Hormone optimization/therapies—including thyroid, estrogen, testosterone, progesterone, DHEA, DHT, pregnenolone, human growth hormone, IGF-1, HCG, insulin, cortisol, 25-hydroxyvitamin D
Preventive medicine protocols—including early detection and prevention of age-related disorders, such as cardiac disease, diabetes, osteoporosis, hyperlipidemia, etc.
Precision Medicine: Emerging therapies—e.g. the use of autologous stem cells and emerging diagnostics (such as genetic screening and telomerase)
Additional content as it relates to Age Management Medicine
82 AMA PRA Category 1 Credits — by participating in the AMMG Certification Program you will be eligible to earn 82 AMA PRA Credits. To receive those credits, you must complete all participation requirements as outlined.
Telomerase, also called terminal transferase, is a ribonucleoprotein that adds a species-dependent telomere repeat sequence to the 3′ end of telomeres. A telomere is a region of repetitive sequences at each end of a chromosome. Telomeres protect the end of the chromosome from DNA damage or from fusion with neighboring chromosomes.
Telomerase is a reverse transcriptase enzyme that carries its own RNA molecule (e.g., with the sequence 3′-CCCAAUCCC-5′ in Trypanosoma brucei) which is used as a template when it elongates telomeres. Telomerase is active in gametes and most cancer cells, but is normally absent from, or at very low levels in, most somatic cells.
Telomerase restores short bits of DNA known as telomeres, which are otherwise shortened when a cell divides via mitosis.
In normal circumstances, where telomerase is absent, if a cell divides recursively, at some point the progeny reach their Hayflick limit, which is believed to be between 50–70 cell divisions. At the limit the cells become senescent and cell division stops. Telomerase allows each offspring to replace the lost bit of DNA, allowing the cell line to divide without ever reaching the limit. This same unbounded growth is a feature of cancerous growth.
Some experiments have raised questions on whether telomerase can be used as an anti-aging therapy, namely, the fact that mice with elevated levels of telomerase have higher cancer incidence and hence do not live longer. On the other hand, one study showed that activating telomerase in cancer-resistant mice by over-expressing its catalytic subunit extended lifespan.
A study that focused on Ashkenazi Jews found that long-lived subjects inherited a hyperactive version of telomerase.
The aging process results in multiple traceable footprints, which can be quantified and used to estimate an organism’s age. Examples of such aging biomarkers include epigenetic changes, telomere attrition, and alterations in gene expression and metabolite concentrations.
More than a dozen aging clocks use molecular features to predict an organism’s age, each of them utilizing different data types and training procedures. Here, we offer a detailed comparison of existing mouse and human aging clocks, discuss their technological limitations and the underlying machine learning algorithms.
We also discuss promising future directions of research in biohorology — the science of measuring the passage of time in living systems. Overall, we expect deep learning, deep neural networks and generative approaches to be the next power tools in this timely and actively developing field.
Strategies for Engineered Negligible Senescence (SENS) is the term coined by British biogerontologist Aubrey de Grey for the diverse range of regenerative medical therapies, either planned or currently in development, for the periodical repair of all age-related damage to human tissue with the ultimate purpose of maintaining a state of negligible senescence in the patient, thereby postponing age-associated disease for as long as the therapies are reapplied.
The term “negligible senescence” was first used in the early 1990s by professor Caleb Finch to describe organisms such as lobsters and hydras, which do not show symptoms of aging. The term “engineered negligible senescence” first appeared in print in de Grey’s 1999 book The Mitochondrial Free Radical Theory of Aging. De Grey called SENS a “goal-directed rather than curiosity-driven” approach to the science of aging, and “an effort to expand regenerative medicine into the territory of aging”.
The arrows with flat heads are notations meaning “inhibits,” used in the literature of gene expression and gene regulation.
The ultimate objective of SENS is the eventual elimination of age-related diseases and infirmity by repeatedly reducing the state of senescence in the organism. The SENS project consists in implementing a series of periodic medical interventions designed to repair, prevent or render irrelevant all the types of molecular and cellular damage that cause age-related pathology and degeneration, in order to avoid debilitation and death from age-related causes.
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