Eat well for a healthy future generation

Eat well for a healthy future generation

London (ISJ) - Mind what you eat, or your children and grandchildren may have to pay the price.

Studies have shown that parental diets, lifestyles as well as maternal care, trauma and exposure to toxins could influence the health and behaviour of their children, writes Dr Eva Sirinathsinghji of the Institute of Science in Society. In some cases, the effect may last for generations.

The findings have major implications for how we understand evolution and, from a medical perspective, how we are able to ensure the health of future generations. Recognising that through maintaining our own health, we give ourselves the potential to secure a healthy life for our children, will likely bring more success than giving into to the fate of our genes and yet-to-be-developed medical interventions to override our genetic ?faults?, Sirinathsinghji writes in an article published on the institute?s website.

The results endorse Lamarckian inheritance ? the idea that an organism can pass on the characteristics that it has acquired during its lifetime to its offspring. These show, not only can we take charge of the health of future generations, but also that mistreating our health and the environment can have much longer-lasting effects than expected. Many environmental chemicals, including pesticides and the household plastics product bisphenol A, commonly called BPA, are well known to have transgenerational effects. Diets too can have the same effects. This is of increasing concern at a time when diet-related diseases are rising globally. It serves as a further warning to people everywhere who are being increasingly exposed to Westernised processed foods high in sugars, fats, and chemicals and low in fibres and nutritional content.

In humans, epidemiological data show that malnutrition in fathers can alter the health prospects of children later in life. Much of this has been found to be mediated through a molecule classified as non-coding RNAs (ncRNA) that go on to influence epigenetic control of gene expression in the genome of offspring, with effects lasting many generations.

According to a study published in�Science,�researchers in China and the US found that a high fat (60%) diet fed to male mice resulted in offspring that by 7 weeks of age suffered impaired glucose and insulin tolerance. To find out what might be responsible for transmitting the information from father to child, they first purified total RNAs from sperm of mice fed both high-fat and control diets and injected them into zygotes. This experiment recapitulated the impaired glucose tolerance, though not impaired insulin tolerance in the offspring, suggesting that additional factors such as DNA methylation in addition to ncRNAs are required for the full inheritance of the metabolic traits.

The researchers performed global RNA sequencing to see if there were any changes in the expression of particular types of RNA species. They found that the sperm of mice on the high-fat diet were enriched for a subset of small RNAs that are 30-34 nucleotides long, deriving from one end of transfer RNAs, termed tRNA derived small RNAs (tsRNAs). Injection of just this form of tsRNA into zygotes again resulted in offspring with impaired glucose tolerance and mild or no insulin intolerance. Analysis of the sperm tsRNAs revealed a total of 10 types of modification, two of which were enriched in the sperm of mice on the high-fat diet. The significance of that is still unknown, but suggests the modifications play a role in RNA stability and/or inheritance.

The researchers then looked at global gene expression in islet cells in the pancreas of the offspring to unravel the cause of the inherited metabolic disease. They found abnormal expression of genes involved in metabolic pathways (including ketone, carbohydrate and monosaccharaide metabolisms) in offspring of males fed the high-fat diets. There were also differences in the methylation patterns (chemical tags on DNA that mediate gene expression) of 28 genes, though none of these matched the dysregulated genes, suggesting that the changes in methylation patterns were not directly related to the changes in transcriptional activity. Injecting the tsRNAs into zygotes identified that it was indeed the tsRNAs themselves that were responsible for the changes in gene expression, with their injection causing gene expression changes in metabolic regulation pathways and others including protein transport. The tsRNA sequences matched the gene promoter regions of many of the dysregulated genes, suggesting that the tsRNAs themselves are directly responsible for the perturbed gene expression.

Source: Institute of Science in Society, London


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