I was having a conversation with my dad recently when he said something that stopped me. “I heard on the news that obesity is genetic and that around 80% of it is inherited.”
Then he followed with a question that concerned me even more. “If that’s true, doesn’t it make you want to give up? If you’ve inherited it, why even try?”
That conversation made me think about how important it is that we communicate science accurately. My dad had heard a statistic on the news and understandably interpreted it to mean that if obesity runs in your family, much of your future weight is already determined.
But that is not what the science tells us. Obesity is complex. Genetics absolutely play a role. But genetic susceptibility is very different from genetic destiny.
And when we communicate the two as though they are the same thing, I believe we risk doing more harm than good.
What does the “80% inherited” statistic actually mean?
A recent study published in PLOS Medicine examined data from up to 85,866 Norwegian children to investigate why body mass index, or BMI, tends to be associated between parents and their children.
At age eight, the researchers estimated that genetic inheritance explained approximately 79% of the covariance between maternal BMI and child BMI. For paternal BMI, the estimate was even higher.
That sounds dramatic until we understand what the researchers were actually measuring.
It does not mean that 79% of an individual child’s obesity is genetically predetermined.
It does not mean that 79% of your body weight is inherited.
And it certainly does not mean that lifestyle, environment, nutrition and health interventions are largely irrelevant. The researchers were investigating why BMI tends to track between parents and children and how much of that relationship could be statistically explained by inherited genetic factors.
That is a very different question. The concept of heritability is also frequently misunderstood. Heritability is a population level statistical measure. It describes how much of the variation in a characteristic between people within a particular population and environment is associated with genetic differences.
An 80% heritability estimate does not mean that 80% of your body weight was caused by your genes. It also does not tell us that the characteristic cannot be modified.
If our genes haven’t suddenly changed, what has?
This is where the obesity statistics become particularly important. According to the latest Australian Institute of Health and Welfare data, in 2022 to 2024 approximately 67% of Australian adults were living with overweight or obesity. Around 33% of adults were living with obesity specifically.
Among Australian children and adolescents aged two to seventeen, approximately 27% were living with overweight or obesity, while approximately 8.5% were living with obesity specifically.
These distinctions matter because the 67% and 27% figures commonly quoted represent overweight and obesity combined.
But the long term trend is still concerning.
In 1995, approximately 56% of Australian adults were living with overweight or obesity. By 2022 to 2024, that figure had increased to approximately 67%.
Obesity alone increased from approximately 19% of adults in 1995 to approximately 33% in 2022 to 2024.
Among Australian children aged five to seventeen, overweight and obesity combined increased from approximately 20% in 1995 to approximately 28% in 2022 to 2024.
Looking further back, Australian data show that among adults aged 25 to 64 living in urban areas, obesity affected approximately 9% of men and 8% of women in 1980. By 1999 to 2000, those figures had risen to approximately 17% of men and 20% of women.
So we need to ask an obvious scientific question. If obesity were predominantly the consequence of genes acting independently of our environment, how could its prevalence change so substantially within only a few decades?
Our population’s genetic architecture has not fundamentally transformed over this period, our environment has. Same genetic susceptibility, different environment.
One of the most interesting pieces of research published in 2026 examined British birth cohorts born in 1946, 1958, 1970 and 2001.
Researchers investigated how genetic susceptibility to higher BMI interacted with the environment experienced by different generations.
At age sixteen, one standard deviation of genetic risk was associated with a BMI difference of approximately 0.46 kg/m² in the 1946 cohort. In the 2001 cohort, the difference was approximately 0.90 kg/m². The association between genetic susceptibility and BMI was therefore almost twice as strong in the younger cohort.
Why? The genes themselves had not suddenly changed. The environment in which those genes were being expressed had changed. This is an important concept known as gene environment interaction. A person may carry genetic variants associated with increased appetite, reduced satiety, greater adiposity or a higher propensity for weight gain.
Whether and to what extent that susceptibility becomes expressed can be influenced by the environment in which that person lives.
Genes may load the biological susceptibility. The environment can influence how strongly that susceptibility is expressed and our environment has changed enormously. Modern life is very different from the environment humans occupied for most of our evolutionary history.
- Highly palatable and energy dense foods are widely available.
- Food can be purchased virtually anywhere and at almost any time.
- Portion sizes and food availability have changed.
- Many occupations require considerably less physical activity.
- Transport requires less movement.
- Screen based leisure has increased.
- Sleep can be disrupted by work patterns, technology and lifestyle.
- Food marketing is sophisticated and pervasive.
Socioeconomic circumstances can influence access to nutritious foods, opportunities for physical activity and healthcare. The Australian Institute of Health and Welfare recognises obesity as a complex condition influenced by interacting biological, behavioural, social, commercial and environmental factors.
That distinction matters. Acknowledging environmental factors is not about removing personal responsibility. It is about understanding the physiology and epidemiology properly. Our food environment can influence how much we eat.
One of the most interesting controlled feeding studies in this area was conducted by researchers at the US National Institutes of Health. Twenty adults lived in a research facility and were assigned to either an ultra processed diet or an unprocessed diet for two weeks before crossing over to the other diet. Participants were allowed to eat as much or as little as they wanted.
During the ultra processed phase, participants consumed approximately 500 additional calories per day compared with the unprocessed phase. They gained approximately 0.9 kilograms during the ultra processed phase and lost approximately 0.9 kilograms during the unprocessed phase.
Importantly, their genetics had not changed, their food environment had. It was a small, short term study and should not be interpreted to mean that every processed food causes obesity. But it provides an elegant demonstration of an important physiological principle.
The environment in which we make our food choices can influence energy intake even when we believe we are simply eating according to hunger.
