Kokosöl und Alzheimer, Kokosöl und Gehirn
Hvad lige præcis menes der, når Alzheimers sygdommen anses som en type 3 diabetes? Amy Berger besvarer dette spørgsmål i sin bog The Alzheimer's Antidote, hvor hun har sammenskrevet, det vi ved om Alzheimers for at lede os tættere på årsagen: mangel på brændstof i hjernen. Hvordan og hvorfor dette forekommer er forklaret i bogen, samt ændringer i kost og livsstil, der kan modvirke processen.

Stofskiftelidelser er en kendt risikofaktor i Alzheimers. Insulinresistens er en faktor i begge og leder til højere niveauer af insulin i blodet (hyperinsulinisme). Glukose er hjernens primære brændstof. Et træk ved Alzheimers sygdommen er en mindskelse i omsætningn af glukose i hjernen. I nogle har reduktionen været på 45 procent og er altid lokaliseret i de områder af hjernen, der er forbundet med læring og hukommelse. Som hjernecellerne bliver mindre i stand til at omsætte glukose som brændstof, sulter de. Berger bemærker, at nogle forskere har fundet dette som den fremherskende unormalitet ved Alzheimers.

Ketones are another source of fuel for the brain but are only produced when insulin levels are low, such as when a person is on a low carbohydrate diet or fasting. Research has found that the brains of people with AD are capable of taking up ketones and will benefit cognitively. This super-fuel will not be used, though, by a brain that is flooded with glucose.

Another marker is the presence of the amyloid-beta (Aβ) plagues found in the brains of people with AD. These plaques occur in everyone but are cleared away routinely. In the case of AD patients, the plaques are not cleared and continue to grow and solidify, interrupting communication between cells. The process for clearing the plaques is the work of an insulin degrading enzyme. The targets for this enzyme are first insulin and then the plaques, so excess insulin occupies the enzyme, which then allows the plaques to build up.

Beyond these and other metabolic processes affected by excess glucose and insulin, the author explains the benefits of higher fat intake, especially the omega 3s and 6s in proper ratio, and medium-chain fatty acids as found in coconut oil. A fat-like substance, whose levels we can monitor in blood tests is cholesterol. Berger's enlightening discussion of the role of cholesterol in proper functioning of the brain will definitely encourage the reader to rethink that low cholesterol diet.

We have been taught that cholesterol found in plaques in the arteries is a result of too much cholesterol in the diet, when in fact the cholesterol is a repair material for vessels damaged by hyperinsulinemia and other conditions. Trauma, infections, and low thyroid, among others will cause levels to rise. Simply put, we need cholesterol. Cholesterol is a component of cell membranes and mitochondria. In the brain, it is used to form the myelin sheath that protects neurons. Cholesterol is required by the body to produce choline, which is used to make acetylcholine, a neurotransmitter involved in memory and learning. Coenzyme Q10 is involved in the production of energy in the mitochondria and is formed by the synthesis of cholesterol. In light of this information, Berger makes clear the damage being done by the push for lower cholesterol diets and routine prescribing of statin drugs.

Berger also includes a discussion of the so-called Alzheimer's gene ApoE4. Cholesterol is vital for healthy brain function, which uses about 25 percent of the body's cholesterol. The apolipoprotein E genes (ApoE), among thousands of other tasks, provide the molecules that allow non-water-soluble substances to travel the blood stream. This is how cholesterol is delivered to the brain. Along the way these molecules will suffer damage from encounters with substances such as excess insulin. Of the ApoE genes, the ApoE4 appears to be the most susceptible to this damage. A person having the ApoE4 gene will not necessarily develop AD, but it is a risk factor. To reduce that risk, the author suggests the low carbohydrate/high fat diet described in the book.

A good portion of the book is dedicated to the diet that can improve brain function of those with AD. The goal is to shift the body's energy source away from carbohydrates to fats. Gone are the prohibitions against animal proteins and fats, in fact their consumption is encouraged. Glycemic control is of upmost importance so, for example, foods such as beans, which have long served as alternatives to animal proteins in other diets, are discouraged for their carbohydrate content.

Another goal of this diet is to utilize ketones for energy. Not to be confused with diabetic ketosis, nutritional ketosis occurs when the blood glucose levels are low. One advantage of this is that the lower insulin levels in the blood will allow the insulin degrading enzyme to clear away the Aβ plaques in the brain. For those having difficulty lowering their glucose levels, the author recommends medium-chain fatty acids such as coconut oil and palm kernel oil to be included in the diet. It is even possible to order ketone supplements.

Lifestyle choices can also affect cognitive function. The importance of exercise, adequate sleep, nutritional supplements, and stress reduction are also discussed. Berger states that the use of low carbohydrate, ketogenic diet therapy research is still in its infancy, and there are no guarantees this approach will work for everyone. She suggests giving the diet and lifestyle changes three months before deciding whether or not there has been improvement.

The information in this book is pointing us in a new direction, which is away from the standard American diet and nutrition advice that has likely exacerbated the development of many diseases including AD. In the Foreword to this book, David Perlmutter, MD, states what is at the root when he says that our food choices interact with our genes for better or worse. Food as instructions to our DNA is something we have some control over, and Berger has well described how and why we should make smarter choices.

This well-referenced book has a wealth of information that informs us of the damage to our brains caused by excess carbohydrate intake, which is so common in diets now. Many of the physical processes described are complex, but the author has used metaphors to assist the lay person so that the book is accessible to everyone. Whether the problem is AD or other forms of memory loss and cognitive decline, this book could be a real game-changer.