Longevity Meme Newsletter, November 30 2009

November 30 2009

The Longevity Meme Newsletter is a weekly e-mail containing news, opinions, and happenings for people interested in healthy life extension: making use of diet, lifestyle choices, technology, and proven medical advances to live healthy, longer lives.



- Overpopulation: Too Many Malthusians
- The Latest Rejuvenation Research
- Fear of Aging is Absolutely Rational
- Discussion
- Latest Healthy Life Extension Headlines


In short: overpopulation doesn't exist, but far too many people think that it does. Throughout recorded history, from Roman times on, speakers have stepped forward to claim that more people will cause disaster, that resources will run out, and that present consequences of mismanagement are in fact the result of too many people. Each time those Malthusians were demonstrated to be completely wrong, just as the hysteria over overpopulation is wrong today:


"Malthusianism is, in essence, yet another facet of some peoples' inability to see change in the world around them. Some folk see only what is, refusing to acknowledge what will be. Which is a strange state to be in given the rampant pace of technological advancement at present. New and better resources to meet any level of demand will be developed, and thanks to the operation of markets, entrepreneurs, and competition, will be developed well in advance of need. That is what we humans excel at accomplishing. More people in the world means more demand for resources, more rewards for those who find new and better ways to satisfy those demands, more opportunity for development, more minds working on science and technology, more new and improved resources developed to replace old ones."


The latest issue of the Rejuvenation Research journal is online:


"In this issue, Michael Fossel lays out the case for a focus on telomere biology: In 1990, telomere length was shown to correlate with cellular senescence; this discovery was followed by a series of papers affirming a causal relationship between telomere length and cell senescence. Further work demonstrated that telomere elongation reverses cellular senescnce in both cells and reconstituted human tissues. Since telomerase, the enzyme that elongates telomeres, is absent (or only transiently active) in normal human somatic cells, the result is a gradual decrease in telomere length with age in most human tissues. The implied potential for in vivo human telomere enlongation raises two critical clinical issues: (a) Does telomere shortening play a key role in human diseases and, if so, (2) is telomere enlongation an effective clinical intervention."


The degenerations of aging are dreadful. To fear them is rational:


"[Some people try to] accommodate aging; play a game of give and take, and strive to accept what happens as their physiology decays. Which is madness. The relationship between humanity and aging should better fit a war story, not a tale of slavery and acceptance. How are we going to dig ourselves out of this pit if all we do is pretend that things will be fine - or if not fine, at least acceptable?

"Aging is a horror, but it isn't supernatural. It is the result of physical processes operating on the biological systems of our bodies. Physics, chemistry, biology. These are biological systems that can be repaired, replaced, and restored: medicine, therapies, biotechnology. But we need to develop the means to achieve that end: technologies capable of repairing and reversing aging are foreseen, proposed, and carefully described - just not yet researched and developed. If we all sit back and accept the suffering that lies ahead, then medicines to fight aging will never be developed. It seems an easy choice to me, but I still hear those talking heads telling us that aging is just fine, and we should give in to it."


The highlights and headlines from the past week follow below.

Remember - if you like this newsletter, the chances are that your friends will find it useful too. Forward it on, or post a copy to your favorite online communities. Encourage the people you know to pitch in and make a difference to the future of health and longevity!




There is good reason to believe that increased leucine in the diet and exercise can counteract some of the muscle loss characteristic to aging: "Loss of muscle mass is an unfavourable consequence of aging and many chronic diseases. The debilitating effects of muscle loss include declines in physical function and quality of life and increases in morbidity and mortality. Loss of muscle mass is the result of a decrease in muscle protein synthesis, an increase in muscle protein degradation, or a combination of both. Much research on muscle wasting has tended to focus on preventing muscle protein breakdown, and less attention has been paid to providing adequate stimulation to increase muscle protein synthesis. In this review, we present evidence to suggest that interventions aimed at increasing muscle protein synthesis represent the most effective countermeasure for preventing, delaying, or reversing the loss of skeletal muscle mass experienced in various muscle wasting conditions. Based on results from acute and chronic studies in humans in a wide variety of wasting conditions, we propose that resistance exercise training combined with appropriately timed protein (likely leucine-rich) ingestion represents a highly effective means."

