Nutrition for Macular Degeneration

Lutein and zeazanthine are plant chlorophyll “helper” molecules or carotenoids, which green plants use to soak up excess light energy which could otherwise damage their chlorophyll molecules during photosynthesis. Much in the manner of oxygen becoming “singlet free Oxygen” in humans, which is a free radical atom that seeks to react aggressively with our cellular molecules and cause damage, so also chlorophyll in plants exposed to excess light can become triplet chlorophyll which has the capacity to damage the plant’s cellular molecules. Xanthophyll and its precursor zeaxanthine are lutein type plant pigments which buffer this excess light energy, exposing themselves to the light and absorbing it. These yellow pigments are found in high concentrations in the xanthophyll pigment of our macular, the so called “macular lutea” or “yellow spot” so named by the ancients who could identify easily the yellowish pigmented spot at the back of the eye. Radiant light is focussed on the macular by the combined corneal and lens optics of the eye, and the blue and ultraviolet light is particularly high in energy and is “buffered” a little by these plant derived pigments. The theory that ingestion of “carotenoids” which are similar molecules to lutein and zeaxanthine, might prevent macular degeneration relates to the idea that these substances protect the macular from oxygen free radical damage, and that somehow that must occur more frequently in dietary states where a deficiency of these foods exists. The idea has modern support in the AREDS trial which showed a benefit of beta carotene, and this was later substituted for lutein and zeaxanthine with even better results in AREDS 2 trial (Age Related Eye Disease Study). Eating nasturtium flowers and lots of Kale might provide a diet enriched in these substances, but dietary supplementation with 10mg lutein and 2mg of zeaxanthine has been recommended and is available in tablet form from a number of outlets.

Selenium is a non metallic mineral commonly used for it’s reddish colour to counterbalance the yellowish tinge that develops in glass manufacture. It is found in high concentrations in some mineral deposits which when flooded can occasionally lead to poisoning of water sources by excess selenium. It is a “co enzyme” of glutathione reductase which is an important human defence mechanism combatting oxidative damage to molecules where light and oxygen create oxygen free radicals. No clear evidence of disease from selenium deficiency has been outlined, yet theoretically some believe that dietary supplementation with selenium may assist the body to defend against oxidative damage and prevent the worsening of macular degeneration. It is contained in some multivitamins for that purpose.

Vitamin C 500mg/d and E 400iu/d are similarly involved in reduction of oxidative damage and listed as part of the AREDs formula. However vitamin e potentially could contribute if taken as a supplement in the diet to a slightly lower lifespan, as calculated from pooling the results of various studies. Nevertheless it is still a part of the AREDs formula.

Zinc 80mg/d was found to be no different to zinc 25mg/d when the studies AREDs and AREDs 2 were compared, either with regard to preventing macular damage or with regard to the side effects of gastrointestinal upset, or genitourinary inflammations. However, confusingly, the recommendation was to stay with the higher dose. This has sent the industry into cartwheels trying to package the 80mg into either one tablet daily (available in some contries) or two tablets daily (as in Australia) even though the study should support the lower dose. Consequently there is confusion as to whether patients need to take two tablets or one tablet daily, and the answer is that 25mg of zinc daily, seems to be as effective and no better or worse than 80mg/ daily. The zinc can chelate copper out of the bloodstream and give rise to anaemia if taken in excess, so some formulations contain a minute dose of copper to prevent this. It is important to remember to check that other multivitamins taken do not contribute to an overall daily intake of zinc that is excessive for this reason, and the upper limit of daily zinc considered safe is somewhere around 200mg/d but varies depending on the literature.

Essential fatty acids are a hot topic, but they fizzled out in the AREDs 2 study, showing no benefit in preventing visual loss or progression to late stage macular degeneration, despite a number of nutritional studies supporting a diet enriched by at least a twice weekly dose of fish, especially oily coldwater fish such as salmon and mackerel. These essential fatty acids are EPA eicosapentanoic acid, and DHA docosahexanoic acid and they originate from the diatoms, plankton and seaweeds and algae beloved of the marine food chain. They are also beloved, by the way, of the Japanese, whose natural rates of macular degeneration are low. Exactly what these fatty acids do that is so good is a little difficult to understand, but basically they are slippery and slimy and help plankton behave that way in the sea. They are important structurally in the cell membranes of these basic life creatures, and are passed up the food chain in the oceans and are highly important dietary elements for fish. The human body has a very limited capacity to manufacture these ‘essential’ fatty acids, but can do so to a small extent from alpha linoleic acid, ALA found in many plant seeds and the oils derived therefrom, for example flaxseed, and other seed oils. However some of these oils are difficult to cook with, smoking a lot and not easy to buy or eat, and in general, the recommendation to eat fish twice a week to stave off macular degeneration remains good advice. The nomenclature of the essential fatty acids is that they contain a double bond, which means that the carbon atom in part of their long carbon chain, is not fully hydrogenated at all available positions, having therefore a double bond with the next carbon, and that this occurs either five (pentanoic) or six (hexanoic) carbons back from the terminal methyl end (CH3) of the carbon chain, therefore is “unsaturated”. Saturated fats, typically derived from eating meat and dairy products, do not have this double bond. Polyunsaturated fats have lots of double bonds. Natural double bonds have a “cis” configuration” which is “bent”, in other words the carbon chain kinks at that point, and this is generally a good thing in our diet. “Trans” double bonds are not kinked but straight, and are generally a result of impurities derived from cooking polyunsaturated fats to turn them into saturated ones by hydrogenating or oxidising them, which we do to make them nicer to eat, being able to melt at close to body temperature, or to stay on the shelf without going rancid (spontaneous oxidation). Due to legal action by activists mainly in the United States, a number of changes to food production have occurred since about 2006, such that the levels of trans fatty acids in processed foods is dropping to less than about 6%, which for legal reasons has become defined as “nil”. This is considered better from a cardiac standpoint, in particular.