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Obesity & Endocrine-Disrupting Chemicals: Bisphenols & Phthalates (2024 Review)

In the quest to understand the alarming rise in obesity rates worldwide, recent research has pointed towards a surprising culprit: endocrine-disrupting chemicals (EDCs), such as bisphenol A (BPA) and phthalates.

These chemicals, ubiquitous in our environment, have been linked to significant disturbances in the hormonal regulation of body mass and adipose tissue function.


  • Endocrine Disruptors & Obesity: EDCs like BPA and phthalates are associated with increased risk of obesity and related metabolic disorders.
  • Mechanisms of Action: EDCs can interfere with hormonal regulation, promote adipogenesis, disrupt appetite signals, and induce chronic inflammation.
  • Critical Exposure Periods: Prenatal, neonatal, pubertal, and reproductive periods are particularly sensitive to the obesogenic effects of EDCs.
  • Transgenerational Impact: EDCs can have epigenetic effects, potentially leading to obesity in future generations.

Source: International Journal of Molecular Sciences (2024)

Endocrine-Disrupting Chemicals (EDCs): BPA & Phthalates

Endocrine-Disrupting Chemicals (EDCs) are substances that can interfere with the normal functioning of the endocrine system in animals and humans.

They are found in a variety of everyday products and can impact health in multiple ways.

Bisphenol A (BPA)

BPA is primarily used in the production of polycarbonate plastics and epoxy resins.

It is commonly found in plastic bottles, food can linings, medical devices, and dental sealants.

BPA can leach into food and beverages, especially when plastic containers are heated or damaged.

BPA mimics estrogen, a primary female sex hormone, and can disrupt normal hormonal activities.

Its estrogenic activity can affect puberty, fertility, and increase the risk of hormone-related cancers like breast and prostate cancer.

BPA exposure is also associated with obesity, as it can influence fat cell production, and has been linked to Type 2 diabetes and cardiovascular diseases due to its role in insulin resistance and arterial stiffness.


Phthalates are a group of chemicals used to make plastics more flexible and harder to break.

They are commonly found in PVC plastics, cosmetics, personal care products (like nail polish, hair spray), toys, vinyl flooring, and medical devices.

Phthalates can be released into the environment and enter the human body through ingestion, inhalation, and skin contact.

Phthalates are known to disrupt the endocrine system, particularly affecting reproductive health.

They have been linked to decreased sperm count in men and reproductive problems in women.

Their role in obesity is attributed to their ability to influence the function of hormone receptors, such as estrogen and androgen receptors, leading to obesity and insulin resistance.

How Endocrine Disruptors like BPA & Phthalates Cause Obesity (Possible Mechanisms)

EDCs contribute to obesity and associated metabolic disorders through various mechanisms:

Impacting Adipogenesis

EDCs like BPA and certain phthalates can activate the peroxisome proliferator-activated receptor (PPAR) pathway, a key regulator in the development of fat cells (adipocytes).

They can stimulate the conversion of stem cells into adipocytes, increasing the number and size of fat cells, which contributes to increased fat storage in the body.

Disrupting Appetite Control

EDCs can alter the function of hormones involved in hunger and satiety, such as leptin and ghrelin. By interfering with these signals, EDCs can lead to increased food intake and disrupted energy balance.

Changes in thyroid hormone function due to EDCs can also affect metabolism and appetite control.

Inducing Chronic Inflammation

EDCs can trigger inflammation in adipose tissue, contributing to the development of obesity and insulin resistance.

Chronic exposure to EDCs can lead to a state of low-grade inflammation, exacerbating the risk of metabolic disorders.

Affecting Gut Microbiome

EDCs can disrupt the gut microbiota composition, which plays a crucial role in metabolism and energy homeostasis.

Altered gut microbiome due to EDC exposure can lead to increased energy harvest from food, insulin resistance, and inflammation, all of which contribute to obesity.

Critical Periods of Exposure & Transgenerational Impact

Critical Periods: The developmental stages like prenatal, neonatal, and early childhood periods are particularly sensitive to EDC exposure. During these times, the endocrine system is developing, and interference can have lasting effects on body weight regulation and metabolic health.

Transgenerational Impact: EDCs can induce epigenetic changes (alterations in gene expression without changing the DNA sequence), which can be passed down to subsequent generations. This can predispose offspring to obesity, even if they are not directly exposed to the EDCs.

