NEWSLETTER 25:                                                                        Edited November 19, 2008. Updated October 2011

In THE NEWS October 2010

In his recent published 19th book: "Stop Alzheimer Now",Bruce Fife, ND, the director of the not-for-profit organization "The Coconut Research Center", demonstrates how a (non-pharmaceutical) induction of ketosis diet by cococnut oil consumption improves the brain function of Alzheimer patients and can reverse the course of the condition.


 In this newsletter we discuss the genetics of Alzheimer's disease (AD) and the hypothesis of a possible causal link between lifestyle and nutritional changes that have occurred over the last 100 years and the proliferation of AD. Further, we suggest some preventive steps.                     


1 - Alzheimer Disease (AD) was first described in 1906.

2 - AD runs in families

3 - AD cases started to multiply in the second half of the twentieth century as if it were an epidemic

4 - Until now there is no cure, the nutritional approach, however, is promising.

5 - Is nutritional prevention possible?



1 - Alzheimer's Disease was first described in 1906.

The condition was first described by Prof. Alzheimer in the beginning of the twentieth century. The patient described by Prof. Alzheimer had what we now describe as "early onset" AD because it appears before the age of 61 years. This is in opposition to the "late onset" form of the condition, previously described as "Senile Dementia" that develops after the age of 61 years. Today both forms are termed Alzheimer's disease altough they differ by several factors. In the early onset form the brain damage is more extensive and the evolution much faster than in the late onset form. Also in the early onset form chromosomal alterations are described ( in chromosome 21 and 14) that are missing in the later onset form. The actual increase of AD cases are late onset forms.

Today's AD numbers are staggering; About 5,000,000 people in the U.S.A. alone have the late onset condition and estimations see an increase of 350,000 cases per year in that country. (Every second, someone in America develops AD). That number 5,000,000 is expected to climb to 18,000,000 over the next 50 years.

See the video of a comprehensive description of late onset AD by Dr Gus Alva.

The consequences for society and for the families are worrisome: The actual cost of Alzheimer disease (AD) for the society is around $248 billion yearly and it could quadruple before 2050. As for the family of AD patients since there is no cure for the condition, the management of the declining patient is essential and constitute a severe burden for the spouse or the caregiver with all its psychological, social, physical and financial load.


2 - AD runs in families

AD runs in families. However AD has a proven genetic chromosomial origin in only 2% of the cases, the “early onset AD”, where chromosomal DNA mutations have been identified.

There is no such chromosomal mutation described for the 98 other percent of the AD cases, the “late onset AD” also inaccurately named the "Sporadic Form AD”.

Then how is AD transmitted in the majority of AD cases? There must be at least one or maybe several vectors ensuring the inheritance of the condition or the transmission of some predisposing factors.

Could it be a virus?  Don't scoff at it. Until not so long ago gastric ulcers were attributed to stress and a myriad of other causes until the discovery of the main causative agent: the germ Helicobacter pylori.

Until someone shows up with the proof that a virus is involved in the epidemic development of AD we are limited to utilize and try to understand the significance of what we already know about the condition and the new information provided by research.

The inheritance of AD. A recent publication may provide an explanation for the transmission of the “late onset AD”;

(quote):"Our new study shows that subjects with a mother with Alzheimer show similarities with Alzheimer's patients. They have metabolic reductions in the brain regions that are typically affected by AD, which worsen over time."

Lisa Mosconi, the author of this breakthrough discovery describes the metabolic reductions as glucose related and declares its inheritance to be of maternal origin only:

(quote):"... a reduction in glucose brain metabolism among individuals with a maternal history of the disease, but not among those with a paternal history or with neither parent affected" (end quote).

Mitochondrial inheritance

Glucose—the essential fuel of brain cells is processed in the mitochondria of the brain cells. The mitochondria are the power units of all our cells. The processing of glucose and other fuel in the mitochondria produces the energy cells need to function.

The reduction of glucose metabolism observed by Lisa Mosconi "in the brain regions that are typically affected by AD" indicates a defect in the mitochondria of the brain cells in those brain regions.

The reason the reduction in glucose brain metabolism was found exclusively "among individuals with a maternal history of the disease" is that all our mitochondria are inherited from our mother only. 

