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How too much insulin in the blood promotes type 3 diabetes which is dementia

When it comes to preventing type 2 diabetes or what has now found to be type 3 diabetes, you might take a look at the book Brain Grain by David Perlmutter, MD with Kristin Loberg. Perlmutter also is author of The Better Brain Book. In his book, Grain Brain, Dr. Perlmutter explains the difference in dietary habits. Then compare what it says with Dr. Hyman's The Blood Sugar Solution. Dr. Mark Hyman reveals that the secret solution to losing weight and preventing not just diabetes but also heart disease, stroke, dementia, and cancer is balanced insulin levels. Compare the vegan diet to the Paleo diet in Brain Grain. There also are books about the vegan Paleo diet. See, The Vegan Paleo Cookbook - The Natural Caveman Diet by Heather Lieberman, published in 2013, and Paleo Diet vs. Vegan Diet: Which diet really works for weight loss and better health? by Ken Tyler, published in 2014.

Which carbs could kill your brain?

What happens when Alzheimer's disease is linked to type 3 diabetes? See, "Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed" and "Is Alzheimer's Type 3 Diabetes? -" Or check out, "What Is Type 3 Diabetes? (with pictures)." Or see, "Symptoms Of Type 3 Diabetes - Diabetes Insight" and "Why Is Alzheimer's Disease Called Type 3 Diabetes?."

You may want to check out, "Do Carbs Kill Your Brain? - Chris Kresser." One issue is whether more vegans get neurological diseases such as Alzheimer's or whether processed wheat and sugar is the real culprit, not a glass of juice from green leafy vegetables or getting fats from flaxseed versus bacon fat.

You need a certain ratio of different types of fats in your diet for brain health

You should know that the omega 3 fatty acid content of flaxseeds is 57% compared to the seed's omega 6 fatty acid content of only 14%. Compare that with walnuts, whose omega 6 fatty acid content is a whopping 52% compared to its omega 3 fatty acid content of just 10%.

The issue is whether you're getting enough fats for your brain without clogging your carotid and coronary arteries. But are we really eating too many berries and apples full of that fructose that's rushing the insulin through bloodstreams that prematurely age organs and arteries? Or is the culprit too much processed sugar and too many syrups baked with trans fats?

According to the September 26, 2007 news release, "Discovery supports theory of Alzheimer's disease as form of diabetes," researchers found that insulin, it turns out, may be as important for the mind as it is for the body. Research in the last few years has raised the possibility that Alzheimer’s memory loss could be due to a novel third form of diabetes.

In 2007 scientists at Northwestern University discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer’s disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer’s removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for “amyloid ß-derived diffusible ligand.”)

With other research showing that levels of brain insulin and its related receptors are lower in individuals with Alzheimer’s disease, the Northwestern study sheds light on the emerging idea of Alzheimer’s being a “type 3” diabetes

The findings, published online in 2007 by the FASEB Journal, could help researchers determine which aspects of existing drugs now used to treat diabetic patients may protect neurons from ADDLs and improve insulin signaling in individuals with Alzheimer’s. (The FASEB Journal is a publication of the Federation of American Societies for Experimental Biology.)

In the brain, insulin and insulin receptors are vital to learning and memory. When insulin binds to a receptor at a synapse, it turns on a mechanism necessary for nerve cells to survive and memories to form. That Alzheimer’s disease may in part be caused by insulin resistance in the brain has scientists asking how that process gets initiated.

“We found the binding of ADDLs to synapses somehow prevents insulin receptors from accumulating at the synapses where they are needed,” said William L. Klein, according to the September 26, 2007 news release, "Discovery supports theory of Alzheimer's disease as form of diabetes," Klein (as of the date of the news release) is a professor of neurobiology and physiology in the Weinberg College of Arts and Sciences, who led the research team. “Instead, they are piling up where they are made, in the cell body, near the nucleus. Insulin cannot reach receptors there. This finding is the first molecular evidence as to why nerve cells should become insulin resistant in Alzheimer’s disease.”

ADDLS are small, soluble aggregated proteins. The clinical data strongly support a theory in which ADDLs accumulate at the beginning of Alzheimer’s disease and block memory function by a process predicted to be reversible

In earlier research, Klein and colleagues found that ADDLs bind very specifically at synapses, initiating deterioration of synapse function and causing changes in synapse composition and shape. Now Klein and his team have shown that the molecules that make memories at synapses -- insulin receptors -- are being removed by ADDLs from the surface membrane of nerve cells.

