Lifeboat Foundation

America’s water is under threat from many sides. It faces pollution problems, outdated infrastructure, rising costs, and unprecedented droughts and rainfall patterns as the climate changes. Yet at a recent event hosted by the Columbia Water Center, the tone was cautiously optimistic, and the conversation centered on solutions.

“If we have aging infrastructure that’s falling apart, and we’re dealing with climate variability and change, isn’t that a good opportunity to actually do something?” suggested Upmanu Lall, director of the Columbia Water Center.

For decades, the U.S. has been a leader in water management. Now we’re falling behind; in the latest infrastructure report card, dams, drinking water and wastewater all received D ratings. But Lall thinks the country could get an A. Here are some of the solutions, presented at the event, that could help to get us there.

https://www.youtube.com/watch?v=YNDyHZp6wWw

http://toosickandnaked.com/2018/05/07/25-the-future-of-medic…-bioquark/

Aging is characterized by the progressive increase in chronic, low‐grade inflammation termed “inflammaging,” which is believed to play an important role in the mechanism underlying aging.

Necroptosis is a newly identified programmed cell death pathway that is highly proinflammatory due to the release of cellular components that promote inflammation. To determine whether necroptosis might play a role in inflammaging, we studied the effect of age and dietary restriction (DR) on necroptosis in the epididymal white adipose tissue (eWAT), a major source of proinflammatory cytokines. Phosphorylated MLKL and RIPK3, markers of necroptosis, were increased 2.7‐ and 1.9‐fold, respectively, in eWAT of old mice compared to adult mice, and DR reduced P‐MLKL and P‐RIPK3 to levels similar to adult mice. An increase in the expression of RIPK1 (1.6‐fold) and MLKL (2.7‐fold), not RIPK3, was also observed in eWAT of old mice, which was reduced by DR in old mice. The increase in necroptosis was paralleled by an increase in 14 inflammatory cytokines, including the pro‐inflammatory cytokines IL‐6 (3.9‐fold), TNF‐α (4.7‐fold), and IL‐1β (5.1‐fold)], and 11 chemokines in old mice. DR attenuated the expression of IL‐6, TNF‐α, and IL‐1β as well as 85% of the other cytokines/chemokines induced with age. In contrast, inguinal WAT (iWAT), which is less inflammatory, did not show any significant increase with age in the levels of P‐MLKL and MLKL or inflammatory cytokines/chemokines. Because the changes in biomarkers of necroptosis in eWAT with age and DR paralleled the changes in the expression of pro‐inflammatory cytokines, our data support the possibility that necroptosis might play a role in increased chronic inflammation observed with age.

A relatively easy way to boost intestinal stem cell (ISC) function might simply be fasting, according to a new study by a team of MIT biologists.

Stem cells supply the specialized cells that make up our tissues and organs; every time existing cells are lost for whatever reason, stem cells that can differentiate into that particular type of cell jump into action to compensate for the loss. However, this ability declines over time as aging progresses; indeed, stem cell exhaustion is one of the hallmarks of aging, and it affects our body by decreasing the regenerative capacity of its tissues, leading to immune dysfunction, muscle wasting, and even neurodegenerative diseases.

The lining of your intestine suffers from this problem as well. It consists of a fast-renewing tissue that typically renews itself entirely in a handful of days, and it is responsible for absorbing nutrients as well as keeping away unwanted substances; maintaining its regenerative abilities is therefore important for everyone, old or young; however, for older people, this is more challenging. However, a relatively easy way to boost intestinal stem cell (ISC) function might simply be fasting, according to a new study by a team of MIT biologists [1].

Continue reading “Fasting might boost intestinal stem cell function” »

Today, we have an interview with Dr. Nichola Conlon, one of the speakers at the Undoing Aging 2018 Conference in Berlin, hosted by the Forever Healthy Foundation and SENS Research Foundation.

Introducing Nuchido

Dr. Conlon is the CEO of Nuchido, a new company that is set to launch later this year and was encouraged in part by four recent breakthroughs in biogerontology, which each showed rejuvenation in mammals [1–9]. These studies, which were all published in leading peer-reviewed scientific journals, showed that rejuvenation of aged animals was possible via different mechanisms of action.

A human study of the mitochondrial antioxidant MitoQ shows promise in addressing some aspects of vascular aging.

Antioxidant-based therapeutics to forestall the effects of aging have had a long history, ever since the elaboration of the free radical theory of aging by Denham Harmon in 1956. However, this long history has also had mixed results, with studies alternately showing efficacy, a lack of efficacy, or even negative health effects for some applications of antioxidants. Many of these studies analyzed the results of taking high doses of naturally occurring antioxidants. In general, high doses are necessary due to the poor bioavailability of many of these naturally occurring compounds.

The poor bioavailability of Coenzyme Q10, a naturally occurring antioxidant that is found in cells and decreases with age, spurred scientists to develop a synthetic form. This form, dubbed MitoQ, is very similar in structure to the naturally occurring form, only it has a triphenylphosphonium moiety that allows this derivative to be two to three orders of magnitude more permeable to membranes, particularly the membranes of mitochondria. It is within mitochondria that MitoQ appears to be doing most of its work by soaking up reactive molecules, generated as byproducts of respiration, that can oxidize and damage lipids and proteins.

Continue reading “Antioxidant MitoQ Combats Vascular Aging in Human Study” »