Eurogene

Yesterday I ordered a book from Amazon called “Outsmart Your Genes” – this was prompted by a tweet from @genesherpas:   Just got my copy http://www.outsmartyourgenes.com/ my Friend Brandon Colby MD's great work. It is a must read for all. That means AnneW too. It wasn’t too expensive and it may be interesting – it also could be part of a slick marketing campaign, a few days previously a press release announced the launch of “Existence Genetics LLC, the world’s first predictive medicine company…”. With the website of the book linking to the Existence website , the twitter and facebook links, and so on, it does look like: @dgmacarthur The "Outsmart your genes" book that @ GeneSherpas is spruiking looks like extended ad for author's company: http://bit.ly/8Zanrd We’ll see, I’ll update when I read the book, meanwhile I learnt some Australian slang as well… First of all – there is nothing wrong with any of the above, it’s all fine and I have not much t...

This article in today’s Independent prompted me to finish off and post this – as far as good nutritional advice is concerned confusion reigns. 1. Sat fats are OK after all 2. Recently we were informed that the “5 a day” advice did not prevent cancer ( see previous post ) 3. We read that >400 IU / day vitamin E increases mortality thanks to a 2005 meta-analysis (Conclusion: “High-dosage (≥400 IU/d) vitamin E supplements may increase all-cause mortality and should be avoided”) 4. In 2007, a widely cited meta-analysis proved “the myth of antioxidant supplements” – they simply do no good and may even do harm 5. The subject of this post – 2 major studies show that vitamin E and Selenium, despite early promise, do not protect against prostate cancer ( SELECT and PHS ) 6. According to one author of the SELECT study –  “The prospects for cancer prevention through micronutrient supplementation have never looked worse” So how much of all this is true...

Headlines all over the press today were “ 5 a day doesn’t prevent cancer ”. So after all these years set in stone it’s all been a waste of time? Hard to tell really, the paper in question is all about cancer but as the Walter Willett editorial points out the same study group provided evidence that 5 a day reduces stroke and heart disease by 30%. But maybe that’s not right either, maybe Dr Aragon in Woody Allen’s Sleeper was right (this is from an interesting article about nutritional genomics by the way): The study: Fruit and Vegetable Intake and Overall Cancer Risk in the European Prospective Investigation Into Cancer and Nutrition (EPIC) by Boffetta et al , published online in the Journal of the National Cancer Institute. It involved almost 500,000 people in a prospective study looking at nutrition and cancer between 1992-2000. Over 30,000 developed cancer but the detailed analysis revealed only a minor F&V protective effect of a few percent, if any at all. Disappointing to...

Personal genetics is moving faster than ever, we began with a few variants in an affordable genetic test, now we have hundreds of thousands, soon it will be sequencing of all our genes (exome sequencing) and finally, the whole genome by 2011, 2012, 2013? Who’s prepared to predict? What’s the use of it though – the technology is moving much more rapidly than the knowledge of the effects of genetic variation and we still only really have a few “clinically useful” applications? A problem that has not yet been fixed is the oversight of commercial services, the fact that there are not yet any new specific regulations to deal with personal genetics is probably just as well because by the time any law is passed it would be likely to be out of date. The lack of really effective clinical utility and the existence of commercial interests increases the confusion though. It’s hard to sell something that is interesting, “fun”(?), quite expensive, but not actually that useful to the majority right...

This post does not have much in the way of personal genetics but is not completely unrelated. If personal genetics is going to work then it will have to involve lifestyle changes especially diet, not just for weight loss but for health. As far as obesity is concerned there have been plenty of GWAS and many genes associated, hopefully the results will be be useful for understanding mechanisms because a gene panel for predicting obesity does not seem to be terribly useful right now, it’s one of the phenotypic traits that most people are aware of without any genetic testing. One much sought after goal though is to use genetics to predict what sort of weight loss diet will be most effective – there are some tantalising studies and there is one company, Interleukin Genetics , that recently introduced a weight loss panel. They claim to be able to select the best diet but until they actually publish their work that they refer to we cannot judge. For now the only weight loss use of nutrigenet...

Celiac disease is a digestive disease that damages the small intestine and interferes with absorption of nutrients from food. People who have celiac disease cannot tolerate gluten, a protein in wheat, rye, and barley. Gluten is found mainly in foods but may also be found in everyday products such as medicines, vitamins, and lip balms. When people with celiac disease eat foods or use products containing gluten, their immune system responds by damaging or destroying villi—the tiny, fingerlike protrusions lining the small intestine. Villi normally allow nutrients from food to be absorbed through the walls of the small intestine into the bloodstream. Without healthy villi, a person becomes malnourished, no matter how much food one eats. Celiac disease is both a disease of malabsorption—meaning nutrients are not absorbed properly—and an abnormal immune reaction to gluten. Celiac disease is also known as celiac sprue, nontropical sprue, and gluten-sensitive enteropathy. Celiac disease is gen...

A paper was published in JAMA a few days ago ( Paynter et al, Association Between a Literature-Based Genetic Risk Score and Cardiovascular Events in Women ) showing that a genetic score based on 101 CVD related SNPs was not effective as a screening tool. So what happened to the promise of GWAS? One or two SNPs are not enough but we were told that when we get to panels of 30, 40 or more then we would see something real and useful, apparently we are not, so is it over? Is the fate for GWAS that of the candidate gene studies where initial positives were generally shown to be chance? Maybe not. But maybe this study is proving, just like with candidate gene studies, that it is naïve to think that “blind” association studies of genes with complex diseases will provide useful results – these are diseases where the causes are many-fold involving genetics, behaviour and environment, but where in general just the disease end-point and the genetics are actually measured. The Paynter paper use...