In mammals, is insulin resistance/type 2 diabetes always a bad thing? Or might it serve a purpose in mammalian biology? Let’s explore.
What causes the body to become insulin resistant? Absence of light and cold climates. If you don’t believe me, get a glucometer and monitor your blood sugar levels pre and post consumption of 50g of sugar mid day, out in the sun. Then try consuming 50g of sugar in the evening when the sun has fully set and measure again. Take note of: 1) peak blood sugar values, and 2) time for blood sugar to return to baseline. The reason for this is because the pancreas is an organ that is active during the day in light. Pancreatic activity decreases in the evening to rest for the next day.
Every mammal becomes insulin resistant in the winter time. It begins at the end of summer/beginning of autumn when light cycles shorten very quickly, and temperatures fall. Why might this be beneficial rather than detrimental to animals? Because insulin resistance leads to high blood sugar, and easy fat gain when carbohydrates are consumed which are still abundantly available in autumn. How can this be a good thing? 1) High sugar in the blood acts as anti-freeze and signals hibernation and 2) When winter hits, our only source of fuel is fat. Insulin resistance essentially shuts down glucose metabolism for the winter in favor of fat burning.
After successfully surviving the winter, the excess fat accumulated from autumn is gone, and blood sugar levels are low, essentially reversing the insulin resistance and obesity, and turning the glucose metabolism back on for summer.
Why have doctors failed to understand this mechanism in modern humans? If we all become insulin resistant in the autumn, and continue to fuel our bodies with carbohydrates throughout winter, might this be the reason we develop type 2 diabetes? Knowing this, can’t we cure type 2 diabetes, and/or prevent it from ever occuring? Yes we can.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282240
https://www.ncbi.nlm.nih.gov/pubmed/10456206
https://www.ncbi.nlm.nih.gov/pubmed/6350027
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3854349
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