Antioxidants Studies

As everyone knows, eating and drinking are necessary for life. Less well known, however, is the fact that the body generates what are called free radicals in the process of turning food into energy. Free radicals are chemicals that are capable of damaging cells and genetic material. But eating is not the only way free radicals spring into being. The food we eat and the sunlight we feel also generate free radicals.

To be sure, free radicals come in many shapes, sizes, and chemical configurations. The characteristic feature of this chemical is that it soaks up electrons from bodily substances that yield them, which can leave the “loser’s” structure or function radically altered. Free radical damage can change the instructions coded in a strand of DNA; it can also make a circulating low-density lipoprotein (LDL, sometimes called bad cholesterol) molecule more likely to get trapped in an artery wall. Free radicals also have the potential to alter a cell’s membrane, changing the flow of what enters the cell and what leaves it.

Fortunately, we aren’t defenseless against free radicals. The body puts up natural defenses against free radicals by making molecules that smothers the errant chemicals. We also extract free-radical fighters from food. Often called “antioxidants”, certain kinds of food give electrons to free-radicals without themselves turning into electron-scavenging substances. There are many different substances that can act as antioxidants. The most familiar ones are vitamin C, vitamin E, beta-carotene, and other related carotenoids, along with the minerals selenium and manganese. They’re joined by glutathione, coenzyme Q10, lipoic acid, flavonoids, phenols, polyphenols, phytoestrogens, and many more.

However, the term “antioxidant” can be misleading. These substances do not emit chemical properties that fight so much as they emit properties that facilitate. Indeed, some substances that act as antioxidants in one situation may be prooxidants—electron grabbers—in a different chemical milieu. Another big misconception is that antioxidants are interchangeable. This is not true. Each anti-oxidant has unique chemical behaviors and biological properties. It is believed, and has been strongly corroborated through scientific study, that anti-oxidants evolved as parts of elaborate networks, each substance having a different role to play. It follows that no single substance can fulfill the function of every other substance.

Health Benefits of Antioxidants: What’s the Buzz?

Antioxidants came to public attention in the 1990s. It was then that scientists began to understand that free radical damage was involved in the early stages of artery-clogging atherosclerosis, and that the chemicals may contribute to cancer, vision loss, and a host of other chronic conditions. A number of studies stated that people with low intakes of antioxidant-rich fruits and vegetables were at greater risk for developing these chronic conditions than were people who ate sufficient amounts fruits and vegetables. Clinical trials tested the impact of single substances, especially beta-carotene and vitamin E, on cancer, heart disease, and similar maladies. But even before the results of these trials were in, the media, and the dietary supplement and food industries began promoting the benefits of “antioxidants.” Foods such as frozen berries and green tea were hyped as being rich in antioxidants. The consequences of this publicity were predictable: certain foods were labeled as rich in antioxidants and were marketed as such in stores; the makers of dietary supplements began touting the disease-fighting properties of all sorts of antioxidants.

In the meantime, the results of the actual trials were mixed. Most have not found the hoped-for benefits. And research teams reported that vitamin E and other antioxidant supplements didn’t protect against heart disease or cancer. One study even showed that taking beta-carotene may actually increase the chances of developing lung cancer in smokers. However, some of the trials reported benefits. One such study found that taking beta-carotene is associated with a modest reduction in the rate of cognitive decline.

The rather most, if not downright disappointing, results of the antioxidant trials have not stopped the commercial interests from misrepresenting the benefits of antioxidants in order to make money. Antioxidant supplements are a $500 million dollar industry that continues to grow. Antioxidants are still added to breakfast cereals, sports bars, energy drinks, and other processed foods, and they are promoted as additives that can prevent heart disease, cancer, cataracts, memory loss, and a host of other conditions. The claims made by the food and dietary supplement industries often distort the data. It is true that the package of antioxidants, minerals, fiber, and other substances found naturally in fruits, vegetables, and whole grains help prevent a variety of chronic diseases; but there is no solid evidence that high doses of antioxidants can accomplish the same feat. The conclusion is clear: randomized, placebo-controlled trials—which, when performed well, provide the strongest evidence—offer little support that taking vitamin C, vitamin E, beta-carotene, or other single antioxidants provides substantial protection against heart disease, cancer, or other chronic conditions. The results of the largest such trials have been mostly negative.