Endocrine Disrupting Chemicals & Obesity (2024 Review)

Maria Dalamaga et al. published a review paper focusing on the association between endocrine-disrupting chemicals (EDCs), such as bisphenol A (BPA), phthalates, and their analogs, and obesity.

They summarized evidence on the role of obesogenic EDCs, specifically BPA and phthalates, in obesity development; discussed mechanisms by which EDCs may cause obesity; analyzed effects of EDCs on obesity in critical chronic periods of exposure; and discussed preventive measures that can be taken to combat exposure.


  • Literature Search and Review: The review used the MESH terms “obesity” and “endocrine-disrupting chemicals” in the PubMed NIH database until 20 October 2023, yielding 670 outputs. After excluding irrelevant and non-English studies, 609 manuscripts were included.
  • Analysis: The review integrated data from mechanistic, animal, and epidemiological studies, including meta-analyses.


  • Adipogenesis Impact: EDCs, particularly BPA and phthalates, promote formation of new fat cells, influencing adipocyte size and number.
  • Epigenetic Modulation: These chemicals impact epigenetic pathways during development, enhancing susceptibility to obesity.
  • Neuroendocrine Signal Alteration: EDCs affect hormones regulating appetite and satiety, potentially leading to increased food intake.
  • Inflammatory Response Induction: EDCs promote chronic low-grade inflammation in adipose tissue.
  • Gut Microbiome Dysregulation: They alter gut microbiota composition, influencing metabolism and weight gain.
  • Thermogenic Adipose Tissue Dysfunction: EDCs affect the function of fat cells involved in thermogenesis and energy balance.
  • Critical Exposure Periods: Prenatal, neonatal, pubertal, and reproductive periods are highlighted as crucial for exposure.
  • Transgenerational Effects: Low doses of EDCs may lead to epigenetic transgenerational inheritance of obesity.


  • Cross-Sectional Nature of Studies: Many human studies are cross-sectional, which limits the ability to draw causal inferences.
  • Single Measurement Issues: Most human studies rely on single-time measurements, which might not accurately reflect long-term or cumulative exposure to EDCs.
  • Potential Dietary Confounding: The association observed between EDC exposure and obesity might be confounded by dietary factors, as higher exposure often coincides with consumption of processed, high-calorie foods.
  • Differing Effects of EDCs: There are variations in the effects of different EDCs, and their impact might differ based on gender, age, and other demographic factors.
  • Lack of Standardization in Biomonitoring: There’s a need for standardized methods for assessing EDC exposure and its health implications.
  • Substitute Compounds: Replacing BPA and phthalates with other compounds might not eliminate health risks, as substitutes could have similar or unknown endocrine-disrupting properties.

Detailed Results: Endocrine-Disrupting Chemicals & Obesity

Adipogenesis & Fat Cell Development

EDCs like BPA and phthalates significantly influence the differentiation of pre-adipocytes into mature adipocytes.

They regulate genes involved in fat cell development, notably PPARγ, leading to increased fat storage.

Epigenetic Impact

Exposure to EDCs alters epigenetic regulation in developing cells. For example, BPA reduces global DNA methylation and activates adipocyte differentiation.

These epigenetic changes predispose individuals to obesity, even after the cessation of direct exposure.

Neuroendocrine Disruption

EDCs interfere with hormones controlling hunger and fullness. BPA, for instance, has been linked to increased levels of orexigenic neuropeptides like NPY and AgRP, enhancing appetite.

This disruption could lead to increased calorie intake and weight gain.

Inflammatory Responses in Fat Tissue

EDCs, especially BPA, induce inflammatory cytokines in adipose tissue, contributing to chronic inflammation, a known factor in obesity development.

This inflammation is associated with metabolic syndrome and insulin resistance.

Gut Microbiome Alterations

Changes in gut microbiota composition due to EDC exposure impact metabolic processes and can promote weight gain.

Studies have shown that BPA can decrease gut microbiome diversity, leading to imbalances that favor obesity.

Impact on Thermogenic Fat

EDCs affect brown and beige adipocytes, which are crucial for thermogenesis and energy balance.

Dysfunctional thermogenic adipose tissue due to EDC exposure could lead to impaired fat burning and energy regulation.

