Nutritional Implications Related to Alzheimer's
New research has found that chronic inflammation is a contributing cause of Alzheimer's. It is important to cut down on foods which contribute to inflammation in the body such as sugar, refined grains, meat, and dairy. Learn more.
The MIND Diet
The Mediterranean-DASH Intervention for Neurodegenerative Delay, according to a 2015 study from Rush University182, has been found to reduce the chances of developing Alzheimer's disease by 53%, and even for those who do not follow the diet closely, a risk reduction in 35% was found. The diet takes elements from both the popularized Mediterranean diet, (which is high in whole grains, vegetables, fish and healthy forms of fat), and the DASH diet for hypertension reduction (which is high in fruit, vegetables, and low-fat dairy products).
The study was based on years of accumulated information from past research about what nutrients support healthy brain functioning and on what people with healthy brain functioning have been eating. The researchers asessed the connections between diet and Alzheimers in 923 patients, aged 58-98, over a 4 1/2 year period.
Here are the elements of the MIND diet for a single day:
- 3 servings of whole grains - for example, brown rice rather than white, whole wheat flour rather than white flour
- A salad in addition to one other vegetable
- A glass of wine
- Nuts as a snack on most days - not too many
- Blueberries or strawberries - berries are the single food that are important in this diet, especially blueberries.
- Chicken or fish and avoid red meat
- Beans (every other day)
- Avoid butter (less than 1 tablespoon daily) & cheese (less than a serving a week)
- Avoid pastries and sweets
- Avoid fried and fast foods (less than a serving a week)
- Avoid processed foods (anything that comes already made in a package)
Researchers have found that the reason vitamin D may be helpful is that it is important in the regulation of macrophages, the cells that are responsible for cleaning waste from the body, which includes the plaque that causes Alzheimer's. The strengthed macrophages open a chloride channel that assists in removing amyloid beta the primary plaque component.179
A number of assessments including 2 in 2009 and 2014181 have tied vitamin D deficiencies to poorer performance in cognitive functioning using standardized tests such as the Rey-Osterrieth Complex Figure (ROCF) test, the Camden Topographical Recognition Memory (CTRM) test and the Digit Symbol Substitution Test (DSST). In the 2014 evaluation British researchers retested over 4800 people who had been tested for cognitive functioning in 1958 and retested in 2008 - fifty years later. Of these 4646 also had the levels of vitamin D measured after 45 years. Strong correlations were found between low vitamin D levels on poor cognitive functioning.
Vitamin D3 & Curcumin
Research has demonstrated that the combination of vitamin D3 and curcumin is effective in helpfing macrophages to absorb and remove amyloid beta from the body. 180
In a preliminary study, people who used antioxidant supplements (vitamin C or vitamin E) had a lower risk of Alzheimer's disease compared with people who did not take antioxidants. Other preliminary research shows that higher blood levels of vitamin E correlate with better brain functioning in middle-aged and older adults. The possible protective effect of antioxidants may be explained by the observation that oxidative damage appears to play a role in the development of dementia. Large amounts of supplemental vitamin E may slow the progression of Alzheimer's disease. A double-blind trial found that 2,000 IU of vitamin E per day for two years extended the length of time people with moderate Alzheimer's disease were able to continue caring for themselves (e.g., bathing, dressing, and other necessary daily functions), compared with people taking a placebo.
Astaxanthin lowers levels of the enzyme PLOOH (phospholipid hydroperoxidases) which accumulates in red blood cells of people suffering from dementia. It may help prevent dementia, including Alzheimer's. A 2011 study in the British Journal of Nutrition demonstrated that taking 6 mg or 12 mg of astaxanthin daily for 12 weeks lowered levels of PLOOH by 40 percent.178 As an antioxidant, astaxanthin is many times more effective than Vitamin E in neutralizing single oxygen free radicals and far exceeds the free radical scavenging power of vitamin C, CoQ10, beta-carotene and green tea.
Omega-3 Fatty Acids
Austrialian researchers confirmed that an omega-3 rich diet may help prevent Alzheimer's by regulating the amounts of zinc in the brain. Zinc is regulated by DHA, found in omega-3 rich diets. Zinc can rise to toxic levels in the brain when DHA levels are low in neuronal cells.177.
A 2015 study published in the Alzheimer's Association journal (4 years, 819 subjects including control, mild impairment, Alzheimer's) reports that supplementation with fish oil reduced the amount of brain atrophy in patients who were mildly impaired or had been diagnosed with Alzheimer's and also improved cognitive functioning. It further reported that the greatest benefits in this regard were among 'normal' patients - suggesting that fish oil supplementation is helpful to protect the brain against decline in later years.183
Several clinical trials have found that acetyl-L-carnitine supplementation delays the progression of Alzheimer's disease, improves memory, and enhances overall performance in some people with Alzheimer's disease. However, in one double-blind trial, people who received acetyl-L-carnitine (1 gram TID) deteriorated at the same rate as those given a placebo. Overall, however, most short-term studies have shown clinical benefits, and most long-term studies (one year) have shown a reduction in the rate of deterioration. A typical supplemental amount is 1 gram TID.
