By Linda Clark, MA, CNC | Contributing Writer
- Vol. 15, No. 2. Summer, 2013
It is no secret that as a nation, the United States is getting fatter.
Over the past 50 years, the prevalence of obesity in adults has nearly tripled, from 13.4% in 1962 to 35.7% in 20101-3
. The economic, social, and medical burden this places on our society cannot be overstated. It is a healthcare crisis of immense proportions.
For good reason, we have become a nation obsessed with weight. We now have weight loss programs of all types and we are inundated with information from the media about trimming our waistlines. With all of this attention, one would think that obesity would be on the decline. Clearly it is not.
It may be that we’re focused on the wrong thing.
For decades, the prevailing thought has been that Americans are obese because we eat and drink too much, exercise too little, and are destined by genetics to gain weight. Even though these are factors, emerging science is pointing to another equally important driver of the obesity epidemic: the change in our environment and the prevalence of toxins that adversely affect metabolism.
A better reckoning with environmental factors could help us understand a phenomenon we’ve all observed in clinical practice: the individual who simply cannot lose weight despite diligent adherence to appropriate dietary regimens, vigilance against over-eating, and careful attention to food choices and regular exercise.
The old rule of “calories in, calories out” simply doesn’t apply to many individuals: something other than caloric consumption and burn rates is affecting their metabolism.Culture of Chemicals
More than 80,000 chemicals are currently used in U.S. commerce,4
with 22,000 of these being introduced in the last four decades.5
Only 200 of these chemicals have been tested for safety, and only five are partially regulated through the Toxic Substances Control Act.4
Yet dozens of studies have shown the deleterious effects of these environmental pollutants, pesticides, plastics, and food additives.6
The CDC regularly assesses Americans’ exposure to environmental chemicals through the National Health and Nutrition Examination Survey (NHANES). Its fourth report (published in 2009) found there was “widespread exposure” among study participants to industrial chemicals, such as flame retardants.7
Bisphenol A (found in plastics) and perfluorooctanoic acid (found in non-stick coatings) were also present in most of the participants’ blood and urine samples.7
The EPA also conducted a study on the US population’s exposure to toxic chemicals. Run from 1970-1989, this study tested adipose tissue, because many chemical toxins are fat-soluble and will accumulate in this kind of tissue. The survey documented a “significant prevalence of pesticide residues in the general population”8 of all ages.9-10
Our “culture of chemicals” even affects newborns. In 2004, the Environmental Working Group led a study that examined umbilical cord blood from 10 babies at U.S. hospitals.11
They found at least 287 chemicals in the cord blood, including pesticides, flame retardants, perfluorochemicals, and waste from burning coal, gasoline, and garbage.11
Looking at these study results, it is easy to conclude that we are all carrying a significant toxic load. Because toxins are stored in adipose tissue, overweight and obese individuals are carrying an even greater toxic burden than those who are lean.Altered Adipogenesis
A new understanding has emerged in the past few years that this burden of toxicity may explain the rise in obesity, and the problem that many people have with losing weight.
Researchers have found that certain environmental chemicals act as endocrine disruptors that alter fat production and energy balance, leaving some people more susceptible to weight gain.12-16
These compounds work in different ways. Some alter adipogenesis—the process of creating fat cells—causing people to have a greater numbers of fat cells, a larger size of their existing fat cells, or abnormal fat cell distribution.15
Other toxins alter levels of the appetite-regulating hormone leptin, or increase the activity of estrogen.13,15
One of the first statements of this toxin-obesity hypothesis emerged from a meta-analysis published in 2002 in the Journal of Alternative and Complementary Medicine
The author concluded that the obesity epidemic can’t entirely be explained by changes in food intake, exercise, or even genetics.
She argued that calorie consumption has actually declined throughout the 20th
century and that decreases in physical activity do not statistically correlate with the extreme rise in obesity in the past few decades.12
Concluding that human exposure to chemicals “may have damaged many of the body’s natural weight-control mechanisms,” she noted that this impact, “may play a significant role in the worldwide obesity epidemic.”12
Another seminal article examined specific cases where an association had already been shown between environmental chemical exposure and obesity13
—such as studies linking childhood obesity with maternal smoking during pregnancy.17-18
The author also highlighted the potent endocrine-disrupting capabilities of tributyltin, a chemical compound that causes female marine invertebrates to take on male sex characteristics.19-20 Weight Gain & Weight Loss Resistance
The altering of fat cells and the disruption of hormone levels are just two of many mechanisms by which environmental toxins can act as endocrine disruptors. They can also increase inflammatory cytokine activity, cause oxidative stress, and impact energy metabolism.
