Cancer cells do not “grow on plants”: what science really says about diet, meat and cancer

Claim 1: “Cancer cells grow on plants, not fat.”

Fact-check: This claim implies that plant foods are the main or exclusive fuel for cancer cells, and that fats (and by extension meat) do not support tumor growth. In reality, cancer cells are metabolically flexible: they primarily use glucose but can also use amino acids (from protein) and fatty acids (from fat) regardless of whether those nutrients came from plants or animal products (source).

The phrasing also blurs the difference between “plant foods” and “carbohydrates.” Whole plant foods (like vegetables, fruits, and pulses) are rich in carbohydrate, but so are refined sugars and starches, which are a very different category nutritionally; animal foods, which supply amino acids and fatty acids can also be used by cancer cells as fuel (source). By framing the issue as “plants versus fat” rather than total energy balance, body weight, metabolic health and food quality, the claim oversimplifies complex cancer biology and misleads people into thinking that vegetables, fruit and whole grains are inherently dangerous if they have cancer.

How do cancer cells actually grow?

Cancer starts when mutations and other changes allow a cell to ignore normal growth controls, divide uncontrollably and eventually form a mass of abnormal cells. As tumors grow, they recruit new blood vessels (angiogenesis) that deliver glucose, amino acids and fatty acids from the bloodstream; these fuels come from all macronutrients in the diet, not from “plants” in particular, which is why scientists do not describe cancer as “growing on plants” but as using energy and building blocks from the whole diet (source, source, source, source, source).

Does eating plants “feed” cancer or put patients at risk?
No clinical guideline recommends (source, source) that people with cancer avoid plant foods as a group; oncology nutrition guidance generally encourages a plant‑forward eating pattern unless there are specific medical reasons to restrict fibre temporarily (for example, certain bowel complications). Observational studies (source, source) in cancer survivors show that dietary patterns rich in fruit, vegetables, whole grains and legumes are often associated with better overall survival and lower recurrence risk.

Cancer cells do need glucose, but the body can make glucose from many sources—carbohydrates, some amino acids and even glycerol from fats—so cutting out vegetables does not “starve” tumours of glucose while sparing the rest of the body. At the same time, plant foods provide vitamins, minerals, fibre and phytochemicals that support immune function and gut health which can be compromised on a very restrictive, meat‑only diet.

Evidence on plant-based diets and cancer prevention
Large cohort studies (source, source) and international reviews consistently (source, source) find that plant‑rich dietary patterns—high in vegetables, fruit, whole grains, legumes and nuts—are linked to lower risk of several cancers, particularly colorectal cancer. The 5th edition of the European Code Against Cancer advises people to “eat a healthy diet” by prioritising whole grains and other fibre‑rich foods and by limiting red meat and avoiding processed meat to reduce cancer risk.

Fibre, the colon, and the immune system
Dietary fibre is almost absent from meat, eggs and dairy but abundant in whole plant foods such as whole grains, legumes, vegetables, fruit, nuts and seeds. In the colon, fibre is fermented by gut microbes into short‑chain fatty acids like butyrate, acetate and propionate, which help maintain the intestinal barrier, dampen inflammation and may inhibit tumour development (source). Epidemiological analyses report that higher intakes of dietary fibre and whole grains are associated with lower colorectal cancer incidence, while low fibre intake and heavy reliance on refined grains and animal products without plant foods are linked to higher risk.

Fibre deficiency can disturb the microbiome, promote degradation of the protective mucus layer in the colon and increase susceptibility to inflammation, which may raise colorectal cancer risk over time (source). Several prospective studies and meta‑analyses (source, source), including EPIC (source) and pooled cohorts, find that higher fibre intake is associated with reduced colorectal cancer risk, and the European Code Against Cancer explicitly cites foods containing dietary fibre as protective. A carnivore diet, by eliminating virtually all fibre, runs counter to this evidence and may adversely affect long‑term colon and immune health unless it is very carefully managed and medically supervised.

Claim 2 (implied by the anecdote): Following a carnivore diet can cure/prevent cancer

In the video posted by Matt Fradd Tammy Peterson suggests that following a carnivore diet helped her survive cancer. 

