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Aging

You can have a test done to find out what your actual biological age is at myDNAge

See also Anti-aging, Longevity / Lifespan / Healthspan, Regenerative Medicine

Overview

In the field of the biology of aging, no one believes in the free-radical theory of aging anymore, it's archaic.

Age Wave,  by Ken Dychtwald, 1987: “In the coming years, American culture will shift from being focused on youth to being increasingly concerned with the needs, problems, and dreams of middle-aged and older population.

The coming “age wave” will challenge and shake every aspect of our personal, social and political dynamics. How will we alter ourselves in response will be an issue of mounting concern; indeed, it may prove to be the single most controversial issue in the twilight of this century.”

1987:

The Futurist, Nov/Dec 1993: “Health-care facilities will be pushed to the limit in the years ahead by an increase in the number of elderly people. By 2030, the United States will have twice as many senior citizens as it does today, 70% of them women.”

1/3 of seniors who die (2016) die with some form of dementia (Dr. Brant Cortright, The Neurogenesis Diet and Lifestyle; Upgrade your Brain Upgrade your Life)

What’s Happening with Age?

What are we trying to gain back?

Classical theories on aging:

But these may not be the proximate cause of aging. These are the consequences of the aging process. Is there a higher “master controller”? Epigenetics.

In aging cells we see increased damage, less cell repair, less clearance, less cell renewal. Cellular senescence leads to less proliferation of damaged cells which is anti-cancer. There's also less tissue function, more inflammation.

NAD is absolutely essential to repairing broken DNA. Broken DNA happens 125 times a day in every cell of the body in single stranded breaks and about 25 times a day in double stranded breaks. And more if you have EMF exposures. NAD is about 50% of what it was in our 20's and 30's by the time we're 60. At 70 its about 10%. At age 80 it's almost gone. Research done at Better Humans is now being conducted to enhance NAD as we age.

The famous aging researcher Leonard Hayflick once observed that aging is an increase in molecular disorder.

One recently proposed theory that builds on this basic concept, and ties many aging concepts together into one model, has been dubbed the ‘green theory’ of aging. This model proposed that aging is the result of damage to large key molecules, especially proteins, that has accumulated as a result of toxic metabolic byproducts (including damage caused by oxidation). A primary determinant of healthspan is therefore the efficiencies of either the protection against toxic products, the removal of these toxic products, including phase I/II detoxification by the liver, or the repair of this large molecule damage. Protect, detoxify and repair is the catch-cry of preserving cellular health into old age.

Source: Principles and Practice of Phytotherapy, 2nd Edition, 2013 by Kerry Bone and Simon Mills. Indicated by (Bone & Mills)

Yale study finds nearly half of older adults improved with age. A long-term Yale study is challenging one of the biggest myths about aging. Nearly half of adults over 65 improved physically, mentally, or both over time, despite the common belief that aging means constant decline. Researchers found that people with more positive attitudes about getting older were significantly more likely to show these gains.

Superagers keep youthful memories but their DNA does not explain why. SuperAgers defy Alzheimers genetics. Scientists expected SuperAgers might simply inherit fewer Alzheimer’s-related risks, but their genes looked much like those of typical older adults. Their extraordinary memories may instead come from still-unknown protective forces involving the brain, body, lifestyle, and environment.

Summary of PDF: Getting Old through the Blood

Authors: Francesco Angelini et al.
Published: 2017 in Frontiers in Cardiovascular Medicine

This review examines how circulating proteins, microRNAs, and regenerative cells may influence aging, cellular senescence, and cardiovascular repair. The authors focus particularly on how the blood environment changes with age and affects endothelial progenitor cells (EPCs), mesenchymal stromal cells (MSCs), and cardiac progenitor cells (CPCs).

Main themes

Important circulating factors

FactorRelationship to aging
IGF-1Levels generally decline with age. It can support cardiac cells, promote survival, and improve EPC function, but excessive or prolonged signaling may activate pathways associated with senescence.
GDF-11Initially proposed as a “rejuvenating” factor that declines with age and reverses cardiac aging. However, later studies produced conflicting results, so its anti-aging role remains unresolved.
PAI-1Generally rises with age and is produced by senescent cells. It can reduce IGF-1 availability, promote cell-cycle arrest, and impair survival of regenerative cells. PAI-1 inhibition showed promising anti-senescence effects in experimental models.
miR-34aIncreases with age and suppresses SIRT1, promoting endothelial and progenitor-cell senescence, inflammation, and reduced angiogenesis.
miR-146aAssociated with aging and inflammatory signaling. Increased levels may impair progenitor-cell survival and regenerative capacity.
miR-21Linked to “inflammaging,” cardiac fibrosis, fibroblast senescence, and dysfunction of vascular progenitor cells.

Cardiovascular regenerative cells

The review highlights three cell populations:

Overall conclusion

The authors propose that aging is influenced not only by changes inside individual cells but also by the systemic blood environment. Circulating molecules could eventually serve as:

  1. Biomarkers of biological aging and cardiovascular risk
  2. Therapeutic targets for reducing senescence
  3. Tools for improving cell-based regenerative therapies

However, the evidence—especially for GDF-11 and several proposed anti-aging interventions—was still preliminary in 2017. The review does not establish that manipulating these factors extends human lifespan. Instead, it identifies promising biological pathways for future research into healthier aging and cardiovascular regeneration.

