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Obesity

Overweight and obesity are considered a risk to health and are defined as abnormal or excessive fat accumulation. Body mass index (BMI) is a simple index of weight for height that is commonly used to classify overweight and obesity in adults and is defined as a person's weight in kilograms divided by the square of his height in meters (kg/m2). BMI over 25 is considered overweight, and over 30 is considered obese [1].

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Obesity figures in the world continue to increase, having grown to epidemic proportions [2]. From 1975 to 2016, the prevalence of overweight and obesity tripled [1]. Approximately 2 billion adults are now overweight, whilst 650 million are obese [2]. Obesity prevalence increased in every single country of the world, although the rates of overweight and obesity vary considerably among regions and  countries. In countries such as Argentina, Australia, Canada, Chile, New Zealand, Spain, Saudi Arabia, United Kingdom, United States, >60% of the population is overweight or obese [4]. While obesity was once considered a problem of high-income countries, in low- and middle-income countries, rates of overweight and obesity are rising especially in urban areas [3]. Over 5 million people die each year as a result of being overweight or obese (according to the global burden of disease data from 2019 [5].

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While an imbalance in energy intake and expenditure is often considered to be the blame, other factors contribute. An analysis of obesity trends (the National Health and Nutrition Examination Study) found that from 1988 to 2006 for the same caloric intake and physical activity, the average BMI was higher. Obesity represents a multifactorial and multidimensional problem. Important factors to consider include stress, lifestyle, and hypercaloric diets [3], However, these factors are not the only ones responsible for obesity. There is a relationship between pollution and obesity. In 2006, it was found that endocrine-disrupting chemicals (EDCs) and metabolism-disrupting chemicals (MDCs) influence adipogenesis and contribute to obesity [4]. [5], [6],[7]. Environmental chemicals that contribute to obesity are referred to as obesogens and are defined functionally as chemicals (natural, pharmaceutical, or xenobiotic) that promote obesity directly by increasing the number of fat cells or the storage of fat into existing fat cells [2], [8].

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Approximately 50 chemicals have been identified that contribute to obesity le [10], [11]. Regular exposure to these contaminants can have long-term effects on adipose tissue, metabolic activity, hormones, and ultimately weight. A significant impact appears to be in utero and during early life when the metabolic system is developing [12]. Prenatal exposure may put people at risk for becoming obese later in life [3].

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Obesogens can be found in many things, from water bottles to microwaveable popcorn, and from non-stick pans to shower curtains. People interact with them on a daily basis, both intentionally and unintentionally, at home, school, and work. They are an unnecessary and mostly preventable potential hazard to health, which can have a large impact on how individuals gain and lose weight.

3 Essentials

  1. Avoid food and beverages stored in plastic. Use glass, silicone, ceramic or stainless steel instead. If you do use plastic, avoid heating plastic containers in the microwave or dishwasher, as this can cause the plastic to break down and release BPA.

  2. When selecting personal care products, opt for products in glass, metal, or paper containers as opposed to plastic.

  3. Read labels and choose personal care products and household cleaning supplies that do not contain the ingredients listed above.

Additional Key Recommendations

  1. Use a water filter to reduce chemicals in drinking water.

  2. Eat organically where possible to reduce pesticide exposure.

  3. Avoid pesticide use around the home garden.

  4. Use natural cleaning products, such as vinegar, baking soda, and lemon juice.

References

  1. World Health Organization, “Obesity and overweight,” WHO, 2022. https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight (accessed Dec. 11, 2022).

  2. A. Martínez-Esquivel, D. J. Trujillo-Silva, and V. G. Cilia-López, “Impact of environmental pollution on the obesogenic environment,” Nutr. Rev., vol. 80, no. 7, pp. 1787–1799, Jun. 2022, doi: 10.1093/nutrit/nuac003.

  3. M. D. Griffin, S. R. Pereira, M. K. DeBari, and R. D. Abbott, “Mechanisms of action, chemical characteristics, and model systems of obesogens,” BMC Biomed. Eng., vol. 2, no. 1, p. 6, Dec. 2020, doi: 10.1186/s42490-020-00040-6.

  4. F. Grün and B. Blumberg, “Environmental obesogens: organotins and endocrine disruption via nuclear receptor signaling,” Endocrinology, vol. 147, no. 6, pp. s50–s55, Jun. 2006, doi: 10.1210/en.2005-1129.