The protein mTOR is one of many flagged as important to longevity by studies of calorie restriction biochemistry. Here it is implicated in the decline in stem cell function with age: "Age-related declines in hematopoietic stem cell (HSC) function may contribute to anemia, poor response to vaccination, and tumorigenesis. Here, we show that mammalian target of rapamycin (mTOR) activity is increased in HSCs from old mice compared to those from young mice. mTOR activation through conditional deletion of Tsc1 in the HSCs of young mice mimicked the phenotype of HSCs from aged mice in various ways. These [included] a relative decrease in lymphopoiesis [and] impaired capacity to reconstitute the hematopoietic system. In old mice, rapamycin increased life span, restored the self-renewal and hematopoiesis of HSCs, and enabled effective vaccination against a lethal challenge with influenza virus. Together, our data implicate mTOR signaling in HSC aging and show the potential of mTOR inhibitors for restoring hematopoiesis in the elderly."

The New Scientist surveys current efforts to build regenerative therapies based on the pluripotency of embryonic stem cells: "Tissue grown from human embryonic stem cells, the most prized, and most controversial, cells ever grown in a lab, could at last make it into the human body. After a decade of scientific and political wrangling, several therapies are now edging towards human trials. Which will be first? ... The first human embryonic stem cells (hESCs) to make it into the human body could be ones that save sight. Last week, Advanced Cell Technology (ACT) of Worcester, Massachusetts, applied for permission to inject stem-cell derived retinal pigment epithelial cells (RPEs) into the eyes of 12 patients with Stargardt's macular dystrophy, a rare inherited condition which leads to blindness in middle age. ... Last week came the first report of human skin made from hESCs. Although the cells have so far only been tested on mice, the idea is to use skin grown from these stem cells as temporary grafts for people with burns, while they wait for a permanent graft to be grown from their own tissue."

Via EurekAlert!: "A cancer vaccine carried into the body on a carefully engineered, fingernail-sized implant is the first to successfully eliminate tumors in mammals ... The new approach [uses] plastic disks impregnated with tumor-specific antigens and implanted under the skin to reprogram the mammalian immune system to attack tumors. The new paper describes the use of such implants to eradicate melanoma tumors in mice. ... [This approach] redirects the immune system to target tumors, and appears both more effective and less cumbersome than other cancer vaccines ... Conventional cancer vaccinations remove immune cells from the body, reprogram them to attack malignant tissues, and return them to the body. However, more than 90 percent of reinjected cells have died before having any effect in experiments. ... The [implants] are 8.5 millimeters in diameter and made of [a] biodegradable polymer. Ninety percent air, the disks are highly permeable to immune cells and release cytokines, powerful recruiters of immune-system messengers called dendritic cells. These cells enter an implant's pores, where they are exposed to antigens specific to the type of tumor being targeted. The dendritic cells then report to nearby lymph nodes, where they direct the immune system's T cells to hunt down and kill tumor cells."

Here is an intriguing line of thinking: if we can identify unambiguously beneficial components of our metabolism, why not make artificial replicas and flood the body with them? "The particles that ferry cholesterol through the bloodstream are popularly known as 'bad' or 'good': bad if they deposit cholesterol on vessel walls, potentially clogging them; good if they carry the cholesterol on to the liver for excretion. Now scientists have created tiny particles in the laboratory that mimic those good carriers, scooping up the cholesterol before it can grow into dangerous deposits of plaque. The surfaces of these new particles are coated with fats and proteins so they can bind tightly with the sticky cholesterol to transport it through the bloodstream. ... Researchers have endowed these artificial particles with the same properties as natural particles that circulate in the blood, [called] high-density lipoproteins, or HDL ... The artificial carriers can clean up sites where plaques can otherwise rupture, leading to strokes and heart attacks."

The real killer in cancer is its spread within the body: metastasis. A reliable method of eliminating metastasis would go a long way to making cancer just a bad, treatable condition rather than the end of life for a quarter of us. Here is one approach: researchers have "found a way to capture tumor cells in the bloodstream that could dramatically improve earlier cancer diagnosis and prevent deadly metastasis. ... researchers can inject a cocktail of magnetic and gold nanoparticles with a special biological coating into the bloodstream to target circulating tumor cells. A magnet attached to the skin above peripheral blood vessels can then capture the cells. ... By magnetically collecting most of the tumor cells from blood circulating in vessels throughout the whole body, this new method can potentially increase specificity and sensitivity up to 1,000 times compared to existing technology ... Once the tumor cells are targeted and captured by the magnet, they can either be microsurgically removed from vessels for further genetic analysis or can be noninvasively eradicated directly in blood vessels by laser irradiation through the skin that is still safe for normal blood cells."

