For easier reading here is a science media report that doesn’t mess up too badly:
There is probably more to talk about with this in view of Type 2 diabetes and obesity?
One thing I was wondering was about a “window” of metabolic grace where a Type 2 diabetic exhausts their pancreatic beta cells, but does not destroy them, then loses body fat from diabetic disease to re-instate insulin sensitivity, which allows a pancreatic re-boot for better ongoing health. You can tell I am typing this without having thought it through.
No Franko, that would be humans or still just human dependent on usage. Adverb or noun. I know you’ve spoken of foraging recently, you haven’t been making cane toad stew have you? Humen is a specific section of the Pearl River is the only reference I could find unless this is a Bogan adaptation of English I’m unaware of.
This will further aggravate feminists Franko, I don’t recommend this language adaptation.
I’ve been eating fungi. I think they are field mushrooms? It’s that time of year here. Moisture has returned to the soil and the fungi are reproducing. There are hippies in the forest trancing.
@David_Stilley Do you think woman is a contraction of woe-man? Or is it a contraction of whoa-man? Like pulling up a horse before it runs off a cliff?
See also the draw backs when playing with stem cells?
”…Dr. Melton’s research group attracted a great deal of excitement in 2014 when it publisheda way of producing large quantities of insulin-producing cells from human stem cells. These cells successfully normalized blood glucose when implanted in rodents, but only those without a functioning immune system. If implanted in an animal with a normally functioning immune system, the cells would likely have been attacked as “foreign.” …” …More
[4] Richard Morris: “…Every moment your glucose is above about 110 mg/dl you are decreasing the beta cells in your pancreas that make your insulin through glucotoxicity and every moment under 110 if you have any beta cells they are increasing through mitosis.
The problem is you can’t make new beta cells from stem cells because apparently there are no stem cells in your pancreas, so you have to rely on existing ones dividing and multiplying. Once you have too few you may never have enough to make enough insulin for you, and once you have to inject insulin it becomes a whole lot more complicated.
So the longer you are an uncontrolled diabetic, the less the chance you’ll make it back. But there is hope, I made it back after a decade of steadily worsening diabetes. …” …More
The realisation that is only now beginning to percolate through scientific thinking is that Type II diabetes is just as much an insulin problem as Type I, the difference being that Type I is an inability to produce insulin resulting from an autoimmune disorder, whereas Type II is an excessive production of insulin resulting from insulin resistance, resulting from an overload of glucose. Type III, Alzheimer’s disease, is insulin resistance of the brain, or more accurately, a defect of the glucose metabolism of the brain resulting from an overload of glucose.
In untreated Type I, the urine overflows with glucose, because the body has no other way of getting rid of it. It was this feature of the disease that was most apparent to the ancients (“diabetes” is derived from an Egyptian word meaning “syphon”). The discovery of insulin and its use in treating Type I diabetics dates to just under a century ago.
In untreated Type II, the most easily measured feature is the serum glucose level, but Dr. Joseph Kraft always maintained that it should really be diagnosed on the basis of insulin production. Until Berson and Yalow developed their radioassay technique for measuring serum insulin, the only way to get an idea of what was going on with the body’s insulin was to run an oral glucose tolerance test (OGTT) and infer the insulin behaviour from the the pattern of glucose readings. Dr. Kraft discerned several different patterns and was convinced that he could use them to diagnose Type II diabetes about twenty years earlier than waiting for problems with the serum glucose level to become manifest.
Type III, Alzheimer’s disease, was originally diagnosed from scans or autopsies showing neurofibrillary tangles and amyloid plaque in the neurons of the brain, and it was long believed that they were the cause of the disease. Recent research, however, has shown that the tangles and the plaque are indicators of the problem, but not the cause, the real cause being an acquired defect in the glucose-metabolising pathway in the neurons. The brain essentially begins to starve, because it cannot make use of the fuel it is receiving. This is why Alzheimer’s disease patients often respond well to MCT’s and ketones: their fat-metabolising pathway still works and can nourish the brain.
The cause of much of the metabolic damage in types II and III seems to be the excessive levels of insulin required to manage the excessive intake of glucose, in the form of both carbohydrates and sugars. (Diabetes was first observed among the rich of India about two thousand years ago, when sugar first began to be extracted from sugar cane. It only became prevalent among the general population in the nineteenth century, when mechanical production of sugar from cane and beets lowered the price of sugar to a level that common folk could afford. In the U.S., the development of the diabetes epidemic follows by about twenty years the development of the candy and soda-pop industries after the Civil War.)
So giving people insulin to manage their blood glucose levels is actually exacerbating the problem; the solution is actually to stop causing the problem by lowering glucose intake (i.e., sugar and carbohydrate) to safe levels. Eliminating sugar alone can start reversing fatty liver within days, and lowering carbohydrate intake to ketogenic levels has actually led to a documented reversal of Type II diabetes in many cases.
Type I diabetics must receive insulin if they are to live, regardless of their sugar intake. A ketogenic diet can be very helpful, since it promotes healthy serum glucose levels, making it easy to manage the insulin dosing. If Type II diabetes goes untreated for enough decades, yes, the β-cells of the pancreas can eventually burn out, but that is especially unlikely in anyone being treated medically for the disease. (If nothing else, exogenous insulin takes some of the burden off the β-cells.) Nevertheless, a ketogenic diet is a more appropriate treatment for Type II, since the problem is an excessive burden on the pancreas resulting from over-consumption of sugar and other carbohydrates. It only makes sense to reduce the burden. Type III is irreversible if unchecked for long enough, unfortunately, but both exogenous and endogenous ketone bodies can still be of help even in advanced cases.
Interestingly enough, experiments in mice have shown that if both the α- and the β-cells of the pancreas are destroyed, so that the animal is producing neither glucagon nor insulin, the animal does not develop diabetes, no matter how much sugar is included in its diet. So there is obviously more to the story of glucose management than we currently understand.
