Is Alzheimer’s Disease Preventable?

Alzheimer’s disease is a very large, extremely costly, growing epidemic that affects older individuals.   The average per-person Medicaid spending for seniors with Alzheimer disease and other dementias is 19 times higher than the average per-person Medicaid spending for all other seniors. If no changes are made, Alzheimer’s disease will cost an estimated $1.2 trillion (in today’s dollars) in 2050. Costs to Medicare and Medicaid will increase nearly 500 percent.

Home care is difficult; institutional care is often required because victims become unable to care for themselves and are frequently hostile. Today, approximately 5.5 million Americans are living with Alzheimer’s disease, including an estimated 200,000 under the age of 65. Nearly two-thirds, 3.2 million, are women. Of Americans aged 65 and older, 1 in 9 has Alzheimer’s disease.


What is Alzheimer’s disease?

Alzheimer’s disease (AD) is a form of dementia that can be defined as a cluster of symptoms and signs exhibited by difficulties in memory; disturbances in language and other cognitive functions; changes in behaviors; and disorder in conduct of daily living. AD is the most common form of dementia, accounting for up to 75 percent of all dementia cases. AD was first recognized as an ailment in about 1950.

Alzheimer’s Deaths Are Under-Reported

Deaths from AD increased 68 percent between 2000 and 2010, while deaths from other major diseases decreased. The numbers of deaths attributed to AD are significantly under-reported. The official number of deaths caused by AD during the year 2010 in the USA was 83,494. However, a detailed study done in 2014 found that AD deaths in 2010 were likely to have been as high as 500,000. The reason for this discrepancy is that AD deaths are frequently attributed on official death certificates to other diseases that occur concurrently with AD. Type-2 diabetes (T2D) is the disease most often a companion of AD. Other associated diseases are obesity, stroke, heart disease, and cancer. All of these diseases, including AD, are classified as non-infectious, chronic inflammatory diseases.

National Policy

Current national policy clearly states that there is no cure or effective treatment for AD. Even so, essentially all governmental research funding is aimed at discovering new drugs and better diagnostic methods. National policy appears to have no interest in learning how to prevent AD, even though medical treatments are proven to be ineffective and patient care costs are economically unsustainable and growing steadily.

Is Alzheimer’s Disease Preventable?

All diseases have causes, and all diseases can be prevented by discovering the cause and then eliminating that cause. Thus, AD is believed to be preventable. One supporting fact is that AD does not affect all of the American population. The existence of an unaffected group is consistent with the idea that a disease is preventable.

Another supporting fact is that AD tends to occur concurrently with one or more of America’s leading chronic diseases that are known to be preventable, namely heart disease, stroke, T2D, cancer, and obesity. That all of these diseases are now also acknowledged to be chronic inflammatory diseases is strongly supported by the following statement from a 2008 paper by C. N. Serhan:

Uncontrolled inflammation is now appreciated in the pathogenesis of many diseases that were not previously considered classic inflammatory diseases. These include atherosclerosis, cancer, asthma, and several neurological disorders, such as Alzheimer’s disease and Parkinson’s disease.

There is sound evidence that all non-infectious chronic inflammatory diseases are caused by the modern American diet; therefore, it is likely that AD is also caused by the modern American diet.

Chronic Inflammation and the Modern American Diet

A review of the scientific literature indicates that AD is a chronic inflammation of the brain caused by one or more of five specific dietary problems that are elements of the modern American diet. These are: a dietary excess of high glycemic carbohydrates (sugar and starches); a dietary excess of vegetable fats and oils (omega-6 fatty acids); a dietary deficiency of magnesium; dietary deficiencies of vitamins B6, B12, and folic acid; and a dietary deficiency of long-chain omega-3 fatty acids (e.g. fish oil).

High Glycemic Carbohydrates

In America, wide use of dietary sugar and starch increases blood insulin levels that, in turn, cause whole body inflammation. In biochemical terms, high insulin levels stimulate the delta-5 desaturase enzyme. When this enzyme is stimulated, it increases conversion of omega-6 arachidonic acid (AA) to inflammatory lipid mediators (eicosanoids) that result in whole body inflammation.

Vegetable fats/oils

The large excesses of vegetable fats and oils (omega-6 fatty acids) in the American diet also stimulate the delta-5 desaturase enzyme. This results in the conversion of AA to pro-inflammatory eicosanoids, which increase whole-body inflammation. Many studies show that when continued over time, long-term inflammation induced by dietary sugar, starch, and vegetable fats/oils is a major underlying cause of chronic inflammatory diseases.

Magnesium Deficiency

Although magnesium is an essential mineral that is indispensable for life, a very large fraction of the US population is deficient in dietary magnesium. This deficiency increases with age. Magnesium deficiency is associated with a number of chronic diseases, such as T2D, stroke, cardiovascular disease, hypertension, and AD.

Aging is linked to magnesium deficiency because intestinal absorption and increased urinary losses increase with age. Further, aging and magnesium deficiency are associated with increased production of oxygen free radicals and increased whole body inflammation. Long-term magnesium deficits have been shown to increase the risk of cardiovascular diseases, insulin resistance, T2D, and neuropsychiatric disorders, including AD.

Magnesium deficiency significantly increases the harmful effects of T2D. Although modern medicine believes that resistance to insulin is the reason that rising blood insulin levels fail to transfer glucose to the body’s cells, biochemical science tells us that the problem is not insulin’s failure to deliver glucose to the cells. Rather, it says that insulin ushers glucose to the cells but that cells cannot accept the glucose provided by insulin because they do not have the magnesium they require to open the door to the glucose being delivered. Dietary deficiency of magnesium is the problem.

This is significant for understanding why T2D and AD often occur in the same patient. Magnesium deficiencies in T2D patients cause very high insulin levels because of the failure of cells to accept glucose. The insulin levels rise in an effort to move the glucose. As a result, as mentioned earlier, high insulin levels stimulate the delta-5 desaturase enzyme and cause it to increase its conversion of arachidonic acid (AA) to inflammatory eicosanoids.

High Homocysteine Levels

The relationship between elevated blood levels of homocysteine and heart disease was first proposed by Kilmer McCully in 1969. Homocysteine has an important biochemical role in the methyl transfer cycle. It is now known that proper regulation of homocysteine metabolism, which is crucial for cardiac health, requires participation of three B vitamins; B6, B12, and folic acid. These three B vitamins are often referred to, along with trimethylglycine, as homocysteine regulators. High levels of homocysteine have been found to cause chronic inflammation.

Relevant Scientific Literature

In 2005, a research paper by Serhan opened the door to the fact that the body utilized essential fatty acids to biosynthesize lipid mediators that controlled inflammation, pain, and healing. In short, the body has a precise biochemical system to heal itself. In this paper, Serhan described the biochemistry wherein the body converts arachidonic acid, an omega-6 fatty acid, to anti-inflammatory, pro-healing lipoxins (LX’s). Importantly, he also reported that aspirin, utilizing arachidonic acid, induced the production of aspirin-triggered lipoxins (AT-LX’s) that were somewhat more potent than the natural LX’s.

In 2005, a study by Lukiw, Serhan, et al. indicated that the concentration of DHA (docosahexaenoic acid), a dietary essential fatty acid, was below normal in the Alzheimer brain. This deficiency was thought to be due to free radical lipid peroxidation of DHA, decreased dietary intake of DHA, or impaired DHA transfer to the brain. Referenced epidemiological studies suggested that diets enriched in omega-3 fatty acids were neuroprotective; follow-up biochemical investigations using animal models indicated that a metabolite of DHA, the docosanoid, NPD1, was the biochemical that promoted survival of stressed human brain cells.

The Brain in Alzheimer’s Disease

Alzheimer’s disease is popularly known for the amyloid plaques and neurofibrillary tangles found in autopsies of the brains of victims of AD. However, the role these aberrations play in the causation of AD is not known.

AD victims tend to have a pro-inflammatory profile, namely overweight or obese; T2D; high blood sugar; high cholesterol; and high blood pressure. The AD brain shows many indicators of severe inflammation, such as increasing numbers of inflammatory cytokines. Cytokines are a family of messenger biochemicals that promote or inhibit systemic inflammation. In addition to increasing numbers of inflammatory cytokines, severe brain inflammation is evidenced by activated glial cells; oxidative free radicals; and pro-inflammatory lipid mediators derived from arachidonic acid via activated COX-2 enzymes.