  5. J. J. Heindel and B. Blumberg, “Environmental obesogens: mechanisms and controversies,” Annu. Rev. Pharmacol. Toxicol., vol. 59, no. 1, pp. 89–106, Jan. 2019, doi: 10.1146/annurev-pharmtox-010818-021304.

  6. U. Shahnazaryan, M. Wójcik, T. Bednarczuk, and A. Kuryłowicz, “Role of obesogens in the pathogenesis of obesity,” Medicina (Mex.), vol. 55, no. 9, p. 515, Aug. 2019, doi: 10.3390/medicina55090515.

  7. J. J. Heindel et al., “Metabolism disrupting chemicals and metabolic disorders,” Reprod. Toxicol., vol. 68, pp. 3–33, Mar. 2017, doi: 10.1016/j.reprotox.2016.10.001.

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  18. B. S. Rubin, C. M. Schaeberle, and A. M. Soto, “The case for BPA as an obesogen: contributors to the controversy,” Front. Endocrinol., vol. 10, p. 30, Feb. 2019, doi: 10.3389/fendo.2019.00030.

  19. R. Naomi et al., “Bisphenol A (BPA) leading to obesity and cardiovascular complications: a compilation of current in vivo study,” Int. J. Mol. Sci., vol. 23, no. 6, p. 2969, Mar. 2022, doi: 10.3390/ijms23062969.

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  21. K. Y. Kim, E. Lee, and Y. Kim, “The association between bisphenol A exposure and obesity in children—A systematic review with meta-analysis,” Int. J. Environ. Res. Public. Health, vol. 16, no. 14, p. 2521, Jul. 2019, doi: 10.3390/ijerph16142521.

  22. M. R. Bernier and L. N. Vandenberg, “Handling of thermal paper: Implications for dermal exposure to bisphenol A and its alternatives,” PLOS ONE, vol. 12, no. 6, p. e0178449, Jun. 2017, doi: 10.1371/journal.pone.0178449.

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  24. B. Liu et al., “Association of bisphenol A and its substitutes, bisphenol F and bisphenol S, with obesity in United States children and adolescents,” Diabetes Metab. J., vol. 43, no. 1, p. 59, 2019, doi: 10.4093/dmj.2018.0045.

  25. L. Kolatorova et al., “Parabens and their relation to obesity,” Physiol. Res., pp. S465–S472, Nov. 2018, doi: 10.33549/physiolres.934004.

  26. P. Hu et al., “Methylparaben and butylparaben alter multipotent mesenchymal stem cell fates towards adipocyte lineage,” Toxicol. Appl. Pharmacol., vol. 329, pp. 48–57, Aug. 2017, doi: 10.1016/j.taap.2017.05.019.

  27. P. Hu et al., “Effects of parabens on adipocyte differentiation,” Toxicol. Sci., vol. 131, no. 1, pp. 56–70, Jan. 2013, doi: 10.1093/toxsci/kfs262.

  28. L. Mathiesen, G. Zuri, M. H. Andersen, and L. E. Knudsen, “A proposed study on the transplacental transport of parabens in the human placental perfusion model,” Altern. Lab. Anim., vol. 41, no. 6, pp. 473–482, Dec. 2013, doi: 10.1177/026119291304100610.

  29. N. Aubert, T. Ameller, and J.-J. Legrand, “Systemic exposure to parabens: Pharmacokinetics, tissue distribution, excretion balance and plasma metabolites of [14C]-methyl-, propyl- and butylparaben in rats after oral, topical or subcutaneous administration,” Food Chem. Toxicol., vol. 50, no. 3–4, pp. 445–454, Mar. 2012, doi: 10.1016/j.fct.2011.12.045.

  30. L. Richter, A. Cordner, and P. Brown, “Non-stick science: Sixty years of research and (in)action on fluorinated compounds,” Soc. Stud. Sci., vol. 48, no. 5, pp. 691–714, Oct. 2018, doi: 10.1177/0306312718799960.

  31. A. Ramírez Carnero, A. Lestido-Cardama, P. Vazquez Loureiro, L. Barbosa-Pereira, A. Rodríguez Bernaldo de Quirós, and R. Sendón, “Presence of perfluoroalkyl and polyfluoroalkyl substances (PFAS) in food contact materials (FCM) and its migration to food,” Foods, vol. 10, no. 7, p. 1443, Jun. 2021, doi: 10.3390/foods10071443.

