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Longevity News Digest

Funding Aging Research

Optimal Protein Amount¦ and Why This is Critical

Dear Future Centenarian, 

I grew up brainwashed into thinking that more protein is better. Protein shakes. Protein bars. Protein powder on everything. Pump some iron¦ and pound the protein.

I was hard-wired with this belief until fairly recently. In fact, I was eating protein bars up until about 5-6 years ago. And I didn™t back off on animal protein until a couple of years ago. I™m still cutting back.

Why? Because excessive protein, especially animal protein, prematurely ages you. It can make you sick too. Very sick.

It can even kill you.

Here™s why:

An essential amino acid called methionine is found in animal protein, often in excessive amounts. Research is showing that an overabundance of methionine can contribute to early mortality. Conversely, moderately restricting methionine has been linked to longer mean and average lifespan in mammals.

Newest total protein research recommends you limit yourself to one-half gram of protein per pound of lean body weight. As it turns out, protein has a stimulatory effect on mammalian target of rapamycin (mTOR)”a pathway that seems to be largely responsible for the pathology seen in cancer growth.

When you limit protein to just what your body needs, mTOR remains inhibited, which helps lessen your chances of cancer growth.

Unless you train extremely hard, your optimal daily need is no more than that one-half gram of protein per pound of lean body mass. Athletic types may need about 25% more. Same for pregnant women. And some elderly people whose digestive systems may not assimilate protein as well anymore, may need a bit more to help offset muscle wasting. But most people rarely need more than 40-70 grams of protein a day.

Do you know how to measure your lean body mass? Determine your body fat percentage and subtract from 100. So if your body fat is 20% you would have 80% lean body mass.

Then multiply that by your weight to get your lean body mass number.

Let™s say you weigh 150 pounds and your lean body mass is 80%. You would multiply 150 by .8, and your lean body mass would be 120. One-half gram times 120 would equal 60. That™s your maximum daily protein intake.

Now let™s look at how much protein is found in common foods:

Meat, fish, eggs, dairy products, legumes, and nuts all have substantial amounts of protein.

Red meat, pork, poultry and seafood average 6-9 grams of protein per ounce. So one recommended 3oz serving gives you about 18-27 grams of protein. One egg averages about 6-8 grams. Therefore, a two egg omelet delivers 12-16 grams plus cheese (6-12 grams per ounce on average) as well as the other ingredients.

Seeds and nuts contain on average, 4-8 grams per quarter cup, most beans about 7-8 grams per half cup of cooked beans, most cooked grains 5-7 grams per cup, most vegetables about 1-2 grams per ounce “ and most fruits contain less.

Monitor your meals for a few days to see how much protein you get now. Aim for mid-range (you might experiment with low-range), and hopefully lots of it comes from plant-based sources. If not, adjust accordingly.

Too little complete protein can be worse than too much though. You need high-quality protein to help ensure healthy heart and muscle tissue, hormones, enzymes, and many other vital body structures. I supplement with hemp protein powder. Hemp is one of the more complete proteins on the market.

More Life,
David Kekich
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Latest Headlines from Fight Aging!

Oxytocin and Muscle Regeneration in Aging - Monday, June 16, 2014
Researchers have discovered an unexpected effect of oxytocin on muscle regeneration.

One has to wonder just how much the fact that use of oxytocin is already approved by regulators factors into this work: there is a strong incentive for researchers to look for new marginal effects in the existing set of approved drugs and compounds rather than work on radically new and better medical technologies.

This is because regulators impose vast costs on novel technologies, but only very large costs on reuse of existing treatments in new ways, and this structure percolates all the way back up the research chain due to its effects on funding. This is just one of many detrimental distorting effects of regulation on the course, speed, and effectiveness of medical research.

Read More https://www.fightaging.org/archives/2014/06/oxytocin-and-muscle-regeneration-in-aging.php

An Example of Alzheimer's Mechanisms Beyond Amyloid - Monday, June 16, 2014
The prevailing focus in Alzheimer's disease (AD) research is on removal of amyloid, solid aggregates of misfolded proteins, considered the main agent of harm. More sophisticated researchers consider why there is more amyloid in the brains of Alzheimer's patients, and the elderly in general, and how that comes about and how it might be prevented.

