A recent South Korean study of over 4,000 patients found something interesting about type 2 diabetes mellitus:
The researchers studied over four thousand people for ten years, some of whom developed type 2 diabetes during that time period. So now there are two groups of patients in the study: those who developed type 2 diabetes, and those who did not.
As the patients aged, the natural insulin in their systems was less effective over time, and this was true for everyone. But for those patients who did not develop diabetes, their bodies just cranked out more insulin. For the diabetics, their pancreases just went haywire instead.
This is important because most health articles you might have read (including all that dumb paleo stuff - I'm talking to you, Mr. One-Reader-Per-Month-Who-Comes-By-Way-Of-Mark's-Daily-Apple) emphasize the importance of increasing a body's insulin sensitivity by eating fewer carbohydrates. But while that may help, this new research suggests that the more important problem is not insulin resistance, but rather pancreatic malfunction.
Everyone experiences insulin resistance to some degree. Only diabetics experience reduced beta-cell functionality.
At least, that's my reading of it.
During 10 years of follow-up, 1093 (27%) of 4106 participants developed prediabetes and 498 (12%) participants developed diabetes. Compared with participants who remained NGT, those who progressed to diabetes had a lower IGI60 (unadjusted data 5.1 μU/mmol (95% CI 0.5 – 56.1) vs 7.9 μU/mmol (0.5 – 113.8); p < 0.0001) and lower ISI (unadjusted data 8.2 (2.6 – 26.0) vs 10.0 (3.2 – 31.6); p < 0.0001) at baseline. Participants who had NGT at 10 years showed a decrease in ISI (adjusted data 10.1 (9.9 – 10.3) vs 7.4 (7.3 – 7.6); p < 0.0001) but a compensatory increase in IGI60 (adjusted data 6.9 μU/mmol (6.5 – 7.2) vs 11.7 μU/mmol (11.2 – 12.1); p < 0.0001) compared with baseline. By contrast, participants who developed diabetes showed a decrease in ISI (adjusted data 8.4 (8.0 – 8.7) vs 3.0 (2.8 – 3.2); p < 0.0001) but no significant compensatory increase (p = 0.95) in IGI60. A genetic variant near the glucokinase gene (rs4607517) was significantly associated with progression to prediabetes or diabetes (hazard ratio 1.27, 1.16 – 1.38; p = 1.70 x 10 − 7).Okay, that's a lot of numbers and gibberish for the lay-person, so let me offer one interpretation of the findings.
The researchers studied over four thousand people for ten years, some of whom developed type 2 diabetes during that time period. So now there are two groups of patients in the study: those who developed type 2 diabetes, and those who did not.
As the patients aged, the natural insulin in their systems was less effective over time, and this was true for everyone. But for those patients who did not develop diabetes, their bodies just cranked out more insulin. For the diabetics, their pancreases just went haywire instead.
This is important because most health articles you might have read (including all that dumb paleo stuff - I'm talking to you, Mr. One-Reader-Per-Month-Who-Comes-By-Way-Of-Mark's-Daily-Apple) emphasize the importance of increasing a body's insulin sensitivity by eating fewer carbohydrates. But while that may help, this new research suggests that the more important problem is not insulin resistance, but rather pancreatic malfunction.
Everyone experiences insulin resistance to some degree. Only diabetics experience reduced beta-cell functionality.
At least, that's my reading of it.
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