Aging-Associated Mental Impairment Protocol

Recommended Products:
ACETYL-L-CARNITINE 500 MG 100 CA...
DHEA 15 MG 100 CAPSULES
MELATONIN 3 MG 60 CAPSULES
METHYLCOBALAMIN 5MG 60 SUBLINGLO...
PHOSPHATIDYLSERINE 100 MG 100 CA...
PREGNENOLONE 50 MG 100 CAPSULES
SUPER ALPHA LIPOIC ACID W/BIOTIN...
SUPER COENZYME Q10 COQ10 W/TOCOTRIENOLS 100 M...
GINKGO BILOBA EXTRACT 120 MG 100 ...
SUPER GLA / DHA 180 SOFTGELS

In another double-blind study, 22 elderly patients with central nervous system degenerative disorders were treated with vinpocetine or placebo (Manconi et al. 1986). The patients received 10 mg of vinpocetine, three times a day for 30 days; then they received 5 mg, three times a day for 60 days. Another 18 elderly patients were given matching placebo tablets for the 90-day trial. Vinpocetine-treated patients scored consistently better in all evaluations of the effectiveness of treatment, including measurements on the CGI and SCAG scales and the MMSQ. According to CGI assessments, severity of illness decreased in 73% of the patients in the vinpocetine group at day 30 and in 77% of patients at day 90. Improvement was seen in 77% and 87% of the patients at days 30 and 90, respectively. Patients also showed statistically significant improvement for all SCAG items (except for one) at days 30 and 90. The physicians rated the improvement in 59% of the vinpocetine-treated patients as "good" to "excellent." There were no serious side effects associated with the treatment drug (Manconi et al. 1986).

Vinpocetine safety and efficacy were demonstrated in a study of infants who experienced severe brain damage caused by birth trauma. In the infants treated with vincopetine, vinpocetine caused a significant reduction or disappearance of seizures. The vinpocetine group also showed a decrease of the phenomena of intracranial hypertension and normalization of psychomotor development (Dutov et al. 1991).

The damaging effects of glutamate-induced excitotoxicity have been well established. A vitamin B12 metabolite called methylcobalamin has been shown to specifically protect against this type of neuronal injury. Vinpocetine has been documented to partially protect against excitotoxicity induced by a wide range of glutamate-related neurotoxins (Miyamoto et al. 1989; Erdo et al. 1990).

Ginkgo biloba
As previously stated, an inevitable consequence of aging is a reduced flow of blood to the brain. Common causes are chronic inflammation, arteriosclerosis, and increased blood "stickiness." The results of cerebral vascular disease can range from mild cognitive impairment to ischemic stroke. The third leading cause of death in the United States is stroke. Unfortunately, the effects of ischemic stroke result in many otherwise healthy people becoming institutionalized.

Ginkgo biloba extract has demonstrated specific mechanisms of action that counteract age-related vascular disorders. Human clinical studies show that ginkgo helps to slow down or restore cognitive dysfunction in those who have vascular dementia or Alzheimer's disease.

The first large-scale United States clinical study on ginkgo appeared in the Journal of the American Medical Association (JAMA) (Lebars et al. 1997). This study demonstrated that, compared to placebo, ginkgo helped prevent short-term memory loss in patients with early diagnosed Alzheimer's disease. The researchers concluded that ginkgo improved cognitive performance and social functioning in these patients.

Ginkgo is a popular prescription drug in Europe and a dietary supplement in the United States. Hundreds of scientific studies demonstrate ginkgo's favorable effects in the human body. However, the primary benefit of ginkgo may be to help prevent the consequences of premature brain aging.

The brain depends on a steady supply of oxygen and glucose for proper functioning. It uses 20% of all the oxygen taken in through the lungs. Without enough oxygen, brain cells are irreparably damaged.

In a critical review of 40 clinical studies using ginkgo extract for "cerebral insufficiency" or age-related dementia, virtually all trials reported positive results (Kleijnen et al. 1992). The methodological quality of the eight most well-designed studies were found to be comparable to a U.S. Food and Drug Administration (FDA)-approved pharmaceutical used for the same indication.

