Metabolic Theory of Cancer: Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.5B)

Okay!

I left off last time saying that we have two big issues to address with regard to hypoxia as a cause or exacerbating factor in cancer: 

1. What causes tissue to become hypoxic?
2. Is there a role for hyperbaric oxygen therapy in fighting cancer?

  

Let’s tackle them in order.

To be honest with you, I still don’t know which comes first: low oxygen, or mitochondrial dysfunction. The fact is, even when there’s plenty of oxygen available, if the mitochondria are malfunctioning, they can’t use it. But what if what’s causing the mitochondria to malfunction is insufficient oxygen? (I told you last time this stuff is complicated!)

It almost doesn’t matter, right? The bottom line is, whether the tissue is hypoxic or not, the mitochondria are not using whatever oxygen might be present. (Well, they’re using some of it. Remember, kids, when it comes to biology and biochemistry, there are very rarely any absolutes, yes or no, on or off. Things aren't binary, but rather, there's a balancing act. Even cancer cells have some mitochondria that are okay; it’s just that the majority of them are messed up.)

I just have a hard time wrapping my head around it all. Think about angiogenesis: the creation of blood vessels specifically so that the cancerous tissue ensures it has a steady supply of fuel and nutrients. But what does blood carry besides fuel and nutrients? OXYGEN. So you would think that angiogenesis would give cancer cells more oxygen, not less. So going one step further, this being the case, it seems like the mitochondrial dysfunction comes first, because theoretically, there should be sufficient oxygen delivery to the cancer cells, what with all those blood vessels they created for their own nefarious purposes. So there is sufficient oxygen (“normoxia”), yet we have hypoxia-inducible factors out the yin-yang upregulating all sorts of nasty pathways and reactions in these cells to keep themselves alive because they think they’re hypoxic. And the reason they think they’re hypoxic is because the mitochondria aren’t using the oxygen. (That’s my logic, anyway. I told you there was going to be a lot of wild speculation here, and so it begins.)

Metabolic Theory of Cancer: Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.5A)

Graphic adapted from Seyfried et al., 2015

OH. EM. GEE!!!!!

It’s baaa-aaaaack!

Today is June 1, 2016. Looking back through the blog archives, I saw that the previous post in this series on the metabolic theory of cancer was published on June 1, 2015. Yes, kids, it’s been a year. A full year! An entire year to the day. If you have been waiting and waiting (and waiting!) for me to get back to this and address some key concepts we haven’t gotten to yet, believe me, nobody wanted me to get back to this more than I did. I absolutely did not plan on it taking a year. But alas. Hopefully, in that time, you’ve learned a thing or two about insulin, stubborn fat loss, and the use of ketogenic diets for Alzheimer’s disease and other neurological conditions. In fact, I am in the process of adding a new installment to the “ITIS/It’s the Insulin, Stupid” series, but when I saw that I was coming up on the one-year anniversary of neglecting the cancer series, I knew I had to get my rear in gear and just DO IT. I really wanted to do the insulin post first, but considering the date, I thought it would be apropos for me to do this one instead.

Also, just to let you know, since the writing of that last post, I have had the honor of meeting Drs. Seyfried, D’Agostino, and Poff in person. {Squee!!}  I also got to meet Dr. Cunnane, Dr. Newport, Dr. Rho, and Dr. Maffetone. Holy moly…it was a nonstop conference of metabolism rock stars.

I am most definitely going to get to the mamma-jamma, granddaddy of all topics we’ve been waiting for in this cancer series—the ketogenic diet—but please be patient. I’ve very recently had more work stuff come up (in a good way), and I am feeling a bit overwhelmed. I will write about ketosis. I can’t promise when, exactly, that will happen, but I promise it won’t take a year. (Maybe just a couple weeks, considering I’m already working on it.)  ;-)

If you’re new to my blog and have no idea what’s going on right now, the series I’ve written on the metabolic theory of cancer is a “fan favorite” – at least, among the people who like to geek out on the science with me. The cancer series is representative of when my blog becomes a free course in (very basic) biochemistry and physiology, and is peppered with links and quotes from the scientific literature. If you prefer my rants, shakedowns of food labels, and other casual-type posts, no prob! Whatever floats your boat. But for those of you who need to kill lots of time at your desk job, or who perhaps need help falling asleep, you might want to start way back at the beginning and work your way toward today’s post. (Actually, that’s sarcasm. The truth is, I think this stuff is fascinating, and perhaps some of my best work. I swear, that hexokinase 2 stuff STILL blows my mind.)

