Certain people can be more obese than others, the difference is mainly due to being genetically predisposed to obesity. Associated genes within the genome of our bodies can be linked to our BMI (body mass index) and can predispose people to obesity.
Higher obesity rates correlate with higher metabolic diseases (e.g., diabetes, cholesterol, blood pressure, cardiovascular diseases, etc). Obesity is an uncontrolled medical condition locking the body into a state of constant uncontrolled hunger, cravings, and hormone imbalances.
Genetic obesity is rare and directly linked to a person’s DNA (deoxyribonucleic acid), or their genetic blueprint that describes who they are on a biological level. If our genes are forcing us to overeat, it is because these genes are familial (passed down through people in our family generations).
Obese pregnant women can have a great impact on their child, putting them at risk to also become obese (developing a metabolic disease). The only effective treatment options for genetic obesity today include bariatric surgery. Contact us today.
What is genetic obesity
Genetic obesity is when a person has an excessive amount of body weight and experiences uncontrolled eating due to having a genetic mutation in their DNA. A mutation is a change that occurs within a gene, making it unable to normally function.
- Genes are functional units of DNA, which contain instructions for our individual growth and development.
- Genetics works to determine hunger hormone levels (e.g., ghrelin) released into the bloodstream in addition to how the brain chooses to interact with hunger hormones.
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Our genes impact our hormones. Digestive system hormones such as ghrelin, GLP-1 (prevents appetite) and peptide YY (signals satiety/fullness) alert the brain when nutrient levels become low. Leptin (from fat) signals to the brain regarding energy levels and available fat storage. Food intake is controlled by the brain’s neuropeptides (neuropeptide Y; neurons or brain cells), acting in response to bodily hormonal signals.
- Ghrelin (responsible for hunger) is highly correlated with obesity.
- To stimulate more fat storage in the body, ghrelin increases when leptin levels are low, telling a person it is time to eat or else the body will resort to using its fat storage for energy when carbohydrate levels become very low.
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Genetic causes of obesity
The effects of genetic obesity start in childhood, cause a person to experience uncontrolled hunger and a lack of satiety (fullness), continuing throughout a person’s life. There are a large number of obesity susceptibility genes (52+).
The most common individual genes that can be responsible for causing genetic obesity in people include:
- POMC: proopiomelanocortin (deficiency); impacts body weight by inducing strong hunger sensations uncontrolled by satiety. POMC gives instructions to the MC4R pathway in the brain.
- PCSK1: proprotein convertase subtilisin or Kexin type 1; can also cause POMC deficiency and controls the synthesis of insulin.
- MC4R: melanocortin-4, a receptor pathway that regulates hunger and is linked to genetic obesity.
- PWS: Prader-Willi syndrome causes feeding issues, endocrine issues/ people grow to a shorter height, developmental delay, adrenal problems, etc.
- LEPR: leptin receptor (deficiency); Monogenic (this is the only gene affected when deficient), a rare morbid obesity disease; leptin receptor protein regulates body weight by allowing people to feel full after eating. A LEPR deficiency results in uncontrolled hunger and a lack of feeling full.
- BBS: Bardet-Biedl syndrome; can cause vision impairment, growth of additional fingers/toes, kidney problems, learning disabilities, or even delayed puberty.
- ALMS1: Alstrom syndrome causes signal disturbances in the MC4R pathway; patient symptom manifestation includes a shortened height, vision/hearing impairment, liver/kidney disease, dilated heart muscle, etc.
- PPARG: peroxisome proliferator activated receptor gamma; increases fat development and lipid uptake.
- PTEN: phosphatase and tensin homolog; controls the rapid increase in the number of cells present in the body (increases risk of cancer).
- SIM1: single minded homolog 1 (loss of function); promotes energy balance.
- FTO: fat mass and obesity susceptibility gene or “the fat gene”; increases food intake and contributes to a higher BMI. People can even have two copies of this gene exaggerating obesity.
