By Marika Sboros

Divergent views on cancer treatment make some oncologists green around the gills. It’s as if specialists believe it’s their way or the highway to certain death.

Yet patients still die from complications of conventional treatment. That’s when they aren’t complaining that treatment is worse than the disease. Of course, treatment can be lifesaving. But you have only to read Siddhartha Mukkerjee’s The Emperor of all Maladies to know how hit-and-miss orthodox medicine can be against cancer.

Canadian nephrologist (kidney specialist) Jason Fung says aspects of the genetic model of cancer are as unlikely as humans mutating and gaining the ability to shoot laser beams out of their eyes or to stick to walls like a spider. Yet we accept unlikely feats from cancer cells daily. Here, Fung argues for cancer as not just a genetic but also an endocrine disease.

It’s one of the most exciting avenues of research internationally. It can make orthodox treatment safer and more effective. It is the focus of a ground-breaking world-first conference, Rethinking Cancer in Paris on September 21. Speakers are prominent doctors and scientists globally working in the field.

It tells the amazing story of Air France captain Jean-Jacques Trochon who “intelligently postponed” chemotherapy and radiation for kidney cancer. Trochon believes his decision is why he is living with, not dying from, cancer.

Dr Jason Fung

Of course, critics may say that Fung should stick to what he knows best – kidney disease. However, there’s good reason that he started researching dread disease.

Kidney disease is one of the most common complications of diabetes. It is also common in patients with “diabesity”. That’s what now call the common co-morbidities of obesity and diabetes.

Thus, many of Fung’s patients are obese, diabetic or both. As he argues, research shows a strong relationship between cancer and obesity. Fung has also spent several years arguing why hyperinsulinemia is the root cause of obesity and type 2 diabetes.

It makes sense then that he thinks it may play a role in dread disease development, too. He believes that diet is as important as genetics in fighting it. Here’s why:

By Jason Fung

Richard Nixon declared war on cancer in 1971. It’s been close to half a century and the war is hardly close to being won. If you simply look at how many people have cancer, things look quite bleak. However, this is not quite accurate.

Cancer screening has increased significantly in the past decades – with increasing adoption of procedures such as mammography and colonoscopy. As you detect the disease earlier, there seems to be more cancer in society.

But there is actually the same amount of cancer; you are just finding more of it.

So, the most unbiased assessment is to simply count the number of deaths, although this, too is not entirely accurate. One of the most important risk factors for the development of cancer is age. And as life expectancy increases, cancer mortality as a percentage also increases.

You can adjust crudely for age, though, and the results are not good.

Click here to read: Cookbook authors dish up scientific cancer ‘cure’


In heart disease, for example,  advances in surgery, angioplasty, smoking cessation and medications (beta blockers, aspirin, and ACE inhibitors) have combined to reduce death rates from heart disease over the last 40 years. But the news in cancer is far more bleak.

While the cancer death rate in those less than 65 has improved, it has barely budged in those over 65, which constitutes the vast majority of disease. As a percentage of death, cancer was 18% in 1975 and 21% in 2013. Not good.

The fact that cancer is far more prevalent in the older age group (>65 years) made this worse. Doctors have made progress in the younger ages, where cancer is more likely to be a genetic mutation. But not in the older age group.

This is despite the tremendous progress researchers have made in medical genetics. We’ve sequenced the entire genome of man. We’ve even sequenced the entire genome of multiple cancers with the wildly expensive and optimistic Cancer Genome Atlas.

You can even get personalised genetic screens for various diseases.

We are now able to develop specific antibodies against virtually any protein in the body. But none of this actually helped.

Where did we go wrong? The big mistake (spoiler alert) was the perception of cancer as a disease of accumulated genetic mutations. When you approach a problem from the wrong angle, you have no chance of seeing the solution.

If you are running in the wrong direction, it doesn’t matter how fast you go. No, cancer is not just a genetic disease. You must approach it as an endocrine (hormonal) disease.

The public and the majority of oncologists (cancer specialists) and researchers commonly perceive cancer as a genetic disease. This is called the somatic mutation theory (SMT). We know that cancer cells contain many different mutations in genes known as oncogenes and tumour suppressor genes.

Click here to read: Cancer therapy of the future? It’s already here – Fettke


Experts believed that cancers develop because of a collection of genetic mutations that happen randomly. That is, a cell slowly, over decades collects a number of random mutations that give it super-powers, like becoming immortal, gain the ability to evade the body’s defences and gain the ability to spread outside its normal boundaries.

It also gains the ability to grow new blood vessels when needed, mutate and develop resistance to chemotherapy etc.

When you think about it that way, it seems about as unlikely as humans mutating and gaining the ability to shoot laser beams out of our eyes or to stick to walls like a spider.

I mean, I’d rather have claws like Wolverine than grow cancer. And it’s just as unlikely. Yet we accept this unlikely feat from cancer cells each and every day.

Click here to read: Seyfried on real cause, right diet to beat dread disease


But there are many lines of evidence that prove that cancer cannot simply be a genetic disease. Diet is a prime example. There is consensus that obesity contributes to certain cancers.

No single substance in the diet, though, shows a strong enough correlation to mark it clearly as a carcinogen, other than some rare stuff like aflatoxin. Not dietary fat, red meat, or carbs can be clearly linked to cancer. Yet together, an estimated one third of British deaths from the disease may be preventable by dietary measure.

An American expert panel also recently came to a similar conclusion.

The exact nature of those dietary changes is debatable since no standard, widely consumed food is known to be particularly mutagenic (causing genetic mutations, like ionising radiation).

Migration studies are a clear example of the environmental influence on cancer rates. Japanese immigrants to the United States almost immediately develop the risk of an American.

Since their genetic make-ups are largely unchanged, any change in risk is largely environmental/ dietary. Compare the risk of a Japanese person in Japan (Osaka 1988) to a Japanese person in Hawaii.

The risk of prostate cancer has gone up by 300-400%! The risk of breast cancer more than triples.

So here’s the paradox. If the risk of a Japanese woman in Hawaii is three times the risk of a Japanese woman in Japan,  why on earth would we consider cancer to be primarily a genetic disease? That makes no sense at all.

If we think it is caused by a collection of random genetic mutations, then why are the genes mutating like crazy in Hawaii? Is it bathed in ionising radiation? There’s lots of cancer in Hawaii, but where are the freakishly strong people who fly?

Compare the cancers found in developing versus developed nations. There are huge discrepancies that simply cannot be a genetic effect. Cancer of the oesophagus, for example, is almost purely found in developing nations. But these risks change based upon migration.

If we use the somatic mutation paradigm, we will miss important effects that could potentially lead to prevention/ treatment.

You know what else shows a very strong migration effect? Obesity. While studies are generally difficult to do, the available data suggest that immigration carries huge risk. For example, immigration from Pakistan to Norway increases Body Mass Index by 4.9 (that’s a huge increase).

Caucasian immigrants to Canada are 15% less likely to be overweight, but this risk gradually increases with duration of living in Canada. By 30 years the risk is identical. 30 years is a very short time to see any type of genetic mutation, but plenty for dietary issues.

There are clearly other variables here – like the exposure to carcinogens (asbestos), or viruses (Human Papilloma Virus) – that may explain the variability in rates.

The point is simply this: The somatic mutation theory is almost certainly wrong. These mutations are unlikely the primary driver.

This myopic focus on genetic mutations has consumed vast quantities of resources (money and research efforts and brain power) and it all leads to a complete dead end. We are barely better off in 2017 than we were in 1971 with regards to the disease in adults.

That’s sad, but true. Only when we face these sobering facts can we start looking for the true nature of cancer elsewhere – as a metabolic, endocrine disease.