Altering (gene) Behaviour

Our life depends upon a combination of our very own chromosomes and our environment (apart from all the events that happen and the choices we make).

But while the chromosomes with their genes (genome) are considered as the blueprint of life, many of those life experiences — the foods we eat, or the toxins we’re exposed to — indirectly affect the genes and tell them what to do.

The cause is the epigenome, a code of chemical markers, attached to genes that are being composed from the products we ingest. They act by turning off some genes and let others do their work, like a kind of traffic lights which are switched on to go or stop. Some of the epigenome is stable over generations others can change quickly; meaning lifestyle choices such as diet and drug abuse could have lasting effects on how our own body works or the bodies of our offspring.

A study published in 2009 on epigenetics and autism found that some children with autism had markers turning off a gene needed to respond to a certain hormone important in social interaction, suggesting that turning off that one gene could cause the social problems people with autism have. In fact, nowadays it has been discovered that in autistic people more than 400 markers differ to normal controls. Interestingly the differences are mainly seen at the location of genes known to play a role in neurosocial behaviour.

Twins are a good example of how environment can affect our genes. Identical twins have identical genes, but sometimes one twin has autism or cancer while the other remains healthy. One of the conclusions particularly concerning autism is, that the critical times in setting the traffic lights are considered the prenatal and neonatal development (apart from puberty where a lot of physical changes take place, too). Studies also show that as twins’ age, their epigenomes become less and less alike, caused by differences in behavior.

The chemicals that make up epigenetic markers ultimately come from the diet. Folic acid, for example, is needed to produce the markers that turn off many unwanted genes.

The classic experiment published in 2003 showed how diet can affect these markers. It showed that when pregnant mice eat lots of folic acid and other vitamins, they have mostly lean, brown offspring. If those mothers ate a diet without folic acid and instead they had more fat, yellow offspring resulted, which were prone to diabetes.
The genome of the offspring was the same — but the mother’s diet determined how they could use those genes.

Another researcher used the same types of mice to examine how Bisphenol A, a toxin common in plastics, affects the epigenome of unborn mice. He reported in a paper in 2007 that mice whose diet included Bisphenol A produced more fat, yellow offspring, but eating folic acid counteracted those negative effects.
Of course I am not saying that folic acid is a miracle drug.  Neither have I touched upon the subject of the problem of drawing conclusions from animal studies, nor of the question of vulnerability, because it is obvious that not everybody develops autism, for example.

But it is interesting and worrying at the same time that ingesting food can stop us making lifestyle choices because it has caused ill health through interfering in the communication of our very own blueprint with environment.

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