What if our diet can cause cancer? An overlooked theory on carcinogenesis

Medical science has failed to cure cancer. It’s time to rethink the cause of cancer.

Most of us have been taught to think the origin of cancer is a genetic mutation. A stray radiation particle, or some toxin, causes an unlucky DNA mutation. That mutation gives rise to a cancer cell, which divides and divides until it takes over our body and kills us.

We’ve since learned that the story is a little more complicated. That our immune system can fight off cancer, and does so all the time. Only when the immune system fails does cancer spread and become lethal. Our ideas obout how cancer begins, however, are still the same.

But what if that origin story is also wrong?

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Lauren Smith

Saved my life

I would like to thank you for literally saving my life. Back in February, I had to be hospitalized while on vacation in Phoenix with an A1C of 11% and had to start taking 2 types of insulin and 2 other meds. I read the Fatburn Fix in April, and followed the program to a tee, and I’m down by 15 pounds, 6.8 A1C, and only one once weekly diabetes medicine. 

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What if cancer originates in something far less random, and far easier for us to prevent and avoid?

Dr. Thomas Seyfried, a cancer researcher at Boston College, says it’s time to rethink cancer’s origins. He has spent decades undermining the idea that these random unlucky mutations cause cancer. His view, which he’s supported with a massive academic book on the topic, is that cancer is not genetic but metabolic. If we want to beat cancer, we need to discard the old idea that genetic mutations cause cancer.

When I first heard Dr. Seyfried discuss his research, way back in 2012, it immediately caught my attention. This could explain why chemotherapy doesn’t work that well: because chemotherapy doesn’t correct the underlying metabolic problem. It could also explain why people with no family history of cancer, who never smoke, eat organic, and do “all the right things” nevertheless develop cancer. So I started looking into it.

I soon found that Seyfried’s idea is not new. It’s built on foundational work that’s been all but forgotten.

Dr. Otto Warburg Discovered Damaged Mitochondria Can Cause Cancer

Mitochondria are kidney bean-shaped little organelles inside our cells (see image above). They do a really important job: give our cells energy. Nearly a century ago, Nobel Prize-winning scientist Otto Warburg observed that cancer cells had mitochondria that behaved abnormally. They used glucose to generate energy much more often than healthy cells. Healthy cells burn mostly fat for fuel, particularly between meals. Glucose is supposed to be the cellular backup fuel for times when oxygen is used up, like when running for your life.

The process of using glucose to generate energy without oxygen is called fermentation. As in fermenting grapes to make wine, fermenting malt to make beer, or fermenting milk to make cheese. Fun fact: the organisms creating these delicious foods don’t require oxygen. Another fun fact: when you’re exercising really hard, that burn you feel in your muscles is a sign that your cells have resorted to fermentation. The phenomenon eventually came to be known as the Warburg effect.

How Scientists Tested Dr. Warburg’s Theory of Carcinogenesis

Here’s an excerpt from Dark Calories, where I explain the experiment that convinced me Dr. Warburg and Dr. Seyfried are right: (You can read some of this original research for yourself here.)

He [Dr. Seyfried] described an elegant sequence of experiments that could disprove the gene theory of cancer once and for all. [Scientists] performed microsurgery on cancerous cells, showing that mitochondria from cancer cells transmitted cancer, while mutated DNA from cancer cells did not. They also designed experiments to test where the DNA mutations came from. Those experiments showed that mitochondrial dysfunction was causing DNA mutations rather than the other way around. This is irrefutable evidence that cancer comes down to mitochondrial dysfunction, not DNA mutation, exactly as Warburg predicted. And it demands we use a radically different strategy for beating cancer than what we’ve been pursuing for the past three-quarters of a century. We’ve been killing rapidly dividing cells when what we should be doing is healing our broken metabolism. 

~Dark Calories Chapter 8: “Reason for Hope”

I remember learning about the Warburg effect in school. But I didn’t learn it was linked to cancer.

Why are doctors not taught that the Warburg effect can cause cancer?

It so happened that Dr. Warburg was German. After WWII, all things German were considered politically incorrect. With the discovery of DNA’s structure in the 1950s, the world’s focus shifted to DNA mutations. So for geopolitical reasons and prejudice, Dr. Warburg’s groundbreaking ideas went underground, fading from our collective memory. A crazy part of being human is that we tend to do stuff for reasons that have nothing to do with logic.

By misunderstanding cancer’s origins, we’ve also been treating cancer wrong.

Not only have we been thinking about carcinogenesis wrong. We’ve been thinking about anti-cancer therapies all wrong. Because if cancer begins primarily with mitochondrial damage and metabolic dysfunction, then cancer treatments should target those broken mitochondria. Instead, most chemotherapy has, for decades, targeted rapidly dividing cells, hoping to kill more of the cancer cells than healthy human cells. This shotgun approach has many unintended side effects, including hair loss, extreme nausea, and immune suppression. Due to the immune suppression and fluid losses, these treatments sometimes result in patient death. And still, after all that, often the cancer cells survive.

Dr. Seyfried says a much smarter approach would be to starve cancer cells of glucose with a very low-carb, ketogenic diet.  His experiments show this idea works pretty well. Not 100%, but much better than standard care. He’s successfully used a low-carbohydrate ketogenic diet to stall and even reverse tumor growth in laboratory animals, and others have replicated the work.

This research is so incredible that multiple organizations are now spreading the word. What this means is, if you have cancer and you want to learn more, you can get help.

Key Nonprofits Supporting Keto for Cancer

HOWEVER: Dr. Seyfried and all these organizations are overlooking something vital.

And it might just help the keto diet work even more effectively.

Sugar Probably Doesn’t Cause Cancer As Much as You Might Guess

The fact that cancer needs sugar has led many people to believe sugar is essentially a carcinogen. In fact, you’ll see statements to that effect from some of the prominent people supporting keto for cancer. They’ve developed an interesting hypothesis to support the idea that sugar can cause cancer. The hypothesis works more or less like this: 1. Diets high in refined sugars cause hyperglycemia (high blood sugar). 2. High blood sugar causes inflammation, which can harm mitochondria. 3. High blood sugar also elevates insulin. 4. Elevated insulin causes inflammation. 5. That inflammation also degrades mitochondrial health.

Certainly cutting sugar once you have cancer is important. But as far as causing cancer in the first place, the evidence is, in my view, relatively weak.

The weakest link is the idea that insulin promotes inflammation. The thinking is that excessive insulin overstimulates something called the MAPK pathway, which promotes cell growth and inflammation. Therefore, high circulating insulin levels actively promote a pro-inflammatory environment in the vascular system, contributing to cardiovascular disease and fat storage. But linking this to mitochondrial dysfunction is highly speculative.

The idea that sugar causes insulin resistance is also a bit overstated, in my view. High blood sugar levels can cause a problem known as glycation, which can promote inflammation. Glycation occurs even at normal blood sugar levels, but it scales exponentially with hyperglycemia. But our blood sugar levels only remain high for extended periods once we already have full-blown diabetes.  In other words, a healthy person can eat a lot of sugar, but won’t experience nearly as much glycation as someone with diabetes, which means they won’t suffer much inflammation from their sugar consumption.

What’s more, not all inflammatory responses are the same. Hyperglycemia elevates certain cytokines involved in fighting infection. But experiments linking hyperglycemia to meaningful insulin resistance are lacking. In other words, it’s not clear that the kind of inflammation driven by hyperglycemia can actually cause insulin resistance.

Much more plausible, I think, is the link between seed oils and cancer. Because seed oils contain oxidized fatty acids that can directly damage mitochondria.

My Theory on How Seed Oils May Cause Cancer

In my peer-reviewed paper, The Energy Model of Insulin Resistance, I describe a mechanism by which seed oils cause mitochondrial oxidative stress, which powerfully promotes inflammation.  I also argue that before you develop cancer, you develop insulin resistance. But doctors don’t look for insulin resistance; we only look for signs of diabetes, so children and adults with insulin resistance usually don’t know they have it. If you want to get screened, I teach you how to do that here. You want to know if you are insulin resistant becuase, if you have insulin resistance, not only does it mean you are at risk of developing type 2 diabetes, it also means you have a much higher risk for cancer.

But doctors are not trained on any of this. So to arrive at answers myself, I’ve spent many years studying the work of scientists such as:

• Martin Grootveld, who reveals how cooking certain fatty acids transforms them into toxins that can cause cancer.

• Denham Harmon and other free radical biologists. These experts identify oxidative stress as a driver of mitochondrial and cellular dysfunction.

• Gerhard Spiteller, whose research shows how saturated fat has been wrongly blamed for diseases caused by the PUFA fats in seed oils.

• And of course Dr. Seyfried, who we’ve been discussing here.

Among others. I cite their work, and many others, in my paper and in my books.

In my view, these sorts of experts need to be better integrated into medical science. They should operate together, but they remain isolated. Medical science should bring experts from these fields into cancer conferences. But they don’t. And until these structural shifts take place, if you want to be healthy, you need to take matters into your own hands.

(My books integrate this overlooked research into the science of human health. And the book that most directly discusses seed oils and cancer is my latest, Dark Calories.)

What Evidence Links Seed Oils to Cancer?

We do not have randomized clinical trials showing that removing seed oils from people’s diets prevents cancer. Such trials would be extraordinarily difficult to conduct given the decades-long development of many cancers. But the absence of that particular kind of evidence does not mean there is “no evidence.”

We know that processed foods and fried foods increase cancer risk. Even though seed oils are ubiquitous ingredients in processed foods, very few people are even asking whether seed oils might cause cancer. There are some; here are a few examples:

• Repeatedly heated frying oil has been linked to various cancers. You may not reheat your cooking oil, but the restaurants you go to do. And so do the makers of chips, crackers, and other junk foods.
• Even without reheating, high-PUFA refined oils are linked to cancer.
• Breathing the volatiles released during the frying of refined high-PUFA oils has been linked to lung cancer.

We also have a kind of logical algorithm that links these oils to cancer. There is evidence that polyunsaturated fats oxidize more easily than the saturated fats we’ve largely removed from our diets. There is evidence that heating high-PUFA oils generates reactive aldehydes and other lipid oxidation products (discussed below). There is evidence that these compounds can damage proteins, DNA, antioxidant systems, and mitochondria. There is evidence connecting mitochondrial dysfunction with metabolic dysfunction and carcinogenesis.

This is all indirect, sure. But bear in mind that the evidence linking alcohol to birth defects is similarly indirect.

And we also have what I would consider pretty direct, damning evidence coming primarily from Dr. Martin Grootveld’s lab.

Cooking with Seed Oils Generates Carcinogens, Directly Linking Seed Oils to Cancer

Dr. Martin Grootveld at De Montfort University in Leicester, England, has spent decades studying what happens chemically when cooking oils are heated.

His work has particular relevance to refined seed oils high in polyunsaturated fatty acids, or PUFA, including:

• soybean oil
• corn oil
• canola oil
• sunflower oil
• safflower oil
• grapeseed oil

Polyunsaturated fatty acids are chemically vulnerable to oxidation. Dr. Grootveld has repeatedly shown that when high-PUFA oils are heated, particularly during frying, their fatty acids undergo lipid peroxidation and generate a complex mixture of lipid oxidation products. Among these are highly reactive molecules called alpha, beta-unsaturated aldehydes. These include compounds such as acrolein and 4-hydroxynonenal (4-HNE), along with numerous other reactive aldehydes.

Aldehydes from Seed Oils Can Damage Mitochondria

Reactive aldehydes are like molecular vandals, on a mission to leave their mark on everything they touch. They can bind to proteins, DNA, and other cellular structures. They can impair antioxidant defenses, alter enzyme function, promote oxidative stress, and damage mitochondria. And research clearly demonstrates that these exact reactive aldehydes powerfully disrupt mitochondrial function and cause mitochondrial DNA damage.

In other words, foods made with high-PUFA oils can generate compounds capable of producing precisely the kinds of cellular injuries that become especially interesting if mitochondrial dysfunction is an initiating event in cancer. Not surprisingly, some of the aldehydes are known carcinogens. For example, crotonaldehyde, which is one of the most carcinogenic compounds in cigarette smoke.

This creates a connection that I believe deserves far more scientific attention. Seyfried’s work asks us to reconsider the cause of cancer. Grootveld’s work identifies a common dietary exposure capable of generating compounds that can damage mitochondria. And my own work on insulin resistance provides another piece of this puzzle.

(Dr. Grootveld liked Dark Calories so much that he invited me to take an honorary position at his university, and now we are working on several papers together!)

Population-Wide Evidence Also Links Seed Oils and Cancer

Seed oils have become ubiquitous in the modern food supply. They’re used extensively in restaurant cooking and frying and appear in countless packaged foods. For many people, exposure isn’t occasional. It occurs meal after meal, year after year. On a population-wide basis, the more seed oil we eat, the more metabolic disease we get. (Graph here.) The more metabolic disease we get, the more cancer we get.

This doesn’t mean seed oils are the only cause of cancer. Cancer is clearly multifactorial. Nor does it diminish established cancer-prevention measures such as avoiding tobacco. It means we need to broaden our conception of what a carcinogen does.

Who Wants a Paradigm Shift?

The prevailing paradigm has encouraged us to look primarily at nuclear DNA mutations. But cells are systems, and mitochondria sit at the center of cellular energy production, redox regulation, metabolism, and survival. Perhaps the better avenue of investigation is not simply: Does this substance mutate DNA? But rather: What does this substance do to the cell that ultimately makes cancer possible?

When we ask the question that way, the relationship between our modern food supply, mitochondrial injury, metabolic disease, and cancer becomes much harder to ignore. At the very least, the possibility deserves far more attention in cancer prevention than it currently receives.

References

Grootveld’s work https://pubmed.ncbi.nlm.nih.gov/35071288/