Ultra marathon runners could possibly see up to 16yr added lifespan

New Victorian research reveals that running long-distance runs can slow the ageing process by protecting the part of the body that stops the genes from fraying.
Runners in The Federation University Australia study had an average age of 43, but their biological age was just 27.
-link

Though previously in this blog we saw that benefits peaked at sub8mph 10miles per week and that exceeding 8mph or 20-25 miles per week could possibly damage the heart neutralizing some of the benefits.   Yet it is said that low intensity exercise does not have such a cap on adding benefits(more research is needed.), which suggest walking for most of ultramarathon distances would be optimal.   That is 10-15 miles per week with 2-3 days of resting per week at no more than 8mph and several hours of walking to achieve the ultramarathon distance.

 The findings, to be presented at the Australian Society for Medical Research National Conference, found ultra-marathon runners clocking up 40-100 km a week had 11 per cent longer telomeres.-link

Yet lifestyle changes

 Ten of the patients embarked on lifestyle changes that included: a plant-based diet (high in fruits, vegetables and unrefined grains, and low in fat and refined carbohydrates); moderate exercise (walking 30 minutes a day, six days a week); stress reduction (gentle yoga-based stretching, breathing, meditation). They also participated in weekly group support.  -link

 might allow similar benefit with much less exercise

The group that made the lifestyle changes experienced a “significant” increase in telomere length of approximately 10 percent. -link

But might not both interventions be combined and yield greater results?

video on google agi

Windfarms could likely save money and lives

Offshore wind farms could tame hurricanes before they reach land, Stanford-led study says Wind farm could reduce peak hurricane wind speeds by up to 92 mph and decrease storm surge by up to 79 percent

Computer simulations by Stanford Professor Mark Z. Jacobson have shown that offshore wind farms with thousands of wind turbines could have sapped the power of three real-life hurricanes, significantly decreasing their winds and accompanying storm surge, and possibly preventing billions of dollars in damages.-link

It seems that wind farms beside looking cool and generating power in a green manner can help save live and money from natural disasters.  Those opposed to them are going to have to argue why they're in favor of lost lives and money just for cosmetic appearances.

Video on programmed aging

Interesting book

"Evolution of Desire is the first book to present a unified theory of human mating behavior. Now in a revised and updated edition, Buss's classic presents the latest research in the field, including startling new discoveries about the evolutionary advantages of infidelity, orgasm, and physical attractiveness."

CR monkey studies video

Marathon improves mortality but it seems excess can wipe the benefits or does it?

 But while a study of 52,600 runners showed that pounding the pavement can yield a 19 percent lower mortality rate, that benefit was wiped out for those tallying 20 to 25 miles a week. Not exactly sure how those stats work because we all die eventually.-link

I'm planning to do about 12-15 miles per week as part of my training regimen

 ...As cardiologist Paul Thompson says in the WSJ piece, "The guys advancing the hypothesis that you can get too much exercise are manipulating the data... They have an agenda."
 ...
 Wen and colleagues reply that yes, they do have data -- and it doesn't show what O'Keefe et al. hope:
...
We were not able to identify an upper limit of physical activity, either moderate or vigorous, above which more harm than good will occur in terms of long-term life expectancy benefits...-link

It seems there are counterpoints to the arguments for moderation but still extremes should likely be cautiously avoided

Moderation seems to provide benefits with about 7mph being optimal at 10-15 miles per week with less than 7 days of running that is with resting days.

 
Regarding pace, individuals who ran six and seven miles per hour had a significant 21% and 27% lower risk of all-cause mortality, whereas those who ran eight or more miles per hour had a nonsignificant 7% lower risk of all-cause mortality.-link

There may be hope for damaged hearts

 In an act of transformation worthy of any magician, scientists have converted scar tissue in the hearts of living mice into beating heart cells. If the same trick works in humans (and we’re still several years away from a trial), it could lead us to a long-sought prize of medicine – a way to mend a broken heart.-link

Witcher 3 gameplay trailer

short comment

Fisetin seems intriguing as a substance for aiding brain function and cr mimetic.  But it is still not cost effective for a reasonable dose, and more research is needed, imho.