  32. X. Lim, “Can microbes save us from PFAS?,” ACS Cent. Sci., vol. 7, no. 1, pp. 3–6, Jan. 2021, doi: 10.1021/acscentsci.1c00013.

  33. A. J. Lewis, X. Yun, D. E. Spooner, M. J. Kurz, E. R. McKenzie, and C. M. Sales, “Exposure pathways and bioaccumulation of per- and polyfluoroalkyl substances in freshwater aquatic ecosystems: Key considerations,” Sci. Total Environ., vol. 822, p. 153561, May 2022, doi: 10.1016/j.scitotenv.2022.153561.

  34. W. Qi, J. M. Clark, A. R. Timme-Laragy, and Y. Park, “Per- and polyfluoroalkyl substances and obesity, type 2 diabetes and non-alcoholic fatty liver disease: a review of epidemiologic findings,” Toxicol. Environ. Chem., vol. 102, no. 1–4, pp. 1–36, Apr. 2020, doi: 10.1080/02772248.2020.1763997.

  35. J. Aaseth et al., “The role of persistent organic pollutants in obesity: a review of laboratory and epidemiological studies,” Toxics, vol. 10, no. 2, p. 65, Feb. 2022, doi: 10.3390/toxics10020065.

  36. M. Han et al., “Association of triclosan and triclocarban in urine with obesity risk in Chinese school children,” Environ. Int., vol. 157, p. 106846, Dec. 2021, doi: 10.1016/j.envint.2021.106846.

  37. J. Lankester, C. Patel, M. R. Cullen, C. Ley, and J. Parsonnet, “Urinary triclosan is associated with elevated body mass index in NHANES,” PLoS ONE, vol. 8, no. 11, p. e80057, Nov. 2013, doi: 10.1371/journal.pone.0080057.

  38. Y. Hu et al., “Association between triclosan exposure and obesity measures among 7-year-old children in northern China,” Ecotoxicol. Environ. Saf., vol. 239, p. 113610, Jul. 2022, doi: 10.1016/j.ecoenv.2022.113610.

  39. M. Prasad et al., “Impact of glyphosate on the development of insulin resistance in experimental diabetic rats: role of NFκB signalling pathways,” Antioxidants, vol. 11, no. 12, p. 2436, Dec. 2022, doi: 10.3390/antiox11122436.

  40. L. N. Vandenberg et al., “Is it time to reassess current safety standards for glyphosate-based herbicides?,” J. Epidemiol. Community Health, vol. 71, no. 6, pp. 613–618, Jun. 2017, doi: 10.1136/jech-2016-208463.

  41. N. E. De Long and A. C. Holloway, “Early-life chemical exposures and risk of metabolic syndrome,” Diabetes Metab. Syndr. Obes. Targets Ther., vol. Volume 10, pp. 101–109, Mar. 2017, doi: 10.2147/DMSO.S95296.

  42. C. N. Martini, M. Gabrielli, J. N. Brandani, and M. D. C. Vila, “Glyphosate inhibits PPAR gamma induction and differentiation of preadipocytes and is able to induce oxidative stress,” J. Biochem. Mol. Toxicol., vol. 30, no. 8, pp. 404–413, Aug. 2016, doi: 10.1002/jbt.21804.

  43. C. N. Martini, M. Gabrielli, and M. D. C. Vila, “A commercial formulation of glyphosate inhibits proliferation and differentiation to adipocytes and induces apoptosis in 3T3-L1 fibroblasts,” Toxicol. In Vitro, vol. 26, no. 6, pp. 1007–1013, Sep. 2012, doi: 10.1016/j.tiv.2012.04.017.

  44. F. Jiang, Y. Peng, and Q. Sun, “Pesticides exposure induced obesity and its associated diseases: recent progress and challenges,” J. Future Foods, vol. 2, no. 2, pp. 119–124, Jun. 2022, doi: 10.1016/j.jfutfo.2022.03.005.

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Where Do They Come From?

These obesogenic chemicals are everywhere: in personal care products, household cleaners, food packaging, water and dust, furniture, electronics, and pesticides [14]–[17].