Heart Disease and Antioxidants

Vitamin E, beta-carotene, and other so-called antioxidants are not a panacea for heart disease and should not be promoted as such. In the Women’s Health Study, 39,876 initially healthy women took 600 IU of natural source vitamin E or a placebo every other day for 10 years. The results of the study showed that the rates of major cardiovascular events and cancer were no lower among those taking vitamin E than they were among those taking the placebo; however, a 24 percent reduction in total cardiovascular mortality was observed, which can be considered a quite significant result.

Earlier large vitamin E trials, conducted among individuals with previously diagnosed coronary disease or at high risk for it, generally showed no benefit. In the Heart Outcomes Prevention Evaluation (HOPE) trial, the rates of major cardiovascular events were essentially the same in the vitamin E (21.5 percent) and placebo (20.6 percent) groups, although participants taking vitamin E had higher risks of heart failure and hospitalization for heart failure. (3) Another trial, the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI), showed mixed results; there were no preventive effects after more than three years of treatment with vitamin E among 11,000 heart attack survivors. Nevertheless, some studies suggest potential benefits among certain subgroups. A recent trial of vitamin E in Israel, for example, showed a marked reduction in coronary heart disease among people with type 2 diabetes who have a common genetic predisposition for greater oxidative stress. In any case, Beta-carotene, as was shown in the Physicians’s Health Study, does not provide any protection against heart disease or stroke.

There have been combinations, but the findings are complicated and unclear. In the Supplementation en Vitamins et Mineraux Antioxydants (SU.VI.MAX) study, 13,017 French men and women took a single daily capsule that contained 120 milligrams of vitamin C, 30 milligrams of vitamin E, 6 milligrams of beta-carotene, 100 micrograms of selenium, and 20 milligrams of zinc, or a placebo, for seven and a half years. The vitamins had no effect on overall rates of cardiovascular disease. In the Women’s Antioxidant Cardiovascular Study, vitamin E, vitamin C, and/or beta-carotene had much the same effect as a placebo on myocardial infarction, stroke, coronary revascularization, or cardiovascular death, although there was a modest and significant benefit for vitamin E among women with existing cardiovascular disease.

Cancer and Antioxidants

There is also no conclusive proof that antioxidants help prevent cancer. Scientists need more time to determine the impact of antioxidants on the risk of getting cancer. In the long-term Physicians’ Health Study, cancer rates were similar among men taking beta-carotene and among those taking a placebo. Other trials have also largely showed no effect, including HOPE. The SU.VI.MAX trial showed a reduction in cancer risk and all-cause mortality among men taking an antioxidant cocktail but no apparent effect in women; it is possible that this is a result of the men in the study having low blood levels of beta-carotene at its beginning. A randomized trial of selenium in people with skin cancer demonstrated significant reductions in cancer and cancer mortality at various sites, including colon, lung, and prostate. The effects were strongest among those with low selenium levels at baseline.

Age-Related Eye Disease and Antioxidants

The effects of antioxidants on age-related eye disease may be one of the most hopeful leads scientists have. A six-year trial, the Age-Related Eye Disease Study (AREDS), found that a combination of vitamin C, vitamin E, beta-carotene, and zinc provided some protection against the development of advanced age-related macular degeneration in people who were at high risk of the disease. Lutein, a naturally occurring carotenoid found in green, leafy vegetables such as spinach and kale, may also protect vision. It is too early to tell what the impact of lutein supplements may be. The trials of such substances have been relatively short, and their ability to slow or prevent age-related macular degeneration has not been ascertained. A new trial of the AREDS supplement regimen plus lutein, zeaxanthin, and fish oil is underway, and it could yield better information.

Potential Hazards of Antioxidants

There have been a few studies which showed that the consumption of antioxidants, as opposed to being beneficial in all instances or at least harmless in fact can interfere with the health of the consumer. The first trial which showed this possible negative effect was undertaken in Finland where heavy smokers were fed beta-carotene. Because of their smoking habits there was a already a lung cancer risk but it was noticed that a significant increase in the incidence of lung cancer amongst the trial group as opposed to the placebo. The trial was stopped so conclusive results are hard to deduce.

A different test which was conducted with heavy smokers exposed to asbestos being fed beta-carotene and vitamin A. This too shows an increase in the incidence of Lung cancer. It must be emphasized that not all trials of Beta-carotene have been negative. A physicians health study which only had a few smokers did not show any significant differences even when followed up after 18 years.

In a separate study showing possible negative effects of a variety of health supplements showed a higher incidence of skin cancer in women being fed supplements of Vitamins C & E, Beta-carotene, selenium and zinc.

