The diagnosis arrives as a shock. The biology rarely does. Cancer — like most chronic degenerative disease — happens in a body that has been depleted, inflamed, and under-resourced for long enough that its surveillance systems stop catching what they should. Understanding that is not about blame. It is about agency.
Someone close to me was recently diagnosed with skin cancer. A small lesion, operable, caught in time. On one level the explanation is obvious — fifty years of occupational outdoor work, significant UV exposure, the kind of accumulated skin damage that was simply never on the radar of a generation that did not think in those terms.
But I found myself thinking about the fuller picture. Because the skin lesion did not arrive in isolation. It arrived in a body carrying eleven medications, years of proton pump inhibitor use, chronic grief and depression following a bereavement, a diet that had shifted from real food to convenience meals as cognitive decline made cooking impossible, disrupted sleep, declining mobility, social isolation, and a wound elsewhere on the face that had taken the better part of six months to heal. That wound, and its stubborn refusal to close, was already telling a story about immune function, nutrient status, and the body's dwindling repair capacity. The cancer diagnosis was, in a sense, the same story told louder.
I am not suggesting the cancer was caused by grief, or by lansoprazole, or by ready meals. I am suggesting that those things — accumulated over years — created a terrain in which the body's natural cancer surveillance mechanisms were progressively undermined. And that distinction matters enormously, because one version of that story leads to fatalism and the other leads to action.
"The diagnosis arrives as a shock. The biology rarely does. Cancer happens in a body that has been depleted for long enough that its surveillance systems stop catching what they should."
The conventional oncology model is predominantly a seed model. It focuses on the tumour — its genetics, its mutations, its markers, its response to treatment. That is not wrong. Tumour biology matters. But it is incomplete in a way that functional medicine has been pointing at for decades.
The soil model — what we call terrain theory — asks a different question: why did the seed find purchase here, in this body, at this time? Every human body produces abnormal cells continuously. Estimates suggest we each generate somewhere between hundreds and thousands of potentially malignant cells every single day as a normal byproduct of cellular replication. The vast majority of those cells are identified and eliminated by the immune system before they ever become clinically relevant. The question is not why cancer cells exist. They always exist. The question is why the surveillance system stopped catching them.
This is not a new idea. The soil versus seed framework in cancer biology traces back to Stephen Paget's 1889 paper on the "seed and soil" hypothesis of metastasis — the observation that cancer does not spread randomly but preferentially to environments that support its growth. More recently, the work of researchers like Thomas Seyfried has reframed cancer as a metabolic disease rather than purely a genetic one, with mitochondrial dysfunction as a central driver. Neither position has displaced the other. The honest picture holds both.
What functional medicine adds to this conversation is the clinical detail of what actually creates a permissive terrain — and, critically, what you can test for and address before that terrain becomes dangerous.
Natural killer cells — NK cells — are your first line of cancer surveillance. They patrol the body continuously, identifying cells that display abnormal surface markers and eliminating them before they can replicate. They do not require prior sensitisation the way T cells do. They act fast, they act early, and they are your most important defence against early-stage malignant change.
NK cell activity is not fixed. It is profoundly influenced by your nutritional status, your stress load, your sleep quality, your inflammatory burden, and your toxic load. Every one of those variables is modifiable. Every one of them is testable. And every one of them was compromised in the person whose story opened this post.
The nutrients required to run adequate immune surveillance are not exotic. They are the fundamentals that modern life — and modern medicine's approach to managing chronic disease — systematically depletes.
DNA repair is an active, energy-intensive process. Every time a cell replicates — which happens billions of times daily across your body — the copying process introduces errors. Your cells have sophisticated proofreading and repair mechanisms to catch and correct those errors before they become mutations. Those mechanisms require specific nutrient cofactors to function. Remove the cofactors, and the proofreading slows down.
Zinc is required for the activity of over 300 enzymes, including several directly involved in DNA repair and immune cell function. Selenium is essential for glutathione peroxidase — one of your primary antioxidant defences against oxidative DNA damage. Folate and B12 are required for proper DNA methylation and synthesis; deficiency in either increases the rate of DNA strand breaks and chromosomal abnormality. Magnesium is a cofactor for DNA polymerase — the enzyme that performs the actual repair work.
Now consider what long-term proton pump inhibitor use does to those nutrients. PPIs — lansoprazole, omeprazole and their relatives — are among the most widely prescribed drugs in the world, and among the most aggressive nutrient depleters we see in clinical practice. They suppress gastric acid production, which impairs the absorption of B12 (requires intrinsic factor in an acid environment), magnesium (actively absorbed in the small intestine, impaired by reduced acid), zinc (requires acid for ionisation and absorption), and iron. Long-term PPI use — years, not weeks — creates a slow but consistent drain on the very nutrients your immune surveillance system depends on.
This is not a theoretical concern. It is documented in the prescribing literature. What is less discussed is the cumulative clinical consequence when that depletion runs for a decade or more alongside other factors compounding it.
A wound that takes six months to heal is not just slow healing. It is a visible marker of zinc insufficiency, impaired immune response, and compromised tissue repair capacity — the same systems required for cancer surveillance. The skin is telling you something about what is happening systemically.
