Scientists Extend Mouse Lifespans by 60%: Why Not Humans?
Just as my 98 year old great uncle couldn't imagine space travel, longevity research may amaze us. With 20+ ways to extend mouse lifespan by up to 60%, it's hard to believe humans can't benefit.
On most of the animals tested, slowing or reversing aging seems to have worked. There are now about twenty different ways of extending mouse lifespan by 10% to 60%, many involving modest genetic alterations.
Aging research has long been overshadowed by anti-aging cosmetics and snake oil remedies. But there is a legitimate scientific field exploring aging at the molecular level. And it’s gaining traction:
The White House announced a clinical trial on slowing ovarian aging.
The New York Times has covered longevity breakthroughs.
There’s a bipartisan Congressional Longevity Caucus.
Alphabet has a division (Calico Labs) that invests heavily in longevity.
Nonprofits are popping up (like the Alliance for Longevity Initiatives) that advocate to prioritize aging research.
The Science of Aging
So far, the methods of extending longevity in mammals aim to reduce cellular damage. Some research indicates that the primary differences between young and old bodies are: (a) levels of damage, and (b) the disarray of biological systems and organs reacting to that damage. In humans, this is still theoretical, as there haven't been sufficient studies on it yet.
Epigenetics, which studies how genes are expressed based on environment and lifestyle, has made strides over the past decade in unlocking more about aging.
According to FightAging.org, which compiles longevity research, the main pathways expected for human age reversal might be:
“Senolytic” therapies that destroy harmful "zombie" cells that accumulate with age, potentially reversing tissue damage (human trials are underway).
Immune system restoration, already successful in treating multiple sclerosis, could be adapted for age-related immune decline.
Amyloid clearance therapies, successful in trials for Alzheimer's and heart disease, remove harmful protein buildups.
And other pathways: Glucosepane cross-link removal could address tissue stiffening, while thymus rejuvenation and mitochondrial repair focus on improving immune function and cellular energy. Researchers are also exploring cancer prevention by disrupting telomere maintenance and rejuvenating stem cells to enable ongoing tissue repair.
The Bottlenecks
Funding in this field is limited and largely directed towards incremental advances rather than groundbreaking research according to scientists in the field. Longstanding issues that likely contribute:
Aging isn't classified as a disease. Federal funding is restricted to disease-specific research.
The National Institute on Aging plans to spend only 9% of its 2024 budget ($4.4 billion) on aging biology, with 60% going to neuroscience research.
Clinical trials can't focus solely on lifespan extension due to aging's non-disease classification.
Partly because of lack of federal funding, the bulk of the research funding is within private sector. Private sector funding is focused on smaller interventions that have higher certainty, instead of slower essential research. Additionally, a private-led drug pipeline without Big Pharma is very difficult without huge investors. Thus, drugs will likely be limited because early-stage drug development companies cannot typically run late-stage trials and commercialize drugs; these skills are vastly different.
Only a small subset of aging research targets repairing damage in aged cells, rather than just understanding or slowing aging. This narrow focus could delay practical reversals in humans.
Aging research also falls victim to systematic weaknesses in our medical research system. Metformin, a common diabetes drug, shows promise in slowing aging and reducing age-related disease risks. Yet, despite its potential for widespread benefits, scientists struggle to secure the $45-70 million needed for comprehensive trials. The challenges? It's a generic drug (so no company will profit) and it addresses multiple issues preventatively rather than treating a single condition.
Interestingly, as progress stalled in Alzheimer's research, some subsets of scientific research seem to be shifting to studying aging itself as the best method to treat single diseases.
Even if the first aging-focused drug is developed via a focus on a single disease, it would still help a lot of people. An aging-focused drug would also delay or help other ailments, much like how statins work today. Although primarily prescribed for reducing cholesterol, statins also reduce heart attacks and strokes. Analysis indicates statins led to 40,000 fewer deaths, 60,000 fewer hospitalizations for heart attacks, and 22,000 fewer strokes in 2008 compared to 1987.
From the late 1930s to the 1980s, all-cause mortality in the US declined by about 2-3% per year - except for the years right after the antibiotic revolution where declines hit 8% a year. Tech leaps led to huge mortality rate declines. Now, since the 1980s, we’ve hit a plateau. Could an all-purpose statin-like aging drug again boost life expectancy?
However, to even hope to get an aging drug this decade, one biotech startup CEO writes we’d need “multiple well-funded ($100M+) shots” on the goal, where the other shots continue to be funded even if the first attempts fail.
What You Can Do Now for Longevity
Everyone know sleep, exercise, low-stress, and strong social bonds correlate strongly with longer, healthy lives. But the only thing so far that shows evidence for slowing aging is unpleasant: Calorie Restriction Optimal Nutrition (CRON). You eat fewer calories, particularly by eating tons of different vegetables, a few lean proteins, ensuring you’re getting all the macronutrients and vitamins that people need (i.e. omega-3s, etc.).
I try to follow this. There’s even an app (CRONometer) that tracks vitamins and minerals from foods. If you’re interested, "The Longevity Diet" book is my go-to guide.
But What About Overpopulation?
Critics worry that if people live longer lives, societal resources would be even more strained from rises in population. However, according to some meta-analyses, overpopulation fears seem exaggerated. Population levels don’t make as much of a dent on emissions; what we really need are breakthroughs in carbon efficiency. And more people working, inventing, and existing longer could mean scientific breakthroughs happen faster.
Imagine: Your dad, vibrant at 90, playing with his great-grandkids. Your mom, sharp as a tack at 85, starting a new business.
That's not science fiction. That's the future we could build.
We've poured billions into space. Why? Because we believed it would work. Now it's time to aim that ambition closer to home. At ourselves. At the people we love. The obstacle is not the technology, it’s our imagination and priorities.
Every breakthrough was once "impossible." Flight. Vaccines. The internet.
Now it's our turn. Our moonshot.