A human ovule contains about 100,000 mitochondria while a spermatozoon has only 16. None of the mitochondria from the spermatozoon penetrate the ovule during fecundation. Only the nucleus of the spermatozoon enters the ovule.

Mitochondrial gene inheritance

It is a well known fact that each of us inherits the same amount of chromosomial genetic material (DNA) from both our parents (well not exactly: the X (the female) chromosome is bigger than the Y (the male) chromosome which makes that daughters only (with two XX's in their genome) receive equal chromosomial genetic material from both parents, while the sons (XY) have a little more from their mother). But wait: this is only valid for the genetic material contained in the chromosomes because mitochondria have their own DNA. It is called mtDNA and that genetic material comes with the mitochondria from the mother only. We all received more DNA from our mother than from our father.

A study from the University of Virginia (UV) supports the view that the defect in glucose handling by the mitochondria involves an alteration of their mtDNA;

(quote):" They found that the defective mitochondrial genes in AD cybrid cells caused increased damage from oxygen free radicals (oxidative stress), because of the inefficient processing of oxygen into water. This led to the activation of cell death pathways, which resulted in the over secretion of beta amyloid peptides and the forming of plaque-like areas in the cells ...... ........Our findings in these AD patients firmly link together defective mitochondrial genes and abnormal beta amyloid metabolism, which is the biochemical hallmark of the disease" (end quote) .

The mtDNA inherited from the mother with the mitochondria explains
the maternal only inheritance of 98% of the AD cases.

DNA and mDNA alteration and repair

DNA and mtDNA alterations occur all the time as well as DNA and mtDNA repair

Both the chromosomial DNA and the mitochondrial mtDNA have repair capacity. However the mtDNA repair mechanism is less effective because mtDNA lacks the regulatory function histone provides to the chromosomial DNA,which makes the mitochondria particularly sensible to oxidative damage and the integrity of their genome very dependent on an efficient oxidative defense system to avoid mitochondrial function loss and ultimately cell death.

Furthermore, the intimate connection between mtDNA and the inner membrane of the mitochondria makes mtDNA exquisively sensitive to any alteration of the membrane.

( quote):"Mitochondrial DNA is a particularly vulnerable target for damage due to its association with the inner mitochondrial membrane, where significant amounts of ROS (added: ROS stands for Reactive Oxygen Species) are produced, and its lack of protective histones" (end quote).

It is obvious that:

Alzheimer's Disease starts progressing when the damage becomes greater than the repair

and cells slide toward destruction

3 - AD cases started to multiply in the second half of the twentieth century as if it were an epidemic

The twentieth century witnessed great changes in human lifespan, nutrition and lifestyle. We are not enough aware of it and if we sometimes notice it, we rapidly forget about it without realizing how profound those changes still affect all of us.

a) Human Lifespan.

During the twentieth century the human lifespan in developed countries has increased significantly. In the US the life expectancy is now 78.14 years. In the beginning of the twentieth century it was around 40 years. Since the symptoms of AD start to appear around 60-65 years of age, the almost doubling of the life expectancy has significantly contributed to the actual increase in number of AD cases. While an extended lifespan explains why we may see more cases of AD today it says nothing about the cause of the condition.

b) Nutrition

During the twentieth century the composition of our diet has changed drastically. Two important changes are the invasion of refined and "industrial" food.

1 - Sugar is an example of a refined product that has changed our diet.

Two hundred years ago refined sugar started invading an already starch-rich diet. Fifthy years ago the consumption of refined sugar in the U.S. was about 50 pounds per year for an adult and more—about 85 pounds per year, for a teenager. Since then the consumption has jumped more than 25 percent. The actual consumption of refined sugar for an average American adult is at least 64 pounds per year. For a teenager it is now more than 100 pounds per year.

(Quote) “Sugar consumption is off the charts” reports Michael F. Jacobson executive director of the Center for Science in the Public Interest, “Added sugar found largely in junk foods such as soft drinks, cakes and cookies—squeeze healthier foods out of the diet. Sugar now accounts for 16 percent of the calories consumed by an average American and 20 percent of teenagers calories.” (more)

Glycation of molecules with a slow turnover (like brain cell components) is a factor of senescence—the aging of cells, tissue and organs at a faster pace than expected for the age of the person. More about Glycation


2 - The switch from animal fat to vegetable oil has completely changed the composition of fatty acids in our diet.

The switch from animal fat to vegetable oil has completely changed the composition of fatty acids in our diet.
The switch has resulted in a 65% drop in saturated fatty acids (inclusive the suppression of the medium chain
fatty acids), a 45% drop in mono-unsaturated fatty Acids, and a sixfold increase in omega-6 essential fatty acids.
The switch also suppressed the omega-3 essential fatty acids in the diet while multiplying by a whooping 150
the trans fatty acid content of the diet.

During hundreds of thousands of years the only fat humans could eat was animal fat and fruit fat (coconut, palm, olive) because there was nothing else available.

There is no record of an epidemic-like development of heart disease, stroke and degenerative conditions and there is no account of any prevalence of obesity, cancer, diabetes, arthritis, Alzheimer's disease, allergy and autoimmune conditions during those hundreds of thousands of years. The only epidemics occurring in the past were outbreaks of infectious diseases

More about this topic
In another newsletter we have explored (1) the similarities and the differences between animal and human fat and oils. - Then, to illustrate the economic and politic triggers that substituted vegetable oils for animal fat, we have (2) a glimpse at the history of margarine - Finaly, we look at (3) the health consequences of an excessive vegetable oil consumption.

In Brief:
The change resulting from the switch from animal fat to vegetable oil can be summarized as follow:

The fatty acids we find in food become part of our cell membranes.

Since de early years of the twentiesth century and on top of the transfat invasion, the introduction of a massive dose of linoleic acid in the diet has significantly increased the exposure of cell and mitochondrial membranes to oxidative stress. Indeed, animal fat contains about 45% of fatty acids with one double bond and less than 10% of fatty acids with more than one double bond. In contrast, vegetable oil has about 60% of fatty acids with each two double bonds and only 20 % of fatty acid with one double bond . The double bonds are the weak spots in a fatty acid molecule. Double bonds are the structures where oxidative damage occurs.

The switch from animal fat to vegetable oil resulted in a more than 300 percent increase of double bonds in the membranes of our cells and in the membranes of cell components like the mitochondria and consequently in a more than 300 percent increase of cell membrane and mitocvhondrial DNA (mtDNA) exposure to oxidative damage.

Four generations have been flooded with trans fatty acids, and to top it off,
the latter two with an excess of linoleic acid.

In Details:

For the details of how the switch from animal fat to grain oil has disrupted our metabolism, see "The Oiling of America, a Fat Mistake".


Good News :

the tide may be changing and research is on its way investigating the disastrous consequences of about 100 years of transfat plus 50 years of linoleic acid poisoning of our diet, we have had to wait until October 2008 to see the first publication about the effect of an arachidonic acid derivate on a mouse model of alzheimer's disease. (arachidonic acid is made exclusively from linoleic acid.


(quote): The most striking change discovered was an increase in arachidonic acid and related metabolites in the hippocampus, a memory center that is affected early and severely by Alzheimer’s disease. Arachidonic acid is thought to wreak havoc in the brains of the mice by causing too much excitation, damaging neurons. By lowering arachidonic acid levels, the researchers found they could allow neurons to function normally." (end quote)


c) Acquired Mitochondrial Damage


Considering the dietary changes that have occurred over the last century and their delerious effect on the quality and the function of the brain mitochondria (explained in the previous chapter), it is obvious that AD can appear in people with NO maternal AD inheritance and that if the person acquiring mitochondrial defect happens to be a woman she me start a new AD maternal inheritance line by transmitting damaged mitochondria to her children.


d) A Big Lifestyle Change: The Event of Artificial Light

A factor that also may have played a role in the onset of the AD epidemic is the event of artificial light.

In the latest years of the nineteenth century electricity became available for public and private use as a source of artificial light. It was a change in lifestyle that was accepted as a great improvement. Nobody realized at that time—and there is still little awareness of it today, that using artificial light after sunset has forever disrupted the natural circadian rhythms of day and night.

It may seem far-fetched at first that something apparently as trivial and unrelated to our topic as the event of artificial light could play a role in the onset of the AD epidemic. However when one considers that circadian rhythms regulate the production of the hormone melatonin, that a disruption of melatonin secretion is described in AD patients and that multiple symptoms present in AD patients are also attributed to a melatonin defect, a possible link between artificial light and the AD epidemic becomes more believable.

