Dear Future Centenarian,
Do you sometimes or often…

  • Hold grudges?
  • Feel sorry for yourself?
  • Feel jealousy?
  • Hate?
  • Dwell on problems?
  • Ask: “Why me?”
  • Envy others?
  • Pursue happiness through accumulating “things” such as money, cars, bigger houses, and any other possessions you have or want?
  • Let illness or pain push your career or relationships out of your schedule?
  • Worry about aging?
  • Worry about dying?
  • Get immersed in politics?
  • Try to appease or impress others?
  • Complain?
  • Argue?
  • Let yourself be easily led or manipulated?
  • Get overly emotional?
  • Feel superior?
  • Feel inferior?
  • React without thinking?
  • Feel indecisive?
  • Lie to others and yourself?
  • Spend much time thinking about (living in) the past?

I know I do. I’ll bet you do too. You would have to be superhuman or a saint to not own ANY of the above character traits.

But the closer you get to eliminating most or all of these traits could influence your health and how long you live.

The opposite leads to unhealthy outcomes.

So, how do you go about managing the emotions that lead to these traits? After all, aren’t we wired at birth with the propensity to develop them, regardless of our desires?

The answer is “No.”

We develop these and other detrimental traits and allow them to control our lives… and our longevity. Or we take control our lives and live lives full of happiness and fulfillment.

It’s a process. I’ve been working on it for a long time, just watched the video below which my cousin Rich sent to me, and I had to share it with you.

It won’t tell you, A-Z, how to eliminate all destructive traits, but it is a great introduction on how to get a flying head start.

If you want to, you’ll apply some of the knowledge you’ll get from the video to help ensure your path to health, happiness and longevity.

Click on the link below. now.

More Life,
David Kekich



Weekly News

Slow Progress Towards Autologous Cell Therapies for Parkinson’s Disease

Cell therapies for Parkinson’s disease have been under development for a very long time indeed, decades at this point. The condition is characterized by aggregation of ?-synuclein and loss of the small but critical population of dopamine-generating neurons in the brain.

The latter is the proximate of cause of the loss of motor control and depression observed in patients. These cells are particularly sensitive to the combination of toxic ?-synuclein biochemistry, mitochondrial dysfunction, chronic inflammation, and other contributing factors that manifest in this condition – and in aging in general.

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Epidemiological Evidence for Herpesvirus Infection to Increase the Risk of Alzheimer’s Disease

There is much debate these days over the contribution of persistent infection (such as by herpesviruses) to the development of Alzheimer’s disease.

Not everyone with the evident risk factors, such as obesity, frailty, chronic inflammation, and so forth, progresses from mild cognitive impairment to full blown Alzheimer’s disease. Why is this?

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The Binarized Transcriptomic Aging Clock

Patterns of epigenetic regulation of gene expression (and thus RNA and protein levels) change constantly in response to cell state and environment.

Some of those changes are characteristic responses to the damage and dysfunction of aging. Since the demonstration of the first epigenetic clocks, those that predict age based on an algorithmic combination of the status of DNA methylation at CpG sites on the genome, researchers have produced any number of new clocks based on mining epigenomic, transcriptomic, proteomic, and other databases for correlations with age.

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Arguing the Direction of Causation in Atherosclerosis and Clonal Hematopoiesis

A major challenge in the study of aging and age-related disease is establishing the direction of causation.

A great many mechanisms of aging are known, but it is difficult to firmly establish the relationships between them. The body is made up of many interacting systems, and changes in any one system tend affect the others, directly or indirectly.

Equally, any two specific aspects of aging can be quite disconnected from one another but nonetheless proceed in parallel because they are both influenced by a third underlying mechanism. For example, the chronic inflammation of aging is a systemic problem, driving dysfunction in tissues throughout the body and accelerating the onset and progression of a wide range of age-related conditions.

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Today’s research materials are an example of this point. Here, researchers debate the direction of causation between atherosclerosis and

Piperlongumine Reduces Aortic Calcification in Mice

Piperlongumine, an extract of long peppers, was shown to be senolytic a few years ago. The compound is capable of selectively destroying senescent cells by sensitizing them to oxidative damage, provoking apoptosis.

The accumulation of senescent cells is one of the causes of aging, and means of clearance are thus potentially valuable. For those considering introducing more long peppers into their diet, note that a senolytic dose of piperlongumine would require ingesting an impossibly large weight of pepper.

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Tsimane and Moseten Hunter-Gatherers Exhibit Minimal Levels of Atrial Fibrillation

Epidemiological data for the Tsimane and Moseten populations in Bolivia shows that they suffer very little cardiovascular disease in later life, despite a presumably greater lifetime burden of infectious disease (and consequent inflammation) than is the case for people in wealthier regions.

The differences in lifestyle are fairly straightforward: a much greater level of physical activity throughout life, and a diet that is high in fiber and low in all of the terrible things, like processed sugars, that people in the wealthier regions of the world tend to consume these days.

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Bioactive Lipids and the Cell Membrane in Aging

Researchers here discuss, in some detail, what is known of age-related changes in the levels of various lipid molecules in cell membranes. There is evidence for these changes to be disruptive to cell function, and thus a meaningful contribution to age-related degeneration.

Like many of the areas of interest in the study of aging, this has the look of a form of disarray that is downstream of the molecular damage that lies at the root of aging. Nonetheless, it is suggested that supplementing the levels of specific lipids, where they decline with age, may be beneficial enough to be worth the effort.

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Higher Cardiovascular Health Score Correlates with Lower Epigenetic Age Acceleration

Epigenetic age acceleration is the degree to which epigenetic age is higher than chronological age. Epigenetic age is assessed via one of the epigenetic clocks, measuring the status of DNA methylation at numerous CpG sites on the genome.

Some changes in DNA methylation patterns are characteristic of aging, a reaction to the accumulation of damage and dysfunction in aged tissues. People with lower epigenetic ages are, on balance, less burdened by the damage and dysfunction of aging than their peers.

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Too Much of a Focus on What is Easy, Too Little on What Could Greatly Increase Lifespan

It is comparatively easy to build companies that sell customized mixes of various supplements shown to modestly slow aging in mice, and the same goes for companies that offer personalized advice on health matters relating to aging.

Neither of these options are going to do much to meaningfully extend the healthy human life span.

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CAR-T Therapy Continues to Perform Well for Patients Unresponsive to Chemotherapy

CAR-T immunotherapy involves equipping T cells extracted from a patient with a chimeric antigen receptor (CAR), expanding them in culture, and then reintroducing these genetically engineered T cells into the patient.

The artificial receptor allows the T cells to aggressively respond to the patient’s cancer, as it is targeted to a cell surface feature that is characteristic of cancer cells. Different cancers have different features, and thus different CARs are used. CAR-T therapies were first trialed for blood cancers, and continue to do well on this front, as noted here.

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A Popular Science View of Mitochondrial Uncoupling

Mitochondrial uncoupling diverts the output of the electron transport chain into heat rather than the production of ATP. Induction of higher than usual levels of uncoupling is a calorie restriction mimetic strategy: it produces some of the same gains in health and longevity as the practice of calorie restriction, with some overlap in the processes affected and metabolic changes produced.

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Age-Associated B Cells Contribute to Autoimmunity and Chronic Inflammation

The immune system becomes disordered and dysfunctional with age in numerous different ways. The B cell component accumulates inflammatory and problematic cells that are known as age-associated B cells.

Here, researchers show that these errant B cells produce antibodies that provoke autoimmunity. B cell aging is a problem with a solution demonstrated in animal models: just destroy all B cells.

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FOXO1 Influences Proteosomal Function via Regulation of the Expression of a Proteasome Subunit

The proteasome is a complex structure in the cell that is responsible for breaking down unwanted proteins.

Like other recycling processes, proteasomal function is connected to life span in short-lived species. Better cell maintenance in response to stress and damage improves cell function, organ function, and longevity.

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Age-Related Vision Impairment Correlates with Mortality

Researchers here note an association between vision impairment and mortality in later life. This has the look of a correlation that exists because aging is a global process at work throughout the body.

It stems from the accumulation of a few classes of cell and tissue damage. That damage causes downstream consequences that spread out into a complex, diverse array of degeneration and diseases. If vision is failing more rapidly in any given individual, then the odds are very good that this is also the case for other, more critical systems in the body.

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An Approach to Allow Much Faster Bioprinting of Tissue

Now that some groups, such as Volumetric, are working on ways to print tissue with blood vessel networks, ways to more efficiently bioprint larger volumes of tissue will be necessary.

Costs must come down in order for the technologies to spread and evolve more rapidly. The road to bioprinting of entire replacement organs lies ahead, given (a) a robust solution for the production of tissues containing small-scale blood vessels, and (b) bioprinters that can turn out tissues reliably and rapidly.

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