In this interview at Ending Age-Related Diseases 2020, Steve Hill of Lifespan.io discusses the longevity of humanity with David Wood of the London Futurists. The topics include the public opinion of people who seek longevity; accelerating technology in respect to aging; ways of gaining mainstream appeal, such as humanitarian and economic arguments; his book on superabundance and transhumanism; and future scenarios, both good and bad.
As Functional Medicine docs, we’re committed to working with the body’s own capacity for health. Dr. Josh Mitteldorf offers a contrarian strategy, one which he says is grounded in a new breed of evolutionary medicine.
He tells us that diseases of old age are qualitatively different from the diseases we get when we’re younger, different because in old age, our bodies are part of the problem, not part of the solution.
Aging, says Josh, is the body deliberately destroying itself (for the sake of the population), via inflammation and apoptosis and autoimmune diseases. In this interview, Josh and I find common ground talking about hormesis. In Josh’s theory, the fact that the body lives longer when stressed (e.g. caloric restriction) is proof that the body isn’t trying its hardest to stay young when it’s not stressed.
It may sound like philosophy, but there are real consequences for the future of medicine.
We associate getting older with a loss of energy. On the molecular level, this is quite literally true, because one of the hallmarks of aging is mitochondrial dysfunction. Mitochondria are often referred to as “the powerhouse of the cell,” because they convert nutrients from the food we eat into usable energy, in the form of ATP. But as we age, mitochondria become less effective at generating the energy we need for various chemical processes.
So why does this happen? As with most things in biology, there are definitely multiple factors at work here. But one likely reason is a failure of quality control. As we age, mitochondrial autophagy (aka mitophagy) declines, and our body starts to accumulate broken and dysfunctional mitochondria. This becomes most obvious in tissues that consume a lot of energy, like skeletal muscle. Hence, mitochondrial dysfunction is linked to poor muscular strength in older people. If we could find a way to ramp up mitophagy, perhaps we could retain excellent mitochondrial function throughout our golden years.
In this episode of humanOS Radio, Dan Pardi welcomes Dr. Davide D’Amico to the show. Davide is a research scientist in the field of metabolism and aging. He was previously a post-doc at the Auwerx Laboratory of Integrative Systems Physiology at the École Polytechnique Fédérale de Lausanne (EPFL), where he investigated the role of mitochondrial function in health, disease, and the aging process.
Aging is arguably the leading risk factor for chronic diseases in the modern world. We have historically thought of aging as an inexorable decline of function, driven by the passage of time – something that we simply have to accept, and that cannot be changed.
But what if aging were actually a modifiable risk factor?
Your chronological age, meaning the length of time that you have been alive, obviously cannot be changed. But we know that biological aging can vary significantly, even among individuals who are of similar chronological age. If we can better understand the fundamental mechanisms that underlie biological aging, we might be able to devise interventions that could prevent or delay age-related diseases.
One of the relevant processes is cellular senescence. Cellular senescence is a phenomenon through which normal cells irreversibly cease to divide in response to genomic damage. Senescent cells accumulate in the body as we get older, and they actually do a lot of bad stuff in the body. Senescent cells secrete pro-inflammatory factors, like cytokines, which induces a state of chronic low-grade inflammation. But it gets even worse. These senescent cells can also drive other healthy neighboring cells into senescence. So senescent cells are basically microscopic zombies!
This has driven interest in identifying senolytics – compounds that can selectively kill senescent cells (while leaving normal cells alone).
In this episode of humanOS Radio, Dan talks to Paul Robbins. Paul is the principal investigator at the Robbins Lab at Scripps Research Institute. Notably, his lab has been screening for drugs that can safely and effectively clear out senescent cells.
This research has produced some remarkable results in animal models. For example, he and colleagues found that older mice that were given senolytics became faster and stronger, and experienced a 36% increased median post-treatment lifespan, compared to a control group.
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