Why we need an integrative, individualized approach to weight loss

Obesity has surpassed epidemic proportions. One in three adults in the U.S. are overweight or obese,1 and if current trends continue, a whopping 57% of children in the United States will be obese by the time they turn 35.2

Researchers continue to search for dietary and lifestyle interventions that can effectively prevent and treat obesity, and test them in controlled trials. The Look AHEAD trial, published in 2010, was perhaps the most successful weight loss trial to date, achieving an average of 9% weight loss after 1 year and maintaining 5% weight loss after 4 years using an intensive lifestyle intervention.3 However, this pales in comparison to bariatric surgery, which is currently able to achieve an average five-year weight loss of 23%.

With all we know about nutrition science, is this really the best we can do? Will 57% percent of the United States require invasive bariatric surgery or face the many comorbidities associated with obesity?

Not necessarily. But it will require some major changes in how we address obesity.

There are four reasons why dietary treatment has not been shown (in controlled weight loss trials) to be an effective alternative to bariatric surgery:

  1. Nutrition dogma and resistance to new paradigms
  2. Excessive focus on calories and not enough focus on quality of food
  3. The underlying causes of obesity are not being addressed
  4. Behavior change is difficult

Nutrition dogma and resistance to new paradigms

It’s inevitable to form personal dietary beliefs when you study nutritional sciences. We can only hope that researchers in the field can put aside their biases and be open-minded to new evidence and new paradigms. Unfortunately, many nutritional scientists developed their personal dietary beliefs decades ago, and are still stuck in a mindset where whole grains are the panacea of health, a calorie is a calorie, and saturated fat and cholesterol are to blame for obesity and cardiovascular disease.

This is despite several recent large-scale, non-industry funded meta-analyses suggesting that saturated fat has no association with heart disease, 4–6 controlled trials that show that dietary cholesterol has little effect on circulating blood cholesterol levels,7,8 and the recent discovery that the sugar industry hid evidence and bribed researchers to shift the blame to fat back in the 1960s.9,10 I’ve also yet to see a study on the benefits of whole grains that isn’t comparing them to refined grains.

Moreover, industry influence abounds, both in original research and at the policy level. One study found that 67% of weight loss studies between 1966 and 2003 were funded by industry.11 This is not all that surprising, given how expensive weight loss trials are. As for policy, the Dietary Guidelines for Americans (DGAs) are determined by the USDA, the same federal agency that subsidizes corn, wheat, soybeans, dairy, and sugar. Is it any surprise that they also recommend eating plenty of these foods?

In 2010, the USDA set up the Nutrition Evidence Library (NEL) in an attempt to bring some sanity and standardization to the evaluation process and reduce bias in developing the DGAs. But in the 2015 report, the NEL was not consulted for over 70% of the topics discussed.12  This included some of the most controversial issues in nutrition science. Instead, they relied on systematic reviews from the American Heart Association (AHA) and the American College of Cardiology (ACC), both of which are heavily influenced by the food and drug industries. Furthermore, the DGAs offer zero information on how to construct a healthy weight loss diet. Yet many weight loss trials are built around the recommendations in the DGAs. (To read more about my take on nutrition policy, click here).

Excessive focus on calories: overfed but undernourished

Nutrition science is also far too focused on calories. Five hundred calories of sugar do not have the same effect on the body as five hundred calories of grass-fed beef. Food affects epigenetics, hormones, metabolic rate, and inflammation, and is the raw building material for our cells.

Yes, eating 3,500 calories a day will probably lead to weight gain. But what we need to be focusing on is why someone is able to eat so many calories a day, not developing diets that painfully restrict calories and lead to poor adherence.

Anthropological studies have found that hunter-gatherer populations are virtually free of obesity and associated comorbidities.13–15 This soon changes if they become exposed to a Western diet of highly processed and refined foods.

In other words, it’s pretty easy to eat 3,500 calories a day worth of cereal, pasta, cookies, and sugary beverages. It’s much harder to eat this many calories worth of meat, vegetables, starchy tubers, fruit, nuts, and seeds in their whole form. The latter is more satiating, greater in volume, and incredibly dense in micronutrients.

Many weight loss “experts” overlook micronutrients, saying they can’t possibly be more important than total calorie intake or the ratios of fat, carbohydrate, and protein, and are therefore irrelevant. Yet several vitamin and mineral deficiencies have been associated with obesity, including antioxidants, vitamin A, vitamin D, B vitamins, iron, magnesium, selenium, and zinc.16 In many cases, animal studies have confirmed that deficiency alone is sufficient to cause weight gain and/or metabolic abnormalities:

Micronutrient deficiencies - effect on health, adiposity, and weight gain

It’s amazing to me that despite all of this evidence, there are still many nutrition scientists who believe that a calorie is a calorie.

