What Chimpanzees and the Amish Reveal About Cancer

In medicine, one of the most useful things you can find is a natural control: a group whose biology or way of life isolates a variable you could never test in an experiment. When it comes to cancer, two natural controls keep pulling at me, because they point to the same uncomfortable conclusion. Most cancer may be something we do to ourselves.

The chimpanzee control

Let's start with our closest genetic relative, the chimpanzee. The Chimpanzee Sequencing and Analysis Consortium reported in 2005 that humans and chimpanzees share roughly 99% of our DNA [1]. If cancer were mostly written into our genes, you'd expect chimps to get it at close to our rate, but they don't. In a 2006 comparison of cancer genes across the two species, Puente and colleagues noted that the common epithelial cancers (breast, prostate, and lung), which together cause more than 20% of human deaths, show up in great apes at rates below 2%, even though the cancer-related genes themselves are more than 99% identical between us [2].

It's worth asking why a species that shares all but 1% of their genome with us rarely gets cancer, even when held in captivity with longer lifespans. That leaves two possibilities: either that 1% genetic difference accounts for almost all the malignancy that plagues us, or something outside the genes is doing the damage.

The usual objection is that we get more cancer simply because we live longer, and cancer is a disease of age. It's a fair point, and the chimpanzee control answers it. Chimps in captivity, spared predators, starvation, and infection, live well beyond their wild life expectancy, so they get the extra years and still don't develop our cancers, which means longer life on its own doesn't explain the gap.

The human control: the Amish

Species-level genetics is one powerful control, and environmental isolation is another. The Amish offer a striking human comparison: a population living inside the modern United States but largely outside its processed diet, its chemicals, its sedentary habits, and its tobacco. In a 2010 study of Ohio Amish, Westman and colleagues found substantially lower overall cancer incidence than in the surrounding non-Amish population, with tobacco-related cancers cut most sharply [3]. It's the same country, the same era, and the same medical care within reach, yet the rates are very different, and the variable that changed wasn't the genome but how they live.

What the broader evidence says

These are illustrations, not proof on their own, so it matters that the larger body of research points the same way. The cleanest test is twins. In a landmark 2000 study in the New England Journal of Medicine, Lichtenstein and colleagues followed tens of thousands of twins in Sweden, Denmark, and Finland and concluded that inherited genes make only a minor contribution to most common cancers; the environment, broadly defined, does the heavy lifting [4]. A 2016 analysis in Nature by Wu and colleagues got to a similar place from a different direction, estimating that extrinsic factors, the influences beyond the random bad luck of cell division, contribute substantially to most cancers [5].

The honest phrasing is the old one. Genes load the gun, but the environment pulls the trigger. For most cancers, the trigger matters more than the gun.

What "environment" actually means

Environment is a vague word, so it helps to name the levers. The drivers with the strongest evidence are the ones the Amish largely avoid and the modern world hands out in abundance: tobacco, alcohol, obesity and the insulin resistance that travels with it, chronic inflammation, ultra-processed food, and certain chemical exposures. We've written about several of these, including how excess fat tissue behaves like a cancer-promoting organ and how the gut microbiome may sit between modern food and rising colon cancer in young adults. None of these existed at scale in the world our genome evolved for.

Where this leaves you

Two cautions keep this honest. First, not all cancer is preventable. Some is genuinely inherited, some is the bad luck of random mutation, and the chimp comparison has limits, because captive chimps aren't studied as closely as humans and their tumors may go underdiagnosed. Read the "less than 2%" figure as a strong signal, not a precise measurement. Second, none of this is a reason to skip screening or to treat a diagnosis as something a person earned. Plenty of careful people still get sick.

But the direction of the evidence is empowering rather than fatalistic. If most cancer risk were locked in your genes, there'd be little to do but wait. The natural controls suggest the opposite. The same handful of changes that seem to protect the Amish, and that our biology appears built for, are the ones within reach: don't smoke, drink little, stay lean and insulin-sensitive, move your body, and eat food close to a form your great-grandparents would recognize. You can't change your genome. You can change almost everything that pulls its trigger.

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References

1. Chimpanzee Sequencing and Analysis Consortium. Initial sequence of the chimpanzee genome and comparison with the human genome. Nature. 2005. PMID: 16136131
2. Puente XS, Velasco G, Gutiérrez-Fernández A, et al. Comparative analysis of cancer genes in the human and chimpanzee genomes. BMC Genomics. 2006. PMID: 16438707
3. Westman JA, Ferketich AK, Kauffman RM, et al. Low cancer incidence rates in Ohio Amish. Cancer Causes Control. 2010. PMID: 19779840
4. Lichtenstein P, Holm NV, Verkasalo PK, et al. Environmental and heritable factors in the causation of cancer: analyses of cohorts of twins from Sweden, Denmark, and Finland. N Engl J Med. 2000. PMID: 10891514
5. Wu S, Powers S, Zhu W, Hannun YA. Substantial contribution of extrinsic risk factors to cancer development. Nature. 2016. PMID: 26675728