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A Matter Of Mind

Toward the Lifestyle Management of Alzheimer’s Dementia

Dr. Ralph Ofcarcik, Ph.D.
Director of Nutrition Services

“I stared at him, with grief and helplessness. Then, looking into his eyes, I wondered . . . where have you gone? “ These were the near-exact words of an emotionally battered resort guest who had spent the last 2 years caring for her dying father, a victim of Alzheimer’s disease (AD). AD is brutal, without mercy, frequently terrorizing the victim, certainly draining to family caregivers. Some say it is the ultimate life curveball.

More than just senior moments and normal aging, Alzheimer’s disease is about encroaching morbidity tied to memory loss, difficulty with familiar tasks and thinking in the abstract, trouble understanding language, and unpredictable mood/personality changes. Progression of the disease may proceed over the course of a few years up to two decades. Most victims, however, rarely succumb to the disease, dying instead of pneumonia and other causes.

Currently, AD affects 4 to 5 million Americans, or approximately 1 out of every 10 seniors over the age of 65. Unfortunately, the risk about doubles every 5 years with nearly half of those over the age of 85 developing the disease. Although there is a small genetic link (about 10% of all AD is familial), most cases are sporadic with increase risk associated with head trauma, brain inflammation, race (Asians, Caucasians, and Native American Crees and Cherokees are at highest risk), long-standing hypertension, elevated serum homocysteine, Down syndrome, mercury or aluminum toxicity, and excessive exposure to electromagnetic fields. Age by far, however, age has to be regarded as the most significant risk factor.

Alzheimer’s disease occurs when the neurotransmitter acetylcholine is denatured, causing a subsequent decline in nerve cell-to-nerve cell communication. Ultimately, neurons (nerve cells) die, first in the hippocampus, with short-term memory loss the inevitable consequence. Later, language skills and judgment decline as neuron lethality increases in the cerebral cortex. The visible consequence of AD are two unique types of abnormal lesions thought to cause nerve cell death: 1. Beta-amyloid plaques - clumps of protein fragments and other tissue that form outside and over neurons, and 2. Neurofibrillary tangles – twisted protein fibers that develop inside the nerve cells. Ninety-nine years ago, German physician Alois Alzheimer performed a brain autopsy on a 51-year-old woman said to have suffered from a rare dementia. He presented his findings at a medical meeting noting the plaques and tangles consistent with today’s characterization of AD. He also questioned if the lesions were the cause or merely an artifact of the affliction. The answer has yet to be determined.

Prevention
Prevention of Alzheimer’s should always a goal aggressively pursued, particularly in families with an established familial link. Although causal relationships have yet to be established, epidemiology is providing some provocative clues into the relationship of lifestyle to AD onset. For instance:

• Societies that consume lesser fat and calories, China and Nigeria in particular, have a lower incidence of AD.
• Low intakes of linoleic acid (from butter and other dairy products) is associated with reduced risk of Alzheimer’s disease.
• Populations consuming more fish are at lesser risk.

In the laboratory, there is near-convincing evidence that free radicals are involved in the onset and progression of AD. Thus, a higher consumption of antioxidants may help with prevention.

Pharmacologic Treatment
Current drug therapy for mild-moderate Alzheimer’s disease targets the preservation of acetylcholine, accomplished to some degree by four U.S. FDA-approved drugs:

• Tacrine (Cognex) introduced in 1993
• Donepezil hydrochloride (Aricept) approved in 1996
• Rivastigmine (Exelon) available since 2000
• Reminyl (Razadyne) on the market since 2001

For moderate to severe AD, there is memantine HCl (Namenda), a drug which slows the decline in cognitive function.

Genome research has targeted key genes which appear to amplify the disease’s progression. Using this new technology, progress is being made which may soon lead to the development of designer drugs capable of limiting or curbing gene expression. The outlook, currently, is positive for both the treatment AD and (possibly) Parkinson’s disease.

Natural Pharmacologic Treatment
Can natural medicine help? . . . possibly. For example:

• Recent research on fish oil has discovered that DHA (one of the two touted omega-3 fatty acids in fish) inhibits the production of beta-amyloid proteins. It also stimulates the synthesis of another protein (NPD1) that slows neuron lethality1.
  
• Vitamin E, although a disappointment in cardiology, has shown promise in the treatment of Alzheimer’s disease. In one two-year, double-blind, placebo-controlled study of 341 AD patients, supplementation with 1000 IU’s of vitamin E per day increased survival time and improved clinical characteristics2.

In another investigation, 633 subjects over the age of 65 initially without AD were tracked for 4.3 years. Twenty-seven individuals had been taking vitamin E and/or vitamin C supplements and continued throughout the study. Eventually, ninety-one of the participants developed Alzheimer’s disease but did not include any of the vitamin consumers – a statically significant result3. Thus, it is probable that taking vitamins E and C may help in the prevention of AD.

• Ginkgo biloba, long prized for its positive effect on memory and cognition, has the most impressive published science from botanical medicine in the treatment of AD. Clinical investigations strongly support the use of ginkgo as a preventative measure. In studies lasting from 1 to 12 months (and in doses of 120-240 mg), ginkgo supplementation has resulted in delay of AD symptoms, bolstered cognition, improved social behavior, and positive changes in daily living4,5.

• A few human studies have found nicotine (from tobacco) to enhance memory and attention span in AD patients. Concurrent animal research supports the hypothesis, demonstrating memory improvement and inhibition of amyloid peptide formation in response to nicotine. Although far from definitive, the potential for nicotine therapy looks promising6.

Noted Victims of Alzheimer’s Disease
Among the victims of Alzheimer’s disease are some familiar names from the past . . . Rosa Parks, for instance. Ditto for Rita Hayworth, Ronald Reagan, Henry Ford Sr., Charles Bronson, Arlene Francis, Perry Como, Barry Goldwater, Sugar Ray Robinson, Norman Rockwell, Aaron Copeland, Beatrice Lillie, etc., etc. “Nothing is at last sacred but the integrity of your own mind” wrote Ralph Waldo Emerson, an extraordinary analyst of the ordinary. Emerson is believed to have died of Alzheimer’s disease in 1882.

RESEARCH CITED

1Cole GM, Lim GP, Yang F, et al. Prevention of Alzheimer’s disease: Omega-3 fatty acid and phenolic anti-oxidant interventions. Neurobiol Aging. Oct 30, 2005.

2Sano M, Ernesto C, Thomas RG et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer’s disease. N Engl J Med. 1997;336:1216-1222.

3Morris MC, Beckett LA, Scherr PA, et al. Vitamin E and vitamin C supplement use and risk of incident Alzheimer’s disease. Alzheimer Dis Assoc Disord. 1998;12:121-126.

4Ernst E, Pittler MH. Ginkgo biloba for dementia: a systematic review of double-blind, placebo-controlled trials. Clin Drug Invest. 1999;17:301-308.

5Le Bars PL, Kieser M, Itil KZ. A 26-week analysis of a double-blind, placebo-controlled trial of the Ginkgo biloba extract. Dement Geriar Cogn Disord. 2000;11:230-237.

6Mantle D, Pickering AT, Perry AK. Medicinal plant extracts for the treatment of dementia: a review of their pharmacology, efficacy and tolerability. CNS Drugs. 2000;13:201-213.