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As it turns out, abdominal fat plays both chicken and egg when it comes to its causal relationship with diabetes; each problem encourages the other.
Researchers have outlined several ways in which abdominal fat (and general obesity) poses challenges to the body’s production and processing of insulin.
The good news is that the vast majority of these issues are at least partially reversible.
The connections between abdominal weight, insulin, fatty acids, and inflammatory compounds (among other factors) are numerous and often complex. This synopsis will at least outline these relationships.
Before diving into the specifics, it’s important to capture just how strong this correlation between body weight and diabetes really is.
This systematic review from the University of Birmingham (UK) reports a “strong association between measures reflecting abdominal obesity and the incidence of type 2 diabetes” with a pooled odds ratio of 2.14.
This means that diabetics were 2.14 times more likely to display abdominal obesity than non-diabetics.
As far as the measures in mention, the Birmingham researchers and many other studies use waist circumference, waist-hip ratio, CT scans (for abdominal fat), and a few other factors to correlate weight status with diabetes or other diseases.
While this simple correlation—“x causes y”—is helpful for expressing the urgency of the situation, it doesn’t exactly dive into specifics.
In other words, what’s happening here?
What is it about abdominal fat that worsens diabetes?
Let’s go down the list.
The connection between systemic inflammation and diabetes risk is largely agreed upon among experts.
According to this article from the R&D department of the Airedale NHS Foundation Trust (UK), “Visceral (gut) fat deposits are associated with the development of adipose cells that are enlarged and dysfunctional (adiposopathy, or ‘sick fat’). Dysfunctional adipose tissue secretes pro-inflammatory biomarkers including prostaglandins, C-reactive protein (CRP), and cytokines such as interleukins (e.g. interleukin-6), tumour necrosis factor alpha (TNF-α), and leptin.”
Here’s the translation:
One cytokine in particular that has garnered a reputation for jacking up diabetes rates is interleukin-6.
The reason this particular compound is so troubling is that such a high percentage of its overall production comes from belly fat.
According to this academic article from the Diabetes Clinic of Cyprus, “Adipose (fat) tissue produces approximately 15-35% of total human circulating levels of IL-6,” and “Visceral adipose tissue produces three to four times more IL-6 than subcutaneous adipose tissue.”
The study goes on to solidly correlate interleukin-6 and some of its equally nefarious cousins (interleukins 1, 18, and 8) with type 2 diabetes onset.
Thankfully, the authors noted that plasma levels of interleukin 6 steadily declined with weight loss, a silver lining we’ll get to in a moment.
Perhaps the most direct link between body fat (regardless of where/how it is distributed) and insulin resistance is the fact that circulating fatty acids raise the amount of insulin required to control elevations in blood sugar.
It’s not important for today’s purposes to dive into the expert-level biochemistry; the point is that insulin cannot ferry glucose into muscle tissue as effectively when fatty acids are too abundant.
So far, most of the findings we’ve reviewed have hinted at abdominal fat’s roles in type 2 diabetes onset, but that doesn’t mean type 1 diabetics get off scot-free.
Yes, type 1 diabetes normally involves a lack of insulin production from an early age, not a trained resistance to insulin, but abdominal obesity can absolutely worsen the prognosis for type 1 diabetics.
For example, this finding authored by gastroenterology and hepatology experts in Poland references how patients with type 1 diabetes still demonstrate greater insulin resistance with weight gain; patients of lower weight required lower insulin doses.
Moreover, the above effects of adipose tissue still hold.
Even if blood sugar is well-controlled with insulin, continuing to gain weight will make this harder and harder.
The takeaway is this: abdominal weight gain and/or obesity may be less likely to cause type 1 diabetes, but it can complicate it just as effectively as it does type 2 diabetes.
We can say unequivocally that smart and safe dieting and exercise programs will always help with insulin tolerance, weight, and general health.
No matter how busy you are, how old you are, and how much you weigh, if you’re breathing, you can exercise.
In skilled nursing facilities and retirement homes across the country, there are 100-year-old tenants riding stationary bikes at this very moment.
It’s our want to clamor for a pill or a gadget that will do the hard work for us, but there simply is no substitute for exercise when it comes to addressing insulin resistance, losing weight, and improving physical health in just about every way.
Of equal importance is the role of nutrition in preventing and/or managing diabetes.
Choose safer sweets, load up on fiber, get the macronutrients in, and take control of your situation once again.
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