Chronic low-grade inflammation is probably the single most important terrain factor in cancer development. The relationship is bidirectional and self-reinforcing: inflammation promotes tumour growth, and tumours exploit inflammatory signalling to evade immune detection.
The mechanism runs through NF-κB — a master transcription factor that regulates inflammatory gene expression. Chronic NF-κB activation, driven by persistent inflammatory stimuli, promotes cell survival, inhibits apoptosis (programmed cell death — the mechanism by which abnormal cells are supposed to eliminate themselves), and creates the kind of microenvironment in which abnormal cells are more likely to survive and replicate than to be cleared.
What drives chronic NF-κB activation? Poor diet — particularly refined carbohydrate, seed oils, and ultra-processed food — is a primary driver. Gut dysbiosis and intestinal permeability generate a continuous stream of bacterial endotoxins (lipopolysaccharide) into the bloodstream, each one triggering an inflammatory response. Visceral fat is metabolically active and pro-inflammatory, secreting cytokines including TNF-α and IL-6 that sustain systemic inflammation. Chronic psychological stress activates the same inflammatory pathways through cortisol dysregulation and sympathetic nervous system activation.
A diet that has shifted from real food to convenience meals — high in refined carbohydrate, low in vegetables, fibre, and polyphenols — is an inflammatory diet. Over time, in a body already carrying other burdens, it creates exactly the kind of permissive terrain that the seed model of cancer cannot fully account for.
The inflammatory cascade and what drives it — including the cholesterol-inflammation distinction — is covered in depth in Follow the Money: Seven Health Narratives That Got Distorted.
The relationship between psychological stress and immune function is one of the best-documented areas in psychoneuroimmunology, and one of the most consistently underweighted in clinical practice.
Cortisol is immunosuppressive by design. In acute stress, that suppression is adaptive — it prevents the immune system from overreacting during a crisis and allows energy to be redirected to immediate survival responses. The problem is chronic cortisol elevation, or the HPA axis dysregulation that follows prolonged stress, which maintains that suppressive effect on NK cell activity, T cell proliferation, and antibody production over months and years.
Grief is one of the most physiologically demanding experiences a human body can undergo. Bereavement studies consistently show measurable immune suppression — reduced NK cell cytotoxicity, decreased lymphocyte proliferation, elevated inflammatory markers — in the months following significant loss. The clinical significance of that immune window, and its duration, is not something conventional medicine routinely addresses. There is no bereavement immune support protocol. There is antidepressant prescribing, which addresses the symptom of mood but does nothing for the underlying HPA axis dysregulation or the nutritional depletion that accompanies it.
Depression itself — independent of grief — is associated with elevated inflammatory cytokines, HPA axis dysregulation, and reduced immune surveillance. The clinical picture of someone who is grieving, depressed, isolated, and on multiple medications managing cardiovascular disease is a picture of sustained immune suppression. Not dramatic, not acute — just a slow, consistent erosion of the body's ability to catch and clear abnormal cells.
The majority of cellular repair, immune reconstitution, and growth hormone-mediated tissue regeneration happens during sleep — specifically during slow-wave and REM sleep stages. This is not a metaphor. It is physiology. Melatonin, produced during darkness, has direct antioxidant and anti-tumour properties independent of its sleep-regulatory role. Melatonin suppresses NF-κB activation, inhibits aromatase (relevant to hormone-sensitive cancers), and directly scavenges reactive oxygen species.
Poor sleep — whether from insomnia, sleep apnoea, disrupted circadian rhythm, or in this case the cognitive disorientation of dementia that makes the transition to bed impossible — systematically reduces melatonin production and interrupts the repair cycles that immune surveillance depends on. Studies consistently show that people sleeping less than six hours per night have significantly reduced NK cell activity compared to those sleeping seven to nine hours. One study found a 70% reduction in NK cell activity after a single night of four hours' sleep.
Falling asleep on the sofa because the coordination required to go to bed has been lost is not a minor inconvenience. Clinically, it is a nightly interruption to the most important repair window the body has.
Eleven medications is a significant detoxification burden. Every drug requires hepatic processing — phase I and phase II liver detoxification — and many have nutrient-depleting effects that compound each other. Statins deplete CoQ10, essential for mitochondrial energy production and antioxidant defence. Diuretics deplete magnesium, potassium, zinc, and B vitamins. Beta-blockers deplete CoQ10 and melatonin. PPIs, as already discussed, deplete B12, magnesium, zinc, and iron. ACE inhibitors deplete zinc.
The cumulative nutrient depletion from eleven concurrent medications in an elderly patient eating a nutrient-poor diet is not routinely assessed. It is not on the discharge letter. It is not part of the annual medication review. But it is real, it is measurable, and it creates a body that is running its most fundamental cellular processes — including DNA repair and immune surveillance — on an increasingly depleted substrate.
The skin as a detoxification organ is a real concept, not a wellness cliché. When the primary detoxification pathways — hepatic phase I and II, renal clearance, gut elimination — are overwhelmed or compromised, the skin bears a greater proportion of the excretory burden. Chronic skin conditions, poor wound healing, and skin lesion susceptibility are all consistent with a detoxification system under excessive load.
