By Jim English
The human brain is one of the most elegant and complex structures ever conceived. Comprising over ten billion neurons and supportive cells, no other organized structure – organic or silicon – can begin to match the sheer complexity and processing power of the human brain. It regulates virtually all life systems while simultaneously generating the thoughts, dreams and feelings that define us and shape our perception of reality.
Every thought, concept, opinion, belief and emotion arises from the untold millions of chemical and electrical reactions that occur in the brain every second. And generating the power to drive all of this activity places a huge demand on the body’s energy reserves. Though it accounts for a mere two percent of body’s weight, the brain greedily consumes more than twenty percent of the body’s available energy in the form of oxygen and glucose.
The Aging Brain
By age seventy most people will have lost about ten percent of their original brain cells to the effects of “normal” aging. This continual loss of brain cells is further aggravated by damage from other age-related conditions, including hypertension, arteriosclerosis (hardening of the arteries), diabetes, and cerebrovascular diseases (CVD) such as cerebrovascular insufficiency, strokes and multi-infarct dementia (MID).
Dementia is defined as the loss of cognitive or intellectual functions. Unlike occasional forgetfulness, dementia is marked by a profound impairment of memory and the loss of complex abilities required for problem-solving, decision making, spatial orientation, and even the ability to put simple words together to communicate.
Dementia is a permanent, progressive disease that mostly affects the elderly, who, over time, may lose the ability to function normally and require round-the-clock care. It is estimated that up to 8 percent of all people over 65 suffer from some form of dementia, and these numbers double every additional five years, with an estimated 20 percent to 50 percent of people in their 80s suffering from some form of dementia.
There are close to fifty different causes of dementia, including neurological disorders (Alzheimer’s disease), vascular disorders (multi-infarct disease), inherited disorders (Huntington’s disease), and infections (viruses such as HIV).
One factor shared by all of these disorders is a reduction in the flow of blood and oxygen to the brain. In addition to depriving brain cells of fuel, reduced circulation contributes to increased production of free radicals that inflict additional damage to cell membranes, further accelerating brain cell death. The continued loss of brain cells to the ravages of age and debilitating effects of degenerative diseases only speeds up the process of mental deterioration. As memories fade the ability to form new thoughts and solve problems is further reduced. Depression, incontinence, disorientation, speech disturbances, tremor, muscle weakness, tinnitus (ringing in the ears), and loss of both visual acuity and coordination also worsen as these conditions progress.
Alzheimer’s disease (or “senile dementia of the Alzheimer type”) is a chronic and progressive degenerative neurological condition that afflicts over four million people in the United States, accounting for up to 60 percent of all cases of dementia. Alzheimer’s commonly appears after age fifty, and from age sixty-five on, the risk of developing the disease doubles with every additional five years of age. As if these numbers weren’t bad enough, they are expected to increase in the coming decades, draining health care resources, and leaving almost no family untouched.
Aging adults face loss of cognitive powers and mental functions. Research supports the role of a number of potent anti-aging therapies to slow brain aging and preserve cognitive function.
While there is currently no cure for Alzheimer’s, ongoing research shows that several nutrients may help to halt the destructive progression of dementia and improve cognitive function of patients suffering from Alzheimer’s and other forms of dementia.
Hope for Aging Brains
While medical researchers and pharmaceutical companies race to patent new (and profitable) treatments for Alzheimer’s and other degenerative brain conditions, a number of existing nutritional compounds have already been proven to safely support healthy brain function while protecting and prolonging cognitive ability. Supported by numerous double-blind controlled trials in Europe and the U.S., these supplements can slow down the age-related loss of higher-level cognitive functions that can appear in healthy individuals as young as fifty years of age.
Acetyl-L-Carnitine (ALC) is a cognitive enhancer and neuroprotective agent that protects against a wide range of age-related degenerative changes in the brain and nervous system. ALC is an ester of carnitine that modulates cellular concentrations of free coenzyme A and acetyl-coenzyme A, two compounds integrally involved in numerous cellular functions, including the transfer of fatty acids across mitochondrial membranes for energy production.
ALC is found in various concentrations in the brain and its levels are significantly reduced with aging. ALC also significantly reduces damaged fats, such as lipofuscin, in the brains of aged rats. In addition to accumulating in the aging brain, lipofuscin also accumulates in the skin as “aging spots,” those brownish pigmented blemishes that accumulate in the backs of hands of many people over fifty. The reduction of these deposits following consumption of ALC may be evidence of a slowing in the aging process in the brain.
ALC also has the ability to cross into the brain where it acts as a powerful antioxidant, preventing the deterioration of brain cells that normally occurs with age.
ALC also has the ability to cross into the brain where it acts as a powerful antioxidant, preventing the deterioration of brain cells that normally occurs with age. Because of this protective effect, ALC may be beneficial in the prevention and treatment of free-radical mediated diseases, such as Alzheimer’s and Parkinson’s disease.
Alzheimer’s disease primarily affects cholinergic function. ALC has been shown to promote both the release and synthesis of acetylcholine. Additionally, ALC promotes high affinity uptake of choline, which declines significantly with age.
In addition to ALC’s cholinergic-enhancing properties, researchers have shown that ALC has numerous beneficial effects on dopaminergic neurons. The decline of the dopaminergic neurotransmission system is most evident in Parkinson’s disease patients.
ALC has been shown to improve age-related changes of dopamine receptors, including improved release and binding of dopamine. Research has shown that ALC can prevent dopaminergic neuron death caused by MPTP, a neurotoxin that mimics neurological symptoms similar to Parkinson’s disease, by selectively killing dopaminergic neurons.
Choline is a precursor to acetylcholine, a cholinergic neurotransmitter that declines with advancing age. Individuals predisposed to Alzheimer’s disease and other dementias, infants and children, diabetics, and athletes (who often have reduced plasma-choline levels after training or competition) may be at increased risk of choline deficiency.
Choline has been shown to have considerable potential for preserving the integrity of neuronal structures and in preventing some of the alterations in the central nervous system during aging. Choline supplementation appears to prevent the age-induced decline of the dendritic network composed of neurons that fire impulses to the cells. Choline increases the number of dendritic spines in the cerebral cortex of old mice and improves the animals’ learning performance.
Under conditions of increased demand for acetylcholine production, excess choline availability becomes a limiting factor for acetylcholine synthesis. When this additional exogenous choline supply is unavailable, cholinergic neurons are able to use free choline taken from a choline “reservoir” to continue the synthesis of acetylcholine.
This process, termed “autocannibalism,” can lead to a decrease in the quantity and quality of membrane in these cells. Indeed, cholinergic neurons’ ability to use this alternative source of choline appears to contribute to their vulnerability in Alzheimer’s disease.
Researchers believe defects in choline-metabolism may play a central role in the development of Alzheimer’s disease as defects in choline transport exist in the cells of Alzheimer’s victims. Defects in choline metabolism may also be influential in Down’s syndrome, normal aging, Huntington’s disease, amyotropic lateral sclerosis, the familial dysautonomias, and the post-polio syndrome.
DMAE (dimethylaminoethanol) is a nutrient found abundantly in fish and in human brains. In the brain, DMAE is converted into choline, the precursor to acetylcholine. Because acetylcholine conducts nerve impulses within the brain, the increased acetylcholine synthesis seen after DMAE supplementation may improve memory and learning skills, elevate mood, prevent memory loss in elderly adults, and increase physical energy.
Studies suggest DMAE may work by inhibiting choline metabolism in peripheral tissues, causing free choline to accumulate in the blood, enter the brain and stimulate choline receptors. As the immediate precursor to choline, DMAE assists in the building and repair of cell membranes, particularly in the brain and central nervous system.
As the immediate precursor to choline, DMAE assists in the building and repair of cell membranes, particularly in the brain and central nervous system.
Animal studies have demonstrated that DMAE stimulates brain neurons and improves working memory performance. In one study, rats treated with DMAE demonstrated significant improvements in remembering how to negotiate a maze. In another study, mice trained to negotiate a maze demonstrated improved memory retention when treated with DMAE.
DMAE’s ability to stimulate acetylcholine synthesis has led researchers to explore its effects in senile dementia and Alzheimer’s. In a promising study, 14 senile dementia patients were treated with DMAE for four weeks. The dosage was gradually increased to 600 mg, three times daily, during the first two weeks, with no adverse effects. Although the patients experienced no improvement in cognitive function or memory, ten of the 14 patients experienced reduced depression, irritability and anxiety and increased motivation and initiative.
Phosphatidylserine (PS) is a naturally-occurring phospholipid nutrient that has been shown to improve cognitive functions and enhance mental ability. PS is essential to the healthy functioning of the human brain where it affects an assortment of nerve cell functions, including: conduction of nerve impulses; accumulation, storage and release of neurotransmitters; the activity and number of receptors involved in synaptic discharge; and the biological maintenance of cellular ‘housekeeping’ functions.
Supplementation with PS has been proven to slow, halt, or in many cases, even reverse cognitive degeneration due to Age-Related Cognitive Decline (ARCD), and dementing illnesses like Alzheimer’s disease. PS has been scientifically established to be among the most effective substances to consistently result in dramatic cognitive improvements and enhancements of other higher brain functions.
PS is extremely bioavailable and crosses the blood-brain barrier with ease. Once in the brain, the PS molecule as a unit merges smoothly into the nerve cell membrane where it is available to facilitate cell-level energy and homeostasis, as well as enhance neurotransmitter production, release, and action. PS also serves as a precursor reservoir for the related phospholipids, phosphatidylethanolamine and phosphatidylcholine.
