Alzheimer’s disease is the most common form of dementia and is usually diagnosed in people over age 65 but it can occur earlier. A progressive form of senile dementia, it damages areas of the brain involved in memory, intelligence, judgment, language and behavior. The disease is characterized by the presence of neurofibrillary tangles and beta-amyloid plaques in the nerve cells. The cause of Alzheimer’s disease is currently unknown but there are some factors that may increase its likelihood, including high blood pressure, severe head injury and the prior occurrence of Alzheimer’s disease in a first degree relative, such as a parent, brother or sister. Biochemical differences observed in Alzheimer’s patients, coupled with the effects of different diets on the frequency of the disease, have also suggested a dietary association which we will examine.

The Bottom Line

For those readers who would like to get straight to the bottom line, here it is. There is growing evidence to suggest that eating a predominantly plant-based diet reduces the risk of getting Alzheimer’s disease. As the animal and caloric content of the diet increase, so also does the risk of Alzheimer’s, except in the case of eating fish or taking supplements rich in the omega 3 fatty acid DHA, which may confer some protection. For more details, please read on.

Plasma Homocysteine Levels in Alzheimer’s Disease

In a rigorous prospective study of 1092 elderly subjects who were initially free of dementia, it was found after 8 years of follow-up that 111 of the subjects developed dementia, most cases being Alzheimer’s disease (1). It was discovered that an elevated level of plasma homocysteine could be a predictor of the disease with the risk nearly doubled for those with the highest concentrations. The authors concluded that “an increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer’s disease.” An association has also been reported between elevated levels of plasma homocysteine and cognitive impairment (reduced mental capacity) (2). The investigators found serum homocysteine to be “an early and sensitive marker for cognitive impairment”. Thirty-nine percent of their patients with mild cognitive impairment had pathological serum homocysteine levels. Homocysteine is formed in the liver from the amino acid methionine, a building block of protein, and this amino acid is present in 2-3 times higher concentrations in dietary animal protein compared to plant protein.

Association between Different Diets and the Incidence of Alzheimer’s Disease

Dietary studies have shown that there is a greater risk for Alzheimer’s disease in people who consume diets high in cholesterol, saturated fats, and total calories, and low in fiber, vegetables, and fruits (3 – 5). In a prospective study of Seventh Day Adventists, subjects were matched for age, sex and zip code and those who ate meat were more than twice as likely to become demented as their vegetarian counterparts in the matched group. The discrepancy was further widened when past meat consumption was taken into account (6).

In a study of 4,740 Utah residents, it was found that supplements containing the antioxidant vitamins C and E might offer protection from Alzheimer’s disease. At the beginning of the study, people taking the vitamin supplements were 78% less likely to be diagnosed with Alzheimer’s disease. Four years into the study, those who had been taking the supplements were 64% less likely to have the disease suggesting that the antioxidants might protect the aging brain from oxidative damage associated with the pathological changes of Alzheimer’s disease (7).

A recent study of 2,258 non-demented individuals in New York has shown that adherence to the Mediterranean Diet is associated with a reduced risk of Alzheimer’s disease (8, 9). This diet is characterized by a high intake of vegetables, legumes, fruits, and cereals; a high intake of unsaturated fatty acids (mostly olive oil), and a low intake of saturated fatty acids; a moderately high intake of fish; a low to moderate intake of dairy products (mostly cheese or yogurt); a low intake of meat and poultry; and a regular but moderate intake of alcohol, mainly wine and with meals. The study found that the greater the adherence to the diet, the lower the risk of Alzheimer’s disease. There was a significant dose – response relationship. Compared to those with the lowest scores of adherence, those with middle scores were 15% less likely to develop Alzheimer’s disease, and those with the highest scores were 40% less likely to have the disease. In a complex analysis in which adjustments were made for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, smoking, medical comorbidity and body mass index, adherence to the diet remained the main predictor of Alzheimer’s disease. Those who adhered most to the diet also tended to smoke less and had a lower calorie intake.