Reproductive errors

The highest level they found was 1 in 6000 sperm in one man – but any couple could have a child with Apert syndrome. It just comes down to how the genetic dice fall. "Every now and then you are going to have a dad who is unlucky," says Wilkie.-link

Luck, especially one involving such high odds and such bad outcome, shouldn't play a role in the generation of new citizens. Sequencing should occur to ensure only healthy embryos are implanted and go through development.

News on iron

Iron deficiency may increase stroke risk by making the blood more sticky, scientists have discovered. Every year, 15 million people worldwide suffer a stroke. Nearly six million die and another five million are left permanently disabled. The most common type, ischaemic stroke, occurs because the blood supply to the brain is interrupted by small clots. In the last few years, several studies have shown that iron deficiency, which affects around two billion people worldwide, may be a risk factor for ischaemic stroke in adults and in children.-link

Too much iron is bad, and too little is bad too.  Biological enhancements will hopefully one day allow the body to store a large reserve safely, and eliminate easily excess. For now it's best to check iron levels and ensure excess and deficiency is avoided, as the present bodies are fragile.

Article on lifestyle and telomeres

Lifestyle Changes May Lengthen Telomeres, A Measure of Cell Aging
The group that made the lifestyle changes experienced a “significant” increase in telomere length of approximately 10 percent. Further, the more people changed their behavior by adhering to the recommended lifestyle program, the more dramatic their improvements in telomere length, the scientists learned.
By contrast, the men in the control group who were not asked to alter their lifestyle had measurably shorter telomeres – nearly 3 percent shorter – when the five-year study ended. Telomere length usually decreases over time.-link

An interesting finding showing lifestyle changes may lead to increases in telomere length.

"Curing Aging through Telomere Biology."

"Curing Aging through Telomere Biology." From the Independent Pharmacy Business Growth Conference, February 23, 2012 in Orlando, FL.

Magnetic Refrigeration technology

In contrast to other oxidative modifications of amino acids, methionine sulfoxide can be enzymatically reduced back to methionine in proteins by the peptide methionine sulfoxide reductase system, composed of MsrA and MsrB. The expression of MsrA and one member of the MsrB family, hCBS-1, was analyzed during replicative senescence of WI-38 human fibroblasts. Gene expression decreased for both enzymes in senescent cells compared to young cells, and this decline was associated with an alteration in catalytic activity and the accumulation of oxidized proteins during senescence. These results suggest that downregulation of MsrA and hCBS-1 can alter the ability of senescent cells to cope with oxidative stress, hence contributing to the age-related accumulation of oxidative damage.-link

Methionine intake has been linked to lifespan, methionine is said to be easily damageable.  Methionine sulfoxide reductases help deal with this damage, yet it seems that senescence results in downregulation of these protective enzymes.   Some say the regular aging process also results in reduction of production of these enzymes, along with the said increase in membrane peroxidation index, the cells would become more damage prone with increasing age.   It is said every ten years, after approx maturity, there's a doubling of mortality.   Why are changes that increase cellular damage taking place?  It's clear that such changes might exceed the maintenance mechanisms of the cells and be behind this increased probability of death.

Why Are Macadamia Nuts King of the Nuts?

Omega-6 essential fatty acids are found in abundance in polyunsaturated vegetable oils like sunflower, safflower, soybean, cottonseed, grapeseed and corn. They are also high in nuts like pine, walnuts and brazil as well as seeds like sesame, sunflower and pumpkin. One problem with omega-6 fatty acids is they get converted into arachidonic acid by the body. And arachidonic acid is in turn used to generate pro-inflammatory cells and hormones.-link

 An article on macadamia nuts and macadamia and coconut oils.   Eating a handful of nuts daily is said to be healthy and add about 3 years in general to lifespan(exercise is said to add about 5 years.).   This article covers macadamia, a nut that is high on monounsaturated fat and low on polyunsaturated fat and low on protein. 

A nice interview with Hugo de Garis on youtube

Final Fantasy Art

An enemy from final fantasy, excellent art.

