Oncology 2.0: A New Approach to Prevention and Treatment of Cancer

Part 1 of 2 on Optimizing Diet and Metabolic Health to Reduce Cancer Risk

Prologue (I’m getting better at this recording stuff):

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As an oncologist, I’ve spent my career treating cancer patients, guiding them through some of the most difficult moments of their lives. I’ve witnessed firsthand the incredible power of modern medicine, from targeted therapies to immunotherapies and precision treatments that have transformed cancer care. But I’ve also seen the frustration and helplessness that come with the realization that conventional medicine doesn’t always have all the answers.

A turning point for me came in recent years when I began looking at cancer through a different lens. I started to see cancer not just as a genetic disease but as one deeply influenced by metabolism and the immune system. When these systems are disrupted, cancer finds a way to thrive. This shift in thinking led me to ask a new set of questions. Could we do more than just treat cancer once it appears? Could we reshape our understanding of metabolism and immune function to prevent cancer in the first place? Could optimizing these systems make existing treatments work better?

This question isn’t just scientific, it’s deeply personal. Like so many others, I have lost loved ones to cancer. As I dug deeper into the research, I realized that the way we eat, move, and live plays a profound role in whether cancer takes hold, how aggressive it becomes, and how well we respond to treatment.

The next few articles will be about understanding cancer in a new way, as a disease shaped by genetics, metabolism, and immune function working together. More importantly, it is about what we can do right now to reduce our risk and improve outcomes.

Photo by National Cancer Institute

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Cancer Isn’t One Disease—It’s Many

One of the biggest misconceptions about cancer is that it is a single disease. People often ask me, will there ever be a cure for cancer? It is an understandable question, but it misses an important point. Saying we will cure cancer is like saying we will cure infections. Just as infections can be bacterial, viral, or fungal, each requiring different treatments, cancer is not one thing. It is an umbrella term for hundreds of different diseases, each with its own unique characteristics.

I see this every day in my clinic. Some cancers grow at a terrifying pace, creating an immediate threat that requires urgent treatment. Others progress so slowly that a patient might live with them for years without symptoms. Some cancers respond beautifully to targeted therapy, melting away with a single pill, while others barely flinch at even the most aggressive treatments. The difference comes down to biology. Every cancer has a distinct origin, a unique molecular profile, and behaves in its own way. Treating them all as if they were the same leads to ineffective treatments and missed opportunities for precision medicine.

“Instead of looking for a universal cure, we should shift our focus toward understanding the root causes of each type of cancer and tailoring treatments to the individual.”

Precision oncology has already made great strides in this area, allowing us to target cancer based on its molecular characteristics rather than treating it as a single entity. But beyond just treatment, we need to think about how to keep the host not only alive but thriving. This means addressing metabolism, immune function, and the broader environment in which cancer develops. The more we move away from the idea of curing cancer and toward the idea of controlling it, preventing it, and personalizing treatment, the more progress we will make.

Rethinking Cancer: From Genetic Mutations to Metabolic, Immune, and Microenvironmental Dysfunction

For decades, cancer research has focused on Oncology 1.0—the idea that cancer is a genetic disease, caused by random mutations that lead to uncontrolled cell growth. This model has shaped how we screen for cancer, develop treatments, and think about risk.

There is truth to this. Mutations do play a role. But if cancer were purely a genetic disease, then every mutated cell would become a tumor. That’s not what happens. There is more to this story.

Oncology 2.0: Cancer as a Disease of Metabolism, Immunity, and the Host Microenvironment

The latest research suggests that cancer is not just about bad genes—it’s about a broken system that allows mutated cells to survive, grow, and evade immune destruction. This involves:

• Metabolic dysfunction – Cancer cells alter how they produce and use energy, often shifting toward glucose fermentation instead of oxidative metabolism (The Warburg Effect).

• Mitochondrial damage – The energy-producing centers of cells become inefficient, pushing cells toward uncontrolled growth.

• Chronic inflammation – The immune system, instead of eliminating cancer, creates an inflammatory environment that promotes tumor progression.

• Insulin and growth factors – High insulin levels and excess growth signals drive unchecked cellular proliferation.

