Can We Really Slow Aging Down?

The new field of gero-science helps us know what to do to make aging malleable.

From the new Anti-Aging Symposium called:

Extending human health span and longevity: a symposium report

Research compiled from these guys below:

• Sticky Ink, Inc, New York, New York.

• Albert Einstein College of Medicine, Bronx, New York.

• University of Minnesota Medical School, Minneapolis, Minnesota.

• Yale School of Medicine, New Haven, Connecticut.

• University of Washington, Seattle, Washington.

• National Institute on Aging, National Institutes of Health, Bethesda, Maryland.

• University of Connecticut School of Medicine, Farmington, Connecticut.

• Life Biosciences, Boston, Massachusetts.

• Wake Forest School of Medicine, Winston-Salem, North Carolina.

• University of Texas Health Sciences Center San Antonio, San Antonio, Texas.

• Mayo Clinic, Rochester, Minnesota.

• USC Leonard Davis School of Gerontology, Los Angeles, California.

• The Buck Institute for Research on Aging, Novato, California.

• Lawrence Berkeley National Laboratory, Berkley, California.

For many years, it was believed that the aging process was inevitable and that age-related diseases could not be prevented or reversed.

The geroscience hypothesis shows that aging is, in fact, “malleable” (as you can see from the video above, I’ve been saying for years) and, by targeting the hallmarks of biological aging, it is indeed possible to alleviate age-related diseases and dysfunction and extend longevity.

Aging is malleable.

We can “stretch” it in the direction we choose, depending on the actions we take.

Or nutrients and/or drugs that we swallow.

This field of geroscience aims to prevent the development of multiple disorders with age, thereby extending the health span, with the reduction of morbidity toward the end of life.

Experts in the field have made remarkable advancements.

Anti-Aging Glossary

Senescent cells: These are old cells with irreversibly damaged DNA; they strongly resist apoptosis. Thus, they are not eliminated and continue to secrete pathogenic proinflammatory molecules.

Senolytics: This is a class of compounds that promote the removal of senescent cells from the body.

For example, rapamycin which tamps down a pathway called the mTOR pathway is being looked at to slow down aging. Most of the docs at my clinic in Florida, including myself, are on this.

Autophagy: This is a process that promotes protein degradation, which is attenuated with aging and that impedes the aggregation of proteins harmful to cell function, particularly those of the central nervous system.

Rampamycin is also supposed to boost autophagy. So does ozone and whole blood irradiation which I try to do monthly, at least.

Proteostasis: This is the dynamic regulation of protein homeostasis.

Epigenetics: This is the field of biology that studies phenotype changes that are not caused by changes in DNA sequencing and that continue to affect cellular division.

For example, hormone replacement helps beneficial epigenetic changes in some. Such as testosterone therapy tamping down the expression of the Alzheimer’s vulnerability gene and thereby protecting cognition in those that might be at genetic risk. I write about this in detail in SEXY BRAIN (how sex steroid hormones rule the brain, so to speak).

Metabolome: This refers to small molecules that make up the building blocks of all organismal features, from cell membranes to metabolic cycles to genes and proteins.

Experiments on old mice that have undergone genetic modification of senescent cells or the administration of "senolytic cocktails" composed of dasatinib plus quercetin protected the animals from the effects of viral infections.

This suggests the vulnerability of aging can be modified through treatment.

What anti-aging meds are studies evaluating?

Growth hormone and type 1 insulin-like growth factor (IGF-1): Older adults are often prescribed growth hormone.

However, get this!

Recent data suggest that doing so is “not” advantageous to this patient population because it antagonizes proteostasis and other cell maintenance mechanisms in older age.

Experimental studies and studies conducted on centenarians suggest that “low growth hormone and IGF-1 levels” contribute to longevity!

Metformin is among the therapeutic agents under investigation in cutting-edge clinical research. Its effect on aging will be studied in the Targeting Aging with Metformin (TAME) clinical trial. This trial is the first to study aging outcomes.

The goal is to create a regulatory framework that future therapies can follow to achieve FDA approval.

Promising anti-aging therapeutic platforms:

1st aims to produce adenosine triphosphate, levels of which decline dramatically with aging.

2nd aims to promote autophagy to remove cellular waste to treat neurodegenerative diseases.

3rd reprograms the “epigenome” to a younger state. (To Benjamin Button your genes, HRT has a lot to do with this in my opinion).

4th heal mitochondrial dysfunction (again, hormone therapies along with nutrients and diverse colorful plant food help with this).

For example, Humanin, a mitochondrial healing peptide, has been demonstrated to exert protective effects on the heart, brain, and liver.

PS mitochondrial proteins are suppressed by growth hormone and IGF-1.

Mantra for anti-aging if you don’t have access or courage to do the above:

• Eat less.

• Move more.

• Eat more plant food.

• Think more positive connecting thoughts.

• Avoid processed anything, even health foods.

• Sleep as though your life depended on it.

• Have community.

• Don’t forget the critical vitamin F, fun.

• Explore senolytics.

Knowledge is power.

Especially to slow down the Mack Truck of Aging.

Dr. B.

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Reference:

Extending human healthspan and longevity: a symposium report. Ann N Y Acad Sci. 2022 Jan;1507(1):70-83. doi: 10.1111/nyas.14681. Epub 2021 Sep 8. PMID: 34498278.

SEXY BRAIN Berkson DL Awakened Medicine Press 2017.