Adverse effects of weight loss: Are persistent organic pollutants a potential culprit?

Rouhou, Mouna Cheikh; Karelis, Antony D.; St-Pierre, David H.; Lamontagne, Lucie

doi:10.1016/j.diabet.2016.05.009

Cited by 20 publications

(11 citation statements)

References 119 publications

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“…For WL Phase 1, we report most individual PCBs and total PCBs in serum increased similarly in men and women following the 12-week WL intervention, which was accompanied with significant weight and fat loss. This finding is consistent with previous studies [ 11 , 14 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ] and extends them by directly comparing PCB changes in obese men and women following a P-CR diet. Another beneficial effect of P-CR is plasma oxidative stress measured by lipid peroxidation (TBARS) was decreased, whereas total antioxidant capacity (TAC) was boosted after WL (Phase 1).…”

Section: Discussionsupporting

confidence: 92%

Serum Polychlorinated Biphenyls Increase and Oxidative Stress Decreases with a Protein-Pacing Caloric Restriction Diet in Obese Men and Women

Zuo

Ward

et al. 2017

IJERPH

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The purposes were to compare the effects of a: (1) 12-week P-CR weight loss (WL) diet (Phase 1) between obese men and women and; (2) 52-week modified P-CR (mP-CR) vs. heart healthy (HH) weight maintenance (WM) diet (Phase 2) on serum PCBs and oxidative stress biomarkers (thiobarbituric acid reactive substances, TBARS; total antioxidant capacity, TAC) in 40 obese participants (men, n = 21; women, n = 19). Participants received dietary counseling and monitoring of compliance. PCBs, TBARS, and TAC were assessed at weeks −1 (CON), 12 (WL), and 64 (WM). Following WL (Week 12), concomitant with reductions in TBARS (0.24 ± 0.15 vs. 0.18 ± 0.11 µM; p < 0.01), PCB serum concentrations (86.7 ± 45.6 vs. 115.6 ± 65.9 ng/g lipid; p < 0.01) and TAC (18.9 ± 2.6 vs. 19.9 ± 2.3 nmol/mL; p < 0.02) were increased similarly in men and women. At the end of WM (Week 64), a significant effect of time × group interaction was observed for % change in PCB 170 and 187; whereby mP-CR values were higher compared to HH (PCB170: 19.31% ± 26.48% vs. −6.61% ± 28.88%, p = 0.02; PCB187: −3.04% ± 17.78% vs. −21.4% ± 27.31%, p = 0.04). PCB changes were positively correlated with TBARS levels (r > 0.42, p < 0.05) and negatively correlated with body weight, fat mass, and abdominal fat (r < −0.46, p < 0.02). Our results support mobilization of stored PCBs as well as enhanced redox status following a 12-week P-CR WL diet. Additionally, a 52-week mP-CR WM diet demonstrated an advantage in preventing weight gain relapse accompanied by an increase in circulating PCBs compared to a traditional HH diet.

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Section: Discussionsupporting

confidence: 92%

Serum Polychlorinated Biphenyls Increase and Oxidative Stress Decreases with a Protein-Pacing Caloric Restriction Diet in Obese Men and Women

Zuo

Ward

et al. 2017

IJERPH

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“…Low levels of DNA methylation at gene promoters might generate active adipogenic genes, thereby permanently increasing adipocyte number and favoring central fat deposition in the presence of energy imbalance. The hyperactivity of adipogenic genes fosters to create an altered metabolic set point, thereby influencing latent effects on the risk of obesity and obesity-related outcomes, and likely accounting also for the very common issue of weight regain after weight loss [27]. Of interest, novel molecular approaches evaluating the phenotypic discordance in monozygotic twins, such as genome-wide methylation assays, point out that epigenetic changes induced by lifestyle are likely operating distinctly during adolescence/adult life for each individual in the pathogenesis of obesity and related comorbidities [4].…”

