Diabetes 2 Winter Hibernation Gone Astray and Diabetes 1 Summer Drought gone astray.. A SEASONAL EXPLANATION FOR DIABETES.
HIBERNATION DIABETES 2
With weight gain the body interprets this as the person heading for deep freezing winter where food will become scarce or unavailable (as with hibernation). Fat stores have to increase to carry him or her through the deep freeze, and what is happening in the plant world exactly matches that of the animal world. The plants provide precisely the right nutrients for the animals for that time of year and vice versa, the bowel flora of the animal's faeces, the composition of it's urine is precisely right for the plants. More nitrogen is locked up in the animals and more carbon is locked up in the plants and I'd reckon that the carbon:nitrogen ratio shifts between the seasons. More muscle mass in in the animal relative to fat in summer means more nitrogen to carbon in summer. Have to think about the plants, eg lignin.
Coming on a winter freeze he or she has to conserve energy by being less active, as is taking place throughout the entire forest, hence the shift in the number of insulin receptors from muscle cells to fat cells. (peripheral resistance to insulin in diabetes 2) The simple sugar sucrose in the berries and other fruits, necessary for fast reactions in summer has been replaced by an increase in the more slowly ingested starch. The glucose from the breakdown of starch is being increasingly converted to fat in fat cells and of course liver (fatty liver) rather than glycogen in muscle cells as they atrophy. Soon glucose, even from starch, won't be available or needed as the animal ceases eating and goes into ketosis and ketones will replace glucose as a fuel in so much of the animals tissue. What glucose the animal must have will come from gluconeogenesis, a part of going into ketosis in this context. Gluconeogenesis is the process whereby the liver MAKES glucose from the bodies own tissues, from 3 sources, lactic acid from the muscle glycogen (although that dissapears one starch stops being eaten), amino acids from from the breakdown of muscle protein, glycerol (glycerine) and fatty acids. Fatty acids from fat cells are broken down to ketones, some of which drive what is called the TCA cycle to provide the energy to drive gluconeogenesis and the rest are exported from the liver as fuel for most of the body as cells adapt to ketones. There are 3 different ketones, acetone, betahydroxybutyic acid and acetoacetic acid. When muscle glycogen runs out and to conserve muscle protein for essentials, then fatty acids and glycerol from fat cells become the sole source of raw material for gluconeogenesis. Cortisol is the hormone responsible for mobilising the muscle protein as well as fatty acids and glycerol from fat cells.
Thus the big muscles developed by the spring and summer activity are now atrophying as big muscles are no longer needed. As the large fat deposits are needed for fuel during the long fast so the muscles act as a reservoir of amino acids for cell repair, peptide hormone synthesis etc., although this will be minimal as the animal lies asleep, only rousing every now and then. Bone breaks down to provide not just calcium and phosphate, but all of the minerals the body needs, copper, zinc, selenium etc The hibernating animal stops urinating to conserve water. I think hibernating animals can store urea, the nitrogen of protein breakdown, in a crystal form, so a range of other things, eg uric acid, can probably be stored in a crystaline form for recycling as the animal COMES OUT of hibernation.
NOW TO THE POINT.
There is NO FUEL STORAGE going on at all in the hibernating animal. Thus there is no point in hanging onto a lot of cells in organs involved in stimulating any sort of storage, e.g. beta cells of the pancreas and cells of the thyroid. So why not get rid of them as they are just wasting fuel AND CAN BE RECYCLED. Apoptosis or cell suicide is the shot as everything in the cell is broken down to bite sized chunks for other cells to use. Their is no energy wasting inflammatory reaction with apoptosis. Enter auto-immune 'disease', only a disease in the concrete jungle which bears absolutely no resemblance to pristine wilderness. (DIABETES IN THE CONCRETE JUNGLE)
I first focussed on this idea when I read about gene clusters DR3 and DR4? associated with auto immune disease. I had already built a model of an animal in the wild of a temperate zone or a human in a temperate zone and these gene clusters were found in people from Central Europe who had diabetes 1 They were active in the pancreas and thyroid, both endocrine organs. Temperate zone equals big swings in temperature, snow in the winter and hot in the summer.
SUMMER DROUGHT DIABETES 1
Then I began to focus on the advantages of trimming these organs with the sudden onset of a life threatening drought in summer when the animal did NOT have big deposits of fat on it's body, but did have big muscles. THE REVERSE OF WINTER. If the mechanism of storage didn't fight with those of release from storage, then the transition to ketosis would be much quicker, easier and smoother. Very little or no adrenalin needed to initiate gluconeogenesis, just cortisol, so no water wasting sweat and energy wasting anxiety from hunger. The animal would quickly become soporific, go lay in the shade under a tree and sleep a lot of the time. Sort of summer hibernation.
So Diabetes 1 could be this summer model gone awry in the concrete jungle. I believe that beta cells of the pancreas are vulnerable to big swings in osmotic pressure caused by big swings in blood sugar, for the same reason that neurons of the brain are vulnerable i.e. they don't have insulin receptors on them and thus don't store glycogen. I have never been able to confirm this idea, but I can't see how they can and regulate blood sugar if they store it as glycogen. They wouldn't produce insulin yet have insulin receptors on them Doesn't add up. Loss of weight in pre-diabetic 1 equals drought adaption but with lots of sugar thrown in to initiate reactive hypoglycaemia plus expression of gene clusters DR3 and DR4. Thus auto immune 'attack', is perhaps apoptosis PLUS necrotic cell death and inflammatory immune reaction. Dunno. All impure speculation of course.
THE CURE
Ok, if the hibernating animal provides a model for Diabetes 2 then it MUST BE REVERSABLE, ie CURABLE, following the path of the animal coming OUT of hibernation. The right ketone diet modelled on what this animal eats once it resumes eating. That's next, as soon as I clean it up.
Saving 
