At long last it’s looking as though researchers have now got down to the final genetic key that causes excess fat in our fat cells to be either burned off or to accumulate. If this is not disproved by other teams in the next . . . few months then this will be one of theTreatment for obesity–but not yet imminent major medical disoveries of our times,
Researchers at Massachusetts Institute of Technology and Harvard Medical School have unveiled a new pathway in our genes that control the precise human metabolism involved. It involves the workings of two genes that lie distantly along a chromosome and are called IRX3 and IRX5. It appears that these two are the master controllers as to whether the heat energy produced by, say sugar — the worst offender in our diet if too much is consumed — is actually released as body heat and then subseqeuntly radiated or remains stored as fat.
In risky individuals one of the four bases (thymine) that make up our DNA in the IRX3 and IRX5 genes is replaced by another base (cytosine). This represses the heat-releasing mechanism. If the cytosine can somehow be replaced with thymine in an individual then he or she will be able to easily control moderate increases in body fat — otherwise impossible, or only temporarily achieved by obsesity-inclined people and even then only with great discipline.
News of the breakthrough appeared in my newspaper today on the front page under a headline “Hope of jab to cure obesity” but I desisted writing about it until I’d read a more weighty account in ScienceDaily. Having read it — and absorbing what detail I was able to in what is a highly complex area of science — it confirms my initial doubts about whether it will ever be treated with an injection because this isn’t mentioned in the ScienceDaily. Rather it’s a case where it’s likely to be treatable by gene-editing — a very precise method of changing one DNA base of a gene with another — something I’ve written about before in this blog. Or, otherwise, if it can be identified in a foetus before it goes full term.
If so, then gene editing is not likely to be practical for a very long time to come and may never be applicable for all those who already suffer from obesity. Instead it may lend itself to the new technique I’ve also written about previously. This is by testing a pregnant women’s urine, testing it for specific proteins which will characterise a foetus that is carrying double-copies of faulty versions of IRX3 and IRX5 genes. If this is found to be so and the mother-to-be decides that she doesn’t want a child who will ultimately be predisposed to being overweight and consequently prone to mid-life killer diseases such as type 2 diabetes, heart diseases and various cancers then she can abort that particular foetus.
In short it’s looking as though this will have to be part of a systematic programme that I wrote about recently (“Breeding better quality children”, 15 August) that I think will inevitably come about in due course — but, would judge, not imminently.