Quote from jobo on September 18, 2019, 3:10 am

Good summary and great effort. 

Quote from lil chick on September 18, 2019, 5:20 am

I assume you are going to break it up into paragraphs?  (grammar nazi here lol).  Here is a whack at it: 

...

Finland has 22-times the rate of Alzheimer’s as does Russia right next door. The Finnish people historically eat far more cod than Russians do. On the other side of the Atlantic, Canadians in the Eastern Provinces had a spectacular 30% decline in Alzheimer’s since the mid-90’s when cod-fishing was banned and they began to eat less of it. Cold-water cod of the North Atlantic have ten-times the amount of Vitamin A than warmer-water cod of the Pacific. Finns and Eastern Canadians shared in an excess intake of Vitamin A via consumption of North Atlantic cod.   The correlation of Vitamin A to these Alzheimer’s disease-rates is much stronger than any genetic-causation hypothesis. Differences in west Canada’s Alzheimer’s numbers also confirm this new thesis.

Medical science has long-documented the toxicity of Vitamin A in numerous research studies. One member of this family of molecules is Retinoic Acid - right up there with Thalidomide on the list of poisons that cause birth-defects. It’s a well-researched teratogen, proven to be so thousands of times over. Retinol is another form of Vitamin A that is also toxic. The National Institutes of Health reports a mere 12-milligrams a day of this molecule can cause liver-damage. Retinol easily metabolizes into Retinoic Acid in our bodies and the chemical difference between them is only one atom of oxygen. Retinoic Acid is estimated to be at least ten times as dangerous as Retinol and is used in chemotherapy for its toxicity.

What problems has Retinoic Acid been proven capable of causing in human cells and tissues? Protein misfolding. Epithelial tissue inflammation. Pathological stem-cell differentiation. Depletion of stem-cells. Mitochondrial dysfunction. Exaggerated immune response. It can cause all of the symptoms of the misunderstood autoimmune conditions – over 50 named to date. The immune-system is doing its job but is aggravated and tricked by cellular-damage due to poisons. The sub-clinical nature of the toxicity, accumulated over years of excess Vitamin A intake, has helped mask the culprit.

The exponential increase in many chronic diseases points logically and directly to an environmental cause. It took an engineer in Alberta Canada named Grant Genereux about 4 hours of reading to distill the essential insight about Vitamin A as a factor in his eczema. He now has over 5 years-worth of ongoing research into understanding how eliminating Vitamin A and Carotenoids from his diet cured him of chronic kidney disease, eczema, failing eyesight, painful joints, and unexplained fatigue.

He discovered North America’s average VA consumption is rising dramatically, along with these diseases – particularly since 1973 when our foods began being fortified with a form of VA called Retinyl Palmitate. The answers to these disease epidemics have been in the medical-research literature for decades. The fact that literally the entirety of modern medical science missed this all-too-obvious sub-clinical toxicity story is undoubtedly the biggest blunder in medical history.

Vitamin A is implicated in causation of the autoimmune diseases. It is implicated in all kinds of cancers. It is implicated in autism. It is implicated in Alzheimer’s, osteoporosis, obesity and much more, including heart disease. Any part of the body that has epithelial tissue can suffer chronic damage from Retinoic Acid. Note the 7000 lawsuits against Hoffman-Roche for Accutane (Retinoic Acid) damages, many youth suffering Crohn’s as a result of taking it.

Systemic toxicity is likely why cells in a variety of organs – not just the liver - create their own proteins to bind (wrap) Retinol and Retinoic Acid. These binding-proteins may provide cell protection from these reactive molecules. This is a new concept presented by Grant, and when validated, it will overturn conventional views that retinoid binding-proteins are made solely for transport. Their function is looking more like that of antibodies.

Grant has scientifically overturned results of animal-studies that were botched long ago and which actually proved the opposite of what was claimed. Researchers didn’t know about Retinoic Acid in the 1920’s or that it was in the rat-chow they designed. They inadvertently poisoned their animals and thought they had proven Vitamin A deficiency. These poor critters died miserably of acute auto-immune conditions in ten weeks or less. Grant raised mice that were vigorous and healthy on a zero-A diet long past ten weeks. Others are repeating this simple experiment successfully at home.

