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How to prevent heart disease naturally
On This Page Eat A Heart Healthy Diet Increase Your Fiber Choose Low-Fat Protein Sources Foods to Avoid Get Regular Exercise Choose Quality Supplements You can avoid heart disease by following a healthy lifestyle. Here are ideas to help you live a heart-healthy lifestyle. While Heart disease is a leading cause of death in […]
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What To Know About Nitric Oxide
Numerous dietary supplements are marketed as “nitric oxide boosters. These supplements do not include nitric oxide itself, but they include ingredients that help create nitric oxide in your body. Two of one of the most typically used components are L-arginine and L-citrulline. L-arginine is a conditionally necessary amino acid, indicating it just needs to be […]
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Keeping Your Immune System Healthy
On This Page Stress and Your Immune System Sugar May Not Be All Sweet for Immunity Exercise for Immunity Sleep Is Important Take a Nap Nitric Oxide May Help With so much emphasis on Covid 19 and keeping your immune system healthy I thought it might be a good idea to look at some […]
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Reversing High Blood Pressure the Natural Way
On This Page What is High Blood Pressure Diet and Lifestyle Sugary Food A Hypertension Problem Hypertension and Diet | Bottom Line American College of Cardiology Stay on top of heart failure symptoms Self-help for atrial fibrillation Grapefruit juice and statins What is High Blood Pressure Blood pressure is the measure of the force of […]
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Fight Aging! Newsletter, March 4th 2019
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Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more.
This content is published under the Creative Commons Attribution 4.0 International License. You are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!
To subscribe or unsubscribe please visit: https://www.fightaging.org/newsletter/
Contents
Request for Startups in the Rejuvenation Biotechnology Space, 2019 Edition
Upregulation of Autophagy to Treat Age-Related Disease
Upregulation of the Ubiquitin-Proteasome System as a Potential Mode of Therapy
Is Somatic Mosaicism in Brain Tissue an Important Contribution to Neurodegeneration?
Upregulation of Autophagy to Attenuate Age-Related Declines in Muscle Regeneration
Exercise Performance a Better Predictor of Mortality than Chronological Age
Greater Activity in Middle Age Correlates with Reduced Risk of Dementia
Narrowing Down the Senescent Cell Populations Responsible for Osteoporosis
Funding Development of Rejuvenation Therapies is the Most Effective Form of Altruism
A Higher Epigenetic Measure of Age Correlates with Increased Breast Cancer Risk
A Guide to Logical Fallacies for Rejuvenation Research Advocates
A More Serious Trial Failure for Gensight's Allotopic Expression Implementation
Clever-1 Inhibition Reduces the Subversion of the Immune System Carried Out by Tumor Associated Macrophages
Acid Sphingomyelinase in Age-Related Blood-Brain Barrier Dysfunction
Aneuploidy and Cellular Senescence in Aging
Request for Startups in the Rejuvenation Biotechnology Space, 2019 Edition https://www.fightaging.org/archives/2019/02/request-for-startups-in-the-rejuvenation-biotechnology-space-2019-edition/
I am a little late with the 2019 list of projects in rejuvenation biotechnology that I'd like to see startups...
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Fight Aging! Newsletter, March 4th 2019
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Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more.
This content is published under the Creative Commons Attribution 4.0 International License. You are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!
To subscribe or unsubscribe please visit: https://www.fightaging.org/newsletter/
Contents
Request for Startups in the Rejuvenation Biotechnology Space, 2019 Edition
Upregulation of Autophagy to Treat Age-Related Disease
Upregulation of the Ubiquitin-Proteasome System as a Potential Mode of Therapy
Is Somatic Mosaicism in Brain Tissue an Important Contribution to Neurodegeneration?