“We think this is a major factor in the memory deficiencies caused by ADDLs in Alzheimer’s brains,” said Klein, in the news release. Klein is a member of Northwestern’s Cognitive Neurology and Alzheimer's Disease Center. “We’re dealing with a fundamental new connection between two fields, diabetes and Alzheimer’s disease, and the implication is for therapeutics. We want to find ways to make those insulin receptors themselves resistant to the impact of ADDLs. And that might not be so difficult.”

Using mature cultures of hippocampal neurons, Klein and his team studied synapses that have been implicated in learning and memory mechanisms. The extremely differentiated neurons can be investigated at the molecular level. The researchers studied the synapses and their insulin receptors before and after ADDLs were introduced.

Researchers discovered the toxic protein causes a rapid and significant loss of insulin receptors from the surface of neurons specifically on dendrites to which ADDLs are bound. ADDL binding clearly damages the trafficking of the insulin receptors, preventing them from getting to the synapses

The researchers measured the neuronal response to insulin and found that it was greatly inhibited by ADDLs. “In addition to finding that neurons with ADDL binding showed a virtual absence of insulin receptors on their dendrites, we also found that dendrites with an abundance of insulin receptors showed no ADDL binding,” said co-author Fernanda G. De Felice, according to the news release. De Felice is a visiting scientist from Federal University of Rio de Janeiro who is working in Klein’s lab. “These factors suggest that insulin resistance in the brains of those with Alzheimer’s is a response to ADDLs.”

“With proper research and development the drug arsenal for type 2 diabetes, in which individuals become insulin resistant, may be translated to Alzheimer’s treatment,” said Klein. “I think such drugs could supercede currently available Alzheimer’s drugs.”

Klein, Grant A. Krafft, formerly at Northwestern University’s Feinberg School of Medicine and now chief scientific officer at Acumen Pharmaceuticals, Inc., and Caleb E. Finch, professor of biological sciences and gerontology at the University of Southern California, reported the discovery of ADDLs in 1998. Krafft is a co-author of the FASEB Journal paper. Northwestern and USC hold joint patents on the composition and use of ADDLs in neurodisorders.

The patent rights have been licensed to Acumen Pharmaceuticals, based in South San Francisco, for the development of drugs that treat Alzheimer’s disease and other memory-related disorders. In addition to Klein, De Felice and Krafft, other authors on the paper are Wei-Qin Zhao, a former visiting scientist at Northwestern, now with Merck & Co., Inc. (lead author); Hui Chen, from the National Center for Complementary and Alternative Medicine at the National Institutes of Health; Michael Quo, from Blanchette Rockefeller Neurosciences Institute; and Sara Fernandez and Mary Lambert, from Northwestern University.

Reduced insulin in the brain triggers Alzheimer's degeneration

Also take a look at the March 23, 2006 news release, "Reduced insulin in the brain triggers Alzheimer's degeneration." Researchers in that study explained how the neuroendocrine disorder is distinct from other types of diabetes. By depleting insulin and its related proteins in the brain, researchers at Rhode Island Hospital and Brown Medical School have replicated the progression of Alzheimer's disease – including plaque deposits, neurofibrillary tangles, impaired cognitive functioning, cell loss and overall brain deterioration – in an experimental animal model. The study demonstrates that Alzheimer's is a brain-specific neuroendocrine disorder, distinct from other types of diabetes.

In the study, brain deterioration was not related to the pancreas, which regulates insulin for the body. When pancreatic insulin is deficient or the body fails to respond to it, the result is Type 1 or Type 2 diabetes. Previous work by the researchers with postmortem brain tissue of Alzheimer's patients showed a strong link between insulin depletion in the brain and Alzheimer's disease, raising the possibility that Alzheimer's is a neuroendocrine disorder, or a Type 3 diabetes.

