Tuesday January 17 2012
Vitamin D (which you can get from sunlight) may have helped people's eyesight (just don't stare at the sun)
“More vitamin D a day could keep glasses away,” according to The Independent. The newspaper reported that “boosting vitamin D intake could help to prevent age-related diseases, in particular loss of vision and blindness”. Unfortunately, this article and others have inferred too much from the results of a very small, short-term laboratory study of eye-ageing problems in animals.
This widely reported news story centres on research in which “middle-aged” mice were treated for six weeks with vitamin D. The researchers examined the mice’s vision and looked for signs of inflammation in their eyes and whether proteins associated with normal ageing had built up. The accumulation of these proteins and inflammation can increase the risk of people developing age-related macular degeneration (AMD), a major cause of blindness in people aged over 50 in countries such as the UK. The researchers found that there was less inflammation and build-up of the protein amyloid beta in the retinas of mice treated with vitamin D.
However, the researchers did not specifically look at a mouse model of AMD and this study has limited relevance to humans. Therefore, it’s not possible to say, based on the study’s results, whether vitamin D has any effect on age-related vision loss or AMD in humans.
Where did the story come from?
The study was carried out by researchers from University College London and was funded by Biotechnological and Biological Sciences Research Council and the Rosetrees Trust. It was published in the peer-reviewed medical journal The Neurobiology of Aging.
All the newspapers reported that this study was carried out in mice. Several included quotes from the researchers as saying that human trials of vitamin D supplementation were needed before it was possible to say whether vitamin D had any beneficial effect on vision and preventing eye disease.
What kind of research was this?
This animal research looked at the effect of six weeks of injections of vitamin D in safflower oil on age-related changes to the eyes of mice. The effects were compared with control mice that received injections of safflower oil only.
The researchers were particularly interested in whether the vitamin D treatment prevented inflammation and the accumulation of proteins, thought to be a cause of age-related macular degeneration in humans. However, the study did not directly assess whether vitamin D prevented age-related macular degeneration (or whatever the mouse equivalent is). As with all animal research, the direct relevance of this research to humans is limited.
What did the research involve?
Seven 12-month-old female mice were injected with vitamin D and safflower oil under their skin every three days for six weeks. A control group was injected with safflower oil only, at the same frequency.
Before treatment, the researchers recorded how well the mice’s eyes responded to visual stimuli by recording the electrical signals made by the retina cells when the mice were exposed to flashing lights.
After the treatment, the researchers dissected the mice’s eyes and stained them for a protein, amyloid beta, which accumulates with ageing. They also stained for a protein called C3d, which is a marker of inflammation. Finally, they counted the number of inflammatory cells (macrophages) in and around the retina and looked at their shape, which showed whether these cells were active or not.
What were the basic results?
After the treatment period there were significant differences in how mice’s retinas responded to stimuli between the control and treated mice.
The researchers found that in the eyes of the vitamin D-treated group of mice there were fewer macrophage cells, and their shape suggested that they were less active in terms of causing inflammation. The mice treated with vitamin D had less build-up of the protein amyloid beta in their eyes than the control mice. The control mice experienced more inflammation, as judged by looking at the amount and form of the inflammation marker C3d.
After the treatment period, there were significant differences in how mice’s retinas responded to stimuli between the control and treated mice.
How did the researchers interpret the results?
The researchers said that the reductions in inflammation and the levels of amyloid beta in the retina of mice treated with vitamin D were reflected in a “significant improvement in visual function, revealing that vitamin D is a route to avoiding the pace of age-related decline”. They added that “excess amyloid beta and inflammation are risk factors leading to age-related degeneration (AMD), the largest cause of blindness in those older than 50 in developed countries”. The researchers also said that epidemiological studies have shown that vitamin D may protect against AMD. From this, they infer that “vitamin D enrichment is likely to represent a beneficial route for those at risk [of AMD]”.
This small animal study showed that injections of vitamin D over six weeks decreased the accumulation of one age-related protein and decreased inflammation in the retina of seven mice compared to seven control mice. The response of the eye to light stimuli differed between the two groups of mice.
The newspapers and the research article itself said that this research suggests that vitamin D supplementation may represent a beneficial route for those at risk of a type of vision loss called age-related macular degeneration (AMD). However, the aim of this animal study was not to see whether vitamin D treatment prevented AMD (or a mouse model version it). It is far too early to say whether this vitamin D could prevent AMD as there have not yet been trials in humans.
The study had looked at how the treatment affected the retina’s electrical response to visual stimuli, but it is difficult to say whether this helped the mice’s vision. It’s not yet possible to say, based on this research alone, whether getting extra vitamin D through diet, sun exposure or supplements would have any effect on human vision.