Vitamin B1 is involved in nerve transmission in parts of the brain (called cholinergic neurons) that deteriorate in Alzheimer's disease. The activity of vitamin B1-dependent enzymes has been found to be lower in the brains of people with Alzheimer's disease. It has therefore been suggested that vitamin B1 supplementation could slow the progression of Alzheimer's disease. Two double-blind trials have reported small but significant improvements of mental function in people with Alzheimer's disease who took 3 grams a day of vitamin B1, compared to those who took placebo. However, another double-blind trial using the same amount for a year found no effect on mental function.
Some researchers have found an association between Alzheimer's disease and deficiencies of vitamin B12 and folic acid; however, other researchers consider such deficiencies to be of only minor importance. In a study of elderly Canadians, those with low blood levels of folate were more likely to have dementia of all types, including Alzheimer's disease, than those with higher levels of folate. Little is known about whether supplementation with either vitamin would significantly help people with this disease.
Nonetheless, it makes sense for people with Alzheimer's disease to be medically tested for vitamin B12 and folate deficiencies and to be treated if they are deficient.
In a preliminary report, two people with a hereditary form of Alzheimer's disease received daily doses of coenzyme Q10 (60 mg), iron (150 mg of sodium ferrous citrate), and vitamin B6 (180 mg). Mental status improved in both patients, and one became almost normal after six months.
Phosphatidylserine (PS), which is related to lecithin, is a naturally occurring compound present in the brain. Although it is not a cure, 100 mg of PS TID has been shown to improve mental function, such as the ability to remember names and to recall the location of frequently misplaced objects, in people with Alzheimer's disease. However, subsequent studies have not validated these results. In one double-blind trial, only the most seriously impaired participants received benefits from taking PS; people with moderate Alzheimer's disease did not experience significant improvements in cognitive function. In another double-blind trial, people with Alzheimer's disease who took 300 mg of PS per day for eight weeks showed better improvement in overall well-being than those who took placebo, but there were no significant differences in mental function tests. In another double-blind trial, 200 mg of PS BID produced short-term improvements in mental function (after six to eight weeks), but these effects faded toward the end of the six-month study period.
A further concern is that the PS used in these studies was obtained from cow brain, which has been found in some instances to be infected with the agents that cause mad-cow disease. The human variant of mad cow disease, called Creutzfeldt-Jakob disease, is rare but fatal and is thought to be transmitted to people who consume organs and meat from infected cows. A plant source of PS is also available. However, the chemical structure of the plant form of PS differs from the form found in cow brain. In a preliminary study, plant-derived PS was no more effective than a placebo at improving the memory of elderly people.
A double-blind trial of 20 to 25 grams per day of lecithin failed to produce improvements in mental function in people with Alzheimer's disease. However, there were improvements in a subgroup of people who did not fully comply with the program, suggesting that lower amounts of lecithin may possibly be helpful. Lecithin supplementation has also been studied in combination with a cholinesterase inhibitor drug called tacrine, with predominantly negative results.
DMAE (2-dimethylaminoethanol) may increase levels of the brain neurotransmitter acetylcholine. In one preliminary trial, people with senile dementia were given DMAE supplements of 600 mg TID for four weeks. The participants did not show any changes in memory, though some did show positive behavior changes. However, a subsequent double-blind trial found no significant benefit from DMAE supplementation in people with Alzheimer's disease.
In vitro studies have shown that zinc can cause biochemical changes associated with Alzheimer's disease. For that reason, some scientists have been concerned that zinc supplements might promote the development of this disease. However, in a study of four people with Alzheimer's disease, supplementation with zinc (30 mg per day) actually resulted in improved mental function. In a recent review article, one of the leading zinc researchers concluded that zinc does not cause or worsen Alzheimer's disease.
A small, preliminary trial showed that oral NADH, or nicotinamide adenine dinucleotide, (10 mg per day) improved mental function in people with Alzheimer's disease. Further studies are necessary to confirm these early results.
