In fact, a Japanese researcher went so far as to claim that it could make you blind.

Rats fed MSG suffered vision loss and had thinner retinas than those not given the flavouring, he discovered.

This is not the first scare about MSG, found extensively in Chinese food. The American drugs agency, the Food and Drug Administration, is also concerned about MSG’s effects on the nervous system.

The Japanese research team pointed out that a very moderate intake of MSG should not impair vision, although exactly what is moderate is still uncertain.

To find out more about food additives, and what they can do to our health, read the WDDTY Good Digestion Guide. Order it from our website: http://www.wddty.co.uk/shop/details.asp?product=345

The findings, prepared by the University of Melbourne, go against other studies showing that antioxidants could slow the progress of the disease.

In this study, researchers gave 1193 healthy volunteers either a placebo or 500 IU of vitamin E every day for four years. Macular degeneration, or age-related maculopathy (AMD), occurred in 8.6 per cent of the vitamin E group vs 8.1 per cent of those given a placebo.

However, another study found that physicians who took either vitamin E or multivitamins had 13 or 10 per cent reductions, respectively, in the risk of AMD, while a new study testing a range of antioxidants found a slowing down of the disease, but only in those who had already developed AMD.

Perhaps, said the Melbourne researchers, people need to take vitamin E for longer, or perhaps the benefits are only seen in specific groups, such as smokers (BMJ, 2002; 325: 11-4).

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

It’s true that medicine is concerned that UV light causes cataracts, although most sunglasses block UVA and B spectrum light as well.

It’s been posited that the brain needs full-spectrum sunlight to stimulate the pathways and organs in the brain, and some specialists have found that sunglasses affect the eyes’ natural reflexes and interfere with vital biological interactions.

So what’s the answer? As usual, it’s to be found in the question. It is important to protect the eyes but, like the sun, put your hat on.

* In a recent study, one third of 773 individuals involved in a road accident as a driver, bicycle rider or pedestrian experienced some level of anxiety, depression, fear of travel or post traumatic stress disorder (PTSD) 3 to 12 months later and, in most cases, persisted. After one year, about half the group had phobic travel anxiety, nearly 60 per cent had general anxiety, and half were diagnosed with PTSD (Am J Psychiatry, 2001; 158: 1231-8).

* New research in nearly 1300 men suggests that, during a severe asthma attack, men are less likely than women to notice the symptoms of the attack. The reason for this is unclear, but it may be that men perceive less discomfort because of greater lung size and muscle strength, or because they generally develop asthma at an earlier age than women. Men also tend to only seek medical attention when symptoms are too severe to ignore, the researchers noted (Ann Emerg Med, 2001; 38: 123-8).

* What’s lurking in that paddling pool? Physicians in Canada have found the first outbreak of a new type of Pseudomonas infection called ‘hot foot syndrome’. This discovery was made when 40 children, aged 2 to 15, developed intense pain in the soles of their feet within 40 hours of using the same wading pool. A hot, red swelling began after a few hours, along with pain so severe that the children were unable to stand up. Three children were given oral cephalexin (an antibiotic) while the others were treated with cold compresses, analgesics and foot elevation. In all cases, the condition resolved within 14 days, although it recurred in three children after they revisited the same pool (N Engl J Med, 2001; 345: 335-8).

A study carried out at Moorfields eye hospital in central London found that soft contact lens users, particularly those using extended wear lenses, had far more risk of developing a bacterial eye infection than those wearing hard lenses.

The infection, known as microbial keratitis, an inflammation of the cornea, can lead to blindness if that part of the eye is perforated or scarred.

The study, published in the Lancet, found users of extended wear contacts most at risk 21 times more likely to develop the infection than hard lens wearers.

Ordinarily soft lenses had a 3.6 times risk, and polymethylmethacrylate hard lenses a risk 1.3 times that of regular hard lenses.

Soft lenses and extended wear lenses are increasingly prescribed these days because they are easy to fit.

The British College of Optometrists is so concerned about these results that it had advised opticians that extended wear lenses should only be prescribed when they are the only medical option.

Any practitioner failing to warn his patients of the risk would be acting unethically, said the college.

These vegetables are rich in certain carotenoids which appear to slow the development of AMD (age related macular degeneration), the leading cause of blindness in people over the age of 65.

Researchers believe it is the elements in the vegetables called lutein and zeaxanthin that may help prevent AMD. This would mean that carrots, the most common of the carotenoid family called beta carotene, would not work as a preventative because they are very low in those elements.

If this is true, other vegetables such as kale, mustard greens and turnips would also help fight AMD, although they were not tested by researchers.

They also believe that high intakes of vitamin C, preferably through foods, may also help. A diet rich in the entire antioxidant family of A, C and E may provide protection, but it could be because of another nutrient found in the foods, rather than the antioxidants themselves. This means that supplements would not help.

The study team, known as the Eye Disease Case Control Study, led by Dr Johanna Seddon, discovered that smokers were at the highest risk of developing AMD, although that risk was reduced if the smoker had high intakes of lutein and zeaxanthin.

They examined 356 people with advanced AMD against 520 people with other eye diseases. Those in the group with the highest intakes of carotenoids were 43 per cent less likely to develop AMD than those with a diet low in carotenoids (JAMA, 9 November 1994).

Carotenoids may also reduce the risks of heart disease, especially among nonsmokers. This finding, by a research team from the University of North Carolina, puts carotenoids back on the map after beta carotene had been found by earlier studies not to be a preventative.

But the North Carolina team has discovered that beta carotene accounts for only 25 per cent of the carotenoids found in the blood. They tested the serum of 1,899 men without any known major illnesses, such as heart disease. Men with the highest levels of carotenoids had a risk of just 0.64 per cent of developing a heart condition, and this fell further to 0.28 per cent among those who did not smoke.