- ADIPOQ: adipocyte, C1q, and collagen domain-containing; made by fat tissue and increases energy output.
- INSIG2: insulin induced gene 2; controls synthesis of fatty acids and cholesterol.
Does genetics play a role in obesity
Yes, genetics can affect obesity, especially when shared variants or mutations exist within family members. Only 2-15 % of all obese individuals are impacted by genetic obesity. Genes can influence the amount of body fat people have, where the fat is stored in the body, and food choices (preferred tastes).
Genetics and obesity: Facts vs Myths
One myth surrounding genetic obesity is that it can be cured with minor lifestyle changes, while one genetic obesity fact is that bariatric surgery has been shown to be the most effective treatment for it.
- Genetically obese patients are a distinct group of people affected by obesity who commonly exhibit severe obesity and cannot expect recovery by less invasive weight loss methods (e.g., diet or exercise).
|Genetic Obesity Myths||Genetic Obesity Facts|
|There’s only one kind of bariatric surgery, which is gastric bypass.||There are several different bariatric surgery options such as the gastric sleeve, gastric bypass, and the duodenal switch.|
|Genetic obesity is a hoax. Obesity is only influenced by our lifestyle choices.||Obesity is a multifactorial illness, caused by lifestyle choices, nutrition and to some degree, our genes. Genetic obesity has been scientifically proven to be monogenic (one gene is impacted) or polygenic (more than one gene is impacted) in nature.|
|Genetically obese people can lose weight the same way anyone else can. No need for surgery!||Genetically obese people are a minority of the obese population whose familial genes predispose them to obesity. Currently, surgery has been the only effective option for them.|
|Genetically obese and obese people tend to physically be around the same size.||False, the majority of genetically obese patients tend to be much larger than obese patients and considered morbidly obese (BMI 40+). Obesity has a BMI of 25-35 kg/m2.|
|Genetically obese people are irresponsible and just make poor eating decisions.||False, genetically obese people have hormones in their bodies that are genetically programmed to be imbalanced, causing stronger hunger sensations and an inability to achieve satiety (fullness).
Their brain is set to believe their body is in starvation mode. Uncontrolled hormones do not allow them to control their eating decisions.
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Genetic obesity treatment options
Currently, treatment options for genetic obesity include bariatric surgery because it has been proven the most effective.
Other previous attempts of pharmacological drug therapeutics aimed at suppressing appetites, such as Sibutramine or Meridia (a monoamine reuptake inhibitor) have been FDA withdrawn in 2010. Since Meridia caused high risk cardiovascular issues (posed a 16% higher risk) in hypothalamic obesity.
Bariatric surgery for genetic obesity
Genetic obesity is often considered a life-threatening form of obesity since it tends to cause severe or morbid obesity, where bariatric surgery has been helpful. The only available last resort treatment for many patients who suffer genetic obesity has been bariatric surgery.
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Gastric bypass for genetic obesity
Gastric bypass has been successful in treating more MC4R genetic mutations than gastric sleeve surgery. MC4R has a 0.5-5.8 % prevalence in the genetic obese. One case showed 76% long-term weight loss in a 5-year follow-up of an MC4R patient after having a gastric bypass.
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Gastric sleeve for genetic obesity
Only two cases of genetic obesity in BBS patients have been studied recently for gastric sleeve results.
- In a 2020 study, a female (age 37) reported in a 3-year follow-up after gastric sleeve surgery that her BMI decreased to 27.5 kg/m2 (from 40.8 kg/m2!). This is a 32.6% BMI reduction.
- Another study reported a BBS boy (age 14) experienced a 28% weight loss in body weight after a year of gastric sleeve surgery.
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Genetic obesity and bariatric surgery success rate
Much of the success obtained by bariatric surgery in treating genetic obesity comes from the fact it fixes their hormone levels enough to alter their brain’s response to better control eating.
Overall, when looking at success rates of bariatric surgery and genetic obesity, it is important to understand that each individual affected by genetic obesity may suffer monogenic obesity or polygenic obesity. Recent studies aim at analyzing monogenic forms, targeting the results for only one affected gene.
