A High Level Popular Science View of the Longevity Industry

The article I'll point out today is an entirely unremarkable, high level tour of the most discussed, most notable portions of the longevity industry and related research efforts. Twenty years ago, we'd all have been delighted to see the media both noticing translational aging research at all, and then actually taking seriously the prospect of treating aging as a medical condition. We've come a long way to now see summary discussions of work on the treatment of aging as business as usual, not really worth mentioning. Still, articles like this miss near all of the really interesting projects, and that is the way of high level overviews. What is most talked about today is only rarely what is most important tomorrow, or at least given a few years to see how and where the dust settles.

Articles of this sort also tend to feature people who believe that only marginal progress towards greater longevity is possible in the foreseeable future; that may or may not be true, but to even answer that question a great deal more support for clinical trials of presently available options is required. The first viable senolytic drugs have been known for going on a decade, low-cost and readily available for anyone who wants to try them. Yet there is no rush to run clinical trials that would answer whether or not they are as impressive in human aging as they are for mice, and the vast majority of older people have no idea that this option is even on the table.

Interested in living healthier longer? Longevity science explained

After age 65, most people have two or more chronic diseases. U.S. adults in their 60s and 70s take up to five different prescription medications at a time. And what helps one condition may worsen another. At about 76, the U.S. life expectancy, the adult will probably die from one of these diseases. All of these chronic conditions share a risk factor: age. It may be the process of aging itself that makes us vulnerable to these diseases, which affects our health span (how long we stay healthy) and life span (how long we live.) As we get older, we lose strength and mobility as our bodies undergo molecular changes that eventually undermine their integrity and resiliency. Scientists refer to these changes as hallmarks. These include chronic inflammation and the accumulation of senescent cells that stop multiplying because of damage or stress but don't die as they are supposed to.

Some researchers believe that through addressing aging itself, diseases related to aging can be pushed back and possibly prevented. This would mean living healthier, longer. "The important implication is that we can study the biology of aging, start to learn about it and we have a potential to intervene in that biology to have a positive impact on disease outcomes and health." The field is known by many names: longevity, geroscience, anti-aging. Regardless of the name, it's still in the early stages. Several drugs may have the ability to postpone or prevent the onset of debilitating diseases. Animal studies have demonstrated their potential, and now clinical trials are beginning to assess whether their promise holds true in humans. "I think it's certainly legitimate to ask why we haven't done that previously. And in part it's because we really haven't had the knowledge base to be able to do that."

One promising drug is rapamycin. It's an antifungal approved by the FDA as an immune suppressor to prevent organ recipients from rejecting a new organ. Rapamycin inhibits a protein called mechanistic target of rapamycin (mTOR). The protein senses nutrients and then controls cell outputs regulating many processes in the cell. Giving rapamycin to yeast, worms, flies and mice prolonged their lives, studies have shown. Scientists began exploring rapamycin's anti-aging effects in people, and studies suggest this immune-suppressing compound can actually improve immune function in older adults boosting their response to flu shots and lowering their odds of getting severely ill during cold and flu season.

As we age, immune function both declines and increases. Though the ability of our immune system to respond to pathogens declines, it can also overreact by striking in the absence of any threat. This can result in healthy tissues and organs being attacked, which can lead to chronic inflammation linked with various kinds of diseases. So, what is causing the inflammation itself? One possible culprit is senescent cells that stop dividing but don't die. They accumulate as we get older and give off inflammatory signals, which contribute to some age-related diseases.

If a drug is ever to be used as an anti-aging therapy, it'll need to be tested in healthy people who are aging naturally the way that new drugs for a certain illness are tested on people who have that disease. However, aging isn't officially defined as a disease. One clinical trial aims to prove that aging is something that can be targeted and treated. It involves metformin, long used to treat Type 2 diabetes. In a trial called Targeting Aging With Metformin (TAME), researchers will track 3,000 adults 65 to 80, who will take the drug for six years. The goal is to see if metformin can prevent or delay three age-related diseases: dementia, heart disease, and cancer. This will show if metformin can increase health span. If the trial succeeds, it may show that drugs to target aging don't need to be expensive and can be available to more people, not just the rich.


I thought the Mayo clinic was doing human trials with D&Q.

Are there any bio hackers out there who are taking D&Q?

Why would there be so many companies focusing on novel senolytics if D&Q work?

Posted by: matt at September 6th, 2023 5:53 AM

'Why would there be so many companies focusing on novel senolytics if D&Q work?'

- patentability
- better selecivity
- better tissue coverage
- better side effect profile

Posted by: Jonrs at September 6th, 2023 8:02 AM

I think this may be the study you mentioned Matt?:


I'm still waiting for some sort of discussion from the authors, but from my layman's perspective, it looks like this experiment was pretty disappointing:

It DECREASED Tao (the one good thing I see)

It INCREASED Amyloid-Beta

it INCREASED il-6 senescence marker

it DECREASED "moca" cognitive assessment

This was a test on a whopping sample-size of 5 people for Alzheimers, but still, not looking like something that worked so well.

Posted by: Gregory Schulte at September 6th, 2023 12:11 PM
Comment Submission

Post a comment; thoughtful, considered opinions are valued. New comments can be edited for a few minutes following submission. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.