• Immune evasion – The body’s defense system becomes suppressed or misdirected, allowing tumors to thrive.

• Host microenvironment dysfunction – The tissues surrounding a tumor—blood vessels, immune cells, connective tissue—can either help fight cancer or create conditions that allow it to grow.

• The microbiome’s role – Gut bacteria influence immune function, inflammation, and metabolism. An unhealthy microbiome may create conditions that increase cancer risk and affect treatment response.

Instead of seeing cancer as one rogue cell gone bad, we need to think of it as a systemic failure—a breakdown in the delicate balance between genes, metabolism, immunity, the microenvironment, and the microbiome.

Why This Matters

This shift in understanding isn’t just theoretical—it changes how we think about cancer prevention and treatment.

• If metabolic dysfunction fuels cancer, then improving metabolic health through diet, exercise, and fasting may reduce cancer risk.

• If chronic inflammation creates a cancer-friendly environment, then lowering inflammation may be as important as killing cancer cells.

• If immune dysfunction allows cancer to grow, then strengthening the immune system could be key to preventing it.

• If the microbiome influences cancer risk, then gut health and microbial balance may play a bigger role than we ever realized.

What’s Next: A Deep Dive Into Diet, Cancer Prevention, and Treatment

Understanding that cancer is more than just a genetic disease changes everything. If cancer thrives in a disrupted metabolic and immune environment, then improving these systems could be one of the most powerful ways to reduce cancer risk and improve treatment outcomes.

In the next article, we will take a deep dive into the research behind diet and cancer prevention, exploring how nutrition-based interventions may help prevent cancer from developing and support treatment in those already diagnosed.

We will examine some of the most studied dietary strategies, including:

• Intermittent fasting and fasting-mimicking diets. These approaches have been shown to activate autophagy, lower IGF-1 levels, and enhance mitochondrial function. Some studies suggest they may help slow tumor growth and even improve responses to chemotherapy. We will look at the evidence behind fasting windows, extended fasts, and how fasting may make cancer cells more vulnerable to treatment while protecting normal cells from toxicity.

• The ketogenic diet. By reducing glucose availability and shifting cells toward ketone metabolism, this diet has been explored as a way to starve cancer cells that rely heavily on glycolysis. Research suggests potential benefits in glioblastoma, pancreatic cancer, and some other malignancies. We will analyze the clinical trials that have tested ketogenic diets in cancer patients and discuss whether it is a realistic and sustainable intervention.

• The Mediterranean and anti-inflammatory diets. These eating patterns emphasize whole foods, healthy fats, and polyphenol-rich plant compounds that may help reduce systemic inflammation and support gut microbiome health. While they may not have the same direct metabolic effects as fasting or ketogenic diets, research suggests they may play a role in reducing cancer risk over time. We will break down the data and discuss how they compare to more aggressive metabolic approaches.

• Caloric restriction and metabolic flexibility. Some studies suggest that restricting overall calorie intake or cycling between different metabolic states may slow tumor progression and enhance the body's ability to repair itself. We will explore whether caloric restriction is feasible for cancer prevention and how a flexible metabolic approach could provide similar benefits without extreme dietary limitations.

• Nutritional support for mitochondrial health. The energy centers of our cells play a critical role in both cancer metabolism and immune function. Certain nutrients, such as omega-3 fatty acids, CoQ10, NAD+, and alpha-lipoic acid, may help optimize mitochondrial performance. We will explore whether targeted nutritional strategies can enhance energy production in healthy cells while limiting the metabolic flexibility of cancer cells.

This next article will not be about dietary trends or unproven fads. We will focus on what the science actually says about how these dietary interventions influence cancer risk, progression, and treatment response.

Cancer does not develop in isolation. It grows in an environment shaped by metabolism, immune function, and lifestyle factors. By making informed, research-backed dietary changes, we may be able to reduce cancer risk, support better treatment outcomes, and improve overall health in the process.

Stay tuned as we take a closer look at the data on diet and cancer, breaking down what truly works, what doesn’t, and how to turn these insights into practical and sustainable choices for better health. In the meantime, if you haven’t read these posts on basics of nutrition and exercise in cancer, I recommend starting here:

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