A quote often attributed to Albert Einstein says:

The definition of insanity is doing the same thing over and over again and expecting a different result.”

The bottom line is, we can’t just restrict caloric intake or increase energy expenditure through exercise and expect weight loss to occur smoothly and be easily maintained when someone has an underlying metabolic issue.

Addressing the underlying cause

We desperately need an integrated, individualized approach to weight management; one that addresses:

1) Micronutrient deficiencies: As discussed in the previous section, micronutrient deficiencies can contribute to weight gain, adiposity, and altered expression of metabolic genes. Moreover, studies have found that obese individuals may have greater micronutrient needs than lean individuals, yet most popular weight loss diets are below even the recommended daily intake for several vitamins and minerals.34,35

2) Gut health: Obesity is associated with an altered gut microbiota, and transplanting fecal material from an obese mouse into a lean mouse is sufficient to cause rapid weight gain.36 Heavier individuals also tend to have increased gut permeability, or “leaky gut”, where bacteria and large molecules from the gut are able to pass into the bloodstream. Leaky gut has been shown to result in an inflammatory response that can initiate insulin resistance and obesity.37 Therefore, addressing gut health and repairing the gut barrier needs to be a key component of treatment in obesity.

3) Food sensitivities: An estimated 25% of the U.S. population are lactose intolerant, yet dairy is a key component of the Dietary Guidelines for Americans (no doubt due to lobbying by the dairy industry) and in many weight loss diets. An individual who continues to eat a food when they are intolerant will induce local gut inflammation and systemic inflammation, which can contribute to insulin resistance. Indeed, antibodies against various food antigens have been correlated with inflammation in obese adolescents,38 and personalized elimination diets based on measured antibody responses have been shown to be effective for weight loss. In one study, individuals lost 19 pounds in 6 months on an elimination diet compared to 2 pounds lost on a standard weight loss diet.39

4) Environmental toxins: Exposure to endocrine disruptors like bisphenol A have been shown to predispose children to weight gain.40 Organic pollutants have also been strongly implicated in the etiology of obesity and diabetes.41

5) Inflammation: this is perhaps the greatest force driving obesity and metabolic syndrome, and is a commonality among all four factors listed above. Inflammatory markers have been shown to predict future weight gain and the development of type 2 diabetes.42,43

6) Hormone imbalances: Active thyroid hormone (triiodothyronine, or T3) regulates energy metabolism, thermogenesis, and plays a crucial role in lipid and glucose metabolism, food intake, and fatty acid oxidation.44 Thyroid stimulating hormone (TSH) is a potent stimulator of leptin secretion.45 Hypothyroidism is associated with obesity, weight gain, and an inability to lose weight.

7) Lifestyle: Chronic sleep deprivation and disruption of the circadian rhythm has been shown to cause increased food intake, impaired glucose tolerance, weight gain, and other metabolic abnormalities.46,47 Combine this with a sedentary lifestyle, chronic stress, and constant access to food, and you basically have the recipe for obesity and diabetes.48

Behavior change is hard

Lastly, we need an approach to weight management that is focused on positive behavior change. According to the CDC, four of the top five behaviors for preventing chronic disease include getting regular physical activity, consuming moderate amounts or no alcohol, not smoking, and obtaining daily sufficient sleep. (The fifth is maintaining a healthy body weight.) In 2013, less than a quarter of Americans engaged in all four of these positive behaviors.49

The reality is, behavior change is difficult. Even if you know the underlying causes of your inability to lose weight and know exactly what diet and lifestyle changes you need to get there, you might lack the motivation and self-discipline to be able to go the distance. People need help making lifestyle habits that stick.

This is where a support system comes in. An intensive lifestyle intervention, with regular counseling, has been shown to be effective at increasing behavior change.3 We need healthcare practitioners that can identify the root cause of disease working alongside health coaches and dietitians that can help encourage people to form new healthy habits.

Conclusion

To sum up, dietary interventions could be equally as effective as bariatric surgery, but to achieve this requires a revolution of our current approach.

We need an integrative, individualized approach that is not rooted in nutrition dogma, recognizes that not all food is equal, addresses the underlying cause of disease, and supports people in forming and maintaining healthy habits. Only then will we have any hope of preventing and reversing the obesity epidemic.

That’s all for now! Be sure to subscribe below so you don’t miss the next article in this series, where I share my 8 simple steps to weight loss.

