Lifeboat Foundation: Safeguarding Humanity
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Category: life extension

Timestamps:

0:00 How the Rose lab more than doubled the lifespan of Drosophila.
17:20 Use of machine learning (ML) and multi-‘omics to characterize aging, and use of ML to develop interventions.
37:04 Adherence to an ancestral diet in Drosophila extends healthspan relative to their evolutionary recent diet.
40:35 The importance of measuring objective markers of health to determine if one’s diet is best for them.
44:04 Does aging stop, and use of biomarker testing to help decipher/optimize that.
53:33 The importance of characterizing aging for both Drosophila and its co-associated microbiome.
1:00:35 Why a massive, wide-scale, Manhattan-project approach for increasing human lifespan is necessary.

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Now researchers have used US economic, health, and demographic data to put a price on just how valuable such an intervention could be. In a paper in Nature Aging, they showed that treatments that slow down aging could be worth US$38 trillion for every extra year of life they give people.

This isn’t the first time someone has tried to pin a number on the benefits of slowing aging. The authors reference a 2013 study in Health Affairs, which estimated that a 2.2-year increase in life expectancy could be worth as much as $7.1 trillion over 50 years.

The new study uses a different methodology, though, known as value of statistical life. This is the measure used by various US agencies and represents how much people would be willing to pay to reduce their risk of dying. It incorporates concepts like health, consumption, and leisure, and therefore measures not just quantity but quality of life.

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Immortality DNA strands found in humans.

Distributed stem cells (DSCs), which continuously divide asymmetrically to replenish mature tissue cells, adopt a special form of mitotic chromosome segregation. Chromosome segregation is nonrandom instead of random. DSCs cosegregate the set of sister chromosomes with the older of the two template DNA strands used for semiconservative DNA replication during the preceding S phase. Neither the responsible molecular mechanisms nor the cellular function of nonrandom segregation are known. Here, we report evidence that immortal strand chromosomes have a higher level of cytosine 5-hydroxymethylation than mortal chromosomes, which contain the younger DNA template strands. We propose that asymmetric chromosomal 5-hydroxymethylation is a key element of a cellular mechanism by which DSCs distinguish older DNA template strands from younger ones.

Immortal strands are the targeted chromosomal DNA strands of nonrandom sister chromatid segregation, a mitotic chromosome segregation pattern unique to asymmetrically self-renewing distributed stem cells (DSCs). By nonrandom segregation, immortal DNA strands become the oldest DNA strands in asymmetrically self-renewing DSCs. Nonrandom segregation of immortal DNA strands may limit DSC mutagenesis, preserve DSC fate, and contribute to DSC aging. The mechanisms responsible for specification and maintenance of immortal DNA strands are unknown. To discover clues to these mechanisms, we investigated the 5-methylcytosine and 5-hydroxymethylcytosine (5hmC) content on chromosomes in mouse hair follicle DSCs during nonrandom segregation. Although 5-methylcytosine content did not differ significantly, the relative content of 5hmC was significantly higher in chromosomes containing immortal DNA strands than in opposed mitotic chromosomes containing younger mortal DNA strands.

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Circa 2010

In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits, and impairments in disorders such as Alzheimer’s disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and β-amyloid likely contribute to impaired neurogenesis in AD. Since factors such as exercise, enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seem promising.

There is a progressive decline in the regenerative capacity of most organs with increasing age, resulting in functional decline and poor repair from injury and disease. Once thought to exist only in high turnover tissues, such as the intestinal lining or bone marrow, it now appears that most tissues harbor stem cells that contribute to tissue integrity throughout life. In many cases, stem cell numbers decrease with age, suggesting stem cell aging may be of fundamental importance to the biology of aging (for review, see Ref. [1]). Therefore, understanding the regulation of stem cell maintenance and/or activation is of considerable relevance to understanding the age-related decline in maintaining tissue integrity, function, and regenerative response.

The adult brain contains neural stem cells (NSCs) that self-renew, proliferate and give rise to neural progenitor cells (NPC) that exhibit partial lineage-commitment. Following several cycles of proliferation, NPC differentiate into new neurons and glia. NSCs are increasingly acknowledged to be of functional significance and harbor potential for repair of the diseased or injured brain. The dramatic decline in neurogenesis with age is thought to underlie impairments in learning and memory, at least in part. Aging is also the greatest risk factor for Alzheimer’s disease (AD), a neurodegenerative disease characterized by progressive loss of memory and cognitive decline. Alterations in neurogenesis have been described extensively in animal models of AD, and key proteins involved in AD pathogenesis are shown to regulate neurogenesis.

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To date, there have been no metrics for accurately assessing individuals’ inflammatory status in a way that could predict these clinical problems and point to ways of addressing them or staving them off, Furman said. But now, he said, the study has produced a single-number quantitative measure that appears to do just that.

You’re as old as your immune system.

Investigators at the Stanford University School of Medicine and the Buck Institute for Research on Aging have built an inflammatory-aging clock that’s more accurate than the number of candles on your birthday cake in predicting how strong your immune system is, how soon you’ll become frail or whether you have unseen cardiovascular problems that could become clinical headaches a few years down the road.

In the process, the scientists fingered a bloodborne substance whose abundance may accelerate cardiovascular aging.

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A serving of mushrooms is just 0.08 kg of CO2 emissions—only lentils have a lower per serving CO2 emission level.

One common question J.P. and I get over and over again is about the problem of overpopulation—if human life extension is a humanitarian goal worth pursuing, won’t there be an inevitable environmental crisis? One worse than what we’re already facing?

When we covered the ethics of life extension we partially answered this question based on what we know about population and consumption trends now (tl;dr: we’re more likely to face a crisis of under population than overpopulation). That said, it’s practically impossible to be able to fully forecast environmental trends 50200, and further years into the future. We noted, “Spanners actually need to address it because we will have to continue living through the consequences of climate change if we don’t.”

In other words, if you’re interested in indefinitely extending your own life, sustainable eating should be a priority today because you’ll most likely be alive in the trash-filled, resource-scarce world of tomorrow.

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Ageing is an incredibly complicated process, so much so that we do not yet understand exactly how complicated it is. It is in fact so complicated, that it could actually be incredibly simple. Confused? Well, imagine if you were a structural engineer who was trying to understand why a building collapsed. From an initial inspection of the rubble, it may be extremely difficult to work out exactly what went wrong. Was the building made from inferior materials? Was it built incorrectly? Was its destruction deliberate? Did it just fall apart due to age? All of these are possible, but what was the true cause for its destruction? Well, that is the same mystery we are trying to solve in longevity research. We can see the damage that is caused by ageing, but what is the cause? Is it a general accumulation of damage, or are there single points of failure which have knock on effects that affect the entire body? A cascade failure if you will.

Of the many different changes that occur during the ageing process, one of the most well-known and understood is the decreased capacity for our body to produced chemical energy, which has a knock-on effect throughout the body. This results in a general decrease in our ability to carry out cellular functions and will therefore effective everything from muscle strength to DNA replication and repair. This decrease in energy output has been linked to defects in our mitochondria, but in addition to these physical defects that occur in these small organisms, we now know that they also suffer a decreased capacity to carry out their function due to lacking a critical coenzyme called Nicotinamide adenine dinucleotide (NAD). Anyone who has taken a high school level biology class will probably recognise this enzyme as part of the electron transport chain in respiration.

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