One last thing here. Try to imagine WWII POW’s fed a cup of rice a day for three years surviving with their eyesight, organs and skin intact. That’s not supposed to happen, since rice is a food with almost zero Vitamin A.

There’s a lot of practical advice at Grant’s blog where zero and low Vitamin A consumers are sharing their experiences. Three very informative books are free to download at his website. Geographic evidence he’s mapped is as compelling as the science he’s uncovered. He also takes a close look at the various comorbidities of Alzheimer’s for further confirmation of this causation-thesis. It’s worth your time to delve deeper than this summary can provide. The books read like detective novels and are difficult to put down. Do it for someone you love @ Ggenereux.blo

Quote from MaryAnn on September 18, 2019, 2:41 pm

Hi  @hillcountry

This is a great summary!  The only thing I would change is to leave out the part about retinoic acid binding proteins being like antibodies. Antibodies are a distinct class of molecules that bind to foreign proteins in the body, they don't bind to chemicals, such as retinoic acid, only proteins. Adding this part about antibodies might make the whole theory suspicious to a scientist. I was a bit taken back when I first read the post about antibodies, but since I'm already a "believer" it wasn't so big a deal. 

Quote from hillcountry on September 19, 2019, 4:25 am

Thanks jobo, lil chick, and MaryAnn. I've made changes, added a bit, and it still fits on one sheet of paper!! See what you think. I really appreciate your insights, suggestions and encouragement. Latest revision is at the top of this thread.

Quote from hillcountry on September 19, 2019, 7:13 pm

Thanks Grant, for discovering and passing along this very interesting paper. It's going to be a valuable addition to the handouts at Alzheimer's Walks coming up in Michigan. The simplicity of it is a great access-point for someone new to the idea. 

Here's the text of the 1992 study - Vitamin A and Alzheimer's Disease by John M. Lewis in the journal Neuroepidemiology.     I left the reference-markers out, as well as the list of references at the end. Maybe I'll figure out a way to link to the study via the    Al Taubman Medical Library at the U-M campus where it's archived. 

Alzheimer’s disease, a devastating illness for its victims, has also proved to be a formidable challenge for its investigators. The disease remains largely a mystery, even after many years of intensive and painstaking research. Epidemiologic study of Alzheimer's disease has proved to be particularly difficult, and has produced only a limited amount of data. The author has selected some of this epidemiologic data for comparison with scientific material from other sources, and will attempt to interconnect all of the information in a manner which may have significance for the etiology of Alzheimer's disease. Presented for consideration are the following epidemiologic data on Alzheimer's disease.

Old age is the major risk factor for Alzheimer's disease; nearly one of every two Americans will be afflicted by age 85.

Alzheimer's disease seems to have a strange predilection for those who have tried to maintain good health.

American women are significantly more likely to get Alzheimer's disease than are American men. White Americans are significantly more likely to get Alzheimer's disease than are black Americans.

Individuals with rheumatoid arthritis are significantly less likely to get Alzheimer's disease than are those without rheumatoid arthritis.

Also presented for consideration are the following scientific data not specifically related to Alzheimer's disease. Vitamin A, consumed either as a single supplement or as a constituent of multivitamin preparations, is a fat-soluble agent which can accumulate in the body and, in large doses, is a known neurotoxin.

If the validity of these statements may be accepted, the author proposes a single simple hypothesis which can account for each of the selected epidemiologic statements on Alzheimer's disease. It is possible that this hypothesis may help to explain the entire complex of Alzheimer's disease. This hypothesis would suggest that there may be a causal relationship (though not necessarily an exclusive one) between the development of Alzheimer's disease and the long-term mild over-dosage with vitamin A. Such a relationship would easily explain and interconnect all of the seemingly disparate epidemiologic data previously considered:

Through diet and supplements the elderly are exposed to elevated doses of vitamin A over many years, hence the extraordinarily high prevalence of Alzheimer's disease (47.2%) in those 85 years of age or older.