!AJAMA, 9 November 1994.

However, although hypertension in the eye’s blood vessels is a key risk factor for glaucoma, not all rises in eye pressure inevitably cause visual damage: in some people, the optic nerve is strong enough to withstand the increased pressure. Equally, those with particularly weak optic nerves can develop glaucoma even if their eye-pressure readings are normal.

Who are most at risk? Anyone can develop glaucoma, but the risk is significantly greater for those over 40, and doubles for those who are 75-80. It is suggested that age-related changes to various parts of the eye may be responsible for the loss of fluid regulation within the eye.

Race is another important factor. In a study funded by the US National Eye Institute, researchers at the Johns Hopkins University, in Maryland, found that glaucoma is three to four times more likely in people of Afro-Caribbean origin than in white Europeans, and it strikes at a younger age (Arch Ophthalmol, 2004; 122: 532-8).

Other high-risk groups include family members of those already diagnosed with the condition, and people who are extremely shortsighted, diabetic or suffering from high blood pressure.

Glaucoma can also be due to drugs (Drug Saf, 2003; 26: 749-67), including:
* corticosteroids (these mainly cause or worsen POAG)
* sulpha-based drugs
* antidepressants
* anticoagulants
* antihistamines/antacids (H1-/H2-receptor antagonists).

Ironically, drugs such as adrenergic agonists and cholinergics, which are often used to treat glaucoma, can also sometimes bring the condition on.

As prevention is always better than cure, those who belong to these high-risk groups should have their eyes regularly checked – that means going to your optician’s for that annual eye test – and their eye pressure monitored.

The drugs used to treat people who are HIV positive are probably some of the most toxic in use. They include DNA chainterminator drugs, originally designed for cancer chemotherapy, such as AZT, ddl, ddC, an untold number of broad spectrum antibiotics such as Septrin, and numerous anti fungals like fluconazole and ketoconazole.The reasoning behind this onslaught of toxic treatment is the much held but completely unproven belief that HIV and HIV alone is the primary cause of AIDS. In order to increase the lifespan of an infected person, it is believed that the human immunodeficiency virus must be blasted out of the cells of the unfortunate host, using cytotoxic agents. The fact that not one single person with an AIDS diagnosis has been saved by this method appears to have escaped attention.

The majority of people taking drugs like AZT, ddl and ddC are persuaded by their clinicians to do so either because they have exhibited a particular T-cell count or because they have supposedly succumbed to one or other of the diseases classified as belonging to AIDS. These include diseases such as tuberculosis, cytomegalovirus (CMV), pneumocystis carinii pneumonia (PCP), toxoplasmosis and Karposi’s sarcoma, which in fact infect far greater numbers of people worldwide who are not HIV positive.

PCP, the most feared of these opportunistic infections, is usually successfully treated with antibiotics in acute cases. However, the tendency is to continue giving the patient antibiotics as a prophylaxis (just incase measure) against future attacks or to asymptomatic HIV patients to avoid an initial attack.

In people with HIV antibodies the state of their health is measured by the number of T-cells present per ml of blood; 200 is considered a level at which the patient is at risk from the opportunistic infections associated with AIDS. Although no direct correlation has ever been demonstrated, people are pressured into starting AZT and similar drugs on the basis of T-count alone, even though their health frequently is excellent.

Septrin, the drug of choice for prophylaxis, is normally advised when T-cell counts reach the magic threshold of 200. However, Septrin is itself extremely toxic if taken for any length of time, even at low dosage (see Drug of the Month, p 7).

Many of its side effects are similar to the list of symptoms doctors expect to see in people with HIV infection. These include anemia (caused by the drug’s interference with body’s use of folic acid), loss of appetite and consequent weight loss, nausea, vomiting, diarrhea, numbness, and pins and needles in the arms and legs, convulsions, systemic lupus erythematosus and meningitis.

Even the milder symptoms are pretty awful, including: skin rashes, conjunctivitis, nettle rash, drug fever and chills, serum sickness symptoms (fever, swollen glands, painful joints), inflammation of the arteries, and ulcers of the eyes, mouth and urethra.

In medical literature, PCP has always been recognized as a disease of immune damage most frequently brought about by malnutrition or nutrient malabsorption (which are side effects of Septrin), but it has also become recognized over the past 20 to 30 years as a complication associated with cancer chemotherapy, like AZT.

When patients report these side effects to their doctor they are more than likely to be told that what they are experiencing is a result of HIV infection. The patient is then put on another form of medication to deal with what are mainly drug side effects.

One of the most disturbing aspects of these forms of medication is their ability to destroy essential micronutrients in the body and their toxic effect on bowel flora. AZT, for instance, is known to completely destroy E coli in the gut (Physicians Desk Reference 1992). One of the most frequent responses following the use of the drug is an overgrowth of candida albicans, which in turn leads to nutrient malabsorption, yet another supposed symptom of HIV infection.

The ability of doctors to make their patient’s symptoms fit the facts as they understand them is amply demonstrated by the reactions of doctors to patients exhibiting all the symptoms of diseases against which they have been vaccinated. The practitioner’s belief in the power of vaccination is so overwhelming that even though the diagnosis is inescapable, the doctor will go to enormous lengths, even to the point of invention, to explain away the illness.

HIV blindness, as I call it, works in a similar way. Doctors are so convinced that all the symptoms they observe in their HIV positive patients are related to HIV infection that they are unable or unwilling to examine the possibility that what they are actually observing is being caused by the very drugs they are prescribing.

Their only perceived recourse is to prescribe further medication with the added danger of even more severe side effects. The result is a toxic avalanche which completely overwhelms the ability of even a moderately damaged immune system to protect the host or to recover its function in the long term.

The outcome is death; the cause, the certificate reads, AIDS.