Conclusions to be drawn from the above studies, amongst others, is that it is known that although free radicals have been shown to contribute to the incidence of heart disease, cancer, Alzheimer’s and even vision loss, there is no automatic conclusion that can be drawn that antioxidants will fix the problem. And certainly not when consumed away from their normal context.

Studies to date do not show conclusive evidence one way or another but there is certainly no strong evidence to suggest that antioxidants are effective against disease. A rider must be mentioned and that is that the trials conducted till now have been short in duration, conducted with people some of whom had an existing disease.

There has been a noticeable benefit to the consumption of beta-carotene on cognitive ability after 18 years. This is exceptional as it is the only study to have continued so long. (Physicians health follow up study) Nevertheless there is abundant evidence suggests that eating whole fruits, vegetables, and whole grains—all rich in networks of antioxidants and their helper molecules—provides protection against many of these scourges of aging.

Clarification with regard to supplemental studies

There are any number of studies conducted on any number of vitamins and other dietary supplements that are often contradictory. The picture presented to the consumer is confusing and will often seem frustrating in that instead of clarifying things these studies muddy the waters.

Examining exactly what the vitamins trial study did will often go some way to explaining the varying results. Here are a few items to check when looking at apparently conflicting vitamins studies.

  • What was the precise dosage taken by the participants and how long was the study’s duration. This is significant as few studies will have identical dosages and identical time spans. A study in Vitamin D showed that a dosage of 700 plus IU per day had a significant protection against fractures whereas a study of people taking only 400 IU per day showed no such effect. The same applies to the duration as the build up of the protective mechanisms is not a short process.
  • The age, health and life styles of the participants. Studies drawn from young, active gym going participants is likely to differ significantly from heavy drink and smoking office workers. Exercise and other lifestyle choices such as diet affect out health and how the body responds to vitamins.
  • At what stage is was the supplement fed to a study participant. If studying the effect of a supplement on someone already suffering from a disease it may be found that something taken at the onset has a differing effect from something taken when a disease is far advanced. An example being that Folate supplements are only effective against neural tube defects in the early stages of pregnancy.
  • How were the results tabulated and calculated. This is a significant problem as measurement as to benefit may and probably will vary widely. Heart disease is a wide subject and a measurement of coronary thrombosis may miss out on the incidence of strokes.

Too Much Iron and Manganese Lead to Higher Risk for Parkinson’s

Too much iron and manganese in the diet may put people at increased risk for Parkinson’s disease, find researchers publishing in the June 2003 issue of Neurology.

Investigators from the University of Washington in Seattle believe the two minerals, common in foods such as spinach, beans, nuts, and whole grains, may impact Parkinson’s risk through their effect on the brain. Both iron and manganese are known to cause oxidative stress, which releases toxic substances known as free radicals and can cause degeneration of brain cells that produce dopamine. The loss of these brain cells plays a crucial role in the development of the disease.

The study involved 250 people with recently diagnosed Parkinson’s and 388 people without the disease. All were questioned extensively about their diets during their adult lives. Participants were then placed into categories depending on how much iron and manganese they consumed and also whether they were regular users of multivitamin or iron supplements.

Researchers found those in the top 25 percent of iron consumption were 1.7-times more likely to have Parkinson’s than those in the bottom 25 percent. Those with higher than average consumption of both minerals were 1.9 times more likely to have the disease. Participants with higher iron intake and a history of daily supplement use were 2.1-times more likely to have Parkinson’s. Those with higher manganese consumption and daily supplement use were 1.9-times more likely to have the disease.

However, the investigators do not suggest people limit their intake of foods rich in iron and manganese, noting the health benefits of eating these nutrient-rich foods probably outweigh the increased risk of Parkinson’s.

Harvey Checkoway, Ph.D., from the University of Washington in Seattle, says, “Our findings may improve understanding of how Parkinson’s disease develops. But there are most likely numerous environmental, lifestyle, and genetic factors that determine who will develop the disease. It’s too early to make any recommendations about potential dietary changes.”

SOURCE: Neurology, 2003;60:1761-1766

Who is at risk for Alzheimer’s?

We’re all at risk now by virtue of the fact that we are part of an aging population. It’s clear that the biggest risk for Alzheimer’s disease is aging. That’s why we know so much about it now. In this century the population is aging more successfully than ever before.

Alzheimer’s wasn’t as prevalent because we weren’t living as long?

Yes. At the turn of the century the average age life expectancy for males in some European cities was only 40 or 50-years-old. Now it’s 20 or 30 years more than that. So we didn’t see the population coming into the age that put them at risk for developing the disease.