Increasing membrane unsaturation with aging and longevity

It has now been documented that there is an age-associated increase in membrane PI and lipoxidation-derived molecular damage (see Table ​Table1).1). In general, PI increases during aging in an organ-dependent way.  -http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3865700/

As seen on the above quote it seems that membranes peroxidation index tends to become less favorable with the passage of time, at least in some organisms.   Given that differences in membrane peroxidation index have been associated with differences in lifespan between species and within species this suggest it may be causal.

In the following we see further evidence:

The results showed significantly lower PI and lipoxidation-derived protein damage in brain and spleen from exceptionally old animals when compared to old specimens, and in a range analogous to adult animals. Therefore, low susceptibility to lipid peroxidation and maintenance of adult-like molecular lipoxidative damage could be key factors for longevity achievement.-http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3865700/

 The animals that exhibited most vigorous long term survival seemed to have lower PI similar to younger adults.   While the authors suggest it may be a key to longevity, I would say it may also be a key to indefinite longevity.   It may or may not be the case that if PI is lowered enough the existing biological maintenance and repair mechanisms may be enough to grant negligible senescence.   I would predict that organisms showing negligible senescence would show such peroxidation resistance, that is they would have a lower PI and it may even be significantly lower(depending on threshold or break even point for indefinite homeostatic balance/maintenance), and a quick wikipedia search shows just that in at least one organism

 Abstract:
Summary: The deleterious reactive carbonyls released upon oxidation of polyunsaturated fatty acids in biological membranes are believed to foster cellular aging. Comparative studies in mammals and birds have shown that the susceptibility to peroxidation of membrane lipids peroxidation index (PI) is negatively correlated with longevity. Long-living marine molluscs are increasingly studied as longevity models, and the presence of different types of lipids in the membranes of these organisms raises questions on the existence of a PI-longevity relationship. We address this question by comparing the longest living metazoan species, the mud clam Arctica islandica (maximum reported longevity = 507 year) to four other sympatric bivalve molluscs greatly differing in longevity (28, 37, 92, and 106 year). We contrasted the acyl and alkenyl chain composition of phospholipids from the mitochondrial membranes of these species. The analysis was reproduced in parallel for a mix of other cell membranes to investigate whether a different PI-longevity relationship would be found. The mitochondrial membrane PI was found to have an exponential decrease with increasing longevity among species and is significantly lower for A. islandica. The PI of other cell membranes showed a linear decrease with increasing longevity among species and was also significantly lower for A. islandica. These results clearly demonstrate that the PI also decreases with increasing longevity in marine bivalves and that it decreases faster in the mitochondrial membrane than in other membranes in general. Furthermore, the particularly low PI values for A. islandica can partly explain this species' extreme longevity.

^ Munro, D., and Blier P.U. (2012). The extreme longevity of Arctica islandica is associated with increased peroxidation resistance in mitochondrial membranes. Ageing Cell 11(5): 845-55. doi: 10.1111/j.1474-9726.2012.00847.x. Epub 2012 Jul 25.-wikipedia
 

Funny picture.

A funny exchange relating to the waifu online phenomenon.

video on ai singularity

Programmed aging

In 2002, Severin and Hyman showed that a natural signal molecule (yeast pheromone) sex-specifically kills S. cerevisiae cells [3]. I suggested that this phenomenon can be regarded as a precedent of programmed death of a unicellular organism [4]. Later it was found in our group that the mechanism of such death strikingly resembles apoptosis of higher organisms [5]. To explain the pheromone effect on yeast in terms of the traditional concept of non-programmed death of organisms, Kirkwood and Melov [1] assumed that yeast cells form in fact a multicellular organism. Such an explanation is hardly sufficient since (i) programmed death phenomena are now also described in bacteria [6-9] and (ii) an additional function of a pheromone as an inducer of the organism's death program was discovered in a mammal, the small marsupial Antechinus stuartii.Male of this rodent uses pheromone to attract females and then to kill himself after run [10]. To define all cases of programmed death of organisms, in 1997 I suggested the term "phenoptosis" [11] (for discussion, see [7,9,12]).-link

Article on programmed aging theories.   In the above snippet, we see that in unicellular organisms and in some multicellular organisms programmed death can occur, strengthening the case for aging being programmed.

