Moderate exercise improves life expectancy: "Undertaking regular jogging increases the life expectancy of men by 6.2 years and women by 5.6 years, reveals the latest data from the Copenhagen City Heart study ... the study's most recent analysis (unpublished) shows that between one and two-and-a-half hours of jogging per week at a 'slow or average' pace delivers optimum benefits for longevity. ... SThe study, which started 1976, is a prospective cardiovascular population study of around 20,000 men and women aged between 20 to 93 years. The study, which made use of the Copenhagen Population Register, set out to increase knowledge about prevention of cardiovascular disease and stroke. Since then the study, which has resulted in publication of over 750 papers, has expanded to include other diseases ... The investigators have explored the associations for longevity with different forms of exercise and other factors. For the jogging sub study, the mortality of 1,116 male joggers and 762 female joggers was compared to the non joggers in the main study population. All participants were asked to answer questions about the amount of time they spent jogging each week, and to rate their own perceptions of pace (defined as slow, average, and fast). ... The first data was collected between 1976 to 1978, the second from 1981 to 1983, the third from 1991 to 1994, and the fourth from 2001 to 2003. For the analysis participants from all the different data collections were followed using a unique personal identification number in the Danish Central Person Register. ... These numbers have been key to the success of the study since they've allowed us to trace participants wherever they go. ... Results show that in the follow-up period involving a maximum of 35 years, [risk] of death was reduced by 44%."

Link: http://www.eurekalert.org/pub_releases/2012-05/esoc-rjs050212.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

I'm a little late in pointing out the latest issue of Cryonics, the magazine published by cryonics provider Alcor, is presently available as a PDF.

The March-April issue of Cryonics features an extensive treatment of protecting one's cryonics arrangements against inflation through life insurance. Insurance agent and Alcor member Rudi Hoffman makes the case for "superfunding" your cryonics arrangements to keep pace with the rising costs of advanced medical procedures. The author explains the differences between the major forms of life insurance (term life, whole life, universal life, etc.), gives advice on how to evaluate the various bells and whistles insurances companies offer, and provides guidance how to read those long policy illustrations. This issue continues the recent focus on identity-destroying brain disorders by offering an article by Alcor staff member Mike Perry about the latest developments in Alzheimer's Disease diagnosis. Alcor CEO Max More reports on the upcoming Alcor conference and both book reviews deal with the topic of immortality, albeit from a different perspective.

The main topic of the issue ties into the ongoing discussion on maintaining Alcor's reserve of funds at a sufficient level for the long term - which is essentially a battle against the predatory inflation produced by the self-serving actions of politicians and political appointees. The political class can be expected to create ever more money from nothing, continually reducing the value of money in circulation and savings accounts, because it is the most effective way to tax the masses - all other forms of taxation generate far more unrest, resistance, and non-compliance, and are thus much more self-limiting in the revenue they can generate.The battle against the inflation resulting from depreciation of the currency is fought by all entities that must tie contracts inked today to outlays required years from now:

As evidenced by recent exchanges on the Alcor Member Forums, our members have a wide variety of suggestions for how to close the substantial funding gap that has been produced by Alcor's practice to date of not raising cryopreservation minimums for existing members. If there is one area of strong agreement, however, it is that all members who are underfunded for today's cryopreservation minimums and who can afford to change or upgrade their life insurance, should do so. This will not just reduce Alcor's funding shortfall but it will also allow the member to secure new cryopreservation and storage technologies that cannot be offered without charging an additional amount. Surplus funding can also be allocated to a personal revival trust or to Alcor's hardship fund to help members with poor funding and/or challenges to pay annual dues.

The March-April issue of Cryonics magazine features an extensive review of life insurance options by Alcor member and life insurance agent Rudi Hoffman. Rudi introduces the topic by presenting the disturbing long-term effects of (medical) inflation. Not all of Alcor's services may be subject to the kind of cost increases we see in medicine but it is prudent to plan using conservative assumptions. After this sobering introduction, Rudi runs us through the various forms of life insurance, their pros and cons, and how to read those long, intimidating policy illustrations. We at Alcor hope that many of you will make efforts to update your cryonics funding to make it easier to solve the underfunding problem and to assist with the really hard cases.

Alcor has its cultural roots firmly in the non-profit world and mindset, as you can see from the above material. This is admirable, but would produce challenges in any organization that must have continuity over decades of serving the same customers. Prices must change to suit the times, and business models must take that into account.

It has occurred to me once or twice over the years that, setting aside the cultural history, an organization similar to Alcor might be best suited to growth and stability as a for-profit subsidiary of a large insurance company. Many of these challenges could be met by a strong relationship with a group that manages insurance and accounts with customers that span many years. In any case, this is another of the possible business models that has yet to be explored in cryonics - and is unlikely to be explored until such time as the industry grows larger.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Chronic inflammation is a bad thing - it greatly increases your risk of suffering age-related disease, and may be one of the more important mechanisms linking excess fat tissue to risk of disease and lowered life expectancy. Here is more evidence to show that being overweight exposes a person to greater inflammation: "Postmenopausal women who were overweight or obese and lost at least 5 percent of their body weight had a measurable reduction in markers of inflammation. ... Both obesity and inflammation have been shown to be related to several types of cancer, and this study shows that if you reduce weight, you can reduce inflammation as well. ... Women in the trial who were assigned to a weight loss intervention had a goal of 10 percent weight reduction during the course of one year achieved through a diet intervention with or without aerobic exercise. ... The researchers measured levels of C-reactive protein, serum amyloid A, interleukin-6, leukocyte and neutrophil in 439 women. At the end of one year, C-reactive protein reduced by 36.1 percent in the diet-alone group and by 41.7 percent in the diet and exercise group. Interleukin-6 decreased by 23.1 percent in the diet group and 24.3 percent in the diet and exercise group. ... there were greater reductions in these measures among women who lost at least 5 percent of their body weight. They also found that exercise alone, without a dietary weight loss component, had little effect on inflammation markers."

Link: http://www.eurekalert.org/pub_releases/2012-05/aafc-wll042412.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

An introduction to what is known of telomeres can be found at the Scientist: "The ends of linear chromosomes have attracted serious scientific study - and Nobel Prizes - since the early 20th century. Called telomeres, these ends serve to protect the coding DNA of the genome. When a cell's telomeres shorten to critical lengths, the cell senesces. Thus, telomeres dictate a cell's life span - unless something goes wrong. Work over the past several decades has revealed an active, though limited, mechanism for the normal enzymatic repair of telomere loss in certain proliferative cells. ... Telomeres shorten as we age. By analogy to the cellular mitotic clock, telomeres have been postulated as a marker of 'genetic age,' and telomere length has been marketed as a simple predictor of longevity. Assays of telomere length have been bundled with recommendations for lifestyle modification and for drug therapy, neither based on appropriate clinical studies. Simple but appealing arguments relating telomeres and aging are currently controversial, likely simplistic, and potentially harmful. Telomere length does indeed reflect a cell's past proliferative history and future propensity for apoptosis, senescence, and transformation. Cellular aging, however, is not equivalent to organ or organismal aging. ... Studies in humans have attempted to relate telomere length to life span. In the provocative initial publication from the University of Utah in 2003, individuals around 60 years of age who had the longest telomeres lived longer than did subjects with the shortest telomeres, but the main cause of death in the latter group was, inexplicably, infectious disease; the persons with shorter telomeres did not have a higher rate of cancer deaths. Moreover, these findings have not been confirmed in other studies of older subjects. In another study evaluating a different population, telomere length failed to predict survival, but interestingly it correlated with years of healthy life. In a Danish study of people aged 73 to 101 years, telomeres correlated with life expectancy in a simple univariate analysis, but only before the researchers corrected for age, suggesting that the correlation was driven simply by the fact that younger subjects had longer telomeres. And a Dutch study of 78-year-old men found that while telomere lengths eroded with age, they failed to correlate with mortality."

Link: http://the-scientist.com/2012/05/01/telomeres-in-disease/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The April 2012 edition of Rejuvenation Research includes the proceedings of the SENS5 conference, so there's a lot of material you'll have already seen there. The sole open access paper is worth reading as an update on research into the use of Z-Phe-Ala-diazomethylketone (PADK) to boost lysosomal function. The lysosome, you will recall, is a form of roving recycling unit that exists within the cell. Its task is to break down waste and unwanted materials - and that function is vital, as demonstrated by the many ultimately fatal conditions caused by lysosomal dysfunction. Unfortunately for all of us, lysosomal functionality deteriorates with age. This is most likely due in large part to accumulating waste materials, such as lipofuscin, that lysosomes cannot break down. They instead bloat and malfunction.

One body of research aiming to fix this issue is organized and advocated by the SENS Foundation, and focuses on ways to safely break down the waste materials that cannot be handled by lysosomes. For example, through biomedical remediation and the use of tailored bacterial enzymes. Meanwhile, other research groups have worked on boosting lysosomal activity in various ways, which seems to have generated some benefits where successful. For example, reversing decline in liver function, and restoring mental capacity in mice engineered to generate the signs of Alzheimer's disease.

It is that second example that is the subject of this open access paper, showing that enhancing lysosomal activity can potentially help with aggregates of damaging material outside cells, as well as the state of the cell interior:

Positive Lysosomal Modulation As a Unique Strategy to Treat Age-Related Protein Accumulation Diseases

Knowing the link between lysosomal dysfunction and selective pathogenesis, one logical step toward therapeutic intervention is the enhancement of enzymatic activity in lysosomes. [Some age-related diseases] may be slowed or reversed by the positive modulation of the lysosomal system. Many studies suggest that lysosomal activation occurs with age and in diseased brains, but not to the necessary extent that would prevent the gradual loss of neuronal integrity and brain function.

Enhancement of lysosomal function has been proposed as a plausible strategy to reduce protein accumulation events in age-related disorders, including those events in Alzheimer disease, Parkinson disease, and Huntington disease. Several of the studies indicate that induction of protein degradation processes is an attempt to clear amyloid peptides and tau species, as well as ?-synuclein and mutant huntingtin. Another potential therapeutic strategy that may involve the endosomal-lysosomal system is the disaggregation of extracellular A? peptide, with the idea that the disaggregation would promote uptake of monomers and small oligomers into neurons and microglia where they are trafficked to lysosomes for degradation.

...

Of the list of lysosomal modulatory agents [provided in the paper] only PADK, diazoacetyl-dl-2-aminohexanoic acid methyl ester, glycyl-phenylalanyl-glycine-aldehyde semicarbazone, and bafilomycin A1 have been reported to elicit protection against protein accumulation pathology under appropriate low-dose conditions.

...

From the in vitro and in vivo findings, unique lysosomal modulators represent a minimally invasive, pharmacologically controlled strategy against protein accumulation disorders to enhance protein clearance, promote synaptic integrity, and slow the progression of dementia.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm