Obesity – Are Genes Destiny?

              Are genes destiny regarding the development of obesity or, is there a more nuanced set of factors that contribute to obesity? The way that that we understand obesity has moved a long way from just being told to eat less and exercise more. In this blog I would like to discuss the state of the evidence for how genetics affects weight and help you understand how this relates to your children and your family. The more we know about the intersection between our genetics and risk for obesity the more chance we have to modify our risk for both ourselves and our families. For a long time now, we have known the basic structure of DNA and we know from recent studies that weight is highly affected by heritable factors1-2. But, if our DNA hasn’t changed in the last couple of decades (it hasn’t – DNA evolution plays out over a longer timescale) then why has the rate of obesity increased so significantly?

        One factor is epigenetics. Epigenetics is the science of how individual genes get turned off and on. This has a big effect on how the “book” of our DNA is “read” by the body. If human DNA is like the book, then epigenetics is the study of why and how the book opens only on the pages that the body needs to read. This is an especially important topic for parents and families because epigenetics is starting to tell us a lot more about the way that our environment interplays with our genes, to affect our weight, our children’s weight and their children’s weight.

       Now, sometimes these changes are inherited sometimes they just occur in response the certain stimuli. And, there are times at which the genes in our bodies are ripe for turning off and on genes that affect Obesity. One of these times is the period before a baby is conceived up until that child is 2years old. Certain systems can be laid down around this time that will play out through-out a child’s life. In this time children can become pre-disposed to becoming obese through maternal and paternal “stress” and fetal programming. Several biochemical factors are at play during this period which can lead to disrupted relationships with food including increases in cortisol, insulin and cytokines.

          It’s a good time to say here, that it’s important to bear in mind just how much we still have to learn about the many, many genes related to obesity and, out of the high number of obesity related genes there has been a low prevalence of genes that singularly cause severe obesity – around 5% of severely obese children are thought to have a single gene mutation increasing their susceptibility to obesity3. What is seen most often in the scientific literature is a “polygenic obesity”4 in other words one gene alone doesn’t code for obesity but rather it takes a lot of genes saying the same thing for them to code for obesity in a person.

          Another set of circumstances that can affect weight is the micro-biome. The understanding of obesity susceptibility and the microbiome is still evolving. However, what we do know is that the micro-biome is different in those individuals who have obesity compared to those who don’t. There are plenty of factors that we know have long-term effects on the developing microbiome such as mode of birth and early anti-biotic use. Overuse of antibiotics in particular has been linked to the onset of obesity5 so I will be interested to see what comes of further research.

       As the industries of the world have found new materials to use in manufacturing, us and our families have become exposed to new chemicals. Some of which have been shown to cause obesity in animals and mice models. Again, here further research is necessary and, in terms of overall risk of being exposed to these chemicals we are well protected as consumers by regulatory bodies, and known dangerous chemicals are banned or restricted as quickly as possible.

         In conclusion, the complexity of protecting children and families from obesity is vast. Families must look at this issue holistically as there are a number of factors that we can consider to increase risk of obesity in relation to our genetics. Does it mean that we can’t change that with healthy eating and good lifestyle behaviors? Certainly not, and, if you as parents and families can support children to live life healthy lives then maybe they can change their destiny and become the healthiest versions of themselves.

References
1. Farooqi I.S. 2005 Genetic and hereditary aspects of childhood obesity. Best Pract. Res. Clin. Endocrinol. Metab. 19 3 359 74
2. Llewellyn C H, van Jaarsveld C H M, Boniface D, Carnell S, Wardle J. 2008 Eating rate is a heritable phenotype related to weight in children. Am. J. Clin Nutr, 88 6 1560 6
3. Perrone L. Marzuillo P. Grandone A. del Giudice EM. Chromosome 16p11.2 deletions:another piece in the genetic puzzle of childhood obesity. Ital J Pediatr. 36 43 43
4. Chirita Emandi, A. Puiu, M. Micle, I. Obesity in rare diseases and genetic factors in the “frequent”childhood obesity. Romanian Journal Of Rare Diseases. 2011 1 22 8
5. Podolsky SH. Historical perspective on the rise and fall and rise of antibiotics and human weight gain. Ann Intern Med. 2017;166;133-138

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Angus Milton

Nutrition Expert

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