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Metabolic diseases, inherited: Also called inborn errors of metabolism, these are heritable (genetic) disorders of biochemistry. Research by scientists from Oxford University and the University of Exeter in Britain into the genetic origins of disease, funded by the Wellcome Trust and published Friday in Science, led to the discovery of the FTO gene. For this research, the genomes of 2,000 people with type 2 diabetes were compared with the genomes of 3,000 healthy individuals. Fifty percent of people are likely to carry one high-risk copy and one low-risk, putting them at a 30-percent greater vulnerability of developing obesity. The extra weight in each case was found to come neither from greater height nor from developed muscle but exclusively from extra body fat. The scientists point out that FTO is not the only gene that will have an impact on obesity. This news will come as a relief to people who pay attention to their diet -- and who cannot understand with their eating and exercise habits why they should be carrying extra weight -- that their genes may be responsible.
So in this spring season when there's no reason to bypass the produce aisles and head for the ready-made food shelves in the supermarket, think green.
Out shopping, grab bunches of vegetables that are in their infancy, like broccolini, the smallest french beans, snow peas and more, and steam them just until they've lost their stiffness and still have a bit of crunch.
Then toss them in a glug of excellent olive oil and sprinkle with a pinch of sea salt and freshly ground black pepper.
For the protein, per serving lay two slices of prosciutto ham, then a 4-ounce fillet of firm white fish on a piece of greaseproof paper large enough to wrap around and enclose it. Put a couple of fresh springs of tarragon on top and two or three thin slices of lemon on that, season to taste, then bring any of the ham round and over the fillet, fold up the paper tightly to close, then microwave for 4 minutes for a 1-inch thick fillet, or until opaque.
Serve on top of a mixed mound of the steamed vegetables and relish the flavor and the start of a new way of life.


Diseases such as type 2 diabetes, Crohn’s disease and even smoking addiction has been passed on to us by our ancestors.
Researchers have discovered that the modern human population carries more than a fifth of archaic Neanderthal human DNA.
The two separate human subspecies co-existed on earth thousands of years ago, until the Neanderthals became extinct around 30.000 years ago. This finding allows scientists to study over 20% of the Neanderthals genomes without having to extract the genetic material from fossils.
The researchers found that non-Africans carried 1 to 3% Neanderthal DNA, but the total amount in current humans reached about 20%. The Neanderthal genes that live on today, make keratin and protein used for the skin, nails and hair. Professor Chris Stringer, a leading expert in human origins at London’s Natural History Museum said the findings added a twist to the debate about how early humans related to the Neanderthals. Examples include albinism, cystinuria (a cause of kidney stones), phenylketonuria (PKU), and some forms of gout, sun sensitivity, and thyroid disease. It's the main cause of heart disease, type 2 diabetes and cancer and has been described as a greater danger than smoking, alcohol and poverty.
They established that particular versions of FTO appeared more frequently among people with type 2 diabetes.
They were found to have two copies of the high-risk version and to carry an average of 7 pounds excess weight, with 15 percent more body fat.
Nor does inheriting a variant of the gene automatically mean that a person will become overweight.
It would be a mistake for anyone carrying more body fat than they should to persist in their present poor habits while waiting for some drug to come along that will magically make them thin and healthy.


Neanderthals have been dead for tens of thousands of years, but their genetic code still lives on.
Scientists have compared genetic variants of the DNA of 176 people from sub-saharan Africa, a toe bone from a 50,000 year old Neanderthal woman and 846 people from non-African heritage. These are only a very few of the hundreds of known inborn errors of metabolism. Advances in the diagnosis and treatment of inborn errors of metabolism have improved the outlook for many of these conditions so that early diagnosis, if possible in infancy, can be helpful. With the lowest danger of becoming obese are the 34 percent of people who have two low-risk copies.
We were one of the first groups to identify the role of the phospholamban gene in determining QT interval in the general population and showed that a combined risk score using 11 of the QT-associated loci only explain about 10% of the heritability of QT. Curious as to whether FTO had an influence upon obesity, they tested their hypothesis on a vastly increased sample of 37,000 people.
There is a massive -- the word is deliberately chosen -- difference between 7 pounds excess weight and 20, 50 and 100-plus pounds excess weight.
We are now involved in a much larger collaboration – the QT Interval International Consortium of Genome-wide Association Studies (QT-IGC). We have previously shown that NOS1AP gene variants play a role in modulating QT intervals in healthy subjects, and other groups have shown that severity of presentation in LQTS is also modulated by NOS1AP variants. We have recently identified common variants in 22 loci, which are associated with QRS duration and cardiac ventricular conduction.
As part of the Cardiovascular Trait Consortium we have been able to nominate a list of genes we are most interested in working on, mostly selected based on published and unpublished Genome Wide Association Studies (GWAS) for which mutant mice will be made at Harwell.



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