Fasting as an evolved mechanism for repair on internal organs | Valter Longo
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In the past, fasting was imposed by the environment during times of famine. Dr. Longo proposes that the human body evolved a natural self-repair mechanism that is switched on during fasting and allows for the repair of damaged cells and organs. In the modern-day with no imposed fasting, these cycles of renewal may remain dormant. In this clip, Dr. Valter Longo discusses how cellular repair mechanisms may have evolved during times of fasting, but are latent in times of food abundance.
Rhonda: So first the threshold between, you know, like you're mentioning the threshold between when you're actually getting rid of intracellular compartments through autophagy, clearing away protein aggregates, pieces of DNA and things like that, but also, and damaged mitochondria, but also the clearing away of complete cells, and particularly damaged cells, which is very interesting to me, because as you mentioned, you've shown this now and there's two different animal models for autoimmune disease, one was multiple sclerosis and the other was the, I think type 1 diabetes.
Valter: Yeah, ours was not, that one particularly wasn't, was not autoimmune. We're doing the autoimmune. There's type 1 induced by, pharmacological induced.
Rhonda: Okay. So it has potential for...
Valter: Yeah, but I can tell you, we've now confirmed it with all the autoimmune diseases. So I think it's going to be applicable to many autoimmune diseases.
Rhonda: So this is what's so cool because, I mean, the, you know, the potential for this type of fasting to cause cells that are preferentially damaged to be cleared away by apoptosis, which makes sense. I mean, I spent six years studying apoptosis and cells that are damaged preferentially die, I can tell you from doing multiple, multiple experiments.
Valter: Even during development, right? In development. I mean, that's the way that the good and the bad are...
Rhonda: Right. It's also how cancer cells are primed to die as well, because cancer cells are damaged. They are mutated and completely damaged, and that may be also why they're very sensitive to stress.
Valter: Yeah, and also, I mean, something that is a speculation but we're starting to think more and more, or at least I'm starting to think more and more, is that...You know, I always say if you cut yourself, it doesn't matter where you cut yourself or if you hurt your head, the system repairs it, right? Or repairs almost anything.
And so what about the inside? You know, is it possible that we never developed a way to fix damaged organs and various systems? So we're starting to think that maybe fasting represents that opportunity to fix the inside, right? And maybe, and just maybe, because everybody had to do it by force, they were forced to do it because there was no food at some point of your month, almost unavoidably you probably were with no food. And so because it was almost unavoidable, it was probably something that...you know, I always also think about sleep, right? And in sleep you feel so tired that you have to sleep. Because obviously people wouldn't have gone to sleep just on their own right?
But in the case of fasting, because it was imposed by the environment, I suspect that maybe we never developed something that forces you to fast. And so now that we eat all the time, which completely lost this auto-repair mode, right? And this could be remarkable because imagine if we had this ability if you have damaged liver, that fixes it. If you have damaged immune cells that are autoimmune, that clears it. And so you never develop defense against autoimmunity because fasting always took care of it.
Now all of a sudden you get rid of fasting, and all these things start building up, whether it's insulin resistance, or liver damage, fatty liver, etc., etc., right?
So, this could be really...and people always are surprised when we say, you know, we're publishing on all these different diseases, but if that's true, then that make sense, right?
Rhonda: Right.
Valter: Because for example, in multiple sclerosis, you see on one side it kills the immune cells. It then turns on the stem cells, then turns on the oligodendrocytes, progenitor, and replace...I mean, it's very...it's like, how the hell does it know how to do all of this? And it does it all in such a sophisticated manner. But if it was an evolved process, that would make a lot of sense.
Rhonda: The thing that's so interesting is how the stem cells, you know, the clearing away of these damaged cells through apoptosis, activating these stem cells which then have to repopulate whatever organ or tissue we're talking about, how they actually can make normal life cell. You're talking about in the case at least for autoimmunity or type 1 diabetes or multiple sclerosis, how they make their immune cells normal, that is so...
Valter: Yeah, but that makes sense, right? Because if you turn on a stem cell, you imagine now that the...you're not going to turn on a damaged stem cell, there's got to be a selection process to pick the...So the stem cell is now of course going to give rise to normal white blood cells, right? They wouldn't have any way to make an autoimmune cell. So, I mean...yeah. So because that happens I think in the differentiated cell, the clonal, so you expand already the differentiated cell. So even I think theoretically that makes perfect sense that once you turn on the stem cell, the hematopoietic stem cell, you will make a healthy...Now, you can always turn the healthy cells into autoimmune cell, but at least initially you will make a healthy one, and that's exactly what we see happening.
Programmed cell death. Apoptosis is a type of cellular self-destruct mechanism that rids the body of damaged or aged cells. Unlike necrosis, a process in which cells that die as a result of acute injury swell and burst, spilling their contents over their neighbors and causing a potentially damaging inflammatory response, a cell that undergoes apoptosis dies in a neat and orderly fashion – shrinking and condensing, without damaging its neighbors. The process of apoptosis is often blocked or impaired in cancer cells. (May be pronounced “AY-pop-TOE-sis” OR “AP-oh-TOE-sis”.)
An immune disorder characterized by an immune response to and subsequent destruction of the body’s own tissue. The causes of autoimmune diseases are not known, but a growing body of evidence suggests they may be due to interactions between genetic and environmental factors. Autoimmune diseases affect approximately 7 percent of the population in the United States and are more common in women than in men. Examples include type 1 diabetes, Hashimoto’s thyroiditis, lupus, and multiple sclerosis.
An intracellular degradation system involved in the disassembly and recycling of unnecessary or dysfunctional cellular components. Autophagy participates in cell death, a process known as autophagic dell death. Prolonged fasting is a robust initiator of autophagy and may help protect against cancer and even aging by reducing the burden of abnormal cells.
The relationship between autophagy and cancer is complex, however. Autophagy may prevent the survival of pre-malignant cells, but can also be hijacked as a malignant adaptation by cancer, providing a useful means to scavenge resources needed for further growth.
An immature cell that can develop into all types of blood cells, including white blood cells, red blood cells, and platelets. Hematopoietic stem cells are found in the peripheral blood and the bone marrow and give rise to both the myeloid and lymphoid lineages of blood cells. The process by which blood cells are produced is known as hematopoiesis.
Myeloid cells include monocytes, macrophages, neutrophils, basophils, eosinophils, erythrocytes, and megakaryocytes to platelets. Lymphoid cells include T cells, B cells, and natural killer cells.
A peptide hormone secreted by the beta cells of the pancreatic islets cells. Insulin maintains normal blood glucose levels by facilitating the uptake of glucose into cells; regulating carbohydrate, lipid, and protein metabolism; and promoting cell division and growth. Insulin resistance, a characteristic of type 2 diabetes, is a condition in which normal insulin levels do not produce a biological response, which can lead to high blood glucose levels.
A physiological condition in which cells fail to respond to the normal functions of the hormone insulin. During insulin resistance, the pancreas produces insulin, but the cells in the body become resistant to its actions and are unable to use it as effectively, leading to high blood sugar. Beta cells in the pancreas subsequently increase their production of insulin, further contributing to a high blood insulin level.
Tiny organelles inside cells that produce energy in the presence of oxygen. Mitochondria are referred to as the "powerhouses of the cell" because of their role in the production of ATP (adenosine triphosphate). Mitochondria are continuously undergoing a process of self-renewal known as mitophagy in order to repair damage that occurs during their energy-generating activities.
A type of glial cell that is involved in the production of myelin, providing support and insulation to axons in the central nervous system. A single oligodendrocyte can extend its processes to 50 axons, wrapping approximately 1 micrometer of myelin sheath around each axon.
Undifferentiated descendants of stem cells. Unlike stem cells, progenitor cells can differentiate into cells of a particular lineage only and they cannot divide and reproduce indefinitely. Progenitor cells show potential in the fields of plastic and reconstructive surgery, ophthalmology, and heart and blood disorders.
A cell that has the potential to develop into different types of cells in the body. Stem cells are undifferentiated, so they cannot do specific functions in the body. Instead, they have the potential to become specialized cells, such as muscle cells, blood cells, and brain cells. As such, they serve as a repair system for the body. Stem cells can divide and renew themselves over a long time. In 2006, scientists reverted somatic cells into stem cells by introducing Oct4, Sox2, Klf4, and cMyc (OSKM), known as Yamanaka factors.[1]
- ^ Takahashi, Kazutoshi; Yamanaka, Shinya (2006). Induction Of Pluripotent Stem Cells From Mouse Embryonic And Adult Fibroblast Cultures By Defined Factors Cell 126, 4.
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