Findings from many controlled clinical trials indicate that PS consistently ameliorates memory loss and other cognitive decline related to aging. In 14 double-blind clinical trials, conducted with subjects aged 50 and older, PS benefited all degrees of cognitive impairment. In one trial subjects with age-related cognitive decline (ARCD), PS reversed the decline of name-face acquisition skills by a statistical 12 years; i.e., from average scores attained by 64-year-old subjects to average scores attained by 52-year-olds. As the investigators noted, it’s as if they had “rolled back the clock” measuring “cognitive biological age” by roughly 12 years, in terms of overall cognitive status.
Findings from many controlled clinical trials indicate that PS consistently ameliorates memory loss and other cognitive decline related to aging.
In double-blind trials conducted with more severely afflicted subjects, PS brought about statistically and clinically significant improvements in measures of recall, learning, concentration, adaptability, mood and sociability. In other double-blind trials, PS improved neuro-physiological measures such as EEG (electroencephalogram) and reflexes (as judged by flicker-fusion response time).
In another trial conducted with young male volunteers, PS significantly improved EEG alpha rhythm (which often declines with age and memory loss). In older subjects with severe cognitive impairment, PS dramatically enhanced brain glucose consumption (assessed via positron emission tomographic [PET] imaging) and partially restored the 24-hour rhythm of TSH (thyroid-stimulating hormone) secretion in aged men. Also, in elderly subjects, PS enhanced the hypothalamic-pituitary-adrenal (HPA) stress-coping axis, as assessed by the dexamethasone suppression test.
A number of clinical studies have shown that Ginkgo biloba can protect brain cells from damage caused by free radicals while improving blood circulation and oxygen delivery, particularly through the microcapillaries. In one study, researchers measured a fifty-seven percent increase in blood flow through capillaries within sixty minutes of giving Ginkgo to volunteers.
A second study by German scientists involved 60 patients diagnosed with cerebral insufficiency and depression. Patients receiving Ginkgo extract began to show marked improvement after only two weeks, with a significant reduction of many of their symptoms.
In another clinical trial of 166 patients over the age of sixty, researchers found that patients suffering from cerebral insufficiency showed a significant improvement following three months of treatment, confirming the efficacy of Ginkgo extract in cerebral disorders due to aging.
Researchers have also found that Ginkgo can be especially helpful when given to Alzheimer’s patients at the first sign of symptoms. In one published study, German scientists gave a daily dose of 120 mg of Ginkgo to twenty elderly patients exhibiting various early symptoms of dementia. The results were dramatic, and the patients receiving Ginkgo showed impressive improvements on a variety of clinical tests, as compared to patients receiving a placebo.
In one large study published in 1996, German researchers tested Ginkgo extract on a group of 222 patients, aged fifty-five or older, who were diagnosed with mild to moderate dementia caused by either Alzheimer’s disease or multi-infarct dementia. Patients were given either 240 milligrams of Ginkgo biloba extract, twice a day before meals, or a placebo, for the duration of the six-month long trial.
At the conclusion of the study the researchers reported that patients receiving Ginkgo showed a remarkable overall improvement in their condition, including a 300 percent increase in memory and attention as compared to those receiving the placebo pills.
The researchers concluded their report by stating that, in cases of dementia, Ginkgo extract could improve a patient’s quality of life while preserving independence and postponing the need (and expense) of full-time care.
Ginkgo and Multi-Infarct Dementia
The second most common cause of dementia in older people is multi-infarct dementia (MID), a condition that accounts for about fifteen percent of all cases of dementia. Multi-infarct dementia usually affects people between the ages of 60 and 75, and men are more likely to have multi-infarct dementia than women. MID is typically caused by a series of mini-strokes, also referred to as transient ischemic attacks (TIAs), that can occur when an artery in the brain either becomes blocked or ruptures. Strokes are generally caused by high blood pressure, high blood cholesterol, diabetes, and heart disease. Of these causes, the most important risk factor for multi-infarct dementia is untreated high blood pressure. In fact, it is extremely rare for a person to develop multi-infarct dementia without also having high blood pressure.
While these mini-strokes may or may not be noticed at the time, the effect on the brain is the same – brain cells become damaged by a lack of oxygen and die. Over time a series of mini-strokes can begin to destroy substantial portions of the brain that control speech and visual processing.
As with Alzheimer’s disease, Ginkgo has been shown to help patients suffering from MID by enhancing memory, alertness and overall quality of life. Additionally, given the underlying disorders that cause blood vessels to rupture, Ginkgo can also benefit patients suffering from MID by restoring elasticity and strength to stiff, weakened blood vessels.
Baby boomers and aging adults face a loss of cognitive powers and impaired mental functions. Research supports the role of a number of potent anti-aging therapies to slow brain aging and preserve cognitive function. Rather than waiting for signs of an irreversible decline in mental abilities or other more serious cognitive problems, it would be prudent to take steps to support the brain’s ability to heal and self-repair. In short, we can take steps now to slow age-dependent brain cell changes, preserve vital functions, and maintain mental health and vigor.