diabetes may not have a single origin story—it may have two
For decades, medicine has treated Type 2 diabetes as a single condition with a single story — yet the human body, it turns out, may tell two. Researchers at Concordia University have found that men and women accumulate and expand fat tissue through fundamentally different mechanisms, and that these differences may trace distinct biological pathways toward the same disease. The finding invites a quiet but consequential rethinking: that what we call one epidemic may in fact be two, bound together by name but divergent in origin.
- Type 2 diabetes has grown from 108 million cases in 1980 to 422 million by 2014, yet medicine still cannot fully explain why excess weight tips some people into disease and spares others.
- Men accumulate fat around their organs while women store it beneath the skin — a difference that sets off entirely separate cellular chain reactions, each with its own inflammatory and hormonal logic.
- Fat cells themselves behave differently by sex: men's cells swell larger, women's cells multiply in number, and women's risk surges after menopause when estrogen's protective influence fades.
- A review of nearly 200 scientific papers by Kerri Delaney and Sylvia Santosa at Concordia University found cellular evidence suggesting visceral fat drives diabetes in men while subcutaneous fat drives it in women.
- Current treatment protocols apply the same medications and lifestyle guidance to all patients regardless of sex — an approach that may be leaving real therapeutic precision on the table.
Type 2 diabetes is one of the defining health crises of our era, growing from 108 million diagnoses in 1980 to 422 million by 2014. Yet despite its scale, medicine has never fully resolved a central mystery: why does excess weight push some people into disease while others remain unaffected? Two researchers at Concordia University set out to examine one compelling theory — that where fat is stored in the body may be the decisive variable.
PhD candidate Kerri Delaney and associate professor Sylvia Santosa reviewed nearly 200 scientific papers, searching for patterns in how fat tissue behaves differently in men and women. What they found, published in Obesity Reviews, suggests that diabetes may not have a single origin — it may have two. Men tend to accumulate abdominal fat around their organs, known as visceral fat, while women deposit it just beneath the skin as subcutaneous fat. These aren't merely anatomical curiosities: the two fat types expand through different mechanisms, interact differently with immune and inflammatory systems, and carry different timelines of risk. Men become vulnerable earlier in life; women's risk accelerates after menopause, when estrogen's protective role disappears.
At the cellular level, the researchers found observable differences in immune cells, hormones, and signaling patterns that appeared to align with their hypothesis — visceral fat expansion driving diabetes in men, subcutaneous expansion driving it in women. The practical stakes are significant. Medicine currently prescribes the same treatments to all diabetes patients regardless of sex, but if the disease originates through different biological pathways, then tailoring medications to match those pathways could meaningfully improve outcomes. The research doesn't yet offer that clinical precision, but it points toward a future where what we call one disease is understood as two related conditions that have long shared a name.
Type 2 diabetes has become a global epidemic. In 1980, roughly 108 million people carried the diagnosis. By 2014, that number had swelled to 422 million—a fourfold increase in just over three decades, with the sharpest climb happening in low- and middle-income countries. Yet despite how common the disease has become, medicine still lacks a complete picture of how it actually develops. Researchers know obesity and diabetes are linked, but the precise mechanism—why excess weight tips some people into disease and not others—remains elusive.
Two researchers at Concordia University decided to examine a specific theory: that the location where a person stores fat might be the key variable. Kerri Delaney, a PhD candidate, and Sylvia Santosa, an associate professor, combed through nearly 200 scientific papers looking for patterns in how fat tissue behaves at both the surface and cellular level, and how those behaviors might differ between men and women. Their work, published in the journal Obesity Reviews, suggests that diabetes may not have a single origin story—it may have two.
The human body is not neutral about where it deposits fat. Men and women store excess weight in fundamentally different places. When a man gains abdominal fat, much of it accumulates around his organs—what researchers call visceral fat. A woman's abdominal fat tends to settle just beneath the skin, known as subcutaneous fat. This distinction matters because the two types of fat appear to behave differently. They expand through different mechanisms. In men, fat cells grow larger. In women, fat cells multiply and increase in number. The tissues interact with the body's inflammatory and immune systems in distinct ways. And there is a temporal element: men become susceptible to diabetes earlier in life, while women's risk rises sharply after menopause, when the protective hormone estrogen disappears.
Delaney and Santosa hypothesized that these differences in fat storage and expansion might explain why diabetes develops through different pathways in each sex. They looked for evidence at the cellular level—examining immune cells, hormones, and cell signaling patterns in the microenvironments where fat tissue lives. What they found was suggestive: observable differences in how these cellular systems operate in men versus women, differences that seemed to align with the theory that visceral fat expansion drives diabetes risk in men, while subcutaneous fat expansion drives it in women.
The implications are practical. Currently, doctors treat Type 2 diabetes the same way in men and women. They prescribe the same medications, recommend the same lifestyle changes, follow the same protocols. But if the disease actually originates from different biological mechanisms in each sex, then the treatment approach might need to change too. Santosa points out that diabetes medications work through specific biological pathways. If those pathways differ between men and women, then tailoring which drugs get prescribed to which patients—based on their sex and how their particular fat tissue is behaving—could improve outcomes. The research does not yet provide that level of precision, but it points toward a future where medicine stops treating diabetes as a single disease and starts recognizing it as two related but distinct conditions that happen to share a name.
Citas Notables
The big question is, how do the different depots uniquely contribute to diabetes development, and is this contribution different in men and women?— Kerri Delaney, lead researcher
Currently, the treatment of diabetes is similar for men and women. If we understood the differences between them better, we could consider these mechanisms in recommending treatments based on how diabetes medications work.— Sylvia Santosa, associate professor
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Why does it matter where the fat is stored? Isn't excess weight excess weight?
Because the location changes how the fat tissue talks to the rest of the body. Visceral fat—the kind men tend to accumulate—sits right next to the organs and seems to trigger different inflammatory responses than subcutaneous fat, which is further from vital systems.
So you're saying men and women are literally developing the disease through different biological routes?
That's the hypothesis. The fat expands differently, the immune cells respond differently, the hormonal environment is different. It's the same disease name, but possibly different origins.
And menopause plays a role in this?
Yes. Estrogen appears to be protective in some way. When women lose it at menopause, their diabetes risk climbs. Men don't have that hormonal buffer, so they're vulnerable earlier.
If this is true, what changes in how doctors treat people?
Right now, everyone gets the same diabetes medication and the same advice. But if the underlying mechanism is different, you might prescribe differently. A drug that works well for visceral fat expansion might not be the best choice for subcutaneous fat expansion.
How confident are researchers in this theory?
They've reviewed nearly 200 papers and found cellular-level evidence that supports it. But they're careful to say more research is needed. This is a framework, not yet a clinical protocol.
What's the next step?
Probably more targeted studies in men and women separately, looking at how specific medications affect each type of fat tissue, and whether personalizing treatment based on sex actually improves outcomes.