Melatonin is a hormone secreted by the pineal gland. Melatonin regulates several biological functions the list of which is still growing as new connections are described. Among others, it is now well established that melatonin counteracts the lipid peroxidation of cell membranes and protects chromosomal and mitochondrial DNA (mtDNA).

In animal experiments melatonin has been found to restore the secretor function, Ca2+ signals and mitochondrial potential of cells the same mitochondrial functions  that are defective in AD.

Melatonin is a potent anti-oxidant and anti-inflammatory agent and has been found in animal experiment, to reduce amyloid plaque deposit and cell death.

Insomnia and abrupt mood change, both considered forerunners of the condition may appear years before full blown AD and are related to a reduced melatonin presence.

The secretion of melatonin crumbling with age may well be a tipping point where the effect of the inherited or acquired mitochondrial damage becomes irreversible and AD starts developing


4 - Until now there was no cure. The nutritional approach, however, is promising

Clinical Trials for Possible Pharmaceutical Prevention and Treatment of AD:

More than 400 clinical trials have been performed or are in progress to investigate possible prevention and treatment for the condition. The National Institute on Aging Alzheimer's Disease Education & Referral Center publishes information about such 49 trials IN THE U.S.A. Most of the trials look at the possible effect of pharmaceutical drugs, Statins (of course) included.
One such study (at the University of Virginia) concludes: (quote):" Finding out what causes AD's damage to brain cells provides possible avenues for new research, and hopefully the development of drugs that will reduce the abnormal oxidative stress in the mitochondria. If we can lessen cell death in AD brains, we should be able to slow the progression of the debilitating symptoms of this tragic disease." (end quote)

A promising nutritional approach:
It as become evident that in Alzheimer, like in other neurodegenerative conditions, brains immune system is over-stimulated. Refined sugar and the omega-6 to omega-3 imbalance of our diet are factors of that over-stimulation. Another factor involved is the disturbance of mitochondrial energy production possibly the result of acquired or inherited mDNA damage, related to mitochondrial membrane oxidation.
This is where a nutritional approach appears promising:
1 - Reducing sugar intake and correcting the omega-6 to omega-3 imbalance of our diet shall reduce the over-stimulation of brain's immune system.
2 - The disruption of the mitochondrial energy production can be alleviated by causing the body to produce more ketones from a supply of medium chain fatty acids, like the lauric and myristic acid abundantly present in coconut oil. Lauric acid is also a potent anti-imflammatory agent.

5 - Is nutritional prevention possible? 

Among the more than 400 trials already performed or in progress only one, the PREADVICE clinical trial looks at prevention of AD with nutraceuticals: vitamin E, C and selenium. The 5 years PREADVICE clinical trial is directed by William Markesbery the director of the University of Kentucky Alzheimer's Disease Research Center (ADRC)

(quotes) " So far, vitamin E has emerged as one of the weapons we have against dementia. There are several other things you can do to lower your risk of getting Alzheimer's, but vitamin E taken in conjunction with vitamin C is important—a previous study showed that vitamin E is one factor that slows, slightly, the progression of the disease. The important thing for individuals at risk is to take vitamin E and vitamin C along with folic acid prior to getting the disease." AND "There is prior evidence that enhanced levels of selenium in the brain might increase antioxidant defense mechanisms against Alzheimer's disease. Taken together, Markesbery says, these two natural antioxidant supplements might work better than alone in fighting oxidative stress" (end quotes)

The timing of vitamin E supplementation for treating Alzheimer’s might be an important factor in its effectiveness. Vitamin E given to young transgenic mice before the formation of telltale plaques reduced up to half the levels of amyloid deposited in the brain.

It is comforting that at least one trial focusses on antioxidative elements of the diet for the prevention of AD. Vitamin E is a very good choice. Vitamin E is a fat soluble vitamin and as such can protect cell and mitochondrial membranes from oxidation. Selenium is also a very good choice because this trace-mineral, as well as manganese, is involved in DNA and mt DNA repair:

(quote) "To defend against ROS (added: ROS is short for reactive oxygen species), mitochondria metabolize superoxide and hydrogen peroxide with manganese containing superoxide dismutase and selenium-containing glutathon peroxidase, respectively" (end quote). Furthermore, a 2007 New Zealand study found an association between low hair selenium levels and cognitive decline as measured by the Timed Up and Go test (TUG)

Prevention of AD involves much more than only supplementing with vitamin E, C, manganese and selenium.