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Sources of obesogens. This figure shows just some of the major classes of obesogens along with some sources of exposure. Exposure to obesogens occurs at home and work; via the air, water, food, and skin contact [10].

Bisphenol A (BPA) (2,2-bis(4-hydroxyphenyl)propane) is just one compound on a growing list of possible obesogens; however, it may play a significant role in the obesity pandemic due to the widespread nature of BPA exposure.[18]. BPA is a chemical produced in large quantities for use primarily in the production of polycarbonate plastics and epoxy resins [19], [20]. Diet is considered the main source of BPA exposure in humans, as it is used in food cans, food storage containers, and reusable bottles such as baby bottles and water bottles [18], [21]. But it is also in composites and sealants in dentistry [21]. BPA exposure can also occur via inhalation of air and dust [18]. Evaluations have also revealed the presence of BPA in products that come in contact with skin including cosmetics and thermal paper [22].

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In many thermal papers used as cash register receipts and tickets for airlines and trains, BPA is applied to the printing surface to be used as a heat-activated developer. In these papers, the coating includes milligrams of unbound BPA per gram of paper. When a laser is directed on the paper, the heat causes BPA to react with the thermal paper dye, producing a colour-developing complex. Whereas BPA used in plastics and can linings are found largely in a polymerised form like polycarbonate or PVC, BPA applied to thermal paper is free, thus relatively large exposures from these materials may occur after normal handling [22].

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When BPA enters the body via the oral route, it is absorbed into the mesenteric blood vessels, transported to the liver, and rapidly metabolised in a process referred to as ‘first pass metabolism’. Such processes mean that the majority of BPA that circulates in the bloodstream following oral exposure is in the conjugated form (e.g., BPA-glucuronide, BPA-sulphate) although some unconjugated BPA does reach circulation. In contrast, when BPA enters the body via alternative routes (e.g., dermal or inhalation), it circumvents first-pass metabolism, allowing significantly more unconjugated BPA to circulate in the bloodstream. These toxicokinetic data suggest that the route of exposure can have a large influence on the concentration of BPA that circulates as unconjugated BPA [22]. The non-oral exposures, although they are considered to occur at significantly lower levels, may be more potent as they avoid the first pass metabolism of BPA by conjugation and therefore dermal sources may have far higher toxicological relevance than expected [18].

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A 2020 analysis of 15 studies found a significant link between BPA levels and obesity. A dose–response analysis revealed that 1-ng/mL increase in BPA increased the risk of obesity by 11%. The similar results were for different type of obesity (hyperplastic (increased fat cell number) and hypertrophic obesity (increased fat cell size)), gender, and age [23].

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Common sources of BPA:

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  • Food and beverage containers: BPA is commonly found in plastic food containers, water bottles, and can linings.

  • Cash register receipts: BPA is often used in the thermal paper used to print receipts.

  • Medical devices: BPA is used in some medical devices such as dental sealants, prosthetics, and catheters.

  • Electronics: BPA can be found in some electronic devices, such as CDs, DVDs, and cell phones.

  • Household items: BPA can be found in some household items such as water pipes, dental fillings, and some types of flooring.

  • Toys: BPA has been used in some toys, particularly in certain types of plastic toys.

  • Water: BPA has been found in some water sources, including bottled water, and water from PVC pipes.

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It is important to note that BPA is not always listed as an ingredient in products, so it can be difficult to determine if a product contains BPA. However, there are some products that are labelled as "BPA-free," which can help consumers make more informed decisions when purchasing products.

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Mechanism of action of bisphenol A and associated obesity. Mechanism of BPA-induced weight gain may be due to its estrogenic activity. BPA binds to estrogen receptors (ERα and ERβ) and subsequently induces a perturbation in peroxisome proliferator-activated receptor gamma (PPARγ) signaling. BPA increases the number and size of adipocytes by regulating the expression of genes such as fatty acid binding protein 4 (FABP4), cluster of differentiation 36 (CD36) and proprotein convertase subtilisin/kexin type 1 (PCSK1). In addition, the estrogenic effect of BPA inhibits adiponectin secretion. Meanwhile, in utero and adult exposure to BPA affect the hypothalamic Agouti-related peptide (AgRP) and neuropeptide Y (NPY) neurons. These potent neuropeptides have a stimulating effect on the appetite. BPA that accumulates in the gut may contribute to gut bacterial dysbiosis. BPA exposure reduces gut small chain fatty acid (SCFA) and increases systemic lipopolysaccharide (LPS) levels, leading to chronic low-grade inflammation and subsequently altered lipid homeostasis [19].

