Dr. William Grant provided this thorough review of Alzheimer's disease and, as mentioned in his bio below, he published the first paper linking diet to Alzheimer's disease and identifying the major dietary components that are risk and risk reduction factors.
Before you get into the article, I'd like to point out that one of the dietary recommendations that Dr. Grant mentions is fish. While fish would be an extremely healthy food, I would not recommend it eating it to reduce your risk of Alzheimer's because, unfortunately, most all fish is contaminated with mercury and other pollutants. Unless you can verify via lab testing that the fish you are eating is mercury-free, I would not eat it.
However, an excellent alternative to eating fish is taking high-quality fish oil or cod liver oil, either in the form of Carslon's liquid or Living Fuel Omega 3 and E. Eating plenty of fish oil is an important part of preventing Alzheimer's (and a host of other diseases as well).
Following are additional steps you can use to reduce your risk of Alzheimer's. These inexpensive and natural methods can be easily implemented by anyone, and you can keep them in mind as you read the article below:
By William B. Grant, Ph.D.Sunlight, Nutrition and Health Research Center (SUNARC)www.sunarc.org
[Peer-reviewed by Dr. Russell Blaylock]
Fish and Fish Oil Reduce AD Risk
The role of fish in reducing the risk of AD was further discussed in 36 and confirmed by a French team 37, as well as by a team at the Rush Alzheimer's Disease Center in Chicago 9,38. The French team extended their work on fish and AD, finding that those who ate fish at least once a week had a relative risk of AD of about 0.7 compared to those who didn't 39. Fish consumption was found inversely correlated with cognitive impairment among middle-aged Dutch, while cholesterol was positively associated 40. The benefits of the primary n-3 fish oils, DHA and EPA, appear to include providing the lipids required for proper brain development and maintenance 41,42 and reducing inflammation 43.
Fatty Acids and AD
It should be noted that one of the first signs of impending AD is what is called cognitive impairment (CI). Thus, studies of dietary links to CI are useful regarding AD, and, indeed, they find much the same results as the AD studies e.g., 11,12. Such results, as well as some for AD, indicate that there are good fats and bad fats, as mentioned above.
However, the ratio of n-6 to n-3 fatty acids is also important, with a ratio of LA to ALA (n-6 to n-3) of about 4:1 being optimal 44,45. This value is nearer to the 1:1 or 2:1 ratio found in the diet of our ancestors than the 10:1 to 25:1 found in present day Western diets 46.
Also, extra virgin olive oil, with its strong antioxidant properties, is a good choice. Virgin olive oil should be considered a risk reduction factor for AD since it has plenty of phenols with high antioxidant capabilities 47. These compounds have been suggested to be very useful when free transition metal ions are involved in oxidation processes 47, as is the case in AD (see discussion below).
Obesity Increases Risk of AD
In addition, there has been further support of the finding that total energy consumption is a risk factor for AD 48,49. Mark Mattson has long championed the idea of caloric restriction for reducing the risk of AD 50, and a recent paper identified obesity as a risk factor for AD 51 with the comment that it was likely related to diet 52. The epidemic of obesity in the United States aa ppears to be linked to increased consumption of convenience food, which is energy-dense 13. These foods are rich in sweeteners (fructose and sucrose), other refined carbohydrates, and animal products high in fat. Sugar is also implicated as a risk factor for AD through the finding that type 2 diabetes mellitus is associated with increased risk of AD 53,54.
Wine Consumption
Two recent studies reported that risk of AD decreased markedly with wine consumption for mild and moderate drinkers 39,55. The risk ratio for AD for moderate drinkers was 0.53 (95% C.I. 0.30-0.95) compared to non-drinkers 39.
Very similar results were found for up to three glasses of wine per day, but not for other alcohol beverages in another study 55. Also, these results were limited to those who did not have the APOEe4 allele.
It is likely the antioxidants in wine that were responsible for this result. Wine has been proposed as an explanation for the "French paradox" regarding coronary heart disease 56. However, another possibility for the brain is that resveratrol in red wine is responsible. A recent paper reported that resveratrol was able to significantly induce heme oxygenase 1, thereby reducing the oxidative stress on neurons 57. Resveratrol also exerts an anti-oxidative action by enhancing the intracellular free-radical scavenger glutathione 58. Resveratrol is also available from grape juice, but is not as readily absorbed as from wine 59,60.
Why Antioxidants are Useful for Alzheimer's Disease
Since AD is to some extent a disease of oxidative stress, it would be expected that antioxidants would reduce the risk of developing AD. That is indeed the case. One prospective study found that a high intake of flavonoids found in tea, fruits, and vegetables reduced the risk of AD by about half 61. A prospective cohort study in Rotterdam found that high consumption of vitamins C and E reduced the risk of AD by 20 percent to 40 percent, with the most pronounced benefit found for smokers 62. Antioxidants are, of course, useful in reducing the risk of a large number of degenerative diseases 63.
An observational study found peripheral levels and activities of all antioxidants reduced in those with mild cognitive impairment and AD 64. A recent study reported that those taking large amounts of vitamins C and E in combination had one-quarter to one-third the risk for AD as those not taking the vitamin supplements 65.
Cholesterol and AD
Cholesterol has been a known risk factor for AD since the early 1990s 23. Cholesterol is often elevated by a diet high in fats 66 and/or high in sugars 67. The role of cholesterol in the etiology of AD was recently reviewed 68,69. The mechanisms are still under review 70,71.
Paradoxically, however, it may be the high-density lipoprotein (HDL) rather than the low-density lipoprotein (LDL) cholesterol that is the bad actor 72, the reverse of the case for heart disease. In heart disease, LDL can clog the arteries, and oxidized LDL can break off the arterial walls and block blood flow to the heart. Thus, use of statins, which act primarily to reduce LDL cholesterol, may not reduce the risk of developing AD 73.
Since cholesterol is implicated as a risk factor for AD, statins, which reduce serum cholesterol levels, especially the LDL fraction, may be useful in reducing the risk of AD 74. Some studies support this hypothesis e.g., 75 and others are underway 76.
Homocysteine Increases the Risk of Alzheimer's
Homocysteine is another risk factor for AD. Homocysteine was first identified as a risk factor for arteriosclerosis from autopsy studies by Kilmer McCully 77. For his important pioneering work, he was dismissed from Harvard and black-listed for several years. Homocysteine levels are elevated when there are deficiencies of vitamin B6, folate, and vitamin B12 78,79. A prospective study found that elevated homocysteine levels were associated independently with increased risk for AD 80.
Conversely, patients with AD have been found to have elevated levels of homocysteine 81,82. Also, patients with stroke and VaD have elevated levels of homocysteine 81.
The Role of Metal Ions Including Aluminum
Metal ions are also involved in the pathology of AD. It is well known that aluminum is elevated in the brains of AD patients 83. Less well known, but well documented, is that transition metal ions (e.g., copper, iron, and zinc) are also elevated, while base cations (e.g., calcium and magnesium) are at lower concentrations 83.
I have attributed this phenomenon to a high consumption of acid-forming foods, such as animal products, which are high in protein (amino acids) and fat (fatty acids). These acids may dissolve the aluminum or transition metal oxides in the food we eat and, thus, permit the ions to be absorbed into the blood 49,84.
There is also the possibility that aluminum from aluminum soft drink cans can be ingested, since carbonated drinks are highly acidic and can leach out aluminum 85. In addition, some soft drinks also contain moderate levels of fluoride, and, in combination with aluminum, can be a risk factor for AD 86.
These transition metal ions and aluminum ions increase the production of free radicals such as hydroxyl 87, both in the body and in the brain, and, thus, are involved in oxidative damage to the brain 88-95. It has been suggested that the transition metal ions can be removed from the body by chelation in a manner that reduces the oxidative damage to the brain 96; a clinical intervention using clioquinol, a metal-protein-attenuating compound (MPAC) that inhibits zinc and copper ions from binding to beta-amyloid, thereby promoting beta-amyloid dissolution and diminishing its toxic properties 97.
William B. Grant has a Ph.D. in physics from U.C. Berkeley and has worked at the level of senior research scientist in the fields of optical and laser remote sensing of the atmosphere and atmospheric sciences at SRI International, the Jet Propulsion Laboratory, and the NASA Langley Research Center. He is the author or coauthor of over 60 physics, instrument development, and atmospheric sciences articles in peer-reviewed journals, has edited two books of reprints, and contributed half a dozen chapters to other books. He published the first paper linking diet to Alzheimer's disease and identifying the major dietary components that are risk and risk reduction factors. He has also studied the links between dietary sugars and heart disease and obesity, diet and breast, colon and prostate cancer, and UVB/vitamin D and cancer and autoimmune diseases. He recently retired from NASA and founded Sunlight, Nutrition and Health Research Center (SUNARC) (www.sunarc.org), where he will continue and extend his health research and educational efforts.
William B. Grant has a Ph.D. in physics from U.C. Berkeley and has worked at the level of senior research scientist in the fields of optical and laser remote sensing of the atmosphere and atmospheric sciences at SRI International, the Jet Propulsion Laboratory, and the NASA Langley Research Center. He is the author or coauthor of over 60 physics, instrument development, and atmospheric sciences articles in peer-reviewed journals, has edited two books of reprints, and contributed half a dozen chapters to other books.
He published the first paper linking diet to Alzheimer's disease and identifying the major dietary components that are risk and risk reduction factors. He has also studied the links between dietary sugars and heart disease and obesity, diet and breast, colon and prostate cancer, and UVB/vitamin D and cancer and autoimmune diseases. He recently retired from NASA and founded Sunlight, Nutrition and Health Research Center (SUNARC) (www.sunarc.org), where he will continue and extend his health research and educational efforts.
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