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As a followup to de Wolf's post on the self-sabotaging misconceptions that lead people away from successfully arranging cryopreservation upon death, you'll find an unfortunate and cautionary tale over at Depressed Metabolism. Even with the best of intentions and good preparation, life - and especially the actions of other people who think they know best - can still sabotage your efforts to take advantage of cryonics and thereby ensure a chance at future restoration:

I have been informed that Marcelon (Marce) Johnson died on 01/21/2009, was cremated, and not cryopreserved.

I understand this information may come as a surprise and as a disturbing shock to many people, especially those who loved and knew Marce, as I did. I thus feel an obligation to explain how this happened and to provide some closure to this story for the many people who helped, or tried to help, avert this catastrophe.

While Marce was alive I was unable to share the full story of what was happening. Now that she is dead and gone I believe it important and the responsible thing to do to relate the story as best I know it.

Read the whole thing, learn from it, and amend your own plans as appropriate.

One should always read the science press with a skeptical eye: scientists are just like the rest of us in that they sometimes get things wrong and often don't know everything of interest in a field. That latter point is especially true as most fields of research in the life sciences have expanded far beyond the awareness capacity of a single busy professional. So it's very helpful to have some background knowledge yourself, to help sort out the relevant from the potentially flawed.

Take this recent work on calorie restriction for example, which is announced as a potential proof that calorie restriction is not going to be useful in healthy humans:

"Our study questions the paradigm that caloric restriction is universally beneficial," Sohal said. "Contrary to what is widely believed, caloric restriction does not extend (the) life span of all strains of mice."

By measuring the animals' metabolic rate, Sohal and his colleagues came to a deceptively simple conclusion: Caloric restriction is only useful when, as in the case of the obese mice, an animal eats more than it can burn off.

"Your energy expenditure and your energy intake should be in balance," Sohal said. "It's as simple as that. And how do you know that? By gain or loss of weight.

"The whole thing is very commonsensical."

For humans of normal weight, Sohal strongly cautions against caloric restriction. In a 2003 study, he and Forster found that caloric restriction begun in older mice - both in DBA and leaner C57 individuals - actually shortened life span.

Given the very large number of studies showing strong positive effects on health and longevity in individuals of normal weight through calorie restriction, one should immediately be cautious in looking at this sort of claim in a single paper. Over at the Immortality Institute, calorie restriction expert Michael Rae dives in to take it apart in more detail:

These guys have really made some extremely unreasonable leaps of reasoning.

First, yes, it's true that DBA/2 mice are resistant to the effects of CR on lifespan -- that's been shown repeatedly, since at least the early 80s, and not just by Sohal; and (per this study) yes, they apparently have some aesthetically happy genetic perk, that allows them to eat ad libitum without gaining any weight, while other mice gain weight as one would expect.

But so what? First, as Anthony noted, while they have demonstrated these two facts, they haven't done anything to prove that this resistance to weight gain in response to an AL diet is what *causes* their resistance to the age-retarding effects of CR in this strain.

Second, as Matt notes, these are sickly mice

...

in [their prior referenced 2003] study, they violated almost every rule of adult-onset CR in the book: they administered CR as shock therapy instead of stepwise to allow for gradual adaptation, and they didn't boost the %protein in the diet to ensure that they got the full rodent 'RDA' of the AL mice. Weindruch and Walford's big 1982 breakthru', showing that you COULD actually make CR work in adults, was based precisely on not making those mistakes - and it's been repeated numerous times since.

...

the current study doesn't come anywhere close to proving what Sohal is evidently asserting about it.

For those of us without this level of background knowledge, the weight of science test is the best way to go: only start to pay serious attention to a claim when it has a cluster of papers backing it. One paper standing in opposition to dozens or hundreds of others is either wrong or the first sign of a change of viewpoint - for an observer outside the scientific community there's no harm done in dismissing it in either case. If change is underway, there will be more papers and studies to support the new viewpoint in due course.

