Alzheimer’s Prevention with dietary supplements, diet, food – Is prevention or cure possible with the use of natural methods?
Do anticholinesterase medications increase lifespan or do they have too many side effects?
December 11 2016

Alzheimer’s prevention – healthy vegetable juices
Preventing Alzheimer’s disease may be possible by drinking more vegetable and fruit juices, particularly vegetable juices since they have less fructose. These juices have tons of beneficial antioxidants.

Alzheimer’s disease prevention, role of junk or fast foods
Mice fed junk food for nine months show signs of developing the abnormal brain tangles strongly associated with Alzheimer’s disease. A diet rich in fat, sugar and cholesterol could increase the risk of this most common type of dementia. Susanne Akterin, a researcher at the Karolinska Institute’s Alzheimer’s Disease Research Center, says a high intake of fat and cholesterol in combination with genetic factors… can adversely affect several brain substances, which can be a contributory factor in the development of Alzheimer’s disease.

Dietary supplements
Q. I just got
Mind Power Rx for my mother, who has early stage Alzheimer’ s disease. Then today I noticed an Alzheimer’s article on Galantamine. Would it be OK to give her both supplements together, or do they have the same basic function?
Mind Power Rx should be tried on its own for a month or so. After stopping Mind Power Rx for a week you can switch her to galantamine for a month and see which works better. It is nearly impossible to predict which supplements or drugs will be of help to an Alzheimer’s patient, but it is quite likely that nutritional therapy can help early Alzheimer’s patient retain their memory longer.

Would the herb yohimbe bark aggravate symptoms of Alzheimer’s disease?
We don’t recommend the use of this potent herb for this disease.

Is acetyl cysteine a good supplement for Alzheimer’s prevention or as a daily pill to take to prevent Alzheimer’s memory loss?
It’s difficult to say without seeing results of clinical trials. We will update this article on Alzheimer’s disease as more studies are published.

Research has been done on mice with induced Alzheimer’s. It was found that niacinamide completely reversed ALZHEIMER’S in the mice (as reported by Dr. David Williams in his newsletter Alternatives). That this has not been applied to humans, as far as I know, seems worse than negligence attributed to greed (i.e., not pursued because there’s no big-bucks payoff). The neglect seems more criminal than merely neglectful.
What happens in mice may not necessarily happen in humans.

Alzheimer’s prevention – copper
High copper levels in tap water may play a role. Those at risk for Alzheimer’s (i.e. family history) may consider drinking distilled water.

Lower homocysteine, use folate and B vitamins
The controversy continues regarding the role of homocysteine in causing Alzheimer’s disease and whether the use of B vitamins are effective for Alzheimer’s prevention. Findings from a longitudinal study indicate an inverse association between folate intake and the risk of Alzheimer’s disease. There is evidence that elevated homocysteine levels may raise the risk of Alzheimer’s disease, says Dr. Jose A. Luchsinger, from Columbia University Medical Center in New York. In their study, reported in the Archives of Neurology for January, the researchers assessed the occurrence of Alzheimer’s disease in 965 dementia-free older adults who completed a food frequency questionnaire and then were followed for 6 years, on average. Dietary and supplemental folate, vitamin B6, and vitamin B12 intake were estimated from the questionnaire responses. A total of 192 subjects were diagnosed with Alzheimer’s disease during follow-up. Subjects in the highest quartile of Folic acid intake (at least 487 µg/day) were 50% less likely to develop Alzheimer’s disease than those in the lowest quartile (no greater than 293 µg/day), the report indicates. By contrast, levels of vitamin B6 and B12 were not associated with the risk of Alzheimer’s disease. Interestingly, high folate intake was only “modestly associated with lower homocysteine levels,” Dr. Luchsinger noted, “suggesting that other mechanisms may be involved” in the possible anti-Alzheimer’s effect. Archives of Neurology 2007.

