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Age-related macular degeneration (AMD), is a major cause of central vision loss in the elderly. Treatments are limited and hope lies in reducing the risk of the disease and preventing its development. A study reported at the Annual Meeting of the Association for Research in Vision and Ophthalmology, in Florida, May, 2003, provides new data supporting the effects of diet and nutrients, in lowering the risks of having a type of AMD that leads to blurred vision, and in severe cases, blindness. The study, carried out by Dr. JP SanGiovanni and colleagues, from the National Eye Institute, in Bethesda MD, showed, that after taking into account other nutrient and non- nutrient factors, that may affect the risk of AMD, a higher intake of omega n-3 polyunsaturated fatty acids (LCPUFA) and fish was associated with decreased risk of having neovascular AMD.

Approximately 1.7 million people over 64, suffer from the severe form AMD, that leads to blindness. The macula is an area located in the center of the retina and is responsible for fine and detailed central vision. The degenerative changes associated with AMD include alterations in the retinal tissues and atrophy of the cells, that account for a number of different types of AMD, and the formation of new blood vessels (neovacularization) under the retina, that accounts for another type, called neovascular AMD, where leaking blood vessels distort the retina and cause blurred vision and loss of eyesight.

The Age-Related Eye Disease Study (AREDS), reported at the meeting, was a case control retrospective study of 4,513 participants, aged 60 to 80 years. Subjects completed a self-administered food questionnaire, and provided information on the frequency and portions of fish intake in the last year, as well as other health and lifestyle data. The types of fish considered, included fried fish or fish sandwiches, tuna salad or tuna casserole, oysters, other shell fish and broiled or baked fish. People without AMD served as control groups for each of the four different types of AMD tested.

The results showed that highest total fish consumption (compared to no intake), of more than two servings a week, of broiled or baked fish or of tuna, reduced the risk of having neovascular AMD, but not other types of AMD, by approximately 50%.

When assessing AMD risk in relation to intake of omega-3 fatty acids, that are high in marine products, the results showed that risk for neovascular AMD, but not other types of AMD, was significantly decreased, by approximately 60%, for people with the highest intake of total omega-3 fatty acids (highest quintiles versus lowest quintiles). A similar risk reduction (approximately 53%), was found with intake of docosahexaenoic (DHA), an omega-3 fatty acid, that is selectively taken up and retained in the photoreceptors of the eye.

The studies indicate an independent association between fish intake and omega-3 fatty acids intake and neovascular AMD, showing that high intake of fish, or omega-3 fatty acids, halves the risk of having the disease.

—Carmia Borek, Ph.D.

Four antioxidants, used in combination, protect against cell abnormalities of the type seen in aging and Alzheimer’s disease (AD). They also increase life span. Researchers in Australia and the U.S. report that giving mice supplemental vitamin E acetate, ginkgo biloba, pycnogenol and ascorbyl palmitate (fat-soluble vitamin C) at doses a human would take, reduces by ten times the number of “inclusion bodies” in brain cells. Inclusion bodies can best be described as abnormal structures that appear in aging cells.1 The inclusion bodies in this study cross-reacted with beta amyloid, an abnormal protein found in Alzheimer’s patients’ brains–which means that the abnormal structures could contribute to a person getting AD. Not only does the supplement combination reduce inclusion bodies, it reduces them in an area of the brain affected by Alzheimer’s disease. In addition to keeping their brains functional, the supplements (which all have antioxidant properties) also made the mice live longer. At 270 days, 55% of the supplement-treated mice were alive versus 22% of the animals who didn’t get the combination. This is the first time it has been proven that a combination of antioxidants can protect the hippocampus against inclusion bodies, an aspect of aging and dementia that’s not well studied.

The results could have important implications for people with a genetic predisposition to Alzheimer’s. Mutations in a gene that makes a protein called “apolipoprotein E” increase the risk of the Alzheimer’s type of dementia. ApoE, as it is known, is one of the proteins that associates with fat (similar to “LDL” or “HDL” cholesterol). Research shows that at least one form of ApoE is an antioxidant, and it reduces Alzheimer’s-related proteins that interfere with brain function. When it is missing because of a genetic mutation, the brain is more susceptible to free radical damage and Alzheimer’s.2

The mice used in the study didn’t have any ApoE. They are genetically deficient–similar to some people who develop Alzheimer’s. But the study shows that the supplement combination was able to overcome the deficiency and provide significant protection. Researchers in Japan have demonstrated that both ApoE and antioxidants reduce the formation of amyloid beta fibrils, abnormal proteins found in the brains of people with dementia.3

–Terri Mitchell

Some types of heart disease can progress to congestive heart failure. This is a very serious, life-threatening complication involving the left chamber of the heart known as the left ventricle. Mortality can be predicted by a measurement of left ventricular end-diastolic volume. The higher the volume, the less likely a person will be to survive heart surgery.

Researchers in Canada approached the problem of high diastolic volume by attempting to reverse underlying biochemical abnormalities with specific supplements. They were successful.1

One of the biochemical abnormalities in congestive heart failure is an energy deficit. The heart, which moves constantly, has a high demand for energy. Normally, demands are met by mitochondria–tiny power plants inside cells. People with congestive heart failure, however, have a profound lack of energy, and two factors crucial for producing it are deficient: carnitine and coenzyme Q10. Studies show that supplementing the diet with these two factors has beneficial effects, including better survival. Also, a study published in 1995 indicates that L-carnitine supplements reduce abnormal enlargement of the left ventricle after a heart attack.2

In addition to the energy deficits, calcium build-up is a problem in congestive heart failure. This is a very serious problem inasmuch as the amount of calcium inside cells is critical to how they perform. If the muscle cells of the heart are overloaded with calcium, heart muscles can’t contract properly. Taurine, an amino acid, is a natural calcium regulator in heart cells. Studies in hamsters show that supplemental taurine reduces calcium build-up, and helps protect heart tissue.

Thirty-eight people with congestive heart failure participated in the Canadian study. All were scheduled for heart surgery, and all had an ejection fraction under 40%. Half were given a drink with 3 grams of taurine, 3 grams of L-carnitine, and 150 mg of coenzyme Q10 everyday. Half were given a placebo. Most had surgery about three weeks later.3

The results indicate that the three supplements reduce left ventricular end–diastolic volume, an important indicator of survival. This is the first double-blind, controlled study of this type in humans. In a previous, non-controlled study, 13 of 15 people who were classified as III or IV in severity were upgraded to class II after taking 4 grams of taurine a day.4

–Terri Mitchell