Other nutracenticals may be useful in prevention of AD. A shortage of vitamins of the B group, particularly a deficiency of vitamin B12, folic acid and vitamin B6 is a factor of arteriosclerosis. Supplementing the diet with vitamins of the B group may avoid the reduction of brain blood supply frequent in older people and an aggravating factor for AD. Vit B, vit B12 and folate concentrations correlate negatively with AD lesions. The mechanism of action may well be the vascular degradation (arteriosclerosis) associated with higher levels of Homocysteine

Then we have vitamin D which is a vitamin (or rather a steroid hormone) that has been neglected until recently. It is as if the compound were discovered again. New light is shed on vitamin D's multiple functions. (See a video about the vitamin D deficiency pandemic). People with AD like all elderly are low on vitamin D and supplementation makes good sense as well as sunbathing an hour twice weekly. (One hour full body exposure = 10,000 IU of vitamin D)

It is obvious that-due to their anti-oxidant property, vitamin E and C as well as the trace minerals selenium and manganese should play a greater role than the vitamins of the B group and than vitamin D in the prevention of AD . Their importance in protecting brain components should not bring us to forget another potent anti-oxidant and anti-imflammatory molecule which is always deficient in AD patients: the hormone melatonin. Melatonin is produced by the pineal gland situated in the brain. Melatonin is secreted during sleep. Its production crumbles with age. Older people complain of sleepiness and AD patients most. They wander around at night and are sleepy during the day.

Melatonin is considered as the "sleep hormone" because it induces sleep. However this is a trivial effect of the molecule only. The main role of melatonin is to protect brain cells: (Quote) " The researchers treated the cells with melatonin then induced cell death in rat cells similar to the way amyloid plaque causes cell death in humans. They found that cells pre-treated with melatonin had a reduced rate of death. In addition, melatonin effectively suppressed nitric oxide formation, prevented intracellular calcium overload that can occur with amyloid plaques, and significantly reduced membrane rigidity."(end quote)

Melatonin supplementation may well become as important in AD prevention as vitamin E, C, selenium, manganese, the vitamins of the B group and vitamin D. (quote):"These results supported the hypothesis that oxidative stress was an early event in AD pathogenesis and that antioxidant therapy may be beneficial only if given at this stage of the disease process. In sharp contrast to conventional antioxidants, melatonin crosses the blood-brain barrier, is relatively devoid of toxicity, and constitutes a potential therapeutic candidate in AD treatment."(end quote)

In AD prevention it makes good sense to limit the damaging effect of oxidation (and glycation) of brain cell components by supplementing the diet with the molecules cited above. However it makes equally-if not more sense, to avoid the damage to brain cells by reducing the consumption of foods that most inflict it.

The foods to avoid in AD prevention and for the reasons explained previously are refined sugar, high fructose corn syrup, all vegetable oils and-of course, all manufactured food containing them.

Research by Bruce Fife, ND indicates coconut milk and coconut oil supplementation
may also help prevent Alzheimer disease


a - AD risk assesment

1 - The five A.D. risk factors

a) The maternal inheritance factor witch we like to name the Mosconi factor since the maternal inheritance of AD was first described by Lisa Mosconi, Ph.D.,M.S.
People whose mother or maternal grandmother has AD are at risk of developing the condition after they reach sixty years.

b) The chromosomial factor. People that carry the chromosomal alterations described in the early onset AD form and found in about 0.04% of the population are at risk of developing the condition well before they reach 60 years.

c) The lifestyle factor . The risk of developing AD is greater in people with sleep problems.

d) The diet factor: The risk of developing AD is greater in people on a diet containing an excess of sugar, trans fatty acids and vegetable oils and deficient in medium chain fatty acids, long chain omega-3 essential fatty acids, anti-oxidants, minerals (particularly selenium, and manganese) and vitamins (particularly vitamin C, D, E and the vitamins of the B group).

e)The vascular factor. Arteriosclerosis of the carotide artery reducing brain blood supply aggravates AD damage.

If you are without any maternal inheritance factor for AD but with sleep problems and a bad diet that may alter the composition and the function of your brain mitochondria you may develop the condition.