But bisphenol S (BPS), the second most prevalent bisphenol viewed as a replacement to BPA, has recently been demonstrated to increase postnatal body weight after neonatal exposure and also increase adipogenesis in vitro, thus raising concerns as to its applicability as a replacement chemical [20]. Another BPA substitute, Bisphenol F (BPF), has been positively associated with higher risk of obesity in children and adolescents [24].

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Phthalates: (pronounced "THAL-ates") are a group of chemicals that are used as plasticisers, solvents, and fixatives in a variety of products, including plastics, cosmetics, fragrances, and personal care products. They are colorless, odorless liquids that can be easily mixed with other materials. Phthalates are commonly used to make plastics more flexible and durable.

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Common sources of phthalates:

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  • Plastic products: Phthalates are commonly found in products such as plastic food wrap, food containers, household cleaning product containers, shower curtains, and vinyl flooring.

  • Cosmetics and personal care products: Phthalates are sometimes used as solvents and fixatives in fragrances and as emollients in lotions, creams, nail polish, and other personal care products.

  • Food and beverages: Phthalates can leach into food and beverages from packaging materials, particularly plastic containers and bottles.

  • Household products: Phthalates are sometimes used in household products such as cleaning agents and air fresheners.

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Parabens are a group of chemicals used as preservatives in the food, cosmetic and pharmaceutical industries. Generally, this group of components is characterised by fungistatic, anti-yeast and anti-mould activities, as well as antibacterial properties. They are known to possess estrogenic effects, and therefore have been classified as endocrine disruptors. In addition to the classical endocrine organs, other tissues have endocrine activity, including adipose tissue. Several chemicals are known to cause obesogenic effects, and parabens are currently being studied in this context [25]. Hu et al. 2017 [26] recently experimentally confirmed their previous observations reported in 2013 [27] that parabens promoted adipocyte differentiation in vitro and increased adiposity. Parabens may enter the human body through ingestion, absorption through the skin and inhalation. Their metabolism differs between these exposure pathways. Transdermal absorption is dependent on the length of the paraben alkyl- substituent, with the absorption decreasing with an increasing side chain [25]. They are later metabolised by esterases, conjugated and excreted in the urine and bile [25].  As a result of daily topical application of paraben-containing cosmetics, parabens may accumulate in the body [28]. Following oral exposure, parabens are metabolised by esterases in the intestine and liver and excreted in the urine as well as in the bile and feces [29].

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Common sources of parabens:

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  • Personal care products: Parabens are commonly used as a plasticiser in personal care products such as shampoos, conditioners, lotions, deodorants, and baby wipes. They can be found in both natural and synthetic products.

  • Cosmetics: Parabens are also commonly used in cosmetics such as lipsticks, foundations, powders, blushes, and eye shadows. They are used to prevent the growth of bacteria and other microorganisms that can cause spoilage and infection.

  • Food products: Parabens are sometimes used as preservatives in food products such as baked goods, processed meats, and beverages.

  • Pharmaceuticals: Parabens are also used as preservatives in some pharmaceutical products, including some creams, ointments, and eye drops.

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Per- and polyfluoroalkyl substances (PFAS) also known as “forever chemicals”, are a large, complex group of synthetic (manmade) chemicals that have been used in consumer products around the world since about the 1950s [30]. They are ingredients used as oil and water repellents and coatings in various everyday products. For example, PFAS are used to keep food from sticking to packaging or cookware, make clothes and carpets resistant to stains, and create firefighting foam that is more effective [30], [31]. PFAS molecules have a chain of linked carbon and fluorine atoms [30]. Because the carbon-fluorine bond is one of the strongest, these chemicals do not degrade easily in the environment, and accumulate over time [32], [33].

