FAT? – I’m Not To Blame It’s My Genes!
Michael Ash BSc(Hons) DO ND FDipION reviews a selection of papers exploring the intersection between our genetic code and the style of food ingested in ever increasing amounts, in which fat and sugar make up the dominant components.
It’s clear from numerous studies that a sedentary lifestyle and a diet high in fat and sugar have profound effects on human mortality and morbidity through adverse weight gain. The enormous human genome project, started in 2000 has also thrown up a number of markers in our approximately 21,000 genes related to an historical adaptive need to store fat when food was scarce and starvation an ever present threat. Some have interpreted this by saying that the reason they are obese or cannot lose weight is down to their genes, and that this may in turn abrogate them from actively altering lifestyle patterns, others have questioned the accuracy or validity of this causal relationship. ,
Certainly people metabolise food differently and some people gain weight more easily than others. Nonetheless, anyone placed in a food-rich environment that encourages inactivity will gain weight, whatever fat genes the person may have. At the same time, in nearly all environments, highly motivated people can maintain lower weight levels. This demonstrates that social pressure, self-control, specific situations – even seasonal variations – combine with physical make-up to determine weight.
A study in the April edition of the FASEB Journal may throw some explanatory light on the question of nature Vs nurture in relation to body mass management. Supported by another study in the Am J Clin Nutr out in March this year a causal relationship between genes, appetite and food selection is beginning to emerge. Some may say this is just common sense but clarity of explanation has the opportunity to offer a clear strategy for food and weight outcomes.
Admittedly the FASEB group examined mice not humans but their study revealed a pathway, that really makes sense. Eating a diet high in fat and sugar causes an increased gene expression in those genes long part of our makeup and designed to store fat, in anticipation of a lean winter. Those fat and sugar laden diets available on any high street, and many homes actually get you twice; conversion of the foods to energy without tissue storage is one problem, the other is the meals are programming your genes to train you to become highly efficient two legged fat repositories.
The receptor involved is the kappa opioid receptor, and once activated it appears to promote increased fat storage useful in the past when food delivery was inconsistent. Another receptor also linked to addiction was revealed in Nature Neuroscience where researchers from Scripps discovered that after a period of time being fed on high fat and sugar foods rats would ignore significant deterrents including electric shocks to get their daily ‘fix’ of junk food. The stimulation centres in their brain became conditioned to the junk food high, the identified site is called the dopamine D2 receptor. D2 reacts to the neurotransmitter dopamine released naturally in the presence of pleasurable experiences such as sex, cocaine and it seems certain junk food.
The heavier the rats became the greater their desire to overeat.
High corn fructose syrup, a very common form of sweetener found in junk food (up to 40% of USA caloric sweeteners) was shown in another rat based experiment to increase the abdominal girth and elevate triglycerides, suggesting the form of sugar used also has direct implications.
Could this be the unholy mix of genes and environment colluding to benefit the manufacturers of fatty, sugar rich foods, and contributing to the rapid loss of leanness across wide swathes of the western world’s population? Watson and Crick may have described the double helix of DNA but food manufacturers have learnt how to manipulate gene expression to their commercial advantage without the need for the human genome experiment to confirm what many have described for years. Patterns of behaviour in people suffering from obesity are consistent with addictive hedonic behaviour and altering them may require strategies developed for drug abuse resolution.
From a nutritional therapy perspective the use of food concentrates such as B6, l-phenylalanine, Mg, 5-HTP and fatty acids may be considered as a step wise intervention into assisting with relevant receptor management along with food and lifestyle counseling and to help prevent relapses in dietary selection. I also recently described how the use of a multivitamin and mineral contributed to increased weight loss in women.
 Herbert A, Gerry NP, McQueen MB, Heid IM, Pfeufer A, Illig T, Wichmann HE, Meitinger T, Hunter D, Hu FB, Colditz G, Hinney A, Hebebrand J, Koberwitz K, Zhu X, Cooper R, Ardlie K, Lyon H, Hirschhorn JN, Laird NM, Lenburg ME, Lange C, Christman MF. A common genetic variant is associated with adult and childhood obesity. Science. 2006 Apr 14;312(5771):279-83. View Abstract
 Scuteri A, Sanna S, Chen WM, Uda M, Albai G, Strait J, Najjar S, Nagaraja R, Orrú M, Usala G, Dei M, Lai S, Maschio A, Busonero F, Mulas A, Ehret GB, Fink AA, Weder AB, Cooper RS, Galan P, Chakravarti A, Schlessinger D, Cao A, Lakatta E, Abecasis GR. Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits. PLoS Genet. 2007 Jul;3(7):e115. View Full Paper
 Czyzyk TA, Nogueiras R, Lockwood JF, McKinzie JH, Coskun T, Pintar JE, Hammond C, Tschöp MH, & Statnick MA (2010). kappa-Opioid receptors control the metabolic response to a high-energy diet in mice. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 24 (4), 1151-9 PMID: 19917675
 Cottone P, Sabino V, Roberto M, Bajo M, Pockros L, Frihauf JB, Fekete EM, Steardo L, Rice KC, Grigoriadis DE, Conti B, Koob GF, Zorrilla EP. CRF system recruitment mediates dark side of compulsive eating. Proc Natl Acad Sci U S A. 2009 Nov 24;106(47):20016-20. Epub 2009 Nov 9. View Abstract
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Thursday 19th November 2015
This evening seminar will take the gathering understanding of the role of our mitochondria as sentinels of metabolic and immune dysfunction and how lifestyle including food and food concentrates are able to either increase or decrease their viability. As our understanding of the molecular influence of food continues to grow, significant understandings become all the more important in our delivery of advice and recommendations. You may think that this subject is too esoteric or removed from every day clinical life, but never has an area of application been more relevant to almost all the clients or people that you support. Delivered in an easy to appreciate format with clinical applicability, we feel confident that this will enhance your confidence and improve your outcomes. We will be recording the event for people attending and those unable to travel..Click for further information
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