Editor’s note: The biological explanations in this article are key to understanding the metabolic view of cancer advocated by some researchers and clinicians. It is presented as a synthesis of certain findings and views related to cancer prevention. Needless to say, there is a wide range of views on this topic not covered here. This article is offered as information only. It is not meant as advice, medical or otherwise. Qualified health professionals should be consulted regarding any health conditions.

For decades, cancer has been framed chiefly as a genetic disease—mutations in key genes driving cells to grow when they should not. But according to a growing body of researchers, that view is at best a partial picture of how cancer develops. 

These clinicians and researchers believe that a cell’s metabolic state—the way it extracts energy from nutrients and interprets growth signals—shapes the environment in which mutations like cancer arise, take hold, or are held in check. In other words, though genes influence possibilities, the metabolism helps decide which possibilities thrive.

What does “metabolic” mean?

By “metabolic,” we refer to the cell’s energy and signaling system: how a cell uses fuel (glucose, fat, ketones), how well cells’ mitochondria produce that energy, and how cues from substances such as insulin guide cells to grow or repair.

When this system is steady, cells find and fix mistakes in their DNA—the instruction manual they live by—and clear out waste on schedule. Cells do this constantly to keep mutations from piling up.

But when the system falls out of balance, growth signals run longer, and repairs slip. That’s when the body’s terrain becomes friendlier to cancer. High insulin, struggling mitochondria, and lingering inflammation are common drivers of this imbalance.

Note that this metabolic understanding doesn’t replace the genetics model of cancer. Rather, it complements it. Genetics identifies the mutations that can drive disease. The metabolic lens adds context: fuel use and signaling set conditions that either restrain those mutations or help them expand. They also influence DNA repair and how effectively the immune system polices abnormal cells.

Four imbalances at the root of cancer risk

From a metabolic perspective, the question to ask is which everyday habits push our metabolic system out of balance, and which ones help restore it. The answer to that key question starts with understanding four imbalances that show up again and again in our bodies at the cellular level.

First, too much easy fuel: For example, after a person downs a scone and a sugary drink, blood sugar surges and insulin levels increase. Insulin is a growth signal that tells cells to take in sugar and build. When it stays high, cells keep burning glucose and postponing repair.

Second, signal overload: Frequent grazing keeps insulin and other growth signals nudging cells to “build” all day, instead of letting them idle and repair themselves between meals. Late-night eating sends a mixed message—the food says “go,” while the body clock says “rest”—so growth signals stay active when cleanup processes should be running instead.

Third, slow cleanup: Cells do their recycling during deep sleep and the nightly fasting window between the last bite today and the first bite tomorrow. Short sleep and snacking until bedtime compress that window. For instance, dessert at 10:30 p.m. and breakfast at 7 a.m. leaves little time for thorough cleanup, so damaged proteins and worn-out mitochondria accumulate and repair falls behind.

Fourth, added “noise”: Ongoing stress keeps stress hormones (like cortisol) high and sleep shorter and lighter, while long sitting idles the leg muscles that normally pump blood. Together, they raise background inflammation levels and slow oxygen delivery to tissues, which creates a body terrain that’s friendlier to cancer.

Why these imbalances matter for cancer prevention

The good news is that small, everyday choices can shift the cells’ fuel and signal balances back toward health. That’s the promise of a metabolic understanding: practical, doable steps that help cells spend more time in repair and less time in constant “go” mode.

Four factors that influence a cell’s balance, in plain language

To keep the rest of this article understandable, let’s start by defining the four main factors of a metabolic energy system. 

These are insulin resistance (signals), mitochondrial health (power), inflammation (background stress), and autophagy (cleanup). Each of these helps explain whether cells spend more time building or repairing, and why that matters for cancer prevention.

Insulin resistance

Insulin is a hormone that tells cells to take in sugar and build. Stated simply, insulin resistance means cells stop responding well, so the body releases more insulin to get the same job done. Higher, frequent insulin levels keep the growth signals set on “on,” which tilts the cells toward building and away from repair. 

Chronically higher insulin, often alongside higher IGF-1 (see section on IGF-1 below), keeps growth signals “on” via the cells’ growth circuits that direct cells to grow and divide and to delay cleanup. 

This elevated insulin state pushes cells toward proliferation. It also inhibits apoptosis, which is the body’s way of removing damaged cells, and reduces autophagy, which is the cell’s housekeeping process that clears damaged proteins and organelles. Basically, cell hygiene drops dramatically. 

When growth stays “on,” cells delay repair and cleanup. DNA damage is more likely to slip through, reactive byproducts build up, and faulty cell parts linger in the body. Over time, more errors persist, and some cells gain growth advantages that can drive precancerous changes.

In short, a growth-first state means less cell cleanup, which increases mutations and the survival of abnormal cells. This raises the odds that precancerous patches progress toward cancer.

IGF-1

IGF-1 stands for insulin-like growth factor. It’s a hormone made mainly in the liver in response to human growth hormone (HGH). As the name suggests, its structure and function resemble insulin, but its role is more about growth and development than blood sugar control. 

IGF-1 is responsible for: 

• Cell growth and survival: It stimulates cells to divide, differentiate, and avoid programmed cell death (apoptosis).
  
• Tissue repair and development: It plays a key role in building muscle, bone, and connective tissue.
  
• Metabolic effects: Like insulin, it helps cells take in glucose and amino acids, but its influence is longer-lasting and more tied to growth signaling than to immediate energy use.

