Obesogens: What veterinarians should know (#380)

While diet and exercise are often blamed for rising obesity rates, accumulating evidence points to a less visible culprit—endocrine‑disrupting chemicals (EDCs) that interfere with metabolism at critical points in development.

A striking subset of these have been dubbed obesogens, a term first coined in 2006 by Felix Grün and Bruce Blumberg of UC Irvine.

What Are Obesogens?

Obesogens are EDCs that reprogram fat cell development, alter metabolic set‑points, and disrupt appetite or satiety signals.

They can promote fat accumulation by:

• Increasing the number and size of adipocytes

  
  

• Modulating insulin sensitivity and lipid metabolism

  
  

• Recalibrating hypothalamic regulation of hunger and fullness

Common examples include bisphenol A (BPA), phthalates, perfluorinated compounds, and tributyltin (TBT)—a compound originally used in marine paints and industrial coatings.

Bruce Blumberg’s Key Findings

Blumberg’s foundational animal studies revealed that even low-dose exposure to TBT in utero led mice to develop significantly more fat cells and increased weight as adults—even without dietary differences. This effect sometimes persisted across generations through epigenetic reprogramming.

Further, his work and that of others showed that developmental exposure to certain EDCs may permanently alter metabolic regulation, making weight gain easier and weight loss harder—even with caloric restraint and exercise.

The Obesogen Economy: Create the Problem, Sell the Cure

Here lies a particularly uncomfortable truth.

Many of the same multinational corporations now aggressively marketing injectable weight-loss drugs are also deeply embedded in petrochemical manufacturing—the very industrial backbone from which obesogens like BPA, phthalates, and PFOAs emerge. These substances infiltrate consumer products, food packaging, flame retardants, agricultural chemicals, and cosmetics.

In other words: corporations helped create the problem—and now profit from treating it.

This dual corporate role is rarely scrutinized.

Pharmaceutical divisions tout breakthrough therapies for obesity and metabolic disease, while their sister companies churn out chemicals that disrupt metabolic health at a population level.

It's a self-sustaining loop of exposure, illness, and monetized treatment.

And because upstream prevention—like regulating EDCs—offers little profit incentive, the focus remains squarely on pharmaceuticals rather than public health.

This raises a pressing ethical question:

Should corporations be allowed to profit from both sides of the metabolic disorder equation?

Mechanisms of Action

The ways obesogens work are complex—and often subtle:

• Targeting nuclear receptors such as PPARγ (master regulator of fat cell differentiation) and RXR, causing inappropriate activation of adipogenesis

  
  

• Reprogramming metabolic set‑points in fetal or neonatal life, effectively increasing the ease of fat storage later in life

  
  

• Interference within the hypothalamus, modifying signals for appetite and satiety via leptin, ghrelin, and neuropeptide pathways

  
  

• Epigenetic alterations passed to subsequent generations—a concept known as “generational toxicology,” often overlooked in traditional risk assessments

Health and Policy Implications

• Obesity and metabolic disorders like type 2 diabetes, NAFLD, and cardiovascular disease may be linked in part to obesogen exposure, with billions in societal costs

  
  

• Regulatory frameworks rarely account for developmental vulnerability or epigenetic inheritance, limiting the effectiveness of traditional toxicity assessments

  
  

• Most studies remain in animal models; while human data are limited, the biological plausibility and parallels justify precautionary vigilance

What Can We Do—or Advocate For?

• Awareness & Education: Inform clients, patients, and colleagues about how exposure to plastics, pesticides, flame retardants, and industrial chemicals may contribute to metabolic risk—even in animals.

  
  

• Precautionary Measures: Simple lifestyle shifts—like reducing plastic use, avoiding canned foods, choosing glass or stainless containers, and filtering water—can lower obesogen load.

  
  

• Policy & Advocacy: Push for updated chemical regulations that incorporate developmental sensitivity and generational effects—shifting from treatment toward prevention.

  
  

• Follow the Money: As veterinarians, scientists, and citizens, we must examine where research funding, marketing strategies, and regulatory lobbying come from. Transparency matters.

Rick’s Commentary

Bruce Blumberg’s research reframes obesity not just as a lifestyle issue but as a consequence of chemical exposures embedded in modern life.

Obesogens challenge us to rethink prevention, to integrate environmental factors into metabolic health, and to confront a system where some companies profit both from the cause and the cure.

If we truly want to address obesity—whether in humans or animals—we must look beyond the medications and into the plastic, the packaging, and the policies that shape health before a single calorie is consumed.

Recommended Source

Endocrine disrupters as obesogens https://pmc.ncbi.nlm.nih.gov/articles/PMC2713042/

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