Diet and obesity

Map of dietary energy availability per person per day in 1961 (kcal/person/day).
Map of dietary energy availability per person per day in 1979-1981 (kcal/person/day).[1]
Map of dietary energy availability per person per day in 2001–2003 (kcal/person/day).[1]
  no data
  <1600
  1600-1800
  1800-2000
  2000-2200
  2200-2400
  2400-2600
  2600-2800
  2800-3000
  3000-3200
  3200-3400
  3400-3600
  >3600

Diet plays an important role in the genesis of obesity. Personal choices, advertising, social customs and cultural influences, as well as food availability and pricing all play a role in determining what and how much an individual eats.

Dietary energy supply

Average per capita energy consumption of the world from 1961 to 2002

The dietary energy supply is the food available for human consumption, usually expressed in kilocalories per person per day. It gives an overestimate of the total amount of food consumed as it reflects both food consumed and food wasted. The per capita dietary energy supply varies markedly between different regions and countries. It has also changed significantly over time.[2] From the early 1970s to the late 1990s, the average calories available per person per day (the amount of food bought) has increased in all part of the world except Eastern Europe and parts of Africa. The United States had the highest availability with 3654 kilo calories per person in 1996.[3] This increased further in 2002 to 3770.[4] During the late 1990s, Europeans had 3394 kilo calories per person, in the developing areas of Asia there were 2648 kilo calories per person, and in sub-Sahara Africa people had 2176 kilo calories per person.[3][5]

Average calorie consumption

Change over time of the macronutrient composition of the US male diet.
Change over time of the macronutrient composition of the US female diet.
USDA chart showing the increase in soda consumption and the decrease in milk consumption from 1947 to 2001.[6]

From 1971 – 2000, the average daily number of calories which women consumed in the United States increased by 335 calories per day (1542 calories in 1971 and 1877 calories in 2000). For men, the average increase was 168 calories per day (2450 calories in 1971 and 2618 calories in 2000). Most of these extra calories came from an increase in carbohydrate consumption rather than an increase in fat consumption.[7] The primary sources of these extra carbohydrates were sweetened beverages, which now accounts for almost 25 percent of daily calories in young adults in America.[8] As these estimates are based on a person's recall, they may underestimate the amount of calories actually consumed.[7]

Fast food

As societies become increasingly reliant on energy-dense fast-food meals, the association between fast food consumption and obesity becomes more concerning.[9] In the United States consumption of fast food meal has tripled and calorie intake from fast food has quadrupled between 1977 and 1995.[10] Consumption of sweetened drinks is also believed to be a major contributor to the rising rates of obesity.[11][12]

Portion size

A comparison of a typical cheeseburger 20 years ago (left) which had 333 calories with a modern cheeseburger (right) which contains 590 calories as per the National Heart, Lung, and Blood Institute

The portion size of many prepackage and restaurant foods has increased in both the United States and Denmark since the 1970s.[7] Fast food servings, for example, are 2 to 5 times larger than they were in the 1980s. Evidence has shown that larger portions of energy-dense foods lead to greater energy intake and thus to greater rates of obesity.[13][14]

Meat Consumption

A 2010 study published in the American Journal of Clinical Nutrition closely tracked 373,803 people over a period of 8 years across 10 countries. At its conclusion, the study reported that meat consumption is positively associated with weight gain in men and women.[15] In response, the National Cattlemen's Beef Association countered that increased meat consumption may not be associated with fat gain.[16] However, a subsequent response controlled for just abdominal fat across a sample of 91,214 people found that even when controlling for calories and lifestyle factors, meat consumption is linked with obesity.[17] Further population studies, reviews, and meta-analysis studies have corroborated the claim that greater meat consumption is linked to greater rates of obesity.[18][19]

