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Anti-Aging or Anti- Immune System Aging?
“…delaying senescence and thus age-related diseases. Rare human mutations can cause accelerated aging diseases. Environmental factors may affect aging – for example, overexposure to ultraviolet radiation accelerates skin aging…”
When PeopleBeatingCancer.org uses the term “anti-aging” it is the biological sense. That is to say, I’m not talking about younger skin or the fountain of youth. Chemotherapy has been shown to age patients.
Therefore, chemotherapy-induced aging is one of the many long-term side effects that I now live with. My goal then, is to research and identify non-toxic therapies shown to slow my cellular aging.
And if my skin looks better aka younger as a result, so be it :-).
All kidding aside- at least on the issue of skin aging. I admit to sitting in the sun way too much as a kid. Every time I sustained a sunburn, I increased my risk of skin cancer according to research.
My high-dose autologous stem cell transplant aged my cells and my lifestyle aged my cells. And both high-dose chemo as well as sun burns increased my risk of skin cancer aka melanoma.
Possible fixes? Stop all chemotherapy and radiation. Fine. That’s easy. Secondly, I no longer sit in the sun. Ever. Thirdly, I eat and supplement with foods that research has shown can slow my cellular senescence.
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David Emerson
- Cancer Survivor
- Cancer Coach
- Director PeopleBeatingCancer
Recommended Reading:
- Multiple Myeloma Chemotherapy- When Cancer Treatment Might Kill You
- Multiple Myeloma Therapy- Clear Human Papilloma Virus (HPV) Naturally
- Myeloma Stem Cell Transplant- Vaccination Post Transplant? Yes or no?
Senescence
“Senescence (/sɪˈnɛsəns/) or biological aging is the gradual deterioration of functional characteristics in living organisms. The word senescence can refer to either cellular senescence or to senescence of the whole organism. Organismal senescence involves an increase in death rates and/or a decrease in fecundity with increasing age, at least in the latter part of an organism’s life cycle.
Senescence is the inevitable fate of almost all multicellular organisms with germ–soma separation,[1][2] but it can be delayed…
…the existence of species having negligible senescence and potentially immortal organisms such as Hydra, have motivated research into delaying senescence and thus age-related diseases. Rare human mutations can cause accelerated aging diseases.
Environmental factors may affect aging – for example, overexposure to ultraviolet radiation accelerates skin aging…”
Causes, consequences, and reversal of immune system aging
“The effects of aging on the immune system are manifest at multiple levels that include reduced production of B and T cells in bone marrow and thymus and diminished function of mature lymphocytes in secondary lymphoid tissues. As a result, elderly individuals do not respond to immune challenge as robustly as the young. An important goal of aging research is to define the cellular changes that occur in the immune system and the molecular events that underlie them. Considerable progress has been made in this regard, and this information has provided the rationale for clinical trials to rejuvenate the aging immune system…
Conclusions and perspectives
As indicated above, a tremendous amount is now known regarding the cellular changes that occur in the aging immune system and the molecular events that underlie them. Thus, it is not unreasonable to expect that this information will continue to be translated into therapies to rejuvenate the aging immune system.
It is likely that the effects of aging on the immune system will not be uniform between individuals. Thus, an ultimate goal would be to identify key biomarkers and establish simple laboratory tests to define each person’s aging profile. Such information could then be used to develop a personalized approach in which targeted interventions could be directed to the individual’s specific aging deficit. However, whatever standard of care is ultimately adopted for stimulating immunity, the emphasis should not necessarily be placed on increasing life span. Rather, the aim is to increase health span, defined as years of healthy living (117).”
Omega-3 fatty acids and protein metabolism: enhancement of anabolic interventions for sarcopenia
“Purpose of review: The increased age observed in most countries, with the associated higher rates of chronic illnesses and cancer, and a diffuse sedentary lifestyle, will increase the number of patients with clinically relevant anabolic resistance, sarcopenia and its complications. The need for solutions to this major health issue is, therefore, pressing.
Recent findings: The metabolic derangements and other consequences associated with sarcopenia can be slowed or even prevented by specific nutritional interventions. New evidence is available about the efficacy of omega-3 fatty acid dietary supplementation to improve protein metabolism and counteract anabolic resistance through indirect effects.
Studies show that the anabolic stimuli from substrates (e.g. amino acids or proteins), hormones (e.g. insulin) and/or physical activity in skeletal muscle can be enhanced by long-term fish oil administration.
Summary: The review of data from recent studies on this topic suggests that dietary omega-3 fatty acid supplementation, in association with an anabolic stimulus, could potentially provide a safe, simple and low-cost intervention to counteract anabolic resistance and sarcopenia.
This intervention may contribute to prevent cachexia and disabilities. Supplementation should be given in the earlier stages of sarcopenia (e.g. precachexia). Further research should, however, be performed to better understand the mechanisms involved and the best dosage and timing of administration…”
Anti-aging tricks from dietary supplement seen in mice
“In human cells, shortened telomeres, the protective caps at the ends of chromosomes, are both a sign of aging and contribute to it. Scientists at Emory University School of Medicine have found that the dietary supplement alpha lipoic acid (ALA) can stimulate telomerase, the enzyme that lengthens telomeres, with positive effects in a mouse model of atherosclerosis…”