In most of the studies [reviewed by Kleijnen et al. (1992)], a daily dose of 120-160 mg of ginkgo extract was given over a period of 4-12 weeks. Compared to the placebo group, significant improvement was observed in typical symptoms such as memory difficulties, confusion, fatigue, anxiety, dizziness, tinnitus, and headaches in the ginkgo extract group.

No serious side effects were reported in any of the assessed 40 trials, and the nonserious side effects were no different from those reported in patients treated with placebo (Kleijnen et al. 1992). This satisfying fact was also confirmed by the conclusion of DeFeudis et al. (2000) (in a summary of the ginkgo literature) that there is generally very little risk associated with products containing a properly standardized ginkgo extract.

In European studies, progressive degenerative dementia such as Alzheimer's disease has been treated with ginkgo extract. The results of these European trials were so impressive that the German government approved ginkgo biloba extract for treatment of dementia.

Free radicals are considered to be the reason for the excessive lipid peroxidation and cell damage observed in Alzheimer's disease (Cecchi et al. 2002). The main effect of ginkgo extract in these conditions appears to be related to its potent antioxidant properties. In a JAMA report, the efficacy and safety of ginkgo extract was tested on patients with Alzheimer's disease and multi-infarct dementia (vascular) (Lebars et al. 1997). This 52-week, randomized double-blind, placebo-controlled multicenter study included 202 patients with mild to moderately severe cognitive impairment. The daily dose given was 120 mg. Measures of outcome included the Alzheimer's Disease Assessment Scale-Cognitive subscale (ADAS-Cog), the Geriatric Evaluation by Relative's Rating Instrument (GERRI), and the Clinical Global Impression of Change (CGIC).

Whereas the ginkgo group maintained its cognitive baseline over the year-long study and improved slightly in social functioning, the placebo group worsened over time in both aspects. The conclusion was that ginkgo appeared to be capable of stabilizing and in a substantial number of cases improving the cognitive performance and the social functioning of demented patients. This corresponds to a delay of 6 months to a year in the progression of the disease. Regarding the safety of ginkgo, there were no significant differences compared with placebo in either the number of patients reporting side effects or in the severity of these effects.

In a German double-blind placebo-controlled study, Maurer et al. (1997) provided further support. In this study, 20 outpatients aged 50-80 and experiencing mild to moderate dementia of Alzheimer's type were treated with a daily dose of 240 mg of ginkgo extract for 3 months. Attention and memory performance of the patients (measured by SKT test) showed significant improvement after 3 months of treatment. The extract was well tolerated with no adverse effects.

Ginkgo biloba has consistently shown that it can help protect against a variety of insults associated with restricted blood supply to the brain (cerebral vascular insufficiency). Ginkgo's three major pharmacological features are improving blood supply by dilating and toning blood vessels; reducing blood-clotting through antagonism of platelet-aggregating factor (PAF); and preventing membrane damage by means of its antioxidant activities.

Can Ginkgo Boost Memory in Healthy People?
While ginkgo has shown significant benefit in persons who already have neurological disease, there is a debate about the acute memory-boosting ability of ginkgo in healthy people. In a study that was widely publicized in the media, a group of healthy adults was given 40 mg of ginkgo extract three times a day or a placebo for 6 weeks. The results showed no difference in memory scores, self-reported perception, or rating by spouses, friends, and relatives after 6 weeks. The implication from the study is that ginkgo provides no short-term benefits in people with healthy cognitive function (Solomon et al. 2002).

However, this report contradicted a similar study conducted on healthy people who received 180 mg a day of ginkgo for 6 weeks (Mix et al. 2002). Compared to placebo, this study showed that ginkgo improved one memory score and significantly improved self-perception of memory. In this positive study, those who received ginkgo rated their overall ability to remember as "improved" compared to those receiving the placebo. This correlates well with previous studies indicating a potential short-term benefit to ginkgo supplementation.

It is known that ginkgo has improved clinical conditions in those diagnosed with severe neurological disease. Based on its multiple mechanisms of action, ginkgo may reduce the risk of developing senile dementia both of vascular and Alzheimer's types. Therefore, the question raised by the one negative study is whether ginkgo can help improve memory in healthy people. Most research shows a benefit, but the most important effect of ginkgo for healthy aging people may be in preserving cognitive function.

