Tuesday 27 January 2009

Human trials for stem cell therapy

Stem cells research to find a cure for macular degeneration is set to take a big step forward in the United Kingdom. British scientists said earlier this week that they will apply this year to start the first human trials. It will be the first time embryonic stem cells therapy is used on human beings to treat the eyes.

This possible breakthrough comes after the United States approved human trials of embryonic stem cells tests on paralysis treatment. So far, embryonic stem cells therapy has been tested only on animals. But the success of those tests have given scientists confidence to start trials on humans.

The application for the trials is expected to be made later this year and scientists are hopeful that the trials proper will start next year or 2011.

For more about this exciting development, click here.

Thursday 22 January 2009

Useful website

Check out this very comprehensive website on macular degeneration, set up by a registered nurse in the United States. It is packed with useful information, including tips on how to continue driving with low vision.

The website is called WebRN-Macular Degeneration.com. Click here to get to the website.

Tuesday 20 January 2009

Reminder: Membership renewal

Dear MDS members,
A gentle reminder to renew your membership. Membership subscription is just S$10. You can either call Anne at 6238-7387 or renew it in person during the first MDS event of 2009.
The event is a talk on artificial vision by our adviser, Associate Professor Au Eong Kah Guan, on Feb 28 (Sat) at the Mt Elizabeth Medical Centre, Seminar Room 1, Level 2. It will be from 2 to 4pm. Check out our website for more information.

Wednesday 7 January 2009

Beating the global myopia threat

A spreading pandemic of myopia among the world’s urban children may be avoided if children spend at least two to three hours each day outdoors. Australian scientists from The Vision Centre say there is persuasive evidence that increased exposure to daylight can prevent the permanent short-sightedness and eye damage which now afflicts up to 80-90 per cent of children in cities in East Asia such as Singapore and Hong Kong.


The finding demolishes long-held beliefs that short sight is due mainly to reading, and overuse of TVs and computers by youngsters, or is primarily linked to genetic factors. Myopia affects over 1.6 billion people worldwide, is spreading rapidly among city populations and, in its most severe form, can cause blindness by middle-age.

“The prevalence of myopia in the Australian population is dramatically lower than in other urban societies round the world – yet we do just as much reading and computer work,” says Professor Ian Morgan of the ARC Centre of Excellence in Vision Science (The Vision Centre) and Australian National University.

The team’s conclusions are borne out by new research in Singapore and the United States, which has reached similar conclusions.“Looking at children of Chinese origin, we found only 3 per cent of those in Sydney suffered from myopia, compared with 30 per cent in Singapore, where there is an epidemic. Yet, if anything, the children of Chinese origin in Sydney read more than those in Singapore. This clearly suggests that myopia was triggered by something in the environment, rather than the genes. The critical factor seemed to be the fact that the children in Singapore spent much less time outdoors.”

Comparing myopia levels among people of Indian origin, the team noted 5 per cent short-sightedness among rural Indians, 10 per cent among city Indians – and 65 per cent among Indians living in Singapore. “We’re seeing large increases in myopia among children in urban societies all around the world – and the outstanding common factor may be less and less time spent outdoors.

“Humans are naturally slightly long-sighted. We see that in rural populations all round the world. But when you start intensive schooling, and spend little or no time outdoors, you get this dramatic rise in myopia. In some East Asian cities 80-90 per cent of children are affected – and governments and the World Health Organisation are very worried about it.”

“The idea that ‘reading makes you short-sighted’ has been popular for a couple of hundred years. But recent data shows that the time spent indoors is a more important factor. Children who read a lot, but still go outdoors, have far less myopia.”

Professor Morgan explained that myopia is essentially an eye that has grown too long, and once it is too long, you can’t shorten it again: “So you have to stop it happening in the first place.

“Our hypothesis is that the light intensity experienced outdoors – which can be hundreds of times brighter than indoor light – causes a release of dopamine, which is known to block the growth of the eyeball. This prevents it taking on the distorted shape found in myopic people. We are now testing this idea.”

Professor Morgan explained that one of the potential problems with using increased time outdoors to prevent myopia is the potential for increasing skin cancers and for causing eye damage later in life. “Our hypothesis is that the protective effect is based on visible light, acting through the eye. We will be testing this over the next few months and the next stage will be a randomised clinical trial.”

If proven correct, then the prevention of myopia through increased time outdoors will be compatible with "Sun Smart" practices.