Vitamin C benefits article

No clinical trials on the primary prevention of heart disease by vitamin C have yet been published. Instead, trials have investigated secondary prevention—the prevention of plaque progression, heart attacks, strokes, and/or mortality in people who already have heart disease. An abstract of one controversial study in 573 people, part of the Los Angeles Atherosclerosis Study in 2000, claimed that supplemental—but not dietary—vitamin C was associated with thickening of the carotid arterial wall. In contrast, an earlier study in Circulation of over 11,000 people reported that supplemental vitamin C in men and women and supplemental vitamin E in women were associated with reduced carotid artery wall thickness. Evidence on the primary prevention of heart disease by vitamin C is limited to epidemiological studies, which correlate dietary factors with disease risk. A meta-analysis of nine such studies with a total of about 293,000 subjects followed for 10 years was published in the American Journal of Clinical Nutrition in 2004. At baseline, the subjects were older than 35 years and did not have heart disease. Intake of dietary and supplemental antioxidants was estimated from questionnaires, which may not truly assess actual dietary intake and supplement use over time. Although the investigators found that vitamin E did not reduce the risk for heart disease, they did find that the intake of more than 700 mg/day of supplemental vitamin C significantly reduced the risk of heart disease by about 25%. Dietary vitamin C had little effect on heart disease risk. The report noted that these results are aligned with previous studies that found a protective effect for an intake of vitamin C greater than 500 mg/day. The biochemical mechanism responsible for vitamin C’s salubrious effects remains uncertain, but may be related to its ability to lower blood pressure, its function as an antioxidant to help attenuate oxidative stress, or its ability to relax arteries, resulting in better blood flow.

• The verdict: The majority of studies that investigated the role of vitamin C in heart disease have reported beneficial effects. This new meta-analysis offers further confirmation that supplemental vitamin C lowers the risk of heart disease. -link

A nice article reviewing recent studies on vitamin C and E.

toxins on seafood

Domoic acid accumulates in seafood and is toxic to the brain. Research indicates that the toxin damages kidneys at concentrations that are 100 times lower than what causes neurological effects.-sciencedaily

Interesting articles on previously unknown dangers of seafood.

More benefits of astaxanthin

The ability of astaxanthin to inhibit the growth of colon cancer cells was studied at Catholic University School of Medicine in Rome, Italy. Astaxanthin inhibited cell growth in a dose and time dependent manner by arresting cell cycle progression and by promoting the death of cancerous cells. Astaxanthin resulted in a 220% increase in the expression of the well known anti-cancer gene p 53, and a 160% and 250% increase respectively in the anti-cancer genes p21 and p27. Astaxanthin strongly upregulated apoptosis through gene modification, and increased phosphoylation of the p38, JNK, and ERK1/2 genes by 160%, 242%, and 280% respectively. Growth inhibitory effects of astaxanthin were also observed in HT-29, LS-174, WiDr, and Sw-480 cells. These results document axtaxanthin as highly effective against colon cancer. (Cancer Letter, May 5)

Learn more: http://www.naturalnews.com/026309_astaxanthin_cancer_research.html##ixzz2sTSPBd1q

Benefits of astaxanthin.  In the particular quote we see it seems that this antioxidant exhibits anticancer activity, which is good to know as not all antioxidants seem to do so. 

 In Caenorhabditis elegans (Nematodes, used to research metabolic pathways of longevity^[37][38]), 0.1-1mM of astaxanthin is able to increase lifespan by 16-30% in all nematodes except the DAF-16 deficient ones.^[39] This enhanced lifespan was associated with increased nuclear accumulation of DAF-16 (the nuclear target of the Ins/IGF-1 signalling pathway^[40]) and increased antioxidant defenses which were thought to be due to DAF-16 gene product expression (superoxide dismutase enzymes in particular^[41]).^[39]http://examine.com/supplements/Astaxanthin/

It seems the substance can increase lifespan in some invertebrates.

