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  1. All, The idea that rapid weight loss can result in release of toxins stored (relatively harmlessly) in body fat cells gets bandied about pretty regularly. In fact I've done it myself several times in just the last couple days (here and here). I've never actually looked for evidence to support this conventional wisdom, which has left me with a nagging feeling of dis-ease. I try not to make claims that I can't back up with evidence. So I figured I would look into it and start a new thread to collect the evidence and encourage discussion about it. Coincidently (or perhaps not?!), Al Pater posted this new study [1] today, which bears directly on the topic. In it, researchers followed 32 women who had just given birth and were breast feeding to see how the level of persistent organic pollutants (POPs) in their breast milk changed as a function of postpartum weight loss. All the women lost at least some weight in the 24 weeks of the study, and sure enough, the amount of POPs in their breast milk was highly correlated with the amount of weight they lost: Among these women, the concentration of PCB 153 in HM was significantly (p = 0.04) higher at follow-up than at baseline. Weight loss was significantly positively associated with changes in concentrations of all studied POPs (2.0-2.4% increase per percent weight loss). Since these women probably weighed in the neighborhood of 140-180 lbs to start with, it appears that the level of toxins in their breast milk went up by about 1-2% per pound of weight loss. Since not all of the toxins released end up in breast milk (especially in men and non-lactating women!) I would expect the increase in toxin load circulating in the blood per pound of weight loss to be higher than that. So [1] definitely supports the idea that rapid weight loss increases circulating toxin load. But even more direct and conclusive evidence of dieting-induced toxin release is study [2]. In [2], researchers followed 45 morbidly obese women for 6 months following either bariatric surgery or intensive dieting. These women were really heavy to start with - average BMI around 40. And they lost quite a bit of weight (-32lbs of body weight on average) in a relatively short period of time (six months). But in fact that translates into 1.23lbs per week of weight loss, which is very close to the maximum rate of weight loss we recommend around here, ~1lb per week. So what did they find? A very large increase in the same Persistent Organic Pollutants (POPs), to the tune of a 50% increase on average: In patients who lost weight, serum [total POP] levels displayed an increase after 6 months of approximately 50%. ... [T]he increase in [Total POP] serum levels after 6 months of weight loss was more pronounced in patients losing relatively more visceral adipose tissue. So even the kind of "slow-and-steady" weight loss we recommend of 1lb of weight per week results in a dramatic increase in toxin load that persists for at least six months. And visceral fat loss is a bigger factor contributing to toxin release than subcutaneous (love-handle) fat loss. In satisfying agreement with the 1-2% increase in POPs per pound of weight loss observed in [1], this study found that an average of 32lbs of weight loss resulted in a 50% increase in average serum POP level, which equates to ~1.5% increase in circulating POPs per pound of weight loss. So in general even 1lb of weight loss per week may be too rapid... Ah. That feels better. My cognitive dissonance is subsiding... Now I can go back to those two posts and insert a link to this thread. And now we have a place to point next time anyone makes the statement that rapid weight loss releases toxins into the blood. --Dean ------------ [1] Chemosphere. 2016 Jun 6;159:96-102. doi: 10.1016/j.chemosphere.2016.05.077. Environmental organic pollutants in human milk before and after weight loss. Lignell S, Winkvist A, Bertz F, Rasmussen KM, Glynn A, Aune M, Brekke HK. Abstract Many persistent organic pollutants (POPs) are banned because they accumulate in organisms and are toxic. Lipophilic POPs are stored in maternal adipose tissue and concentrations in human milk (HM) may increase during weight loss. Our aim was to examine associations between weight loss and concentrations of chlorinated POPs in HM in lactating women participating in a weight loss study. We analysed POPs (PCB 28, PCB 153, HCB, DDE) in HM at 12 and 24 weeks postpartum from 32 women who participated in a randomized, 2 ? 2 factorial trial of diet and exercise for postpartum weight loss. Participants donated milk before and after the intervention period. We examined associations between weight loss and change in POP concentrations and estimated the intake of POPs by their breastfed infants. Most (n = 27) women lost weight during intervention, 0.45?0.30 kg/week (mean?SD). Among these women, the concentration of PCB 153 in HM was significantly (p = 0.04) higher at follow-up than at baseline. Weight loss was significantly positively associated with changes in concentrations of all studied POPs (2.0-2.4% increase per percent weight loss). Estimated mean intakes of POPs (ng/day) remained stable because infant milk consumption decreased during the study period. As infants gained weight, estimated mean intakes per kg body weight decreased 17-22%. Changes in concentrations of POPs in HM correlated positively with maternal weight loss, but it is unlikely that the balance between the benefits and risks of breastfeeding will change if the weight loss is restricted to 0.5 kg per week. KEYWORDS: Human milk; Obese; Overweight; POPs; Postpartum; Weight loss PMID: 27281542 ------------ [2] J Clin Endocrinol Metab. 