Cancer &
the Fire.

You can't change the seed. You can tend the soil.

More than a century ago a surgeon, Stephen Paget, noticed that cancers don't spread at random — they take root where the ground suits them. He called it "seed and soil": the tumour cell is the seed, but whether it grows depends on the soil it lands in. That's the honest frame for this whole chapter. Cancer needs a seed — the genetic damage, largely a matter of chance, ageing and exposure. But it also needs soil, and the metabolic state of the body is a large part of that soil.

The public argument is a false either/or: "cancer is genetic bad luck" versus "cancer is metabolic and therefore preventable." Both are partly true, and the useful picture holds them together. Cancer begins with genetic damage — that's not in dispute, and this series doesn't pretend the mutations are imaginary. But which damaged cells actually grow into a tumour, and how fast, depends heavily on the environment they sit in: the growth signals reaching them, the inflammation around them, the fuel available.

This chapter is about that environment — the soil — because it's the part that's modifiable, and it's under-discussed. After tobacco, excess body fat and the metabolic dysfunction that travels with it are among the leading preventable contributors to cancer in the developed world — the settled view of the International Agency for Research on Cancer, which identified around thirteen cancers for which excess body fatness is an established risk factor.[1]

The growth signal.

Insulin is, at its core, a signal that says "times are good — grow and store." It doesn't send that only to fat and liver. Chronically high insulin, and the IGF-1 it raises, act on cells throughout the body through the same PI3K–AKT–mTOR pathway — the one whose discoverer, Lewis Cantley, and whose central oncogene, PIK3CA, sit at the heart of modern cancer biology.[2] The message that pathway carries is exactly what a would-be tumour wants to hear: proliferate, and resist the built-in signal to die.

High insulin does three growth-promoting things at once, all familiar from earlier chapters: it drives that PI3K pathway directly; it lowers the IGF binding proteins, so more IGF-1 runs free; and it lowers SHBG, freeing more sex hormone — which feeds hormone-sensitive cancers like post-menopausal breast and endometrial.[2] The same three levers the PCOS and menopause chapters turned — here shifting the soil rather than the ovary.

The terrain evidence — and the timing.

The evidence that the terrain matters is strong and mainstream. The IARC working group identified around thirteen obesity-linked cancers — colorectal, post-menopausal breast, endometrial, kidney, liver, pancreatic and more.[1] A 2026 analysis linked measured insulin resistance to twelve cancer types.[3] Markers of insulin secretion like C-peptide predict some cancers independent of glucose,[4] and Mendelian-randomization studies support a causal role for IGF-1 in several — not all — of them.[5]

The liver loop.

One cancer ties straight to a chapter you've met. Liver cancer is rising fast, and a growing share now arises from fatty liver — MASLD — rather than alcohol or viral hepatitis; in several countries metabolic fatty liver is becoming a leading driver of liver-cancer incidence.[7] The fatty-liver chapter's fat-making and selective insulin resistance are, followed far enough, one of the roads to this cancer. The fire that fills the liver with fat is, in a proportion of people, the same fire that later drives the tumour.

Why cancer eats sugar.

You may know cancer cells guzzle glucose — it's how a PET scan finds them, by lighting up where labelled sugar is devoured. That's the Warburg effect, named for Otto Warburg, who won a Nobel for the machinery of respiration and then argued, too strongly, that cancer is fundamentally a metabolic disease. The modern understanding is subtler. For here, the point is only this: a tumour's hunger for glucose is real, visible in every oncology department, and part of why the metabolic terrain isn't incidental to cancer but woven through it.

If the metabolic terrain is part of the soil, improving it is a genuine, if partial, lever on lifetime cancer risk — the same lever as the rest of the series, aimed here at prevention.

• Lower the insulin load — reducing refined carbohydrate and not overfeeding lowers the chronic insulin and IGF-1 signalling that fertilises the terrain. The most on-mechanism lever, reaching the whole metabolic cluster at once.
• Build and keep muscle, and move — exercise improves insulin sensitivity directly and independently lowers the risk of several of these cancers.
• Do the boring, proven things — don't smoke, keep alcohol low, and — this matters — attend the cancer screening you're offered. Prevention and early detection are partners, not rivals.

The soil is partly yours to tend.

You cannot choose the seed. But the soil is partly yours to tend, and a body kept out of chronic high insulin is a less fertile ground for the cancers that answer to that signal. Prevention, not a promise; terrain, not treatment. And never a reason to refuse the medicine that fights an established cancer.

You cannot choose the seed — but the soil is partly yours to tend. Risk, not fate; prevention, not treatment.