Upregulation of Autophagy to Attenuate Age-Related Declines in Muscle Regeneration
Exercise Performance a Better Predictor of Mortality than Chronological Age
Greater Activity in Middle Age Correlates with Reduced Risk of Dementia
Narrowing Down the Senescent Cell Populations Responsible for Osteoporosis
Funding Development of Rejuvenation Therapies is the Most Effective Form of Altruism
A Higher Epigenetic Measure of Age Correlates with Increased Breast Cancer Risk
A Guide to Logical Fallacies for Rejuvenation Research Advocates
A More Serious Trial Failure for Gensight's Allotopic Expression Implementation
Clever-1 Inhibition Reduces the Subversion of the Immune System Carried Out by Tumor Associated Macrophages
Acid Sphingomyelinase in Age-Related Blood-Brain Barrier Dysfunction
Aneuploidy and Cellular Senescence in Aging
Request for Startups in the Rejuvenation Biotechnology Space, 2019 Edition https://www.fightaging.org/archives/2019/02/request-for-startups-in-the-rejuvenation-biotechnology-space-2019-edition/
I am a little late with the 2019 list of projects in rejuvenation biotechnology that I'd like to see startups...
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Higher Epigenetic Measure of Age Correlates with Increased Risk of Cancer
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Epigenetic clocks use patterns of DNA methylation that correlate with age. Numerous studies have shown that people with epigenetic age higher than chronological age have a raised risk of disease. This works the other way as well; patient populations with a range of age-related diseases tend to have higher epigenetic age measures than their healthier peers of the same chronological age. The study noted here is the most recent in a growing body of evidence to suggest that epigenetic clocks measure something potentially useful about aging.
What exactly it is about aging that epigenetic clocks measure is still an open question, however. The patterns of DNA methylation were discovered by analysis of epigenetic data by age, not built from an understanding of the underlying processes. It is quite possible that they reflect only a fraction of the important processes in aging, which is fine when aging proceeds in a unified way, all processes roughly aligned with one another, but the utility of such clocks will end when it becomes possible to address any one specific process of aging via rejuvenation therapies. Take clearance of senescent cells, for example: at this point no-one has the first idea as to what that will do to epigenetic clock measures, and until data is established the clocks aren't all that helpful for developers working on senolytic therapies to selectively destroy senescent cells.
Scientists speculate that biologic age may be tied to environmental exposures. If so, it may be a useful indicator of disease risk. They used three different measures, called epigenetic clocks, to estimate biologic age. These clocks measure methylation found at specific locations in DNA. Researchers use these clocks to estimate biologic age, which can then be compared to chronologic age. The researchers used DNA from blood samples provided by women enrolled in the Sister Study, a group of more than 50,000 women in the U.S. and Puerto Rico. The study was specifically designed to identify environmental and genetic risk factors for breast cancer. The research team measured methylation in a subset of 2,764 women, all of whom were cancer-free at the time of blood collection.
"We found that if your biologic age is older than your chronologic age, your breast cancer risk is increased. The converse was also true. If your biologic age is younger than your chronologic age, you may have decreased risk of developing breast cancer. However, we don't yet...
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Upregulation of Autophagy to Attenuate Age-Related Declines in Muscle Regeneration
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As a companion piece to another recently published open access paper, noted earlier this week, today's review paper considers the therapeutic upregulation of autophagy as a possible approach to reduce the deleterious impact of aging on muscle regeneration. Autophagy is the name given to a collection of cellular housekeeping processes responsible for ensuring that excess and broken cellular components are transported to a lysosome for recycling. Lysosomes are membrane-bound vesicles packed with enzymes capable of breaking down near all structures and molecular waste they are likely to encounter. The remnant molecules are released back into the broader cell as raw materials.
Autophagy is known to decline with age. Many of the approaches shown to slow aging in short-lived laboratory species either involve increased autophagy, or, as is the case for calorie restriction, appear to depend on increased autophagy for the beneficial effects on health and life span. Increased autophagy is a feature of many forms of cellular stress response: heat, cold, lack of nutrients, oxidative damage, and so forth. Mild or short-lived stress or damage can provoke a reaction that lasts for a while and produces an overall gain in cell function. Since autophagy removes damaged components, it limits the opportunity for damage to spread and produce downstream effects. When that is happening in every cell in the body on a regular basis, the result is a longer life span.
Unfortunately, what we know of the effects of calorie restriction in mice and humans tells us that stress responses such as upregulated autophagy have a much larger effect on life span in short-lived species than they do in long-lived species such as our own. Calorie restriction can increase maximum mouse life span by 40%. In humans an effect size of more than five years would be surprising, given that any reliable gain much larger than that would have been discovered in antiquity and very well explored by now. Which is not to say that calorie restriction is worthless: it produces a larger reliable gain in long term health - for basically healthy people - than any readily available, well understood medical technology. Given the advent of senolytics as a rejuvenation therapy, that statement probably won't remain true for very much longer, but it is worth considering.
Autophagy as a Therapeutic Target to Enhance Aged Muscle Regeneration
Skeletal muscle has remarkable regenerative...
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Clever-1 Inhibition Reduces the Subversion of the Immune System Carried Out by Tumor Associated Macrophages
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Cancers subvert the immune system in order to protect themselves while they grow. One of the ways in which this happens is activities of macrophage cells that become associated with the tumor tissue. Cancer cells influence the macrophages into dampening the local immune response, preventing the immune system from effectively targeting the tumor. Researchers here find a way to reduce the impact of this process, and note that it synergizes well with the currently popular checkpoint inhibitor approach to rousing the immune system to attack cancerous cells.
One reason behind many unsuccessful cancer treatments is the cancers' ability to hijack the immune system to support its own growth. This is assisted by the so-called tumour-associated macrophages that can be educated by cancer cells to dampen anti-tumour immune responses. Macrophages are phagocytes that form the first line of defence towards invading pathogens and they have a crucial role in maintaining tissue homeostasis. Macrophages have a large repertoire of functions in immune activation and resolving inflammation.
Researchers investigated the possibility to utilise tumour-associated macrophages to increase the immunological detection and killing of cancer cells. Previously, it was observed that Clever-1 controls leukocyte trafficking between tissues. A new study found that blocking Clever-1 function on macrophages activated the immune system and was highly effective in inhibiting cancer progression. By inhibiting Clever-1 functions, tumour-associated macrophages that normally impair adaptive immune cell activation, such as cancer cell killing by cytotoxic T cells, were managed to be re-educated so that they had increased ability to present antigen and secrete pro-inflammatory cytokines leading to increased activation of killer T cells.
The antibody therapy targeting Clever-1 worked in the studied tumour mouse models as efficiently as the PD-1 antibody therapy that is in clinical use. The PD-1 antibody maintains the functionality of the killer T cells. It is notable that the Clever-1 antibody therapy targeting macrophages also increased the activity of the killer T cells efficiently. In certain mouse models of cancer, a combination of anti-Clever-1 and anti-PD-1 therapies prevented tumour growth and formation of metastases more effectively than either treatment alone.
Link:
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A More Serious Trial Failure for Gensight's Allotopic Expression Implementation
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Gensight Biologics uses allotopic expression of a mitochondrial gene, ND4, to attempt to treat the inherited blindness condition Leber hereditary optic neuropathy, in which this gene is mutated and dysfunctional. An altered copy of ND4 is introduced into the cell nucleus, and the protein produced is delivered back to the mitochondria where it is needed for correct function. A fairly standard gene therapy is used to deliver this payload into the retina. Unfortunately, after promising results from earlier trials and technology demonstrations, their late stage trials are failing.
It remains to be seen as to why this is the case. Earlier work makes it clear that the technology works in principle. It is possible that intervening too late cannot clear out enough of the damage already done, and that damage makes further decline inevitable, or recovery difficulty. This is a systemic problem for many conditions, given the way in which the structure and enormous cost of clinical trial regulation pushes companies towards the late stage of the disease, rather than earlier, preventative treatment. Equally, it may be that this formulation of the allotopic expression gene therapy isn't achieving a great enough coverage of retinal cells to produce reliable benefits. There are many possible reasons for failure.
A phase 3 trial of GenSight Biologics' Leber hereditary optic neuropathy (LHON) gene therapy has missed its primary endpoint. The AAV gene therapy was no better than placebo at improving vision at 48 weeks, leading GenSight to look to future updates to salvage the study. GenSight designed GS010 to improve the vision of patients with a particular mutation in the mitochondrial ND4 gene and moved the gene therapy into a pair of phase 3 trials in 2016. One trial enrolled patients who had suffered vision loss for 6 to 12 months. The other recruited people whose vision loss began less than six months ago. Both trials missed their primary endpoints.
The latest clinical setback involves LHON patients with six months or less of vision loss enrolled in the RESCUE trial. As in the other study, GenSight set out to link GS010 to a 15-letter improvement over placebo on a vision test. Each subject received GS010 in one eye and a sham injection in the other. This time around, the eyes treated with GS010 deteriorated by 19 letters over the first 48 weeks of the trial, compared to a 20-letter decline in the control cohort. The top-line figures hide a...
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How Proper Sleep Lowers Infection
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Previous research1 has shown that sleep deprivation has the same effect on your immune system as physical stress. When volunteers stayed awake for 29 hours straight, their white blood cell counts were found to increase during the sleep deprivation phase.
This is the same type of response you typically see when you're sick or stressed. In a nutshell, whether you're physically stressed, sick or sleep-deprived, your immune system becomes hyperactive and starts producing white blood cells — your body's first line of defense against foreign invaders like infectious agents.
Elevated levels of white blood cells are typically a sign of disease. In other words, your body reacts to sleep deprivation in much the same way it reacts to illness. Your immune system, in turn, plays a key role in controlling inflammation in your body, and if it's not working optimally, your ability to fight off the infection will be impaired. As reported by Science Daily:2
"Sleep improves the potential ability of some of the body's immune cells to attach to their targets … The study,3,4 led by Stoyan Dimitrov and Luciana Besedovsky at the University of Tübingen, helps explain how sleep can fight off an infection, whereas other conditions, such as chronic stress, can make the body more susceptible to illness."
When Ga(s)-Coupled Receptor Agonists Are Activated, Immune Function Declines
When your immune system senses a foreign invader, such as a virus, white blood cells known as T cells (among others) are dispatched. Sticky proteins called integrins allow the T cell to attach to the infected target and kill it.
Dimitrov and his team decided to investigate5 the effects of signaling molecules called Ga(s)-coupled receptor agonists. While these signaling molecules are known to have immunosuppressive effects, it was not known whether they might inhibit the activation of integrins in T cells specifically, which is what they sought to determine here.
What they discovered was that certain Ga(s)-coupled receptor agonists did indeed prevent T cells from activating integrins once the target was identified. Ga(s)-coupled receptor agonists exhibiting this effect included:
Adrenaline and noradrenaline (hormones)
Prostaglandin E2 and D2 (proinflammatory molecules)
Adenosine (a neuromodulator)
Sleep Helps Your Body Fight Infection
Levels of adrenaline and prostaglandin are known to decrease during sleep, and both have been shown to suppress integrin activation, so the team...
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Upregulation of the Ubiquitin-Proteasome System as a Potential Mode of Therapy
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There are numerous cellular maintenance processes responsible for breaking down various component parts of the cell, proteins, and forms of metabolic waste. Autophagy, for example. Another is the ubiquitin-proteasome system. Broken or excess proteins are tagged with a ubiquitin molecule, which ensures they are broken up for raw materials by a proteasome. Proteasomes come in a variety of flavors, and all are very complex multi-protein structures. Like other forms of cellular maintenance, the pace at which the ubiquitin-proteasome system operates is regulated and responds to environmental cues such as lack of nutrients resulting from calorie restriction or the oxidative stress that results from mitochondrial activity during exercise.
Greater cellular maintenance leads to better cell function, a reduction in downstream damage caused by the presence of damaged proteins. Analogous to the search for ways to upregulate autophagy, factions within the research community have looked for ways to artificially boost the activity of proteasomes. Research programs tend to start by using exercise or calorie restriction to help understand how exactly the ubiquitin-proteasome system functions, and how proteasomal activity is regulated, and then proceed to find ways to intervene at the point of regulation. The research materials here are a snapshot of one such development program.
As is the case for upregulation of autophagy, we should expect upregulation of proteasomal activity to produce only modest benefits in humans. This is only one among many mechanisms by which exercise or calorie restriction produces benefits to health and longevity, and we know the scope of those interventions. While the health benefits in humans are certainly worth it when the treatment is free, it is arguably the case that we shouldn't be investing billions into this class of therapeutic development. We should prefer programs with a much greater potential benefit, those capable of rejuvenation rather than just a modest slowing of aging.
Exercise, fasting help cells shed defective proteins
Malfunctions in the cells' protein-disposal machinery can lead to the accumulation of misfolded proteins, which clog up the cell, interfere with its functions, and, over time, precipitate the development of diseases, including neurodegenerative conditions such as amyotrophic lateral sclerosis and Alzheimer's. The best-studied biochemical system used by cells to remove junk...