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Dietary intake is an important source of PFAS exposure. PFAS contamination in food accounts for the majority of non-occupational exposure to PFAS, accounting for over 90% of exposure. Multiple causes can lead to the contamination of food by PFAS. As PFAS are bio-accumulative and persistent in environment, food derived from animals, in particular seafood, may contain PFAS due to the exposure of animals to the environment. Plant-based food can also be contaminated by being watered by PFAS contaminated water or grown in soil amended by contaminated biosolids. Direct exposure to food packaging can be another possible cause of contamination, as a great number of PFAS are widely used in food packaging as oil and/or water repellents, especially in fast food packaging. The migration of PFAS from food packaging to food has also been extensively reported. Interestingly, the dietary exposure of PFAS is correlated with high consumption of foods in paper containers. PFOA residues in polytetrafluoroethylene (PTFE)-coated non-stick cookware (commonly known as Telfon) could likewise be a potential source of PFAS exposure through food. Besides these dietary sources, the accumulation of PFAS in human milk, which is the most important source of PFAS exposure for infants, has also been well-studied, and a growing body of literature has suggested a link between postnatal exposure to PFAS and health effects in childhood, adolescence, and adulthood [34].

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In addition to drinking water and food, it has been reported that humans can also be exposed to PFAS by indoor air, indoor dust, and direct contact with PFAS-treated consumer products [34]. Exposure to PFAS can also occur through a variety of other sources and pathways, including but not limited to drinking water, food, indoor air, and dust. Water contamination is considered one of the major sources, especially those near certain locations including industrial sites, military fire training sites, and wastewater treatment plants [34].

 

The role of PFAS in obesity has yet to be fully clarified, although some data derived from epidemiological studies suggest that PFAS exposures are associated with overweight and obesity. Higher levels of PFAS were found in mothers with obesity when compared to those of a normal weight. Moreover, prenatal exposure to PFAS has been linked with obesity, metabolic disorders, and alterations in children’s growth. In a large multicentre prospective cohort study, the “European Youth Heart Study” performed in young participants (N = 369), scientists found that PFAS exposure predicted adiposity at 15 and 21 years of age. A recently published cross-sectional study in US children from 12–18 years of age (N = 2473) showed a dose-dependent association between obesity and PFAS exposure. Nonetheless, the European Food Safety Authority reported in 2020 that there is insufficient data to support a link between PFAS exposure and obesity, thus the explanation for this association requires further research [35].

 

Common sources of PFAS:

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  • Non-stick cookware: PFAS are commonly used in non-stick cookware such as Teflon pans. When these pans are heated, they can release PFAS into the air and food.

  • Food packaging: PFAS are used in food packaging to make it resistant to grease, oil, and water. This includes products such as fast-food wrappers, microwave popcorn bags, and pizza boxes.

  • Stain and water-resistant fabrics: PFAS are used to make fabrics, carpets, and furniture stain and water-resistant. This includes products like stain-resistant carpeting, upholstery, and outdoor gear.

  • Firefighting foam: PFAS are used in firefighting foam to extinguish fires involving flammable liquids such as oil and gasoline. The foam can contaminate groundwater and soil when it is used and disposed of.

  • Personal care products: Some personal care products such as dental floss and some cosmetics may contain PFAS.

  • Industrial applications: PFAS are used in a variety of industrial applications such as electronics manufacturing, metal plating, and oil recovery.

  • Water: found in some drinking water.

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Triclosans and triclocarban antimicrobial chemicals commonly found in many household, personal care, and consumer products. These chemicals are present in over 2,000 products such as soaps, toothpastes, detergents, clothing, toys, carpets, plastics, and paints [2]. While triclosan is more commonly used in liquid soaps, triclocarban is mainly used in soap bars [1]. However, the U.S. Food and Drug Administration (FDA) states that there is currently no evidence that triclosan or triclocarban improves consumer health or prevents disease when used in personal care products like hand soap [3]. It is worth noting that the FDA has banned the use of triclosan and triclocarban in over-the-counter antiseptic wash products, citing concerns about their potential effects on the endocrine system and the environment [3]. However, these chemicals are still allowed to be used in other consumer products. There have been some studies that suggest a possible link between triclosan or triclocarban exposure and obesity [36]–[38].

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Common sources of triclosans and triclocarbans:

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  • Personal care products: Triclosan and triclocarban are commonly used in personal care products such as soaps, toothpaste, mouthwash, deodorants, and shaving cream. They are added to these products to prevent the growth of bacteria and other microorganisms.

  • Textiles: Triclosan and triclocarban are used in textiles such as clothing, bedding, and towels to prevent the growth of bacteria and other microorganisms that can cause odour and staining.