Potential Implications of this Review (EDCs & Obesity)

  • Public Health Strategies: These findings highlight the need for public health policies to limit EDC exposure, especially in vulnerable populations like children and pregnant women.
  • Product Manufacturing Reforms: There’s a pressing need for safer alternatives in product manufacturing, moving away from EDCs like BPA and phthalates.
  • Clinical Practice: Awareness in clinical settings regarding EDC exposure can guide preventive strategies and patient education, particularly in managing obesity and related metabolic disorders.
  • Research Focus: Further research is warranted to explore safe alternatives to these chemicals and to understand the long-term implications of EDC exposure.
  • Regulatory Actions: Regulatory bodies might need to reassess current permissible levels of EDCs in consumer products considering their long-term health impacts.
  • Consumer Awareness: Educating consumers about the potential risks associated with EDCs can lead to informed choices and potentially reduce exposure levels.

Strategies to Reduce Exposure to Endocrine Disruptors (Ideas)

1. Choose Safer Containers

Avoid plastic containers, especially for food and drinks. Opt for glass, stainless steel, or BPA-free plastics.

Be cautious with canned foods, as many have linings containing BPA. Look for brands that advertise BPA-free cans.

2. Check Personal Care Products

Read labels on personal care items. Avoid products with ingredients like “phthalate,” “DBP,” “DEP,” “DEHP,” and “fragrance,” which can indicate hidden phthalates.

3. Food Preparation & Storage

Avoid heating food in plastic containers, which can cause chemicals to leach into food. Use ceramic or glass for microwave cooking.

Store foods in glass or BPA-free containers.

4. Limit Processed & Packaged Foods

Processed and packaged foods are more likely to contain EDCs.

Choose fresh or frozen foods and minimize consumption of packaged snacks and fast food.

5. Be Careful with Receipts

Many receipts are coated with BPA. Handle them minimally and wash hands afterward.

6. Dust & Vacuum Regularly

Regular cleaning reduces dust that can contain EDCs.

Use a vacuum with a HEPA filter and damp mop floors frequently.

7. Choose Safe Toys

Buy toys labeled phthalate-free, especially for young children who put toys in their mouths.

Advanced Strategies for Detoxification of EDCs & Epigenetic Targeting

  • Nutritional Detoxification: Diets rich in fiber, antioxidants, and essential nutrients may help the body detoxify harmful chemicals. Foods like cruciferous vegetables, berries, nuts, and seeds are beneficial.
  • Pharmacological Agents: Research into drugs that can bind and neutralize EDCs in the body is ongoing. These would work by either blocking the action of EDCs or facilitating their excretion.
  • Epigenetic Therapies: Future treatments might include epigenetic drugs that can reverse the DNA methylation or histone modifications caused by EDCs. Gene editing technologies like CRISPR could potentially be used to correct epigenetic changes induced by EDC exposure.
  • Gut Microbiome Modulation: Probiotics and prebiotics might be used to restore or maintain a healthy gut microbiome, which can be disrupted by EDCs.
  • Advanced Filtration Systems: Investing in advanced water filtration systems at home can reduce exposure to EDCs found in water supplies.
  • Safer Material Research: Development of new materials that don’t rely on EDCs for production. Bio-based plastics and green chemistry are areas of active research.
  • Nanotechnology: Nanoparticles could be designed to target and bind EDCs in the body, rendering them inert or facilitating their removal.

Takeaway: Endocrine-Disruptor Chemicals & Obesity

The review underscores a significant link between exposure to endocrine-disrupting chemicals (EDCs) like bisphenol A and phthalates, and the development of obesity.

These EDCs contribute to obesity through various mechanisms including adipogenesis, epigenetic modifications, disruption of neuroendocrine signals, induction of inflammation in adipose tissue, alteration of gut microbiome, and affecting thermogenic fat tissues.

Their impact is particularly concerning during critical developmental stages, suggesting that exposure in early life can have long-lasting effects.

The findings call for urgent public health measures, changes in manufacturing practices, and increased consumer awareness to mitigate these risks.

While the study presents compelling evidence, it also highlights the need for more research to fully understand these complex interactions and to find safer alternatives to these widespread chemicals.

Overall, the study adds to the growing body of evidence about the potential health risks posed by common EDCs.


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