Lifeboat Foundation

The inside of a mitochondria is made up of a folded membrane, which has evolved to produce the greatest surface area possible between two parts of the mitochondria known as the intermembrane space (the outer part) and the mitochondrial matrix (the inner part). To drastically oversimplify this entire process, the mitochondria uses glucose (and ethanol if it’s available) to pump hydrogen ions (with the occasional deuterium and tritium ion) across the membrane which separates these two compartments of the mitochondria (known as the cristae) into the intermembrane space. These hydrogen ions then flow back into the mitochondrial matrix through a very special protein called ATP synthase, which uses the electrostatic potential energy of the hydrogen ion to manufacture ATP.

Unfortunately, as we get older this inner membrane starts to decay and become smaller. As the cristae starts to shrink, there is less space for ATP synthase, which means there is less ATP produced, which ultimately means that our cells do not have enough energy to maintain all of our cellular functions. As you can imagine, this lack of energy is catastrophic for the health of the cell, and will eventually lead to either cell senescent (where the cell essentially becomes dormant), or complete cell death.

Numerous different suggestions have been put forward as to explain why exactly why mitochondria decay in this way, including mutations within the DNA of the mitochondria (they have their own chromosomes), as well as the build up of oxidative agents within the cell itself which cause direct damage to the mitochondria. However, a group of scientists lead by Dr Hazel Szeto have discovered that the decay of the mitochondrial cristae is linked to declining levels of a phospholipid (fat) called cardiolipin. It turns out that as we age, oxidative agents within our body destroy this phospholipid, which is essential for maintaining the folded inner membrane of the mitochondria.

Several different causes of aging have been discovered, but the question remains whether there are common underlying mechanisms that determine aging and lifespan. Researchers from the Max Planck Institute for Biology of Ageing and the CECAD Cluster of Excellence in Ageing research at the University Cologne have now come across folate metabolism in their search for such basic mechanisms. Its regulation underlies many known aging signaling pathways and leads to longevity. This may provide a new possibility to broadly improve human health during aging.

In recent decades, several cellular signaling pathways have been discovered that regulate the lifespan of an organism and are thus of enormous importance for aging research. When researchers altered these signaling pathways, this extended the lifespan of diverse organisms. However, the question arises whether these different signaling pathways converge on common metabolic pathways that are causal for longevity.

We probably cannot slow the rate at which we get older because of biological constraints, an unprecedented study of lifespan statistics in human and non-human primates has confirmed.

The study set out to test the ‘invariant rate of aging’ hypothesis, which says that a species has a relatively fixed rate of aging from adulthood. An international collaboration of scientists from 14 countries, including José Manuel Aburto from Oxford’s Leverhulme Centre for Demographic Science, analyzed age-specific birth and death data spanning centuries and continents. Led by Fernando Colchero, University of Southern Denmark and Susan Alberts, Duke University, North Carolina, the study was a huge endeavor requiring monitoring wild populations of primates over several decades.

Jose Manuel Aburto says, Our findings support the theory that, rather than slowing down death, more people are living much longer due to a reduction in mortality at younger ages. We compared birth and death data from humans and non-human primates and found this general pattern of mortality was the same in all of them. This suggests that biological, rather than environmental factors, ultimately control longevity.

With heart donors in short supply, artificial hearts have literally been a lifesaver for many heart patients. Here’s all you need to know about them.

Stem cell biologist Hugo Vankelecom (KU Leuven) and his colleagues have discovered that the pituitary gland in mice ages as the result of an age-related form of chronic inflammation. It may be possible to slow down this process or even partially repair it. The researchers have published their findings in PNAS.