Is there evidence that a carnivore diet helps during cancer treatment?

Current research focuses primarily on ketogenic diets (very low carbohydrate, high fat, moderate protein), not on strict carnivore diets that eliminate nearly all plant foods. A recent meta‑analysis of ketogenic diets in cancer patients found improvements in fat mass, visceral fat, insulin, blood glucose, inflammation markers and some quality‑of‑life scores, but it did not demonstrate clear survival benefits or prove that avoiding all plant foods is necessary.

Expert reviews describe ketogenic diets in cancer care as still experimental and debated, because human studies so far are small, mixed in their results and limited to specific tumor types, so they do not yet show a clear, consistent anti‑cancer benefit. These reviews also stress that such diets are very restrictive and must be carefully supervised to avoid malnutrition, since cutting out many carbohydrate‑rich foods can reduce intake of fibre, several B‑vitamins (such as thiamine and folate), vitamin A, vitamin E, calcium, magnesium, iron and potassium, all of which are important for maintaining weight, muscle mass, immune function and tolerance of treatment. Many ketogenic protocols used in trials still include non‑starchy vegetables, nuts and other plant foods, which directly contradicts the idea that people with cancer should completely “stay away from plants”, and there are currently no robust randomised controlled trials showing that an all‑meat, plant‑free carnivore diet improves cancer control or survival compared with balanced, guideline‑based diets.

Saturated fat, cholesterol and cancer risk

High intakes of saturated fat are strongly linked to cardiovascular disease and can contribute to obesity and insulin resistance, which themselves increase risk for several cancers, including post‑menopausal breast, colorectal and endometrial cancers (source). Diets centered on fatty meats and high‑fat dairy tend to be high in saturated fat and cholesterol and low in fibre, which can worsen lipid profiles and inflammation, particularly over years (source, source).

Meta‑analyses of ketogenic diets in cancer patients note changes in LDL and total cholesterol and emphasise careful monitoring, especially in populations already at high cardiovascular risk. In prevention guidelines, organisations stress maintaining a healthy body weight, limiting saturated fat and favoring unsaturated fats from plant oils, nuts, seeds and fish rather than relying heavily on animal fat.

How strong is the evidence that red and processed meat increase cancer risk?

In 2015, the International Agency for Research on Cancer (IARC) classified processed meat (such as bacon, sausages, ham and some deli meats) as “Group 1 carcinogenic to humans” based on sufficient evidence that it causes colorectal cancer. Red meat (beef, pork, lamb, veal, mutton, horse, goat) was classified as “Group 2A probably carcinogenic to humans” based on limited evidence in humans and strong mechanistic evidence.

A 2011 meta‑analysis, updated by a more recent 2025 meta‑analysis, found that higher consumption of red and processed meat was associated with roughly 15–22% increased risk of colorectal cancer, reinforcing earlier findings that risk rises with greater intake. Other analyses (source, source) report that red meat is a risk factor for colon, colorectal and rectal cancer in Asian populations, and that replacing red and processed meat with fish can modestly reduce colorectal cancer risk. Public health bodies like the WHO and the American Institute for Cancer Research emphasise that “Group 1” classification reflects certainty that a cause–effect relationship exists, not that processed meat is as dangerous as tobacco on an absolute scale; risk rises with amount and frequency.

Are there flaws or limitations in meat–cancer studies?

Most meat and cancer data come from observational cohorts, which can be affected by residual confounding (for example, people who eat more processed meat may smoke more or exercise less) and measurement error in self‑reported diet. However, many studies adjust for smoking, alcohol, BMI and other lifestyle factors, and still detect a dose‑response relationship between processed meat and colorectal cancer, which strengthens the likelihood of a true association (source).

There is also mechanistic support: processing can introduce nitrites, N‑nitroso compounds, polycyclic aromatic hydrocarbons and heterocyclic amines, which can damage DNA in the gut, while high heme iron in red meat can promote oxidative stress and formation of carcinogenic compounds in the colon. Even with limitations, the convergence of epidemiology, mechanistic data and consistent findings across populations is strong enough that major bodies worldwide recommend limiting processed meat and moderating red meat.