Lifeboat Foundation

Meet the Harvard genetics genius who says we can stop growing old today – even without futuristic drugs.

Guppies, a perennial pet store favorite, have helped a UC Riverside scientist unlock a key question about evolution:

Do animals evolve in response to the risk of being eaten, or to the environment that they create in the absence of predators? Turns out, it’s the latter.

David Reznick, a professor of biology at UC Riverside, explained that in the wild, guppies can migrate over waterfalls and rapids to places where most predators can’t follow them. Once they arrive in safer terrain, Reznick’s previous research shows they evolve rapidly, becoming genetically distinct from their ancestors.

Prof. Steve Fuller is the author of 25 books including a trilogy relating to the idea of a ‘post-’ or ‘trans-‘human future, and most recently, Nietzschean Meditations: Untimely Thoughts at the Dawn of the Transhuman Age.

During this 2h 15 min interview with Steve Fuller we cover a variety of interesting topics such as: the social foundations of knowledge and our shared love of books; Transhumanism as a scientistic way of understanding who we are; the proactionary vs the precautionary principle; Pierre Teilhard de Chardin and the Omega Point; Julian and Aldous Huxley’s diverging takes on Transhumanism; David Pearce’s Hedonistic Imperative as a concept straight out of Brave New World; the concept and meaning of being human, transhuman and posthuman; humanity’s special place in the cosmos; my Socratic Test of (Artificial) Intelligence; Transhumanism as a materialist theology – i.e. religion for geeks; Elon Musk, cosmism and populating Mars; de-extinction, genetics and the sociological elements of a given species; the greatest issues that humanity is facing today; AI, the Singularity and armed conflict; morphological freedom and becoming human; longevity and the “Death is Wrong” argument; Zoltan Istvan and the Transhumanist Wager; Transhumanism as a way of entrenching rather than transcending one’s original views…

Continue reading “Prof. Steve Fuller on Transhumanism: Ask yourself what is human?” »

If used to make non-heritable genetic changes, CRISPR gene-editing technology holds tremendous promise for treating or curing a wide range of devastating disorders, including sickle cell disease, vision loss, and muscular dystrophy. Early efforts to deliver CRISPR-based therapies to affected tissues in a patient’s body typically have involved packing the gene-editing tools into viral vectors, which may cause unwanted immune reactions and other adverse effects.

Now, NIH-supported researchers have developed an alternative CRISPR delivery system: nanocapsules. Not only do these tiny, synthetic capsules appear to pose a lower risk of side effects, they can be precisely customized to deliver their gene-editing payloads to many different types of cells or tissues in the body, which can be extremely tough to do with a virus. Another advantage of these gene-editing nanocapsules is that they can be freeze-dried into a powder that’s easier than viral systems to transport, store, and administer at different doses.

In findings published in Nature Nanotechnology [1], researchers, led by Shaoqin Gong and Krishanu Saha, University of Wisconsin-Madison, developed the nanocapsules with specific design criteria in mind. They would need to be extremely small, about the size of a small virus, for easy entry into cells. Their surface would need to be adaptable for targeting different cell types. They also had to be highly stable in the bloodstream and yet easily degraded to release their contents once inside a cell.

TVs and radios blare that “artificial intelligence is coming,” and it will take your job and beat you at chess.

But AI is already here, and it can beat you — and the world’s best — at chess. In 2012, it was also used by Google to identify cats in YouTube videos. Today, it’s the reason Teslas have Autopilot and Netflix and Spotify seem to “read your mind.” Now, AI is changing the field of synthetic biology and how we engineer biology. It’s helping engineers design new ways to design genetic circuits — and it could leave a remarkable impact on the future of humanity through the huge investment it has been receiving ($12.3b in the last 10 years) and the markets it is disrupting.

On its surface, the plan was simple: gene-hack mosquitoes so their offspring immediately die, mix them with disease-spreading bugs in the wild, and watch the population drop off. Unfortunately, that didn’t quite pan out.

The genetically-altered mosquitoes did mix with the wild population, and for a brief period the number of mosquitoes in Jacobino, Brazil did plummet, according to research published in Nature Scientific Reports last week. But 18 months later the population bounced right back up, New Atlas reports — and even worse, the new genetic hybrids may be even more resilient to future attempts to quell their numbers.

Age is not the definitive factor it’s made out to be when it comes to our health. We can use our age as a baseline for tracking our health and longevity, but it isn’t stagnant. For example, certain types of testing can help us compare our biological age to our calendar age in order to tinker with our wellness routine and achieve the milestones we’re after. With the right steps, we can slow down and even sometimes reverse the aging process.

When it comes to our biological age, or the measure of how well our body is actually functioning for whatever life stage we are in, there are many things that impact it. Diet, lifestyle patterns like exercise and sleep, and stress are all involved in forming our biological age, along with many other factors like blood sugar, inflammation, and genetics. This week on The Doctor’s Farmacy, I’m joined by Dr. David Sinclair to explore the topic of longevity and anti-aging and how he reduced his own internal age by more than 20 years. Dr. Sinclair is a professor in the Department of Genetics and co-director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School, where he and his colleagues study longevity, aging, and how to slow its effects.

Continue reading “Death is Inevitable but Aging is Not” »

Medications that mitigate inflammation caused by a variety of diseases including rheumatic arthritis may also compromise a person’s immune system, but a new approach points to a possible solution to this problem.

Researchers have discovered a mechanism that might alleviate inflammation by suppressing the migration of a type of white blood cells called neutrophils. The cells migrate within tissues in order to kill pathogens but may also cause excessive inflammation, resulting in tissue injury and other adverse effects.

The scientists identified a genetic molecule called miR-199, a type of “microRNA,” which reduces the migration of neutrophils, therefore potentially relieving inflammation without compromising the immune system.

In experiments in mice, Johns Hopkins Medicine researchers say they have developed a way to successfully transplant certain protective brain cells without the need for lifelong anti-rejection drugs.

A report on the research, published Sept. 16 in the journal Brain, details the new approach, which selectively circumvents the immune response against foreign cells, allowing transplanted cells to survive, thrive and protect brain tissue long after stopping immune-suppressing drugs.

The ability to successfully transplant healthy cells into the brain without the need for conventional anti-rejection drugs could advance the search for therapies that help children born with a rare but devastating class of genetic diseases in which myelin, the protective coating around neurons that helps them send messages, does not form normally. Approximately 1 of every 100,000 children born in the U.S. will have one of these diseases, such as Pelizaeus-Merzbacher disease. This disorder is characterized by infants missing developmental milestones such as sitting and walking, having involuntary muscle spasms, and potentially experiencing partial paralysis of the arms and legs, all caused by a genetic mutation in the genes that form myelin.