"We have demonstrated that a loss of insulin in the brain triggers the onset of Alzheimer's, probably because as the brain loses insulin, the cells that require insulin to function and survive also eventually die. The consequences are increased oxidative stress, brain deterioration, loss of cognitive function, and a buildup of plaques and tangles in the brain – all hallmarks of Alzheimer's, said senior author Suzanne M. de la Monte, MD, MPH, a neuropathologist at Rhode Island Hospital, according to the March 23, 2006 news release, "Reduced insulin in the brain triggers Alzheimer's degeneration." de la Monte (at the date of the news release) also is a professor of pathology and clinical neuroscience at Brown Medical School in Providence, RI. "We now know that if you specifically target insulin and its actions in the brain, you could develop new treatments for this disease," de la Monte explained. The study is published in (Volume 9, Issue 1) of the Journal of Alzheimer's Disease (

Neurodegeneration: Impairments in insulin/IGF signaling and deficiencies in the corresponding growth factors can occur in the central nervous system (CNS) independent of Type 1 or Type 2 diabetes

Researchers injected the brains of rats with Streptozotocin (STZ), a compound that when metabolized, destroys beta cells in pancreatic islets and produces diabetes. When injected directly into the brain, the treatment caused neurodegeneration, while the pancreatic islet cells remained intact. That is because insulin depletion produced by STZ was confined to the brain, just like what occurs in most cases of Alzheimer's.

"This study provides definitive evidence that impairments in insulin/IGF signaling and deficiencies in the corresponding growth factors can occur in the central nervous system (CNS) independent of Type 1 or Type 2 diabetes," the authors write.

As a result of the treatment, insulin and its IGF-I receptors were significantly reduced in the brain, triggering a cascade of neurodegeneration. Both insulin and IGF-I activate complex signaling pathways downstream, prompting energy metabolism and growth required for learning and memory, and inhibition of oxidative stress, which unchecked could trigger neurodegeneration.

As insulin was depleted, neurons died and the brain dropped to half its size, a result of atrophy which is a prominent feature of Alzheimer's. At the same time, there was an increase in astrocytes and microglial cells, which are responsible for neuroinflammation, another critical and consistent feature of Alzheimer's and probably related to the increased amyloid deposition in the brain, the researchers say.

Also, there was increased activation of a kinase called GSK-3 beta

This kinase is overactive in Alzheimer's and triggers tau phosphorylation, which is known to be at the core of neurofibrillary tangles. The researchers had previously shown that tau is regulated by insulin and insulin-like growth factor (IGF-I). In the current research, they found that as insulin and IGF-I were depleted in the brain, the expression of GSK-3 beta increased, leading to oxidative stress and cell death.

While the link between insulin and tau had been established, researchers also looked at the connection between insulin and amyloid precursor protein gene expression, as increased levels could account for amyloid accumulation, or the buildup of plaques in the brain. They found that amyloid beta deposits in vessels and plaques did build up in the brain, and they suggest that these abnormalities occurred due to increased oxidative stress.

Another feature of Alzheimer's affected by impaired insulin signaling, acetylcholine deficiency, is linked to dementia and has long recognized as an early abnormality in Alzheimer's

The enzyme that makes acetylcholine, choline acetyltransferase (ChAT), was previously found to be regulated by insulin and IGF-1. In brains with Alzheimer's, impairment of insulin and IGF-I signaling mechanisms correlate with deficits in acetylcholine production. In this study, ChAT was markedly reduced in the experimental Alzheimer's model.

"Our previous work has shown that many of the important features of Alzheimer's – such as the accumulation of phosphorylated tau and the death of neurons – were somehow linked to insulin deficiency in the brain. This study shows that insulin is the controlling factor in all of these features of Alzheimer's disease," de la Monte explained in the news release. "The evidence suggests that impaired insulin and IGF signaling must be addressed in order to make significant progress in the treatment and prevention of Alzheimer's disease," she says. Grants from the National Institutes of Health supported this study.

Dietary habits and neurological disease

If you look at the scientific studies published in various medical and technical journals, the published studies describing Alzheimer's disease as type 3 diabetes began around 2005, according to the book, Grain Brain.

Links between poor diet and Alzheimer's have been published in many books and articles that show the main differences between our diet and the 75% fat diet of pre-agricultural hunters and gatherers. How high in fat should a diet be for the general population trying to wean itself from processed fats and sugars?

The pre-agriculture ancestral diet was 75% fat, 20% protein, and 5% carbs. Today's diet is 60% carbs, 20% fat, and 20% protein. Numerous physicians and other scientists think Alzheimer's disease can be prevented by using food as medicine, by changing the food we eat. But what foods work best on the general population compared to patients with special-need diets?

What diabetes and the brain have in common

If you go back to cave people days, when glucose was difficult to find except when the season permitted people to gather a few wild berries and other fruits in temperate zones and sweeter fruits such as bananas in tropical areas, evolution designed the human body to turn the fuel from food into energy for cells to reproduce and function the way nature programmed cells to work.

For almost the entire existence of our species, glucose - the body's major source of energy for most cells - has been scarce

You can read about fat being the major source of brain energy for ancestral peoples before agriculture in Dr. Perlmutter's book, Grain Brain. What's important for the general public to consider is that when the cave people ate a diet of 75% fat, that diet made it possible to develop ways to store glucose and convert other things into it.

The body can manufacture glucose from fat or protein if necessary through a process called gluconeogenesis. The problem with gluconeogenesis is that it takes a lot of energy. What takes less energy is the way the human body converts starches and sugar into glucose. It's easier to change sugar into glucose and takes less energy by the body to get the glucose to the brain and muscles.

The process by which human cells accept and utilize glucose

You have sugar molecule in your body from the food you're eating. Now your cells are going to make insulin, a hormone so that the glucose can get into your cells in the first place. Insulin is made by your pancreas. You need enough insulin to move the glucose/sugar in your blood into your muscles, fat, and liver cells. It's your basic fuel, working like fuel in an engine to make it move. It's your energy.

If your cells are normal, they are highly sensitive to insulin. But if you have insulin resistance, the cells aren't as healthy and not so sensitive to insulin. So the body makes more and more insulin to the point where you get symptoms of having too much insulin in the blood. You don't want abnormally high levels of insulin in your bloodstream.

If you keep eating foods that quickly turn to sugar in your blood, like eating too much fruit, your cells get exposed to too much insulin. For example, if you eat fruit in the morning your body will process it differently than if you eat fruit in the afternoon or evening, when the body processes fruit more like sugar. Eating a bowl of blueberries at dinner time can keep you up all night constantly urinating from too much insulin in the blood or too high blood glucose levels.

Insulin resistance

Modern societies feed their populations too much food that's so highly processed, full of refined sugars and syrups or processed, heated fats. The result is too high insulin levels or insulin spikes. The insulin levels surge beyond normal levels. What happens is the cells eventually adapt by reducing the number of receptors on their surfaces to respond to insulin. Now, we have insulin resistance. Sometimes the symptoms are called low blood sugar related to diet.

By eating too much fruit, too much sugar, or too much bread, pasta, pastry, potatoes, and other starchy foods that quickly turn to sugar in the blood, your cells desensitize themselves to insulin, causing insulin resistance.

What happens with insulin resistance is that your cells ignore the insulin pouring out into your bloodstream. So the glucose in your bloodstream is not taken up by your cells. You may start to feel symptoms of low blood sugar because your cells are not getting glucose from your blood. The result is that your pancreas responds by pumping out more insulin.

Now higher levels of insulin become needed for sugar to go into the cells. The cycle happens again and again until you change your diet. Some people develop type 2 diabetes. Diabetics have high blood sugar. With type 2 diabetes, the sugar stays in the blood causing toxic sugar damage to the rest of the body such as nerve damage, heart disease, and as researchers say, Alzheimer's disease. The sugar causes inflammation that runs through the body. It's sugar in the blood causing problems from heart disease to neurological dementia for many.

If you follow the chain of events, you can see how it back engineers to insulin and blood sugar issues

Insulin does more than moves glucose into cells. Insulin also stimulates growth. For some people, it's weight gain. For thin people with low blood sugar exacerbated by diets with too much sugar or eating too many fruits at the expense of other foods that don't turn to sugar quickly in the blood. Is your body abusing foods that quickly turn to sugar over a period of years? Too many kids are pre-diabetic or already have type-2 diabetes.

What's going to happen to their brain and artery health when they become senior citizens? Your genes ultimately have their own time table when type 2 diabetes develops. But all this is reversible by diet. Food can be medicine if it has the ability to prevent the cycle, or slow down the time table of the genes on what happens next. When it comes to nutrition, does one size fit all?

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