Transcription
From the non-expert to the expert, there's been quite the push to understand how cancer can be stopped through fasting. With some, there is this belief that cancer can be starved out of the body and that fasting is the cure to all cancers. But is there any truth to that notion? What I'd like to do throughout this video is introduce you to some of the general molecular mechanisms that drive cancer without getting lost in the details. In doing so, I hope to present something that you may never have heard: the differential stress resistance hypothesis. From there, we'll discuss how fasting affects cancer cells, and then I'll make an argument for why fasting might be an appropriate therapy against cancer.
The only promise that I need from you is to keep in mind that there's much more to cover than what I can peripherally touch on here, but I hope to offer some revelations that you may never have heard before. I won't bog this conversation down too much by discussing the details about cancer itself, but we know that cancer's hallmark is unregulated cell division. Your cells undergo regulated cell division, meaning that you have molecules inside your cells that prevent cell division when it isn't needed. These molecules are often called tumor suppressor proteins; the most famous is p53. However, in many cancers, these tumor suppressor proteins are mutated, meaning that their structure is altered in such a way that they can no longer perform the function that they were intended to fulfill, which is to stop cell division. If key suppressor proteins are inactivated, then we could get unregulated cell division, a requisite of cancer formation.
However, for cells to divide, they require massive amounts of energy and substrates, or building blocks, for the production of a whole new cell. Imagine having to create a clone of yourself; it would mean making two of every part of you—your liver, your kidneys, your heart, and so on. Well, on a microscopic scale, your cells have to do the same, which means mass consumption of the necessary molecules like nutrients. Now, what would happen if you were to stop consuming nutrients, also known as fasting? Research has started delving into this topic.
Well, actually, let's listen to just one of these researchers: "Fasting and fasting cycles could protect the mice from chemotherapy side effects, but it was not clear whether this effect also applied to cancer cells. So if we protected the host by also protecting the cancer cells, the study would be worthless. Without chemotherapy, in a number of different cancers, we saw that the fasting cycles were almost as effective as chemotherapy." So fasting is where researchers have started to focus some of this attention, which is especially evident in a hypothesis generated based on this notion. The hypothesis, as I teased earlier, is called the differential stress resistance hypothesis. I'm going to abbreviate it as the DSR hypothesis, if you don't mind.
The DSR hypothesis essentially states that because cancer cells are genetically programmed to divide uninhibited, it may offer them an advantage in growth. But if supplies, a.k.a. nutrients, run low, cancer cells are disproportionately negatively affected compared to our normally regulated healthy cells. This distinction, this propensity for growth, leads them to be far less adaptable to shifting to a preservation state—a state of non-growth—which our normal healthy cells are perfectly capable of doing because they don't live in the extreme growth state. Normal healthy cells will slow cell division and focus on gene repair as well as autophagy, a process of self-cleansing, while cancer cells will still be trapped pushing growth. Yet the nutrients aren't as available to facilitate that growth. In doing so, they produce significant oxidative stress or damaging molecules that can cause the cancer cell to incur so much damage that they are forced to die.
As one example, a study looking at fasting on breast cancer showed that breast cancer cells that were starved, counterintuitively, increased their protein production, meaning the cells collected large amounts of molecules presumably for cell division, as explained earlier, but could not undergo cell division. Therefore, they were stuck holding on to excess protein molecules that they would otherwise have used on the production of a new cancer cell. Granted, this is speculation, but it is further corroborated when looking at tumor size. The black line is the tumor size when fasting is not implemented; however, when animals with cancer undergo fasting, represented by the blue line, there is a significant reduction in tumor size.
So we have some preliminary evidence that fasting at least slows the growth of some tumors in cancer cell division. But does it also kill cancer cells? Well, one of the mechanisms by which cells die is by self-promoting damage to themselves through proteins known as caspases. These caspases, when activated, destroy components of the cell, thereby causing so much harm to that cell that the cell dies. Again, looking at breast cancer cells, cancer cells that are starved or fasted experienced increased levels of this activated caspase, indicated by a darker splotch compared to the control, which is the same cells without fasting. This isn't foolproof evidence that fasting kills cancer cells, but it does at least lend some evidence that it stresses the cancer cells toward that direction.
Unfortunately, there are limitations to experiments like this because the body is never completely devoid of nutrients; otherwise, all cells would die. The obvious implication of removing nutrients from cells is that they all die, regardless of the cell type. Still, this shows some sensitivity to fasting, and we do know that in living systems, there is a reduction in tumor size. But fasting does more than just slow cancer cell division and stress cancer cells to promote potential cell death; it may have some additional benefits.
I previously mentioned a protein called p53. This protein is one of the most powerful anti-cancer proteins, acting as a tumor suppressor protein. Essentially, if the genome of your cells is damaged, the p53 protein will block cell division, making it impossible for the cell to materialize new cells with these similar genetic damages. Now, many cancers have mutated, dysfunctional p53, but some still have functional versions. So p53 is not the only factor protecting us from cancer. That said, fasting seems to increase p53 levels in specific situations that we'll discuss shortly.
Incredibly, fasting seems to also trigger the expansion, meaning the division, of lymphoid immune cells. These cells, when triggered, have a voracious appetite for destroying tumors. Additionally, people who fasted tended to experience less fatigue from cancer and cancer therapies than people who didn't. But let's speak to that: cancer therapies. I realize many people feel strongly that traditional medical practices like chemotherapy are nothing but poison. There's something to that because chemotherapy is a poison. Just listen to this: chemotherapy drugs are delivered through pills and injections and use cytotoxic agents, which means compounds that are toxic to living cells. Essentially, these medicines cause some level of harm to all cells in the body, even healthy ones, but they reserve their most powerful effects for rapidly dividing cells, which is precisely the hallmark of cancer.
So yeah, there's no denying that chemotherapy is a blunt weapon against cancer, but it does work in many cases. However, it is possible to combine the approaches—fasting and chemotherapy—for even better results. I should interject here before continuing because I feel some people might click off the video at this point, thinking that they've come here for the fasting alone benefits, and that's good enough. I'll state this plainly to keep this interjection short: fasting alone can be insufficient in battling cancer, depending on the cancer. So I would urge you to listen to the rest of what I'll explain in relation to fasting paired with chemotherapy, even if you are resistant to the idea of chemotherapy.
Speaking in tandem with my interjection, the results that we've described from fasting on a cellular level to a holistic level are simply unignorably supercharged when paired with chemotherapy. As I mentioned, fasting alone is often not sufficient to defeat cancer, but fasting can be an excellent contribution to potent chemotherapy. Why do I say that? Well, I've been a bit disingenuous with you because I've been holding some information back. For example, if we look back at the data on tumor size in animals that were fasted versus not fasted, we saw with the blue line being fasting animals that tumor size was significantly reduced. However, what I didn't show you was the pairing of fasting plus chemotherapy. In red, we see an even greater effect.
Moving away from animal studies, there are positive effects in humans as well. Preliminary studies using fasting and fasting-mimicking diets paired with chemotherapy indicate better tolerability of chemotherapy, as well as some preserved health markers that would otherwise be negatively affected by chemotherapy. Still, these are results in humans that need to be done long-term to determine the actual effectiveness of combating cancer directly, not just the side effects of chemotherapy. Hopefully, it would follow a similar result as this recent study, again in animals, using long-term fasting plus chemotherapy. This data indicates 100% survival of the mice compared to the mice only put on chemotherapy for the same amount of time.
We'll have to see more relatable data as it appears. So with these scraps of information that I've presented here for you, there's certainly more. There might be something to this DSR hypothesis. Fasting and chemo are a two-pronged approach to taking advantage of hyper-aggressive, growth-focused cancer cells, or it may be through another mechanism, like this wickedly cool one: for chemotherapy to work, it needs to enter the cell. Unfortunately, the admittance into the cell may be determined by transporters that either allow or disallow, like a gate or a bridge, the drugs into the cell. However, fasting seems to increase the expression of some of these transporters, thereby making chemotherapy drugs more lethal—not because there is more drug present, but because what is present in the blood can more readily attack the cells because it penetrates the cells to a greater degree.
There's so much information that I've left out because I simply can't cover it in one video, but the bottom line is that fasting can be an effective therapy against cancer. Researchers stress that fasting by itself may have limited effects against cancer in most cases, and I would add that it also depends on the cancer. However, fasting and conventional medical practices combined may provide a powerful avenue by which to combat susceptible cancers. I certainly expect to further investigate this topic in the future with far more detail, but for now, let's hope that you feel a bit more educated on some—and truly only some—of the nuances of fasting on cancer. Speak with you next time, and thanks for listening.