Sources:

  1. Data Briefs – Number 288 – October 2017. (2017). Available at: https://www.cdc.gov/nchs/products/databriefs/db288.htm. (Accessed: 16th December 2017)
  2. Ward, Z. J. et al. Simulation of Growth Trajectories of Childhood Obesity into Adulthood. New England Journal of Medicine 377, 2145–2153 (2017).
  3. Long Term Effects of a Lifestyle Intervention on Weight and Cardiovascular Risk Factors in Individuals with Type 2 Diabetes: Four Year Results of the Look AHEAD Trial. Arch Intern Med 170, 1566–1575 (2010).
  4. Siri-Tarino, P. W., Sun, Q., Hu, F. B. & Krauss, R. M. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am. J. Clin. Nutr. 91, 535–546 (2010).
  5. Siri-Tarino, P. W., Sun, Q., Hu, F. B. & Krauss, R. M. Saturated fat, carbohydrate, and cardiovascular disease. Am. J. Clin. Nutr. 91, 502–509 (2010).
  6. Hooper, L. et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev CD002137 (2001). doi:10.1002/14651858.CD002137
  7. Herron, K. L. et al. Men classified as hypo- or hyperresponders to dietary cholesterol feeding exhibit differences in lipoprotein metabolism. J. Nutr. 133, 1036–1042 (2003).
  8. Herron, K. L. et al. Pre-menopausal women, classified as hypo- or hyperresponders, do not alter their LDL/HDL ratio following a high dietary cholesterol challenge. J Am Coll Nutr 21, 250–258 (2002).
  9. Kearns, C. E., Apollonio, D. & Glantz, S. A. Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents. PLOS Biology 15, e2003460 (2017).
  10. Kearns, C. E., Schmidt, L. A. & Glantz, S. A. Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med 176, 1680–1685 (2016).
  11. Thomas, O. et al. Industry funding and the reporting quality of large long-term weight loss trials. Int J Obes (Lond) 32, 1531–1536 (2008).
  12. Teicholz, N. The scientific report guiding the US dietary guidelines: is it scientific? BMJ 351, h4962 (2015).
  13. Cordain, L., Eaton, S. B., Miller, J. B., Mann, N. & Hill, K. The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. Eur J Clin Nutr 56 Suppl 1, S42-52 (2002).
  14. Walker, A. R. P., Walker, B. F. & Adam, F. Nutrition, diet, physical activity, smoking, and longevity: From primitive hunter-gatherer to present passive consumer—How far can we go? Nutrition 19, 169–173 (2003).
  15. Cordain, L. et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 81, 341–354 (2005).
  16. García, O. P., Long, K. Z. & Rosado, J. L. Impact of micronutrient deficiencies on obesity. Nutrition Reviews 67, 559–572 (2009).
  17. Campión, J., Milagro, F. I., Fernández, D. & Martínez, J. A. Vitamin C supplementation influences body fat mass and steroidogenesis-related genes when fed a high-fat diet. Int J Vitam Nutr Res 78, 87–95 (2008).
  18. Campión, J., Milagro, F. I., Fernández, D. & Martínez, J. A. Diferential gene expression and adiposity reduction induced by ascorbic acid supplementation in a cafeteria model of obesity. J. Physiol. Biochem. 62, 71–80 (2006).
  19. Bonet, M. L. et al. Opposite effects of feeding a vitamin A-deficient diet and retinoic acid treatment on brown adipose tissue uncoupling protein 1 (UCP1), UCP2 and leptin expression. J. Endocrinol. 166, 511–517 (2000).
  20. Ribot, J., Felipe, F., Bonet, M. L. & Palou, A. Changes of adiposity in response to vitamin A status correlate with changes of PPAR gamma 2 expression. Obes. Res. 9, 500–509 (2001).
  21. Mercader, J. et al. Remodeling of white adipose tissue after retinoic acid administration in mice. Endocrinology 147, 5325–5332 (2006).
  22. Cheng, Q., Boucher, B. J. & Leung, P. S. Modulation of hypovitaminosis D-induced islet dysfunction and insulin resistance through direct suppression of the pancreatic islet renin-angiotensin system in mice. Diabetologia 56, 553–562 (2013).
  23. Yanoff, L. B. et al. The prevalence of hypovitaminosis D and secondary hyperparathyroidism in obese Black Americans. Clin. Endocrinol. (Oxf) 64, 523–529 (2006).
  24. Pooya, S. et al. Methyl donor deficiency impairs fatty acid oxidation through PGC-1α hypomethylation and decreased ER-α, ERR-α, and HNF-4α in the rat liver. Journal of Hepatology 57, 344–351 (2012).
  25. Waterland, R. A., Travisano, M., Tahiliani, K. G., Rached, M. T. & Mirza, S. Methyl donor supplementation prevents transgenerational amplification of obesity. Int J Obes (Lond) 32, 1373–1379 (2008).
  26. Chen, M. D., Song, Y. M. & Lin, P. Y. Zinc may be a mediator of leptin production in humans. Life Sci. 66, 2143–2149 (2000).
  27. Mantzoros, C. S. et al. Zinc may regulate serum leptin concentrations in humans. J Am Coll Nutr 17, 270–275 (1998).
  28. Marreiro, D. do N. et al. Effect of zinc supplementation on serum leptin levels and insulin resistance of obese women. Biol Trace Elem Res 112, 109–118 (2006).
  29. Zhao, L. et al. Obesity and iron deficiency: a quantitative meta-analysis. Obes Rev 16, 1081–1093 (2015).
  30. Dongiovanni, P., Fracanzani, A. L., Fargion, S. & Valenti, L. Iron in fatty liver and in the metabolic syndrome: A promising therapeutic target. Journal of Hepatology 55, 920–932 (2011).
  31. Sartori, S. B., Whittle, N., Hetzenauer, A. & Singewald, N. Magnesium deficiency induces anxiety and HPA axis dysregulation: Modulation by therapeutic drug treatment. Neuropharmacology 62, 304–312 (2012).
  32. Pitts, M. W. et al. Deletion of Selenoprotein M Leads to Obesity without Cognitive Deficits. J. Biol. Chem. 288, 26121–26134 (2013).
  33. Beckett, G. J., MacDougall, D. A., Nicol, F. & Arthur, J. R. Inhibition of type I and type II iodothyronine deiodinase activity in rat liver, kidney and brain produced by selenium deficiency. Biochemical Journal 259, 887–892 (1989).
  34. Damms-Machado, A., Weser, G. & Bischoff, S. C. Micronutrient deficiency in obese subjects undergoing low calorie diet. Nutrition Journal 11, 34 (2012).
  35. Calton, J. B. Prevalence of micronutrient deficiency in popular diet plans. Journal of the International Society of Sports Nutrition 7, 24 (2010).
  36. Turnbaugh, P. J. et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027–131 (2006).
  37. Cani, P. D. et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56, 1761–1772 (2007).
  38. Wilders-Truschnig, M. et al. IgG Antibodies Against Food Antigens are Correlated with Inflammation and Intima Media Thickness in Obese Juveniles. Exp Clin Endocrinol Diabetes 116, 241–245 (2008).
  39. Onmus, M. Y., Avcu, E. C. & Saklamaz, A. The Effect of Elimination Diet on Weight and Metabolic Parameters of Overweight or Obese Patients Who Have Food Intolerance. Journal of Food and Nutrition Research 4, 1–5 (2016).
  40. Newbold, R. R., Padilla-Banks, E., Snyder, R. J. & Jefferson, W. N. Developmental exposure to estrogenic compounds and obesity. Birth Defects Res. Part A Clin. Mol. Teratol. 73, 478–480 (2005).
  41. Dirinck, E. et al. Obesity and Persistent Organic Pollutants: Possible Obesogenic Effect of Organochlorine Pesticides and Polychlorinated Biphenyls. Obesity 19, 709–714 (2011).
  42. Engström, G. et al. Inflammation-sensitive plasma proteins are associated with future weight gain. Diabetes 52, 2097–2101 (2003).
  43. Pradhan, A. D., Manson, J. E., Rifai, N., Buring, J. E. & Ridker, P. M. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 286, 327–334 (2001).
  44. Reinehr, T. Obesity and thyroid function. Mol. Cell. Endocrinol. 316, 165–171 (2010).
  45. Menendez, C. et al. TSH stimulates leptin secretion by a direct effect on adipocytes. J. Endocrinol. 176, 7–12 (2003).
  46. Knutson, K. L., Spiegel, K., Penev, P. & Van Cauter, E. The Metabolic Consequences of Sleep Deprivation. Sleep Med Rev 11, 163–178 (2007).
  47. Markwald, R. R. et al. Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain. PNAS 110, 5695–5700 (2013).
  48. Freese, J., Klement, R. J., Ruiz-Núñez, B., Schwarz, S. & Lötzerich, H. The sedentary (r)evolution: Have we lost our metabolic flexibility? F1000Research 6, 1787 (2017).
  49. Liu, Y. Clustering of Five Health-Related Behaviors for Chronic Disease Prevention Among Adults, United States, 2013. Prev. Chronic Dis. 13, (2016).