For example the SENS research program includes periodic removal of all amyloids as a goal because the presence of amyloid is a fundamental difference between old and young tissue, and therefore should be eliminated as a part of any repair-based rejuvenation treatment.

No consensus goes unchallenged in medical science, however, and there are a range of alternative views and proposed mechanisms for the harm caused by Alzheimer's disease, some of which add to the amyloid viewpoint as this one does. That there is further damage caused by amyloid that is not restored by simply removing the amyloid deposits is an incentive to develop periodic amyloid clearance treatments.

These should be applied to healthy people throughout life, so as to prevent amyloid ever rising to the level at which it causes these further harms. All too much of the research community remains entirely committed to the model of waiting until the late stages of disease and then trying to repair everything that goes wrong at that time, however.

Read More https://www.fightaging.org/archives/2014/06/an-example-of-alzheimers-mechanisms-beyond-amyloid.php

Catabodies to Degrade Transthyretin Amyloid - Tuesday, June 17, 2014
A comparatively small number of misfolded proteins form solid aggregates in tissue due to the change in chemical properties caused by this misfolding, and the result is called an amyloid, and a consequent medical condition is called an amyloidosis.

The best known type of amyloid is that associated with Alzheimer's disease, but for many of the others it isn't as clear as how these aggregates cause damage. Nonetheless amyloids all accumulate with age, and thus should be removed by any comprehensive suite of rejuvenation treatments.

One of the other amyloids clearly linked to harm is misfolded transthyretin (TTR), which is implicated as the cause of death in most people who make it to very advanced ages. In the very elderly this form of amyloid clogs the cardiovascular system. There is also an inherited variant of TTR amyloidosis that occurs rarely in younger people due to an unfortunate genetic mutation, and as is often the case in these matters most past research has focused there.

Here is a pointer to a recent paper that results from SENS Research Foundation funded work on one possible way to safely break down transthyretin amyloid, removing its contribution to age-related mortality through the use of catalytic antibodies, thought to be a type of functional component in the innate immune system. If selective antibodies effective at breaking down this form of amyloid are established by searching through the many different types present in humans, then these few proteins can be manufactured in bulk and used as the basis for a treatment.

Read More https://www.fightaging.org/archives/2014/06/catabodies-to-degrade-transthyretin-amyloid.php

Towards a Better Basis For Kidney Regeneration - Tuesday, June 17, 2014
Researchers are step by step establishing a better understanding of kidney regeneration that should improve efforts to spur regrowth and repair through stem cell treatments and other forms of regenerative medicine.

Read More https://www.fightaging.org/archives/2014/06/towards-a-better-basis-for-kidney-regeneration.php

More Quantification of Human Nuclear DNA Mutation Rates - Wednesday, June 18, 2014
Nuclear DNA is essentially a big complicated molecule, and stuck in the middle of the dynamic environment of the cell it accumulates damage due to reactions with other molecules.

Near all of this damage is repaired quickly, but only near all. So we accumulate somewhat random mutations scattered across our cells as we age. There is some debate over whether this is actually a cause of general age-related degeneration over the present human life span versus only a cause of cancer.

This paper looks at human mutation rates in the exome, a classification that includes only small fraction of our DNA, but which is thought to encompass most of the important known mutations associated with various diseases. There is thus an energetic community that studies this small part of the genome.

Read More https://www.fightaging.org/archives/2014/06/more-quantification-of-human-nuclear-dna-mutation-rates.php

Methionine Restriction and FGF21 in Mice - Wednesday, June 18, 2014
All near alternatives to calorie restriction with optimal nutrition are attracting more scientific attention these days, among them intermittent fasting and methionine restriction.

All three of these have been demonstrated to extend life in mice and rats to varying degrees, and the collection of mechanisms involved appears to be somewhat different in each case: overlapping sets of metabolic reactions to low levels of food or reduced amounts of one of a few dietary constitutents such as methionine.

It is interesting to see FGF21 levels mentioned in the methionine restriction study below, as using genetic engineering to increase the levels of FGF21 in mice has been shown to extend life by influencing one of the better known longevity mechanisms in mammals. Everything touches on everything else in metabolism, and the diversity of methods by which aging can be slowed in laboratory species really reflects a smaller number of core mechanisms that can be altered in many different ways.

Read More https://www.fightaging.org/archives/2014/06/methionine-restriction-and-fgf21-in-mice.php

More Sitting, More Cancer - Thursday, June 19, 2014
One of the more interesting results from the study of health and lifestyle choices in recent years is the finding that time spent sitting correlates with increased mortality and a shorter life expectancy regardless of whether or not individuals also exercised.

As for all such statistical investigations, there is a lot of room to speculate as to the web of related associations and which of them are actually contributing meaningfully to differences in health. This metastudy expands on the picture by looking specifically at cancer risk.

Read More https://www.fightaging.org/archives/2014/06/more-sitting-more-cancer.php

Memory Aging and Known Influences on Longevity - Thursday, June 19, 2014
This open access review paper looks over some of the better known ways to modestly slow aging and extend healthy life in laboratory animals and their relationship with the progressive degeneration of memory with advancing age.

Read More https://www.fightaging.org/archives/2014/06/memory-aging-and-known-influences-on-longevity.php

Transthyretin Amyloidosis as a Cause of Lumbar Spinal Stenosis - Friday, June 20, 2014
Transthyretin (TTR) amyloidosis, also known as senile systemic amyloidosis, occurs as a misfolded form of transthyretin forms solid deposits in tissues.

In young people this is only threatening when accompanied by rare genetic mutations that greatly accelerate the process, but ongoing accumulation of this amyloid throughout life happens to everyone. If you live to a very great age and survive all of the other forms of age-related disease, then this amyloid will grow to clog your cardiovascular system and kill you.

Safe removal of this transthyretin amyloid must thus be a part of any future rejuvenation treatment, and so the SENS Research Foundation funds some lines of research, such as work on catabodies that can break down amyloid deposits. Unfortunately this is in general a small, poorly funded area of research - few groups are looking into TTR amyloidosis, which is why non-profits like the Foundation are trying to hurry matters along.

In this open access paper researchers suggest that in earlier old age TTR amyloid causes other issues, in particular a painful form of degeneration known as lumber spinal stenosis - though more work than was accomplished here would be needed for proof. Producing treatments for this manifestation of amyloidosis would probably be more of a motivation for developers to work on ways to remove amyloid, as there are more patients and thus greater potential revenue from a therapy. So it goes.

Read More https://www.fightaging.org/archives/2014/06/transthyretin-amyloidosis-as-a-cause-of-lumbar-spinal-stenosis.php

Vitamin D and Mortality - Friday, June 20, 2014
I rarely discuss supplements in the context of longevity, as there is little to say: the weight of scientific evidence is overwhelmingly against most of what is sold under claims of providing some benefit to long-term health. Much of what is written out there in the world on this topic is written by people who sell supplements, and who therefore have every incentive to lie to you and lie to themselves in order to keep up a revenue stream.

There are just a few exceptions to this state of affairs, where the state of evidence swings in the direction of benefits and few harms for ordinary people who are not vitamin deficient, and one of them is vitamin D.

Even here it isn't that there is an iron-clad case for taking it, just a decent case: there is good evidence for vitamin D levels in blood to correlate statistically with decreased mortality, there is very little sign of any harms from supplementing with vitamin D in animal and human studies, and vitamin D is very cheap.

However it is magical thinking to assume that taking vitamin D to raise levels in blood will have the same effect as a natural variation observed in a population - one could imagine scenarios in which an artificially induced increase in vitamin D levels shuts off some useful process, for example, or in which natural variations in vitamin D levels are a side-effect of a beneficial process that is unaffected by supplementation. So there must still exist evidence to show that supplementing over the long term does actually produce benefits.

The rational person should spend all of five minutes thinking this through, make a decision, and then move on to much more important matters. The potential benefit here is not large in comparison to the potential outcomes of improved medical science over the next few decades, such as work on the SENS vision for rejuvenation biotechnology, so if we're going to spend time on thinking about longevity, far better for that time to go to SENS.

Read More https://www.fightaging.org/archives/2014/06/vitamin-d-and-mortality.php
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DISCLAIMER:  News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.fightaging.org/

David A. Kekich
Maximum Life Foundation
www.MaxLife.org

"Where Biotech, Infotech and Nanotech
     Meet to Reverse Aging by 2033"



 

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