Microglia are cells that are the resident microphages of brain and spinal cord. This means that microglia are the first and main form of active immune defense in the central nervous system. Their job is to protect the brain from infection and inflammation by destroying all foreign bodies and harmful microorganisms. They constantly scavenge the central nervous system for damaged neurons and infectious agents. A signal that will cause the glial cells to react is brain inflammation.

Once activated, microglia are ruthless killers aimed at destroying infected neurons, bacteria, and viruses. In their attempt to destroy infection, the microglia cause widespread collateral damage in the brain. The predicament is that the AD brain tends not to be infected or not to contain bacteria or viruses.   Today’s AD patients suffer from whole body chronic inflammation caused largely by the modern American diet. Importantly, inflammation is the activator of the microglia that are causing brain damage.


Mitochondria are tiny organelles inside of cells that generate essentially all of the body’s energy. The very large human brain, which uses about 20% of the body’s energy, contains millions of mitochondria. In terms of human health, it is significant to note that the mitochondria are able to induce cell suicide (termed apoptosis) when appropriate and, as a result, control the fate of every cell. The mitochondrial triggers in the brain that induce cell suicide are cellular damage, viruses, bacteria, oxygen free radicals, and chronic inflammation.

Biochemical View of the Alzheimer’s Brain

Biochemists generally describe the AD brain as follows: excess amounts of inflammatory eicosanoids and pro-inflammatory cytokines; over-active microglia; excitotoxicity caused by increased calcium flux into neurons; excess amounts of reactive oxygen species; and neuronal degeneration.

As mentioned earlier, epidemiologic studies suggest that diets enriched in omega-3 fatty acids are neuroprotective. Recent biochemical studies indicate that DHA, an omega-3 dietary essential fatty acid, and its docosanoid metabolite, NPD1, a neuroprotectin, are consistently low in the AD brain, and that both DHA and NPD1 deficiencies correlate with cognitive impairment. It is also known that NPD1 exhibits anti-apoptotic, anti-inflammatory, and neuroprotective actions.

NPD1 is derived from the selective oxygenation of DHA by the 15-lipoxygenase-1 (15-LOX-1) enzyme. Bazan reports that NPD1 and the 15-LOX-1 enzyme are deficient in the AD brain. The probable reason is that the very large amount of an omega-6 linoleic acid in the American diet monopolizes 15-LOX-1 enzyme. The source of linoleic acid is dietary vegetable fats and oils.

A study by Merched found that the “Western diet” usurped the ability of the 15-1 LOX enzyme to biosynthesize the lipid mediators that protect against inflammation and inflammatory diseases. These are the lipoxins, resolvins, neuroprotectins, and others that control inflammation and stimulate both healing and the return to homeostasis.

Ramsden found that the 15-LOX-1 enzyme aggressively converts dietary linoleic acid to 9-HODE and 13 HODE. These chemicals are oxidized derivatives of linoleic acid (also termed OXLAMS) that have been implicated in a variety of pathological conditions. Lowering dietary linoleic acid proportionately lowers OXLAMS in humans. Unexpectedly, increasing dietary omega-3 fatty acids appears to have no effect on the conversion of linoleic acid to OXLAMS.

A study in Japan published in 2009 found that OXLAM levels were significantly higher in AD patients than in healthy controls. Further, OXLAM levels in AD patients increased with increasing clinical dementia ratings.

The Remarkable Marriage of AD and T2D

The scientific literature reveals that AD is the result of long term, whole body inflammation including the brain, and that this inflammation is the result of at least one of about a dozen of pro-inflammatory issues, most of which are dietary. Clinical observation has shown that AD does occur more commonly in people who suffer from one or more of America’s major non-infectious, chronic inflammatory diseases. This is not an unexpected finding in view the fact that all of these diseases have a common cause, namely chronic inflammation.

Interestingly, the connection of AD with T2D appears to be the most favored of all such diseases. A number of studies have found that the excess risk for AD in adults with T2D range from about 50% to 100%. The relationship between T2D and AD may be likened to Adam and Eve of biblical times. Adam contributed his rib, which was needed to beget Eve. T2D does not make a literal contribution to AD, but rather a figurative one; the metabolism of T2D produces an environment that is needed for the begetting of AD.