Section: “Obesogenic” Edcs From the Endocrinologic Point Of Viewmentioning

confidence: 99%

Endocrine Aspects of Environmental “Obesogen” Pollutants

Nappi

Barrea

Somma

et al. 2016

IJERPH

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Growing evidence suggests the causal link between the endocrine-disrupting chemicals (EDCs) and the global obesity epidemics, in the context in the so-called “obesogenic environment”. Dietary intake of contaminated foods and water, especially in association with unhealthy eating pattern, and inhalation of airborne pollutants represent the major sources of human exposure to EDCs. This is of particular concern in view of the potential impact of obesity on chronic non-transmissible diseases, such as type 2 diabetes, cardiovascular disease, and hormone-sensitive cancers. The key concept is the identification of adipose tissue not only as a preferential site of storage of EDCs, but also as an endocrine organ and, as such, susceptible to endocrine disruption. The timing of exposure to EDCs is critical to the outcome of that exposure, with early lifetime exposures (e.g., fetal or early postnatal) particularly detrimental because of their permanent effects on obesity later in life. Despite that the mechanisms operating in EDCs effects might vary enormously, this minireview is aimed to provide a general overview on the possible association between the pandemics of obesity and EDCs, briefly describing the endocrine mechanisms linking EDCs exposure and latent onset of obesity.

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“…EDCs have been detected also in biological fluids such as sera (38), urine (35), amniotic fluid (39), and breast milk (40). Some EDCs persist in the body for a long time, such as persistent organic pollutants (POPs), and some (e.g., pesticides) are quickly metabolized and cleared from the organism, although chronic exposure can lead to bioaccumulation (37,41). Nevertheless, the presence of EDCs in amniotic fluid and placenta is alarming, as EDCs can alter the normal hormonal control of fetal development (42).…”

Section: Environmental Factors-the Side Effects Of Civilization Endocrine Disrupting Chemicalsmentioning

confidence: 99%

Polycystic ovary syndrome and environmental toxins

Rutkowska

Diamanti-Kandarakis

2016

Fertility and Sterility

143

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Polycystic ovary syndrome (PCOS) is the most common, heterogeneous, and multifactorial endocrine disorder in premenopausal women. The pathophysiology of this endocrinopathy is still unclear; however, the heterogeneity of its features within ethnic races, geographic location, and families suggests that environment and lifestyle are of prime importance. This work is mainly focused on the possible role of the most common and studied environmental toxins for this syndrome in the pathogenesis of PCOS. Plasticizers, such as bisphenol A (BPA) or phthalates, which belong to the categories of endocrine disrupting chemicals (EDCs) and advanced glycation end products (AGEs), affect humans' health in everyday, industrialized life; therefore special attention should be paid to such exposure. Timing of exposure to EDCs is crucial for the intensity of adverse health effects. It is now evident that fetuses, infants, and/or young children are the most susceptible groups, especially in the early development periods. Prenatal exposure to EDCs that mimic endogenous hormones may contribute to the altered fetal programming and in consequence lead to PCOS and other adverse health effects, potentially transgenerationally. Acute or prolonged exposure to EDCs and AGEs through different life cycle stages may result in destabilization of the hormonal homeostasis and lead to disruption of reproductive functions. They may also interfere with metabolic alterations such as obesity, insulin resistance, and compensatory hyperinsulinemia that can exacerbate the PCOS phenotype and contribute to PCOS consequences such as type 2 diabetes and cardiovascular disease. Since wide exposure to environmental toxins and their role in the pathophysiology of PCOS are supported by extensive data derived from diverse scientific models, protective strategies and strong recommendations should be considered to reduce human exposure to protect present and future generations from their adverse health effects.

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Adverse effects of weight loss: Are persistent organic pollutants a potential culprit?

Cited by 20 publications

References 119 publications

Serum Polychlorinated Biphenyls Increase and Oxidative Stress Decreases with a Protein-Pacing Caloric Restriction Diet in Obese Men and Women

Serum Polychlorinated Biphenyls Increase and Oxidative Stress Decreases with a Protein-Pacing Caloric Restriction Diet in Obese Men and Women

Endocrine Aspects of Environmental “Obesogen” Pollutants

Polycystic ovary syndrome and environmental toxins

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