Talk about the vascular connection

The connection has been known for a long time, ever since Alzheimer described the disease. There’s a small protein called amyloid that gets deposited in the brains of those that suffer from Alzheimer’s disease. There’s always been a question of how it causes the disease and if it has any normal functions. We started to look into that problem several years ago. One of the things we found was that when amyloid comes anywhere near blood vessels, it causes them to constrict and stay constricted. That was a novel finding, and there are several implications. This might be part and parcel of the Alzheimer process, that there may be a tendency of the vessels in the brain to close down and stay closed down. Of course that would have implications for delivering oxygen and nutrients to the nerve cells in the brain.

So this connection happens years before the amyloid?

Yes. One of the interesting aspects of this is that in full-blown Alzheimer’s disease you have aggregations of amyloid that precipitate out. They come out of solution and form plaques in the brain. Our findings occur with much lower concentrations. So the implication is some of the affects that we’re looking at occur many years early on before the disease really becomes full-blown and recognized in the way that we see it clinically.

Would you be able to see the vessels closed on an MRI or something?

I wish we could, but it’s very difficult to do that in humans. We have done animal studies that show that. The animals that produce too much amyloid do close their vessels, and they stay closed. That gives them significant problems.

Is this the same as somebody who has cardiovascular disease? If they have cardiovascular problems, would they be at a higher risk for Alzheimer’s?

If you have a little bit of Alzheimer’s and you have a little bit of cerebral vascular disease or even cardiovascular disease, those things can combine in a way that makes them both work. You can see individuals that have a slight amount of Alzheimer’s disease pathology and normally wouldn’t have any symptoms. If they have cerebral vascular problems on top of that, then they start to display symptoms.

People might see that and say, “If I had a heart attack, then I might be an Alzheimer’s patient later on.” Is that true?

If you have a heart attack then you usually have some form of atherosclerosis or some form of vascular disease. Quite often it extends to elsewhere in the body. Yes, that does put you at risk for increasing the expression of Alzheimer’s disease. In other words, it does put you at risk for having Alzheimer’s symptoms before you normally would if you just had Alzheimer’s alone.

Now that you understand this connection, where do you go from here?

What we’ve been working on for the last couple of years is finding out exactly why the vessels close down. To start with, we thought that it was mediated by free radicals. These substances increase with age and are generally thought to be bad news in a number of conditions. However, what we actually found out is the vessels close down because they began an inflammatory response. It’s the same as when you first scratch yourself the skin blotch is white because there’s an immediate inflammatory response. In fact, the blood vessels in the brain are doing something very similar when they come into contact with amyloid.

How would you treat this?

If we block the actual molecular mechanisms, the chemicals that are switched on inside cells, we can stop the effect. We’ve already demonstrated that in the experimental situation. Now what we have to do is demonstrate that in the clinic. That’s the next step.

Could drugs used for cardiovascular disease be used?

Yes. One of the first drugs we’ve investigated that blocks this effect in the experimental situation has been used for other conditions. It’s never been used for Alzheimer’s disease, but it has been used for cardiovascular disease. It’s that kind of drug that we want to test in a clinical situation.

What are those drugs?

We don’t have the full FDA approval to say.

Do antioxidants help?

As far as the vessel discovery is concerned, antioxidants mop up free radicals, and free radicals seem to make the situation much worse. That was one of the first things we found. So we’re not pursuing that in the clinic.

Using the cardiovascular connection as an identifier, it could be years before we see Alzheimer’s. How do you treat current Alzheimer’s patients if it’s already beyond that?

One of the other groups of patients that we look at are people that don’t have Alzheimer’s disease but are before that stage. They are memory-impaired but don’t have full-blown Alzheimer’s disease. If we follow a group like that, then we know that a certain percentage, quite a high percentage convert to Alzheimer’s disease every year. They would be an ideal population for us to give this medication to. That would be a much better intervention than waiting until folks have full-blown disease. That group is a target population for us.

So people who already have it might not benefit from this?

It’s generally recognized that once you’ve had the disease for five or six years then there’s very little that medical intervention can do now. The real target populations are those folks that are in the very early stages of Alzheimer’s disease or who would develop Alzheimer’s disease in the next several years. Right now those are the groups that we are actively recruiting into our study.

How do you identify those people?

We have sophisticated memory screens that give evaluations. These evaluations look at every aspect of memory and distinguish those effects that are truly pathological from those that are simple forgetfulness, which we all suffer from in one form or another.

Will you identify whether or not the amyloid is present?

