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Continued from page 79 – The Effects of PersistentOrganic Pollutants (POPs) in Weight LossAdipose Tissue: A Storage Site for PersistentOrganic Pollutants (POPs)Research now indicates that the doctor should evaluatethe patient’s levels of POPs prior to weight loss. Thisevaluation is especially important in middle-aged andolder adults since toxins accumulate with age.Persistent organic pollutants, such as polychlorinatedbiphenyls (PCBs), hexachlorobenzene (HCB), andp,p'-dichlorophenyldichloroethylene (DDE) areubiquitous microcontaminants that are lipid solubleand accumulate in stored fat. A type of fat known aswhite adipose tissue (WAT) constitutes 15 to 25% ofbody weight and can increase greatly in the morbidlyobese.1 This tissue serves as a depot for lipophiliccontaminants like POPs. 1 Weight loss can facilitatesignificant releases of these toxicants, often leading toan increase of symptoms which may prevent further oroptimal loss of fat. 2, 3 Though banned, these POPs arean ever-increasing problem that may affect theendocrine, nervous and immune systems; storing themin adipose tissue may be a defense mechanism. Due tothese issues the CDC has expanded their evaluation ofthese toxic compounds in the National Health andNutrition Examination Survey (NHANES). 4 TheNHANES is a program of studies designed to assessthe health and nutritional status of adults and childrenin the United States. Physicians need to be aware oftheir patient’s levels of POPs, how these toxiccompounds are released during weight loss, thepossible effects they can have, and ways to amelioratetheir release. Answering these questions and treatingthese issues may help patients complete weight lossprograms and avoid regaining weight, with thesignificant advantage of reduced toxic burden.Testing Toxin LevelsThe measurement of chemicals and biomarkers hasrevolutionized the field of exposure assessment. TheCenters for Disease Control and Prevention (CDC)published the The National Report on HumanExposure to Environmental Chemicals, whichprovides an ongoing assessment of 148 chemicalsfound at detectable levels in the U.S. population usingbiomonitoring. The blood and urine samples werecollected from a statistically representative sample ofthe U.S. population during NHANES.5 The CDC hastherefore established 95th percentile reference limitsfor many of these organic pollutants, allowingphysicians to compare their patients’ levels against anational standard. 4,6 Certain of these organotoxins cannow be analyzed using private laboratories. 7Current, and anticipated, scientific advances can permitbroader toxicity testing coverage of the universe ofpotentially toxic chemicals to which humans may beexposed. By 2010, it has been predicted that the CDC willbe monitoring nearly 1000 chemicals,8 a significantadvance, yet small considering the estimated 80,000chemicals in use.Main Sources of POPsContrary to common belief, there is still a body burden ofbanned chemicals due to the persistence of thesecompounds in the environment, to their continued use inother countries 9 and to the fact that animal feeds are themain source of POPs in the human food chain. 10 Studiesby LaRocca have shown that the majority of humanexposure to PCBs, for example, is derived from foods ofanimal origin. 11 Storage of these compounds can result inincreased concentrations in fatty tissues, muscles andorgans, which can induce various adverse health effects.In addition to foods of animal origin, POP’s are alsofound in pesticides, building materials, plastics, cosmeticsand perfumes. In other words, most sources surround usin our homes, offices and schools.Toxic Effects of Exposure to POPsThe potential of these pollutants to impair immuneresponses and trigger autoimmune disease is of growingconcern. POPs show structural similarity to thyroidhormones. 12 Some effects of exposure includedevelopmental and reproductive toxicity, dermal toxicity,endocrine effects, hepatotoxicity, carcinogenesis, and theinduction of diverse phase I and phase II drugmetabolizingenzymes. 13-16 Endocrine effects of organicpollutants seem to occur through mimicking the body’snatural steroid hormones, and by interfering with theadipocyte phenotype. 1 Mullerova and Kopecky havedescribed plausible mechanisms for POP interference infat metabolism via modulation of estrogen-regulatedgenes, disordered estrogen biosynthesis in WAT,inhibition of peroxisome proliferator-activating receptors(PPARs) and disruption of other aspects of the fat cell1, 17transcription machinery.Emerging evidence has also demonstrated thatpolyhalogenated aromatic hydrocarbons (PHAH),particularly polybrominated diphenyl ethers (PBDE), alterthyroid hormone homeostasis and cause thyroiddysfunction. Release of organochlorines were found toimpair thyroid status, which may reduce resting metabolicrate (RMR) and decrease in serum T(3), furtherexacerbating weight loss issues. 18Toxicants and Weight LossWeight loss has been shown to mobilize PCBs and otherContinued on page 8180-- Traditional African Clinic July 2013