Furthermore, if you are a women you can also initiate a new maternal AD lineage for your descendants.

2 - Evaluating your A. D. risk

Whatever the relative importance of the five factors described above, the damage they may cause on brain structures can be approached:

a) By a psychological evaluation comprising a mental status exam or by screening with the Geriatric Depression Scale (GDS) . A GDS provided by Drs. Wes Ashford and Anil Sharma of VA Palo Alto Health Care Systemis is available on the web for free. as well as an elementary Alzheimer's Symptoms Quiz (A"Aricept" product promotion by Pfizer). See also a list of symptoms with an an illustration of the brain indicating what symptoms are linked to the part of brain most affected.

b) By brain Positron Emission Topography (PET) measuring the level of glucose metabolism in brain cells.

c) By Magnetic Resonance Imaging (MRI). A new type of automated MRI scan may help detect early signs of AD in the brain decades before the first symptoms of dementia may appear.


b - What can you do to lower your AD risk?

What you can do to reduce your risk is improving or restoring your circadian rhythm, changing your diet by the reduction of vegetable oils, sugar and starch, and supplementing with n-3 EFAs, vitamins, minerals and anti-oxidants

1 - Reset your biological clock

Exposure to artificial light may have disregulated your biological clock. Light reaching your eyes triggers a nerve impulse that travels to the center of your brain and controls your biological clock. Artificial light after sunset disrupts the natural day-night cyclus. Reset your biological clock particularly if you are complaining of poor sleep. Resetting the clock involves avoiding bright light in the evening and getting ALL light out of your bedroom. Your brain produces melatonin only when informed of darkness .

Poor sleep, agitated sleep with anxiety and frequent awakening as well as difficulty to fall asleep are related to a melatonin deficiency.

The following is an excerpta from the "Hormone Handbook" by Dr. Thierry Hertoghe . (quote) "Melatonin deficiency not only includes sleep complains but also fatigue during the day, abdominal pain related to intestinal overactivity, tense muscles, restless leg syndrome, anxiety , lack of serenity, of peace of mind, depression, seasonal affective disorders, irritability and emotional instability, hypertension, premature aging and intense jet lag symptoms when crossing from a time zone to another. (end quote) Dr. Hertoghe also cites Alzheimer's disease in his list of disease susceptibility for people with melatonin deficiency.

USING MELATONIN: Start with 0.1 mg of melatonin under the tongue 15-30 minutes before bedtime. Should this not work, take 0.2 mg the next day. Increase the daily dosage by increments of 0.1 mg until your reach your optimal level. It may take a few weeks before you feel some effect and three months is the average timespan to reset your biological clock.

An overdosage of melatonin produces a short and deep sleep during 3 to 4 hours (with nightmare) followed by strong heart beat, profuse sweating and 24 hours of heavyheadness.

2 - Change your diet

a) Suppress your transfat and excessive linoleic acid intake by staying away from vegetable oils. Instead revert to butter, beef tallow, lard and fruit oils (olive, palm. coconut). Reduce the intake of sugar and of food with a high glycemic index

b) Fry meat, eggs, fish and other food at low temperature in butter or fruit oils (best is coconut)

3 - Take supplements

a) Add fish oil to your vitamin regimen to increase your long chain omega-3 EFAs intake.

b) Make a habit of taking daily one cup of coconut milk, a good mix of vitamins and minerals providing in particular vitamin C: 200 mg/ day, vit D: 2.000 IU/ day, vit B 12: 500 micrograms/ day, vitamin B6: 25 mg/day, Folic acid: 2.5 mg/ day, selenium: 100 microgram/ day per 60 lb bodyweight with a maximum of 300 micrograms per day, manganese: 5 mg/ day, calcium 400 mg/ day

c) Don't forget CoQ10, 100 mg/d the most potent anti-oxidant protecting your mitochondria

d) Take daily at least a tablespoon of coconut oil

4 - Stay away from Statins

They have been found to inhibit CoQ10 and to further damage the mitochondria

5 - Your brain blood supply

Should you have had some brain blood supply problems like a transient ischemic attack, have your carotide arteries blood flow checked

More info

To further document yourself, download a list of 137 URLs of Interest


   Copyright © 2008-2010 Edmond Devroey MD