Since it has been a year (!!) since the last installment, I’ll make it easy for you and list all the posts in order, from first to most recent: 

1. Introduction
2. Cells Behaving Badly
3. Cellular Energy Generation 1 - Glycolysis
4. Cellular Energy Generation 2 - Mighty Mitochondria (Krebs Cycle, Electron Transport Chain)
5. Mitochondrial Dysfunction 1
6. Mitochondrial Dysfunction 2 - They ARE Broken
7. Glycolysis Run Amok & Mutant Hexokinase
8. Aerobic Fermentation (a.k.a. "The Warburg Effect")
9. Cancer Cells are Sugar Junkies
10. Mutations vs. Mitochondria
11. Cancer as a Protective Mechanism
12. Speculation on the Causes of Cancer (Pt.1)
13. Video Lesson! (Thomas Seyfried, PhD)
14. Speculation on the Causes of Cancer -- and How to Mitigate Risk (Pt.2)
15. Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.3 - Viruses)
16. Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.4 - Carcinogens)

Buckle up and hang on tight, everyone. HERE WE GO!

Metabolic Theory of Cancer: Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.4)

We’re in the midst of exploring a few potential causes of cancer, and ways to possibly reduce risk. Up today: carcinogens. (If you’re new here, this post is pretty far down the line in a series that started back in November 2014, in which we are exploring the metabolic theory of cancer. Click here for the first post. Each one will end with a link to the next.) 

I have been saying that sometimes, people can do “all the right things,” and still end up developing some pretty gnarly health issues. I have also said that some of the diet and lifestyle factors we suspect might cause cancer (mostly by way of disrupting mitochondrial function) probably apply less to little kids than they do to older folks. So, aside from what we’ve already covered—viruses, age, and freaky mutations to mitochondrial DNA, what else might be causing cancer in babies and other people with no obvious risk factors?

Metabolic Theory of Cancer: Speculation on the Causes of Cancer -- and How to Mitigate Them (Pt.3)

Graphic modified from Seyfried, et al. 

Cancer as a metabolic disease: 

implications for novel therapeutics. 

Carcinogenesis. 2014 Mar; 35(3): 515–527.

VIRUSES

The potential cancer cause we’ll look at today is viruses. Some cancers are known to be viral in origin, and this makes total sense. Viruses hijack a cell’s replication machinery, right? They hijack the replication mechanisms such that the virus’ own DNA or RNA gets copied like crazy, so we’re left with lots of cells that contain tons of viral DNA/RNA. I am not a microbiologist, nor do I play one on TV. But I have to assume that having lots of viral DNA or RNA floating around in a cell probably isn’t good for mitochondria. Either way, if certain viruses do cause cancer, my guess would be that they do so by affecting mitochondrial function.

As a potential cause of cancer, viruses can strike people of any age. I suspect viruses are one of the primary drivers of cancer in children. I can’t imagine much else causing it. Like I said, older people have had many more years to abuse their mitochondria via diet, lifestyle, and unknown environmental exposures. But little kids? Not so much. Something else has got to be driving cancer in younger people. (And like I've said before, it’s entirely possible there’s a role for maternal & paternal health/diet at the time of conception and during gestation, as well as environmental exposures in utero, but, like the authors of the paper I mentioned in an earlier post said, if you think I’m about to blame the parents of a child with cancer for causing that child’s cancer, you are crazier than a vegan at a Brazilian churrascaria.)