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A 2019 study analyzed results for a few years after gastric sleeve surgery for 18 morbidly obese female patients with genetic obesity (involving only PTEN).
- 1 year after surgery- patients reported a 39.4% total weight loss.
- 2 years after surgery- patients reported a 48.8% total weight loss.
- 3- years after surgery, patients reported 44.9% (this decrease is likely due to some ghrelin levels rising after 2 years from surgery).
A study for 53 females with a PTEN mutation analyzed their change in body weight after one year from different bariatric surgeries.
- 74% of the (53 total) females had a gastric bypass and reported a 32.7% mean reduction in body weight.
- 26% of females had gastric sleeve surgery and reported a 62.8% mean reduction in body weight.
Final Words: Bariatric surgery to treat genetic obesity – Yes or No?
Yes, bariatric surgery can directly benefit genetic obesity. People say “you are being irresponsible with your health”. They say “others have lost weight naturally, why can’t you?”. They say “if you tried harder, you could lose weight on your own” or “my friend lost 50 pounds just 3 months after having a baby, what is your problem?”. We say “they” were wrong.
Making a physical change to our stomach’s size and function via bariatric surgery can really change our future eating habits, leading to long-term weight loss success. You deserve more than just short-term weight loss and you are more than just a number on the scale.
Because you deserve to live an active lifestyle like anyone else, because your family still needs you, because you deserve life happiness and satisfaction, contact Jet Medical Tourism® today to find out how you can take that first step!
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- Jet Medical Tourism®. Gastric Bypass Surgery (RNY or Roux-n-Y). 2020. Web. Accessed: 5. Nov, 2020. https://jetmedicaltourism.com/gastric-sleeve-surgery/
- Misra, A., & Basu, S. From genetics to bariatric surgery and soda taxes: Using all the tools to curb the rising tide of obesity. 2020. PLoS medicine, 17(7), e1003317. https://doi.org/10.1371/journal.pmed.1003317
- Food and Drug Association, FDA. FDA Drug Safety Communication: FDA Recommends Against the Continued Use of Meridia (sibutramine). 2010. Web. Accessed: 5, Nov. 2020. https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-fda-recommends-against-continued-use-meridia-sibutramine
- Vos N, Oussaada SM, Cooiman MI, Kleinendorst L, Ter Horst KW, Hazebroek EJ, Romijn JA, Serlie MJ, Mannens MMAM, van Haelst MM. Bariatric Surgery for Monogenic Non-syndromic and Syndromic Obesity Disorders. Curr Diab Rep. 2020 Jul 30;20(9):44. doi: 10.1007/s11892-020-01327-7.
- Centers of Disease Control and Prevention, CDC. Genes and Obesity. 2013. Web. Accessed: 5, Nov. 2020. https://www.cdc.gov/genomics/resources/diseases/obesity/obesedit.htm#:~:text=Rarely%2C%20obesity%20occurs%20in%20families,people%20in%20various%20ethnic%20groups.
- Cooiman, M. I., Kleinendorst, L., van der Zwaag, B., Janssen, I., Berends, F. J., & van Haelst, M. M. (2019). Genetic analysis in the bariatric clinic; impact of a PTEN gene mutation. Molecular genetics & genomic medicine, 7(6), e00632. https://doi.org/10.1002/mgg3.632
- MacKintosh, M. L., Derbyshire, A. E., McVey, R. J., Bolton, J., Nickkho-Amiry, M., Higgins, C. L., Kamieniorz, M., Pemberton, P. W., Kirmani, B. H., Ahmed, B., Syed, A. A., Ammori, B. J., Renehan, A. G., Kitchener, H. C., & Crosbie, E. J. (2019). The impact of obesity and bariatric surgery on circulating and tissue biomarkers of endometrial cancer risk. International journal of cancer, 144(3), 641–650. https://doi.org/10.1002/ijc.31913