Fish oils? Omega-3 fatty acids?
The following study shows slight benefit in preventing or reducing Alzheimer’s in some patients. Could a higher dose have worked better? Could nutritional therapy be more effective in early Alzheimer’s?
Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial.
Arch Neurol. 2006. Department of Neurobiology, Caring Sciences and Society, Section of Clinical Geriatrics, Karolinska University Hospital Huddinge, Stockholm.
Two hundred four patients with Alzheimer’s disease whose conditions were stable while receiving acetylcholine esterase inhibitor treatment and who had a Mini-Mental State Examination (MMSE) score of 15 points or more were randomized to daily intake of 1.7 g of docosahexaenoic acid and 0.6 g of eicosapentaenoic acid (omega-3 fatty acid-treated group) or placebo for 6 months, after which all received omega-3 fatty acid supplementation for 6 months more. Administration of omega-3 fatty acid in patients with mild to moderate AD did not delay the rate of cognitive decline according to the MMSE or the cognitive portion of the Alzheimer Disease Assessment Scale. However, positive effects were observed in a small group of patients with very mild or early Alzheimer’s disease (MMSE >27 points).

Hypertension and Alzheimer’s disease, high blood pressure
Having hypertension reduces blood flow in the brains of Alzheimer’s patients, making them more vulnerable to the effects of the disease.

Alzheimer’s studies and published trials
Drugs for Alzheimer’s disease, which pharmaceutical companies and campaigners have lobbied the UK government to provide to large numbers of elderly patients with dementia across the country at a cost of over £39m a year, have little effect on their memory and do not lead to Alzheimer’s prevention and progression, according to an important study published 2004. The five-year study, paid for by the NHS and not the drug companies, found that the drugs are a waste of the scarce resources available for the condition, said the lead re searcher Roger Gray, director of Birmingham University’s clinical trials unit

Alzheimer disease test
A chemical designed by doctors in Los Angeles could give unprecedented insight into the ravages of Alzheimer’s disease and provide a new way to test for treatments. Previously the only way to determine if a person suffers from the devastating Alzheimer’s brain ailment has been to remove some brain tissue or with an autopsy. The new study by doctors at the University of California, Los Angeles, is part of a larger quest to find a better method to diagnose the condition using tracers that can be detected with a positron emission tomography, or PET, scan. The chemical, known as FDDNP, attaches to the abnormal clumps of proteins called amyloid plaques and tau tangles that develop in Alzheimer’s sufferers and inhibit messages being processed by the brain. Gary Small and his colleagues discovered that the chemical allowed doctors to pick out which of 83 volunteers had Alzheimer’s, which had mild memory problems, and which were functioning normally for their age. It was 98 percent accurate in determining the difference between Alzheimer’s and mild cognitive impairment. That was far better than the 87 percent success rate for a PET scan test that measured sugar metabolism in the brain, and the 62 percent accuracy rate when doctors used a magnetic resonance imaging scan to gauge brain deterioration. “You can see the telltale FDDNP signal in people years before they get Alzheimer’s,” Small said. His team also found that the distribution of the FDDNP in the brain of Alzheimer’s patients matched the pattern seen in people where the diagnosis is confirmed with an autopsy. One problem plaguing Alzheimer’s tests is that the results are not always clear-cut. For example, some people who seem to have few memory problems can have a positive result on a test.

Rate of Alzheimer’s disease in Japan
To determine the age-, sex-, and subtype-specific incidence of dementia and to assess the effect of education level on the incidence in a Japanese population. 2,286 dementia-free subjects, aged ge60 years, were followed for 5.9 years through biennial two-phase examinations. 206 cases of dementia were newly diagnosed based on DSM IV. The incidence per 1,000 person-years was 12.0 for men and 16.6 for women. Based on NINCDS-ADRDA criteria, 80 cases of probable Alzheimer disease (AD) and 50 cases of possible AD were diagnosed. Based on NINDS-AIREN criteria, 36 cases of probable vascular dementia (VaD) and 40 cases of possible VaD were diagnosed. Age and education showed the most statistically significant effects for all dementia.  AD was the predominant type of dementia in this recent incidence study conducted in Japan, suggesting a reduction in VaD and an increase in AD. Age, sex, and education effects differed by dementia subtype.

Difference between Alzheimer’s and dementia, fact
Alzheimer’s disease is a progressive brain condition that destroys memory and thinking skills, and eventually the ability to carry out simple tasks. In most people, symptoms initially begin after age 60. AD is the most common cause of dementia among older people. Dementia is the loss of mental functioning such thinking, remembering, and reasoning. When it progresses, it can interfere with a person’s daily life and activities. Diagnosing Alzheimer’s disease is usually done clinically after excluding other diseases that cause cognitive decline.