Inherited tendencies to gain excess weight are real. Ignoring them does nobody any good. This article will help you understand what you did and did not inherit, and what to do about it.
Not long ago the general perception was that overweight people had nobody to blame but themselves. They were the ones finishing the biscuits. They kept the freezer stocked. Nobody made them do it.
We now know a great deal more, and the picture is considerably more interesting than that.
The twin and adoption studies, and what they found
Before the genome could be sequenced, researchers had a cleverer way of separating nature from nurture: study people raised apart from the relatives who gave them their genes. What those studies found was more dramatic than almost anyone expected, and it remains the single most persuasive body of evidence in this field.
The Danish adoption study
In 1986, Stunkard and colleagues published in the New England Journal of Medicine a study of 540 Danish adults who had been adopted as infants. Denmark keeps meticulous records, so each adoptee could be matched to both their biological and their adoptive parents.
The question was simple. Whose body did the adoptee end up resembling — the parents who supplied the genes, or the parents who supplied the kitchen?
The result
- A strong relationship between adoptees' weight class and the BMI of their biological parents (mothers p<0.0001, fathers p<0.02)
- No relationship at all with the BMI of the adoptive parents who raised them
The authors concluded that genetic influences have an important role in human fatness, while the family environment alone had no apparent effect.1
Read that again, because it is genuinely startling. Children raised from infancy in a household — eating that family's food, absorbing that family's habits, sitting at that family's table for eighteen years — grew up to resemble the body weight of biological parents they had never met, and not the people who fed them.
Twins reared apart
Stunkard's group followed this in 1990 with a study of identical twins reared apart. Comparing twin pairs separated in infancy against those raised together, they found that the heritability of BMI was around 0.7 — and, crucially, that being reared in different homes made remarkably little difference to how similar the twins ended up.2
Two people with identical DNA, raised in different houses by different families, ended up with strikingly similar body weights. Two people raised in the same house with different DNA did not.
And the overfeeding experiment
The most direct demonstration came from Bouchard's team in Québec, also published in the New England Journal of Medicine. Twelve pairs of identical twins were overfed by 1,000 calories a day, six days a week, for 100 days — under supervision, in a controlled setting, with intake genuinely equalised.
Everyone gained weight. But the amount gained varied roughly threefold between pairs — from about 9 lb to about 29 lb on the same excess. Within each twin pair, however, the gain was remarkably similar, and so was where the fat was deposited.3
This is as close to a controlled experiment on human weight gain as ethics permits. The calories were identical. The outcomes were not, and the variation tracked the genome.
How much of body weight is inherited?
Twin and family studies consistently produce heritability estimates for body mass index in the range of 47 to 90%, depending on the population and method.4 That is a wide range, but even at the lower end it places BMI among the more strongly heritable human traits — comparable to height in some analyses.
When I wrote this article a decade ago, roughly 50 genetic loci had been associated with obesity. That number is now over 500, drawn from studies approaching a million participants.5 Yet even the best polygenic scores built from them explain only about 20% of the variation in BMI — well short of what twin studies imply. The gap between the two figures is one of the more honest admissions in the field: we know inheritance matters enormously, and we still cannot fully account for how.
What has become clearer is the magnitude of the effect. Recent work indicates that people in the highest genetic risk band for BMI are around ten times more likely to develop obesity than those in the lowest — at comparable levels of activity and intake.6 Two people can eat and move similarly and end up in very different places.
Epigenetics: what your parents’ circumstances did to your genes
Beyond the genes themselves, epigenetic changes appear to play a real role. These are chemical modifications sitting alongside DNA that switch genes on or off. Crucially, they can be shaped by the environment — including the environment your mother experienced while pregnant — and some appear to persist across generations.
The Dutch Hunger Winter cohort remains the clearest human example: people conceived during the 1944–45 famine showed altered metabolic profiles and higher rates of obesity decades later, with measurable differences in DNA methylation.7 Their bodies were, in a sense, calibrated for scarcity that never came.
Your body actively defends its weight
The second thing to understand is that our bodies hold onto gained weight through redundant mechanisms wired into the brain. This is not a design flaw. For nearly all of human history, the ability to defend fat stores against famine was the difference between surviving a bad winter and not.
This is also the main reason so few effective drugs existed for so long — and, incidentally, why the GLP-1 medications represent a genuine advance: they work partly by acting on those same brain circuits rather than trying to outmuscle them.
Why this is not an excuse
Here is where I want to be careful, because this material gets misused in both directions.
It is used to dismiss: “it’s all genetic, so nothing I do matters.” That is false. Genes load the gun; environment and behaviour still pull the trigger. The obesity rates of the 1970s and today are drawn from essentially the same gene pool — what changed was everything around us.
And it is used to blame: “if genetics only explains part of it, the rest is your fault.” Also false, and considerably crueller. Two people with identical discipline can face very different difficulty.
What heredity determines is not your weight. It is how hard you have to work for a given weight, and how vigorously your body will resist.
Knowing that changes the plan rather than abandoning it. If you inherited a strong predisposition, you likely need more structure, more measurement, more protein and resistance training to protect lean mass, and more patience — and you should probably expect to need a maintenance strategy permanently rather than temporarily. That is a harder assignment than your neighbour got. It is not an impossible one.
I return to this in the tenth commandment, which is about what these differences should mean for how we treat each other.
References
- Stunkard AJ, Sørensen TIA, Hanis C, et al. An adoption study of human obesity. N Engl J Med. 1986;314(4):193–198. doi:10.1056/NEJM198601233140401 540 Danish adoptees: strong relationship with biological parents' BMI, none with adoptive parents'.
- Stunkard AJ, Harris JR, Pedersen NL, McClearn GE. The body-mass index of twins who have been reared apart. N Engl J Med. 1990;322(21):1483–1487. doi:10.1056/NEJM199005243222102 Identical twins reared apart: heritability of BMI around 0.7, with rearing environment contributing little.
- Bouchard C, Tremblay A, Després JP, et al. The response to long-term overfeeding in identical twins. N Engl J Med. 1990;322(21):1477–1482. doi:10.1056/NEJM199005243222101 The 100-day supervised overfeeding experiment: threefold variation in weight gain between twin pairs on identical excess calories.
- Elks CE, den Hoed M, Zhao JH, et al. Variability in the heritability of body mass index: a systematic review and meta-regression. Front Endocrinol (Lausanne). 2012;3:29. doi:10.3389/fendo.2012.00029 Meta-analysis of twin and family studies, the source of the heritability range quoted.
- Jansen PR, Vos N, Gebrayel P, et al. The utility of obesity polygenic risk scores from research to clinical practice: a review. Obes Rev. 2024;25(11):e13810. doi:10.1111/obr.13810 Current review: over 500 loci identified, best polygenic scores explaining roughly 20% of BMI variance.
- Kaur Y, de Souza RJ, Gibson WT, Meyre D. A systematic review of genetic syndromes with obesity and recent advances in polygenic obesity risk. Obes Rev. 2017;18(6):603–634. doi:10.1111/obr.12531 Background on the magnitude of polygenic risk and its interaction with lifestyle.
- Heijmans BT, Tobi EW, Stein AD, et al. Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci USA. 2008;105(44):17046–17049. doi:10.1073/pnas.0806560105 The Dutch Hunger Winter methylation findings described above.