03 Mar Have You Got The Fat Gene?
Have you ever wondered if your genes are responsible for your weight challenges? The chances are, they may well be playing a role.
While academics have long argued over the extent to which genes affect our weight, more and more evidence is suggesting a strong connection. So have you got the fat gene?
HAVE YOU GOT THE FAT GENE?
For most of us, there is no one single ‘fat gene’ responsible for all of our weight issues. Rather, a number of different genetic polymorphisms combine to create a unique set of challenges for each individual.
A number of different genes impact our desire for food, the types of foods we desire and how our body uses those foods once we’ve consumed them. Below we’ll look a small handful of the genes that can have an effect on our fat storage and appetite. Our appetite is primarily regulated by two hormones, ghrelin (our hunger hormone) and leptin (our satiety hormone). Genes that influence the function of these hormones can make a big difference to our eating behaviour and weight control.
The good news is that understanding your unique genetics can help you understand how to optimise your diet and lifestyle to support healthy gene expression and quieten less helpful genetic tendencies. Your genes are not your destiny. As the saying goes ‘genes load the gut but environment pulls the trigger’.
As a team of nutritionists who specialise in weight loss, we regularly test our clients DNA. This enables us to truly tailored their health, nutrition and lifestyle plan to their unique biology. Find out more about our Intelligent DNA: Weight & Longevity Panel here or to buy the test, click here.
WHAT CAN OUR GENES TELL US?
Our test is the most comprehensive weight and metabolism DNA test available. It looks at over 40 genes and 50 SNPs across six pathways. These including appetite regulation, nutrient sensing, sugar and fat metabolism, cholesterol and bile, mitochondria and inflammation. Understanding your unique genetic traits means you can take a strategic approach to successful weight loss and long term weight maintenance, based on your body’s unique make up.
Below are the specific genes we test for:
Appetite Regulation: BDNF, FAAH, FTO, LEPR, MC4R, NPY, POMC
Nutrient Sensing: ADIPOQ, FOXO3, HIF1A, IRS1, PARP1, PGC1A, PPARA, PPARG, SIRT1, VEGFA
Sugar Metabolism: AMPD1, FABP2, GCK, GLUT2, IRS1, PPARG, TCF7L2
Fat Metabolism: ADRB3, CD36, CPT1A, FABP2, LPL, PLIN1, PPARA, SREBF1
Cholesterol and Bile: CYP7A1, HMGCR, LDLR, SREBF1
Mitochondria and Inflammation: CAT, CRP, FOXO3, GPX1, IFNG, IL6, NRF2, SIRT3, SOD2, TNF, UCP1/2/3
Below are a few more detailed examples of the genes we test for. These examples demonstrate how different genes can affect our weight and the specific strategies that can be implemented to quieten their expression.
MC4R – THE ‘DEATH BY BUFFET GENE’
The MC4R (melanocortin 4 receptor) gene plays a key role in regulating appetite and energy balance in the body. It drives a desire to eat more combined with a reduced metabolism. This receptor in nerve cells of the hypothalamus is triggered by leptin, the satiety hormone. This alerts our brains to the fact we are full. Mutations or variations in the MC4R gene can disrupt this signal, leading to an increased risk of obesity. It’s been referred to as the ‘death by buffet gene’ as people who have this genetic polymorphism can find it hard to stop eating once they’ve started.
Research shows that people with this genetic trait have a strong preference for high fat foods and consuming them is understood to result in a greater serotonin release. However, they typically have less of a preference for sugary foods (study: https://www.cam.ac.uk/research/news/chicken-korma-eton-mess-and-a-genetic-variant-provide-clues-to-our-food-choices). It might also be called the ‘polar bear gene’ as polar bears have inactive MC4R genes that allow them to eat as much as possible to accumulate fat during the summer! Mutations in this gene are one of the most commonly known genetic causes of monogenic obesity. We’ll discuss this in more detail later on.
HOW TO HACK A MC4R POLYMORPHISM
People with MC4R variations can find it helpful to be clear on ideal portion sizes. It’s advisable that they are mindful of their fat consumption and avoid high fat trigger foods. And avoid the all you can eat buffet!
FTO – THE ‘FAT SO’ GENE
The FTO gene is one of the most well-known genetic risk factors for obesity, and variations in this gene can affect several aspects of energy balance, including appetite, metabolism, and weight regulation. The FTO gene increases our production of ghrelin, the hunger hormone. This activates other hormones that help our brains tell us to eat. FTO gene variants result in more frequent eating and snacking. There is a general preference for calorie dense foods in general, both fats and carbs. In fact, this gene alone can account for 3kg of weight gain in a person.
HOW TO HACK A FTO POLYMORPHISM
Getting into a good mealtime routine, avoiding snacking, fasting in the evening and overnight, and taking regular exercise can help to reduce weight gain due to SNPs in this gene.
POMC – THE ‘HUNGRY LABRADOR’ GENE
Another key player in appetite is POMC (Proopiomelanocortin) which is the source of melanocortins for the MC4R receptors. Some genetic variants can reduce POMC, reducing the melanocortin hormones that help to make us feel full. Looking at the animal kingdom again, Labrador dogs lack the POMC gene, explaining their insatiable desire to continue eating.
HOW TO HACK A POMC POLYMORPHISM
People with POMC variants need to support their eating behaviour in a similar way to MC4R variants, but as it can also be influenced by the mood supporting neurotransmitter serotonin. Supplements, habits and behaviours that support serotonin production and improve mood can all be helpful.
FAT GENE EXTREMES
In extreme cases, genetic disorders can lead to significant weight issues.
Prader-Willi syndrome is a rare genetic disorder characterised by a constant sense of hunger, amongst the learning difficulties and physical and behavioural challenges associated. According to the NHS website: Prader-Willi syndrome is caused by some missing genetic material in a group of genes on chromosome number 15. This leads to a number of problems and is thought to affect part of the brain called the hypothalamus, which produces hormones and regulates growth and appetite. This may explain some of the typical features of Prader-Willi syndrome, such as delayed growth and persistent hunger, often leading to obesity.
Prader-wili is considered monogenic obesity. This is when obesity results from the mutation or deficiency of one specific gene. Most of the clients we work with come under the polygenic category where which a larger number of genetic polymorphisms each have a small effect.
TEST TO FIND OUT IF YOU HAVE THE FAT GENE
Our Intelligent DNA: Weight & Longevity Panel can identify the extent to which genetics are impacting your weight. The good news is, your genes are not your destiny. As you’ll have seen from the examples above, much can be done to ‘switch on’ or ‘switch off’ your genes. Our comprehensive test includes a consultation with a nutritionist who will talk you through your results and give you a plan tailored to your unique genetics. Click here to purchase the test or contact us for more information.