Lifeboat Foundation

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Most of our progress in disease treatment and prevention to date has been the product of the linear process of hit-or-miss efforts to find useful interventions. Because we have lacked tools for systematically exploring all possible treatments, discoveries under this paradigm have owed a lot to chance. Likely the most notable chance breakthrough in medicine was the accidental discovery of penicillin — which opened up the antibiotic revolution and has since saved perhaps as many as 200 million lives. But even when discoveries aren’t literally accidental, it still takes good fortune for researchers to achieve breakthroughs with traditional methods. Without the ability to exhaustively simulate possible drug molecules, researchers have to rely on high-throughput screening and other painstaking laboratory methods, which are much slower and more inefficient.

To be fair, this approach has brought great benefits. A thousand years ago, European life expectancy at birth was just in the twenties, since so many people died in infancy or youth from diseases like cholera and dysentery, which are now easily preventable. By the middle of the nineteenth century, life expectancy in the United Kingdom and the United States had increased to the forties. As of 2023, it has risen to over eighty in much of the developed world. So, we have nearly tripled life expectancy in the past thousand years and doubled it in the past two centuries. This was largely achieved by developing ways to avoid or kill external pathogens — bacteria and viruses that bring disease from outside our bodies.

Today, though, most of this low-hanging fruit has been picked. The remaining sources of disease and disability spring mostly from deep within our own bodies. As cells malfunction and tissues break down, we get conditions like cancer, atherosclerosis, diabetes, and Alzheimer’s. To an extent we can reduce these risks through lifestyle, diet, and supplementation — what I call the first bridge to radical life extension. But those can only delay the inevitable. This is why life expectancy gains in developed countries have slowed since roughly the middle of the twentieth century. For example, from 1,880 to 1900, life expectancy at birth in the United States increased from about thirty-nine to forty-nine, but from 1980 to 2000 — after the focus of medicine had shifted from infectious disease to chronic and degenerative disease — it only increased from seventy-four to seventy-six.

Positive life experiences boost brain mitochondrial health, potentially providing protection against certain brain disorders and promoting longevity.

In @MedicalXpress: https://ow.ly/BNn750SrT3c.

In PNAS: https://ow.ly/wT1e50SrT3b.

Continue reading “Psychosocial experiences are associated with human brain mitochondrial biology” »

Cirrus Therapeutics, the University of Bristol, and London’s Global University Institute of Ophthalmology have discovered a new treatment for age-related macular degeneration (AMD), the leading cause of vision loss among older adults.

Featured on the cover of the journal Science Translational Medicine, this research reveals that boosting a specific protein, IRAK-M, in retinal cells could offer a new and highly effective therapy for AMD.

AMD can severely impact a person’s vision. Patients suffering from AMD often start with blurred vision or seeing a black dot in their central vision, which can ultimately expand to the point where there is no useful central vision. Currently, AMD affects approximately 200 million people worldwide, a number projected to rise to 288 million by 2040 with graying populations. The exact cause of AMD is complex and thought to involve a combination of aging, environmental, and lifestyle factors.

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I found the scientific evidence for heat therapy for longevity to be much more convincing than that for cold therapy:

We look at the research around heat therapy, sauna bathing, infrared, and more to see!

In pre-clinical trials, a small molecule effectively regrew neurons, reduced inflammation, and improved memory, speed, coordination, grip strength, and more. The finding could have a profound impact on aging and the diseases that accompany it.

In conducting the research, scientists at the University of Texas MD Anderson Cancer Center, turned their focus to telomerase reverse transcriptase (TERT), an enzyme that is known to help synthesize and extend telomeres, the protective caps at the ends of chromosomes that help cells divide. TERT levels are reduced as we age.

Without sufficient levels of TERT, when our telomeres shrink or get seriously modified, they can lead to a process that continually damages our DNA, which causes cells to release inflammatory compounds that can in turn lead to aging, tissue damage, and cancer.

The enzyme telomerase can prevent telomere attrition from happening by extending the length of telomeres. However, in most multicellular organisms, including humans, telomerase expression is switched off, except in germ cells, some types of stem cells, and certain white blood cells. While this might play a role in preventing cancer, as most cancerous cells must switch telomerase expression back on via mutations to enable runaway replication, numerous studies have shown that increasing telomerase through TERT delays aging and increases longevity of model organisms [1].

The small molecule that could

In the lab, this is usually done by introducing genetic vectors carrying a working copy of the gene that codes TERT. It’s this gene that is switched off in somatic cells. However, gene therapies are complex and expensive, and they are just entering the medical mainstream. What if we could do the same using a small molecule?