Effect of Insulin

The insulin of T2D appears to be a bridge in the relationship between T2D and AD. This effect of insulin is significant for understanding why T2D and AD often occur in the same patient. Magnesium deficiencies in T2D patients cause very high insulin levels. As mentioned earlier, the rise in insulin levels is due to failure to move glucose from the blood stream because the magnesium-deficient cells cannot accept the glucose.

Also, as mentioned earlier, high insulin levels stimulate the delta-5 desaturase enzyme and cause it to increase its conversion of arachidonic acid to inflammatory eicosanoids. The result is that overly high insulin levels in magnesium-deficient T2D patients cause excessive production of inflammatory eicosanoids. The outcome is very high whole body inflammation that promotes T2D as well as the inflammation of the brain that underlies AD.

The Ventricular System of the Brain

The ventricular system consists of four interconnected cavities in the brain.

These are called ventricles. The two larger are termed lateral ventricles. The lateral ventricles produce, circulate, and are filled with cerebral-spinal fluid (CSF). This CSF fills the ventricular system and spinal cord and surrounds the outside of the brain to provide a cushion between the brain and the skull.

Patients with AD: AD patients show an increase in volume in the lateral ventricles, which is also known to occur with age and with several neurological conditions, namely schizophrenia; bipolar disorder; major depressive disorder; as well as AD. However, Nestor, using volumetric MRI measurements of AD disease progression, found that absolute ventricular volumes and ventricular enlargement measured over a six-month interval were greater in subjects with AD compared to age-matched controls.

Patients with T2D: T2D patients show a greater increase in lateral ventricular volume than do normal controls. A total of 55 patients with T2D and 28 matched control participants had two magnetic resonance imaging scans with a 4-year interval. Findings were that patients with T2D had a greater increase in lateral ventricular volume than control participants. The conclusion was that T2D is associated with a slow increase of cerebral atrophy over the course of years.

A Brief Summary: The above two paragraphs present good evidence that both T2D and AD are inflammatory diseases; that T2D increases lateral ventricular volumes; and that increased lateral ventricular volumes are a measure of progression of AD. Hence, logic suggests that to prevent AD the specific causes of chronic inflammation and especially the cause of T2D must be identified and eliminated.

Personal Prevention

Any disease can be prevented by removing its cause.   An effort to prevent AD is of tremendous importance because every person and every family will benefit enormously if it can avoid the tragedy of this protracted, devastating illness. Additionally, an important consequence of a prevention program for AD is that it can also prevent all other chronic inflammatory diseases mentioned earlier: obesity; T2D; cardiovascular diseases; stroke; arthritis; and cancer.

It is reasonable to ask how a single prevention program can put a stop to a range of so many different diseases. First, all of these diseases have the same underlying cause, which is long-term, low-level inflammation. Different diseases occur from the same cause because individuals differ in many aspects, including their responses to chronic inflammation. Examples of these differences are dietary patterns; eating habits; ages; genetic backgrounds; oxidative stress; occupational environments; and harmful habits such as smoking. Various combinations of these differences influence individual biochemistry and physiology that, in turn, determine the actual disease that is expressed.

It has long been known that excess consumption of high glycemic carbohydrates (sugar and starch); imbalances of omega-6 to omega-3 ratios, with emphasis on excesses of omega-6 linoleic acid; and excesses or deficiencies of essential vitamins and minerals are major causes of chronic inflammation. There is no guidance from governmental agencies on disease prevention; therefore, it is urgent that individuals become responsible for their own health. They must learn the basics of healthful nutrition from authors who present sound science rather than flawed dogma and take steps to incorporate the simple basics of good nutrition into their daily fare.

The Ketogenic Diet

A ketogenic (keto) diet is the ideal diet for prevention of chronic inflammatory diseases. It is an anti-inflammatory diet that counters the inflammatory diet that caused the disease. It eliminates sugars and starches (carbohydrates). It includes all varieties of meat (protein) and animal fats.   The keto diet is considered to be a close approximation of the diet on which the human species evolved; primitive man’s diet was mostly of animal origin. That the timing of primitive man’s diet was irregular, depending on the catch, suggests that he also experienced frequent periods of unintended fasting.

