Cognitive Function

Cognitive Function

by Kim Schoenhals

Memory is an integral part of how people define "self" and is constructed of past occurrences, people and places. Memories are commonly discussed at social and business gatherings, drawing people together in the present through the time and distance of the past. But what happens when memories are no longer as clear as they once were, when the memory aspect of cognition is lost due to malfunctions in the brain?

Several diseases of the brain can effectively steal memories from a once healthy person, detracting from that well-constructed sense of self. In addition to memory loss, neurodegenerative diseases such as Alzheimer's and Parkinson's can also affect awareness, judgment and other aspects of cognitive function.

Contrary to popular belief, memory loss is not a normal aspect of aging; rather, it can be a symptom of a serious illness, according to the Alzheimer's Association. Alzheimer's disease--originally discovered in 1906 by the German physician Alois Alzheimer--is one of several disorders that cause the gradual loss of brain cells and is currently recognized as the No. 1 cause of dementia in the United States.

"Dementia is an umbrella term for several symptoms related to a decline in thinking skills," according to the Alzheimer's Association. "Common symptoms include a gradual loss of memory, problems with reasoning or judgment, disorientation, difficulty in learning, loss of language skills, and decline in the ability to perform routine tasks."

Approximately 4 million Americans have Alzheimer's disease, according to the Alzheimer's Association, and by 2050, 14 million Americans will suffer from the disease. In addition, one in 10 people over the age of 65 and nearly half of those over age 85 have Alzheimer's.

As for Parkinson's disease, an estimated 1.5 million Americans are affected by the disease, which was named after James Parkinson, an English physician who described the disease in 1817. Parkinson's disease is a progressive neurological condition that affects a portion of the mid-brain and gradually degenerates its cells, thereby reducing dopamine production. This decrease of dopamine causes the hallmark signs of Parkinson's disease, such as tremor, slow movement, stiffness and balance difficulties. The disease is also known to affect cognition.

Aside from cognitive impairment caused by Alzheimer's and Parkinson's, dementia can occur as a symptom of Huntington's disease or as vascular dementia (a.k.a. multi-infarct dementia). Vascular dementia is a common cause of dementia in the elderly, according to the National Institute of Neurological Disorders and Stroke (NINDS). It occurs when blood clots block small blood vessels in the brain, thereby destroying brain tissue.

While Alzheimer's, Parkinson's and vascular dementia do not have cures or preventive measures, there are medical therapies available to restore cognitive function and slow the degeneration of brain cells. In addition, several natural therapies are suspected to assist this process and return some normalcy to the patient's brain health, as well as slow the rate of cognitive decline.

Antioxidants

As with many health conditions, neurodegenerative diseases are suspected to be caused--at least in part--by oxidative damage. "Accumulation of oxidative damage in neurons either primarily or secondarily may account for the increased incidence of neurodegenerative diseases such as Alzheimer's disease ... in aged populations," according to researchers at the University of Toronto.¹

There is a wealth of research showing the possible protective role of antioxidants in cognitive function, although it has been suggested that additional research is needed. In fact, researchers at the University of California, Irvine, suggested that "oxidative damage impairs cognitive function, and antioxidant treatment can result in significant improvements, supporting the need for further human studies."² A research review out of Paris also noted a protective effect of antioxidants on cognitive performance in humans.³

In support of the protective role antioxidants play in cognitive function, it has been shown that diets rich in fruits and vegetables improve human well-being and delay the development of neurodegenerative disorders.⁴ Researchers at the U.S. Department of Agriculture's (USDA) Neuroscience Laboratory in Boston further noted that foods are an important source of micronutrients--such as vitamin E and vitamin C--that play crucial roles in cell function. "An optimal intake of these nutrients has been associated with decreased risk of developing cognitive impairments associated with aging," they wrote. Some of the same researchers from the USDA Neuroscience Laboratory conducted a research review and determined both vitamins are important for the central nervous system, and decreased concentrations can lead to structural and functional cellular damage.⁵

Like the risk of cognitive impairments, supplementation with vitamins E and C also increases with age. According to the Natural Marketing Institute's (NMI) Health & Wellness Trends Database, four years of trended data from more than 2,000 consumer respondents, 51.6 percent of consumers age 65 and older take vitamin E and 49.4 percent take vitamin C. These percentages showed steady increases from 16.9 percent using vitamin E and 21.3 percent using vitamin C at age 35 and younger.