2015 Dec;100(12):4463-71. doi: 10.1210/jc.2015-2571. Epub 2015 Oct 15. Pivotal Role for the Visceral Fat Compartment in the Release of Persistent Organic Pollutants During Weight Loss. Dirinck E(1), Dirtu AC(1), Jorens PG(1), Malarvannan G(1), Covaci A(1), Van Gaal LF(1). Author information: (1)Department of Endocrinology, Diabetology, and Metabolism (E.D., L.F.V.G.), Toxicology Centre (A.C.D., G.M., A.C.), and Department of Intensive Care Medicine/Clinical Pharmacology (P.G.J.), Antwerp University Hospital, University of Antwerp, 2650 Edegem, Belgium. Full text: http://sci-hub.cc/10.1210/jc.2015-2571 CONTEXT: Polychlorinated biphenyls (PCBs), are implicated as potential endocrine disruptors and obesogens. These lipophilic substances are preferentially stored in the fat compartment and released into the circulation during weight loss. OBJECTIVE: The aim of this study was to examine the contribution of abdominal adiposity, and visceral adiposity in particular, to the increase of serum PCB levels during weight loss. MATERIALS AND METHODS: Fourty-five obese women were prospectively recruited. Twenty individuals received dietary counseling and 25 underwent bariatric surgery. Anthropometric data were collected and intra-abdominal adiposity was assessed by measurement computed tomography scanning of the abdominal fat compartment, delineating the visceral and subcutaneous compartment. Serum levels of 27 PCBs were determined and the sum of all PCBs (ΣPCBs) calculated. Follow-up measurements of anthropometric data, computed tomography scanning, and PCB levels were performed after 6 months in all patients. RESULTS: In patients who lost weight, serum ΣPCB levels displayed an increase after 6 months of approximately 50%. Both correlation and regression analysis, focusing on the relative contribution of the visceral vs the subcutaneous fat compartment, suggested that the increase in ΣPCB serum levels after 6 months of weight loss was more pronounced in patients losing relatively more visceral adipose tissue. This trend could be established in the diet-treated, but not the surgery-treated subgroup. CONCLUSION: Our study suggests that the contribution of PCBs released from the visceral fat compartment might be more pronounced compared with the subcutaneous fat compartment during weight loss. These findings are present in the entire study group whereas subanalysis of the diet vs surgery groups suggested the same effect in the diet group but failed to reach statistical significance in the surgery group. This suggests a possible weight-loss method-specific effect. PMID: 26469381
  2. All, Anyone who has been following discussions around here will realize that I've been criticizing salmon as a healthy food, and Saul has been vehemently defending it, which has lead to some amusing exchanges, e.g. here, here and especially here, where Saul wrote: Well, the evidence just keeps piling up against Saul's sacred cow, er, fish. Background Summary: PCBs are bad sh*t. PCBs (or polychlorinated biphenyls) are man-made organic chemicals widely manufactured and used in a variety of industries, but mostly for cooling and insulating fluid for electrical devices, all over the world up until 1979 when they were banned. Unfortunately, PCBs are very persistent, remaining in the water and soil for many years, and bioaccumulating the in flesh (mostly fat) of animals. Fish, especially fatty fish, seems to be the food in the human diet where the most PCBs bioaccumulate, as illustrated by this graph (data from [2]) of PCB content in 12,000+ food samples from around Europe: Notice that fish oil is off the chart, but people typically only consume a gram or two of FO per day, and this graph represents micrograms per kilograms. Fish itself (all types) was about 5x higher than any other animal products. Fruit, vegetables and cereals had close to zero PCBs. Interestingly though, most exposure in North America comes from beef, dairy and other animal flesh rather than fish, since we eat so much more of them than fish: So how bad are PCBs? Pretty bad across the board, including causing cancer, endocrine disruption, reproductive and neurological effects. See here for more details about all the bad effects PCBs have on human health. With that background, this new study [1] posted by Al (thanks Al!) looked at dietary PCBs levels based on self-reported food-frequency questionnaires from ~36,000 elderly Swedish women, and then followed them for an average of 12 years to see how heart attack risk related to dietary PCB exposure. First, off a helpful chart of demographics of study participants by quartile of dietary PCB intake: As you can see from my highlights, the dietary PCB (and mercury) levels in these women was strongly correlated with fish and long-chain omega-3 intake. Women who ate the most fish had almost 3x the level of PCBs of those who ate the least. So what about heart attacks? Here is what the authors' found: Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01–1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10–2.25) after adjusting for EPA-DHA. Stratification by low and high EPADHA intake, resulted in RRs 2.20 (95% CI, 1.18–4.12) and 1.73 (95% CI, 0.81–3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. In other words, having the highest intake of PCBs (mostly from fish) was associated with a 21% increase in the risk of heart attack relative to being in the lowest PCB intake group. But it was only a 21% increase because EPA/DHA was pulling the other way, helping to prevent heart attacks. If you statistically factor out the EPA/DHA benefits, PCBs alone would raise heart attack risk by 58% in the top vs. bottom quartile group. Analyzed the other way, EPA/DHA intake wasn't associated with fewer heart attacks, largely because of