Is Hoarding in Our Genes? What a Landmark Twin Study Reveals

Where does hoarding behavior come from? Is it something people choose, something they learn, or something encoded in their DNA? A landmark 2009 study published in The American Journal of Psychiatry by Alessandra Iervolino and colleagues tackled this question, and what they found is both surprising and fascinating.

The setup: Twins as nature’s experiment

The researchers turned to one of behavioral science’s most elegant research tools: twins. Identical (monozygotic) twins share virtually 100 percent of their DNA, while fraternal (dizygotic) twins share on average about 50 percent, roughly the same as any two siblings. If a trait like hoarding is heavily influenced by genes, identical twins should resemble each other far more than fraternal twins. If not, then shared family environment and experiences are probably doing most of the heavy lifting.

The study drew on a large sample of 5,022 identical and fraternal twins who completed a validated self‑report measure of compulsive hoarding, drawn from the TwinsUK registry. With this sample size, the researchers had sufficient statistical power to trust their estimates. They used liability‑threshold models and maximum‑likelihood structural equation modeling to tease apart how much of the variance in hoarding could be attributed to additive genetic factors, shared environmental and nonshared environmental factors, conducting the model‑fitting analyses in the female twins, who numbered 4,355.

What they found

A total of 2.3 percent of twins crossed an empirically derived threshold for clinically significant hoarding symptoms on the questionnaire, with notably higher rates in males (4.1 percent; a smaller sample) than in females (2.1 percent). That gender gap is intriguing and still not fully explained, though the authors flag it as worthy of future investigation.

The headline finding, though, was heritability. In female twins, genetic factors accounted for approximately 50 percent of the variance in compulsive hoarding, with nonshared environmental factors and measurement error accounting for the other half. Put differently, about half of the disparity in hoarding symptoms across individuals in this population could be traced to genetic influences, and the other half to individual life experiences and random factors that even twins who grew up in the same household do not share.

What did not show up as a significant contributor in the best‑fitting model? Shared family environment—things like the home you grew up in, the parenting style you experienced, and the cultural messages transmitted at your dinner table—did not explain a detectable proportion of variance in hoarding symptoms in this sample. This finding cuts against the intuitive assumption that hoarding is primarily something people incorporate into their own character from a disorganized parent or a household full of clutter.

Earlier research has shown that hoarding tends to run in families, but family resemblance alone cannot tell you whether genes or shared environment are driving that pattern. This twin study was designed to untangle exactly that, and its answer was clear for women in this cohort: Genes matter enormously, while shared home environment, at least as captured by this model, appears to play a limited role.

Why this matters

For anyone who has ever wondered why one sibling turns into a hoarder while another, raised in the same house, does not, this study offers a compelling explanation. Individual life experiences, including personal traumas, losses, stressful events, and one’s idiosyncratic relationship with objects and attachment, appear to modulate whether a genetic vulnerability actually flowers into a disorder. Genes may help load the gun, but life circumstances have a great deal to say about whether and how the trigger is pulled.

This also has important clinical implications. If hoarding were primarily a learned behavior, interventions focused mainly on restructuring the family environment or correcting early learning would be the obvious starting point for treatment. But a roughly 50 percent heritability estimate suggests we should also be looking closely at neurobiology, what is happening in the brains of people who are genetically predisposed to hoard, and why certain life events push some of them over the clinical threshold while others never cross it.

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Why male heritability could not be estimated

The reason is a practical one rooted in the nature of the TwinsUK registry itself. The registry from which participants were drawn predominantly comprises female twins, a pattern common among volunteer twin registries in the UK and elsewhere, as women tend to participate in health research at higher rates than men.

The male twins in the sample were simply too few in number to support reliable model‑fitting analyses. The authors were transparent about this, noting it as a limitation and flagging the need for future studies to examine heritability in men, particularly given the suggestive finding that male prevalence rates (4.1 percent) were nearly double those of females (2.1 percent), though the male sample was small. That gender gap makes the absence of male heritability estimates all the more frustrating, because it raises the possibility that the genetic architecture of hoarding could differ between men and women, a question this study simply could not answer.

The critical eye: What the study gets right and where it falls short

This was a well‑designed, appropriately powered study from a respected research group, and it provided the first robust population‑based heritability estimate for compulsive hoarding in adults. That said, several limitations are worth examining.

First, the sample composition matters. The model‑fitting analyses, the part of the study that actually estimated heritability, were conducted only in female twins. The authors explicitly concluded that compulsive hoarding is “highly prevalent and heritable, at least in women,” a qualifier that acknowledges the obvious gap. Given that males in this cohort showed higher symptom prevalence, the absence of a parallel heritability analysis in men is a real gap in the science. We simply do not know whether the 50 percent figure applies to men.

Second, the study relied entirely on self‑report via a questionnaire measure rather than clinical interviews. Self‑report instruments, even well‑validated ones, introduce measurement error, and people with hoarding disorder are often poor historians of the severity and impact of their own behavior. This is partly why the authors bundled “measurement error” together with nonshared environmental variance in their model, an analytic choice that makes the environmental component harder to interpret.

Third, the sample came from a volunteer twin registry in the United Kingdom, which skews toward educated, predominantly white, and health‑conscious participants, typical of many volunteer cohorts. Whether these heritability estimates generalize to more diverse populations with different cultural relationships to material possessions remains an open question.

Fourth, the apparent absence of shared environmental effects does not mean the family environment is irrelevant in any absolute sense. Twin models rest on assumptions—such as the equal‑environments assumption—and may miss more complex, nonlinear, or culture‑specific environmental influences, as well as gene-environment correlations, in which genetically influenced traits shape the environments people experience. The safest interpretation is that, in this particular sample and model, shared family environment did not emerge as a major source of variance, not that it never matters.

Finally, a 50 percent heritability, while meaningful, is not destiny. It is a population‑level statistic, not a personal prognosis. It tells us that across a large group, genes explain about half of the differences in symptom levels, at least in females, and the interplay between their specific genetic makeup and life history will determine their outcome in ways no group‑level statistic can fully predict.

The bottom line

Iervolino and colleagues gave us something genuinely important: rigorous empirical evidence that compulsive hoarding is not simply a bad habit, a moral failing, or the predictable product of a cluttered childhood home. It is, in substantial part, a biologically rooted condition with a meaningful genetic signature, shaped and sometimes restrained by the unique life experiences that make each person’s relationship to objects their own.