This is perhaps the closest to an admission we will get from modern science that oxidation of fat is what creates insulin resistance and leads to diseases like type 2 diabetes. This is the first time I have actually seen an admission by mainstream science of the causal link between burning fat and insulin resistance. Usually, what I had seen so far presented things the other way around - i.e. people somehow mysteriously became insulin resistant (genetics is often said to be involved) and after that they preferentially burn fat. Other than the obvious "Ray Peat is right again" and fat oxidation is what directly causes insulin resistance, the only other mechanism I can see for the hibernation causing insulin resistance is the sharp rise in serotonin, which is what allows for the hibernation to set in. Either way, I think this is a very good finding and probably something mainstream medicine will promptly ignore.
My only question is - if insulin resistance in bears is important enough to be studied then why aren't the same studies performed in humans? How difficult / expensive would it be to get 3 groups (1 control, one on fat oxidation diet, one on sugar oxidation diet) and determine which group gets insulin resistant in couple of months?
Anyone care to offer a reason why this experiment has not been done in humans? Or maybe it has been done already?
http://www.newscientist.com/article/dn2 ... FL0DBa0eZQ
"...As the bears put on weight in preparation for the winter, they responded normally to insulin – which prevents the breakdown of fatty tissue. But during hibernation, insulin effectively stopped working. That is a symptom in people with type 2 diabetes, in which high fat levels in the blood induce insulin resistance. This insulin resistance allows the bears to break down their fat stores throughout hibernation, when they will not eat, drink or defecate for up to seven months. They survive on their fat before waking up, and begin to respond normally to insulin when they start to feed again.
http://www.npr.org/blogs/health/2014/08 ... like-we-do
"...Corbit and his team then looked at how the bears responded to insulin at other points during the year — before hibernation, during hibernation and after hibernation. They found that the bears were actually most sensitive to insulin just before hibernation, when they were at their largest. During hibernation, they became extremely resistant to insulin. Then after hibernation, they became sensitive to insulin again."
My only question is - if insulin resistance in bears is important enough to be studied then why aren't the same studies performed in humans? How difficult / expensive would it be to get 3 groups (1 control, one on fat oxidation diet, one on sugar oxidation diet) and determine which group gets insulin resistant in couple of months?
Anyone care to offer a reason why this experiment has not been done in humans? Or maybe it has been done already?
http://www.newscientist.com/article/dn2 ... FL0DBa0eZQ
"...As the bears put on weight in preparation for the winter, they responded normally to insulin – which prevents the breakdown of fatty tissue. But during hibernation, insulin effectively stopped working. That is a symptom in people with type 2 diabetes, in which high fat levels in the blood induce insulin resistance. This insulin resistance allows the bears to break down their fat stores throughout hibernation, when they will not eat, drink or defecate for up to seven months. They survive on their fat before waking up, and begin to respond normally to insulin when they start to feed again.
http://www.npr.org/blogs/health/2014/08 ... like-we-do
"...Corbit and his team then looked at how the bears responded to insulin at other points during the year — before hibernation, during hibernation and after hibernation. They found that the bears were actually most sensitive to insulin just before hibernation, when they were at their largest. During hibernation, they became extremely resistant to insulin. Then after hibernation, they became sensitive to insulin again."
