The people standing athwart epigenetics and yelling “Stop!” probably won’t like epigenomics either.
Obesity may be written not only in the genes, but also on top of them. One of the largest studies so far to probe the human epigenome — the collective name for the patterns of chemical groups that adorn DNA sequences and influence their activity — has found some tags that are linked to differences in body mass index (BMI).
Chemical alterations in a gene thought to be involved in metabolism were identified in the blood and fat cells of more than 2,500 people, scientists reported last month. The work, led by Nilesh Samani at the University of Leicester, UK, is part of an emerging line of research that is probing disease through epigenome-wide association studies (EWAS). Those in the field hope that because many epigenetic changes are influenced by the environment, such studies will reveal mechanisms of disease that have remained elusive. However, many scientists remain sceptical.
Obesity is a stubborn, growing problem in non-starving societies. Billions can be made off diets and treatments that don’t really work. Treatment that did work would be a far smaller industry. But seriously, we need to know more about why some people, surrounded by an abundance of food, don’t eat so as to become obese, but close relatives do. Maybe they have mostly the same genes but are getting different sets of signals. So we shouldn’t be looking for a special “fat gene” but a signalling pattern about when and how much it feels right to eat.
That said, it’s a long road and we don’t know the territory at all well:
Stephan Beck, a medical genomicist at University College London, thinks that epigenomic epidemiology is at the same stage genomic epidemiology was at eight years ago, when most studies were small and rarely identified the same genetic variants for any one disease. That changed in 2007, when the Wellcome Trust Case Control Consortium, an effort by research groups to identify genetic variants linked to common diseases, set standards for GWAS that emphasized the importance of large numbers of patients and reproducibility.
Beck sees signs that EWAS are headed in the same direction. For example, in the past few years several studies have reproduced the finding that a gene called AHRR is epigenetically modified in the blood cells of adult smokers and their newborn children. And some epigenome studies — including the BMI research1 — now verify discoveries made in one group of patients in separate cohorts of the same study. From More.
As with obesity, why do some people become addicted to nicotine, and relatives—surrounded by opportunities to buy and smoke it—never do. Or do it once or twice, get bored, and quit without damaging their lungs. Is there a “nicotine gene” that one relative happened to get and the other happened not to? Or will a science-based answer sound more like epigenomics and less like the selfish gene?
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See also: DNA doesn’t even tell teeth what they should look like
“If DNA really rules, why did THIS happen?”, where human neurons, transplanted into a mouse, had a mouse morphology.
Jonathan Wells: Far from being all-powerful, DNA does not wholly determine biological form (Mutate a fruit fly embryo in every possible way, and observe only three possible outcomes: a normal fruit fly, a defective fruit fly, or a dead fruit fly.)
Jonathan Wells: We are far from a good theoretical model of organisms’ development (We are far from having a complete list of the components, as a matter of fact.)