Both vitamins E and C are also suspected to prevent neurological dysfunction caused by homocystinuria, a metabolic disorder that leads to homocysteine accumulation.⁶ Brazilian researchers investigated the protective effects of vitamins E and C against homocystinuria in a rat model. Animals receiving homocysteine exhibited significantly impaired memory; however, rats chronically treated with vitamins E and C had this effect prevented.

Antioxidants are also believed to protect cognitive function in Parkinson's patients. The National Parkinson Foundation suggests a regimen of a multivitamin/mineral supplement three times weekly alternated with an antioxidant combination (vitamins A, C and E) three times weekly as an "insurance policy" for preserving brain function. In terms of preventing Parkinson's, however, researchers from the Harvard School of Public Health in Boston did not find a protective effect from vitamin E or C supplements or multivitamins, although they did note a protective effect from food-derived vitamin E.⁷

Vitamin E from foods has also been associated with a reduced risk of Alzheimer's disease, according to a study out of Chicago's Rush Institute for Healthy Aging.⁸ Some of the same researchers conducted a subsequent study--a longitudinal, population-based trial of 2,889 community-based residents--and determined that vitamin E intake from food or supplements was associated with less age-associated cognitive decline.⁹

Vitamin E may also affect cognitive function in the young, as demonstrated by animal research out of Japan.¹⁰ Young animals given vitamin E demonstrated an improvement in learning capacity, as well as a reduction in stress-induced memory loss.

Aside from general research on vitamin E in the form of supplements or food, studies have also been conducted on the various isomers of vitamin E, of which there are eight (alpha-, beta-, delta- and gamma-tocopherol and four corresponding tocotrienols). Research out of Spain was conducted to determine what correlation, if any, existed between serum alpha-tocopherol concentrations and cognitive function.¹¹ Of a group of elderly subjects (34 men, 86 women), those with vitamin E intakes lower than half of the recommended daily amount made more mistakes on the Pfeiffer's Mental Status Questionnaire than subjects with higher intakes of vitamin E. Also, subjects who made no errors on the test exhibited significantly higher concentrations of serum alpha-tocopherol.

Animal research conducted with alpha-tocopherol indicated the antioxidant isomer prevented cognition impairment and lipid peroxide accumulation, as well as decreased the number of apoptotic cells in mice.¹²

As for the tocotrienols, NINDS awarded more than $1 million in 2002 to researchers at Ohio State University, Columbus, to investigate how alpha-tocotrienol protects against neuronal cell death. The award was based on preliminary research conducted with a tocotrienol complex (as Tocomin from Edison, N.J.-based Carotech Inc.) that demonstrated tocotrienols cross the blood-brain barrier and protect against neuronal cell death. The ongoing NIH-funded study is meant to elucidate the mechanism by which alpha-tocotrienol exerts its neuroprotective effects.

Like vitamin E, vitamin A has also been studied in terms of cognitive function. Researchers at the University of Cagliari in Italy noted vitamin A deprivation in adult rats for 12 weeks induced severe learning deficits; this impairment was fully restored when vitamin A was re-introduced into the animals' diets.¹³

CoQ10 (coenzyme Q10), a vitamin-like antioxidant compound, has also been linked to improved cognitive function. With age, consumers are more likely to use CoQ10 supplements, according to NMI. While 1.3 percent of consumers aged 35 and younger use CoQ10 on a daily basis, 5.7 percent of consumers age 46 to 55 and age 65 and older, and 5.8 percent of consumers age 56 to 65 take the vitamin-like compound daily.

