Feb
01
2006

Macular Degeneration Risk Less With Vitamins

Age related macular degeneration (AMD) is one of the more frequent reasons for loss of vision in the ageing population. The disease is also the most prevalent reason for blindness in developed countries.
A group of researchers from the Netherlands made it their mandate to investigate, in which proportion antioxidants were useful in the prevention of AMD. Supplementation with vitamins C, D and E was used and also beta-carotene and zinc. The observations were made using questionnaires from the Rotterdam Study (1990-1993).

The group on which the research concentrated consisted of inhabitants 55 years of age or older living in a middle class suburb of Rotterdam. Of 5836 at the baseline with a risk of AMD 4765 had reliable data of their dietary habits. At the end of the study 4170 participated in the follow up.
Dietary intake of vitamin E and zinc was inversely associated with the development of AMD: the group with an intake of vitamin E and zinc had less macular degeneration than those whose diet was deficient. A higher than median intake of all the four nutrients, vitamin E, zinc, vitamin C and beta-carotene showed even more benefit. The risk to develop macular degeneration was reduced by an impressive 31 %.

Macular Degeneration Risk Less With Vitamins

Macular Degeneration Risk Less With Vitamins

These results are of importance to the ageing population and the elderly. A high dietary intake of the four nutrients is important in the risk reduction of age related eye diseases like AMD.

Reference: JAMA. 2005; 294:3101-3107; Vol. 294, No. 24, December 28, 2005

Last edited December 6, 2012

Aug
01
2005

New Drug Reverses Macular Degeneration

Age-related macular degeneration in the past meant blindness for the patient. In more recent years laser surgery could be a sight saver, but it also meant a more invasive treatment.
The arrival of new anti-angiogenic drugs that can reverse age-related macular degeneration has received a lot of attention at the recent Schepens International Society ophthalmology meeting. The new drugs Macugen (pegaptanib sodium injection) and Lucentis (ranibizumab) were showing that they stopped the disease in 95% of cases. They were injected into the vitreous of the eye, and the vision of those patients who took it, actually improved.
Macugen has been approved by Health Canada and will be launched for use in September 2005, according to Pfizer, the company behind the drug therapy.
The research goes back to the 1970’s with the discovery of a process that forms new blood vessels in the body allowing tumors to thrive and metastasize. This research revolutionized the understanding of cancer. The new anti-angiogenic drugs fight a protein that induces angiotensin and is responsible for the abnormal blood vessel growth under the retina. This blood vessel growth causes macular degeneration (the wet form).

New Drug Reverses Macular Degeneration

New Drug Reverses Macular Degeneration

Dr. Judah Folkman, a Harvard professor of cell biology, gave the presentation and he stated that this new approach would be “a lot of hope to patients.”

More information about macular degeneration: http://nethealthbook.com/eye-diseases-and-eye-related-topics/retinal-problems/macular-degeneration/

Reference: The Medical Post, July 5, 2005, page1, 58

Last edited October 29, 2014

May
01
2004

Age-Related Macular Degeneration Can Be Postponed

In a well-controlled study that was published earlier in 2004 Dr. Johanna M. Seddon

has shown that age-related blindness (AMD) is caused from an inflammation in the blood vessels, which is associated with an elevated blood marker, called C-reactive protein (CRP). The authors of this study also showed that the dry form of AMD would tend to deteriorate with age and/or from smoking cigarettes into the more serious wet form, a common cause of blindness.

The inflammatory component of cardiovascular disease is known to be controlled by the use of aspirin (ASA) or the statins, medication that is known to lower the bad LDL cholesterol. It is with this background that the author of the study that I am reviewing here, Dr. Jacque L. Duncan from the University of California at San Francisco, has examined the effects of ASA and of statins on AMD. 326 patients with AMD (204 with dry AMD, 104 with wet AMD from blood vessels forming underneath the retina and 18 with geographic atrophy) were followed between January 1990 and March 2003. Patients were at least 60 years old or older and followed at the San Francisco VA Hospital Eye Clinic.
Dr. Duncan found that patients with blindness due to wet AMD used ASA or statins significantly less than patients with stable AMD. Moreover, he found that patients who had AMD and took statins were 49% less likely to develop wet AMD and if they took ASA the were 37% less likely to develop wet AMD.

Age-Related Macular Degeneration Can Be Postponed

Age-Related Macular Degeneration Can Be Postponed

The study also suggests that there is a link between the inflammatory process that leads to heart attacks and strokes on the one hand and the further deterioration to blindness when dry AMD is not treated on the other hand. The notion that inflammation is the missing link in both of these processes is a relatively new finding.

More information about Macular Degeneration here.

Based on article by Dr. Jacque L. Duncan in the American Journal of Ophthalmology 2004;137: 615-624.

Last edited October 26, 2014

Mar
01
2004

Inflammatory Marker Linked To Blindness

This outline is about “inflammatory marker linked to blindness”. Up to now age-related blindness or “age-related macular degeneration” (AMD) as it is medically called, has been a mystery. Notably, the retina is the light-sensitive area of the eye similar to the film in a camera. Specifically, the “macula” is that part of the retina that has the highest visual acuity. It is important to realize that several studies have been conducted lately regarding age-related blindness. Most compelling evidence sheds more light on this important health hazard of old age. One day these studies might even lead to a cure or powerful preventative measures to avoid AMD from ever developing.

Macular degeneration related to C-reactive protein

Particularly, one such study is the one by Dr. Johanna M. Seddon and co-workers published in the Feb. 11, 2004 issue of the Journal of the American Medical Association. Almost 1000 patients with various degrees of age-related degrees of blindness from the Age-Related Eye Disease Study (AREDS) were classified by the degree of their macular degeneration. As an illustration, I have produced the bar graphs below based on these studies.

Details of AMD in relation to CRP

For one thing, the researchers defined four groups, namely those with no AMD who served as controls. The second group were those with mild AMD, the third group those with moderate AMD. And the fourth group were those with severe AMD who were legally blind. Specifically, they suspected that an inflammatory marker in the blood stream of these patients, called C-reactive protein (CRP), might be present in the more severe cases of blindness when compared to the control group who did not have any inflammatory changes in the macula. Indeed, the bar graphs below show exactly what the test results indicated. Another key point, they also found that smokers (blue bars) tended to have slightly worse blood tests in terms of CRP (more inflammatory substances circulating in the system) within the same severity category of the age-related eye changes.

CRP (mg/L) Levels in Various Degrees of Severity of Age-related Macular Degeneration (AMD)

Inflammatory Marker Linked To Blindness

Inflammatory Marker Linked To Blindness

Risk of AMD depends on value of CRP

The investigators studied the risk for the highest percentile of the CRP tests within various subgroups of AMD. They found several differences as shown in the next table. First there was a low probability to develop AMD in a person with a normal looking macula. The investigators took this risk as the 1.0 point for comparison. In contrast a person with a normal looking macula who smokes has a 1.5-fold risk of developing AMD later. Patients with a moderate degree of AMD have about a 2-fold risk of getting a severe degree of AMD. This is true for smokers and non-smokers. Once the inflammatory cycle has started, the process of causing a moderate degree of AMD is so strong. This means that the effect of smoking will not add that much in comparison.

This is the first study of this kind that established that CRP is useful as a screening for the risk to develop AMD. Physicians already use CRP  as a test for monitoring progress in rheumatoid arthritis or to monitor for the risk of developing a heart attack or stroke.

AMD risk studied by another research group

Another study by Dr. Johanna M. Seddon and co-workers was published recently in the Archives of Ophthalmology. 261 people aged 60 years and older with established AMD were followed for 4.6 years and checked for deterioration. 101 patients had deterioration of their AMD.

Risk of Developing Age-Related Macular Degeneration (AMD) in Highest CRP Percentile
 Inflammatory Marker Linked To Blindness1

Omega-3 fatty acids protect against AMD

The authors analyzed the patients’ diet habits and found that increased fat intake was a high risk factor for deteriorating AMD. Both vegetable and animal fat had a 2-to 3-fold increased risk for deterioration of the AMD to a more severe stage (legal blindness). Fish, omega-3 fatty acid and nuts had a protective effect, but only when omega-6 fatty acid (linoleic acid) intake was low in the same group. The studies showed that the risk of age-related blindness was reduced by 40% when patients ate nuts at least once per week. The authors concluded that a “fat conscious diet” would be good for “maintaining good eye health” and at the same time be beneficial for prevention of heart attacks and strokes.

The authors will do further studies to investigate potential ways of helping patients with AMD and to understand the mechanisms of the disease process better.

References

1. JAMA 2004;291:704-710  2. Arch Ophthalmol – 01-DEC-2003; 121(12): 1728-37