A paper published in Obesity Review
in 2003 looked at the effects of organochlorines (pesticides and plastics) on metabolic rate and weight regulation.21
The authors reviewed 63 studies and found many mechanisms related to weight loss resistance. Primarily, they noted that organochlorines, “have been associated with altered immune and thyroid functions, particularly decreased triiodothyronine (T3) concentrations.”21
Other mechanisms included:
- Inhibition of enzymes in the mitochondrial electron transport chain (which can decrease energy)
- Decreased capacity for fatty acid utilization in skeletal muscle
- Decrease in thyroxine concentrations (as the toxins compete for the same thyroid receptors)
- Inflammation and oxidative stress as a cause-and-effect of toxin release
Furthermore, some herbicides induce hormonal shifts, leading to estrogen excesses and increased fat deposition. These herbicides, including the widely used atrazine, induce aromatase activity by as much as 250%.22
Aromatase is the key enzyme involved in converting androgens to estrogen. Why Can’t I Lose More Weight?
Many people who are trying to lose weight find that they can lose the first 20 or 30 pounds, but then hit a plateau where it is difficult to lose more. Part of this problem stems from the fact that when people do lose weight, toxins stored in fat tissue are released into circulation.
An increase in toxic load during weight loss—added to an already-substantial toxic burden—can create an inflammatory cascade that inhibits the body’s inherent, highly sophisticated detoxification system.23
This inflammatory process can also deplete reserves of glutathione, an important antioxidant, which alters the liver’s detoxification efficiency.23-25
In order to support healthy weight loss and lower the toxic load, we need to ask whether these released toxins can be effectively neutralized, so that they don’t compromise metabolic and hormonal mechanisms? Maximize Detoxification
This may seem like a vicious cycle—the body gains weight because it’s natural metabolism has been disrupted by chemicals, but the process of losing this weight only releases more chemicals to further alter the body’s natural functions.
The important leverage point here is that we can increase the efficiency of liver detoxification. Targeted use of a specialized array of nutrients that act as cofactors for phase I and phase II liver detoxification, can support the liver’s detoxifying abilities while at the same time providing antioxidants to deal with oxidative stress.
Herbs such as milk thistle, dandelion root, and gotu kola; dietary fibers like inulin, and nutrients such as vitamin C, bioflavanoids, B vitamins, and amino acids—to name just a few—should be included as supplemental detoxification support.
A low-allergenic, whole foods diet can also support the body’s natural detoxification processes by reducing immune system activation. Since weight gain is an inflammatory process, it is essential to lower the inflammatory load in the diet, not just by reducing the amount of chemical toxins consumed, but also by eliminating the most allergenic foods. This, in turn, lowers systemic inflammation and improves metabolic efficiency.
I recommend a diet that emphasizes wholesome, fresh foods (preferably organically grown) that includes lean protein, vegetables, vegetable starches and fruit. I also advise elimination of all grains, legumes, nuts, seeds, dairy and eggs. I generally recommend lean sources of proteins, vegetables, vegetable starches and fruit.
Over the years, I have tried many dietary approaches to support detoxification and optimize the body’s natural metabolic system, and I have found this approach to be the most successful. What I particularly like about this approach is that it supports the healthy functioning of a number of body functions, not just detoxification and metabolism.
People can also lower their toxic load through specific lifestyle changes. Some of these include detox baths, skin brushing, drinking filtered water, and changing to stainless steel (rather than coated “non-stick”) cookware. I also recommend switching to more natural, allergen-free household and personal care products.
Self-care cannot be overlooked—developing healthy sleep habits, adding relaxation to the daily routine, and engaging in physical activity all allow for more effective detoxification and improve overall quality of life.
A well-designed detoxification program should not only foster short-term weight loss, but also encourage long-term lifestyle and dietary changes.
The benefits of weight loss cannot be overstated—a reduction in risk for heart disease, obesity, diabetes, and cancer. Yes, we must address the issues of overeating, lack of physical activity, poor food choices, and genetic metabolic issues. However, we can no longer ignore the impact of environmental toxins on weight loss, weight gain, and obesity.
What this means for the clinical picture is to develop and undertake strategies to reduce the toxic burden and optimize detoxification capacity. I have found over the years that a dietary and lifestyle-based detoxification program can produce dramatic shifts in body composition, along with better blood sugar balance, healthier lipid levels, and improved liver enzyme function. People who had previously been unable to lose weight may find that they’re able to break through the weight loss resistance.Linda Clark, MA, CNC, is an adjunct professor at John F. Kennedy University and teaches graduate courses in holistic nutrition, functional endocrinology, nutrition consulting, diet and meal planning, and functional testing for the holistic health master’s program. She holds a master’s degree in holistic health education from John F. Kennedy University and a nutrition consultant certification from Bauman College.
Ms. Clark owns Universal Wellness Associates, a holistic nutrition and wellness practice located in Fair Oaks, California. For the past six years, she has conducted seminars throughout the Western United States as a speaker for Apex Energetics™. She is the author of a booklet called Gluten-Free Life, which is distributed to healthcare professionals across the country. She has also developed the Detox 360™ diet and lifestyle program, distributed by Apex Energetics.
1. Weight-control Information Network. Overweight and Obesity Statistics. Bethesda, MD: National Institute of Diabetes and Digestive Kidney Diseases;October 2012.
2. Ogden CL, Carroll MD. Prevalence of overweight, obesity, and extreme obesity among adults: United States, trends 1960-1962 through 2007-2008. Atlanta, GA: National Center for Health Statistics, Centers for Disease Control and Prevention; June 2010.
3. Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among U.S. adults, 1999-2010. JAMA. 2012 Feb;307(5):491-497
4. Hearings Before the Subcommittee on Commerce, Trade, and Consumer Protection Committee on Energy and Commerce, U.S. House of Representatives. July 29, 2010. (testimony of Steve Owens, Assistant Administrator, Office of Chemical Safety and Pollution Prevention, U.S. Environmental Protection Agency).
5. Schierow L. The Toxic Substances Control Act (TSCA): Implementation and New Challenges. Washington, DC: Congressional Research Service; July 28, 2009.
6. Wilding BC, Curtis K, Welker-Hood K. Hazardous Chemicals in Health Care: A Snapshot of Chemicals in Doctors and Nurses. Washington, DC: Physicians for Social Responsibility; 2009.
7. Centers for Disease Control and Prevention, National Center for Environmental Health. Fourth National Report on Human Exposure to Environmental Chemicals. Atlanta, GA: Centers for Disease Control and Prevention; 2009.
8. Committee on National Monitoring of Human Tissues, Board on Environmental Studies and Toxicology, National Research Council. Monitoring Human Tissues for Toxic Substances. Washington, DC: The National Academies Press, 1991.
9. Kutz FW, Strassman SC, Sperling JF. Survey of selected organochlorine pesticides in the general population of the United States: Fiscal years 1970-1975. Ann N Y Acad Sci. 1979 May 31;320:60-68
10. Strassman SC, Kutz FW. Trends of organochlorine pesticide residues in human tissue. In: Khan MAQ, Stanton RH eds. Toxicology of Halogenated Hydrocarbons: Health & Ecological Effects. New York: Pergamon Press; 1981,
11. Environmental Working Group. Body Burden—The Pollution in Newborns. Washington, DC: Environmental Working Group; July 2005.
12. Baillie-Hamilton PF. Chemical toxins: a hypothesis to explain the global obesity epidemic. J Altern Complement Med. 2002 Apr;8(2):185-192
13. Blumberg B, Grün F. Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling. Endocrinology. 2006 Jun;147(6 Suppl):S50-S55
14. Heindel JJ. Endocrine disruptors and the obesity epidemic. Toxicol Sci. 2003 Dec;76(2):247-249
15. Holtcamp W. Obesogens: Environmental link to obesity? Environ Health Perspect. 2012 Feb;120(2):a62-a68
16. Newbold RR, Padilla-Banks E, Snyder RJ, Jefferson WN. Perinatal exposure to environmental estrogens and the development of obesity. Mol Nutr Food Res. 2007;51:912-917
17. Toschke AM, Koletzko B, Slikker Jr W, Hermann M, von Kries R. Childhood obesity is associated with maternal smoking in pregnancy. Eur J Pediatr. 161:445-448
18. Hill SY, Shen S, Locke Wellman J, Rickin E, Lowers L. Offspring from families at high risk for alcohol dependence: increased body mass index in association with prenatal exposure to cigarettes but not alcohol. Psychiatry Res;135:203-216
19. Blaber SJM. The occurrence of a penis-like outgrowth behind the right tentacle in spent females of Nucella lapillus. Proc Malacol Soc Lond. 1970;39:231-233.
20. Matthiessen P, Gibbs P. Critical appraisal of the evidence for tributyltin-mediated endocrine disruption in mollusks. Environ Toxicol Chem. 1998;17:37-43.
21. Pelletier C, Imbeault P, Tremblay A. Energy balance and pollution by organochlorines and polychlorinated biphenyls. Obes Rev. 2003 Feb;4(1):17-24
22. Sanderson JT, Seinen W, Giesy JP, van den Berg M. 2-Chloro-s-triazine herbicides induce aromatase (CYP19) activity in H295R human adrenocortical carcinoma cells: a novel mechanism for estrogenicity? Toxicol Sci. 2000 Mar;54(1):121-127
23. Mecdad AA, Ahmed MH, El Halwagy MEA, Afify MMM. A study on oxidative stress biomarkers and immunomodulatory effects of pesticides in pesticide-sprayers. Egypt Jour Forens Sci. 2011 Jun;1(2):93-98.
24. Agrawal A, Sharma B. Pesticides induced oxidative stress in mammalian systems: a review. Int J Biol Med Res. 2010;1(3):90-104.
25. Zordoky BN, El-Kadi AO. Role of NF-kappaB in the regulation of cytochrome P450 enzymes. Curr Drug Metab. 2009 Feb;10(2):164-178