I'll post my current understanding of the processes involved and I'd appreciate any input you guys may have:
As far as I can tell, somewhere in our primate evolution, we lost the ability to synthesize vitamin C, and as a result, we also lost the ability to synthesize uricase, the enzyme that breaks down uric acid. 1 Why the former occurred, I couldn't tell you, but it was perhaps advantageous to a greater extent to preserve that glucose for a brain that was ever-increasing in size. The latter was likely lost in response to the former, since uric acid and vitamin c have overlapping roles as a sort of general purpose antioxidant. When vitamin C rises, uric acid falls. 2
The significance of this for us is that if we do something that spikes uric acid outside of its optimal range, like eat a lot of fructose, it will have too much of an antioxidant effect and will create a "reductive stress" if you will. Too much of an oxidant creates an oxidative stress, while too much of an antioxidant has the opposite effect. It exerts its effect where it shouldn't, so instead of effectively coping with the reactive oxygen species in our blood, uric acid oversteps its boundaries and reduces things that we don't want reduced, i.e. endothelial nitric oxide. Insulin resistance arises because insulin needs nitric oxide for glucose uptake. 3
So the question is, once a person has NIDDM, what do they do to correct it? They find themselves in a situation where glucose is pooling in the blood in response to a starchy meal, but is just sitting there because insulin can't shuttle it into the liver and muscle glycogen and activity isn't sufficient to oxidize all of it in muscle mitochondria. It seems to me that, at this stage at least, with regard to diet, any producer of uric acid should be eliminated or at least limited. Obviously fructose is non-essential so it gets pitched first. Any yeast needs to go as it spikes uric acid as well. Even purine-rich meat should probably be limited for a while until things get under control. Glucose is now becoming a fairly potent poison and glycating proteins as it pools in the blood, so low carb is the obvious choice. They then should be eating a diet that is high in fats that are readily converted into ketones like coconut oil along with a nominal amount of meat and some non-starchy vegetables if desired. That should take care of most of the diet end of things.
I would argue that if that's all you did, it would take much longer than necessary in order to bring about a full correction. The answer to this problem also happens to be the answer to the problem of lowering triglycerides (that are probably elevated here as well) and reducing fat mass (which is likely also elevated), namely a high volume of low intensity exercise that is performed in the fasted state. In practice, this means walking as much as possible before every meal. The glucose pool needs to be reduced rapidly via oxidation in the muscle mitochondria. I see no reason why walking in this way wouldn't be sufficient for correcting insulin sensitivity completely and thus reversing the disease. 4
If this continued, there should be an eventual adaptation back toward lipids as the primary energy substrate in muscle mitochondria, and thus no longer a need for starch avoidance, provided that 1) activity continued in the fasted state and 2) serum uric acid levels weren't allowed once again to climb and interfere with endothelial function as it relates to insulin sensitivity. When this insulin sensitivity is restored, the transient blood glucose spikes that would occur subsequent to a meal containing starch would be properly met with an insulin response that shuttled this glucose into liver and muscle glycogen. There would be a healing period that would clearly depend on the duration and severity of the disease, but I don't see why most cases couldn't be corrected in a matter of months if this protocol is followed. This is especially so since walking has been shown to increase mitochondrial density, and thus improve the capacity for the individual to oxidize fat or glucose as needed. 5
Where this would fail obviously is if individuals who have endured this disease are left with some kind of permanent inability to properly handle carbohydrates. I'm not familiar with any such thing, so if you are aware of a compelling reason why starch could never be added back into the diet if desired, I would be very interested to hear what that is.
asked byTravis_Culp (39831)
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on September 23, 2011
at 03:50 AM
I see no reason why walking in this way wouldn't be sufficient for correcting insulin sensitivity completely and thus reversing the disease. 4
Actually there was a study done this year in UK which showed that recently-diagnosed, obese T2 diabetics who went on a 1200 cal diet was able to reverse the disease (google UK t2 diabetes reversal). The study is controversial but the medical establishment seems to be accepting the position that T2 diabetes, in certain cases, can be reversed. The study has been excoriated since 1200 / day is at starvation-level: i.e., it would be de facto ketogenic even if not low carb. Those successful tend to lose weight rapidly (as you would if you stick to 1200 cals) and rid themselves of the fat in their pancreas (fatty pancreas) and liver (fatty liver). What's intriguing is the possibility that the pancreatic beta cells may not have actually "died" when "burnt out" but may be revived by "shocking them out of their dormancy." We still do not know whether these beta cells are dead or lost their functionality temporarily.
What's intriguing is that there are doctors in Asia and India and other countries who do not get published in medical journals ... who claim to have cured T2 diabetes by restoring insulin sensitivity this way: through an extreme diet and exercise... many believe in restricting animal fats (i.e., satruated fat), overall calories, and all sugary snacks. These are anecdotal accounts but I tend to believe them because I've been somewhat successful in restoring my own insulin sensitivity.
It's counterintuitive and finding a right metabolic pathway that induces insulin sensitivity might be within reach. The problem is that these pathways are black boxes and the only way to figure out is to reverse engineer: find someone who reversed his insulin resistance, study what he did, repeat in more T2s through clinical trials, see if you can repeat it, then theorize about what could be happening, and you still can't be sure that the mechanism is actually what happened, not something else.