In terms of prevention,  We can’t do much about this except to make sure our immune systems are up to snuff. I have said before that most of us probably “get cancer” all the time. We have cells behaving badly and doing wacky things left and right, but our immune systems go to work and kick those misbehaving cells to the curb. (Or the cells engage in apoptosis, commit suicide, and save our immune systems the trouble.) So how might we try to ensure our immune systems are up to the task? I was originally going have a separate post (or two or three!) about cancer prevention, but it seems more logical to address potential prevention/mitigation strategies in the same post as I write about putative causes. (I would be embarrassed to admit how much time I’ve spent going back and forth over this issue, about which most of you probably don’t care one way or the other.)

Metabolic Theory of Cancer: Speculation on the Causes of Cancer -- and How to Mitigate Risk (Pt.2)

If the previous post in this series on cancer (before the video) was unsettling, good! It was supposed to be. It was meant to remind us that cancer is a vile beast, and that it can spring up seemingly from out of nowhere. It strikes people who are total health trainwrecks, and people who, by all accounts, are healthy. (That is, except for the cancer...) It strikes old people, young people, fat people, thin people, rich people, poor people, PhDs, high school dropouts, men, women, and everybody somewhere in between.

We are working under the theory that cancer is a metabolic disease. Something damages mitochondrial function to the point that cellular metabolism is derailed, and all the nefarious things cancer cells do can be understood as logical sequelae of broken mitochondria and cells that are fighting to keep themselves alive. (Anyone else hearing “Eye of the Tiger” playing in their head right now? Hehheh. [BTW…to anyone out there in the Philadelphia area, I did the Broad Street Run several years ago and someone on the sidelines about a mile from the finish line had a boom box and they were playing that song, and it was awesome. Especially because the original Rocky is one of my all-time favorite movies, but I digress. Adrian!!])

I left off last time saying that, according to the metabolic theory of cancer, anything that contributes to mitochondrial dysfunction can be considered a potential cause of cancer. I think the reason older folks tend to have higher rates of cancer is simply that their bodies have been exposed to potential cancer-causing dietary, lifestyle, environmental, and unknown factors for longer than younger people’s bodies have been. That stuff’s gotta add up over time, no? Frankly, in this day and age, I think if you make it to 85 without getting cancer, you’re kind of a living miracle.

But recall that I made a point to emphasize that babies and toddlers get cancer, too, so it’s not only a matter of physiological insults building up over time. And it’s not just eating too much vegetable oil, or slurping down too much sugar, or being sedentary, or smoking, or being exposed to too much radiation, or whatever else we might speculate could cause cancer. There are other factors at work here.

Metabolic Theory of Cancer: Video Lesson!

Since I've fallen behind in churning out new posts in the cancer series on this blog, I wanted to share a little something with you to whet your appetite for more, and to remind you of all the amazing things we've covered so far. (I’ll get back to posting once I’ve written a few and have them in the hopper, ready to go, but I hope you’ll agree that finishing my Alzheimer’s book constitutes a “good cause” for having put things on hold.) 

I have quoted a ton from the work of Thomas Seyfried, PhD, and his colleagues & students. Here, you’ll get to see the man, himself, in action. If you’ve followed along in the series so far, you will be able to understand it all. In fact, you’ll know even more details than Dr. Seyfried goes into here. He only had 55 minutes, after all, and he wasn’t speaking to a room of molecular biologists or biochemists, so he kept things pretty general.  

Still, he managed to cover a lot of ground in less than an hour. He touches on the following, which you are now familiar with:

Metabolic Theory of Cancer: Speculation on the Causes of Cancer (Pt.1)

Those of us who are steeped in the ancestral health paradigm sometimes get a little too big for our britches. Because we know a little more about the care and feeding of the human body than the average guy or gal on the street, we tend to think we have an explanation for just about every health-related issue there is. When someone we know is diagnosed with a chronic illness, it’s easy for us to say to ourselves, “If only he had done x, y, and z, this wouldn’t have happened.” Or, “If only she hadn’t done a, b, and c, she wouldn’t have ended up like this.”

And, sure, when it comes to things like type 2 diabetes, heart disease, obesity, difficulty conceiving, and the like, we do have plenty of answers. (Or think we do, anyway.) So we play the blame game. The afflicted individuals brought their conditions upon themselves by engaging in certain behaviors and/or not engaging in others. It’s not that we think they “deserve” whatever conditions they have; it’s just that we can readily identify things they did or did not do, that eventually brought those conditions about. (And in my opinion, in some cases, ignorant doctors hold just as much responsibility as the patients.)

But what about cancer? Anyone out there gutsy enough to say that someone with cancer had it comin’? I’m sure as heck not.

Metabolic Theory of Cancer: Cancer as a Protective Mechanism

“Cancer cells were producing energy in a way that evolution had set aside as an auxiliary pathway, a highly inefficient generator that kicked in when the power went out.” (Christofferson, p.20) 

“Tumors bypass many of the biochemical constraints that regulate metabolism, in order to maximize their survival at great expense to the host.” (Mathupala, Ko, Pedersen, 2010)

The amplified rates of glycolysis “indicate a strategy used by highly malignant tumors to survive as well as thrive within the host using a remarkable set of coordinated molecular mechanisms. These mechanisms, which are very similar to those utilized by some highly successful parasites, indicate a sophisticated strategy devised by tumors to survive even the most inhospitable microenvironments within the host.” (Mathupala, Rempel, Pedersen, 1997)

Throughout this series on the metabolic origins of cancer, I have been hinting that cancer—destructive, devastating, scary cancer—might be an evolutionarily conserved protective mechanism. I realize this is politically incorrect. But when we understand some of the biochemistry and physiology involved, this is actually a fairly logical conclusion to arrive at.   

I have gone to great lengths to explain some of the relevant biochemical pathways involved in how and why cancer cells accomplish all the seemingly horrible things they do. In looking at glycolysis, the shift to hexokinase 2, aerobic fermentation, the upregulation of glucose transporters, and more, we have explored a lot about the how of cancer. And we’ve certainly talked a bit about the why. Today, let’s go a little farther down the rabbit hole of the why, because, as I left off saying last time, if we can figure out why cells become malignant, we might have better odds at preventing cancer. We can certainly develop more effective treatment protocols if we understand the how of cancer, but understanding the why will give us even more of an advantage in devising treatments, as well as creating (potentially) better prevention strategies and strategies to prevent recurrence.    

Metabolic Theory of Cancer: Mutations vs Mitochondria

“Let’s get ready to RUUUUMBLLLLLE!”

“Maybe we’ve mischaracterized the origin of cancer. Maybe cancer is not a genetic disease after all. Maybe we are losing the war against cancer because scientists are chasing a flawed scientific paradigm, and cancer is not a disease of damaged DNA but rather one of defective metabolism.” (Christofferson, xiii)

“If scientists have mischaracterized the origin of cancer, then we have lost three decades trying to target mutations that are a side effect rather than the motor driving the disease. (Christofferson, p.223)

“It is interesting to note that none of the current approaches to brain cancer management discussed at a recent symposium involved strategies to target tumor cell energy metabolism. Several presentations at this symposium discussed the failures associated with current approaches to management. As long as [brain] cancer is viewed as something other than a disease of energy metabolism, the failures will likely continue in our opinion.” (Seyfried et al., 2012)

Metabolic Theory of Cancer: Cancer Cells are Sugar Junkies

“One of the most common and profound phenotypes of cancer cells is their propensity to utilize and catabolize glucose at high rates.” (Mathupala et al, 1997)

“The higher the glucose levels, the faster the tumors grew. As glucose levels fall, tumor size and growth rate falls.” (Seyfried et al., 2012)

“Hyperglycemia was also directly linked to poor prognosis in humans with malignant brain cancer.” (Seyfried et al., 2012)

Cancer cells are sugar junkies.