The pituitary gland is a small, globular gland located underneath the brain that plays a major role in the hormonal system, explains Professor Hugo Vankelecom from the Department of Development and Regeneration at KU Leuven. “My research group discovered that the pituitary gland ages as a result of a form of chronic inflammation that affects tissue and even the organism as a whole. This natural process usually goes unnoticed and is referred to as ‘inflammaging’—a contraction of inflammation and aging. Inflammaging has previously been linked to the aging of other organs.” Due to the central role played by the pituitary, its aging may contribute to the reduction of hormonal processes and hormone levels in our body—as is the case with menopause, for instance.

The study also provides significant insight into the stem cells in the aging pituitary gland. In 2012, Vankelecom and his colleagues showed that a prompt reaction of these stem cells to injury in the gland leads to repair of the tissue, even in adult animals. “As a result of this new study, we now know that stem cells in the pituitary do not lose this regenerative capacity when the organism ages. In fact, the stem cells are only unable to do their job because, over time, the pituitary becomes an ‘inflammatory environment’ as a result of the chronic inflammation. But as soon as the stem cells are taken out of this environment, they show the same properties as stem cells from a young pituitary.”

In a minute and 27 seconds we get the what from an eye regeneration for mice, to monkey trials to start later this year, to human trials by 2023, and full body in a decade.

David Sinclair—a world-leading biologist, Harvard Medical School Professor, and author of The New York Times best-selling book @Lifespan.

Continue reading “When can we begin to apply age reversal gene therapies to humans? Harvards David Sinclair explains” »

The resulting implant consists of cells attached to the scaffold, which permits the targeted delivery of therapeutic cells to the diseased region within the eye. A non-cryopreserved formulation of this cellular therapy is being employed in an ongoing Phase I/IIa clinical trial sponsored by RPT. The cryopreserved formulation enabled by the work of Pennington and colleagues will facilitate anticipated Phase IIb and Phase III clinical trials as well as ultimate commercialization and clinical application of the product.

Scientists at UC Santa Barbara, University of Southern California (USC), and the biotechnology company Regenerative Patch Technologies LLC (RPT) have reported new methodology for preservation of RPT’s stem cell-based therapy for age-related macular degeneration (AMD).

The new research, recently published in Scientific Reports, optimizes the conditions to cryopreserve, or freeze, an implant consisting of a single layer of ocular cells generated from human embryonic stem cells supported by a flexible scaffold about 3×6 mm in size. This implant is currently in clinical trial for the treatment of AMD, the leading cause of blindness in aging populations. The results demonstrate that the implant can be frozen, stored for long periods and distributed in frozen form to clinical sites where it is designed to be thawed and immediately implanted into the eyes of patients with macular degeneration. The capacity to cryopreserve this and other cell-based therapeutics will extend shelf life and enable on-demand distribution to distant clinical sites, increasing the number of patients able to benefit from such treatments.

Continue reading “A frozen leap forward for age-related macular degeneration stem cell-based therapy” »

The World Health Organization classifies processed meat as a Group 1 carcinogen. Processed meat includes ham, sausage, bacon, pepperoni; they’re meats that have been preserved with salt or smoke, meat that has been cured, and meat treated with chemical preserves. Other Group 1 carcinogens include formaldehyde, tobacco, and UV radiation. Group 1 carcinogens have ‘enough evidence to conclude that it can cause cancer in humans.’

There is no question whether or not our current meat production complex is inhumane, unsanitary, or bad for the environment. Almost all chickens (99.9%), turkeys (99.8%), and most cows (70.4%) eaten in the United States are raised on factory farms. There are horrific consequences to this practice.

For example, the EPA estimates agriculture is the biggest contaminator of rivers and streams, to the point where feedlots, crop production, and manure runoff have led almost half (46%) of the U.S.’s rivers to be “in poor biological condition.”

Continue reading “Vegans Diets and Longevity: What Existing Science Actually Says” »

For those who track their diet, eating only the RDA for many nutrients may not optimize health. For example, the RDA for selenium is 55 micrograms per day, but is that amount optimal for reducing risk of death for all causes?

Papers referenced in the video:

Continue reading “Selenium: How Much Is Optimal For Health?” »