Body mass index and risk of adenocarcinomas of the esophagus and gastric cardia. J Natl Cancer Inst. 1998; 90: 150-5.
17. Vaughan TL, Davis S, Kristal A, Thomas DB. Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev. 1995; 4: 85-92.
18. Lew EA, Garfinkel L. Variations in mortality by weight among 750,000 men and women. J Chronic Dis. 1979; 32: 563-76.
19. Michaud DS, Giovannucci E, Willett WC, Colditz G, Stampfer M, Fuchs C. Physical activity, obesity, height, and the risk of pancreatic cancer. JAMA. 2001; 286: 921-9.
20. Wolk A, Gridley G, Svensson M. A prospective study of obesity and cancer risk (Sweden). Cancer Causes Control. 2001; 12: 13-21.
21. Moller H, Mellemgaard A, Lindvig K, Olsen J. Obesity and cancer risk: a Danish record-linkage study. Eur J Cancer. 1994; 30: 344-50.
22. Calle EE, Terrell DD. Utility of the National Death Index for ascertainment of mortality among Cancer Prevention Study II participants. Am J Epidemiol. 1993; 137: 235-41.
23. Physical status: the use and interpretation of anthropometry: report of a WHO Expert Committee. World Health Organ. 1995; 854:1-452.
24. Friedenreich CM. Physical activity and cancer prevention: From observational to intervention research. Cancer Epidemiology, Biomarkers and Prevention.2001; 10(4): 287–301.
25. Kritchevsky D. Diet and cancer: What’s next? Journal of Nutrition. 2003; 133(11):3827–29.
26. Kaaks R, Van Noord PAH, Den Tonkelaar I. Breast cancer incidence in relation to height, weight and body-fat distribution in the Dutch “DOM” cohort. International Journal of Cancer. 1998; 76(5): 647–51.
27. Männistö S, Pietinen P, Pyy M. Body-size indicators and risk of breast cancer according to menopause and estrogen-receptor status. International Journal of Cancer. 1996; 68(1): 8–13.
28. Hill HA, Austin H. Nutrition and endometrial cancer. Cancer Causes Control. 1996; 7: 19-32.
29. Wolk A, Lindblad P, Adami H-O. Nutrition and renal cell cancer. Cancer Causes Control. 1996; 7: 5-18.
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