Continued from page 80 – The Effects of PersistentOrganic Pollutants (POPs) in Weight LossPOPs from lipid stores producing an increase in bloodconcentrations of these potentially toxic organochlorines.2 The level of plasma organochlorine andpesticide compounds is related to total weight lost. 19Thus weight loss strategies that produce significant orquick decreases in weight have been shown to lead togreater increases in plasma organotoxin levels. There isa measured and persistent release of toxins shown inplasma up until a change in BMI greater than 14 kg/m2,when blood concentrations jump sharply. It is thereforeadvisable to calculate a patient’s anticipated change inBMI. An increase in organotoxins may explain whysome patients begin to feel like they are being poisonedduring the first part of a weight loss program, possiblycontributing to the difficulty of sticking with a programor why patients regain weight so quickly. Cliniciansworking in the field of bariatrics encountering weightloss resistance in their patients have speculated that itmay be the result of a toxic interference. 19Minimizing Exposure to POPsMitigating the toxic effects of exposures to POPs (or toany toxic substance) necessitates avoiding orminimizing overall exposure to such compounds.Minimizing exposure to POPs is more efficient,effective and economical than eating /storing/eliminating them from our bodies. High fat animalproducts are a primary contributor to POP intakes.Dairy products, processed foods, and meat are majorcontributors of PCB and dioxin accumulation. 20Consuming fewer animal products and cleaner sourcesare prudent measures. Industrial, toxicant-promotingagricultural practices such as CAFOs contributesignificantly to the increase of toxins in our foodsupply. 10 Lower toxin levels are found in vegans andvegetarians, as well as those who consume greaterquantities of vegetables, fruits, whole grains, nuts,seeds, beans and wild caught young fish. 21Epidemiological research has consistently shown thisdiet to be healthier in many catagories. 22Detoxification ApproachesWith regard to established detoxification programs, theAyurvedic approach has been investigated by morethan 600 studies. 9 Most programs include saunas,supplements, massages, and dietary inclusions andrestrictions. Research has evaluated the levels of PCBsin patients before and after such a detoxificationprogram, and compared levels to controls. Sometechniques have been found very successful atincreasing excretion of organotoxins. Many of thesesteps can be easily included into weight loss programsand provide significant reductions of toxins. Thus it isimportant that clinicians advising their patients on weightloss assess serum toxin levels prior to beginning aprogram. Patients with higher levels of these toxins couldbe advised to add more detoxification protocols to theirweight loss program to promote their increasedelimination during weight loss.References1. Mullerova D, Kopecky J. White adipose tissue: storageand effector site for environmental pollutants. Physiol Res.2007;56(4):375-381.2. Chevrier J, Dewailly E, Ayotte P, Mauriege P, DespresJP, Tremblay A. Body weight loss increases plasma andadipose tissue concentrations of potentially toxicpollutants in obese individuals. Int J Obes Relat MetabDisord. Oct 2000;24(10):1272-1278.3. Redgrave TG, Wallace P, Jandacek RJ, Tso P. Treatmentwith a dietary fat substitute decreased Arochlor 1254contamination in an obese diabetic male. J Nutr Biochem.Jun 2005;16(6):383-384.4. Ruiz P, Faroon O, Moudgal CJ, Hansen H, De Rosa CT,Mumtaz M. Prediction of the health effects ofpolychlorinated biphenyls (PCBs) and their metabolitesusing quantitative structure-activity relationship (QSAR).Toxicol Lett. Sep 2008;181(1):53-65.5. Department of Health and Human Services, Centers forDisease Control and Prevention. Third National Report onHuman Exposure to Environmental Chemicals.http://www.cdc.gov/exposurereport/pdf/thirdreport.pdf.2005.6. Ferriby LL, Knutsen JS, Harris M, et al. Evaluation ofPCDD/F and dioxin-like PCB serum concentration datafrom the 2001-2002 National Health and NutritionExamination Survey of the United States population. JExpo Sci Environ Epidemiol. Jul 2007;17(4):358-371.7. Krewski D, Andersen ME, Mantus E, Zeise L. Toxicitytesting in the 21st century: implications for human healthrisk assessment. Risk Anal. Apr 2009;29(4):474-479.8. Paustenbach D GD. Biomonitoring: is body burdenrelevant to public health? Regul Toxicol Pharmacol.2006;44(3):249-261.9. Herron RE, Fagan JB. Lipophil-mediated reduction oftoxicants in humans: an evaluation of an ayurvedicdetoxification procedure. Altern Ther Health Med. Sep-Oct 2002;8(5):40-51.10. Walker P, Rhubart-Berg P, McKenzie S, Kelling K,Lawrence RS. Public health implications of meatproduction and consumption. Public Health Nutr. Jun2005;8(4):348-356.11. La Rocca C MA. From environment to food: the case ofPCB. Ann Ist Super Sanita. . 2006;42(4):410-416.Continued on page 8281-- Traditional African Clinic July 2013
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