Ketogenic Diet and AD: Interestingly, a literature review by Maalouf indicates that the neuroprotective properties of fasting have been recognized since antiquity and that current evidence suggests that the benefits of calorie restriction and the keto diet might be applicable to many acute and chronic neurological diseases such as AD. A review article by Paoli reports that in the 1960’s, keto diets were a common method of obesity treatment, and a study by Kivipelto found that obesity at midlife is associated with dementia and AD.

A number of studies have noted that keto diets were protective against AD. The suggestion that ketone bodies were the beneficial element in the diet appears to have been confirmed by Jarrett.   He reported that mitochondria in brain cells, when using glucose for energy, emit reactive oxygen species that deplete glutathione, a critical antioxidant, and cause significant inflammation in the brain. However, when mitochondria in the brain are using ketone bodies for energy, as is the case when employing a keto diet, the emission of reactive oxygen species are minimized, glutathione increases, and inflammation of the brain does not occur.

Sources of Information

The internet and bookstores abound with information helpful to anyone interested is following a ketogenic diet. For starters, we offer the following suggestions:

Metabolic Energy Control

The metabolic energy control system of the human organism is designed to be fueled by glucose (carbohydrates) and/or fatty acids (lipids). In a diet in which the macronutrients (carbohydrates, proteins, and lipids) are in reasonable proportion, it is customary for the body to switch back and forth seamlessly between glucose and fatty acids during the day, in response to stage of digestive cycle. In ketogenic nutrition, the dietary fuel is almost solely fatty acids. It is prudent for a person implementing a keto diet to have a general idea of how diet provides energy to the body.


Diabetics – Listen Up

It is essential for people on a keto diet to have a good book on the subject. One we recommend highly is Conquer Type 2 Diabetes with a Ketogenic Diet authored by Ellen Davis and Keith Runyan, M.D.

Ellen has a Master of Science degree in Applied Clinical Nutrition, and Dr. Runyan is a practicing physician specializing in obesity, kidney disease, and diabetes who is himself a type-1 diabetic. Despite their expertise and personal knowledge, they strongly advise that your personal physician be involved in review and application of information in this book.


A Revisit To The Importance Of Dietary Animal Fat The refusal of the government-nutrition cabal to renounce its longstanding proscription against animal fat and, by association, red meat, has seriously compromised the health status of its trusting citizens. This post is included to assure people that fears of animal fat are unfounded.


Alzheimer’s Antidote

Although this book will not be available until March 2017, it is recommended here because it shows great promise of being a valuable resource for both managing and preventing AD. It has had excellent Amazon reviews, and is authored by Amy Berger, MS, CNS, NTP, a highly qualified Certified Nutrition Specialist and Nutritional Therapy Practitioner.

Amy is a US Air Force veteran who now specializes in using low-carbohydrate nutrition to help people reclaim their vitality through eating delicious, wholesome foods, and teaching them that achieving vibrant health doesn’t require starvation, deprivation, or living at the gym. Her motto is, “Real people need real food!” You can read her blog at, where she writes about a wide range of health and nutrition-related topics, such as insulin, metabolism, weight loss, thyroid function, and more.


Editorial Note

Due to the length of the list of citations for this post, it was decided not to include it. Any reader who would like to have the reference for a specific statement, please write a request to the comments section. It will be answered promptly.

2 Responses to “Is Alzheimer’s Disease Preventable?”

  1. I was reading recently about the “Polyol Pathway” and the potential for damage caused by osmotic changes in blood, CSF etc and caused by, primarily sugars and alcohol. It would seem that here is potential for damage to cell membranes from cyclic expansion and contraction. The potential damage to neurons, nephrons and retinal cells suggests there may be a connection with Alzheimer’s. Are you aware of any relevant research related to the retention of sorbitol and fructose in these cell groups?

    • Many thanks, Lew, for mention of the Polyol Pathway. We are sorry that we cannot be of much help to you because of our own lack of information about the pathway, but perhaps there is someone out there in Ketopia-land who can help.

      We checked back to our class lecture notes of many decades ago and learned that the polyol pathway, then known as the sorbitol-aldose reductase pathway, was recognized primarily as a minor method for removing excess dietary glucose from the blood when it threatened to raise blood glucose concentration to dangerous levels. A great deal more has been learned since then, but we have not kept up with it.

      Because of the significance of the polio pathway in diabetic cellular damage , especially in the eye, study of this pathway is of importance. You have asked a good question, Lew.

      Is there anyone out there who can help with information?


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