  • Kitchenware: Triclosan and triclocarban are sometimes used in cutting boards, sponges, and other kitchenware to prevent the growth of bacteria.

  • Toys: Triclosan and triclocarban are sometimes used in toys and other children's products to prevent the growth of bacteria.

  • Pesticides: Triclosan and triclocarban are sometimes used as antimicrobial agents in pesticides to prevent the growth of bacteria and fungi.

  • Medical devices: Triclosan and triclocarban are sometimes used in medical devices such as catheters and surgical instruments to prevent infections.

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Pesticides

 

Glyphosate is a herbicide widely used in agriculture to control weeds. It is marketed in the brand names “Roundup” and “Ranger Pro” [39]. Use of glyphosate-based herbicides (GBHs) increased ∼100-fold from 1974 to 2014 [40]. While glyphosate is not directly obesogenic, it has been linked to disruptions in the gut microbiome, which in turn may contribute to the development of obesity and related health problems. Glyphosate has been identified in surface and groundwater; however, most nonoccupational exposures occur from consuming foods containing glyphosate residues [41]. While the effects of glyphosate on metabolic health in humans have largely not been explored, there are animal and cell culture studies that have investigated the effects of glyphosate on key metabolic pathways. Glyphosate depletes bioavailability of the amino acid tryptophan. This is turn impacts serotonin synthesis (which is derived from tryptophan). Serotonin is potent appetite suppressant, therefore serotonin deficiency could lead to overeating and obesity. Glyphosate has also been shown to increase apoptosis (programmed cell death) and induce oxidative stress in preadipocytes [42], [43]. Oxidative stress ensues due to mitochondria dysfunction and decreased oxidative capacity, which has been shown to impair glucose uptake into adipocytes, promoting hyperglycaemia [42]. Oxidative stress also disturbs the adipokine production by fat cells, which has been suggested to be an early initiation event in the development of metabolic syndromes [41]. Taken together, these studies suggest that further study of the effects of glyphosate on obesity and metabolic syndrome risk requires further attention [44].

 

Organophosphate pesticides are commonly used in agriculture to kill insects. They work by disrupting the nervous system of insects, but they can also affect human health. Studies have linked exposure to organophosphate pesticides to an increased risk of obesity, insulin resistance, and metabolic disorders [45]–[48].

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Pyrethroid pesticides are synthetic chemicals used to control insects. They are widely used in agriculture, as well as in households (e.g., in fly sprays) and public spaces. Some studies have suggested that exposure to pyrethroids may be associated with an increased risk of obesity and metabolic disorders [44], [49]–[51].

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Neonicotinoid pesticides are a newer class of insecticides that are widely used in agriculture. They work by affecting the nervous system of insects. However, there is growing concern that exposure to neonicotinoids may be linked to the development of metabolic disorders such as obesity and diabetes [44], [52]–[54].

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Butylated hydroxytoluene (BHT) is a synthetic antioxidant commonly used as a food preservative. The chemical is added to food to protect nutrients and prevent fats from turning rancid. BHT is also found in cosmetics, pharmaceuticals, jet fuels, rubber, and petroleum products. It has been studied for its potential obesogenic effects in animal models and in humans, and studies have suggested that BHT may have a role in the development of obesity [55], [56]. BHT is banned from food in the European Union and Japan, and also from baby food in the United States.

How They Affect You

Obesogens work by upsetting the body’s “metabolic thermostat”, which makes gaining weight and reducing weight more difficult. The interaction of numerous hormones from fat tissue, the gut, the pancreas, the liver, and the brain is crucial for the body's ability to maintain a balance between energy intake and expenditure through exercise. The amount and size of fat cells, the signals that make individuals feel full, thyroid function, and the dopamine reward system can all be directly impacted by chemicals and pollutants. Additionally, by improving the efficiency with which calories are absorbed from the intestines, they can alter the microbiota in the gut and contribute to weight gain [1], [10].

