Dr. Susan Summerton does an excellent job in keeping our members up to date with current research with the articles she posts on our OWNS facebook page. Below is an article Dr. Summerton recently shared.
Dietary Habits, Fatty Acids and Carotenoid Levels Are Associated with Neovascular Age-Related Macular Degeneration in Chinese
Received: 4 July 2019; Accepted: 22 July 2019; Published: 25 July 2019
Abstract: The role of diet and circulatory carotenoids and docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are implicated in age-related macular degeneration (AMD) but not well studied in Chinese. However, other fatty acids were not comprehensively evaluated if it had additional consequence on AMD. This study investigated the relationship among dietary habits, fatty acids levels, carotenoids and AMD in Hong Kong Chinese adults. In this cross-sectional case-controlled study, plasma fatty acids including, saturated fatty acids (SFA), monounsaturated fatty acids (MUFA) and olyunsaturated fatty acids (PUFA), and carotenoids levels were quantified between patients with neovascular AMD (n = 99) and age-gender-matched controls (n = 198). A food frequency questionnaire was also conducted.
Low blood carotenoid levels and omega-3 PUFAs namely DHA, EPA and α-linolenic acid increased the odds ratio of developing neovascular AMD. High blood omega-6 PUFAs specifically arachidonic acid and eicosadienoic acid, oleic acid (a MUFA) and SFA levels increased the odds ratio of having neovascular AMD. Neovascular AMD group had significantly less omega-3 PUFA rich food (vegetables, nuts, seafood) intake and higher SFA (meat) intake than controls. In short, neovascular AMD was associated with lower circulatory levels of carotenoids and omega-3 PUFAs, and higher level of omega-6 PUFAs, oleic acid and SFAs in the Hong Kong Chinese population. These findings enhance the understandings of dietary impacts on neovascular AMD and provide a context for future nutritional intervention studies.
Cardiac and visual degeneration arrested by taurine supplement
Dr. Stuart Richer shared the article below on a recessive gene mutation that causes retinal degeneration and cardiomyopathy by interfering with taurine. By supplementing with a single nutrient, taurine, researchers were able to reverse cardiomyopathy and halt retinal degeneration in the children studied. “These results are exceptional, because it’s the first time a food supplement given orally has been used to treat the retina and the heart successfully”
A reversible recessive disease?
The scientists speculated that it might be possible to block the progression of the disease by administering taurine to the children. They brought the family to Geneva to conduct detailed investigations into this rare genetic disease. In addition to the progressive visual impairment, which was now unfortunately total in the case of the boy, the doctors diagnosed damage to the cardiac muscle in both children. The little girl fortunately still retained some residual vision.
Since taurine is a food supplement rather than a medicine, the Swiss Ethics Commission agreed that it could be administered orally. “We gave 100 mg per kg of taurine daily to the children to be continued over the long-term, and organized regular ophthalmologic and cardiac monitoring sessions in Pakistan,” emphasizes Emmanuelle Ranza, a doctor and geneticist at University Hospitals Geneva (HUG) and UNIGE who was responsible for the clinical part of the study. The results quickly came about: in three days, the taurine levels in their blood jumped from 6 to 85 μ mol/l, reaching normal thresholds. And, after two years, the cardiomyopathy had completely disappeared in both children! In addition, the degeneration in the girl’s sight was brought to a halt, and there was even an improvement, meaning she could move around by herself. Unfortunately, this development was not possible for the boy, who had already lost his entire retina.
A single patient can change medicine
“These results are exceptional, because it’s the first time a food supplement given orally has been used to treat the retina and the heart successfully,” points out Antonarakis. “This little girl has paved the way for a potential cure for newborns suffering from the same recessive disease. One patient can change the history of medicine!” In fact, researchers estimate that there are possibly 6,000 babies worldwide who might suffer from the same SLC6A6-related disease, and around 300 in Europe and North America. “Our goal now is to detect newborns affected by the condition at an early stage so they can be treated from birth with a taurine supplement and potentially prevent the onset of symptoms,” adds Antonarakis. The geneticists also aim to continue to identify new genes that cause recessive diseases, especially since they now have proof that some of them can be treated effectively.
Taurine is the most abundant amino acid in the retina. Taurine stabilizes cell membranes, functions as a neurotransmitter and osmoregulator, is involved in the conjugation of bile acids, and plays a role in retinal function. Taurine also contributes to cardiac contractility, has antiarrhythmic and anticonvulsant effects, and inhibits platelet aggregation. Taurine may be useful for preventing and/or treating congestive heart failure, diabetes, cirrhosis, nonalcoholic fatty liver disease, myotonic dystrophy, and retinitis pigmentosa. Taurine is present exclusively in animal foods. It is not considered an essential nutrient, because it can be synthesized from methionine via cysteine. However, endogenous taurine synthesis may not always be sufficient to meet the body’s needs. See the article below on taurine and retinal degeneration:
Taurine: The comeback of a neutraceutical in the prevention of retinal degenerations
Taurine is the most abundant amino acid in the retina. In the 1970s, it was thought to be involved in retinal diseases with photoreceptor degeneration, because cats on a taurine-free diet presented photoreceptor loss. However, with the exception of its introduction into baby milk and parenteral nutrition, taurine has not yet been incorporated into any commercial treatment with the aim of slowing photoreceptor degeneration. Our recent discovery that taurine depletion is involved in the retinal toxicity of the antiepileptic drug vigabatrin has returned taurine to the limelight in the field of neuroprotection. However, although the retinal toxicity of vigabatrin principally involves a deleterious effect on photoreceptors, retinal ganglion cells (RGCs) are also affected. These findings led us to investigate the possible role of taurine depletion in retinal diseases with RGC degeneration, such as glaucoma and diabetic retinopathy. The major antioxidant properties of taurine may influence disease processes. In addition, the efficacy of taurine is dependent on its uptake into retinal cells, microvascular endothelial cells and the retinal pigment epithelium. Disturbances of retinal vascular perfusion in these retinal diseases may therefore affect the retinal uptake of taurine, resulting in local depletion. The low plasma taurine concentrations observed in diabetic patients may further enhance such local decreases in taurine concentration. We here review the evidence for a role of taurine in retinal ganglion cell survival and studies suggesting that this compound may be involved in the pathophysiology of glaucoma or diabetic retinopathy. Along with other antioxidant molecules, taurine should therefore be seriously reconsidered as a potential treatment for such retinal diseases.