Sugar consumption

Existing evidence from large-scale cross-sectional and prospective cohort studies supports that consumption of sugar-sweetened beverages is correlated with the childhood and adult obesity epidemic in the United States population (Malik et al. 2006). Sweetened drinks containing either sucrose alone or sucrose in combination with fructose appear to lead to weight gain due to increase energy intake.[20] Fructose might also be preferentially metabolized into fat as feedback inhibition as with glucose is missing.[21] In fact, about half of total added sugar consumed in the United States is in liquid form.[22] Teenage boys showed the greatest consumption of sugar sweetened beverages, upwards of 357 calories per day.[22] In addition to the evidence that humans have a natural propensity towards sugar,[23] there exists additional biological plausibility that explains the correlation of sugar-sweetened beverage consumption and obesity.[24]

A study by the National Center for Health Statistics showed that non-Hispanic black men consumed a larger percentage of their total calories from added sugars than non-Hispanic white and Mexican-American men. Non-Hispanic black men consumed 14.5% of their calories from added sugars compared with 12.8% for non-Hispanic white men and 12.9% for Mexican-American men. Non-Hispanic black women also consumed a larger percentage of their total calories from added sugars than non-Hispanic white and Mexican-American women. Non-Hispanic black women consumed 15.2% of their calories from added sugars compared with 13.2% for non-Hispanic white women and 12.6% for Mexican-American women. No significant differences in percentage of calories from added sugars were found between non-Hispanic white and Mexican-American men or women.[25]

Sugar-sweetened beverages raise concern because they are calorie-dense and yet produce low satiety.[26] There exists a strong correlation between the consumption of liquid calories and total energy intake. Individuals do not tend to decrease solid calories in compensation for increased liquid calories.[24] For example, if there were no compensation for liquid calories, the 40-50g of sugar in each 12 oz. can of soda drunk on a daily basis could lead to a 15-pound weight gain per year.[24] On the national scale, the American Heart Association estimates that approximately half of the total caloric intake increase over the past 30 years is attributable to liquid calories.[27] The high glycemic load of these beverages is also thought to be a contributor to chronic disease, including diabetes and nonalcoholic fatty liver disease.[26][28] Furthermore, there is emerging evidence that suggests sugar may be an addictive substance, further potentiating any individuals’ existing problem of excessive consumption.[23]

The soda industry budget for advertising in 2000 totaled over $700 million in the US, an increase of over $381 million since 1986.[22] Furthermore, standard serving sizes have increased from 8-ounce to 12-ounce bottles between 1977-1996.[22] Price incentives from beverage companies have kept their product prices low.[29]

Social policy and change

Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables.[30]

Participation by adults in the United States Department of Agriculture Supplemental Nutrition Assistance Program (i.e. Food Stamps) is positively associated with obesity, waist circumference, elevated fasting glucose, and metabolic syndrome.[31]

Metabolism

Evidence does not support the commonly expressed view that some obese people eat little yet gain weight due to a slow metabolism. On average obese people have a greater energy expenditure than normal weight or thin people and actually have higher BMRs.[32][33] This is because it takes more energy to maintain an increased body mass.[34] Obese people also underreport how much food they consume compared to those of normal weight.[35] Tests of human subjects carried out in a calorimeter support this conclusion.[36]

See also

References

  1. 1 2 "Compendium of food and agriculture indicators - 2006". Food and Agriculture Organization of the United Nations. Retrieved February 18, 2009.
  2. ↑ "Compendium of food and agriculture indicators - 2006". UN Food and Agriculture Organization. Archived from the original on August 2, 2008. Retrieved January 10, 2009.
  3. 1 2 "Calories per capita per day" (gif). UN Food and Agriculture Organization. Retrieved January 10, 2009.
  4. ↑ "www.fao.org" (PDF). UN Food and Agriculture Organization. Retrieved January 10, 2009.
  5. ↑ "USDA: frsept99b". USDA. Retrieved January 10, 2009.
  6. ↑ "In the Long Run" (pdf). USDA. Retrieved February 17, 2009.
  7. 1 2 3 Wright JD, Kennedy-Stephenson J, Wang CY, McDowell MA, Johnson CL (February 2004). "Trends in intake of energy and macronutrients—United States, 1971–2000". MMWR Morb Mortal Wkly Rep 53 (4): 80–2. PMID 14762332.
  8. ↑ Caballero B (2007). "The global epidemic of obesity: An overview". Epidemiol Rev 29: 1–5. doi:10.1093/epirev/mxm012. PMID 17569676.
  9. ↑ Rosenheck R (November 2008). "Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk". Obes Rev 9 (6): 535–47. doi:10.1111/j.1467-789X.2008.00477.x. PMID 18346099.
  10. ↑ Lin BH, Guthrie J and Frazao E (1999). "Nutrient contribution of food away from home". In Frazão E. Agriculture Information Bulletin No. 750: America's Eating Habits: Changes and Consequences. Washington, DC: US Department of Agriculture, Economic Research Service. pp. 213–239.
  11. ↑ Malik VS, Schulze MB, Hu FB (August 2006). "Intake of sugar-sweetened beverages and weight gain: a systematic review". Am. J. Clin. Nutr. 84 (2): 274–88. PMC 3210834. PMID 16895873.
  12. ↑ Olsen NJ, Heitmann BL (January 2009). "Intake of calorically sweetened beverages and obesity". Obes Rev 10 (1): 68–75. doi:10.1111/j.1467-789X.2008.00523.x. PMID 18764885.
  13. ↑ Ledikwe JH, Ello-Martin JA, Rolls BJ (April 2005). "Portion sizes and the obesity epidemic". J. Nutr. 135 (4): 905–9. PMID 15795457.
  14. ↑ Steenhuis IH, Vermeer WM (2009). "Portion size: review and framework for interventions". Int J Behav Nutr Phys Act 6: 58. doi:10.1186/1479-5868-6-58. PMC 2739837. PMID 19698102.
  15. ↑ Vergnaud, Anne-Claire; Norat, Teresa; Romaguera, Dora; Mouw, Traci; May, Anne M.; Travier, Noemie; Luan, Jian'an; Wareham, Nick; Slimani, Nadia (2010-08-01). "Meat consumption and prospective weight change in participants of the EPIC-PANACEA study". The American Journal of Clinical Nutrition 92 (2): 398–407. doi:10.3945/ajcn.2009.28713. ISSN 1938-3207. PMID 20592131.
  16. ↑ Astrup, Arne; Clifton, Peter; Layman, Donald K.; Mattes, Richard D.; Westerterp-Plantenga, Margriet S. (2010-11-01). "Meat intake's influence on body fatness cannot be assessed without measurement of body fat". The American Journal of Clinical Nutrition 92 (5): 1274–1275. doi:10.3945/ajcn.110.000661. ISSN 0002-9165. PMID 20844064.
  17. ↑ Vergnaud, Anne-Claire; Norat, Teresa; Romaguera, Dora; Peeters, Petra HM (2010-11-01). "Reply to A Astrup et al". The American Journal of Clinical Nutrition 92 (5): 1275–1276. doi:10.3945/ajcn.110.000786. ISSN 0002-9165.
  18. ↑ Lin, Yi; Bolca, Selin; Vandevijvere, Stefanie; De Vriese, Stephanie; Mouratidou, Theodora; De Neve, Melissa; Polet, Anja; Van Oyen, Herman; Van Camp, John (2011-04-01). "Plant and animal protein intake and its association with overweight and obesity among the Belgian population". The British Journal of Nutrition 105 (7): 1106–1116. doi:10.1017/S0007114510004642. ISSN 1475-2662. PMID 21144092.
