Are we there yet ? A familiar cry to all parents , the typical response – nearly – could aptly describe the current position with the emerging science of pharmacogenomics – the concept of using genetic analysis to guide medical treatment. Though currently in an embryonic stage of devleopment this concept is growing rapidly and when it comes to AMD there has been a slew of recent research that could pave the way for a whole new way of treating conditions such macular degeneration. In summary below is a list of genetic associations with AMD that also may have some relevance in treatment/ intervention responses;

Complement Factor H Y402H gene type : correlates with a more aggresive type of wet AMD (predominantly classic type) and poorer outcomes with Photodynamic therapy & Avastin injection therapy in patients who had two copies of this gene variation that is strongly linked to AMD.

Genes for placental growth factor have also been implicated in suboptimal responses to standard wet AMD treatments

Overall 3 AMD gene variants – CFH Y402H, ARMS2 A69S and C3 R80G account for around 76% of risk of AMD development.

Complement factor H variant in particular has also shown some impact on the value of Zinc supplementation in AMD progression with a greater beneficial effect being seen in patients who did not have the high risk CFH gene variant (68% v 11%) in other words patients who have two “bad” copies of the CFH gene are much less likely to gain the standard known benefit that Zinc confers on “average” AMD patients.

Summary : Current research is rapidly buliding up a picture of a range of genetic variants that are implicated in the development of AMD, furthermore gentetic testing may become an invaluable tool in helping to select the appropriate treatment programme for both dry AMD and wet AMD in the very near future.  Nearly There !

Indulging in dark chocolate a little may not be all bad !

Bioflavanoids are widley distributed  plant compounds and are the most important plant pigments for flower colloration – producing yellow and red/blue pigmentation designed to attract pollinator animals. Experimental evidence suggests that they may act as biological “response modifiers” and could play a role against inflammation. From a macular degeneration perspective they also appear to have powerful anti-oxidant properties. Though there is debate as to whether this is direct or indirect – in other words dietary flavanoids may actually work by increasing uric acid levels that result from the metabolism of these compounds.

As such there is no large scale clinical trial investigating the impact of dietary bioflavanoids in the battle against AMD but there does appear to be some role here that clearly requires further investigation.

What should AMD patients do – my suggestion at this stage is to stick with the following measures;

1) Stop Smoking – every research study has shown consistently that smoking is THE single most important factor that patients can actually do something about

2) If you are a non smoker or have not smoked for more than 10 years – Use AREDS style supplementation with either VITEYES AREDS formula or Ocuvite Preservsion AREDS formula.

3) Consider supplementing with Lutein and Zeaxanthin as well

4) If you are a smoker – you may benefit from VITEYES somkers formula

5) To increase dietary intake of FLAVNOIDS – consider adding the following to your diet;

a) Citrus Fruits

b) Red Onions

c) Pulses

d) Tea _ green tea especially

e) Red wine  - in moderation !

f) Dark Chocolate (>70% cocoa) agian in moderation

stem cells under a microscope

A great deal has been written about stem cells – often described as the holy grail of modern medicine. In a condition such as AMD where cell loss and scarring are at the centre of the problem stem cells do in principle offer a way to recover lost function ie eyesight. How do they work ?

Every cell in the body contains a code (the DNA) that in theory contains all the information to make that cell into any kind of cell. Many cells in the body are not programmed to regenerate – this is especially true for the vision receptor cells in the retina, once damaged they cannot regrow. However researchers have found that “embryonic” cells can be coaxed into turning into specialised cells such as photoreceptr cells. Many groups are involved in research trying to regenerate cells.

Professor Coffey’s group in London is working on treating AMD with a single layer of retinal pigment epithelium (support cells for the retina) derived from human embryoinc stem cells. This procedure involves transplantation of these cells into the damaged area of the macula. Human clinical trials may begin as early as 2011 if successful, eye surgeons may be able to perform this procedure as early as 2015.  One problem that still hasnt been fully dealt with is tissue rejection – though the unique structure of the eye makes it a less active part of the body for rejection to occur – it would still be a possibility – clearly much more research is required before these treatments become available – but nevertheless genuinely exciting prospects ahead for AMD sufferers.