Age-related macular degeneration (AMD) refers to the slow deterioration of the cells in the macula, a tiny yellowish area near the center of the retina, which contains light-sensitive cells that send visual signals to the brain. Sharp, clear, ‘straight ahead’ or central vision – used mostly for reading, writing, driving and identifying faces – is processed by the macula. In the most severe forms of AMD, straight lines become crooked and wavy, distinct shapes are blurry and there is a fog in the center of your vision. Your peripheral vision, however, is not affected.
Of all the illnesses of the aging eye – including glaucoma and cataracts – AMD is the only one that is sharply on the rise. Worldwide, some 30 million people have the condition – a figure that is expected to treble over the next 25 years (Bull World Health Org, 1995; 73: 115-21) – and six million Americans have vision loss because of AMD, with another 13-15 million suffering from early signs of it.
Given this new epidemic, new treatments for AMD are always being explored, including retinal cell transplants, drugs that will prevent or slow the progress of the disease, laser treatment, radiation therapy, gene therapy and even a computer chip implanted in the retina that may help simulate vision.
But what medicine has seldom explored is the role of diet in the development of this epidemic or, indeed, its parallels with heart disease. New evidence places the blame squarely at the door of processed food, particularly processed fats.
Recently, a group of researchers from Harvard Medical School and the Harvard School of Public Health set out to determine whether diet had any affect on the development of AMD. They selected 261 participants, aged 60 or older, with early or intermediate AMD and visual acuity of 20/200 in at least one eye. Over the next four and a half years, the researchers studied the participants’ dietary intake and compared it with the progression of their disease. Specifically, they looked at the amount and type of fat the patients were consuming in their daily diets (Arch Ophthalmol, 2003; 121: 1728-37).
What they found was quite extraordinary. Those consuming high-fat diets were three times as likely to progress to advanced forms of AMD compared with those whose intake of fat was lowest.
But the risks relating to the kinds of fats consumed confounded the usual expectations. Although intake of any animal fat was associated with a doubling of risk of the disease, higher levels of animal-fat intake did not increase the risk any further. In other words, you increase your risk of developing AMD by eating meat, but your risk doesn’t increase with the quantity.
The real risk for AMD was associated with vegetable-fat intake, which nearly quadrupled the risk of the disease progressing. These fats included the monounsaturated, polyunsaturated and trans unsaturated fats. And in this case, quantity did matter.
The researchers also noted a doubling of risk with intake of processed foods, which are usually laden with these types of processed vegetable fats.
Other kinds of fats proved protective. Fish and nuts, both rich in omega-3 fatty acids, slowed progression of the disease – so long as your intake of the usual omega-6 fatty acids was also low.
Other clues suggest that processed foods lie at the heart of AMD. This is a disease of the industrialized world. Living in the developed countries is a significant risk factor for AMD. While the condition is the leading cause of blindness among the American, Canadian and English elderly, it is rare in the developing countries where, nevertheless, there is a high incidence of blindness from other eye diseases such as glaucoma and cataracts. These countries do not consume a highly processed diet.
AMD is also a cousin of coronary heart disease, and shares with it several common ancestors, such as atherosclerosis (Am J Epidemiol, 1995; 142: 404-9), hypertension (Arch Ophthalmol, 2000, 118: 351-8) and high cholesterol. AMD also afflicts nearly 40 per cent of those with diabetes (J Longev, 1998; 4: 24-6).
Many other risk factors for heart problems are also risk factors for AMD. These include smoking (especially in women), age (3.8 per cent of Americans have either intermediate or advanced AMD by the time they reach age 50-59 and, by the time they are 70-79, this proportion will have increased to 14.4 per cent) and gender (women appear to be at a slightly greater risk than men).
Increasingly, the evidence points to a role for industrialized food-processing in the onset of heart disease and diabetes. More and more studies of heart patients are finding that they have elevated levels of homocysteine, an amino acid derived from the normal breakdown of proteins in the body. Raised levels of this amino acid are an indication that something has gone awry (see Viewpoint, p 5).
Crucial to this process is the presence of adequate levels of certain B vitamins. Other studies of heart patients have shown that they are deficient in these vitamins, and that adequate B-vitamin supplementation can reduce the incidence of heart attack and angina (Res Commun Mol Path Pharm, 1995; 89: 208-20). Links have also been made between the onset of diabetes and heart disease and deficiencies of chromium.
Natural sugars and grains contain adequate concentrations of chromium to support the metabolism of high-carbohydrate foods. However, virtually all B vitamins and chromium are removed during the refining process of most of the sugars and processed foods that now make up the bulk of the typical Western diet. Diets high in processed carbohydrates are nearly always deficient in chromium.
Another area that medicine has never explored is its own hand in the development of the AMD epidemic. Many of the drugs routinely prescribed for older people may well accelerate eye damage.
Doctors push aspirin because it thins the blood, thereby reducing the risk of blood clots. But, apart from poor effectiveness and the risk of gastrointestinal bleeding, new research suggests that long-term aspirin use can accelerate macular degeneration and contribute to retinal hemorrhage.
More than a decade ago, Dr J.D. Kingham wrote a letter to the prestigious New England Journal of Medicine (1988; 318: 1126-7) in which he noted that, in his clinic, many of the elderly patients who came to him with decreased central vision and macular hemorrhages had a history of recent ingestion of aspirin and other drugs known to affect platelet function or the bloodclotting process.
NSAIDs (non-steroidal anti-inflammatory drugs) have been shown to increase the risk of cataracts – a risk factor for the later development of AMD – by as much as 44 per cent (Ophthalmology, 1998; 105: 1751-8).
Many other common drugs, however, also contribute to a slow and steady degeneration in the eye, and hasten the onset of macular degeneration by making the eye more light-sensitive. These include certain antibiotics, psychotherapeutic medications and NSAIDs (Int J Toxicol, 2002; 21: 473-90). Phenothiazine antipsychotics, antidopaminergics (for motion sickness) and calcium antagonists have also been associated with AMD (Arch Ophthalmol, 2001; 119: 354-9).
However, some of these adverse effects of drugs are temporary. People taking sildenafil (Viagra), for example, often experience transient visual changes, described as ‘blue tint’, which usually lasts for four hours after taking the drug, according to the Viagra package insert.
This greater affinity for blue light is linked to the way that sildenafil affects the rods and cones in the retina, the cells that process colour information.
Aspirin also apparently interferes with many of the nutrients that are specifically essential for eye health.
Taking aspirin can increase the turnover of vitamin C in the body, leading to a possible deficiency (BMJ, 1975; I: 208). Similarly, taking 3 g/day of aspirin has been shown to decrease blood levels of zinc (Scand J Rheumatol, 1982; 11: 63-4). Aspirin also appeared to increase the loss of zinc through the urine in this study, and this effect was noted as early as three days after starting the aspirin regimen.
Aspirin can also enhance the blood-thinning effects of vitamin E in some individuals. In one double-blind study of smokers, those who took aspirin plus 50 IU/day of vitamin E had a statistically significant increase in bleeding gums compared with those who took aspirin alone (Ann Med, 1998; 30: 542-6). This increased risk of bleeding could have a theoretical impact on the eyes.
Physicians themselves are suffering from a kind of ‘blindness’ that prevents them from seeing the obvious role of diet and drugs in the development of AMD. The best a doctor might do for an AMD sufferer is to put down his prescription pad and say: ‘Don’t take two aspirin.’