Age-related macular degeneration (AMD) refers to the slow deterioration of the cells in the macula, a tiny yellowish area near the centre 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 centre of your vision. Your peripheral vision, however, is not affected.
Of all the illnesses of the ageing eye – including glaucoma and cataracts – AMD is the only one that is sharply on the rise. In the UK, registrations for AMD have burgeoned by 30-40 per cent. 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.
The role of 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 flesh foods, but your risk doesn’t increase with the quantity of meat that you eat.
The real risk for AMD was associated with vegetable-fat intake. Consuming high levels of these types of fats 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 more of these you ate, the greater your risk.
The researchers also made another connection that is most unusual in these types of studies. They 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 industrialised 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.
Link with heart disease
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 industrialised 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.
Aspirin accelerates the damage
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 bloodclots. 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 haemorrhage.
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 haemorrhages 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’, that 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 (see box, p 2). In a small study of men and women taking 200 mg of Viagra daily, 64 per cent of those who completed the study reported visual disturbances. The participants were given an electroretinogram, a test that looks at the behaviour of the rods and cones in the retina. While the test results were within normal limits, they also confirmed that taking the drug caused a slightly depressed function in the cone cells.
The hungry eye
Aspirin also apparently interferes with many of the nutrients that are specifically essential for eye health. To understand why this is important, it is necessary to know some basics about how the eye works.
Four types of cells in the human retina capture light and process visual information. One type, the rod cells, regulates night vision. The other three types, called cone cells, control colour vision. This constant processing of visual information can cause a great deal of (normal) wear and tear in the cells of the eye.
To continue to function optimally, our eyes require a constant supply of nutrients. High levels of antioxidants, such as vitamins C and E, beta-carotene and lutein as well as zinc, selenium and copper, are all naturally present in the macula.
Our eyes also require a great deal of oxygen. But where the oxygen-containing environment is especially rich and the metabolic rate is high, as it is in the macula, high levels of oxidative free radicals are also generated. So, in addition to providing nourishment, the antioxidants found in the eyes also protect against free-radical damage.
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.
Gastrointestinal (GI) bleeding is another common side-effect of taking aspirin. Often, this problem will go undetected for rather a long time. The long-term blood loss due to regular use of aspirin can lead to iron-deficiency anaemia.
Another potential problem area is foods containing salicylates, the main ingredient in aspirin (see box above).
But aspirin may have another damaging effect. As well as depleting levels of important nutrients, aspirin can disrupt the normal circadian rhythms.
The hormone melatonin is produced by the pineal gland at night. It helps us to sleep, but it also boosts immunity and, for those at risk of AMD, it helps lower blood pressure (Hypertension, 2004; 43: 192-7) and protects the retinal pigment from oxidative stress (Exp Eye Res, 2004; 78: 1069-75).
NSAIDs (including aspirin) work, in part, by inhibiting prostaglandins, which produce pain and inflammation. They also contribute to the regulation of body temperature and the production of melatonin (J Pharm Pharmacol, 1987; 39: 840-3).
One double-blind study found that nighttime body temperature did not drop to its usual levels after taking either aspirin or ibuprofen (Physiol Behav, 1996; 59: 133-9). This was because taking these NSAIDs at night suppressed normal levels of melatonin. Earlier reports have confirmed that healthy individuals taking NSAIDs experience melatonin suppression and alterations in their normal sleep patterns (Sleep Res, 1992; 22: 165; Physiol Behav, 1994; 55: 1063-6).
Such chronic disruption may allow blood pressure to rise, with negative effects on the eye, as well as expose the retina to greater levels of oxidative stress.
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.’
Pat Thomas and Lynne McTaggart