the PCBs that typically accompany them, it would appear. In fact, those in the highest quartile of DHA/EPA intake had a (non-significant) 11% increase in risk of heart attack. But when they statistically factored out the PCBs, DHA/EPA was (weakly and non-significantly) associated with a 26% reduction in heart attack risk. The relevant data is summarized in this table with my highlights, for anyone who wants to see the details: To summarize, it looks like if you can get DHA/EPA without the accompanying PCBs, it may be a slight win for heart attack risk. But when the DHA/EPA comes as a package deal with PCBs (would you like fries with that?), as it did for these fish-eating Swedish women, it's bad news. And its looks it might be even worse for us skinny folks, since they found: In a stratified analysis, we observed a higher RR [of high dietary PCBs] (2.39; 95% CI, 1.15–4.96) among lean women (waist circumference b80 cm) than among those with abdominal adiposity, however the interaction was not statistically significant (p value = 0.18) and the confidence interval was wide. ... Our results indicate a stronger association between PCB and risk of myocardial infarction among lean women meanwhile no association among women with abdominal adiposity. One likely explanation behind the observation is the higher concentrations of circulating PCBs in blood and lower dilution of PCBs in adipose tissue of lean than of obese woman [22]. Fortunately, it is possible to ensure one gets DHA/EPA without the PCBs, by choosing an algae source of DHA/EPA, like this one, rather than taking one's chances eating fish what one hopes is low in contaminants like PCBs, but which can often be mislabelled. --Dean ------------ [1] Int J Cardiol. 2015 Mar 15;183:242-8. doi: 10.1016/j.ijcard.2015.01.055. Epub 2015 Jan 27. Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction - a population-based prospective cohort study. Bergkvist C(1), Berglund M(2), Glynn A(3), Wolk A(1), Åkesson A(4). Sci-hub.io full text: http://www.sciencedirect.com.sci-hub.io/science/article/pii/S0167527315000820 BACKGROUND: Fish consumption may promote cardiovascular health. The role of major food contaminants, such as polychlorinated biphenyls (PCBs) common in fatty fish, is unclear. We assessed the association between dietary PCB exposure and risk of myocardial infarction taking into account the intake of long-chain omega-3 fish fatty acids. METHODS: In the prospective population-based Swedish Mammography Cohort, 33,446 middle-aged and elderly women, free from cardiovascular disease, cancer and diabetes at baseline (1997) were followed-up for 12 years. Validated estimates of dietary PCB exposure and intake of fish fatty acids (eicosapentaenoic acid and docosahexaenoic acid; EPA-DHA) were obtained via a food frequency questionnaire at baseline. RESULTS: During follow-up 1386 incident cases of myocardial infarction were ascertained through register-linkage. Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01-1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10-2.25) after adjusting for EPA-DHA. Stratification by low and high EPA-DHA intake, resulted in RRs 2.20 (95% CI, 1.18-4.12) and 1.73 (95% CI, 0.81-3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. CONCLUSION: Exposure to PCBs was associated with increased risk of myocardial infarction, while some beneficial effect was associated with increasing EPA and DHA intake. To increase the net benefits of fish consumption, PCB contamination should be reduced to a minimum. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. PMID: 25679993 ------------ [2] EFSA Journal 2010; 8(7):1701. [35 pp.]. doi:10.2903/j.efsa.2010.1701. European Food Safety Authority; Results of the monitoring of non dioxin-like PCBs in food and feed. Free Full text: http://www.efsa.europa.eu/sites/default/files/scientific_output/files/main_documents/1701.pdf ABSTRACT Non dioxin-like polychlorinated biphenyls (NDL-PCBs) are persistent organic chemicals that accumulate in the environment and humans and are associated with a broad spectrum of health effects. Processing and distribution of PCBs has been prohibited in almost all industrial countries since the late 1980s but they still can be released into the environment from electrical appliances, building paint and sealants and waste sites that contain PCBs. In 2002 the European Commission prescribed a list of actions to be taken to reduce the presence of dioxins and PCBs in food and feed and Member States were recommended to monitor the situation. A total of 12,563 food and feed samples collected in the period 1995 - 2008 from 18 EU Member States, Iceland and Norway were retained for a detailed analysis of the occurrence of the six indicator NDL-PCBs (# 28, 52, 101, 138, 153, and 180). Overall, 18.8% of the results for single congeners were below the limit of quantification (LOQ) but their distribution varied highly between food and feed groups. PCB-153 and PCB-138 were the most commonly detected congeners. In food, the highest mean contamination level was observed in fish and fish derived products followed by eggs, milk and their products, and meat and meat products from terrestrial animals. The lowest contamination was observed in foods of plant origin. A similar pattern was observed in feed where high contamination was reported in feed containing fish derived products and comparatively very low levels in feed of plant or mineral origin. The sum of the six NDL-PCBs was on average close to five times higher than the sum of the 12 dioxin-like PCBs. This relationship varied across food groups and is presumably related to the origin of samples and the contamination source. Country-specific clustering has been observed in several food and feed groups.