Most, but not all, studies have found that people with Alzheimer's disease have lower blood DHEA (dehydroepiandrosterone) levels than do people without the condition. Emerging evidence suggests a possible benefit of DHEA supplementation in people with Alzheimer's disease. In one double-blind trial, participants who took 50 mg BID for six months had significantly better mental performance at the three-month mark than those taking placebo. At six months, statistically significant differences between the two groups were not seen, but results still favored DHEA. In another clinical trial, massive amounts of DHEA (1,600 mg per day for four weeks) failed to improve mental function or mood in elderly people with or without Alzheimer's disease. It is likely that the amount of DHEA used in this trial was far in excess of an appropriate amount, illustrating that more is not always better. Other research confirms no benefit to short-term memory.176
Botanical Treatment Options
An extract made from the leaves of the Ginkgo biloba tree is an approved treatment for early-stage Alzheimer's disease in Europe. While not a cure, Ginkgo biloba extract (GBE) may improve memory and quality of life and slow progression in the early stages of the disease. In addition, four double-blind trials have shown that GBE is helpful for people in early stages of Alzheimer's disease, as well as for those experiencing another form of dementia known as multi-infarct dementia. One trial reported no effect of GBE supplementation in the treatment of Alzheimer's disease, vascular dementia or age-associated memory impairment. However, the results of this trial have been criticized, since analysis of the results does not separate those patients with Alzheimer's disease or vascular dementia from those with age-associated memory impairment. A comparison of placebo-controlled trials of ginkgo for Alzheimer's disease concluded that the herb compared favorably with two prescription drugs, donepezil and tacrine, commonly used to treat the condition. Research studies have used 120 to 240 mg of GBE, standardized to contain 6% terpene lactones and 24% flavone glycosides per day, generally divided into two or three portions. GBE may need to be taken for six to eight weeks before desired actions are noticed.
Huperzine A is a substance found in huperzia (Huperzia serrata), a Chinese medicinal herb. In a placebo-controlled trial, 58% of people with Alzheimer's disease had significant improvement in memory and mental and behavioral function after taking 200 mcg of huperzine A BID for eight weeks - a statistically significant improvement compared to the 36% who responded to placebo. Another double-blind trial using injected huperzine A confirmed a positive effect in people with dementia, including, but not limited to, Alzheimer's disease. Yet another double-blind trial found that huperzine A, given at levels of 100 to 150 mcg BID-TID for four to six weeks, was more effective at improving minor memory loss associated with age-related cognitive decline than the drug piracetam. This study found that huperzine A was not effective in relieving symptoms of Alzheimer's disease. Clearly, more research is needed before the usefulness of huperzine A for Alzheimer's disease is confirmed.
Lesser periwinkle contains the alkaloid vincamine. Supplementation with a semi-synthetic derivative of vincamine, known as vinpocentine, showed no benefit for people with Alzheimer's disease in a preliminary study, but vincamine itself was shown to be beneficial in a later double-blind trial.
Refer to the individual herb for information about any side effects or interactions.
Research on saffron components and memory demonstrates significantly improved spacial memory and supports neurotransmission capacity in the brain.184
Research on cannabinoids, found naturally in the body but also present in marijuana, may be helpful in reducing the inflammation-related cause of neurogical deterioration. Note: this does not mean that smoking or eating marijuana is helpful, but that some active ingredients in the plant may be a part of treatment therapy.
176. Merritt, P., et al, Administration of dehydroepiandrosterone (DHEA) increases
serum levels of androgens and estrogens but does not enhance short-term memory in post-menopausal women,
Brain Res. 2012 Nov 5;1483:54-62. doi: 10.1016/j.brainres.2012.09.01
177. Omega-3 fatty acid may help prevent brain cell death, FEBS Letters, volume 584, Issue 3, Pages 612-618, 5 February 2010
178. Antioxidant effect of astaxanthin on phospholipid peroxidation in human erythrocytes, Br J Nutr. 2011 Jun;105(11):1563-71
179. Milan Fiala, et al, Journal of Alzheimer's Disease, March 6, 2012
180. John Cashman, et al., Journal of Alzheimer's Disease, July, 2009
181. Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men J Neurol Neurosurg Psychiatry 2009; 25-Hydroxyvitamin D, APOE e4 genotype and cognitive function: findings from the 1958 British birth cohort, Maddock, J. et al, European Journal of Clinical Nutrition, October 8, 2014.
182. Morris, M.C., et al, MIND diet associated with reduced incidence of Alzheimer's disease, Alzheimers & Dementia, Feb. 2015
183. L.A. Daiello, et al, Association of fish oil supplement use with preservation of brain volume and cognitive function, Alzheimer's & Dementia: The Journal of the Alzheimer's Association, February, 2015.
184. F. Asadi, et al, Reversal effects of crocin on amyloid beta-induced memory deficit: Modification of autophagy or apoptosis markers, Pharmacology, Biochemistry and Behavior, December, 2015; M.R. Khazdair, et al., The effects of Crocus sativus (saffron) and its constituents on nervous system: A review, Avicenna Journal of Phytomedicine, September-October, 2015.