One mechanism of action suggested for CoQ10's role in protecting cognitive function is its ability to improve mitochondrial function. The body's mitochondria are responsible for manufacturing cellular energy in all tissues, including the brain. Research out of the University of Southern California, Los Angeles, demonstrated that oral supplementation with CoQ10 (as Q-Gel from Westbury, N.J.-based Tishcon) increased CoQ10 levels in the test animals' brain mitochondria, as well as the mitochondria of the liver, kidney, heart and skeletal muscle.¹⁴

In terms of bioavailability, a study was conducted by researchers at the Texas Tech Health Sciences Center School of Pharmacy to compare the bioavailability of three CoQ10 preparations.¹⁵ Researchers conducted an open, randomized, multiple-dose, crossover design with dogs, comparing a powder-filled capsule (control Group A) and two softgel formulations: Group B received Q-Gel and Group C received Q-Nol (also manufactured by Tishcon), a water-miscible form of ubiquinol, the reduced form of CoQ10. Results indicated that the relative bioavailabilities of formulations B and C were approximately 3.6- and 6.2-fold higher than that of the control formulation.

In additional animal research, CoQ10 has been found to decrease brain damage in neurological disease. In a mouse model of Huntington's disease, researchers from the Bedford Veterans Administration Medical Center in Massachusetts found oral CoQ10 administration significantly extended survival and delayed the development of motor deficits and neuronal intranuclear inclusions.¹⁶

CoQ10 administration may attenuate neuron damage in Parkinson's disease as well. Researchers at the University of North Dakota, Grand Forks, studied the mitochondrial genetics of Parkinson's disease and noted that in the common form of the disease, a defect of complex I of the mitochondrial respiratory chain is present at a biochemical level.¹⁷ They further noted that the neurotoxin 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP), which causes a Parkinson-like syndrome in humans, acts via an inhibition of complex I.

Additional promising research with CoQ10 and Parkinson's disease came out of the University of California, San Diego.¹⁸ The phase II clinical trial indicated supplementation with 1,200 mg/d of CoQ10 stalled cognitive decline by 44 percent compared to placebo. Lower doses (300 mg/d and 600 mg/d) also reduced the rate of mental decline, but not to the same extent as the high-dose group. [Editor's note: The CoQ10 product used in this study was a special formulation developed by Enzymatic Therapy (www.enzy.com). The company produced a wafer form of its Vitaline CoQ10 with 1,200 mg of natural CoQ10 and 1,200 mg of vitamin E, using a patent-pending manufacturing process to enhance absorption without use of excipients that can be neurologically harmful at high doses.]

Researchers in Poland compared the possible protective effects of CoQ10 with those of the sulfur-containing antioxidant compound lipoic acid for reducing neuronal cell death.¹⁹ The researchers invoked diabetes in rats and then induced cerebral ischaemia in some of them. Then, all animals were either treated with CoQ10 or lipoic acid for seven days. Both treatments were found to diminish neuronal cell loss in diabetes complicated with ischemia.

Percentage of Consumers By Age Group Using Supplements
Source: The Health & Wellness Trends Database
The Natural Marketing Institute, 2003

Lipoic acid has also been compared to acetyl-L-carnitine for its ability to improve age-associated memory decline.²⁰ In a rat study conducted at the University of California, Berkeley, lipoic acid and acetyl-L-carnitine--both of which are mitochondrial metabolites--were found to reduce age-associated memory decline and inhibit the age-associated increase of oxidative damage to lipids, proteins and nucleic acids, as well as elevate the levels of antioxidants and restore mitochondrial enzyme activity. The researchers concluded both compounds protected neuronal cells from oxidative damage. Previous research conducted by the same team indicated orally administered acetyl-L-carnitine or alpha-lipoic acid improved memory, although the combination of the two was found to be more effective.²¹

Independently, acetyl-L-carnitine may also have beneficial effects on cognitive function. Researchers at Yamanashi University in Japan treated mice genetically prone to accelerated senescence with either 100 mg/kg or 400 mg/kg of acetyl-L-carnitine or saline (placebo) three times a week up to four months of age.²² The high-dose treatment was shown to slow the learning and memory deficits seen in the placebo group.

Another group of antioxidant compounds--flavonoids--may also have application in the realm of cognitive function. A research review conducted at King's College in London indicated dietary flavonoids from fruits and vegetables have potential neuroprotective actions, particularly toward deficits seen with aging.²³

Concern With Preventing Memory & Concentration Problems
Source: The Health & Wellness Trends Database
The Natural Marketing Institute, 2003

The polyphenolic constituents of grapes have also been studied in terms of protecting cognitive function. A novel grapeseed proanthocyanidin extract (as ActiVin, from Fresno, Calif.-based San Joaquin Valley Concentrates) was shown to prevent DNA damage in various tissues and partially protect brain tissue against toxin-induced damage.²⁴ A safety and toxicity study of grapeseed extract indicated chronic administration of 100 mg/kg/d of the extract for 12 months was safe in female mice and did not cause any detrimental effects.²⁵

Researchers at the University of Missouri, Columbia, noted from their animal research that grape polyphenols ameliorated neuronal damage caused by oxidative stress from chronic ethanol consumption.²⁶ They also noted that resveratrol, a component of grape polyphenols, demonstrated protective effects against neuron cell death induced by ethanol or other oxidative agents.

B Vitamins and Naturally Occurring Compounds

In addition to the antioxidant compounds, the B vitamins are also thought to play a significant role in protecting brain health. In fact, researchers from the University of Toronto stated the pharmacotherapy of Alzheimer's disease should include supplementation with a B vitamin complex.²⁷

According to data from NMI, older consumers are more likely to take a B vitamin complex than younger consumers. While 11.1 percent of consumers age 35 and younger use a B vitamin complex, 22.9 percent of consumers above age 65 take a daily B complex.

As for specific B vitamins, a deficiency of vitamin B12 (cobalamin) may be associated with poor cognition in elderly subjects, according to a study out of the University of Georgia, Athens.²⁸ Investigators at the University of Pittsburgh found similar results in a group of patients with probable Alzheimer's disease.²⁹ And, researchers at the University of Maastricht in The Netherlands found low cobalamin levels were linked with reduced information processing speed.³⁰ Supplementation with vitamin B12 may improve cognitive function in elderly patients with a B12 deficiency, perhaps due to a reduction in plasma homocysteine levels, as demonstrated by researchers at the University Medical Centre Nijmegen in The Netherlands.³¹

Similar to vitamin B12, folic acid may also affect homocysteine concentrations and cognitive function in the elderly. Researchers at England's Rowett Research Institute noted B vitamin and homocysteine status were associated with cognitive variation in old age, as demonstrated by a review of two large cohorts.³² Specifically, B12 status was positively associated with higher scores on a national reading test, and folic acid was positively correlated with higher scores on verbal learning and digit symbol tests.

Supplementation with vitamin B12, folic acid and vitamin B6 may significantly affect memory performance, according to researchers in Australia.³³ The researchers gave 211 women either a treatment regimen (15 mcg/d of vitamin B12, 750 mcg/d of folic acid and 75 mg/d of vitamin B6) or a placebo for 35 days. Supplementation was shown to affect memory performance, and dietary intake status--as measured by food-frequency questionnaires--was associated with speed of processing, recall and recognition, and verbal ability.

Choline, categorized under the umbrella of the B vitamin family, is actually synthesized by humans, although generally in amounts insufficient to meet metabolic needs--hence its classification as an essential vitamin. Because choline is a ubiquitous nutrient present in all cell membranes, deficiency is generally unheard of. However, patients who require long-term parenteral nutrition (feeding through the veins due to severe intestinal problems) have been known to develop choline deficiency, suggesting the body cannot fully synthesize choline without some dietary intake. Researchers at Northwestern University, Chicago, investigated this phenomenon and learned that patients who received added choline chloride exhibited improved verbal and visual memory compared to patients receiving parenteral nutrition alone.³⁴

Choline chloride may also affect cognitive health when given during pregnancy, as demonstrated by animal research out of Williams College in Massachusetts.³⁵ When pregnant rats were given choline chloride, the animals' offspring had enhanced hippocampal nerve growth factor levels at 20 and 90 days of age, suggesting an underlying mechanism for improved spatial and temporal memory of adult rats exposed to choline in the womb.

A double blind, crossover study of choline supplementation in humans did not have as positive a result.³⁶ Investigators at the Uniformed Services University of the Health Sciences in Bethesda, Md., gave 13 men choline (50 mg/kg), which was shown to significantly increase plasma choline concentrations but did not affect cognitive or physical performance.

The primary dietary source of choline comes from phosphatidylcholine (PC), a phospholipid found in lecithin that is sometimes called lecithin itself. PC provides choline for the synthesis of the neurotransmitter acetylcholine. Researchers at the Institute of Public Health in Cambridge, England, noted that people with Alzheimer's have a relative lack of the enzyme responsible for converting choline into acetylcholine within the brain.³⁷ However, in their meta-analysis of trials involving patients with Alzheimer's or Parkinson's dementia, they did not find sufficient evidence to support the use of lecithin in improving cognitive function. Contrarily, researchers at Guiyang Medical College in China noted that certain lipids in lecithin have been shown to help mental function in patients with Alzheimer's.³⁸

Researchers at the University of Guelph in Canada discovered that patients with Alzheimer's disease, other dementias or general cognitive impairment exhibited lower plasma phospholipid--specifically PC--levels than subjects with normal cognitive functioning.³⁹ Similar data was reported by researchers at the Universite du Maine in France.⁴⁰ Their animal study indicated older rats have reduced fatty acid composition in PC and phosphatidylserine (PS) classes compared to younger animals.

Plant-derived PS is as effective for inducing cognitive benefits as bovine-derived PS, according to researchers in Tokyo.⁴¹ They found that aged male rats given soy-derived PS for 60 days had significantly improved performance in a water maze escape test.

An open trial of plant-sourced PS conducted in Tel Aviv, Israel, also garnered promising results.⁴² For 12 weeks, 18 healthy elderly volunteers with age-associated memory impairment were treated with three daily doses of 100 mg of PS. From the noted improvements, researchers concluded PS may be a viable approach for treating age-related cognitive decline after double blind clinical trials are conducted.

Contrarily, researchers at the Brain & Behaviour Institute in Maastricht, The Netherlands, found no benefit for memory or other cognitive function with soy-derived PS.⁴³ Although, additional research by the same team demonstrated that soy-derived PS is safe for elderly subjects and causes few and mild adverse effects when taken in doses up to 600 mg/d.⁴⁴

Another naturally occurring compound, glycerophosphocholine (GPC), has been studied for its ability to improve cognitive function in subjects of all ages. In terms of the older population, researchers at the University of Perugia in Italy published a meta-analysis of GPC studies and concluded GPC enhanced general mental performance.⁴⁵ In a subsequent review of GPC studies conducted at the University of Camerino in Italy, GPC was shown to benefit vascular dementia and enhance cognition, mood and somatic symptoms in aging subjects.⁴⁶

Melatonin, a naturally occurring hormone, may have application in the realm of cognitive function, as demonstrated by several animal studies. Researchers in Turkey found that melatonin plays a role in central memory.⁴⁷ Additional animal research has suggested melatonin's role in improving memory may be due to its antioxidant properties.^48,49

Investigators at the University of Hong Kong compared the memory-enhancing function of melatonin to that of Ginkgo biloba in an animal model of memory deficit.⁵⁰ They learned that while melatonin did not reverse the induced memory deficit, orally administered ginkgo seemed to protect the animals' brains from induced changes that led to memory deficit.

Prevention/Treatment of Memory/Concentration Problems With Supplements Vs. Food
Source: The Health & Wellness Trends Database
The Natural Marketing Institute, 2003

Botanicals, Etc.

Ginkgo biloba is probably the most well-known herb in terms of cognitive function and has been included in countless herbal formulas for improving memory and cognition. Elderly consumers are more likely to use ginkgo than younger consumers, according to NMI. Nearly 10 percent of consumers age 65 and older reported taking a daily ginkgo supplement, while only 2.6 percent of consumers age 35 and younger said the same.

While its popularity remains healthy, the herb's reputation was tarnished slightly when the Journal of the American Medical Association published a government-sponsored trial in August 2002 that demonstrated no benefits of ginkgo supplementation in elderly subjects without cognitive impairment.⁵¹ The six-week, randomized, double blind trial involved 203 participants, and researchers noted there were no significant differences in tests of learning, memory, attention or concentration between the treatment and placebo groups.

In the same month, however, a similar trial was published in which elderly subjects with no history of dementia demonstrated cognitive improvements with ginkgo supplementation.⁵² Researchers at Liberty University in Lynchburg, Va., randomly assigned 262 elderly volunteers to receive either ginkgo or placebo for six weeks, at which point the patients taking ginkgo exhibited significant improvement on cognition tests compared to those taking placebo.

As for ginkgo's mechanism of action, researchers in Bulgaria determined its effects on learning and memory are perhaps due to its modification of the beta-adrenergic system in the brain.⁵³ Researchers at the University of Southern Mississippi, Hattiesburg, suggested two potential mechanisms of action for ginkgo's role in reducing Alzheimer's degeneration: as an antioxidant and as a stimulant for cell survival machinery.⁵⁴

Ginkgo has also been studied in combination with various other herbs for improving cognitive function. A combination of ginkgo and ginger (Zingiber officinale, as Zingicomb) improved several indicators of learning and cognition, as well as decreased oxidative damage in brain tissue, in an aged rat model.⁵⁵ When combined with Panax ginseng (as G115 by Pharmaton SA), ginkgo (as GK501 by Pharmaton SA) was shown to dose-dependently improve performance on "quality of memory" and "speed of attention" factors in 20 healthy young adult volunteers.⁵⁶ Subsequent research by the same investigators from the University of Northumbria in Tyne, England, found that individual doses of ginkgo and ginseng, as well as the combination product, improved secondary memory performance.⁵⁷ The researchers also noted that the ginseng, when taken alone, improved the speed of performing memory tasks and the accuracy of attention tasks. When combined with vinpocetine--a derivative of the alkaloid vincamine, which is found in the aerial part of the Vinca minor and other plant sources such as the Voaconga and the Crioceras longiflorus--ginkgo improved working memory capacity and processing in 24 healthy adults after two weeks.⁵⁸

A possible mechanism of action for vinpocetine's efficacy in improving cognitive function may be its role as a cerebral vasodilator, meaning it improves blood flow to the brain. A research review published out of Hungary indicated vinpocetine may have a protective effect against chronic cerebrovascular insufficiency by interfering with several aspects of the biochemical and pathophysiological processes of cerebral hypoperfusion.⁵⁹ Another research review noted, "Vinpocetine, found in the lesser periwinkle Vinca minor, is an excellent vasodilator and cerebral metabolic enhancer with proven benefits for vascular-based cognitive dysfunction."⁶⁰

An Ayurvedic botanical, ashwagandha (Withania somnifera) is considered an adaptogen and has also been researched for its potential to prevent cognitive decline. The herb has been shown to positively affect memory and learning abilities in mice, according to Muhammed Majeed, Ph.D., author of Ashwagandha (Indian Ginseng): An Adaptogen (NutriScience Publishers Inc., 2000). It also blocks chemically induced learning and memory disruption. According to Indian researchers at M.L. Sukhadia University in Udaipur, ashwagandha demonstrates anti-stress and neuroprotective effects when applied to the hippocampal region of stressed rats.⁶¹

Green tea and its constituents have also been researched for application in protecting cognitive function--specifically for preventing Parkinson's and Alzheimer's diseases. Researchers at Inha University in South Korea found both tea and its polyphenol (-)-epigallocatechin 3-gallate (EGCG) prevented brain cell loss in mice, leading to the conclusion that both may have potential for preventing Parkinson's disease.⁶² Researchers at the Keimyung University School of Medicine in Korea learned the protective effects and antioxidant properties of EGCG may lend it to the prevention of Alzheimer's disease.⁶³

Aside from botanical ingredients, there are additional nutraceuticals that are suspected to play a role in brain health. Two forms of protein, for example--soy and whey--have each been featured in peer-reviewed venues for their abilities to improve cognitive function. At Soy & Health 2002, two presentations focused on soy's role in mental clarity. Researchers from King's College in London reported on two studies that demonstrated soy's ability to enhance cognition.⁶⁴ The first study compared a low-isoflavone diet to a high-isoflavone diet for 10 weeks, after which time those receiving the high-isoflavone diet demonstrated significantly greater improvements in short- and long-term memory and mental flexibility. The second study compared soy supplementation (using Ashdod, Israel-based Solbar Plant Extract's Solgen, 60 mg/d of total isoflavones) to placebo for 12 weeks--the subjects taking the soy supplement demonstrated improvements in episodic memory and mental flexibility.

Researchers from the University of Alabama, Birmingham, also presented at Soy & Health 2002, and concluded soy acts by modifying brain proteins.⁶⁵ After feeding mice a soy-based or control diet, researchers analyzed the animals' brains and noted several polypeptide spots that were different in intensity or horizontal position--indicating differences in post-translational modifications--between the control brains and treated brains.

Whey protein was featured in the American Journal of Clinical Nutrition for its role in protecting cognitive function.⁶⁶ Researchers from the University of Maastricht recruited 23 high stress-vulnerable subjects and 29 low stress-vulnerable subjects, all of whom completed a memory-scanning task after consuming a diet enriched with either alpha-lactalbumin (a whey protein with a high tryptophan content) or sodium caseinate (control). The high stress-vulnerable subjects taking the whey protein exhibited improvements in memory scanning ability compared to the other subjects.

The omega-3 fatty acids have also been highly researched for their role in cognitive function--specifically for contributing to brain development in the womb. Research out of the University of Connecticut, Storrs, indicated maternal plasma levels of docosahexaenoic acid (DHA) can indicate how well the fetal central nervous system is developing--higher levels of maternal DHA may indicate greater central nervous system maturity in the infants.⁶⁷ And, maternal intakes of omega-3 fatty acids DHA and eicosapentaenoic acid (EPA) have been shown to affect the children's IQs at four years of age.⁶⁸ Researchers concluded maternal intake of long-chain omega-3 polyunsaturated fatty acids (PUFAs) may improve the children's mental development. Contrarily, researchers at the University Hopsital Maastricht in The Netherlands, found no correlation between long-chain PUFA status at birth and cognitive development at four years of age.⁶⁹

Researchers at the University of Waterloo, Ontario, found long-chain PUFAs, such as DHA, as well as the omega-6 arachidonic acid (AA), accrue rapidly in the gray matter of the brain during development.⁷⁰ Their investigation indicated that fatty acid imbalance and specific fatty acid deficiencies can negatively affect development, and omega-3 fatty acid deficiency specifically influences neurotransmitter systems in the brain.

A trial of Alzheimer's patients in Japan indicated dietary supplementation with omega-3 PUFAs may be useful for the prevention of the disease and for the therapy of dementia.⁷¹ They prescribed 900 mg/d of EPA to correct the patients' ratios of omega-6 and omega-3 fatty acids. An improvement in cognition was noted after three months of supplementation, and results lasted for six months.

Cognition--defined as the act or process of knowing, including both awareness and judgment--is an invaluable aspect of human life. When cognitive function declines, quality of life arguably declines with it. Several neurodegenerative diseases are known to affect cognitive function, although contemporary medicine and complementary therapies are known to stall cognitive decline and improve everyday life. In addition, several of these natural products are thought to delay age-associated declines in memory. Trace nutrients, antioxidants, naturally occurring compounds, botanicals and omega-3 fatty acids are all thought to have a significant role in protecting brain health, which can preserve self-identity as well.

For a full list of references to this story, click here.

Share this article: Email, Slashdot, Digg, Del.icio.us, Yahoo!MyWeb, Windows Live Favorites, Furl
Add this article feed to: RSS, My Yahoo, Newsgator, Bloglines