We can’t detect amyloid in the brain. There’s no known way for us to do that at this stage. What we have to do is identify individuals who have memory impairment but don’t have full-blown Alzheimer’s disease and recruit those into our studies knowing that the largest majority of those will in fact develop the disease over a four- or five-year-period.

If I know somebody in my family who has it, what are my chances of developing Alzheimer’s?

One’s risk for the disease is definitely increased if you have a family history. However, the reality of that statement is it’s such a prevalent disorder, if most of us look far enough into our family histories we’ll find a case of Alzheimer’s disease. That’s just another way of saying that as we get to be 80 or 90 we’re all at risk for the disease. However, if you have a strong family history in addition to age, your risk is increased still further.

Are men or women more at risk?

Men and women are equally at risk for the disease. Men tend to die from other things before they get Alzheimer’s disease. So there’s an imbalance in the absolute numbers in the population. If you just take 100 women and 100 men, they’re equally at risk for the disease as they age.

News Source: Ivanhoe Newswire – 1999

Oxidized LDL

The prime focus of most drug research concerning cardiovascular disease has been about lowering cholesterol levels, and that is about all you will hear in their ads on television. However, thousands of studies are now showing how oxidized LDL is much more dangerous and promotes virtually every stage of atherosclerosis; therefore, in addition to lowering its level, it is just as important to keep your LDL cholesterol from becoming oxidized. LDL cholesterol can become oxidized by free radicals. Oxidized cholesterol is more prone to stick to arterial walls and form foam cells that eventually form plaque. Commercial tests are not yet available to measure oxidized cholesterol at affordable prices. Since there is no economical test to determine the degree to which LDL cholesterol is oxidizing in your body, it is bet to quench inflammation, take antioxidants, lower Apo B (apolipoprotein B) levels, and take supplements to reduce small LDL particles.

For example, the higher the calorie, sugar, and fat content of each of your meals, the greater you will experience what doctors call postprandial oxidative stress after you have finished eating. It is an oxidation process. So eating a Mediterranean diet wins again. You can also drink water with lemon or lime, green or black tea, or 2 ounces pomegranate juice with your meals to reduce this oxidation process.

It is also recommended that you take the following in supplement form if you are not getting these nutrients to lower oxidized cholesterol:

• Gamma tocopherol
• Pomegranate juice
• Ubiquinol (CoQ10)
• Grape seed and/or pine bark extracts
• Theaflavin

Apolipoprotein B

Apo B is a measurement of the number of LDL (bad cholesterol) particles in the blood. It is the protein portion of the low-density lipoprotein and transfers cholesterol from the lipoprotein either to the cells to be used or to the liver to be excreted. If the amount of Apo B present is in proportion to the amount needed by the cells, then no problem occurs. However, if you have an excess of Apo B, the excess Apo B will usually deposit cholesterol in arterial walls. Apo B determines whether the cholesterol is used correctly, it determines if cholesterol ends up as plaque. It is believed that LDL particle numbers may predict coronary artery disease risk better than LDL levels. Apo B is mainly genetically determined. Having a large number of LDL particles has been shown to increase heart attack risk even when the total LDL is normal or low and that this measurement is among the most powerful tools for predicting an ischemic event.

To determine the number of LDL particles, it is possible to count apolipoprotein B (Apo B) particles, because Apo B is the major protein particle of an LDL cluster, and each LDL cluster will have only one. It is possible to have an LDL number of 80 (normal), for instance, but an Apo B count of either 50 (normal) or 130 (elevated). (Note that a normal Apo B level would be anything below 60). Unfortunately, a low LDL amount but a high Apo B count is fairly common and increases your risk of cardiovascular disease.

Proper diet, regular exercise, and supplementation are effective in reducing your Apo B level. Avoiding trans fats and reducing saturated fats in your diet are also extremely important in lowering Apo B. below are supplements to lower Apo B:

• Niacin
• Red yeast rice
• Sytrinol
• Pantethine

LDL particle size:

Small LDL particles are far more atherogenic (plaque forming) because they are 40 percent more likely to get stuck in artery walls and form plaque. Studies have shown small LDL triples the likelihood of developing coronary plaque. Small LDL also shows a tendency toward insulin resistance and thus an increased risk of diabetes, especially if you are overweight or obese. Other research has shown that if you have small LDL particles and high C – reactive protein (CRP) levels, your chances of a heart attack are six times higher than normal.

The best way to keep LDL particle size larger and safer is by maintaining a healthy weight. Taking 1,500-3,000 mg of niacin a day (or as directed by your doctor) can also help control LDL size. Research is showing niacin may be the most effective nutrient to take to help eliminate small LDL. It is also best to eat foods that have a low glycemic index (GI) number and thus release sugars more slowly after eating. Note that stain drugs have only a minimal to no effect on LDL particle size. Taking soluble fiber supplements with your other foods can also help in promoting larger LDL particles, as can making sure you are getting enough omega-3 fatty acids and getting regular exercise.

Ascorbate (vitamin C) is a highly potent aqueous-phase antioxidant in plasma, which has been shown in vitro to retard LDL oxidation. USANA Vitamins Supplements Booster C 600™ has a special blend of immunity-supporting ingredients. It contains zinc, echinacea, and elderberry and includes USANA’s own proprietary vitamin C supplement Poly C as well. Booster C 600 is also the perfect seasonal companion to USANA’s other supplements that support immunity health: USANA Proflavanol® C100, USANA® Probiotic, Pure Rest™, and USANA’s Vitamin D supplement.

What are antioxidants and what do they do?

That’s a very good question. They are both natural substances and synthetic substances that help treat free radicals in the body. Free radicals are a natural byproduct of some cellular metabolism. They’re useful for the immune system for killing foreign cells and bacteria; but if the situation gets out of control, they can be harmful to the body. A free radical is a substance that has lost an electron and is therefore an unstable ion. What it wants to do is become stable again. So it attacks a cell that’s close to it and takes an electron from that cell. Then a game of hot potato starts. A cascade of events occur leading to death within a cell. This causes premature aging and can lead to cancer. Antioxidants are substances that protect plants, for instance, in the environment. For example, they protect plants against smog, environmental pollution and ultraviolet radiation. These same properties that protect plants can be used to protect humans. With consumption of nutrients found within plants — such as vitamin C, vitamin E, beta carotene — these natural substances called antioxidants donate electrons and therefore neutralize the harmful effects of free radical damage.

If it works, why aren’t more people taking green tea? Are there any negative effects associated with it?
Green tea has caffeine in it, and caffeine doesn’t agree with certain people. For instance, it can lead to insomnia. It can lead to fibrocystic breast disease in women. It can lead to frequent urination. It can lead to elevated cholesterol and a host of other health problems. It can become addictive. Nevertheless, you will be pleased to know that green tea has one fifth the amount of caffeine that a typical cup of coffee has and one third the amount of caffeine that black tea has. Furthermore, there are extracts available which are virtually caffeine-free. As for why more people don’t take green tea, I don’t think they know about it. The Chinese have known about it for over 4,000 years, but it’s just now becoming available in extract form. People who may not want to drink the six to nine cups of tea that are needed to get maximum benefit can now take it in an extract form — in a capsule form.

A healthy diet may help improve mental funciton

Eating a healthy diet may help protect against dementia as people age, according to a new study.
Researchers from the National Research Council in Milan, Italy studied more than 1,600 men and women over age 70. Participants were questioned about the types of food they ate and took a test to determine their level of mental function. Researchers then evaluated the diets of the individuals and separated them into groups based on mental function.

After evaluating the data, researchers found that a balanced diet with low levels of saturated fat and cholesterol is linked with a lower risk of mental decline. While they are unsure how a healthy diet protects from mental decline, researchers hypothesize antioxidants play a key role. Potent antioxidants such as vitamins C and E are crucial in clearing up free radicals from the body. Researchers say studies also show omega-3 fatty acids may be helpful. Previous studies have shown the ability of omega-3 fatty acids to protect against Alzheimer’s disease.

USANA Vitamins fish oil Supplement USANA BiOmega provides advanced and guaranteed levels of EPA and DHA, two long-chain omega-3 fatty acids important for memory and learning.

In the current study, researchers also found moderate alcohol intake to be associated with better mental function. Researchers say while it may be that moderate drinking habits and good health generally go together, other research that shows moderate alcohol intake is associated with reduced risk of stroke may also mean it has a positive benefit on cognitive capabilities.

Dementia can occur at any age but is more common after age 65. Researchers emphasize dementia is not a normal part of the aging process. According to the San Francisco Alzheimer’s and Dementia Clinic, Alzheimer’s disease is the most common type of dementia. It typically occurs after 65 years of age and affects 4 million adults. Alzheimer’s Disease is the fourth leading cause of death in the United States. From onset until death, the disease generally lasts from 3 to 18 years.

SOURCE: European Journal of Clinical Nutrition, 2001;55:1053-1058