VIDEOS:

Why Do We Age?
The Role of Glycans in Human Aging
Human cell research in space may reveal secrets of aging
"Honest Aging: A New Way of Growing Old" by Rosanne M. Leipzig, MD, PhD
Physiology of Growing Older & Atypical Presentation to the Emergency Department
Aging and AI, What the Future Holds for all of us
Professor David Sinclair What Is Ageing Why It Happens
Dr. David Sinclair on Informational Theory of Aging, Nicotinamide Mononucleotide, Resveratrol & More
Normal and Abnormal Aging and the Brain
Does meditation affect cellular aging?
Aging with Grace: What to Expect as Your Parents Get Older
Are Microbes Making You Older?
How Testosterone is Transforming Aging – Epic Results
Health & Successful Aging w/ PROFESSOR BRIAN KENNEDY
New study reveals how humans age (2019)
What Signs of Aging are Actually Due to Aging?
Research on Healthy Aging
The Science and Clinical Approaches to Aging - Dr. Ahvie Herskowitz (Nov 2019)
Why We Age and Why We Don't Have To | David Sinclair
The Physiology of Human Aging and How to Optimize it with Stephen Harridge
4 Ways to be more Resilient as you Age
Can You Age Backwards?
How to Counter the Inflammation of Aging
Death is Inevitable but Aging is Not
Why do Ears & Nose Grow as you Age?
Epigenetic Regulation of Senescence and Aging
We're One Step Closer to Understanding Aging
"Aging - A Perspective from Proteostasis and the Health of the Proteome"
Myths About Aging: What’s Real?
Professor David Sinclair What Is Ageing Why It Happens
2017- Aging-Related Research - National Poll on Healthy Aging
Why Stressing About Aging Shortens Your Life
What Big Pharma Doesn't Want You to Know About Aging
Healthy Aging Begins and Ends with the Gut
Follow Your Gut: Microbiomes and Aging with Rob Knight - Research on Aging
8 Unexpected Things Aging You Faster (And How to Slow Aging Naturally)
Do You Need More Protein as You Age?
Understanding Molecular Aging with Attila Csordas, AgeCurve Limited
2019 - Technology and Aging: Updates
How Technology can Keep you Weak and Age you Faster
Aging with Resilience
How to Age Well
Does Meditation Affect Cellular Aging?
Dr. Thomas Rau's Aging Well Program
RHR: How to Slow Down Aging—with Sara Gottfried
8 Unexpected Things Aging You Faster
5 Tips in Dealing with Old Injuries as You are Aging
How to Slow Down Aging
Aging Gracefully with Resilience

ARTICLES/STUDIES

Aging Process

Long-lived families reveal a rare genetic clue to healthy aging. Rare gene delays disease 13. A study of long-lived families has identified rare genetic variants that may help people stay healthier for much longer as they age. One standout mutation appears to temper inflammation, potentially delaying disease and extending years of healthy living.

Biological Aging vs. Chronobiological Age – An Important Role for the Mitochondria, Part 2

Klotho, Aging, and the Failing Kidney

Breaking the Rules – Important Molecular Pathway for Control of Aging Discovered

Genes Associated with Earlier and Higher Reproduction Linked to Accelerated Aging

Loss of delta-6-desaturase activity as a key factor in aging Aging is characterized by a wide variety of defects, particularly in the cardiovascular and immune systems. Cyclic AMP levels fall, especially in lymphocytes. Delta-6-desaturase (D6D) levels have been found to fall rapidly in the testes and more slowly in the liver in aging rats. D6D is an enzyme which converts cis-linoleic acid to gamma-linolenic acid (GLA). Other factors which inhibit D6D activity are diabetes, alcohol and radiation, all of which may be associated with accelerated aging. In meat eaters or omnivores which can acquire arachidonic acid from food, the main consequences of D6D loss will be deficiencies of GLA, dihomogamma-linolenic acid (DGLA) and prostaglandin (PG) E1. PGE1 activates T lymphocytes, inhibits smooth muscle proliferation and thrombosis, is important in gonadal function and raises cyclic AMP levels in many tissues. It is a good candidate for a key factor lost in aging. Moderate food restriction, the only manoeuvre which consistently slows aging in homoiotherms, raises D6D activity by 300%. Other factors important in regulating D6D and the conversion of GLA to PGE1 are zinc, pyridoxine, ascorbic acid, the pineal hormone, melatonin, and possibly vitamin B3. GLA administration to humans has been found to lower blood pressure and cholesterol, and to cause clinical improvement in patients with Sjogren's syndrome, scleroderma and alcoholism. These diseases are associated with some features of accelerated aging. The proposition that D6D loss is not only a marker of aging but a cause of some of its major manifestations is amenable to experimental test even in humans. The blocked enzyme can be by-passed by giving GLA directly.

Healthy Aging

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