Belly fat and chronic pain: the waistline plot thickens

Not all fat is unhealthy. But when it does cause health problems … it also drives chronic pain.

And it’s mostly the belly fat that does this — the visceral fat tucked around your organs like foam packing peanuts.

Some people with high body mass index are just fine, while others with a low BMI are still at risk — the “obesity paradox” — usually because they have too much belly fat specifically.

Not all fat is unhealthy. But when it is unhealthy … it is a risk factor for chronic pain.

Like any other tissue, fat is complex and lively stuff, and can be healthy or unhealthy depending on genes, life, and midnight snacks. The harder you push your luck by consuming too many calories, the more likely you are to trigger trouble. Extra visceral fat is the most likely to be stressed and oozing inflammatory signals … which drags the liver into the equation, because it’s right there … which in turn throws the whole system off kilter.

And so belly fat is strongly linked to poor health, including roughly double the risk of chronic pain, even from musculoskeletal conditions like arthritis and tendinopathy. Obesity is more metabolically relevant to pain than biomechanically.

These facts have been coming into focus over the years, and I’ve dipped a toe into this topic a few times before — like that 2024 paper about the extremely impressive effects of semaglutide (Ozempic) on arthritis (one of the best “good news” stories in years).

“Belly fat hurts” is not a complicated bottom line, but it is resting on a bunch of science. Today’s post breaks down two new papers that add more to that foundation.

Obesity as a metabolic disease … but not in everyone

The first paper, by Matthias Blüher, is a state-of-the-science overview of obesity complications. It’s got just one author, and it’s in a minor journal, but it harmonizes well with other recent papers like Busetto et al. in Nature Medicine, a much more prestigious journal — and Blüher focuses more on the biological story. This is just a straight translation of Bluher’s technical overview into something much shorter and more readable for patients and clinicians.

Blüher M. An overview of obesity-related complications: The epidemiological evidence linking body weight and other markers of obesity to adverse health outcomes. Diabetes Obes Metab. 2025 Apr;27 Suppl 2(Suppl 2):3–19. PubMed 40069923 ❐ PainSci Bibliography 49319 ❐

The most important development over the last couple of decades is that we now know that fat mass alone does not explain why obesity is sometimes dangerous — because fat can be metabolically healthy or unhealthy.

It’s not (just) the quantity, it’s the quality, according to Blüher.

Consider two people, both carrying quite a few extra pounds, but one of them is fine, and the other is not. We’re not used to thinking about obesity like that.

Unhealthy fat cells are themselves “fat,” stretched to the limit of their storage capacity, and stressed by it! And so they start to struggle, just like any tissue failing under strain: they bloat, get hypoxic, leak fatty acids, summon immune cells (inflamed), and more. This reminds me of how some people’s tendons get all cruddy and hurty under strain, while others don’t. But tendinitis doesn’t cause trouble anywhere else, and fat definitely does.

Abdominal fat is particularly dangerous because those fat cells tend to get overloaded and stressed, and they are metabolically hyperactive and anatomically positioned to do more harm. They are plugged right into vital organs, directly connected to them by plumbing: the venous drainage for the visceral fat drains into the portal vein, which goes straight to the liver, which then also gets inflamed and triggers a cascade of systemic problems, like insulin resistance and vascular disease at the very least.

Whether fat goes bad depends on how well it can adapt to energy surplus over time. Some people’s underskin fat can keep making new adipocytes and new capillaries, safely storing surplus energy. Others can’t, and run out of that capacity sooner, so other fat cells — chiefly the visceral ones, the main backup system — get into trouble sooner.

The capacity to adapt — whether the subcutaneous is shaped by genetics, sex hormones, and early-life influences. A bunch of stuff out of our control.

We do have some control, however. The thing to do with “bad fat” is to get rid of it — notoriously easier said than done, of course, but diet, exercise, surgery, and medications are all effective to varying degrees. And substantial weight loss can eliminate the danger and even reverse damage already done.

Warning: Obviously some pathology makes weight loss unusually difficult, impossible, or irrelevant. For instance, ascites (fluid in the abdomen) mimics the appearance of visceral fat, making any attempt to lose weight a dangerous, futile distraction.

Although all of this is on good scientific footing, it’s all quite new still. BMI continues to be used as the main basis for diagnosing obesity, even in obesity clinics. Recent formal redefinitions of obesity diagnosis that go beyond BMI exist precisely because doctors still lean too hard on BMI.

Visceral fat is guilty by association with pain

BMI and waist circumference can’t tell visceral fat from fat under your skin, and even less so with age. A newer index — the Metabolic Score for Visceral Fat (METS-VF) — is designed to score visceral fatness based on fasting glucose, triglycerides, HDL-C, BMI, waist-to-height ratio, age, sex, and probably how your pants fit. So Zhu et al. tested METS-VF: does it predict greater odds of chronic pain? Better than BMI? Does systemic inflammation (help) explain any association?

Zhu J, Wang Y, Yu G, et al. Association between metabolic score for visceral fat and chronic pain: a cross-sectional analysis of NHANES 1999-2004. Front Nutr. 2025 May 14;12:1545774. PubMed 40444245 ❐ PainSci Bibliography 49318 ❐

They had data on almost 6000 people — old data, practically vintage (from the early 2000s). About 860 reported chronic pain, and they did have more belly fat: more METS-VF, bigger BMI, wider waists.

And more belly fat (top quartile) had nearly double the odds of chronic pain. That’s nothing like the 4× greater risk of diabetes with obesity, or the 10× risk of mesothelioma from asbestos exposure. But it is enough to take seriously: it’s in the same league as the secondhand smoke and lung cancer link, or poor sleep and hypertension, or sedentariness and mortality.

The rest of the results were disappointing:

• The fancy METS-VF score had no more power to predict pain than BMI and waist size, with the exception of a slight edge with older people.
• Belly fat isn’t particularly good at predicting who will get chronic pain, however it’s measured: somewhat better than random chance, but also far from clinically powerful. It’s useful in research with big groups, but not as a diagnostic test for individuals.
• The link between belly fat and pain was not clearly correlated with inflammation. This is cross-sectional (slice of time) data, so it can’t tell us how the link works, but you can sometimes find “hints” this way. Not this time, though — which is not really a surprise when you’ve only got the roughest possible measure of inflammation (C-reactive protein, CRP).

Despite many advances, it’s still early days on this topic, and Zhu et al. got us closer with a lot of numbers and some good number-crunching. They did confirm a strong association between belly fat and pain — that’s the main thing. It’s hard to get much more out of old cross-sectional data on self-reported pain and CRP as the only biomarker for inflammation.

But this fat-pain link is solidly in “good to know” territory.

I’ve already mixed these citations into my plantar fasciitis book, where they are surprisingly relevant (see also evidence like De Luca et al. that links obesity to tendinopathy specifically, not just any kind of chronic pain). People with bilateral plantar fasciitis tend to struggle the most, and that’s likely because there’s a systemic health issue that affects both feet — like both mechanical and metabolic strain from obesity. The plantar fasciitis book has been updated several times recently and is in particularly good shape right now.

Then I’ll also add them to my article about systemic vulnerability to chronic pain, and subtle systemic inflammation. And then several more books!