In a follow-up study (10) by the New York researchers of almost 2000 people averaging 76 years of age of whom 194 had developed Alzheimer’s disease, the results were confirmed. The investigators analyzed each person’s diet during the previous year and scored it on how closely it followed the Mediterranean diet, including mild to moderate consumption of alcohol and low red meat intake. The more closely a Mediterranean diet was consumed, the lower the risk correlation for Alzheimer’s disease. In an extension of this study, the 194 people who had developed Alzheimer’s disease were followed up prospectively every 1.5 years to determine if there was a relationship between adherence to a Mediterranean diet and longevity with the disease. It was found that higher adherence to a Mediterranean diet was be associated with a lower mortality in these patients (11).

A recently reported study from the same research team showed that adherence to a Mediterranean-type diet and increased physical activity were independently associated with a reduced risk of developing Alzheimer’s disease (12). An important component of the Mediterranean diet is fish and in a prospective study of 815 people, aged 65-94 years, in a biracial community in Chicago it was found that subjects who consumed fish once a week or more had a 60% lower risk for developing Alzheimer’s disease than those who consumed fish less frequently (13). Consumption of omega 3 fatty acids that included docosahexaenoic acid (DHA) also reduced the risk of developing Alzheimer’s disease over the 4 years of the study (13). Animal studies using the TG3 transgenic mouse model of Alzheimer’s disease have shown that dietary supplementation with DHA results in a decrease in amyloid plaques and tau protein in brain cells (14). Interestingly, this effect was diminished when the DHA supplementation was combined with the omega 6 fatty acids, arachidonic acid and docosapentaenoic acid (DPA).

Conclusion

It is clear from the studies described that diet may have a role to play in determining the onset of Alzheimer’s disease. Now it remains to identify those dietary factors responsible for the observed differences in the hope that they may yield useful information regarding the causes, prevention and possible treatment of Alzheimer’s disease. A clinical trial sponsored by the National Institute on Aging (NIA) is currently underway to determine whether administration of the omega 3 fatty acid DHA can slow the progression of Alzheimer’s disease (15).

© Christopher J. Jones M.Sc., Ph.D.

References

1. Seshadri, S et al. (2002) Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer’s Disease. N. Eng. J. Med. 14, 346 (7), 476-483.

2. Gottfries C. G. et al. (1998) Early Diagnosis of Cognitive Impairment in the Elderly with the Focus on Alzheimer’s Disease. J. Neural Transm. 105:8-9, 773-786.

3. Luchsinger, J. A. et al. (2002) Caloric Intake and the Risk of Alzheimer Disease. Arch. Neurol. 59:1258-1263.

4. Morris, M. C. et al. (2003) Dietary Fats and the Risk of Incident Alzheimer Disease. Arch. Neurol. 60:194-200.

5. Ortega, R. M. (1997) Dietary Intake and Cognitive Function in a Group of Elderly People. Am. J. Clin. Nutr. 66:803-809.

6. Giem, P., W. L. Beeson, and G.E. Fraser. 1993. The Incidence of Dementia and Intake of Animal Products: Preliminary Findings from the Adventist Health Study. Neuroepidemiology 12: 28-36.

7. Zandl, P. (2004) Reduced Risk of Alzheimer Disease in Users of Antioxidant Vitamin Supplements. The Cache County Study. Arch. Neurol. 61, 82-88.

8. Scarmeas, N. et al. (2006) Mediterranean Diet and Risk for Alzheimer’s Disease. Ann. Neurol. 59 (6), 912-921.

9. Hitti, M. (2006) Mediterranean Diet may cut Alzheimer’s.

http://www.webmd.com/alzheimers/news/20060418/mediterranean-diet-cut-alzheimers

10. Scarmeas, N. et al. (2006) Mediterranean Diet, Alzheimer Disease, and Vascular Mediation. Arch Neurol. 63:1709-1717.

11. Scarmeas, N. et al. (2007) Mediterranean Diet and Alzheimer Disease Mortality. Neurology 69:1084-1093.

12. Scarmeas, N. et al. (2009) Physical Activity, Diet, and Risk of Alzheimer Disease. JAMA 302: 627-637.

13. Morris, M. C. et al. (2003) Consumption of Fish and N-3 Fatty Acids and Risk of Incident Alzheimer Disease. Arch. Neurol. 60: 940-946.

14. Green, K. N. et al. (2007) Dietary Docosahexaenoic Acid and Docosapentaenoic Acid ameliorate Amyloid-B and Tau Pathology via a Mechanism involving Presenilin 1 Levels. J. Neuroscience, 27, 4385-4395.

15. National Institute on Aging (2007) Study to Determine whether Chronic DHA (Docosahexaenoic Acid) Supplementation slows the Progression of Cognitive and Functional Decline in Mild to Moderate Alzheimer’s Disease. http://clinicaltrials.gov/ct/show/NCT00440050

Alzheimer’s disease is the most common form of dementia, afflicting approximately 5.3 million Americans, and causing the progressive destruction of brain cells and loss of function. Presently incurable, it is the seventh leading cause of death in the United States and is the focus of intensive research efforts (1).

One of the ways to ward off Alzheimer’s disease is to keep our minds active, by pursing new interests and learning new skills. Researchers at Case Western Reserve University in Cleveland, Ohio compared activity levels in normal subjects during the years from age 20 – 60 with those of people who had possible or probable Alzheimer’s disease (2). They found that people who devoted more time to intellectual pursuits during the period from early adulthood (ages 20-39) to middle adulthood (ages 40-60) had a significantly lower risk of getting Alzheimer’s disease. Also, individuals who were more physically active had a lower risk of Alzheimer’s disease but the difference was not as marked as that observed for intellectual activity (2). Research conducted at the Mayo Clinic in Rochester, Minnesota has shown that reading, playing games, working on the computer and engaging in craft activities such as knitting and making a patchwork quilt resulted in a 30 to 50 percent decrease in the risk of developing mild cognitive impairment. (3). Also, subjects who watched television for less than 7 hours a day were 50% less likely to develop memory loss than those who watched for longer. So, from the point of view of benefiting ourselves, it is much better to take classes and be proactive than to sit in front of a television, unless, of course, the program is intellectually stimulating.

References

1) The Alzheimer’s Association: What is Alzheimer’s? http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp

2) Friedland, R. P. et al. (2001) Patients with Alzheimer’s Disease have Reduced Activities in Midlife compared with Healthy Control-Group Members. Proc. Natl. Acad. Sci. 98, 3440-3445

3) Geda, Y. et al. (2009) Cognitive Activities Are Associated With Decreased Risk of Mild Cognitive Impairment: The Mayo Clinic Population-Based Study of Aging. The American Academy of Neurology. http://www.aan.com/press/index.cfm?fuseaction=release.view&release=695 http://www.alzinfo.org/newsarticle/templates/newstemplate-prevention.asp?articleid=346&zoneid=14

© Christopher J. Jones, M.Sc., Ph.D.

Alzheimer’s disease is a progressive and fatal form of dementia. The involvement of aluminum was originally suggested when it was found to be present in neurofibrillary tangles in the brains of some patients who had died from the disease and it has also been shown to cause memory loss if administered intravenously. The jury is still out on whether aluminum is a cause of Alzheimer’s. However, there is no evidence to suggest that we need aluminum for our body to function normally (1). We do not need it in our diet. It is considered non-physiological and yet we are exposed to it from so many sources in our daily lives. I think it is prudent to avoid aluminum as much as possible. In the excellent report (2) and video below, produced by Phyllis Staff after her father had passed away from Alzheimer’s disease, the concerns about aluminum and the steps we should take to minimize our exposure to it are presented.

References

1) Bernardo, J. F., Edwards, M. R. & Barnett, B. (2009) Toxicity, Aluminum. eMedicine from WebMD http://emedicine.medscape.com/article/165315-overview

2) Staff, P. (2009) Elemental Enigma: A Guide to Aluminum and Alzheimer’s Disease. http://www.viewzone.com/alzheimers.html