Click edit button to change this text.

Why we need an integrative, individualized approach to weight loss

Obesity has surpassed epidemic proportions. One in three adults in the U.S. are overweight or obese,1 and if current trends continue, a whopping 57% of children in the United States will be obese by the time they turn 35.2

Researchers continue to search for dietary and lifestyle interventions that can effectively prevent and treat obesity, and test them in controlled trials. The Look AHEAD trial, published in 2010, was perhaps the most successful weight loss trial to date, achieving an average of 9% weight loss after 1 year and maintaining 5% weight loss after 4 years using an intensive lifestyle intervention.3 However, this pales in comparison to bariatric surgery, which is currently able to achieve an average five-year weight loss of 23%.

With all we know about nutrition science, is this really the best we can do? Will 57% percent of the United States require invasive bariatric surgery or face the many comorbidities associated with obesity?

Not necessarily. But it will require some major changes in how we address obesity.

There are four reasons why dietary treatment has not been shown (in controlled weight loss trials) to be an effective alternative to bariatric surgery:

  1. Nutrition dogma and resistance to new paradigms
  2. Excessive focus on calories and not enough focus on quality of food
  3. The underlying causes of obesity are not being addressed
  4. Behavior change is difficult

Nutrition dogma and resistance to new paradigms

It’s inevitable to form personal dietary beliefs when you study nutritional sciences. We can only hope that researchers in the field can put aside their biases and be open-minded to new evidence and new paradigms. Unfortunately, many nutritional scientists developed their personal dietary beliefs decades ago, and are still stuck in a mindset where whole grains are the panacea of health, a calorie is a calorie, and saturated fat and cholesterol are to blame for obesity and cardiovascular disease.

This is despite several recent large-scale, non-industry funded meta-analyses suggesting that saturated fat has no association with heart disease, 4–6 controlled trials that show that dietary cholesterol has little effect on circulating blood cholesterol levels,7,8 and the recent discovery that the sugar industry hid evidence and bribed researchers to shift the blame to fat back in the 1960s.9,10 I’ve also yet to see a study on the benefits of whole grains that isn’t comparing them to refined grains.

Moreover, industry influence abounds, both in original research and at the policy level. One study found that 67% of weight loss studies between 1966 and 2003 were funded by industry.11 This is not all that surprising, given how expensive weight loss trials are. As for policy, the Dietary Guidelines for Americans (DGAs) are determined by the USDA, the same federal agency that subsidizes corn, wheat, soybeans, dairy, and sugar. Is it any surprise that they also recommend eating plenty of these foods?

In 2010, the USDA set up the Nutrition Evidence Library (NEL) in an attempt to bring some sanity and standardization to the evaluation process and reduce bias in developing the DGAs. But in the 2015 report, the NEL was not consulted for over 70% of the topics discussed.12  This included some of the most controversial issues in nutrition science. Instead, they relied on systematic reviews from the American Heart Association (AHA) and the American College of Cardiology (ACC), both of which are heavily influenced by the food and drug industries. Furthermore, the DGAs offer zero information on how to construct a healthy weight loss diet. Yet many weight loss trials are built around the recommendations in the DGAs. (To read more about my take on nutrition policy, click here).

Excessive focus on calories: overfed but undernourished

Nutrition science is also far too focused on calories. Five hundred calories of sugar do not have the same effect on the body as five hundred calories of grass-fed beef. Food affects epigenetics, hormones, metabolic rate, and inflammation, and is the raw building material for our cells.

Yes, eating 3,500 calories a day will probably lead to weight gain. But what we need to be focusing on is why someone is able to eat so many calories a day, not developing diets that painfully restrict calories and lead to poor adherence.

Anthropological studies have found that hunter-gatherer populations are virtually free of obesity and associated comorbidities.13–15 This soon changes if they become exposed to a Western diet of highly processed and refined foods.

In other words, it’s pretty easy to eat 3,500 calories a day worth of cereal, pasta, cookies, and sugary beverages. It’s much harder to eat this many calories worth of meat, vegetables, starchy tubers, fruit, nuts, and seeds in their whole form. The latter is more satiating, greater in volume, and incredibly dense in micronutrients.

Many weight loss “experts” overlook micronutrients, saying they can’t possibly be more important than total calorie intake or the ratios of fat, carbohydrate, and protein, and are therefore irrelevant. Yet several vitamin and mineral deficiencies have been associated with obesity, including antioxidants, vitamin A, vitamin D, B vitamins, iron, magnesium, selenium, and zinc.16 In many cases, animal studies have confirmed that deficiency alone is sufficient to cause weight gain and/or metabolic abnormalities:

Micronutrient deficiencies - effect on health, adiposity, and weight gain

It’s amazing to me that despite all of this evidence, there are still many nutrition scientists who believe that a calorie is a calorie.

