Longevity News Digest
Brush Away Heart Disease
Dear Future Centenarian,Â
Cardiovascular disease continues to be our #1 killer¦ in spite of the fact that it™s largely avoidable.
OK, I understand the psychology of shying away from exercise and the difficulty of resisting deadly highly processed foods that seem to taste the best. But not brushing and flossing regularly? C™mon.
Michael Greve from https://forever-healthy.org contributes this life-preserving information:
A wide array of health problems, including but not limited to obesity, insulin resistance, type 2 diabetes, periodontal disease, stroke, and heart disease all have inflammation as a part of the disease.
The majority of inflammatory diseases start in your gut.
Chronic inflammation in your gut can disrupt the normal functioning of many bodily systems.
When fat cells (adipocytes) interact with environmental agents¦ in this case, bacterial toxins. They then trigger a chronic inflammatory process. Bacterial toxins stimulate fat cells to release molecules called cytokines, which promote inflammation.
All staph bacteria make toxins called superantigens - molecules that disrupt the immune system.
A related news item further highlights the role of inflammation in the development of chronic disease.
According to Medical News Today: œResearchers at Columbia University in New York suggest that if you look after your gums, you could also be reducing your risk of heart disease. They claim that improving dental care slows the speed with which plaque builds up in the arteries. Journal of the American Heart Association October 28, 2013; 2: e000254
This isn™t the first time researchers have found that your oral health can have a significant impact on your cardiovascular and heart health. For example, a 2010 study found that those with the worst oral hygiene increased their risk of developing heart disease by a whopping 70 percent, compared to those who brush their teeth twice a day.Â BMJ2010;340:c2451 May 27, 2010
It™s important to realize that periodontal disease involves both bone and the tissue that is in contact with that bone. From this contact, bacteria and toxic inflammatory compounds can easily enter your blood stream.
Once in your blood stream, these toxic compounds can harm the lining of your blood vessels, which can lead to both strokes and heart attacks. So, reducing inflammation is of primary importance for your overall health, and brushing your teeth regularly is one way to combat chronic inflammation in your body.
Findings such as these offer potent testimony to the fact that heart disease is a condition that can be prevented, most of the time, by leading a healthy lifestyle -- which includes the simple act of brushing your teeth regularly to prevent periodontal disease, and optimizing your gut health by eating foods that allow healthy bacteria to flourish and keep pathogenic bacteria in check.
Latest Headlines from Fight Aging!
More on Klotho and Neurodegeneration - Monday, July 28, 2014
High levels of the protein produced by the klotho gene are associated with longevity in mammals, and recently it has also been associated with greater cognitive performance. Here is another small piece of evidence to add to all that.
Rapamycin and Its Effects on mTORC1 and mTORC2 - Monday, July 28, 2014
The immunosuppressant compound rapamycin has been demonstrated to slow aging in mice, though with unpleasant side-effects, and some debate over whether this is in fact a slowing of aging or just a reduction in cancer incidence.
The present consensus on its mode of operation is that it produces longevity-related effects by suppressing the generation of two protein complexes, mTORC1 and mTORC2, both of which include the mTOR protein that has long been associated with rapamcyin.
Of these two complexes, the effects of lowered levels of mTORC1 are better understood and more clearly beneficial. Here researchers delve into mechanisms associated with mTORC2, which are much more of a mixed bag. For the research groups involved in this work, the goal is to design new drugs that only trigger the beneficial alterations from the full set of those induced by rapamycin.
Considering Mitochondrial DNA Deletions in Skeletal Muscle - Tuesday, July 29, 2014
The organelles known as mitochondria play the role of power plant in the cell, generating energy stores to power cellular operations. As for all cellular components, mitochondria are built of proteins derived from DNA blueprints, but unlike all other cellular components mitochondria have their own DNA, separate from that in the cell nucleus.
They are descendants of symbiotic bacteria, and continue to replicate like bacteria within our cells. Certain types of damage to mitochondrial DNA are one of the contributing causes of degenerative aging: mitochondria missing certain proteins become dysfunctional, ultimately taking over a small fraction of all cells by old age, and causing widespread harm in surrounding tissues.
In this paper researchers consider the process by which one bad mutation in one mitochondrion eventually fills the cell with duplicates of itself. This is one of the areas in which there is plenty of room for argument: does it happen because it confers the ability to replicate more readily, because it allows damaged mitochondria to evade quality control mechanisms, or for some other reason? As is often the case negative results in studies still add information to the overall picture.
Alcor Working on Field Perfusion for Remote Cryonics Cases - Tuesday, July 29, 2014
The state of infrastructure technologies in the cryonics industry is improving slowly over time. Most organizations in the community are volunteer based, which puts a greater burden on the few professional groups to work on research and development.
Nonetheless, cryonics today is a more reliable undertaking than at any point in the past decades of its existence as an option, even if there is still a lot of room for improvement. That improvement can only arrive rapidly given an expansion of the industry, however, something that has stubbornly refused to occur for a long time now.