What is the IGF-1 cancer connection?

High circulating IGF-1 has been linked in studies to increased risks of several cancers (such as breast, prostate, and colorectal cancer). That’s because it pushes cells into more cell divisions, suppresses apoptosis (so damaged cells survive when they shouldn’t), and stimulates new blood vessel growth, which is exploited by tumors to feed themselves.

In short, insulin and IGF-1 form a growth-promoting duo. When both are chronically high—say, from insulin resistance paired with excess growth hormone signaling—they create an internal environment where cancer cells can thrive.

Mitochondrial health

Mitochondria are the cell’s power generators that turn fuel into usable energy. 

Well-fueled, resilient mitochondria support steady energy for DNA repair. They help cells switch fuels smoothly, which avoids the constant “fast sugar” metabolism that pushes growth. Healthy mitochondria also help trigger apoptosis and keep reactive by-products in check, thereby lowering the chance of DNA injury.

In contrast, when mitochondria are strained or damaged, cells rely more on quick sugar burning and become less flexible at using other fuels such as ketones. 

If mitochondria run “tired,” cells lean on quick glucose burning, generate more oxidative by-products, and send fuzzier danger signals. That can blunt apoptosis, leave damaged parts in place, and tilt tissues toward disorder.

Inflammation

Inflammation is the body’s alarm system. Short bursts help healing; constant, low-level alarms nudge cells toward trouble. 

Acute inflammation clears debris and then stands down. That “on, then off” rhythm preserves tissue architecture and helps immune cells recognize and remove abnormal cells before they take hold. 

On the other hand, persistent, low-grade inflammation keeps alarm molecules circulating. This can encourage excessive growth signaling and reduce insulin sensitivity. This condition can create a micro-environment where DNA damage is more likely to persist.

Autophagy 

Autophagy is the cell’s cleanup and recycling cycle. During this window, cells clear damaged proteins and worn-out mitochondria and fix small problems before they get out of control. Short sleep and eating late compress this window, so cleanup falls behind.

Regular autophagy keeps the cells’ “housekeeping” on schedule. This maintains protein quality, removes faulty mitochondria, and reduces clutter that can destabilize DNA. It also supports timely apoptosis, so abnormal cells are less likely to linger.

If cellular cleanup is chronically delayed, damaged parts accumulate and the stress levels in the cell increase. This raises the odds that small cellular errors stick around. 

Researchers and educators shaping the metabolic view

Researchers are finding that everyday choices can nudge metabolic balance in the right direction. What and when we eat (for example, reducing fast-absorbed sugars or using time-restricted eating), how we move, how we sleep, and how we handle long-term stress all contribute to lowering our cancer risk and supporting overall health.

A growing number of respected clinicians and researchers are contributing pieces of this metabolic understanding. Below is a sampling of the leading voices in this field of research and their specific contributions to the subject.

Medical doctors

• Jason Fung, MD: Clinician-educator specializing in fasting and insulin resistance. Here is a primer on what insulin resistance is and why it matters metabolically: What is insulin resistance?
  
• Matthew G. Vander Heiden, MD, PhD: Physician-scientist known for modernizing the role-of-the-metabolism-in-cancer view. Here is a clear overview of his work and why metabolism matters in tumors: Exploring cancer metabolism

Other clinicians and scientists

• Thomas N. Seyfried, PhD: Proponent of the mitochondria-first model of cancer. Here is a short, nontechnical Q&A on his thesis: Cancer as a Metabolic Disease.
  
• Valter Longo, PhD: Researches fasting and the fasting-mimicking diet (FMD). For a news-style summary (preclinical + early clinical context) on fasting-like cycles and cancer therapy: Fasting-like diet turns the immune system against cancer.
  
• Dominic D’Agostino, PhD: Studies ketones and metabolic stress. For an approachable intro talk on why ketones might change tumor biology: Can ketones help fight cancer?
  
• Adrienne C. Scheck, PhD: Explores ketogenic metabolic therapy with standard care in glioma. For a patient-friendly walkthrough: Altering metabolism for brain tumor therapy
  
• Nasha Winters, ND: “Metabolic terrain” systems model in integrative oncology. Here is a concise lay page outlining the Terrain Ten and the approach: The metabolic approach to cancer.
  
• Eric Berg, DC: Practitioner-educator who popularizes insulin resistance and autophagy concepts for the public. Here is a lecture that details his points of view, including action steps he recommends, to assist in preventing cancer: How to Never Get Cancer.
  
• Ivor Cummins (engineer/author): In this lecture, Cummins explores in detail his view on insulin resistance as a common risk driver: The pathways of insulin resistance. 

The road ahead for metabolic cancer prevention

Metabolism fits alongside genetics as a core pillar of modern cancer science. It helps explain how cells use fuel and respond to growth and repair signals, and why everyday habits can tilt that balance toward or away from disease.

The picture is still coming into focus. Trials are testing diet patterns, fasting-mimicking cycles, exercise, and metabolic drugs alongside standard care. Work on insulin and IGF signaling, mitochondrial function, and cellular cleanup is informing how prevention might work in real life.

Emerging studies suggest that everyday habits—especially how we eat, sleep, and exercise—can significantly push our cancer risk in the right direction. As the research base grows, so will a practical toolkit for cancer prevention: clearer, simpler daily habits that put more of the odds on our side.