Can Endometriosis Cause Weight Gain?

If you live with endometriosis or adenomyosis, you may feel like your body has changed—especially around your abdomen. Many patients describe “endo belly,” swelling that comes and goes, and a frustrating sense that they’re gaining weight even when they haven’t changed what they eat.

So, can endometriosis cause weight gain? The most honest evidence-based answer is: endometriosis isn’t proven to directly “cause” fat gain in the way some hormonal conditions can—but it can absolutely contribute to body changes that look and feel like weight gain, and it may be linked to metabolic risk factors in some people.

This article draws from multiple recent studies—population studies, biomarker research, and microbiome and nutrition research—to explain what we know (and what we don’t) about endometriosis, weight gain, and metabolism.

First: “Weight gain” can mean different things

Many people mean “weight gain” when they’re experiencing one (or several) of these:

• Fluid retention and bloating (often cyclical)
• Constipation and GI distension (sometimes IBS-like symptoms)
• Reduced activity due to pain and fatigue
• Changes in appetite, cravings, or stress eating
• Actual fat gain over months/years

Endometriosis can plausibly affect the first four—even if the fifth is not consistently proven as a direct effect.

Endometriosis can cause “endo belly” (bloating) that mimics weight gain

One of the most consistent patient experiences—supported indirectly by research—is that endometriosis often comes with digestive symptoms. A large recent review of “microbiota insights” in endometriosis notes that digestive symptoms are very common and can occur even when there are no visible bowel lesions. That matters because it supports what many patients already know: GI symptoms can be a major part of endometriosis, not just an “extra” problem.

Research linking endometriosis to the gut microbiome is still evolving and human studies don’t agree on one specific “endometriosis microbiome.” But animal and mechanistic work summarized in recent reviews suggests that gut changes and endometriosis may influence each other, and that microbiome-related metabolites (like butyrate) may affect inflammation and lesion biology in models. For patients, the practical takeaway is simpler: bloating and bowel changes are real, common, and not “in your head.” They can change your waistline day to day without reflecting fat gain.

Is endometriosis linked to metabolism or cardiometabolic risk?

This is where the evidence has gotten more interesting in the last couple of years.

Population studies suggest higher odds of “metabolic syndrome” markers in endometriosis

A population-based study from Tehran found that women with endometriosis had higher odds of metabolic syndrome (a cluster including waist size, blood pressure, blood sugar, HDL, triglycerides) compared with women without endometriosis, even after adjusting for several lifestyle factors. The strongest signals were higher odds of low HDL (“good cholesterol”) and high waist circumference.

Meanwhile, U.S. NHANES-based studies have reported associations between endometriosis history and composite metabolic risk scores such as the cardiometabolic index (which combines triglycerides, HDL, and waist-to-height ratio). In those analyses, triglycerides often appear as one of the clearer individual components associated with endometriosis history.

A separate NHANES analysis using lipid accumulation product (a marker combining waist circumference and triglycerides) also found higher values were linked with higher odds of reporting endometriosis.

What this does—and doesn’t—mean

These studies suggest that some people with endometriosis may be more likely to have certain metabolic risk patterns, especially involving central body measures and lipids. But most of this evidence is cross-sectional, meaning:

• It cannot prove endometriosis causes metabolic changes.
• It cannot prove metabolic changes cause endometriosis.
• Shared drivers (inflammation, hormones, medications, sleep disruption, activity limits, genetics) could influence both.

Still, if you’re asking “could endometriosis affect my metabolism?” the best current answer is: it might, indirectly, and it may be connected to cardiometabolic risk for some patients.

Inflammation, fat tissue signals, and why the story is complicated

Endometriosis is increasingly described in modern reviews as a systemic inflammatory and immune-mediated condition, not only a local pelvic disease. That framing matters because chronic inflammation can interact with appetite regulation, fatigue, sleep, and metabolic health.

One example: a 2024 review on adiponectin (a hormone-like protein produced by fat tissue that is often linked to insulin sensitivity and inflammation) describes mixed clinical findings, but a cited meta-analysis suggests people with endometriosis may have lower adiponectin and higher leptin compared with controls. Importantly, that same evidence did not show a clear relationship between adiponectin and disease severity—so this is not a diagnostic tool, and not a simple “low adiponectin causes endometriosis” story. It’s more a clue that metabolism-related signaling and inflammation overlap with endometriosis biology.

The “mental pathway”: pain, stress, sleep, and eating patterns

Even without a direct metabolic effect, endometriosis can push the body toward weight changes through lived reality:

• Chronic pain can reduce daily movement and make exercise unpredictable.
• Fatigue can affect meal prep, cravings, and reliance on ultra-processed convenience foods.
• Stress and mood symptoms can change appetite and increase emotional eating.