When I see a client whose wound will not heal, I am not just thinking about the wound. I am thinking about zinc status, vitamin C sufficiency, protein adequacy, inflammatory load, and immune function. The wound is a window into the system. The same logic applies to recurrent infections, slow recovery from illness, and the kind of progressive health deterioration that gets attributed to ageing when it is actually attributable to accumulated, addressable deficit.
Fifty years of outdoor work and significant UV exposure is a real and documentable skin cancer risk factor. UV radiation causes direct DNA damage — pyrimidine dimers, specifically — that the nucleotide excision repair pathway has to correct. When that repair pathway is running on depleted cofactors, in a body with suppressed immune surveillance and elevated inflammatory load, the probability that some of those DNA errors persist and progress increases substantially.
UV exposure did not cause the cancer in isolation. It provided the initiating damage. The terrain determined whether that damage was caught and corrected, or whether it found purchase and progressed. That is the distinction the seed-only model misses.
This is also why the sunscreen conversation is more nuanced than either the "avoid all sun" camp or the "sunscreen is toxic" camp acknowledges. Appropriate, non-burning sun exposure — supporting vitamin D synthesis, circadian rhythm regulation, nitric oxide production — is beneficial. Burning is not. The answer is not avoidance or lathering with chemical filters regardless of duration. The answer is dose management and a body with sufficient repair capacity to handle the exposure you do get.
The full vitamin D story — Scottish latitude, UVB seasonality, storage versus active hormone form, and the magnesium-K2 axis — is covered in the Vitamin D Trilogy.
I want to be clear about something. The terrain argument is not a blame argument. Saying that cancer happens in a depleted body is not the same as saying the person depleted themselves carelessly. The depletion I have described above was the result of decades of cardiovascular disease management, bereavement, cognitive decline, and the practical impossibility of maintaining optimal nutrition and lifestyle when your world has contracted to the size of a single room and the person who cooked for you is gone.
The terrain argument is an agency argument when it is applied prospectively. Right now, before a diagnosis, while you are reading this with enough cognitive resource to act on it — the terrain factors that undermine immune surveillance are largely modifiable. That is the clinical point worth making.
This is where Test, Don't Guess becomes most relevant. You do not have to guess at your nutritional status, your inflammatory load, your detoxification capacity, or your HPA axis function. You can measure them.
None of those tests requires a GP referral. None of them will appear on a standard NHS panel. All of them speak directly to the terrain factors that determine whether your body is in a state of active surveillance or quiet erosion.
The foundations are not glamorous but they are non-negotiable. Real food — not perfect food, not expensive food, but food that has not been processed into something unrecognisable — provides the nutrient matrix that synthetic supplements can support but cannot replace. Sleep, protected and prioritised, is when repair happens. Movement, even modest and daily, maintains lymphatic flow, supports NK cell activity, and reduces visceral fat-driven inflammation. Stress management — not elimination, which is impossible, but active parasympathetic recovery — addresses the HPA axis dysregulation that suppresses immune function over time.
Where deficiencies are identified through testing, targeted repletion matters. Zinc for immune function and DNA repair. Selenium for glutathione and antioxidant defence. Vitamin D with K2 and magnesium for immune modulation and anti-inflammatory signalling. B12 and folate for methylation and DNA integrity. These are not alternative medicine — they are biochemistry, and the evidence base for their role in immune surveillance is substantial.
"The question is not why cancer cells exist. They always exist. The question is why the surveillance system stopped catching them — and what conditions we spent years creating that made that possible."
The conventional oncology narrative — cancer as random genetic misfortune, managed through surgery, radiation, and chemotherapy — is not wrong. It is incomplete. The terrain matters. The conditions the body has been living in for the years and decades before the diagnosis matters. The nutritional substrate available to the surveillance systems matters. The inflammatory load, the sleep quality, the stress history, the medication burden — all of it matters.
This does not mean that everyone who develops cancer failed to look after themselves. It means that the body's defence systems are not magic. They are biological processes that require specific inputs and conditions to function. When those inputs are chronically insufficient and the conditions are chronically hostile, the probability of a surveillance failure increases. That is not fate. That is physiology.
The most honest thing I can offer after 37 years in clinical practice is this: the people I see who are building genuine health — testing comprehensively, addressing what they find, eating real food, sleeping properly, moving consistently, managing their stress with something more than hope — are building a terrain in which the seed finds very poor soil. They may not eliminate risk entirely. No one can. But they are making the biology work for them rather than passively waiting to find out whether the biology will work against them.
That is what Test, Don't Guess means in this context. Not testing because you are frightened. Testing because you want to know where you actually stand — and because knowing is the only position from which you can act.
If you want to understand your terrain — your inflammatory load, your nutrient status, your HPA axis function, your gut health — start with the Health Pattern Finder. Or book a call and we will look at what the data actually says.
The TDG Five-Test Programme measures the factors that determine whether your body is in active surveillance or quiet erosion — hormones, gut function, organic acids, food sensitivity, and comprehensive blood chemistry. Nine hundred data points. One clinical picture.
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