A Review of Age-Related Macular Degeneration - Wednesday, July 30, 2014
Age related macular degeneration (AMD) is one of the first prospective targets for prototype rejuvenation treatments.
This is because the relationship between the condition and one of the primary forms of change between young and old tissue is both direct and comparatively well understood: certain hardy metabolic waste compounds accumulate in long-lived retinal cells to cause increasing dysfunction over the timescale of a human life span, and this occurs because our cellular recycling machinery cannot effectively break down these compounds.
The best solution is to develop drugs or make use of tools such as bacterial enzymes that can do this for us; comparatively few groups are working on this angle, however.
A Review of Approaches to Delay Sarcopenia - Wednesday, July 30, 2014
Sarcopenia is the name given to age-related loss of muscle mass and and strength, although by the time it is processed through the regulatory system into a formal, final disease definition, it will be restricted to referring to only severe levels of loss.
Average loss of muscle mass and strength will be called normal, just a part of aging, and therefore something that shouldn't be treated - and indeed, that it is forbidden to treat, as in regulatory systems like that of the FDA in the US, everything that is not explicitly permitted is illegal. This is a major systemic problem with the present system of medical regulation, one that has to be changed, and soon. It is no wonder that we see only slow progress in research and fundraising when treating degenerative aging is largely forbidden, especially any focus on causes and prevention rather than patching over late stage consequences after the fact.
Here is an open access review of a range of approaches in mainstream research aimed at slowing the onset and progression of sarcopenia, most of which haven't made it as far as drug development yet. As for so many of these topics it overwhelmingly focuses on alteration of metabolic processes rather than repair of root causes: slowing the progression of damage only, not reversing it.
Resistance to Oxidative Stress in Cells of Long-Lived Species - Thursday, July 31, 2014
Here is a small slice of broader efforts to investigate and understand the range of differences in longevity and cellular biochemistry between species. It seems likely that these research programs will provide additional helpful information beyond that derived from the straightforward study of human biochemistry when it comes to work on treating aging.
More Context on the Goals of Human Longevity, Inc. - Thursday, July 31, 2014
The company Human Longevity was recently founded to work on the genetics of aging and health. My thinking is that genetics is a hot field, and there is much to be done in the general context of medicine, but that insofar as longevity goes it is the wrong place to be looking for large benefits.
Epigenetic and gene expression changes are secondary consequences in aging, not the root cause, and natural genetic variations have a small effect on aging in comparison to what might be possible through repair biotechnologies such as those of the SENS vision.
So for aging the outcome of Human Longevity is likely to be incremental advances in the present day practice of ignoring the comparatively simple causes of degeneration, the accumulation of damage, while trying to patch over the very complex end states by tinkering with enormously complex dysregulations of metabolism and biological systems that occur in response to damage. This is doomed to only marginal success, just like the medicine of today.
Here is a piece that provides more context on where Human Longevity is headed in the near term: undoubtedly useful, just not so much for aging. We all age in the same way, due to the same root causes involving an accumulation of specific, known forms of damage to cells and molecular tissue structures. Fix those causes by repairing them and near all but the most rare and catastrophic genetic variations are irrelevant. They simply don't matter.
TRAP-1 Knockout Improves Health and Extends Life in Mice - Friday, August 1, 2014
Cancer researchers here stumble upon a way to alter mitochondrial function to improve health and extend life in mice.
A range of the known ways to slow aging through genetic alteration work through similar mechanisms to those shown here, creating somewhat dysfunctional mitochondria that can still perform their necessary functions but which generate a raised level of damaging oxidative molecules in the process. This spurs cells to increase cellular housekeeping activities in response, which in turn leads to a net gain in cellular health and function. Over the lifespan of an organism these small differences in every cell add up.
Healthier, Wealthier, and Wiser - Friday, August 1, 2014
It is known that greater health throughout life, greater wealth, greater social status, and greater intelligence are all associated with greater life expectancy. Untangling the nature of these linked correlations is ever a challenge, however, since they all associate with one another as well.
There are any number of plausible explanations as to why the wealthy or the more intelligent live longer, and some interesting speculation besides, such as the association of intelligence with physical robustness, but rarely is there any way to prove these explanations true in the data obtained from population studies. Correlations are what is obtained, and it is then usually a matter of retreating to animal studies where it is possible to structure the work to prove causation - but of course this is somewhere between hard and impossible to achieve for intelligence and social status.
This paper reminds us of the tendency for age-matched cohorts to become on average healthier, wealthier, and wiser over time. This isn't a matter of self-improvement, though any of us can work on that, but occurs because those who were not comparatively healthy, wealthy, and wise are more likely to be dead already.
DISCLAIMER:Â News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.fightaging.org/
David A. Kekich
Maximum Life Foundation
"Where Biotech, Infotech and Nanotech
Â Â Â Â Meet to Reverse Aging by 2033"