Healthy Life Extension
Procrastinating Yourself into the Grave
posted on October 23rd, 2012
Dear Future Centenarian,
Attention Southern California lifeÂ extensionists, futurists, Cryonicists, and other health enthusiasts:
You're invited to this year™s Annual Healthy Longevity Holiday Party!
Kat Cotter and I are hosting it again, and I heard she sent something like the following to some of our friends:
œWe hope you can join us to kick off the holiday season and we look forward to seeing you!
Date: Saturday November 17th
Time: 5:00 PM to 10 PM
Location: The Colony at Fashion Island
(inside the clubhouse)
5100 Colony Plaza, Newport Beach, CA
RSVP to email@example.com
œThis will be a POT LUCK so please bring a dish and something you™d like to drink. Bring a tasty but healthy dish.... If you bring something that needs to be heated, no problem, we have an oven there.
œYou™re welcome to bring GUESTS... the more the merrier! But please ask each person to bring a dish and something they wish to drink. And please RSVP to firstname.lastname@example.org for each so we know how many guests to expect!
œThere is a guarded GATE. Give the attendant your name. He will have the RSVP list and will let you in if you are registered.
œFeel free to call me at 310-528- 6712Â if you have any questions and call me or Dave if you need help finding us that evening. Dave™s cell phone is 213-268-1521. But try me first, since Dave is yet another year older, and he tells me there must be something wrong with his phone, because he can™t hear it ring when there™s background noise.
œHe also wanted me to remind you that it will be fairly close to Christmas, so for convenience, you can bring his present early. If you forget, no problem. He will.
P.S. Dr. Lynn Johnson offers an excellent free ebook for people who subscribe to her newsletter. We all want to maintain healthy telomere length, and since stress management is a major telomere factor, her ebook can help you do just that and have fun in the process. Simply go to http://drlynnjohnson.com, scroll down and click on "Free ebook: Happiness Checklist."
LATEST HEADLINES FROM FIGHT AGING!
SPERMIDINE LEVELS MEASURED IN CENTENARIANS Friday, October 19, 2012
Spermidine has been noted to boost autophagy and promote greater longevity to some degree in laboratory animals. Its activities are in the process of being advanced by some researchers as candidate drug mechanisms for slowing aging. Given that, it makes sense for researchers to investigate spermidine levels in longer lived individuals to see if there is any association:
"Polyamines (putrescine, spermidine and spermine) are a family of molecules deriving from ornithine, through a decarboxylation process. They are essential for cell growth and proliferation, stabilization of negative charges of DNA, RNA transcription, translation and apoptosis.
A SMALL STEP TOWARDS TISSUE ENGINEERED KIDNEYS Friday, October 19, 2012 http://www.fightaging.org/archives/2012/10/a-small-step-towards-tissue-engineered-kidneys.php
Tissue engineers have been inching closer to building a kidney from stem cells in the past couple of years. Here is a recent example of the ongoing work in this field: "Investigators can produce tissues similar to immature kidneys from simple suspensions of embryonic kidney cells, but they have been unsuccessful at growing more mature kidney tissues in the lab because the kidneys' complicated filtering units do not form without the support of blood vessels.
Now, from suspensions of single kidney cells, [researchers] have for the first time constructed "organoids" that can be integrated into a living animal and carry out kidney functions including blood filtering and molecule reabsorption. Key to their success was soaking the organoids in a solution containing molecules that promote blood vessel formation, then injecting these molecules into the recipient animals after the organoids were implanted below the kidneys. The organoids continued to mature and were viable for three to four weeks after implantation."
MORE ON YOUNG BLOOD AND OLD MICE Thursday, October 18, 2012
Some of the effects of aging are driven by signaling changes in important parts of our biochemistry - such as in stem cell niches, collections of cells that provide necessary support to the stem cells that maintain and repair tissue. Niches increasingly act to suppress the stem cells they contain in response to rising levels of cellular and other damage connected to aging.
The stem cells themselves also suffer damage, and this evolved response is likely a way to minimize the risk of cancer at the cost of maintaining tissues, but the declining function of the stem cells so far seems to be far more a property of signals from the niche.
MORE ROBUST DATA ON THE EFFECT OF MITOCHONDRIALLY TARGETED ANTIOXIDANTS ON FLY LIFE SPAN Thursday, October 18, 2012
In recent years a few research groups have been working on a class of antioxidant compounds that can be ingested but nonetheless target themselves to mitochondrial in our cells.
These compounds extend life in laboratory animals, probably by soaking up reactive free radical compounds emitted by mitochondria in the course of their operation, and thus preventing some of the damage that mitochondria cause to themselves. This damage is significant in aging, one of the root causes of degeneration and age-related disease.
THE PLASTICITY OF LIFE SPAN Wednesday, October 17, 2012
We live longer than our ancestors thanks to our greater wealth and more advanced technology: risk of death is reduced at all ages, the level of damage suffered due to infectious disease and other causes is lowered throughout life, and inroads made into means of alleviating age-related disease.
When it comes to effects across a life span, however, our extended lives are so far largely incidental, a side effect of improvements in medicine and quality of life that were introduced to satisfy other, more short-term goals. This shows that aging and life span is very plastic - it can be changed, and is very readily changed.
OVEREXPRESSION OF FGF21 EXTENDS LIFE IN MICE Wednesday, October 17, 2012
An enormously complex web of genes and protein machinery controls the operation of metabolism, a layered nest of interactions and feedback loops. It is thus possible for many different genetic alterations to extend life by working through the same basic mechanism.
The example here involving fibroblast growth factor 21 is a newly discovered change that seems to work through a known life extension method involving suppression of growth hormone, used in the past to extend life by 60-70% in mice.
DOPAMINE AND MEMORY DECLINE IN AGING Tuesday, October 16, 2012
Parkinson's disease is caused by excessive loss of cells in the small population of dopamine-generating neurons. This is an exaggerated version of a loss that we all suffer due to the wear and tear of
Many age-related conditions are of this nature, aggravated or more rapidly occurring versions of the same damage that everyone suffers. So all people lose some of the cells that generate the neurotransmitter dopamine, just not enough for that loss to become a named and known medical condition.
ANOTHER GLENN FOUNDATION LAB ESTABLISHED Tuesday, October 16, 2012
Following on from last week's news, it seems the Glenn Foundation for Medical Research is establishing a brace of new laboratories for the study of aging, joining those formed a few years back.
Which is to say that the Foundation is reinforcing some of the existing leading lights in aging and longevity science, and in the process of delivering sizable grants is setting up new, named research centers. This time it's the turn of researchers at the Albert Einstein College of Medicine:
COMMENTING ON THE LATE LIFE PLATEAU IN AGING Monday, October 15, 2012
One fairly standard definition for aging is an increase in mortality rate over time. You are said to age if you become increasingly likely to die in any given interval of time.
There is an interesting twist, however: researchers have shown that in short-lived species such as flies there appears to be a point in very late life at which mortality rate stops increasing - i.e. aging, by this definition, ceases.
INVESTIGATING NATURAL BLADDER REGENERATION IN RATS Monday, October 15, 2012
Important things remain to be learned of the regenerative capacity of various mammal species - such as the way in which rats can regrow large sections of the bladder.
Researchers investigate mechanisms of natural regeneration with an eye to finding ways to reproduce exceptional examples of regrowth in human biochemistry. Here, scientists suggest that regeneration of the bladder in rodents is a better avenue of investigation than the well-known regeneration of the liver that even we humans are capable of: