Calorie restriction with optimal nutrition is known to extend healthy life span in mammals - this from the wait and see method of study, meaning that all we can say for sure today for humans is that it does great things for your long-term health. Researchers have been digging into the mechanisms of calorie restriction more energetically in recent years, hoping to find the keys that change metabolism to slow aging.

The other side of the metabolic approach to intervening in the aging process is the search for longevity genes - mutations or changes in gene expression that change the processes of metabolism to slow down the accumulation of age-related damage. Scientists have been turning up a handful of new longevity genes every year in the recent past, many connected to the mechanisms of calorie restriction, many not.

After studies demonstrating extended life span through single gene mutations, and studies demonstrating extended life span through calorie restriction, why not studies of both at once? There's a lot of that going on at the moment, as researchers attempt to understand just how many distinct ways exist to improve metabolism and slow aging.

How diet interacts with longevity genes:

In laboratory mice, suppression of growth hormone (GH) signaling by spontaneous mutations or targeted disruption of GH- or IGF1-related genes can lead to an impressive increase of longevity. Hypopituitary Ames dwarf (Prop1 df) and GH receptor knockout (GHRKO) mice live 35-70% longer than their normal littermates.

Many phenotypic characteristics of these long-lived mutants resemble findings in genetically normal animals subjected to calorie restriction (CR). Microarray and RT-PCR studies of gene expression suggest that effects of the "longevity assurance genes " (Prop1 df or Ghr-/-) and CR are overlapping but not identical.

Subjecting Ames dwarf mice to 30% CR starting at 2 months of age leads to a further significant extension of their average and maximal lifespans. In contrast, identical CR regimen has either no or very little effect (depending on gender) on longevity of GHRKO mice. We suspect that this difference in response is related to the fact that CR improves insulin sensitivity in Ames dwarfs but does not further increase the extreme insulin sensitivity of GHRKO mice.

To search for effects of CR associated with extension of longevity, we are studying expression of insulin and IGF1-related genes in the liver, skeletal muscle and heart of normal and GHRKO mice.

Researchers will be working on the mechanisms of metabolic longevity for many years to come - it's a rich vein. It does seem plausible, however, that the biomechanisms of calorie restriction could be completely uncovered and understood within the next five years. The present pace is fast, and a great deal of funding is available in that part of the field.

For all that, if you're one of those folk holding out for a good calorie restriction mimetic (a drug to trigger all the same controlling gene expression changes without the need to diet), it's worth bearing in mind that a fair chunk of the benefits of calorie restriction seems to stem from cutting down visceral fat mass and not triggering an insulin resistance feedback loop through chronic overeating.

Meanwhile, we should all recall that slowing aging buys us little in comparison to methods to repair aging, and that those repair methods will likely be easier to develop in any case. It's a big leap to build a better metabolism when we're so far from fully describing the one we have. A far smaller leap to undo the known changes that turn a young metabolism into an aged, damaged metabolism.

Posted by Reason at 5:35 PM
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Carrying more visceral fat in your body than you need to get by - the standard result of a life involving too many calories and too little exercise - reduces your longevity. It also greatly increases the chances of your later years being unhealthy, painful and expensive. I've looked at a range of mechanisms by which this happens:

• A Gentle Reminder That Fat Will Eat Your Mind
• Fat and Inflammation
• How Excess Fat Tissue Slowly Destroys You
• Fat, Inflammation and Atherosclerosis

Knowing is half the battle, but putting the work in to shed that fat will pay great dividends over the years. Who wants to be frail and incapacited by diabetes and Alzheimer's at 70, versus fit enough to get out and play a game of tennis whenever you feel like it?

Continuing this examination of reasons not to be overweight, I noticed an interesting paper that demonstrates quite directly the cost of visceral fat (visceral adipose tissue in science-speak) on life span.

Visceral Adipose Tissue Modulates Mammalian Longevity

Caloric restriction (CR) can delay many age-related diseases and extend lifespan, while an increase in adiposity is associated with enhanced disease risk and accelerated aging. Among the various fat depots, the accrual of visceral fat (VF) is a common feature of aging, and has been shown to be the most detrimental on metabolic syndrome of aging in humans.

We have previously demonstrated that surgical removal of visceral fat (VF) in rats improves insulin action, thus, we set out to determine if VF removal affects longevity.

We prospectively studied lifespan in 3 groups of rats: ad libitum fed (AL), 40% caloric restriction (CR) and a group of ad libitum fed rats with selective removal of VF at 5 months of age (VF-). We demonstrate that compared to AL, VF- rats had a significant increase in mean and maximum lifespan and significant reduction in the incidence of severe renal disease.

CR animals demonstrated the greatest mean and maximum lifespan the lowest hazard rate of death as compared to AL rats. Taken together, these observations provide the most direct evidence to date that a reduction in fat mass, and specifically VF, may be one of the possible underlying mechanisms of the anti-aging effect of CR.

This conclusion seems likely - but note that sensibly practicing calorie restriction does much more under the hood than just lower the level of fat in your body. Also note that you don't need to be full-on calorie restricted to lose enough visceral fat to greatly benefit from its absence. The difference between an average, healthy body weight and what passes for the norm in much of the developed world today is large enough to make a big difference to health and longevity in later life.

The body is a complex machine, and like all machines, it ages more slowly if you take better care of it. That much should be common sense.

Posted by Reason at 4:20 PM
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Generally speaking, I'm not a big fan of the sort of hyperaggressive tinkering with supplements that passes for action amongst a large portion of the healthy life extension community. It's highly unlikely to improve significantly on simple exercise, calorie restriction and a sane multivitamin. You have no reliable tool to measure how effective your vitamin regimen is in any case, short of waiting for the necessary decades to see how your long term health goes. Furthermore, solid scientific support is sorely lacking for most of the recommendations you'll see out there - a situation far removed from the vast array of detailed support for exercise and calorie restriction. The waters are muddied by less than ethical marketeers with supplements to sell and money to make; it's very hard for the average fellow to figure out what's what.

Quite aside from all that, how exactly is that tinkering with supplements helping to advance the science of repairing age-related damage? Answer: it isn't. Perhaps your energies are better directed elsewhere...

There are, of course, exceptions to all rules. Leucine supplementation for older folk might just be one of those - although there's a little more work to be done to make an airtight case. Take a look back at the Longevity Meme archives:

Preventing Age-Related Muscle Loss:

Muscle in adults is constantly being built and broken down. As young adults we keep the two processes in balance, but when we age breakdown starts to win. However, adding the amino acid leucine to the diet of old individuals can set things straight again. ... After the age of 40, humans start loosing muscle at around 0.5-2% per year. ... The team of researchers believe that the age-related problem results from defective inhibition of ubiquitin-proteasome dependent proteoloysis, a complex degradative machinery that breaks down contractile muscle protein, and that leucine supplementation can fully restore correct function.

Sarcopenia As Dietary Issue

Sarcopenia, age-related muscle loss, is well known as a common result of aging - and the resulting lack of exercise hastens age-related decline in other ways. ... Since nutritional studies show that many elderly individuals eat less protein than the average person, researchers have reasoned that if the elderly simply increased their protein intake, they might slow down muscle loss -- as long as old age doesn't inherently interfere significantly with the ability to make muscles out of the protein in food. ... We wanted to know if there is some reason your grandmother's body, for example, can't stimulate muscle growth in response to eating the same protein-rich meal that you eat, which might over time contribute to muscle loss ... [however] older bodies are just as good as young ones at turning protein-rich food into muscle.

So, maybe leucine, maybe just protein deficiency. A more recent study caught my eye today; it manages to add support to both sides without actually resolving the question either way:

Supplementation with Dietary Leucine to a Protein-Deficient Diet Suppresses Myofibrillar Protein Degradation in Rats

Muscle mass is regulated by the synthesis and degradation of muscle protein, which in turn are affected by aging, several catabolic diseases, and malnutrition. Amino acids, particularly leucine, are known to stimulate muscle protein synthesis and suppress muscle protein degradation, although their long-term effects are unclear. The objective of our research was to elucidate whether long-term feeding of a protein-free or low-protein diet supplemented with leucine suppresses myofibrillar protein degradation.

...

These results suggest that long-term feeding of leucine suppresses the rate of myofibrillar protein degradation and muscle weight loss in rats fed a protein-deficient diet.

Which supports the use of leucine supplementation in a low-protein diet to slow the rate of muscle loss over time, but doesn't tell us whether simply increasing the amount of dietary protein is a better solution. This is probably of interest to folk practicing calorie restriction, given that their intake of protein is reduced (indeed, reduced protein intake may be the driving mechanism for the beneficial metabolic changes brought on by calorie restriction). As I said above, however, this all needs more weight of research.

Posted by Reason at 5:01 PM
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That excess visceral fat you're carrying causes chronic low-level inflammation, which damages you in all sorts of ways. One of those ways is atherosclerosis, which tends to up and kill you without warning. In fact, eating all the food required to gain a large amount of visceral fat causes a feedback loop in your metabolism that spirals down into insulin resistance and diabetes - both of which make the effects of having a lot of visceral fat that much worse and that much more rapid.

But that extra fat won't just make you much more prone to be frail, and it won't just try to kill you - it'll also eat your mind. Researchers are coming to view Alzheimer's disease as analogous to diabetes, a result of lifestyle choices for most, touching on many of the same metabolic processes as diabetes, and the risk factors seem to be much the same.

Big Bellies Linked to Alzheimer's Disease:

The study of more than 6,000 people found the more fat they had in their guts in their early to mid-40s the greater their chances of becoming forgetful or confused or showing other signs of senility as they aged. Those who had the most impressive midsections faced more than twice the risk of the leanest.

Surprisingly, a sizable stomach seems to increase the risk even among those who are not obese, or even overweight

...

The research is the latest evidence that fat in the abdomen is the most dangerous kind. Previous studies have linked the apple-shaped physique to a greater risk of diabetes, heart disease and even cancer. Researchers suspect that those fat cells are the worst because of their proximity to major organs. They ooze noxious chemicals, stoking inflammation, constricting blood vessels and triggering other processes that might also damage brain cells.

"There is a lot of work out there that suggests that the fat wrapped around your inner organs is much more metabolically active than other types of fat right under the skin," Whitmer said. "It's pumping out toxic substances. It's very potent toxic fat."

Another excellent reason to take care of the health basics - a responsible level of diet and exercise - before your body sabotages your mind. The longer you leave it, the more damage you're creating, and the more you're cutting from your likely healthspan.

Posted by Reason at 5:17 PM
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Researchers are working their way closer to a grail of tissue engineering: a fabricator that can print out living organs in three dimensions just like the rapid prototyping devices used today in a variety of industries. Plastics and inks become cells and biomaterials, and the whole works much the same way. Organs are many magnitudes more complex in structure than the plastic prototypes turned out by fabricators in the design industry, but the cells used to build those organs can - in theory - be induced to do most of the small-scale organization for you. Roland Piquepaille notes one of the latest technology demonstrations:

"We will never be able to print a liver with all of its many details," says Forgacs. "But it is not necessary. If you initiate the process, nature will do it for you."

According to MU, "the team used bio-ink particles, or spheres containing 10,000 to 40,000 cells, and assembled, or 'printed,' them on to sheets of organic, cell friendly 'bio-paper.' Once printed, the spheres began to fuse in the bio-paper into one structure." Nature adds that "when they printed out cardiac and endothelial cells, the cells fused into a tissue after 70 hours, and began beating in time like regular heart tissue after 90 hours."

Nature also explains why this project is different from previous ones. "What makes this work different from that done in most other tissue-engineering labs is that Forgacs's team does everything without a scaffold - they don’t start with an object shaped like the tissue or organ they are aiming to create, but instead plan to print the whole thing from scratch, from the vasculature up. This should make it easier to print any type of organ, they say, as they don’t have to develop different scaffolds for each tissue type. 'Often when you implant a scaffold you get inflammation,’ says Forgacs.'"

Researchers are still building the components of organs in the technology demonstrations - we're a few years away from fabrication of even "simple" organs, such as the heart or liver. As I've noted previously, the big hurdle of the moment is getting the blood vessels - the vasculature - right. Blood transport is vital to building living tissue of any meaningful size, and it's a hard problem if all the blood vessels, from microscopic capillary networks on up, have to be designed by hand into the tissue you're printing.

Posted by Reason at 1:12 PM
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Some interesting material from a scientific study of attitudes to healthy life extension and enhanced longevity is posted to Cryonet:

The age of the respondent was related to life-extension attitudes [with] the older respondents tilting in the pro-longevity direction.

Pro-longevity attitudes were strongest in the separated-divorced group and weakest in the single group.

From a utilitarian, economic action viewpoint, that is much as I would expect. I think there's ample circumstantial evidence to suspect that those who claim to be fine with aging and dying will mostly change their minds when they get there. The unpleasant future is all too easily hand-waved away for another day - until that day finally comes home to roost.

The study presented subjects with a range of positive and negative viewpoints on healthy life extension. The viewpoints vary widely in validity, with those on the economic side of the house being particularly bad, but I don't think that's too important when it comes to drawing conclusions from the reactions of study participants:

I. Personal Emotional Rejection (PER) reflects a harsh rejection of life extension with endorsement of items focused on pointlessness and waste, and contrary-to-nature aspects of extending life span. Other items reflect the personal cost of life extension (e.g., delaying commitments or prolonging goals, inducing boredom).

II. Utopian Vision (UV) points to the many advantages of life extension for older people and for society at large.

III. Social Economic Burden (SEB) highlights the economic burdens on the individual and the health-care system flowing from life extension. The highest loading items stress preference for health over longer life and a fear of financial dependency for the individual, and exhaustion of resources for the society.

Age was significant for each of the factors. ... The older the adult, the more likely is he or she to reject the harsh negativity toward life extension reflected by the items loading on factor I. Correspondingly, chronological age is positively associated with endorsement of items that promise a Utopian future with life extension (Factor II). Finally, the outcome for Factor III is somewhat counterintuitive as we observe that older adults are significantly more disposed to endorse anti-longevity items. These items concern the added costs of health-care and social welfare and hence raise the possibility of exhaustion of financial resources.

That last point only reinforces my conviction that economic ignorance is one of the greatest threats to the future of healthy life extension (and indeed to all meaningful advancements in technology). It is a strange world when so many believe that more healthy people working away to produce value and trade with one another will somehow make us all poorer:

• Jealousy, Fear, Envy and Economic Ignorance - Powerful Poisons
• If We Fail, It Will Be From Ignorance
• Death (For Everyone) Before Inequality (For Anyone)

The points that found the most favor in the study might lead us to a little more optimism, however:

Of the positive survey items, these were the most stable across the studies:

Longevity improving life more time for goals
Extending life giving respect to old age
Longevity research as duty to future generations
Long Term Relationship (LTR) quality will increase with longevity
Society will benefit from greater wisdom
Increase budget for this research

Other positive items from the LEQ:

Favor longevity research even if product unaffordable
Extend life to have more leisure time
Estimate satisfaction greater at age 110 than 75
Families benefit from cross-generation interaction

I'm sure you'll recognize a number of these in past material produced by longevity advocates, myself included. Biomedical gerontologist Aubrey de Grey in particular has argued for duty to those yet to live - in his view, who are we to decide that our grandchildren's lives must be as short as our own? By failing to heed the moral imperative to longevity research, we condemn future generations to have no choice in their own longevity.

Posted by Reason at 5:28 PM
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Far too much energy is spent on looking at what presently exists, our present state of being in ever greater detail and fine degree of measurement, when rampant change is the nature of the day. Why are people willing to spend inordinate amounts of time and energy examining and debating which narrowly separated socio-economic groupings of humanity live a year more in health here or year less in health there? This is an age of foaming scientific revolution and rapid progress in biotechnology and medical science, in which all these factors are changing very rapidly. Time spent carefully drawing lines between groups of people - that will be erased almost immediately with the speed of change these days - is time not spent helping to make lives better.

It seems evident to me that I should spend far more effort in relation to progress in the fields that will add decades to healthy life spans in due course, swamping all minor variables of the human condition. Those small differences are insignificant in that context - and will become increasingly so as success in medical research continues.

So why is it that most people care so much more about the shiny, distracting trinkets of the now, a few years more or a few years less than someone else, in comparison to the far more important issue of the desired future and how to get there? I wonder. I seem to recall saying much the same thing in connection with research into telomere length and socio-economic status back in 2006:

[We should] recognize that time is far better spent acknowledging that we're all suffering from a condition that will deliver suffering, pain and death - and then doing something about it rather than simply observing it.

We are all doomed unless we dig ourselves out of the hole of aging via the future of medical technology. What does it matter that some of us are a handful of percentage points more or less doomed than others, largely through our own actions in exercise, diet and other controllable factors? It's still doom, and we'll all be just as rescued by technologies capable of repairing the damage that is aging.

My thinking was steered this way once more by a brace of recent articles on education level and longevity - which is just another correlation in the general pattern of wealth, use of medical resources, good health practices, and all that other fun stuff that fits in with "socio-economic status." I don't see more in the way of separating causation from correlation this time around - and the press is generally much more interested in playing the game called "who has more" in any case. Not a forward-looking group, mainstream journalists, nor much acquainted with context in terms of past and future. They are the voice of the shiny trinkets of the now. See what you think:

Harvard Researcher: Education Key to Longevity

"We looked at life expectancy at age 25," Meara says.

"How many additional years can you expect to live if you arrive at age 25 and your education has stopped at high school, or sooner? Versus how many years, can you expect to live if you've reached aged 25 and you've gone on to at least some college…"

Meara says they found that in 1990, a 25-year-old who only had some secondary school could expect to live for a total of 75 years. In 2000, a 25 year old with some secondary education could also expect to live to the age of 75.

In contrast, for a better educated 25-year-old, they could expect to live to the age of 80 in 1990. Someone with a similar education level in the year 2000, could expect to live to be more than 81 years, 81.6 years to be exact.

Longevity rising for educated:

"If you look in recent decades, you will find that life expectancy has been increasing, which is good, but when you split this out by better-educated groups, the life expectancy gained is really occurring much more so in the better-educated groups," said lead researcher Ellen Meara, an assistant professor of health-care policy at Harvard Medical School.

The answer may lie with tobacco. About one-fifth of the difference in mortality between the groups can be accounted for by smoking-related diseases such as lung cancer and emphysema, Meara said.

A large chunk of the rest of the difference is likely related to exercise habits and excess body fat - obesity is at least as damaging to healthy longevity as smoking, and possibly more so when combined with lack of exercise. We can also throw in psychological stress for consideration; plausible evidence suggests that chronic stress damages biochemistry into more rapid aging over the years.

I could go on - there are all sorts of ways in which we can choose to damage ourselves, or let damage continue at a greater rate due to circumstances we can control. All of this is irrelevant and unimportant, however, when compared to the speed with which medical technologies for the repair of aging are developed. If we can make that happen rapidly enough, we're all rescued. If not, we're all doomed.

Posted by Reason at 5:03 PM
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I'm pleased to note that the Immortality Institute folk will be offering incentive prizes to participants in the Longevity Meme Folding@Home team on a quarterly basis going forward:

The Longevity Meme has teamed up with the Immortality Institute to offer a quarterly prize to people who contribute to the Stanford Folding@home distributing computing project - aimed at curing disease through understanding the basics of protein folding.

...

Winners will be determined by how many points are accumulated over the course of three months as reported at the Stanford Folding@home statistics site. The first quarter of competition begins at 12:00 a.m. Eastern daylight time (U.S.) April 2nd and ends at 12:00 midnight, Eastern daylight time, on June 30th.

The Longevity Meme team has grown and performed very well in the years since its formation. It takes organization and active recruitment to break into the top 200 ranked teams; many of the Immortality Institute regulars have stepped up to provide that organization. Thank you all for helping to make the team a continuing success.

Futures are built, one brick at a time, on the self-organizing collaboration of many interested people. Those collaborative communities are built of many, many overlapping modest goals and projects, just like this one. I hope you'll consider joining in, contributing to the Folding@Home project, and through this effort, learning more about the greater goals of longevity science, curing age-related disease, and ultimately repairing the damage of aging.

Head on over to the Immortality Institute to learn how to register for the prize program or discuss Folding@Home in the team thread.

Posted by Reason at 5:36 PM
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Some research groups are making the case that all roads lead to autophagy, the process of tearing down and replacing worn cellular components, when it comes to enhancing healthy longevity through adjustments to metabolism. Examples include calorie restriction (CR) - which you can manage all by yourself today - or drugs that mimic some of the effects of CR on regulatory mechanisms in our biochemistry, which you're going to have to wait a little longer for. But it's all down to increased autophagy, they say:

The better known life extension mechanisms in lesser animals are all driven by changes in autophagy - or so say the autophagy specialists. It's true that the various hyperspecialized communities of modern biology are overly cloistered and ignorant of one another's research, but the autophagy researchers are assembling compelling evidence for this position: "Here we show that mutational inactivation of autophagy genes, which are involved in the degradation of aberrant, damaged cytoplasmic constituents accumulating in all aging cells, accelerates the rate at which the tissues age in the nematode Caenorhabditis elegans. According to our results Drosophila flies deficient in autophagy are also short-lived. We further demonstrate that reduced activity of autophagy genes suppresses life span extension in mutant nematodes with inherent dietary restriction, aberrant insulin/IGF-1 or TOR signaling, and lowered mitochondrial respiration. These findings suggest that the autophagy gene cascade functions downstream of and is inhibited by different longevity pathways in C. elegans, therefore, their effects converge on autophagy genes to slow down aging and lengthen life span. Thus, autophagy may act as a central regulatory mechanism of animal aging.

Which is interesting, because other research groups are fairly sure that the enhanced longevity provided by these sorts of metabolic adjustment is accomplished through lowered levels of chronic inflammation and free radical generation:

This review focuses on the emerging evidence that attenuation of the production of reactive oxygen species and inhibition of inflammatory pathways play a central role in the antiaging cardiovascular effects of caloric restriction.

The evidence on both sides is compelling, but it can't be both all autophagy and all inflammation and free radical reduction, and it can't be just one or the other. Conflicting evidence and theories with good experimental backing on all sides are usually a good sign that there is something important left to be discovered, some shift in the overall picture of the field. For example, a comprehensively described link between autophagy, inflammatory processes and free radical generation. For now we're still missing a unifying view of the many known metabolic and genetic changes that increase longevity in mammals - how do they work?

Posted by Reason at 7:11 PM
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Here's a short review of the effects of calorie restriction on two important areas in the science of metabolism and aging:

This review focuses on the emerging evidence that attenuation of the production of reactive oxygen species and inhibition of inflammatory pathways play a central role in the antiaging cardiovascular effects of caloric restriction. Particular emphasis is placed on the potential role of the plasma membrane redox system in caloric restriction-induced pathways responsible for sensing oxidative stress and increasing cellular oxidative stress resistance.

We propose that caloric restriction increases bioavailability of NO, decreases vascular reactive oxygen species generation, activates the Nrf2/antioxidant response element pathway, inducing reactive oxygen species detoxification systems, exerts antiinflammatory effects, and, thereby, suppresses initiation/progression of vascular disease that accompany aging.

Chronic inflammation and the generation of reactive oxygen species (or free radicals) are prominent in the present day view of how normal metabolic processes cause the accumulation of biochemical damage that is aging. Look back in the Fight Aging! archives for more:

• Inflammation and the Damage of Aging
• How Age-Damaged Mitochondria Cause Your Cells To Age-Damage You

Calorie restriction reduces the rate at which damage occurs in both of these noted avenues - fewer free radicals, more antioxidant biochemistry to soak up those free radicals, and less inflammation. Given that, it shouldn't be surprising to find that the practice of calorie restriction "makes everything better" when looking at the pace of age-related degeneration. Damage yourself more slowly and your health will last longer.

Posted by Reason at 6:30 PM
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Beware of people bearing either / or choices, especially when both options are terrible. Nothing in life is binary, and there exist no inescapable boxes nor walls that cannot be torn down. You'll always find other choices, other paths forward, if you care to search hard enough.

Here is a charming either / or choice, posed by someone with surprisingly little vision for a medical research:

Controversially, Brown also suggests that wiping out cancer and heart disease might be misguided, because these are swifter, and therefore relatively desirable, ways to die. It would be easy to think him heartless, were it not for his moving and vivid descriptions in the book of watching his own father die from pancreatic cancer. Brown writes how he “returned one last time to the hospice on a vile rainy day - I hadn't seen him for a week - and it was like something from a horror movie. I had never seen someone so dead who was still alive.”

Brown admits “the experience of seeing my father in pain and being in a degraded state was very difficult. But, although it was awful, in the grander scheme, it was a relatively easy death. My father had expressed a fear of dying with dementia, and so that would have been much harder, and that's partly why I believe we shouldn't remove these acute forms of death (like cancer). We'll just be exposing ourselves to longer, more drawn-out forms of death.

It is utterly false to present a choice of working to prevent dementia or working to prevent cancer and heart disease. All can be done - there's no shortage of resources in the world. But this fellow is well with the cage of his preconceived limits: in his world, we must all suffer and die from some age-related disease. Not doing so isn't even a possibility. How odd to hear a researcher argue this point; one might almost think about pushing him back a century to argue about whether consumption or yellow fever is best to be adopted as the death of choice, and therefore no cures should be sought.

We live in an age on the verge of repairing the damage of aging, preventing all age-related disease, and extending the healthy human lifespan through other means besides. How can any medical researcher be debating which age-related degeneration should be left alone as the accepted mode of suffering and death? The strongest bars are found in the cages of the mind that we build for ourselves by accepting the world in its present form.

Ultimately, limits to action and endeavor - and in this case, limits to what can be achieved through medical research - stem from our preconceptions of what those limits should be. An incurable disease, known to all as a death sentence, is only an incurable disease until a group of vision raises the funds, performs the work, and develops a therapy. So too with age-related degeneration, suffering and death. One person's notion of the absolute wall to progress is a red flag to those more inclined to charge ahead and make progress happen.

Posted by Reason at 6:25 PM
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The responsible practice of calorie restriction with optimal nutrition (CR) has nothing whatsoever to do with eating disorders like anorexia. The former is engaged methodically in order to meaningfully and measurably improve your health and longevity, while the latter is engaged carelessly and relentlessly in order to damage oneself, slaved to an impossible ideal.

There is a world of difference between those extremes. That is self-evident to anyone who's taken a serious shot at practicing CR for the health benefits, as well as anyone who's spent any time in the online or offline CR communities. But you'll always find some idiot - and some academic idiots in past years - who can't see eating in a more planned fashion as anything other than a mental illness, no matter how many facts to the contrary are right under their noses. CR practitioners need no help to send idiots packing, but it's nice to see that some of the folk involved in the ongoing CALERIE study of human CR recently published a more scholarly refutation than the idiots deserve.

Is caloric restriction associated with development of eating-disorder symptoms? Results from the CALERIE trial:

This study tested a secondary hypothesis of the CALERIE trial (Heilbronn et al., 2006) that a 12-month period of intentional dietary restriction would be associated with an increase in eating disorder symptoms.

...

All three dietary restriction arms were associated with increased dietary restraint and negative energy balance, but not with increased ED symptoms or other harmful psychological effects. Participants in the three calorie restriction arms lost significant amounts of body weight. The psychological and behavioral effects were maintained during a 6-month follow-up period. ... These results did not support the hypothesis that caloric restriction causes increased eating disorder symptoms in overweight adults. In general, caloric restriction had either benign or beneficial psychological and behavioral effects.

So hopefully we'll be hearing less of the anorexia association nonsense in the years ahead. People who exercise in a planned fashion so as to be healthy don't have to put up with nonsensical accusations of mental illness, so why should people who eat in a planned fashion so as to be healthy?

Posted by Reas