If those five words, strung together in that order, are a surprise to you, then you haven’t been paying much attention so far. If you’ve been keeping up with the previous posts in this series on the metabolic origins of cancer, you will have seen this coming a mile away. (Or, rather, four or five blog posts away.)

Cancer cells love glucose. They need glucose. And they do everything in their power to suck up as much of it as they possibly can, even at the expense of healthy tissue elsewhere in the body. Short of actually taking control of the motor functions of your arms and hands in order to pour you a giant bowl of sugar-frosted breakfast cereal and cram it down your throat, cancer cells do everything they can to ensure they have access to a never-ending supply of glucose. 

In the past few posts, we’ve looked in detail at the main reason why cancer cells do this, and a few mechanisms for how they do it. I have been saying all along that cancer cells are wily little things, and they perform some stunningly impressive feats of metabolic Twister in order to accomplish the nefarious task of keeping themselves alive by gorging on glucose.

Since it’s been a while since the last post, let’s take a quick look back at what we’ve covered so far, regarding cancer cells’ dependence on glucose as their primary fuel.

Metabolic Theory of Cancer: Aerobic Fermentation (a.k.a. "The Warburg Effect")

Did I blow your mind with that mutated hexokinase stuff in the previous post? (To be honest, it blew my mind, when I first read about it. Still does, actually.)

You can see that as we gather more pieces of this puzzle, cancer cells’ voracious appetite for glucose is starting to reveal itself. So is—for lack of a better term— the intelligence of cancer cells. These little buggers are good at doing whatever they need to in order to stay alive, aren’t they? I mean, their mitochondria are broken. But they need fuel. And because the mitochondria are broken, the only fuel they can use successfully is glucose. So they start using this variation of hexokinase in order to make sure that glycolytic metabolism will never stop. Crazy! (Yet ingenious, no?)

As an aside, I have to mention here that cancer seems to be a metabolic condition every bit as much as Alzheimer’s disease is, but they are opposite sides of the same coin: In both conditions, the mitochondria have lost the ability to effectively generate ATP. In Alzheimer’s, the protective mechanism involves cells shutting off the glucose spigot, whereas in cancer, the spigot is turned on full blast and never shuts off.

Last time, we discussed cancer cells ramping up glycolysis in order to feed themselves. And we left off saying that, as a result of this abnormal amount of glycolysis, we have a ton of pyruvate building up. And the fate of this pyruvate, as I’ve mentioned in past posts, is fermentation—an anaerobic process. But cancer cells do something interesting that most healthy cells don’t: they perform incredible amounts of fermentation even in the presence of oxygen.

Metabolic Theory of Cancer: Glycolysis Run Amok & Mutant Hexokinase

“The ability to sustain an enhanced glycolytic rate represents one of the most consistent and profound biochemical phenotypes of many cancer cells.”
                                            -Mathupala et al, 1997.


Through the previous posts in this series, we have woven a path through an introduction to the metabolic origins theory of cancer, some basic facts about cancer cells, cellular energy generation, mitochondrial structure & function, and potential causes of mitochondrial dysfunction. We have also established that there is a large degree of mitochondrial abnormality in cancer cells. We ended things last time by saying that we would explore cancer's next two most striking calling cards. So here we go. More of the metabolic hallmarks of cancer cells. (And finally, you will start to see why all my blabbing on and on about glycolysis and the Krebs cycle were necessary. I promise!)

Before we get into things today, I’d like to thank anyone who’s still along for the ride. I genuinely believe the metabolic theory of cancer holds an incredible amount of promise, and I consider it a privilege to be able to share with you my understanding—however rudimentary—of the science involved. It has occurred to me that, for the purpose of this series, my blog has become a free course in biochem & physiology, rather than the popular stuff with sensationalist, attention-grabbing headlines about adrenal fatigue, digestion, and women’s hormones. I may be getting far fewer page hits than the big boys and various “gurus” out there, but I sincerely think this could be life-saving information. (And frankly, between you and me…just us friends here…I’m kinda tired of all that adrenal/thyroid/digestion stuff, even if I do find it fascinating most of the time.) Based on the number of page hits, not too many folks are interested in this deep dive into the metabolic origins of cancer. Oh well. Their loss. I like writing about this, and I know there are at least one or two of you out there who value it, so I'll keep going. (And I will try not to be discouraged that other people's posts about “Paleo chocolate chip banana bread” and such generate more buzz than this supremely critical information.)

So to anyone out there who’s still with me, thank you. I hope you continue to find it worth your time.

Metabolic Theory of Cancer: Mitochondrial Dysfunction 2 - They ARE Broken

Class is back in session!

We have covered several hallmarks that make cancer cells different from healthy cells. I’ve been saying there are a few more we’ve been holding off on discussing until we laid a bunch of critical groundwork about cellular energy generation. Well, I'm happy to report that we have emerged from the biochemical weeds, and now, we’re ready to start addressing the first of those remaining hallmarks. 

I have been emphasizing all along that mitochondrial dysfunction is at the heart of the metabolic theory of cancer. Understanding the implications of this is so fundamental to our grasp of cancer as a metabolic disease that we have dedicated a couple of (very long) posts to exploring the structure and function of mitochondria. This was essential groundwork to lay, since we can’t understand what might happen when mitochondria malfunction if we don’t know how things are supposed to work when they’re healthy and everything’s groovy.

The rest of the series will focus on the ramifications of broken mitochondria. Most of the hallmarks of cancer cells make perfect sense as the logical results of mitochondria that are incapable of generating sufficient energy (ATP). But there’s a big, gaping hole in things so far. We haven’t actually established that mitochondria are malfunctioning in cancer cells. I’ve been saying so for a while, but what if I’m making that up? What if I’m just saying any old thing that makes sense because I want you to believe the rest of what I’m going to say? (“These aren’t the droids you’re looking for…”)

So today, let the official record show that mitochondria are abnormal in cancer cells. 

But before we get started, if you’ve just stumbled onto things here, you’ll want to fill yourself in on what we’ve covered so far:

• Introduction: Metabolic Theory of Cancer
• Cells Behaving Badly
• Cellular Energy Generation 1 - Glycolysis
• Cellular Energy Generation 2 - Mitochondrial Structure & Function
• Mitochondrial Dysfunction 1

Metabolic Theory of Cancer: Mitochondrial Dysfunction 1

Welcome to the next installment in my ongoing series exploring the metabolic theory of cancer.

If this is your first visit, you might want to check out the posts leading up to this:

1. Introduction
2. Cells Behaving Badly
3. Cellular Energy Generation 1 - Glycolysis
4. Cellular Energy Generation 2 - Mitochondria

Last time, we started exploring the structure and function of mitochondria, our cells’ main energy generators. I have been saying all along that mitochondrial dysfunction—the inability of mitochondria to generate sufficient energy (ATP)—is at the heart of the metabolic origins theory of cancer. Another leg of this table is mitochondrial insufficiency—too few mitochondria, even if they are functioning perfectly well. For today, though, we’ll focus on dysfunction.

The previous post left off saying we would take a look at a few things that can cause structural damage to mitochondria. And let’s remember: since structure determines function, if mitochondrial structure is compromised, then function will be compromised as well.

Metabolic Theory of Cancer: Cellular Energy Generation 2 - Mighty Mitochondria

We meet again!

If you’re new here, we are in the midst of exploring a fascinating theory regarding the etiology of cancer. We’ve already covered some ways in which cancer cells differ from normal, healthy cells, but we’re holding off on looking at three or four of the most striking hallmarks that make cancer cells different from healthy cells until we have a good understanding of how our cells generate energy.

If you’re just tuning in, you’ll want to check out the previous posts in this series:

1. Introduction
2. Cells Behaving Badly
3. Energy Generation 1 - Glycolysis

Last time, we looked at the biochemical pathways known as glycolysis and fermentation, both of which are old and somewhat “primitive,” and are relatively inefficient ways of harvesting ATP from carbohydrates (glucose, specifically). We briefly introduced the more complex pathway called oxidative phosphorylation (OxPhos), also called cellular respiration. Recall that “respiration” is a good way to think of this, since this pathway requires oxygen. OxPhos takes place within specialized structures inside cells, called mitochondria.

If it seems like we’re veering off course to explore all this energy and mitochondrial “stuff,” I promise, these brief forays into cell biology are building a very necessary foundation, without which we won’t be able to make sense of the metabolic theory of cancer. After all, how can we understand cancer as a metabolic disease if we don’t have at least a cursory familiarity with cellular metabolism?

Metabolic Theory of Cancer: Cellular Energy Generation 1 - Glycolysis

 

If you’re just joining us, welcome! You have serendipitously stumbled upon a series in which I am exploring the metabolic origins theory of cancer—its scientific underpinnings, and the therapeutic implications thereof. To bring yourself up to speed, check out the introduction and the second post. (This is the third.)  

Last time, we made a list of several ways in which cancer cells behave differently from healthy cells. I left off saying that we had to hold off on discussing three of the most important of these distinguishing behaviors until we had a working understanding of how our cells generate energy. So that’s what’s on the menu today. (Hope you’re hungry!)

As we get into things, it might seem like we are going far afield, and like this couldn’t possibly have anything to do with cancer. I assure you, there’s a method to the madness, and what we’ll be talking about in the next couple of posts is absolutely essential ground to cover if we hope to understand the metabolic origins theory of cancer.

Metabolic Theory of Cancer: Cells Behaving Badly

If you’re just tuning in, you have landed on a series in which we are exploring the metabolic origins theory of cancer. To find out what this means, take a minute to visit the introductory post. (You can also just read this book review on Amazon for a quick version of what this is all about.)

In this first installment of getting into all this, I think it’s a good idea for us to take a look at some of the ways in which cancer cells distinguish themselves from healthy cells.

• Generally speaking, they don’t die. Healthy cells undergo a kind of programmed suicide when their parts & pieces are damaged or worn out. They’re not supposed to live forever. When they outlive their usefulness, they make a graceful exit. This programmed cell death is called apoptosis, and it is largely absent in cancer cells. Think of it as the reverse Darwin Awards: instead of taking themselves out of the gene pool by doing something really stupid, cancer cells are absolute geniuses at keeping themselves in it—forever. (Until, that is, they grow and spread enough of themselves that they kill their “host,” which, when you think about it, actually does get them a Darwin Award.) Seriously, though, instead of dying as programmed, like good little cells, cancer cells just multiply, and multiply, and multiply, and grow and grow, and spread and spread. 

Metabolic Theory of Cancer: Introduction

If you have followed my blog for any length of time, you are probably accustomed to me having contrarian views. Much of what I believe about nutrition, food, and health, runs counter to the advice we’ve heard from the government, the popular media, and, for the most part, even from our own professional healthcare providers. I have talked many times about my feelings on saturated fat and cholesterol, and I’ll have a few posts coming up on another misunderstood and wrongfully maligned essential nutrient—sodium.

In the meantime, there is another issue—a big, big issue—that I’d like to bring attention to, and I’m going to strike while the iron is hot. On this week’s episode of the Paleo Solution Podcast (which you can check out right here), Robb Wolf is interviewing Travis Christofferson, who wrote a book called Tripping Over the Truth: The MetabolicTheory of Cancer. I first became aware of Travis and his interest in cancer research back in 2013, when he wrote this guest post for Robb’s website. I left a comment, which spurred Travis to check out my blog, where he saw that I do book reviews. Well, he asked me to review the book several weeks ago, and you can now read my glowing review of it on Amazon.

I had intended to write an additional review tailored specifically for my blog audience, but the more I thought about it, the more I realized there is so much fascinating, educational, and potentially life-saving information to be had by digging into this material that there was no way a simple one-post book review would do it justice. So instead, this will be a multi-part series looking at a contrarian—but revolutionary and extremely promising—view on the etiology and potential treatment of cancer.