Genetics still matter
I don’t want the pendulum to swing too far in the opposite direction either. There is strong scientific evidence for a genetic contribution to body weight regulation and obesity susceptibility. Some people genuinely experience stronger biological pressures towards weight gain than others.
Genetic differences can influence appetite regulation, satiety signalling, energy expenditure, fat distribution and other aspects of metabolism. Rare genetic disorders can also directly cause severe obesity.
For many people, however, common obesity is polygenic. This means that numerous genetic variants each contribute small effects to overall susceptibility. Two people can therefore live in very similar environments and have very different weight responses.
This is one reason why telling someone simply to “eat less and move more” fails to acknowledge the complexity of obesity physiology. It is also why comparing one person’s weight loss journey with another person’s can be misleading. The degree of difficulty is not equal for everyone. But greater biological difficulty does not mean biological impossibility.
Lifestyle can interact with genetic risk
Research also suggests that lifestyle can modify the relationship between genetic susceptibility and body weight. A large 2026 analysis followed more than 22,000 women and men for up to 26 years and examined polygenic risk alongside lifestyle factors.
The association between genetic susceptibility and BMI was substantially lower among people with healthier lifestyle patterns compared with those with the least healthy lifestyle patterns. Because this was observational research, it cannot prove that every individual can overcome a particular level of genetic susceptibility through lifestyle alone. Nor should it be interpreted that way.
Some people require considerably more support, including structured nutrition intervention, psychological support, medical treatment or pharmacotherapy. But the findings reinforce an important principle. Genetic risk is not the same as a predetermined outcome. We need to remove blame without removing hope.
There is another side to this discussion that I think is equally important. For decades, people living with obesity have experienced stigma and the assumption that their body weight simply reflects poor discipline or lack of willpower. That is scientifically inaccurate and can be incredibly damaging.
The research showing a strong genetic contribution to obesity susceptibility can help correct that narrative. The recent parent and child study may also help reduce inappropriate blame placed on mothers by suggesting that the relationship between maternal BMI and childhood BMI is largely explained by inherited genetic factors rather than simply the mother’s weight around pregnancy directly causing higher weight in her child.
That is important. But we need to be careful that in removing blame, we don’t accidentally remove hope.
If someone hears:
“Obesity is 80% inherited,” they may interpret that as: “There is very little I can do about it.” That was exactly how my dad interpreted it and I suspect he isn’t alone.
The science is more empowering than the headline. The more accurate message is this:
- You may inherit a greater biological susceptibility to gaining weight.
- You may experience stronger hunger.
- You may require more structure around your nutrition.
- You may regain weight more easily.
- You may need greater clinical support than somebody else.
But your genes do not operate in isolation. They interact continuously with nutrition, physical activity, sleep, medications, health conditions, socioeconomic circumstances, the food environment and many other factors.
For some people, appropriate medical treatment will also form an important part of obesity management. There is no single intervention that will work equally for everyone. That is precisely why we need personalised, evidence based approaches rather than blame or fatalism.
So, Dad, should everyone just give up?
Absolutely not. If anything, understanding your genetic susceptibility should help you make better informed decisions about your health. Someone with a strong family history of type 2 diabetes does not conclude that nutrition, exercise and metabolic health no longer matter. We recognise their increased susceptibility and intervene earlier. We should think about obesity risk in a similarly sophisticated way.
If you know you are biologically more susceptible to weight gain, that information can help you understand why maintaining a healthy weight may require greater attention and support. It is information.it is not a sentence. Obesity is neither simply a failure of willpower nor simply the inevitable consequence of our DNA.
The science sits between those two extremes.
Our genes matter.
Our biology matters.
Our environment matters.
Our behaviours matter.
And access to appropriate healthcare matters. We need health messaging that reduces stigma while preserving agency. Because perhaps the most important message from the science is not that obesity can run in families.
It is that genetic susceptibility is not genetic destiny.
References
- Helgeland Ø, et al. Genetic inheritance explains the association between parental and offspring body mass index: Evidence from up to 85,866 Norwegian children. PLOS Medicine. 2026. Available from: https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1005094
- MedlinePlus Genetics. What is heritability? US National Library of Medicine. Available from: https://medlineplus.gov/genetics/understanding/inheritance/heritability/
- Australian Institute of Health and Welfare. Overweight and obesity: How many Australians are overweight or obese? Australian Government. Available from: https://www.aihw.gov.au/reports/overweight-obesity/overweight-and-obesity/contents/how-many
- Australian Institute of Health and Welfare. Overweight and obesity: Causes of overweight and obesity. Australian Government. Available from: https://www.aihw.gov.au/reports/overweight-obesity/overweight-and-obesity/contents/causes-of-overweight-and-obesity
- Australian Institute of Health and Welfare. Are all Australians gaining weight? Differentials in overweight and obesity among adults, 1989 to 90 to 2001. AIHW Bulletin No. 11. Canberra: AIHW. Available from: https://www.aihw.gov.au/getmedia/e7646b8e-9cc4-4b53-b8e2-46943708f861/bulletin08.pdf
- Johnson W, et al. Changing genetic influences on body mass index across generations: Evidence from British birth cohorts. PLOS Genetics. 2026. Available from: https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1012138
- Hall KD, Ayuketah A, Brychta R, et al. Ultra processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial of ad libitum food intake. Cell Metabolism. 2019;30(1):67 to 77.e3. doi:10.1016/j.cmet.2019.05.008.
- PubMed. Research examining long term lifestyle patterns, polygenic susceptibility and BMI in more than 22,000 adults. 2026. PMID: 42333656. Available from: https://pubmed.ncbi.nlm.nih.gov/42333656