Largely in the mistaken belief that good health will result, a segment of the American population consumes vitamin supplements in addition to the additives supplied in their diet. This presumably health-conscious group is therefore exposed to greatly increased doses of vitamin A, hence the seemingly paradoxical predilection of Alzheimer's disease for this group.

American women consume significantly more single and multivitamin supplements than do American men. This results in a greater cumulative dose of vitamin A, hence a significantly higher prevalence of Alzheimer's disease in American women than in American men

White Americans consume significantly more single and multivitamin supplements than black Americans, resulting in a greater cumulative dose of vitamin A, hence a significantly higher prevalence of Alzheimer's disease in American whites than in American black.

Patients with rheumatoid arthritis are treated coincidentally with the same drugs known to inhibit the toxic effects of vitamin A on laboratory animals. Though human data are unavailable, a similar protective effect might be inferred, hence the significantly lower prevalence of Alzheimer's disease among patients with rheumatoid arthritis than in the normal population.

The concept that hypervitaminosis A may be an etiologic factor in the development of Alzheimer's disease would also help to explain some of the hitherto unsolved riddles associated with Alzheimer's research.

The hypothesis would help to explain the absence of any natural animal model for the disease, on the basis that no animal (except man) chronically overdoses itself with vitamin A.

The hypothesis might well account for the findings in studies of Alzheimer's disease in identical twins. Unexpectedly. several of these studies revealed considerable discordance and were incompatible with a purely genetic mode of transmission of Alzheimer's disease. This discordance might well be explained by different degrees of exposure to vitamin A, most likely in the form of vitamin supplements.

The hypothesis might account for the impression, if not reality, that the incidence of Alzheimer's disease is much higher now than in past years. It was not until 1947 that vitamin A was successfully synthesized on a commercial basis, but after this time it became widely available in foodstuffs and as a supplement.

Granting a latent phase of 2-3 decades, intake of the newly synthesized vitamin A would result in a dramatically increased incidence of Alzheimer's disease beginning in the 1970s.

The hypothesis might explain the impression, if not the reality, that Alzheimer's disease is rare among inhabitants of Third World countries. Known as the •prosperity vitamin', vitamin A has traditionally been a very scarce commodity in poor countries. Inhabitants of these countries derive most of their vitamin A from carotene precursors which do not carry the risk of vitamin A toxicity. Exposure to toxic levels of vitamin A does not occur, and Alzheimer's disease is accordingly rare or nonexistent.

Americans consume excessive amounts of vitamin A in their diet (mostly in the form of food additives) when measured against standards set by the World Health Organization and the Food and Agriculture Organization in 1986. A segment of the American population consumes additional vitamin A in the form of single or multivitamin supplements.

Among Americans consuming vitamin A supplements, the elderly take significantly more than the young, women take significantly more than men, and whites take significantly more than blacks.

Aspirin, corticosteroids, and the nonsteroidal anti-inflammatory drugs have been shown to prevent the toxic effects of large doses of vitamin A on laboratory animals.

The hypothesis might explain the impression, if not the reality, that patients with early-onset Alzheimer's disease deteriorate faster than patients with late-onset disease.

The latter group. more likely to be suffering from the usual aches and pains of old age, are more apt to be chronically medicated with aspirin or other anti-inflammatory agents, which may slow or halt the progression of the disease. The disease proceeds at full speed in the younger and otherwise healthier group.

The hypothesis would account for the generally disappointing results produced by the many epidemiologic surveys on Alzheimer's disease. In the light of the hypothesis, all attempts at case-control studies would have been predestined to fail, since the entire population had already been exposed to the toxin (excessive vitamin A) through food additives; real control groups did not and could not exist.

Moreover. otherwise valid epidemiologic data may well have been confounded by the subjects' use of any of the anti-inflammatory drugs, such as aspirin. These drugs are taken so commonly that their use goes largely unnoticed and unmentioned.