It should be pointed out that there is scientific support for memory enhancement even in young healthy people. Following just a single dose of 600 mg of ginkgo extract, a significant memory improvement was demonstrated in a randomized, double-blind crossover study using Sternberg's memory scanning test. The effect lasted for several hours (Subhan et al. 1984). In a later study on healthy volunteers, Rigney et al. (1999) investigated the effects of ginkgo extract on memory and psychomotor function. In this randomized, double-blind, and placebo-controlled crossover study, 31 volunteers aged 30-59 years were given multiple doses of 50 or 100 mg; a single dose of 120 or 300 mg; or placebo during the day of testing. A psychometric test battery was administered before the first dose and at frequent intervals during the day until 11 hours after the last dose.

The results show that the memory-enhancing effect of ginkgo in healthy volunteers was most evident with the 120-mg dose; more apparent in the oldest age group of 50-59 years; and more pronounced for short-term memory than for other aspects of cognitive functioning. This study is interesting in that it showed that a single daily dose of 120 mg was more effective than smaller multiple doses given throughout the day (Rigney et al. 1999). In the negative study, 40 mg of ginkgo was given three times a day. Taking a 120-mg ginkgo capsule once a day (rather than dividing it into smaller 40-mg doses) might have yielded short-term memory improvement in the JAMA study.

Hundreds of scientific studies have confirmed ginkgo's beneficial effects on the human body. Because of its multiple mechanisms of action, ginkgo provides enormous potential protection against our most feared diseases. Aging humans have much to gain from using ginkgo biloba extract in a dose of 120 mg once a day as a preventive measure to help maintain neurological and circulatory health.

Therefore, that one study failed to show improved memory in healthy people who received 40 mg of ginkgo (three times a day) for only 6 weeks is not relevant to those seeking long-term anti-aging effects. The authors of the negative study acknowledge that higher doses of ginkgo or longer periods of exposure might produce the desired effects (Solomon et al. 2002).

To Protect Brain Cell Membranes

Phosphatidylserine
Because the health of brain cell membranes is crucial to neurological function, one of the reasons for the early popularity of lecithin was that it provided a wide range of "phospholipids" that are essential to cell membrane structure and function. However, newer extracts from soy provide a more concentrated means of protecting brain cell membranes. One of these is phosphatidylserine, which plays an important role in maintaining the integrity of brain cell membranes. The breakdown of brain cell membranes prevents glucose and other essential nutrients from entering the cell. By protecting the integrity of cell membranes, phosphatidylserine facilitates the efficient transport of energy-producing nutrients into cells, enhancing brain cell energy metabolism.

Abnormalities in the composition of phosphatidylserine have been found in patients with Alz-heimer's disease (Corrigan et al. 1998). European studies have also shown enhancement in cognitive function when phosphatidylserine is administered to those in various stages of dementia.

Although it has been approved as a drug to treat senility in Europe, phosphatidylserine is sold as a dietary supplement in the United States. The typical daily dose for a healthy person is 100 mg, whereas those with cognitive impairment sometimes take 300 mg a day.

Innovative Drug Strategies

Piracetam
Piracetam is considered to be the "father" of nootropic drugs (cognitive enhancers). Piracetam has been shown to improve a series of mental activities, especially higher cortical functions. It can improve intelligence, concentration, memory, and creativity. Piracetam is a cyclic derivative (2-oxo-pyrrolidine acetamide) of the amino acid GABA (gamma amino butyric acid). Although GABA is an inhibitory neurotransmitter, piracetam does not appear to act in the same way.

In studies from the 1970s to the 1990s, piracetam was shown to

Enhance memory, particularly when used in combination with choline (Bartus et al. 1981; Pragina et al. 1990; Senin et al. 1991)
Increase attention and cognition (Gallai et al. 1991)
Improve spatial learning (Canonico et al. 1991)
Improve the use of glucose by the brain (Heiss et al. 1988, 1991)
Improve brain circulation (Zykov 1992)
Reduce lipofuscin (age pigment) buildup in the brain (Paula-Barbosa et al. 1991)
Act as an antioxidant (Qian et al. 1992)
In animal experiments and in single photon emission computed tomography (SPECT) studies of patients with acute ischemic stroke, piracetam improved micro-circulation and neuronal metabolism and enhanced transmitter functions (Orgogozo 1998).

Another study found that piracetam provides neurological and functional protection from deficits resulting from a moderate or severe stroke when administered within a few days. This study noted that piracetam is well-tolerated and is effective when taken orally and that other treatments have very limited efficacy (Hitzenberger et al. 1998; Noble et al. 1998; Orgogozo 1998).

Research has demonstrated that piracetam's effect on circulation in the brain translates into improvements in aphasia (inability to speak) and level of consciousness, as well as fewer deaths (Poeck 1998).

A daily dose of 4800 mg of piracetam proved to be very effective in a double-blind study of 60 patients with post-concussional syndrome of 2-12 months' duration. After 8 weeks of treatment, piracetam significantly reduced the occurrence and severity of vertigo, headache, tiredness, decreased alertness, increased sweating, and neurasthenic symptoms (Hakkarainen et al. 1978).

A study showed that after 2 months of oral treatment with piracetam (2.4 g daily) in elderly human volunteers, SPECT imaging of the brain indicated a regional improvement in cerebral blood flow, particularly in the cerebellum. However, no beneficial effects with this drug were spontaneously reported (Dormehl et al. 1999).

Unfortunately, in the United States, piracetam has not been approved by the FDA for any use, despite its long track record and extensive clinical use in Europe. Therefore, piracetam is not available in the United States. Piracetam may be ordered from offshore pharmacies. The recommended dose of piracetam is 2400-4800 mg daily.

Hydergine
Hydergine was discovered in the 1940s and later approved by the FDA to treat individuals over age 60 who manifested signs or symptoms of mental incapacity. Unfortunately, when one study showed that Hydergine was not effective in treating Alzheimer's disease, United States physicians virtually stopped prescribing Hydergine, even though the drug was never approved for the treatment of Alzheimer's disease.

Hydergine remains a popular supplement among health-conscious people seeking to slow age-related mental decline. Studies have revealed several mechanisms by which Hydergine protects against brain aging:

Increases blood supply and oxygen to the brain (Emmenegger et al. 1968)
Enhances metabolism in brain cells (Emmenegger et al. 1968)
Protects the brain from damage during periods of decreased or insufficient oxygen supply (Boismare et al. 1978)
Slows the deposit of age pigment (lipofuscin) in the brain (Amenta et al. 1988)
Prevents free radical damage to brain cells (Cahn et al. 1983)
Increases intelligence, memory, learning, and recall (Ditch et al. 1971)
Enhances the use of glucose by brain cells (Nagasawa et al. 1990)
Normalizes the brain levels of serotonin (Markstein 1985)
Increases superoxide dismutase (SOD) and catalase in the brain while decreasing toxic levels of monoamineoxidase (MAO) (Sozmen et al. 1998)
An article by Cover et al. (1996) discussed specific antibodies that bind to brain cell membranes and then target the cell for destruction and removal by the immune system.
Younger brains have significantly lower levels of these destructive antibodies compared to older brains. Hydergine-treated mice showed a reduction in these destructive antibodies, suggesting that middle-aged people who take Hydergine could retard the development of senile dementia caused by programmed immune destruction. The animals receiving Hydergine in middle age maintained healthy brain cell metabolic activities compared to the control group who did not receive Hydergine.

The scientists concluded that Hydergine therapy begun in middle age could protect against the initiation of the cascade that leads to Alzheimer's disease. The scientists emphasized that once the Alzheimer's disease cascade begins, Hydergine would be of little value because the brain cells have already been marked and targeted for immune destruction (Cover et al. 1996).

An article by Rosen (1975) described a double-blind study that evaluated the effectiveness of Hydergine versus papaverine in the treatment of selected symptoms associated with mental aging. After 12 weeks of treatment, ratings of overall clinical condition and global change showed that the 26 patients given Hydergine improved more than twice as much as the 27 patients given papaverine (Rosen 1975).

The Life Extension Foundation has long advocated the use of Hydergine to prevent the degenerative changes that lead to brain cell aging and Alzheimer's disease. Hydergine appears frequently in the scientific literature as therapy for a wide range of diseases ranging from asthma to stroke. Hydergine may be the most underutilized drug in the United States because of the one study that showed its failure to treat advanced Alzheimer's disease.

For middle-aged persons who have a family history of Alzheimer's disease, a daily dose of 10-20 mg of Hydergine is suggested. For middle-aged persons seeking to slow their rate of brain cell aging, a daily dose of 5-10 mg of Hydergine is suggested.

In 5% of people, Hydergine may induce mild nausea. However, for the remaining 95% for whom Hydergine does not cause nausea, 5-mg Hydergine tablets may be obtained from European suppliers, making taking high doses convenient and very economical.

Deprenyl
Another cause of brain aging is the elevation of an enzyme in the brain called monoamine oxidase (MAO). Monoamine oxidase A and B are the primary enzymes that degrade neurotransmitters in the central nervous system and peripheral tissues. Elevated MAO levels damage brain cells and are a specific cause of age-related neuronal deterioration. Too much MAO has also been shown to cause pathological disorders such as Parkinson's disease (Orru et al. 1999; Abell et al. 2000).

Low-dose deprenyl (selegiline) is thought to protect the brain from aging by specifically inhibiting monoamine oxidase B (MAO B) in the brain. Deprenyl was approved for use in Parkinson's disease in the 1980s and was often combined with L-dopa (levodopa). However, one study raised concerns about combining high doses of deprenyl (10 mg per day) with L-dopa due to an apparent increase in mortality in the deprenyl group (Lees 1995). The results of that paper were hotly debated and several flaws were found in the study design. Later studies showed clinical benefit with deprenyl without a decrease in mortality and no toxic effects, particularly when lower doses were used (5 mg a day or every other day) (LeWitt 1991; Shoulson 1992, 1998).

Deprenyl has long been recommended in very low doses (10 mg a week) as part of an overall anti-aging program because it has been shown to extend lifespan in animal studies. Deprenyl has also been shown to stimulate the efflux of norepinephrine, dopamine, and serotonin in vitro by a direct action on the hypothalamus. Some researchers are proposing that deprenyl may be considered as an alternative to levodopa for starting treatment in Parkinson's disease patients (Caracenia et al. 2001; MohanKumar et al. 2001).

Deprenyl has also been shown to induce rapid increases in nitric oxide (NO) production in brain tissue and cerebral blood vessels and also to protect the vascular endothelium from the toxic effects of amyloid-beta peptide (Thomas 2000). Another study showed that deprenyl protected cells from apoptosis induced by a neurotoxin, N-methyl(R)-salsolinol, and reactive oxygen species, nitric oxide and peroxynitrite (Naoi et al. 2000). Additionally, Zhu et al. (2000) showed that deprenyl significantly improved the cognitive function of rats after traumatic brain injury.

A study of 17 patients with Alzheimer's disease found that the Mini-Mental State Examination scores were significantly higher in those patients receiving selegiline (deprenyl) than in those receiving placebo (Alafuzoff et al. 2000). In India, another study of 32 patients with Parkinson's disease found a significant improvement in memory in patients treated with 10 mg a day of deprenyl as compared to placebo (Dixit et al. 1999).

Scientists who conducted lifespan studies using deprenyl have estimated the ideal dose to slow brain aging in humans to be about 1.5 mg daily. Because deprenyl is usually sold in 5-mg tablets and has a long-acting effect on the brain, most Life Extension members take a low dose of 5 mg of deprenyl twice a week.

However, Hydergine seems to be more effective when higher doses are used. European physicians often prescribe 4.5-20 mg daily of Hydergine without concern for toxicity. Persons seeking protection from neurological aging and wanting to boost cognitive function have used high-dose Hydergine and low-dose deprenyl together for more than 16 years. No adverse effects have been reported when using these two medications together.

Caution: Care should be taken when administering dopamine to patients who have been using deprenyl (selegiline). One journal article noted a drastic increase in systolic blood pressure after a critically ill man using selegiline was given an infusion of dopamine (Rose et al. 2000).

Nimodipine
Nimodipine is particularly recommended for victims of head trauma. Nimodipine (brand name Nimotop) is a calcium channel blocker specific to the central nervous system. It prevents movement of calcium into the cells of blood vessels, thereby relaxing the vessels and increasing the supply of blood and oxygen. It dramatically improves cerebral blood flow.

Nimodipine is an FDA-approved drug that is used to prevent and treat problems caused by a blood vessel around the brain that has burst. But nimodipine has been ignored by most neurologists treating victims of stroke and other age-related neurological diseases.

An article by Pantoni et al. (2000a) described a 26-week, multinational, double-blind, placebo-controlled study of nimodipine in patients with multi-infarct dementia. This study failed to show a significant effect of nimodipine on cognitive, social, or global assessments. However, a lower incidence of cerebrovascular and cardiac events was observed in the nimodipine-treated patients in comparison with the placebo group. A subgroup analysis found that those patients with subcortical vascular dementia performed better on the majority of neuropsychological tests and functional scales in comparison with patients on placebo (Pantoni et al. 2000b). A recommended dose of nimodipine is 30 mg, three times daily.

Centrophenoxine
Centrophenoxine (meclofenoxate) is widely used in Europe in combination with piracetam to improve memory and enhance mental energy. Although Centrophenoxine is readily available in Europe, it is not sold in the United States. Centrophenoxine can be ordered from pharmacies in Europe.

Researchers have proposed several mechanisms for Centrophenoxine, including:
Increasing activity of free radical scavengers, especially in brain and heart tissues (al-Zuhair et al. 1998)
Providing antioxidant action, possibly due to the DMAE (dimethyl-amino-ethanol) it contains (Zs-Nagy 1989)
Increasing acetylcholinesterase activity in the hippocampus and brain (Sharma et al. 1995)
Decreasing the deposition of the age-pigment lipofuscin, which has been shown to cause neuronal damage (Patro et al. 1992)
Inhibiting total MAO (monoamine oxidase), MAO-A and MAO-B, which has been shown to damage brain cells (Stancheva et al. 1988)
Increasing the content of serotonin (5-HT), a key neurotransmitter that can be damaged by elevated MAO (Stancheva et al. 1988)
Significantly increasing the fluidity of brain membranes, which can reverse the dehydration of nerve cells of older animals (Lustyik et al. 1985; Wood et al. 1986)
Centrophenoxine was shown to improve memory retention in aged rats in tests using the maze method for active avoidance with punishment reinforcement and the step-through method for passive avoidance with negative reinforcement. Centrophenoxine increased the number of responses to conditioned stimulus and strongly prolonged the time spent in the light chamber (a measure of improved retention) (Mosharrof et al. 1987).

A double-blind clinical trial of 50 patients with dementia examined the effects of 2 grams a day of Centrophenoxine for 8 weeks: 48% of the Centrophenoxine group displayed improvements in the memory functions versus 28% of the placebo group (Pek et al. 1989). Another study found that Centrophenoxine corrected the blood pressure drop when standing in 25 patients who had orthostatic hypotension due to brainstem ischemia (Stoica et al. 1991).

The recommended dose of Centrophenoxine is 250-1000 mg daily.

Other Factors to Consider

Lifestyle
Taking steps to improve one's overall health is highly recommended to help prevent or minimize age-associated mental impairment. For example, exercising regularly; not smoking; and monitoring blood cholesterol levels can reduce the risk of stroke and heart disease and keep arteries open, supplying the brain with essential oxygen and nutrients. Regular exercise improves some mental abilities by an average of 20-30%. Abstaining from alcohol or drug use, or minimizing it, can also help preserve mental function. Because most persons tend to eat less food as they age, the use of low-fat, nutrient-rich food is recommended. This type of diet will help prevent nutrient deficiencies, which can impair mental function as a result of physical illnesses. Eating large quantities of high-antioxidant fruits, especially berries (blueberries), may significantly provide protection from senility and many other age-related conditions. Mental exercise is another crucial lifestyle component. Forcing the memorization of dates, lists, and telephone numbers can help keep your mind sharp as you age. Engaging in activities that challenge acuity can also provide an "exercise" effect for your brain.

Guarding Against Prescription Drug Side Effects
Adverse side effects can result from either too high or too low doses of medications; unusual reactions to medications; or combinations of medications. It is especially common in the older population for individuals to be taking many different medications prescribed by different doctors, in addition to over-the-counter supplements. Be certain that your primary physician is aware of all prescription and nonprescription medications that you take.

Be Certain that You Are Not Anemic
A large number of aging people are anemic. Their physicians often fail to treat this condition because anemia is so common. Anemia represents a deficiency in the oxygen-carrying capacity of the blood. Blood should be tested annually. If there is any indication of even borderline anemia, seek medical assistance. For complete information about anemia, refer to the Anemia protocol in this book (also see Life Extension website at www.lef.org ).

Keep Blood Pressure in the Low Normal Range
A 30-year study of male twins showed that elevated blood pressure in mid-life predisposed men to accelerated brain aging and an increased risk of stroke later in life. Men with even mildly elevated blood pressure 25 years before showed smaller brain volumes and more strokes compared to their twin brothers who did not have the elevation in blood pressure. This study in the journal Stroke emphasized the importance of aggressively treating elevated blood pressure even when it is not grossly abnormal (DeCarli et al. 1999). Refer to the Hypertension protocol in this book for information about natural methods of controlling blood pressure.

Summary

The brain is the center of personal identity that makes us uniquely human. Decline in brain function is the greatest fear most persons have when thinking about aging.

Age-associated mental impairment can range in severity from forgetfulness to senility to dementia. Age-associated mental impairment can be caused by a wide variety of specific disease processes, many of which are treatable. It can also result from normal brain aging. Whatever its form or cause, age-associated cognitive impairment does not need to be accepted as an inevitable consequence of growing older.

Behavioral modification such as participating in increased physical and mental activity and following a healthy diet can improve mental function both directly and indirectly by enhancing overall health.

Age-associated mental impairment can be treated safely and effectively with memory-enhancing nutrients, hormones, and drugs. These therapies improve cerebral circulation; boost brain cell metabolism; stabilize brain cell membranes; increase acetylcholine; provide structural building blocks to neurons; synchronize brain cell interaction; restore youthful hormone balance; suppress free radicals; and reduce chronic inflammatory processes.

The benefit of taking several different types of agents that protect and enhance neurological function is that these same agents can also prevent age-associated diseases from manifesting in other parts of the body. Nutrients such as coenzyme Q10, acetyl-L-carnitine, and ginkgo, along with hormones such as DHEA, melatonin, and testosterone, can provide dramatic systemic anti-aging effects. A massive body of published scientific research indicates that one can take steps to boost cognitive function today, while simultaneously reducing the risk of Alzheimer's disease, stroke, and other degenerative brain diseases.

There is currently much debate as to whether mild cognitive decline or memory problems are a risk factor for developing more serious neurological disease, such as dementia or Alzheimer's disease. Some studies indicate that a significant percentage of elderly people complaining of mild cognitive impairment will go on to develop Alzheimer's disease. Clinical studies have been conducted in elderly people to see if the decline in cognitive function can be slowed and Alzheimer's disease can be postponed or prevented (Hanninen et al 1997; Richards et al. 1999; Grober et al. 2000; Collie et al. 2001; Goldman et al. 2001a; Goldstein et al. 2001; Petersen et al. 2001).

Perhaps the most important research paper published on age-associated memory impairment stated that memory decline is not a normal feature of aging. What the researchers found was that in persons with mild memory impairment, memory loss tended to progress, whereas persons who were healthy did not experience memory impairment as they aged (Goldman et al. 2001b).

If you have a neurological disorder such as cerebral vascular disease (stroke), Alzheimer's disease, Parkinson's disease, etc., refer to the in-depth protocols in this book that provide innovative treatment options that are often overlooked by conventional physicians.

