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If cancer is predominantly a random process, then why don’t organisms with thousands of times more cells suffer more from cancer? Large species like whales and elephants generally live longer, not shorter lives, so how are they protected against the threat of cancer?

While we have a great deal more to learn when it comes to cancer biology, the general belief is that it arises first from mutation. It’s becoming clear it’s actually an incredibly complicated process, requiring a range of variable factors such as mutation, epigenetic alteration and local environment change (like inflammation). While some students may have spent sleepless nights wondering how many mutated cells they contain after learning the fallibility of our replication mechanisms, the reality is that with such an error rate we should all be ridden with cancer in childhood — but we’re not. Our canine companions sadly often succumb around their 1st decade, but humans are actually comparatively good at dealing with cancer. We live a relatively long time in the mammal kingdom for our size and even in a modern environment, it’s predominantly an age-related disease.

While evolution may have honed replication accuracy, life itself requires ‘imperfection’ to evolve. We needed those occasional errors in germ cells to allow evolution. If keeping the odd error is either preferable or essentially not worth the energy tackling when you’re dealing with tens of trillions of cells, then clearly there is more to the story than mutation. In order to maintain a multi-cellular organism for a long enough period, considering that errors are essentially inevitable, other mechanisms must be in place to remove or quarantine problematic cells.

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Lifespan.io is running a SENS fundraiser to aid research into Mitochondrial repair. This is a new fundraiser platform to help get important regenerative medicine research funded and underway. Let us hope this is the start of how research could be funded and that it opens up faster progress.


Engineering backup copies of mitochondrial genes to place in the nucleus of the cell, aiming to prevent age-related damage and restore lost mitochondrial function.

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Ever since the free radical theory of aging was conceived in the 1950s, antioxidants have been a buzzword in health — saturating the cosmetic industry and contributing to a smoothie blending, supplement popping boom.


Ever since the free radical theory of aging was conceived in the 1950s, antioxidants have been a buzz word in health — saturating the cosmetic industry and contributing to a smoothie blending, supplement popping boom. While antioxidants can certainly play an essential role in health, there is growing evidence that additional supplementation has limited benefit and can actually be harmful in some cases.

Aging has yet to be ascribed to one, singular cause and the free radical theory has struggled to prove itself. While in some organisms reducing oxidative stress can prove beneficial and increasing mitochondria targeted catalase (an important antioxidant enzyme) production in mice showed a modest increase in lifespan, when important enzymes were knocked out in C. elegans (a model organism) there was curiously no reduction and reducing expression of various antioxidant mechanisms in mice also failed to reduce lifespan. While a certain amount of vitamins and antioxidant intake is necessary, as many are co-factors in essential reactions, it seems that aside from nutritional value there is little consensus regarding additional benefits.

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Checkout the latest Longevity Reporter Newsletter (15th August, 2015), covering this week’s top news in health, aging, longevity

This week: ‘Danielle’ — An Eye Opening Simulation Of The Aging Process; How Does Chronic Inflammation Lead To Cancer?; Low Inflammation and Telomere Maintenance Predict Healthy Longevity; 3-D Printing: Could Downloadable Medicine Be The Future?; And more.

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“A protein found in the blood of young animals called GDF-11 is inducing systemic rejuvenation effects on bone, muscle, heart, blood vessels, and brains of older animals.

“GDF” stands for growth differentiating factor. It functions to turn “on” senescent stem cells, which results in a restoration of youthful structure and function to senile tissues. This same protein (GDF-11) is found in young humans as well as animals.

Harvard, Stanford, and other universities are conducting remarkable studies showing age reversal in animal models. Researchers from these centers of medical innovation are optimistic that this approach might be applicable to humans.”


Reversing aging may be humanly possible. It may also be closer than you think.

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A universal therapy that targets mis-folded proteins is a very significant step forward if clinical trials in humans translate from animals. Obviously there is more work to be done but it this is the kind of technology we need in order to intervene against biological aging.

It is not hard to see that a therapy like this followed up by another that regenerates the brain eg, the Conboy Lab work by promoting neurogenesis could be a way to repair and restore the brain to healthy function.


A drug that breaks up different types of brain plaque shows promising results in animals and could prevent Alzheimer’s and Parkinson’s disease.

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