 

The proposed hypothesis might well help to explain the long-suspected but as yet unproven role of aluminum in Alzheimer's disease. Aluminum is a known cytotoxin, but so common in the environment that for all practical purposes it is impossible to avoid exposure to it. Fortunately, only minimal absorption of aluminum occurs through the normal human intestine, and virtually none of it penetrates the healthy blood-brain barrier. The aluminum which does gain intracellular access is believed to be sequestered in lysosomes, where it may be relatively harmless to ongoing metabolic processes. Indeed, it has been estimated that humans could live to 150 years of age before eventually being overwhelmed by and succumbing to the cumulative toxic effects of aluminum. This normal status may be altered in the presence of chronically elevated levels of vitamin A. Large doses of vitamin A (retinol) are believed to exert toxic effects by overwhelming the specific retinol-binding protein system, resulting in the retinol being transported in great excess to inappropriate sites by nonspecific lipoproteins. It might be speculated that excessive doses of the highly membrane-active vitamin A might alter the absorption characteristics of the human intestine, and allow for increased absorption of aluminum. It would not be unreasonable to propose that elevated doses of this known neurotoxin might likewise impair the integrity of the blood-brain barrier, facilitating the passage of aluminum into the central nervous system. And it is known that one of the effects of vitamin A as a toxin is the disruption of biologic membranes, particularly lysosomal membranes. Lysosomal destruction would result in the discharge of sequestered toxins (including aluminum) into the cell, causing cell damage or death. By these various mechanisms, a chronically excessive level of vitamin A might transform the functionally rather harmless aluminum into an active neurotoxin. Aluminum and vitamin A may be interrelated in yet another and quite unexpected way. Vitamin A is destroyed mainly by oxidation, a process that occurs most readily in the presence of copper or iron. These metals were used as cookware for hundreds of years, and would have served to lower the vitamin A content of any food cooked or stored in them. Aluminum cookware was introduced at the end of the last century, and it has to a large extent supplanted iron and copper in this regard because it is light and inexpensive. Aluminum cookware does not hasten the destruction of vitamin A as does cookware of copper or iron, resulting in an increased amount of vitamin A (natural or synthetic) being passed along to the consumer. This would effectively raise vitamin A levels in entire populations. Vitamin A is partially excreted by the kidneys, and levels rise significantly in renal failure. It is possible that hypervitaminosis A may have played an unrecognized role in the development of dialysis encephalopathy, a syndrome occurring in the mid-1970s when renal failure patients were unknowingly dialyzed against fluids containing small amounts of aluminum. These patients exhibited florid central nervous system symptoms which resolved only when aluminum was removed from the dialysate or a functional kidney implanted. Brain aluminum levels in these patients were noted to be high, and the levels remained high even after resolution of the encephalopathy. Perhaps the syndrome was produced by the acutely high levels of both aluminum and vitamin A acting in concert, a condition which subsided when blood levels of one or both components returned towards normal. The duration of exposure may have been too brief to allow for the development of the classic pathological stigmata of Alzheimer's disease, and the insult to the brain may have been limited enough to allow for full recovery. The concept that a vitamin may act as a cofactor with aluminum in the development of Alzheimer-like neurologic disease does not originate with this author. Dr. Ralph Garruto, an investigator of the amyotrophic lateral sclerosis-parkinsonism-dementia complex in the western Pacific, has suggested this very same possibility: It is also probable that other interacting factors such as vitamins, hormones, enzymes, and drugs can dramatically promote or modify the toxic expression of aluminum'. It may also be of interest to note that both aluminum and vitamin A were in common use well before the first described case of Alzheimer's disease in 1907. Vitamin A (in the form of cod-liver oil) was widely prescribed for a number of 'wasting' ailments before the turn of the last century, and aluminum was available in a variety of applications soon after commercial production began in 1886. It is thus conceivable that the very first case of Alzheimer's disease — as well as the millions to follow in our own time — may have resulted from the overuse of vitamin A and the bioavailability of aluminum. The author wishes to Close with an ominous and possibly prophetic quote from Pitt: …people seem curiously reluctant to recognize just how toxic is vitamin A. I have long asserted that considered as a chronic poison vitamin A is probably more harmful than cyanide, but I have usually been disbelieved Vitamin A is an essential substance: for lack of it many people in the world suffer ill-health. Irreversible blindness or death. But it is a very dangerous substance and it needs to be handled with care.