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A Guide to Logical Fallacies for Rejuvenation Research Advocates
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The world has not yet rallied to the cause of defeating aging. Aging remains by far the greatest cause of suffering, pain, and death in this world, and yet it is accepted as set in stone by the vast majority of people. Few think of doing something about it. Little funding goes towards the research and development programs that could plausibly bring aging under medical control, indefinitely extending healthy life spans. Humanity spends more on sports stadiums than it does on addressing the impending death and drawn out, painful decline of everyone presently alive.
All of this is why, even as our community grows and we achieve success in spurring the start of a rejuvenation biotechnology industry, we must continue to aggressively advocate for the cause of rejuvenation research. It is why it is important to stand up and speak out, to argue in public, to make presentations and educate those who do not yet know that aging could be ended, if only sufficient resources were dedicated to that goal. Tools to aid in that work of advocacy and persuasion are always greatly appreciated - such as this long list of logical fallacies with specific examples for our field.
Alleged certainty: this fallacy consists of concluding something is true because "everybody knows" it is. "Everybody knows" that there are too many people on this planet and therefore rejuvenation is a bad idea; "everybody knows" that life-saving treatments, such as rejuvenation, will always be only for the rich; and so on. Whether or not everybody actually knows these things doesn't matter; what does matter is the evidence used to back them up. For example, overpopulation is not at all a black-and-white issue; whether we're overpopulated depends on the metrics that are taken into account. The best way to counter this fallacy may be simply asking for evidence and pointing out that simply claiming that everyone knows something isn't sufficient proof, especially if the topic is not at all uncontroversial.
Appeal to anger: this fallacy attempts to justify an argument based solely on negative emotions. In the context of life extension, this fallacy is rarely committed alone; it usually hinges on other fallacies or weak arguments that are used as premises. For example, someone might be outraged that you worry about life extension when, allegedly, there are much worse problems than aging in the world, and he might use the supposed outrageousness of life extension to gloss over the fact...
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A Higher Epigenetic Measure of Age Correlates with Increased Breast Cancer Risk
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Epigenetic clocks use patterns of DNA methylation that correlate with age. Numerous studies have shown that people with epigenetic age higher than chronological age have a raised risk of disease. This works the other way as well; patient populations with a range of age-related diseases tend to have higher epigenetic age measures than their healthier peers of the same chronological age. The study noted here is the most recent in a growing body of evidence to suggest that epigenetic clocks measure something potentially useful about aging.
What exactly it is about aging that epigenetic clocks measure is still an open question, however. The patterns of DNA methylation were discovered by analysis of epigenetic data by age, not built from an understanding of the underlying processes. It is quite possible that they reflect only a fraction of the important processes in aging, which is fine when aging proceeds in a unified way, all processes roughly aligned with one another, but the utility of such clocks will end when it becomes possible to address any one specific process of aging via rejuvenation therapies. Take clearance of senescent cells, for example: at this point no-one has the first idea as to what that will do to epigenetic clock measures, and until data is established the clocks aren't all that helpful for developers working on senolytic therapies to selectively destroy senescent cells.
Scientists speculate that biologic age may be tied to environmental exposures. If so, it may be a useful indicator of disease risk. They used three different measures, called epigenetic clocks, to estimate biologic age. These clocks measure methylation found at specific locations in DNA. Researchers use these clocks to estimate biologic age, which can then be compared to chronologic age. The researchers used DNA from blood samples provided by women enrolled in the Sister Study, a group of more than 50,000 women in the U.S. and Puerto Rico. The study was specifically designed to identify environmental and genetic risk factors for breast cancer. The research team measured methylation in a subset of 2,764 women, all of whom were cancer-free at the time of blood collection.
"We found that if your biologic age is older than your chronologic age, your breast cancer risk is increased. The converse was also true. If your biologic age is younger than your chronologic age, you may have decreased risk of developing breast cancer. However, we don't yet...
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Processed Foods Lead to Cancer and Early Death
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The struggle with weight gain and obesity is a common and costly health issue, leading to an increase in risk for heart disease, Type 2 diabetes and cancer, just to name a few.