This pathway is hard to measure, but it’s clinically believable and consistent with broader chronic pain research: when pain is persistent, the whole system (sleep, stress hormones, activity, eating patterns) can shift.

In addition, some endometriosis treatments can affect weight-related factors:

• Hormonal treatments may change appetite, water retention, and body composition differently person to person.
• Some people experience mood changes on hormonal contraception; recent reviews of oral contraceptives and psychiatric side effects highlight that mental health effects are possible for a subset, which can indirectly influence eating and activity.

If you feel your eating habits changed after your symptoms worsened—or after starting a medication—this is a valid and important clinical discussion, not a willpower issue.

Does BMI predict symptoms or disease type?

Patients often hear confusing messages: “Endometriosis is associated with lower BMI” versus “Endometriosis and obesity go together.”

Part of the confusion is that research has looked at different things:

• Risk of being diagnosed
• Severity of symptoms
• Anatomical disease types
• Metabolic markers beyond BMI (waist measures, lipids)

A more recent clinical discussion in nutrition-focused literature argues that while older observational studies sometimes showed an “inverse” relationship between BMI and endometriosis diagnosis, this should not be interpreted as obesity being protective. Diagnosis patterns and bias can strongly influence what we see (for example: who gets referred, imaged, or offered laparoscopy).

In other words, BMI alone is a blunt tool. Two people can have the same BMI and very different inflammation, visceral fat, lipid profiles, and symptoms.

Can diet help with endometriosis-related “weight gain” or bloating?

Diet is not a cure, but it can be a meaningful symptom tool—especially for GI symptoms and inflammation-related flares.

A 2025 review on nutrition in endometriosis summarizes evidence that:

• Limiting trans fats and emphasizing anti-inflammatory fats (like omega-3s) is biologically plausible and sometimes supported by observational data.
• Antioxidant supplementation (vitamins C and E) showed pain improvement in at least one randomized trial over 8 weeks.
• Evidence on caffeine is mixed overall, with some signals only at higher intakes.

Another 2025 review focusing on medical nutrition therapy highlights that for people with endometriosis plus IBS-like symptoms, a structured low FODMAP approach may improve abdominal symptoms and quality of life in subgroups—suggesting that the biggest “body change” wins may come when diet is matched to symptom patterns rather than used as a one-size-fits-all plan.

There is also an ongoing randomized trial protocol testing a Mediterranean-pattern anti-inflammatory diet before IVF in endometriosis-related infertility; it’s notable because it measures not only fertility outcomes but also pain, quality of life, inflammation scores, and microbiome features—exactly the areas patients care about. Results aren’t available yet, but it signals where research is heading.

Practical takeaways (without blaming yourself)

If you’re worried about endometriosis and weight gain, consider reframing the question to: “What type of body change am I experiencing—and what are the likely drivers?”

Here are a few practical next steps to discuss with your clinician:

• Track waist changes + symptoms (pain, bowel habits, cycle timing) for 1–2 cycles to separate bloating patterns from true weight change.
• Ask whether it makes sense to screen metabolic health: lipids (HDL, triglycerides), A1c/glucose, blood pressure, waist circumference—especially if you have a family history or other risk factors. Population studies suggest this is relevant for some people with endometriosis.
• If GI symptoms dominate, ask about an IBS-style evaluation and whether a dietitian-supported low FODMAP trial is appropriate (rather than randomly cutting foods).
• If stress eating or mood changes are part of your story, consider treating that as a medical symptom: pain psychology, therapy, or medication changes can be part of endometriosis care.
• Review your medications (hormonal and non-hormonal) with the question: “Could this be affecting appetite, water retention, or mood?”

What we still don’t know (and why your experience can differ from someone else’s)

• We don’t yet have strong prospective evidence that endometriosis directly causes long-term fat gain.
• Microbiome findings in humans are inconsistent, and there’s no validated “endometriosis microbiome test” for clinical use.
• Biomarkers tied to metabolism (like adiponectin) show mixed results and are not ready for diagnosis or treatment decisions.
• Endometriosis is heterogeneous: lesion type, comorbid adenomyosis, pain sensitization, sleep disruption, medications, and genetics can all change the “weight story.”

So if you feel your body is changing, you’re not imagining it—but the cause may be a mix of bloating, inflammation, activity limits, sleep/stress physiology, and sometimes metabolic risk factors, rather than a simple direct effect of endometriosis on fat storage.

The most helpful mindset is “whole-body endometriosis care”: managing pelvic disease and supporting gut health, mental health, sleep, and metabolic screening when appropriate.