Back in full flow for 2009, you'll find a brace of posts on aging research from the past few days over at Ouroboros.

Telomere length and psychological stress:

it should come as no surprise to learn that chronic psychological stress has been associated with accelerated telomere shortening in circulating white blood cells. The problem arises in trying to provide a biological mechanism that links this form of stress to increased telomere loss.

Links between accelerated aging and extended longevity:

I’m sitting in an auditorium listening to a seminar by Laura Niedernhoefer from U. Pittsburgh. She’s telling us that Ercc1-/- mice, which are deficient in nucleotide excision repair, show transcriptional changes that mirror those found in old wildtype or unusually long-lived mutant animals. Her data is strongly reminiscent of recent findings that progeroid DNA repair mutants exhibit transcriptional similarities to aging calorie-restricted and dwarf animals.

Old cells and organ transplants:

Because senescent cells accumulate with age, senescence has been considered a biomarker of aging - that is to say, a measurable feature of a tissue that would allow us to calculate its "biological" or "physiological" age without necessarily knowing the chronological age of the donor. This makes abundant sense: tissues with more senescent cells would have lower proliferative capacity and higher levels of deleterious secreted factors; given two samples of the same chronological age, one could argue that the one containing more senescent cells was "older" in some meaningful way. This idea is central to a recent paper demonstrating that senescence correlates negatively with the efficacy of a transplanted tissue.

More on old cells and transplants:

Another group, working in a mouse model, has shown that older donor tissues express higher levels of the senescence marker p16, which is negatively correlated with proliferative capacity. But the old material doesn’t just start from behind, but also gets worse more rapidly: p16 levels rise dramatically in old grafts following transplantation, much faster than in young grafts, indicating that older cells are more sensitive to the stresses of undergoing transplantation and that they respond to this stress by undergoing senescence.

All organs equal before oxidative damage:

What causes organ failure during aging? Is it stochastic, with individual organ systems deteriorating and failing more or less independently - or is it more like a chain of dominoes, with a primary organ failure in one tissue putting pressure on other tissues and accelerating their decline?

Mitochondrial uncoupling protein extends lifespan:

The most surprising result is that [mutants lacking uncoupling protein] have shorter lives, implying that mitochondrial uncoupling is a key mechanism for controlling oxidative stress throughout the lifespan.

Alcor does a good job at their website clearing up the major myths and answering questions about cryonics, the practice of low-temperature, ice-free storage of the body and brain after clinical death. After you die, the structure of your brain remains intact - if stored, plausible future technology could one day restore you to life. The important thing, the core of what is you, is the data represented by the preserved structure of your brain.

But if you want to benefit from cryonics, you have a little work to do. Like most forms of insurance, it has to be set up in advance and preparations kept up to date if you want to benefit. Over at cryonics blog Depressed Metabolism, Aschwin de Wolf looks at some of the self-sabotaging assumptions that get in the way:

Unfortunately, advances in the science of cryopreservation will not automatically translate into better patient care. Other factors, such as the delay between time of "death" and start of procedures, and the protocols, equipment and personnel of the responding cryonics organizations, matter as well. For example, if a cryonics standby team is not able to get to a patient before 24 hours after cardiac arrest, pumps him full of air during remote blood washout, and ships him back to the cryonics organization at subzero temperatures, that patient will not benefit from advances in human cryopreservation such as rapid induction of hypothermia, neuroprotection and vitrification.

...

Both critics and supporters have made specific probability estimates about how likely cryonics is to work. In its worst form such probability assessments convey nothing more than putting a number on overall feelings of pessimism or optimism.

...

At the time a person really needs cryonics, he may no longer be able to communicate those desires, lack funding to make arrangements, or encounter hostile relatives. A more subtle variant concerns the person who expects that aging will be solved before cryonics will be necessary. This person may or may not be right, but such optimism may not make him more immune to accidents than other people. This mindset is often observed among young "transhumanists" and practicing life extensionists.