This Review examines several emerging features of autophagy and postulates how they may be linked to aging as well as to the development and progression of disease. While autophagy is intimately linked to health, the intricate relationship among autophagy, aging and disease remains unclear. This includes dementia, cancer and heart disease.īut, at the moment, we just don’t know enough about autophagy in humans to make any claims about what we can do to increase it, or any health benefits.īen Lewis, science writer and communicator at the South Australian Health and Medical Research Institute, co-authored this article.Autophagy is a fundamental cellular process that eliminates molecules and subcellular elements, including nucleic acids, proteins, lipids and organelles, via lysosome-mediated degradation to promote homeostasis, differentiation, development and survival. Because of this, it has the potential to address some of the biggest health issues our society currently faces. So far, we know it can slow biological ageing in laboratory animals. However, nothing directly shows it can increase autophagy in humans.Īutophagy has only been widely studied for around 15 years. One prominent product for sale is spermidine, which can increase autophagy in the laboratory, such as in yeast and cultured human cells. So exactly how much fasting is required to increase autophagy in humans is completely unknown: influencer claims of 16, 24 or 48 hours are stabs in the dark. For example, a mouse can only go without food for two to three days before dying, while a human can go without food for weeks. Indeed, work on the mechanisms of autophagy really did win the Nobel Prize in 2016.īut influencers’ claims wildly extrapolate from preliminary data without context. ShutterstockĪs dubious as these claims might seem, a lot of them do tend to stem from a grain of truth. There is no end of advice and nutritional supplements that promise to increase autophagy for healthy ageing. Or, you can buy supplements claiming to increase autophagy with ingredients such as citrus bergamot. These tend to be books or material that explain how to diet your way to more autophagy (using intermittent fasting or keto-diets for example). Given the positive results in animals, and because autophagy is sensitive to nutrition, it is not surprising there is no end of advice and nutritional supplements that promise to increase autophagy for healthy ageing. At best this makes various claims of boosting autophagy and its benefits premature, and at worst, completely incorrect. We simply do not understand enough about autophagy in humans, and there has not been enough time to test whether autophagy-boosting diets or supplements actually work in people. There's no magic way to boost your energy. We’re still not sure about the levels of autophagy in tissues like the brain or whether the autophagy activity we see in the blood matches elsewhere in the body. But even that is limited to blood samples. How would we know if it’s the same in humans?įor us to know if fasting, taking a pill or some other activity affects autophagy in humans (and our health), we need to be able to measure if autophagy is increasing or decreasing.Īnd our group has developed the first test of its kind to measure how autophagy activity varies in humans. Of mice and men: why animal trial results don’t always translate to humans But, and this is the big stumbling block, we don’t really know how it acts in humans. This means diet can potentially modify autophagy. If we decrease nutrition in laboratory cells and laboratory animals, autophagy increases to compensate. And because autophagy is crucial for survival during starvation, it is sensitive to nutrient and energy levels. Decreased autophagy also accelerates signs of dementia and heart disease in mice.Īutophagy degrades cellular components to re-use as an energy source during advanced stages of starvation in mice. For example, genetically engineered mice with less autophagy are more likely to develop tumours. Removing these waste products can potentially affect age-related diseases. Author provided Mice benefit, but do humans?
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