We’re Fundamentally Wrong About The World’s Deadliest Disease.

Is it genetics, or something deeper?

Cancer Cell Illustration from Geneng. News / iStock.

If, after all our work, millions of people keep dying every year, we shouldn’t blame it on the disease. After all, cancer doesn’t care.

Clearly, something’s extremely wrong with how we’re approaching things — and it’s our fault. The only explanation is that we’ve laid a faulty foundation on cancer, and every treatment and piece of knowledge we’ve built on it isn’t reliable.

Why Is This So Complicated?

Cancer is a genetic disease.

In our massive body of scientific knowledge on cancer, we package its origins into what we call the “somatic mutation theory.

Using observations from thousands of papers on cell behaviour, it traces cancer back to bad genes. It makes a rock-solid case, and it’s one of the most well-supported theories in modern biology. Rightly so, because it makes complete sense.

Somatic Mutations.

Over the thousands of years we’ve been documenting cancer, we put together a shortlist of all the ways we suspected someone could get it. After we studied this on enough people and verified our findings with enough research, we named these factors carcinogens:

How we view cancer through the lens of somatic mutation theory.

Let’s say you were analyzing a frog with a tumour. What would happen if you isolated one of its cancer cells, and transplanted its nucleus — containing lots of supposedly cancerous mutations — into a new frog embryo?

Considering the somatic mutation theory, it’d be safe to assume that you’d end up creating some cancer cells. If mutations cause cancer, then the expected source of the issue (the nucleus) should turn its new host into a cancer cell. But, we don’t see that.

“There was unequivocal genomic evidence that the R545–1 NT ES cell was cloned from a tumorigenic nucleus of the R545 tumor cell line. Furthermore, these characteristic genomic alterations were present in all R545–1 NT ES cell derivatives.”

Even after being proven to harbour negative mutations in their nuclear DNA, the mice still didn’t develop cancer. After stress-testing these embryos, they achieved the same results as we saw with the frogs.

Powering Up (Way Too Much).

There’s a growing body of research suggesting a completely different explanation behind why cancer cells go rogue. It starts with a seemingly innocent cellular powerhouse that’s pasted on every biology textbook out there. That’s right — I’m talking about our mitochondria.

Those quiescent cells became cancerous, but there was a lot more to it than just that. After the mitochondria transfer, their nuclear DNA began mutating.

Think about that for a second. Not only did the mitochondria encourage cell growth, but they lead to changes in a completely separate organelle.

Cell Metabolism

As an organelle, the mitochondrion’s only job is to take substances (substrates) from our body and convert them to energy. On the cellular level, though, energy looks a bit different from what powers your desk-lamp or iPhone. Here, the basic currency for energy’s a molecule called adenosine triphosphate, or ATP.

“The prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar.” — Otto Warburg.

He fully believed that damage to mitochondria handicapped the OXPHOS pathway and forced cells into Aerobic Glycolysis.

Also, as a side-effect of the inefficiency of Glycolysis, a cancer cell would need to take in 18x more glucose to get the same amount of ATP.

As expected, another hallmark of cancer is an intense hunger for sugar.

Connecting The Dots

How does all this lead to uncontrolled cell growth? The short answer is that it’s forced, too. Everything’s forced in cancer.

Healthy cells tend to slowly stockpile resources to divide from their environment. That’s why they divide slowly.

Cancer cells handle the situation in their own way. They have to grow bigger, since they’re absorbing so much glucose that they can’t store it all. That’s why cancer cells integrate those excess glucose molecules into their structure and expand. They have to grow, because they’re forced to eat so much more than they should:

A better look at what damaged mitochondria do to your cells. Source

Cancer isn’t genetic. It’s metabolic. This isn’t an alternative explanation to cancer. This is the explanation to cancer.

Why does this matter? Because we might be killing people without even knowing what we’re doing.

If we don’t know even understand how cancer even develops, how can we create reliable cures to it without a fluke? We can’t. This is what we’re missing, and it isn’t rocket science.

I’m not a conspiracy theorist, and I hope this article didn’t come off that way. If this means anything, we’ll have to clear our minds and rethink the situation. At the very least, let’s just think for ourselves.



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