Alzheimer’s disease is a brain disorder that occurs in the later years of life. People with Alzheimer’s develop progressive loss of memory and gradually lose the ability to function and to take care of themselves.
The cause of this disorder is not known, although the problem appears to involve an abnormal breakdown of acetylcholine (an important neurotransmitter in the brain). Some studies suggest it may be related to an accumulation of aluminum in the brain.
Despite this suggestion, aluminum toxicity has been studied in humans, and it is quite distinct from Alzheimer’s disease. Therefore, the importance of aluminum in causing Alzheimer’s disease remains an unresolved issue.
What are the symptoms of Alzheimer’s disease?
Symptoms of Alzheimer’s include a pattern of forgetfulness, short attention span, difficulty in performing routine tasks, language problems, disorientation, poor judgment, problems with thinking, misplacing things, depression, irritability, paranoia, hostility, and lack of initiative.
Dietary changes that may be helpful.
Whether aluminum in the diet can cause Alzheimer’s disease remains controversial. A preliminary study found Alzheimer’s disease patients are more likely to have consumed foods high in aluminum additives (e.g., some grain product desserts, American cheese, chocolate pudding, chocolate beverages, salt, and some chewing gum), compared to people without the disease.
Until this issue is resolved, it seems prudent for healthy people to take steps to minimize exposure to this unnecessary and potentially toxic metal by reducing intake of foods cooked in aluminum pots, foods that come into direct contact with aluminum foil, beverages stored in aluminum cans, and foods containing aluminum additives.
Aluminum is added to some municipal water supplies to prevent the accumulation of particulates. In such areas, bottled water may be preferable. It appears unlikely; however, that avoidance of aluminum exposure after the diagnosis of Alzheimer’s disease could significantly affect the course of the disease.
In population studies, high dietary intake of fat and calories was associated with an increased risk for Alzheimer’s disease, whereas a high intake of fish was associated with a decreased risk. Whether these associations represent cause and effect is unknown.
Lifestyle changes that may be helpful.
Keeping active outside of one’s work, either physically or mentally, during midlife may help prevent Alzheimer’s disease. People with higher levels of non-occupational activities, such as playing a musical instrument, gardening, physical exercise, or even playing board games, were less likely to develop Alzheimer’s later in life, according to one study.
Nutritional supplements that may be helpful.
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 three times per day) 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 taken three times per day.
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.
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 a placebo. However, another double-blind trial using the same amount for a year found no effect on mental function.
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 taken three times per day 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 had better improvement in overall well-being than those who took a placebo, but there were no significant differences in mental function tests. In another double-blind trial, 200 mg of PS taken twice daily 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 three times per day 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 a preliminary report, two people with a hereditary form of Alzheimer’s disease received daily: 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.
Studies in the test tube 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 (10 mg per day) improved mental function in people with Alzheimer’s disease. Further studies are necessary to confirm these early results.
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.
Most, but not all, studies have found that people with Alzheimer’s disease have lower blood DHEA 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 twice daily for six months had a 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.
Herbs that may be helpful.
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 the 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 the 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% flavones 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 twice per day 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 thathuperzine A, given at levels of 100 to 150 mcg two to three times per day 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.
In a double-blind trial, supplementation with an extract of lemon balm (Melissa officinalis) for 16 weeks significantly improved cognitive function and significantly reduced agitation, compared with a placebo, in people with Alzheimer’s disease. The amount of lemon balm used was 60 drops per day of a 1:1 tincture, standardized to contain at least 500 mcg per ml of citral.