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A blueprint for choosing the right fish oil supplement — filled with specific recommendations, guidelines for interpreting testing data, and dosage protocols.
Differential stress resistance is a property that is characteristic of prolonged fasting. During a prolonged fast normal cells develop a tendency to become more resilient to stress, whereas cancer cells are unable to do this as a consequence of oncogenic signaling. Mounting evidence suggests that exploiting this property may be useful towards reducing the toxicity of chemotherapeutics while also maximizing their impact in the treatment of cancer. In this clip, Dr. Valter Longo describes how this was demonstrated in a mouse model and how he believes the same process occurs in humans.
Rhonda: But you did a clinical trial, so are you involved in this clinical trial that you kind of mentioned, like, briefly, which I thought was very interesting? The actual one with fasting, where the cancer patients fasted either before or after the chemo treatment, and I thought it was very interesting that you found, maybe you can talk about it, but you found that their normal cells were more resistant to the stresses of chemo, whereas the cancer cells were more sensitized to that.
Valter: Right, right. So, of course, all of these starts in mice. And in mice, we were able to show very strong effects, what we call differential stress resistance, which is you protect the normal cells, but not the cancer cells. And then, something called differential stress sensitization, where you kill the cancer cells, but not the normal cells.
Rhonda: Can you explain that a little bit, like why that is?
Valter: Yeah. Well, that is, again, because almost every organism, you can start with E. coli, actually, bacteria, and then move to simple organism like yeast, and all the way up to mice, they have starvation responses, right? So, if you starve any system, virtually any system, they'll go into this shielding mode, protected mode, and then, they sit there until food comes around again. So, in this protective mode, they're very resistant to all kinds of things. They're resistant probably because they have to be resistant to the sun, and to chemical produced by other microorganisms that might be surrounding them. And so, then, they happen to also, at least in mice and now we think humans, chemotherapy is also one of the toxins that they're resistant to. So, you starve the normal cells going to the protected mode when you starve a cancer cell though because the oncogenes are the regulatory genes of this protection. The cancer cells, by definition, can never respond, right?
So, they just, normal cells respond no matter what normal cell is, from a muscle cell to hepatocytes, to a brain cell, but the cancer cells don't respond. And that's really what's called differential stress resistance. In the differential stress sensitization, instead, it really has to do with something that, I think, was under-appreciated, which is a cancer cell is viewed as a smart cell. In fact, the cancer cell is a very dumb cell. And why is it dumb? Because it is involved in all this high nourishment environment, right? So, it's involved with a lot of proteins, a lot of amino acids, a lot of sugars, a lot of growth factors, all these things are around all the time. So, by making them available I know the oncologist means well, right? But by making all this available during chemotherapy, you really helping one thing more than anything else, is the cancer, right?
Rhonda: What you're referring to is them telling people to eat a lot of calories.
Valter: Yeah, of course, yes, so they tell them to eat. And so, you know, because the cancer loves sugar, and loves amino acids, right, and depends on sugar and amino acid, the more you give it, the happier it is. And also these nutrients basically, make the normal cells sensitive, right? So, you're making the normal cell sensitive, and you're making the cancer happy, right? Instead of the opposite, which is making the normal cells protected, and make the cancer cells miserable. Why are the cancer cells miserable? Well, because, again, having evolved in this abundance, once you take the abundance away, it's like almost saying imagine somebody that had a very low IQ, you know, been looking for food, you know, and if you make it available, it's easy.
Let's say, thinking about a monkey, let's say a monkey that has got a very low IQ, and, you know, you put it in front of food all around it, and it's gonna have no problem, right? As soon as you take the same monkey with a very low IQ, and you make it extremely difficult to find the food, now that monkey is gonna have a problem. And, you know, and that's how we see the cancer cells. You know, once the amino acids are low, the growth factors and the sugar are low, the cancer is gonna starve. And then, if on top of that, you hit it with chemotherapy, it just has a very low chance of escaping. This is why, in mice, we see cancer-free survival, meaning myself free of cancer only when we combine the starvation or the fasting-mimicking diets with the chemotherapy. We almost never see it when we use each one alone, right?
Rhonda: Mm-hmm.
Valter: We, and many other labs have tried that. You see, which is great, often the fasting, the first thing we can say it's as good as chemo, but you never see, you know, alone, each intervention alone being curative. So, it's very interesting, and this is also very important to point out because a lot of people, tend to either be in the camp of traditional medicine, or in the camp of alternative medicine. And people don't understand that, you know, that both of them are very important, and when you combine it, particularly the alternative integrative medicine that's got a deep scientific foundation, when you combine it, now you have a very powerful system, you know, in your hands. And, you know, whereas each alone doesn't work very well.
A naturally occurring substance capable of stimulating cellular growth, proliferation, healing, and differentiation. Growth factors typically act as signaling molecules between cells. Examples include cytokines and hormones that bind to specific receptors on the surface of their target cells.
A cell of the main parenchymal tissue of the liver. Hepatocytes make up 70-85% of the liver's mass. These cells are involved in: protein synthesis, protein storage, transformation of carbohydrates, synthesis of cholesterol, bile salts and phospholipids.
A gene that has the potential to cause cancer. A proto-oncogene is a normal gene that regulates cell growth and proliferation but if it acquires a mutation that keeps it active all the time it can become an oncogene that allows cancer cells to survive when they otherwise would have died.
An oncogene is a mutated form of a gene ordinarily involved in the otherwise healthy regulation of normal cell growth and differentiation. Activation of an oncogene, through mutation of a proto-oncogene, promotes tumor growth. Mutations in genes that become oncogenes can be inherited or caused by environmental exposure to carcinogens. Some of the most common genes mutated in cancer are the IGF-1 receptor and its two main downstream signaling proteins: Ras and Akt.
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