The following are dietary supplements available in the United States that may benefit persons who have age-associated mental impairment:

Cognitex is a multi-ingredient formula providing nutrients such as vinpocetine, phosphatidylserine, glyceryl phosphorylcholine (GPC), and others discussed in this protocol. Three to six capsules of Cognitex daily are suggested.
Essential fatty acids such as DHA, GLA, and EPA are found in Super GLA/DHA. The recommended dose is six softgels daily of Super GLA/DHA, providing 1000 mg of DHA and 900 mg of GLA, along with 200-400 mg of EPA.
Ginkgo biloba extract, 120 mg daily.
Acetyl-L-carnitine, 2000 mg daily.
Coenzyme Q10, 100-300 mg daily.
Super Alpha Lipoic Acid, 250-500 mg daily.
Life Extension Mix provides broad-spectrum, high-potency antioxidants, vitamins, and minerals. A suggested dose is three tablets, three times a day.
DHEA, 25-50 mg daily. Refer to the DHEA Replacement Therapy protocol before initiating DHEA or pregnenolone replacement.
Melatonin, 300 mcg to 3 mg nightly, a half hour before bedtime.
Phosphatidylserine (PS), 100-300 mg daily.
Vitamin B12 (preferably in the form of methylcobalamin), 1-40 mg daily.
Drugs and hormones requiring a prescription or that may be obtained from offshore pharmacies are:

Testosterone replacement, often indicated in aging males. Refer to the Male Hormone Modulation protocol in this book for complete details.
Estrogen replacement, often indicated in aging females. Increased risk of certain cancers and cardiovascular disease are of concern. Refer to the Female Hormone Replacement protocol for alternatives to estrogen drugs.
One or a combination of the following drugs may be considered:
Piracetam, 2400-4800 mg daily.
Centrophenoxine, 250-1000 mg daily.
Hydergine, 5-20 mg daily.
Deprenyl, one 5-mg tablet, two times weekly.
Nimotop (nimodipine), 30 mg, three times daily.
Chronic inflammation inflicts devastating effects, particularly as humans grow older. The pathological consequences of inflammation are fully documented in the medical literature. For example, in Alzheimer's disease, an inflammatory cascade is involved in many of the destructive processes observed in the neurons of patients, including the formation of toxic beta-amyloid. As this toxic inflammatory process continues, the loss of functioning neurons is accelerated, first resulting in mild cognitive impairment. Many scientists believe that unchecked inflammation is an underlying culprit in the development of Alzheimer's disease.

Because chronic inflammation is so injurious to brain cells, aggressive steps should be taken to suppress the inflammatory cascade. Some of the supplements recommended in this protocol, such as Super GLA/DHA, ginkgo, DHEA, and Life Extension Mix, can significantly reduce chronic inflammatory processes. For more information about drugs and additional therapies that are available to suppress dangerous inflammatory components in blood, please refer to the Inflammation (Chronic) protocol in this book.

As you have learned from this protocol, there are multiple diverse factors involved in the development of cognitive impairment and senility. Therefore, the emphasis should be on incorporating as many supplements, hormones, and drugs as are feasible to guard against the mechanisms involved in neuro-degeneration. For example, while supplements that increase acetylcholine (such as GPC) have become popular agents to improve short-term memory, they do not suppress a chronic inflammatory state nor do they appreciably boost brain cell energy metabolism.

Therefore, to optimally protect your brain from the numerous insults incurred as a result of normal aging and environmental toxins, a multimodal approach is needed that includes the proper dose of the nutrients, hormones, and drugs discussed in this protocol.

For More Information

Contact the National Institute on Aging, (800) 222-2225; the Alzheimer's Association, (800) 272-3900; and the National Institute of Neurological Disorders and Stroke, (800) 352-9424.

Product availability

Cognitex, Super GLA/DHA, ginkgo biloba, vinpocetine, acetyl-L-carnitine, coenzyme Q10, alpha lipoic acid, Life Extension Mix (containing essential vitamins and minerals), DHEA, melatonin, methylcobalamin (vitamin B12), and phosphatidylserine are available. Piracetam, high-dose Hydergine, and Centrophenoxine are available from overseas companies. A list of these companies can be obtained by calling (800) 226-2370. Testosterone patches, gels, or creams; estrogen drugs; and Hydergine, deprenyl, and nimodipine are available in the United States only by prescription.

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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease