FAT? – I’m Not To Blame It’s My Genes!

Reading Time: 6 minutes

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.[1] 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. [2],[3]

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.[4] 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.[5] 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.[6]

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[7] 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.[8] 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.

Father and Son have multiple environmental and genetic factors that will play a role in determining their body mass.

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.


[1] Katzmarzyk PT, Janssen I, Ardern CI (2003) Physical inactivity, excess adiposity and premature mortality. Obes Rev 4: 257–290. View Abstract

[2] 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

[3] 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

[4] 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

[5] Llewellyn CH, van Jaarsveld CH, Johnson L, Carnell S, Wardle J. Nature and nurture in infant appetite: analysis of the Gemini twin birth cohort. Am J Clin Nutr. 2010 Mar 24. View Abstract

[6] Johnson, P., & Kenny, P. (2010). Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats Nature Neuroscience DOI: 10.1038/nn.2519

[7] Watson J.D. and Crick F.H.C. (1953). “A Structure for Deoxyribose Nucleic Acid” (PDF). Nature 171 (4356): 737-738 View PDF

[8] 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

Previous Post
Sparkling Water Saves Lives!
Next Post
Multivitamins & Breast Cancer – Is It Too Little Rather Than Too Much?

4 Comments. Leave new

  • I think that this FASEB article illustrates just how fragmented the field of metabolic research is. Having read ‘Good Calories Bad Calories’ by Gary Taubes recently, his explanation of why sugar (or rather carbohydrate) leads to obesity is much more compelling than the ‘thrifty gene’ concept.

    In short, carbohydrate consumption drives insulin release. This promotes fat storage and impedes conversion of stored triglycerides to free fatty acids for use as fuel.

    This leads to a form of ‘internal starvation’ where the body’s cells are lacking in energy due to the inability of stored fats to flow freely, and the tendency for high circulating levels of insulin to dump fuel into fat cells.

    Therefore, the fat person experiences a lack of motivation to move as the body/brain conserves fuel which is sees as scarce. At the same time, it generates hunger sensations to replenish the ‘missing’ energy stores.

    There’s no doubt in my mind that sugar and processed carbs are at the root of the obesity problem, but fat in the diet is not. Hence why people on law carbohydrate diets lose weight, even when fat and protein calories are unlimited.

    I used to be of the mindset that blamed obese people for their own situation. I now believe their metabolism is ‘broken’ by carbohydrate ingestion and have seen it cured many a time by reduction of carbs in the diet.

    • The role of carbohydrates in gene expression and risk of unwanted fat deposition is becoming better understood, but other more insidious effects are better elucidated. The role of dietary carbohydrate consumption in the development of insulin resistance, a precursor to diabetes has many negative consequences, even in the absence of weight gain. [1]
      An unpleasant manufacturing deceit to squeeze sugars into foods such as breakfast cereals is to use different forms By using 4 – 5 different structural forms it is possible not to list sucrose as the number one ingredient in breakfast cereals. The effect is for manufacturers to compound the sugar/salt/fat combination identified as the most likely to alter gene expression and addiction risk.
      Carbs are as addictive as fats and the role of food selection and consumption is as affected by desire as it is by comprehension. One pattern we are all aware of is that humans are uniquely capable of amassing a long list of explanations for what is, in most cases a simple selection and ingestion matter.
      However, there are an increasing number of people of all ages inadvertently following a misguided approach to food selection based on mass opinion rather than individual requirements. It must be obvious even to the most hardened – ‘you can get all you need from your diet’ evangelist that unique phenotypical variations in gene codes and expressions will combine with lifestyle choices to produce confounding outcomes – in this case unavoidable weight gain.

      [1] Ferrannini E, Balkau B, Coppack SW, Dekker JM, Mari A, Nolan J, Walker M, Natali A, Beck-Nielsen H; RISC Investigators. Insulin resistance, insulin response, and obesity as indicators of metabolic risk. J Clin Endocrinol Metab. 2007 Aug;92(8):2885-92. Epub 2007 May 15. View Full Article

  • Dear Micheal

    while I have read with interest your review, particularly because I am convinced that individual differences can play a role in obesity, I would very much like to understand a little bit more about your claim that certain supplements (e.g. B6 etc) could be beneficial for some obese/overweight people to break the circle of overeating.

    Could you please elaborate on this?

    • Michael Ash
      May 5, 2010 1:55 pm

      Hello Andrea
      I briefly mentioned the role of specific nutrients and also tagged a previous post on a study related to a multi vitamin product that had assisted with weight management. This is an area in which your role as a practitioner can make a big difference, specifically you can add nutrient concentrates to either support or suppress key pathways. I mentioned B6, although single nutrient use would not be recommended for this therapy, as B6 has a strong role in digestive function and also in thyroid support, as well as blood sugar management.

      Vitamin B6 is a coenzyme involved in the metabolism of carbohydrates, fats, and proteins and this particularly helps dieters. Also responsible for the manufacture of hormones, red blood cells, neurotransmitters, enzymes, and prostaglandins and serotonin an important neurotransmitter.

      I hope that the post did not indicate that a random use of single nutrients would solve weight management problems, rather it was a suggestion of nutrients used by the body in the production of neurotransmitters involved in the balance of dopamine.

      A recent trial using a proprietary combination of dietary strategies and supplements called the Control-It strategy was introduced into the UK after a very successful start in clinics in the USA. The benefits are consistent weight loss, better body mass management and overall health benefits beyond that experienced by weight loss alone. You may wish to visit the information here.


Leave a Reply

Your email address will not be published. Required fields are marked *

Fill out this field
Fill out this field
Please enter a valid email address.
You need to agree with the terms to proceed