Few snippets on aging

 Compared to other elderly, membranes from centenarians (> 100 yrs) showed:
1) decreased lipid peroxide levels and reduced susceptibility to peroxidation
2) increased unsaturated/saturated fatty acid ratio
3) higher levels of EPA and DHA, reduced LA and AA
4) higher fluidity 
Membranes from centenarians show some distinct features in comparison with elderly subjects that might act in a protective way against injuries
 -http://www.waiworld.com/waitalk/phpBB3/viewtopic.php?f=20&t=3385

The above is from a thread where the topic of membrane composition, peroxidation and lifespan is covered

I was reading the book Neurons and the DHA Principle, and it seems that neuron's have substantial polyunsaturated fat content in membranes but can overcome this by antioxidant defenses.   Given these are the longest lived cells in the body and can function for over 120 years(oldest human is said to've been free from dementia), it suggests to me that if some lipid soluble antioxidant was found that didn't turn pro-oxidant nor significantly interfered with ROS signalling it could be an overall positive.

The accumulation of lipofuscin-like material may be the result of an imbalance between formation and disposal mechanisms: Such accumulation can be induced in rats by administering a protease inhibitor (leupeptin); after a period of three months, the levels of the lipofuscin-like material return to normal, indicating the action of a significant disposal mechanism.^[3] However, this result is controversial, as it is questionable if the leupeptin-induced material is true lipofuscin.^[4][5] There exists evidence that "true lipofuscin" is not degradable in vitro;^[6][7][8] whether this holds in vivoover longer time periods is not clear.-link

Assuming the cells can't actually digest it, all that would be necessary is some mechanism to export the waste and discard it elsewhere.   Whether such a mechanism exists is a good question, but I think it is likely. 

We report that long-term overexpression of
Parkin can eliminate mitochondria with deleterious COXI mutations
in heteroplasmic cybrid cells, thereby enriching cells for wild-type
mtDNA and restoring cytochrome coxidase activity.-link

Emerging data indicate that selective mitochondrial degradation through autophagy (mitophagy) plays a critical role in mitochondrial quality control. Inhibition of mammalian target of rapamycin (mTOR) kinase activity can activate mitophagy. To test the hypothesis that enhancing mitophagy would drive selection against dysfunctional mitochondria harboring higher levels of mutations, thereby decreasing mutation levels over time-link

The mitochondria has its own dna, it codes for vital functions not redundantly covered in the nucleus.  It is subject to direct exposure to damaging reactive species, so it can become dysfunctional much more easily than the dna in the nucleus.   An obvious question was how can such an organelle subject to far more mutational damage not lead to extinction of most any species.   A method of quality control has been found in female reproductive systems, iirc at the level of discarding cells, again iirc.   But it opened the question as to whether an intracellular method of quality control might also exist(after all neurons last for over a century of high metabolic activity and they don't divide).  As the above two links show it seems very likely there is a method of quality control that can preserve mitochondrial quality.

Link to a nice list and info on resveratrol benefit

 The third story in my “top 10” list is another example of pathway synergy.  Combining exercise with Resveratrol supplementation enhances mitochondrial biogenesis more than is explainable due to summing the effects of the individual interventions.

Stories 2 and 3 convey a very powerful message for anti-aging interventions: combining interventions in seemingly independent pathways may produce positive effects that are much greater than additive.-link

Interesting post on another site about a list on aging things from 2013.  This one, 3rd on the list, shows resveratrol having a positive effect on rodents.

NOTE:  Regards the vitamin findings on the list, I consider them highly suspect even many researchers not associated to big pharma have a tendency to dismiss supplements(probably don't like taking pills even if it's cents a day).  It is also the case that it is extremely unlikely that in a large population none would have a deficiency in at least one nutrient given the diversity of diets, so at least some in the population should see benefits.   In addition those who're given a vitamin and don't normally take one might also engage in additional harmful lifestyle activity which may more than counter the benefits of vitamins and minerals.

Nice quote

"Debating creationists on the topic of evolution is rather like trying to play chess with a pigeon — it knocks the pieces over, craps on the board, and flies back to its flock to claim victory."

- Eugenie Scott

A nice quote on debating creationists.

chocolate...

It is rare for men to make it to centenarian rarer still to supercentenarian(110+), here we see that one of the foods consumed was chocolate. Which reminds of Jeanne Calment who also consumed chocolate. UPDATE: Some sources claim it is possible the age may be off by 10 years which would give 100+ rather than 110+, still impressive but not as impressive.

Nice video on astaxanthin

A video that showcases the benefits of astaxanthin, its production and general info.