Much of the Alzheimer's research community is focused on removing the characteristic buildup of amyloid-beta from the brain. Amyloid and Alzheimer's are linked, so remove the amyloid. As the tools of biotechnology improve, however, matters begin to look more complicated. For example: "recent research demonstrates that amyloid-beta is also necessary to maintain proper brain functioning. ... Without amyloid-beta, a normal product of cellular metabolism, one's ability to learn and remember could be profoundly damaged, so drugs currently in development to eliminate amyloid-beta could be rendered obsolete. ... By studying synapses in brain slices of healthy mice and in neuronal networks growing in vitro, [researchers] determined that there is an optimal amount of amyloid-beta needed to keep the neurons working well. ... if this precise balance is even slightly disturbed, the effectiveness of information transfer between neurons is greatly impaired. ... amyloid-beta peptide, believed to be toxic, regulates the type of information that neurons transfer."

FAT AND DEMENTIA RISK (November 24 2009)
Yet another study showing the risk you run by letting your body amass fat unchecked in middle age: "Women who store fat on their waist in middle age are more than twice as likely to develop dementia when they get older ... Anyone carrying a lot of fat around the middle is at greater risk of dying prematurely due to a heart attack or stroke. If they nevertheless manage to live beyond 70, they run a greater risk of dementia. ... The research is based on the Prospective Population Study of Women in Gothenburg, which was started at the end of the 1960s when almost 1,500 women between the ages of 38 and 60 underwent comprehensive examinations and answered questions about their health and lifestyle. A follow-up 32 years later showed that 161 women had developed dementia, with the average age of diagnosis being 75. This study shows that women who were broader around the waist than the hips in middle age ran slightly more than twice the risk of developing dementia when they got old. However, the researchers could find no link to a high body mass index (BMI). ... Other studies have shown that a high BMI is also linked to dementia, but this was not the case in ours. This may be because obesity and overweight were relatively unusual among the women who took part in the Prospective Population Study."

That investment advisors are discussing the prospects for engineered longevity at all is more of an indicator than what they actually say. Nonetheless, these are words of wisdom: "I was at dinner with some friends and the conversation turned to the topic of undiscovered investment opportunities. One of my nominations for undiscovered investment theme was life extension technology. ... The natural winner in life extension is the biotechnology industry. But not so fast! The real winners may not be available for investment. Here is a case in point. Back in 1979-80, I correctly identified the microcomputer (they were called microcomputers back then as IBM didn't introduce the PC until August 1981), would be the growth industry of the future. I told anyone who listened that the microcomputer would be as common as the office photocopier in five years. I was wrong, it was more common than the photocopier as there were multiple PCs in most offices. Who were the major publicly listed players in the microcomputer then? They were Commodore, Tandy (Radio Shack) and Atari, which was a division of Warner Communications. Apple hadn't gone public yet and hadn't gotten into the business at the time. Microsoft was just a small private concern. This story shows that it is possible to identify a long-term trend, but the winners may not be available to the ordinary investor for quite some time."

From ScienceDaily: "Age-related hearing loss is a very common symptom of aging in humans, and also is universal among mammal species, and it's one of the earliest detectable sensory changes in aging. ... In mice, the new study shows that the damage starts with free radicals, which are key suspects in many harmful changes of aging. Free radicals trigger a process called apoptosis, or programmed cell death, by which damaged cells 'commit suicide.' Apoptosis is often beneficial, as it eliminates cells that may be destined for cancer. Before the study, it was already clear [that] aging was associated with a major loss of hair cells and ganglion cells, so it was plausible that programmed cell death was playing a role in hearing loss. We also thought that oxidative stress - the presence of free radicals - contributes to age-related hearing loss, so we put two and two together and showed that oxidative stress does indeed induce age-related hearing loss. ... [Researchers] found that the suicide program was operating in hair cells and spiral ganglion neurons, and that the suicide program relied on activity in a suicide gene called bak. Activity of the bak gene [is] required for the development of age-related hearing loss. The strongest evidence for this was the fact that a strain of mice that did not have the bak gene did not show the expected hearing loss at 15 months of age."



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