A quote often attributed to Albert Einstein says:

The definition of insanity is doing the same thing over and over again and expecting a different result.”

The bottom line is, we can’t just restrict caloric intake or increase energy expenditure through exercise and expect weight loss to occur smoothly and be easily maintained when someone has an underlying metabolic issue.

Addressing the underlying cause

We desperately need an integrated, individualized approach to weight management; one that addresses:

1) Micronutrient deficiencies: As discussed in the previous section, micronutrient deficiencies can contribute to weight gain, adiposity, and altered expression of metabolic genes. Moreover, studies have found that obese individuals may have greater micronutrient needs than lean individuals, yet most popular weight loss diets are below even the recommended daily intake for several vitamins and minerals.34,35

2) Gut health: Obesity is associated with an altered gut microbiota, and transplanting fecal material from an obese mouse into a lean mouse is sufficient to cause rapid weight gain.36 Heavier individuals also tend to have increased gut permeability, or “leaky gut”, where bacteria and large molecules from the gut are able to pass into the bloodstream. Leaky gut has been shown to result in an inflammatory response that can initiate insulin resistance and obesity.37 Therefore, addressing gut health and repairing the gut barrier needs to be a key component of treatment in obesity.

3) Food sensitivities: An estimated 25% of the U.S. population are lactose intolerant, yet dairy is a key component of the Dietary Guidelines for Americans (no doubt due to lobbying by the dairy industry) and in many weight loss diets. An individual who continues to eat a food when they are intolerant will induce local gut inflammation and systemic inflammation, which can contribute to insulin resistance. Indeed, antibodies against various food antigens have been correlated with inflammation in obese adolescents,38 and personalized elimination diets based on measured antibody responses have been shown to be effective for weight loss. In one study, individuals lost 19 pounds in 6 months on an elimination diet compared to 2 pounds lost on a standard weight loss diet.39

4) Environmental toxins: Exposure to endocrine disruptors like bisphenol A have been shown to predispose children to weight gain.40 Organic pollutants have also been strongly implicated in the etiology of obesity and diabetes.41

5) Inflammation: this is perhaps the greatest force driving obesity and metabolic syndrome, and is a commonality among all four factors listed above. Inflammatory markers have been shown to predict future weight gain and the development of type 2 diabetes.42,43

6) Hormone imbalances: Active thyroid hormone (triiodothyronine, or T3) regulates energy metabolism, thermogenesis, and plays a crucial role in lipid and glucose metabolism, food intake, and fatty acid oxidation.44 Thyroid stimulating hormone (TSH) is a potent stimulator of leptin secretion.45 Hypothyroidism is associated with obesity, weight gain, and an inability to lose weight.

7) Lifestyle: Chronic sleep deprivation and disruption of the circadian rhythm has been shown to cause increased food intake, impaired glucose tolerance, weight gain, and other metabolic abnormalities.46,47 Combine this with a sedentary lifestyle, chronic stress, and constant access to food, and you basically have the recipe for obesity and diabetes.48

Behavior change is hard

Lastly, we need an approach to weight management that is focused on positive behavior change. According to the CDC, four of the top five behaviors for preventing chronic disease include getting regular physical activity, consuming moderate amounts or no alcohol, not smoking, and obtaining daily sufficient sleep. (The fifth is maintaining a healthy body weight.) In 2013, less than a quarter of Americans engaged in all four of these positive behaviors.49

The reality is, behavior change is difficult. Even if you know the underlying causes of your inability to lose weight and know exactly what diet and lifestyle changes you need to get there, you might lack the motivation and self-discipline to be able to go the distance. People need help making lifestyle habits that stick.

This is where a support system comes in. An intensive lifestyle intervention, with regular counseling, has been shown to be effective at increasing behavior change.3 We need healthcare practitioners that can identify the root cause of disease working alongside health coaches and dietitians that can help encourage people to form new healthy habits.

Conclusion

To sum up, dietary interventions could be equally as effective as bariatric surgery, but to achieve this requires a revolution of our current approach.

We need an integrative, individualized approach that is not rooted in nutrition dogma, recognizes that not all food is equal, addresses the underlying cause of disease, and supports people in forming and maintaining healthy habits. Only then will we have any hope of preventing and reversing the obesity epidemic.

That’s all for now! Be sure to subscribe below so you don’t miss the next article in this series, where I share my 8 simple steps to weight loss.

Sources:

  1. Data Briefs – Number 288 – October 2017. (2017). Available at: https://www.cdc.gov/nchs/products/databriefs/db288.htm. (Accessed: 16th December 2017)
  2. Ward, Z. J. et al. Simulation of Growth Trajectories of Childhood Obesity into Adulthood. New England Journal of Medicine 377, 2145–2153 (2017).
  3. Long Term Effects of a Lifestyle Intervention on Weight and Cardiovascular Risk Factors in Individuals with Type 2 Diabetes: Four Year Results of the Look AHEAD Trial. Arch Intern Med 170, 1566–1575 (2010).
  4. Siri-Tarino, P. W., Sun, Q., Hu, F. B. & Krauss, R. M. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am. J. Clin. Nutr. 91, 535–546 (2010).
  5. Siri-Tarino, P. W., Sun, Q., Hu, F. B. & Krauss, R. M. Saturated fat, carbohydrate, and cardiovascular disease. Am. J. Clin. Nutr. 91, 502–509 (2010).
  6. Hooper, L. et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev CD002137 (2001). doi:10.1002/14651858.CD002137
  7. Herron, K. L. et al. Men classified as hypo- or hyperresponders to dietary cholesterol feeding exhibit differences in lipoprotein metabolism. J. Nutr. 133, 1036–1042 (2003).
  8. Herron, K. L. et al. Pre-menopausal women, classified as hypo- or hyperresponders, do not alter their LDL/HDL ratio following a high dietary cholesterol challenge. J Am Coll Nutr 21, 250–258 (2002).
  9. Kearns, C. E., Apollonio, D. & Glantz, S. A. Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents. PLOS Biology 15, e2003460 (2017).
  10. Kearns, C. E., Schmidt, L. A. & Glantz, S. A. Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med 176, 1680–1685 (2016).
  11. Thomas, O. et al. Industry funding and the reporting quality of large long-term weight loss trials. Int J Obes (Lond) 32, 1531–1536 (2008).
  12. Teicholz, N. The scientific report guiding the US dietary guidelines: is it scientific? BMJ 351, h4962 (2015).
  13. Cordain, L., Eaton, S. B., Miller, J. B., Mann, N. & Hill, K. The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic. Eur J Clin Nutr 56 Suppl 1, S42-52 (2002).
  14. Walker, A. R. P., Walker, B. F. & Adam, F. Nutrition, diet, physical activity, smoking, and longevity: From primitive hunter-gatherer to present passive consumer—How far can we go? Nutrition 19, 169–173 (2003).
  15. Cordain, L. et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr 81, 341–354 (2005).
  16. García, O. P., Long, K. Z. & Rosado, J. L. Impact of micronutrient deficiencies on obesity. Nutrition Reviews 67, 559–572 (2009).
  17. Campión, J., Milagro, F. I., Fernández, D. & Martínez, J. A. Vitamin C supplementation influences body fat mass and steroidogenesis-related genes when fed a high-fat diet. Int J Vitam Nutr Res 78, 87–95 (2008).
  18. Campión, J., Milagro, F. I., Fernández, D. & Martínez, J. A. Diferential gene expression and adiposity reduction induced by ascorbic acid supplementation in a cafeteria model of obesity. J. Physiol. Biochem. 62, 71–80 (2006).
  19. Bonet, M. L. et al. Opposite effects of feeding a vitamin A-deficient diet and retinoic acid treatment on brown adipose tissue uncoupling protein 1 (UCP1), UCP2 and leptin expression. J. Endocrinol. 166, 511–517 (2000).
  20. Ribot, J., Felipe, F., Bonet, M. L. & Palou, A. Changes of adiposity in response to vitamin A status correlate with changes of PPAR gamma 2 expression. Obes. Res. 9, 500–509 (2001).
  21. Mercader, J. et al. Remodeling of white adipose tissue after retinoic acid administration in mice. Endocrinology 147, 5325–5332 (2006).
  22. Cheng, Q., Boucher, B. J. & Leung, P. S. Modulation of hypovitaminosis D-induced islet dysfunction and insulin resistance through direct suppression of the pancreatic islet renin-angiotensin system in mice. Diabetologia 56, 553–562 (2013).
  23. Yanoff, L. B. et al. The prevalence of hypovitaminosis D and secondary hyperparathyroidism in obese Black Americans. Clin. Endocrinol. (Oxf) 64, 523–529 (2006).
  24. Pooya, S. et al. Methyl donor deficiency impairs fatty acid oxidation through PGC-1α hypomethylation and decreased ER-α, ERR-α, and HNF-4α in the rat liver. Journal of Hepatology 57, 344–351 (2012).
  25. Waterland, R. A., Travisano, M., Tahiliani, K. G., Rached, M. T. & Mirza, S. Methyl donor supplementation prevents transgenerational amplification of obesity. Int J Obes (Lond) 32, 1373–1379 (2008).
  26. Chen, M. D., Song, Y. M. & Lin, P. Y. Zinc may be a mediator of leptin production in humans. Life Sci. 66, 2143–2149 (2000).
  27. Mantzoros, C. S. et al. Zinc may regulate serum leptin concentrations in humans. J Am Coll Nutr 17, 270–275 (1998).
  28. Marreiro, D. do N. et al. Effect of zinc supplementation on serum leptin levels and insulin resistance of obese women. Biol Trace Elem Res 112, 109–118 (2006).
  29. Zhao, L. et al. Obesity and iron deficiency: a quantitative meta-analysis. Obes Rev 16, 1081–1093 (2015).
  30. Dongiovanni, P., Fracanzani, A. L., Fargion, S. & Valenti, L. Iron in fatty liver and in the metabolic syndrome: A promising therapeutic target. Journal of Hepatology 55, 920–932 (2011).
  31. Sartori, S. B., Whittle, N., Hetzenauer, A. & Singewald, N. Magnesium deficiency induces anxiety and HPA axis dysregulation: Modulation by therapeutic drug treatment. Neuropharmacology 62, 304–312 (2012).
  32. Pitts, M. W. et al. Deletion of Selenoprotein M Leads to Obesity without Cognitive Deficits. J. Biol. Chem. 288, 26121–26134 (2013).
  33. Beckett, G. J., MacDougall, D. A., Nicol, F. & Arthur, J. R. Inhibition of type I and type II iodothyronine deiodinase activity in rat liver, kidney and brain produced by selenium deficiency. Biochemical Journal 259, 887–892 (1989).
  34. Damms-Machado, A., Weser, G. & Bischoff, S. C. Micronutrient deficiency in obese subjects undergoing low calorie diet. Nutrition Journal 11, 34 (2012).
  35. Calton, J. B. Prevalence of micronutrient deficiency in popular diet plans. Journal of the International Society of Sports Nutrition 7, 24 (2010).
  36. Turnbaugh, P. J. et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027–131 (2006).
  37. Cani, P. D. et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56, 1761–1772 (2007).
  38. Wilders-Truschnig, M. et al. IgG Antibodies Against Food Antigens are Correlated with Inflammation and Intima Media Thickness in Obese Juveniles. Exp Clin Endocrinol Diabetes 116, 241–245 (2008).
  39. Onmus, M. Y., Avcu, E. C. & Saklamaz, A. The Effect of Elimination Diet on Weight and Metabolic Parameters of Overweight or Obese Patients Who Have Food Intolerance. Journal of Food and Nutrition Research 4, 1–5 (2016).
  40. Newbold, R. R., Padilla-Banks, E., Snyder, R. J. & Jefferson, W. N. Developmental exposure to estrogenic compounds and obesity. Birth Defects Res. Part A Clin. Mol. Teratol. 73, 478–480 (2005).
  41. Dirinck, E. et al. Obesity and Persistent Organic Pollutants: Possible Obesogenic Effect of Organochlorine Pesticides and Polychlorinated Biphenyls. Obesity 19, 709–714 (2011).
  42. Engström, G. et al. Inflammation-sensitive plasma proteins are associated with future weight gain. Diabetes 52, 2097–2101 (2003).
  43. Pradhan, A. D., Manson, J. E., Rifai, N., Buring, J. E. & Ridker, P. M. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 286, 327–334 (2001).
  44. Reinehr, T. Obesity and thyroid function. Mol. Cell. Endocrinol. 316, 165–171 (2010).
  45. Menendez, C. et al. TSH stimulates leptin secretion by a direct effect on adipocytes. J. Endocrinol. 176, 7–12 (2003).
  46. Knutson, K. L., Spiegel, K., Penev, P. & Van Cauter, E. The Metabolic Consequences of Sleep Deprivation. Sleep Med Rev 11, 163–178 (2007).
  47. Markwald, R. R. et al. Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain. PNAS 110, 5695–5700 (2013).
  48. Freese, J., Klement, R. J., Ruiz-Núñez, B., Schwarz, S. & Lötzerich, H. The sedentary (r)evolution: Have we lost our metabolic flexibility? F1000Research 6, 1787 (2017).
  49. Liu, Y. Clustering of Five Health-Related Behaviors for Chronic Disease Prevention Among Adults, United States, 2013. Prev. Chronic Dis. 13, (2016).

Click edit button to change this text.

By |2017-12-20T15:32:27+00:00December 19th, 2017|