According to the latest available data,1 18.5 percent of American children and nearly 40 percent of adults are now obese, not just overweight. That's a significant increase over the 1999/2000 rates, when just under 14 percent of children and 30.5 percent of adults were obese.
Research has linked growing waistlines to a number of different sources, including processed foods, sodas and high-carbohydrate diets. Risks associated with belly fat in aging adults includes an elevated risk of cardiovascular disease and cancer.2
Researchers have actually predicted obesity will overtake smoking as a leading cause of cancer deaths,3 and recent statistics suggest we're well on our way to seeing that prediction come true as obesity among our youth is triggering a steep rise in obesity-related cancers at ever-younger ages.
Millennials More Prone to Obesity-Related Cancers Than Their Parents
As obesity rates rise, so do related health problems, including cancer. According to a report4 on the global cancer burden, published in 2014, obesity is already responsible for an estimated 500,000 cancer cases worldwide each year, and that number is likely to rise further in coming decades.
As reported in a recent Lancet study5 by the American Cancer Society, rates of obesity-related cancers are rising at a far steeper rate among millennials than among baby boomers. According to the authors,6 this is the first study to systematically examine obesity-related cancer trends among young Americans.
What's more, while 6 of 12 obesity-related cancers (endometrial, gallbladder, kidney, multiple myeloma and pancreatic cancer) are on the rise, only 2 of 18 cancers unrelated to obesity are increasing. As noted in the press release:7
"The obesity epidemic over the past 40 years has led to younger generations experiencing an earlier and longer lasting exposure to excess adiposity over their lifetime than previous generations.
Excess body weight is a known carcinogen, associated with more than a dozen cancers and suspected in several more … Investigators led by Hyuna Sung, Ph.D., analyzed 20 years of incidence data (1995-2014) for 30 cancers … covering 67 percent of the population of the U.S…
Incidence increased for 6 of the 12 obesity-related cancers … in young adults and in...
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Stop Heart Disease Today!
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While many Americans worry about Cancer, Heart Disease is still the number 1 killer in America today. Wouldn’t it be wonderful if there was no more heart disease! Unfortunately with all the modern science available we are still struggling with the problem. Here is a look at one part of heart disease, hypertension. High Blood
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Upregulation of Autophagy to Treat Age-Related Disease
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Regulation of autophagy has been a tremendously popular topic in the aging research community over the past twenty years, so much so that it is very surprising that little progress towards clinical therapies has been made. Search PubMed for autophagy and aging and you'll find a deluge of papers over this time frame, many of which express optimism on the topic of finding ways to upregulate autophagy to improve health and slow the aging process. It is the consensus in the research community that autophagy declines with age, and that there are benefits to be realized through increased autophagy. This may allow many age-related conditions to be treated, slowed, or postponed. All of this is taken as self-evident from the voluminous evidence accumulated to date.
What is autophagy? It is a collection of maintenance processes responsible for recycling broken or otherwise unwanted cellular structures and proteins. In the case of chaperone-mediated autophagy, target proteins are guided by a chaperone protein and imported into a lysosome for disassembly. For macroautophagy, an autophagosome membrane forms around the target structure, moves to a lysosome, and fuses with it. In microautophagy, a lysosome directly engulfs the target without assistance. In all cases, a lysosome is the final destination, a membrane packed with enzymes capable of taking apart near everything it will encounter inside a cell. The component parts are then released for reuse.
Many of the methods shown to slow aging and extend life span in short-lived laboratory species involve upregulation of autophagy. Calorie restriction is the canonical example, but increased autophagy is a common response to many forms of stress. Greater autophagy helps cells to survive, it reduces levels of cellular damage, it improves function. Brief stress can leads to lasting autophagy, and thus intermittent stresses tend to improve health and lengthen life - the process known as hormesis. That said, short-lived animals have much greater plasticity of life span than is the case for long-lived species such as our own. While calorie restriction, which arguably largely acts through autophagy, clearly improves human health significantly, we don't gain anywhere near the life extension observed in mice.
When are we going to see drugs that enhance autophagy? Calorie restriction mimetics such as mTOR inhibitors and the like work to some degree through upregulated autophagy. More rationally designed...
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