The research is being carried out through the ARC Centre of Excellence in Vision Science, the Australian National University and Sydney University, with support from the Australian Research Council, and the National Health and Medical Research Council. The NHMRC-funded Sydney Myopia Study was a large school-based study of over 4,000 Year 1 and 7 students from 55 schools located across the Sydney metropolitan area, carried out by Professor Morgan and his colleagues, Dr Kathryn Rose and Professor Paul Mitchell, at the University of Sydney. The data has been compared to data from the WHO and other national surveys around the world.

Saturday 3 January 2009

Clinical trials short changing us?

By Stephen Daniells
Yet again major randomised clinical trials report that vitamin and mineral supplements don’t work to prevent disease, so should we give up and just eat chips and chocolate?

No! The studies are important, no one is questioning that, but their true value is as a way of enforcing that perhaps randomised clinical trials (RCTs) are not suitable as a stand-alone way of determining if nutrients are beneficial or not.

We are, after all, talking about trials that, in essence, pull a nutrient out of context and follow the same methodology as used for the testing of drugs.

But let's not forget that by following the drug model we are supplementing the diet with one or two nutrients, each at a single dose, for a set period of time. RCTs work by randomly assigning a group of volunteers to receive an active compound, be it a drug or nutrient(s), or a non-active comparison, be it an inactive form of the active compound or a placebo.

For food items that do not normally form part of the usual food chain, RCTs are the best of the best because such compounds can be tested and retested successfully. Probiotics, for example, could fit into this category. But micronutrients that are found in a wide array of foods, in different food matrices, and in (synergistic?) combinations with other nutrients, do not ally themselves to a form of study that isolates one at a fixed dose for a set period of time.

This week’s publication of the results of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) and the Physicians' Health Study II (PHSII) in the Journal of the American Medical Association, are prime examples of the dubious application of the drug model to nutrients.

Guess what the results showed: No effect.

Cue the media headlines, such as the BBC’s “Vitamins 'do not cut cancer risk'”. This is an over-simplification of the situation, and a damaging one. Will consumers read this and can their vitamins as ineffective? (Questions over the quality of the journalism should be put on hold for another day.)

I am no expert, and I don’t pretend to be, but it amazes me time and again when people pump millions of dollars, pounds, or euros into studies that pull nutrients out of context.

The same questions jump to my mind all the time: Where’s the control group? Are the people in the placebo group actually taking supplements on the side? How long is the latency period for the disease in question?

Let’s address these one by one: For many nutritional studies a true control group doesn’t really exist. You cannot remove vitamin C, for example, totally from someone’s diet. It’s both unethical and practically impossible.

The PHSII study authors admit that the population was well-nourished, so could we ever have expected to see an effect? They also admit that this only applies to one dose. So is a study with one dose of one nutrient in a well-nourished population enough to conclude that selenium, vitamin E, and/or vitamin C are ineffective against prostate cancer?

Putting it a different way, ultimately we’re comparing someone with a good diet, with someone with a good diet plus a little extra vitamin C. What if people in the control group had a real love of kiwi fruit?

Next up is the question of whether the placebo group participants are also taking supplements on the side. This may sound silly, but there are plenty of examples in the literature where we see this. After all, if people believe calcium supplements are good for them, then you can’t stop someone from taking them. This is exactly what we saw with the WHI study a few years back that showed no differences between people in the calcium plus vitamin D group, and the placebo group. Turns out many of the participants in the placebo group were also taking calcium pills. Oops!

And then the question of latency is critical. If it can take upwards of 10 to 15 years for a disease to develop, as is the case with colorectal cancer, for example, and the study participants are free of the disease at baseline, then can we be hugely surprised or disappointed if we see no benefits after six years of supplementation? I think not.

But don’t think that just because we are aware of these issues and the limitations that this will have any impact on the view of RCTs.

Let’s look at Europe: the European Food Safety Authority (EFSA) is pinning all the health claims regulations on data from the ‘gold standard’ randomised clinical trial. The message is clear: If you have no RCT data, don’t even think about applying for a health claim.

So where does that leave us?

I would say we are at an important moment in time, and things may be moving in the right direction. At the recent Supply Side West, Professor Jeffrey Blumberg gave an excellent presentation about the over-reliance on evidence based nutrition, based on evidence based medicine, and called for science to be taken in its entirety, including in vitro, animal, and epidemiological studies.

It will be a long way to achieve the paradigm shift but there is hope. Until then, recommendations remain to limit the chips and chocolate.

Stephen Daniells is the science editor for NutraIngredients.com and FoodNavigator.com. He has a PhD in chemistry from Queen's University Belfast and has worked in research in the Netherlands and France.