  19. ↑ Rouhani, M. H.; Salehi-Abargouei, A.; Surkan, P. J.; Azadbakht, L. (2014-09-01). "Is there a relationship between red or processed meat intake and obesity? A systematic review and meta-analysis of observational studies". Obesity Reviews 15 (9): 740–748. doi:10.1111/obr.12172. ISSN 1467-789X. PMID 24815945.
  20. ↑ Tappy, L; Lê, KA (January 2010). "Metabolic effects of fructose and the worldwide increase in obesity". Physiological reviews 90 (1): 23–46. doi:10.1152/physrev.00019.2009. PMID 20086073.
  21. ↑ Lyssiotis, C; Cantley, LC (October 2013). "Metabolic syndrome: F stands for fructose and fat". Nature 502 (7470): 181–182. doi:10.1038/502181a. PMID 24108049.
  22. 1 2 3 4 Woodward-Lopez G, Kao J, Ritchie L (2010). "To what extent have sweetened beverages contributed to the obesity epidemic?". Public Health Nutrition 14 (3): 499–509. doi:10.1017/s1368980010002375.
  23. 1 2 Avena N.M., Rada P., Hoebel B.G. (2008). "Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake". Neuroscience Biobehavioral Review 32 (1): 20–39. doi:10.1016/j.neubiorev.2007.04.019.
  24. 1 2 3 Malik, VS; Schulze, MB; Hu, FB (2006). "Intake of sugar-sweetened beverages and weight gain: A systematic review". The American Journal of Clinical Nutrition 84 (2): 274–288. PMC 3210834. PMID 16895873.
  25. ↑ Ervin, R.B. and C.L. Ogden. (2013). Consumption of Added Sugars Among U.S. Adults, 2005-2010. Hyattsville, Md.: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics.
  26. 1 2 Hu, F., Malik, V. Sugar-sweetened beverages and risk of obesity and type II diabetes: epidemiologic evidence. Physiology and Behavior. 2010; 100: 47-54.
  27. ↑ Johnson, R.K., Appel, L.J., Brands, M., Howard, B.V., Lefevre, M., Lustig, R.H., Sacks, F., Steffen, L.M., Wylie-Rosett, J. Dietary sugars intake and cardiovascular health: a scientific statement from the American heart association. Circulation. (2009) 120: 1011-1020.
  28. ↑ Assy, N. Nasser, G. Kamayse, I., Nseir, W., Beniashvili, Z., Djibre, A., Grosovski, M. Soft drink consumption linked with fatty liver in the absence of traditional risk factors. Canadian Journal of Gastroenterology. (2008). 22(10) 811-816.
  29. ↑ Brownell, K.D., Farley, T., Willett, W.C., Popkin, B.M., Chaloupka, F.J., Thompson, J.W., Ludwig, D.S. The public health and economic benefits of taxing sugar-sweetened beverages. The New England Journal of Medicine. (2009) 361(16) 1599-1605.
  30. ↑ Pollan, Michael (22 April 2007). "You Are What You Grow". New York Times. Retrieved 2007-07-30.
  31. ↑ CW Leung, WC Willett, and EL Ding (Jan 2012). "Low-income Supplemental Nutrition Assistance Program participation is related to adiposity and metabolic risk factors". Am J Clin Nutr 95 (1): 17–24. doi:10.3945/ajcn.111.012294. PMC 3238460. PMID 22170370.
  32. ↑ Kushner, Robert (2007). Treatment of the Obese Patient (Contemporary Endocrinology). Totowa, NJ: Humana Press. p. 158. ISBN 1-59745-400-1. Retrieved April 5, 2009.
  33. ↑ Crowe, Tim. "Monday’s medical myth: ‘my slow metabolism makes me fat’". Retrieved 15 November 2013.
  34. ↑ Adams JP, Murphy PG (July 2000). "Obesity in anaesthesia and intensive care". Br J Anaesth 85 (1): 91–108. doi:10.1093/bja/85.1.91. PMID 10927998.
  35. ↑ Peter G. Kopelman, Ian D. Caterson, Michael J. Stock, William H. Dietz (2005). Clinical obesity in adults and children: In Adults and Children. Blackwell Publishing. ISBN 1-4051-1672-2.
  36. ↑ "mdPassport". Retrieved December 31, 2008.
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