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As heritable as height

Heritability means how much of the difference between people comes down to genes. Here it is for obesity, next to two things nobody blames you for. Tap any of the three.

How much of it is genes

Twin studies. Tap a row.
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Nobody picks the size of their body any more than they pick their height. Both are set largely by the genes you were born with.

How many genes they have found

There is no single obesity gene. There are thousands of them, and each one on its own is tiny. Every one of these studies was done in people, not animals, and they needed hundreds of thousands of people at a time because the effects are so small.

Why does it say spots rather than genes? Think of your DNA as a neighborhood. It runs street after street, and the genes are the houses along them. Every house has an address.

A search like this does not knock on doors. It compares hundreds of thousands of people, narrows down which addresses the difference seems to be coming from, and writes those addresses on a list. That is what a spot is. An address, not a name.

So 941 spots means 941 addresses. Somebody still has to go to each one and work out which house is actually responsible, which is much slower work. Of those 941, 138 have had a house named so far. The rest are addresses with nobody's name on them yet.

GLP-1 Strong

Facts are useful when you have to speak up for yourself

Weight stigma turns up in exam rooms and at family dinners. Knowing what the evidence actually says gives you something specific to say back.

The STRONG framework is a step by step way to respond to it while it is happening: Stop, Think, Respond, Offer Clarity, Navigate, and Grow stronger together. Offering clarity is the step where facts like the ones on this page get used.

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FAQ

Sources

10 references

Every figure above was read from the study that reported it. One thing worth knowing: almost all of this research was done on people of European ancestry, and genetic scores are known to work less well for everyone else. The researchers say so themselves.

  1. Silventoinen K, Jelenkovic A, Sund R, et al. Differences in genetic and environmental variation in adult BMI by sex, age, time period, and region: an individual-based pooled analysis of 40 twin cohorts. The American Journal of Clinical Nutrition. 2017;106(2):457–466. doi:10.3945/ajcn.117.153643. The obesity bar: heritability of BMI 0.77 in men and 0.75 in women aged 20–29, falling to 0.57 and 0.59 in the oldest groups, across 140,379 complete twin pairs in 20 countries. Also the source for heritability being much the same across regions and across the decades from the 1940s to the 2000s.
  2. Jelenkovic A, Hur YM, Sund R, et al. Genetic and environmental influences on adult human height across birth cohorts from 1886 to 1994. eLife. 2016;5:e20320. doi:10.7554/eLife.20320. The height bar: 0.69–0.84 in men and 0.53–0.78 in women across 143,390 complete twin pairs. Same consortium as source 1, modelling both traits the same way in largely the same cohorts, which is what makes the height comparison a like-for-like one.
  3. Willemsen G, Ward KJ, Bell CG, et al. The concordance and heritability of type 2 diabetes in 34,166 twin pairs from international twin registers: the discordant twin (DISCOTWIN) consortium. Twin Research and Human Genetics. 2015;18(6):762–771. doi:10.1017/thg.2015.83. The type 2 diabetes bar: 72 percent (95% CI 61–78) across 34,166 same-sex twin pairs aged 45 and over.
  4. Elks CE, den Hoed M, Zhao JH, et al. Variability in the heritability of body mass index: a systematic review and meta-regression. Frontiers in Endocrinology. 2012;3:29. doi:10.3389/fendo.2012.00029. Why the chart uses twin studies only, and why its obesity figure is higher than the 40 to 70 percent often quoted. Across 88 twin estimates in 140,525 twins, BMI heritability ranged 0.47 to 0.90, against 0.24 to 0.81 from 27 family studies. Averaging the two designs produces a number that matches neither.
  5. Locke AE, Kahali B, Berndt SI, et al. Genetic studies of body mass index yield new insights for obesity biology. Nature. 2015;518(7538):197–206. doi:10.1038/nature14177. The 97 loci, found in up to 339,224 individuals.
  6. Yengo L, Sidorenko J, Kemper KE, et al. Meta-analysis of genome-wide association studies for height and body mass index in ~700,000 individuals of European ancestry. Human Molecular Genetics. 2018;27(20):3641–3649. doi:10.1093/hmg/ddy271. The 941 near-independent variants associated with BMI, which together explain about 6 percent of the variation in an independent sample, the score built from them correlating about 0.22 with actual BMI, and 138 genes prioritized.
  7. Khera AV, Chaffin M, Wade KH, et al. Polygenic prediction of weight and obesity trajectories from birth to adulthood. Cell. 2019;177(3):587–596.e9. doi:10.1016/j.cell.2019.03.028. The score built from 2.1 million common variants and tested in more than 300,000 people, which is the figure behind the third step of the gene count.
  8. Papandonatos GD, Pan Q, Pajewski NM, et al. Genetic predisposition to weight loss and regain with lifestyle intervention: analyses from the Diabetes Prevention Program and the Look AHEAD randomized controlled trials. Diabetes. 2015;64(12):4312–4321. doi:10.2337/db15-0441. The answer to whether these genes mean you are stuck. 91 established obesity-predisposing loci tested against weight loss across four years and against regain, in 1,824 Diabetes Prevention Program and 3,906 Look AHEAD participants. Most were not associated with weight loss or regain, directly or through any interaction with the lifestyle programme.
  9. Kilpeläinen TO, Qi L, Brage S, et al. Physical activity attenuates the influence of FTO variants on obesity risk: a meta-analysis of 218,166 adults and 19,268 children. PLoS Medicine. 2011;8(11):e1001116. doi:10.1371/journal.pmed.1001116. The FTO variant raised the odds of obesity by 1.22 per copy in physically active adults against 1.30 per copy in inactive adults, reported as the association being attenuated by 27 percent. No such interaction was found in the children studied.
  10. Martin AR, Kanai M, Kamatani Y, Okada Y, Neale BM, Daly MJ. Clinical use of current polygenic risk scores may exacerbate health disparities. Nature Genetics. 2019;51(4):584–591. doi:10.1038/s41588-019-0379-x. The source for the ancestry note above: polygenic scores available today are several times more accurate in people of European ancestry than in other ancestries.