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Obesity is a complex medical condition that is associated with various adverse health effects. Increased body mass index (BMI) is a major risk factor for noncommunicable diseases such as:

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  • type 2 diabetes

  • cardiovascular diseases (mainly heart disease and stroke), which are leading causes of death;

  • fatty liver disease - This can lead to liver inflammation, scarring, and eventually liver failure;

  • musculoskeletal disorders (especially osteoarthritis – a highly disabling degenerative disease of the joints);

  • respiratory problems, such as sleep apnoea, obesity hypoventilation syndrome, and asthma, due to the extra weight putting pressure on the lungs and airways;

  • mental health issues - obesity is associated with depression, anxiety, and other mental health problems, which can negatively impact an individual's quality of life;

  • some cancers (including endometrial, breast, ovarian, prostate, liver, gallbladder, kidney, and colon).

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The risk for these noncommunicable diseases increases, with increases in BMI [57]–[61].

 

The most vulnerable period of a child's development to obesogens is the early years. The most vulnerable periods, according to studies, were during foetal development and the early years of life since these were the times when the metabolic system's programming was irreversibly altered, making people more susceptible to weight gain [1]. Childhood obesity is associated with a higher chance of obesity, premature death, and disability in adulthood. But in addition to increased future risks, obese children experience breathing difficulties, increased risk of fractures, hypertension, early markers of cardiovascular disease, insulin resistance and psychological effects [1].

How To Protect Yourself

Recognize the need to become more aware of environmental toxins and their presence in all aspect of life.  Avoid exposure to dangerous toxins and pollutants in purchased food, personal care products, and cleaning products, and your water, especially for pregnant females and babies.  You can do this by, when possible, making sure to use products that declare their chemicals on the label in order to prevent exposure to dangerous chemical toxins and pollutants.

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While some chemical toxins may not be listed on an ingredient declaration, many are. Avoid products containing the following ingredients:

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BPA: a “3 or 7” or “PVC” on the triangle symbol on plastics. The triangle symbol with a number inside, often found on the bottom of plastic containers, is known as the Resin Identification Code (RIC). This code indicates the type of plastic resin used to make the container and is used to help identify which plastics can be recycled. RIC 3 indicates that the plastic is made from polyvinyl chloride (PVC). It may contain additives such as BPA or phthalates. Plastic containers that are made with BPA may be marked with the RIC number 7, but not all containers with this code contain BPA. In addition, the presence of "PVC" in the RIC does not necessarily indicate the presence of BPA.

 

Parabens: -paraben, methylparaben, propylparaben, butylparaben, isopropyl paraben, isobutylparaben

 

Phthalates: phthalate, dibutyl phthalate (DBP) (in nail polish and other cosmetic products), diisononyl phthalate (DINP) (in vinyl flooring, adhesives, synthetic leather), diethyl phthalate (DEP) (in fragrances), diethylhexyl phthalate (DEHP) in PVC pipes), dimethyl phthalate (DMP) (in fragrances), benzyl butyl phthalate (BBP) (in vinyl flooring and adhesives), di-n-octyl phthalate (DNOP) (in PVC pipes, artificial leather), diisodecyl phthalate (DIDP) (in vinyl flooring, wallpaper, synthetic leather).

 

Triclosans/triclocarbans: triclosan, 2,4,4'-trichloro-2'-hydroxydiphenyl ether, triclocarban, 3,4,4'-trichlorocarbanilide, “anti-bacterial”, “odour-fighting”

 

Fragrance

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Use resources such as those listed below to determine whether a product includes recognised toxins. Find out what resources could be accessible in your nation or WHO Region.

  • EWG.org, EWG Healthy Living App, EWG Skin Deep App

  • Think Dirty App

  • Good Guide App

  • Madesafe.org

  • Redify App

  • Dirty Dozen App

 

Other ways to reduce your exposure include:

  • Store food in glass or ceramic.

  • Use stainless steel or glass water bottles.

  • Avoid covering food with plastic wrap[IL1] .

  • Avoid heating food in plastic or roasting/steaming bags.

  • Reduce the number of canned foods that you eat.

  • Use your own reusable coffee mug if you purchase take-away coffee.

  • Use baby bottles that are labelled BPA free.

  • Go straw-less by not asking for a straw at a restaurant or buy your own reusable straws.

  • Avoid handling cash receipts where possible.

  • Do not use any pan with non-stick coating. Use stainless steel, cast iron, ceramic, or ceramic coated cast iron or glass as alternatives.

Work with a naturopathic doctor / naturopath to help you assess for environmental pollutants and to understand how they may be affecting your health. The information on this website is a guide for ways to protect you and your family from environmental pollutants.  It is not meant to replace advice from a healthcare professional.

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