Can You Truly Extend Your Lifespan?
NUTRITION
SUPPLEMENTS
Supplementing with REJUVENINS - Not Antioxidants
Guy R. Schenker
DC
Anti-inflam-aging? The possibility is real; the science of gerontology proves it.
Anti-aging nutrition? Are you interested? Anti-inflam-aging? The possibility is real; the science of gerontology proves it, and achieving an extended lifespan is easily attainable for you, your family, and your patients.
The problem with the study of aging is that researchers took a wrong turn many decades ago. That misdirection was driven by the irrefutable evidence that oxidative free-radical damage, or oxidative stress (OxS), causes tissues to age. Catabolic OxS causes both structural and functional breakdown over time. Researchers jumped to the “obvious” conclusion that OxS is the cause of aging and, hence, the process that shortens lifespan.
However, by the 1990s, so many inexplicable contradictions appeared in the “free radical theory of aging,” leaving researchers in a quandary. Over the past 15 years, gerontologists have righted their course.
Revelation began with the understanding that nearly all pathophysiology includes inflammation. The term “inflam-aging” stalled to appealin research literature. At first, this inflammatory character of aging seemed to corroborate OxS as the underlying cause of aging. Everyone from alternative healthcare providers to health food store shoppers bombarded every symptom and condition with a broad array of antioxidant supplements. The expected benefits were twofold —first, improvement of symptoms and, second, the promise of a long, healthy life.
The first expected benefit was occasionally met. The second? Never. Both animal and human studies show that antioxidant supplements protect tissue structure and function up to a certain age. At a point even younger than middle age, antioxidants’ protective effects begin to wane. Ultimately, a stage of life is reached when antioxidants become counterproductive (a heretical notion to antioxidant-peddling nutritionists!).
The Truth No One Wants to Hear
Finally, the “knife in the heart” of all true believers of the free radical theory of aging was the finding that antioxidant supplementation actually shortens lifespan.
What did gerontologists make of this uncomfortable but irrefutable truth? They can now demonstrate unequivocally that there are actually two separate metabolic pathways driving the aging process. One of those mechanisms detenuines what gerontology tenus “healthspan.” The other aging pathway also influences healthspan, but it exclusively detenuines lifespan.
If OxS is the mechanism driving the aging pathway that detenuines healthspan, what mechanism underlies the aging pathway that limits lifespan? The forces driving lifespan-limiting aging arise intracellularly. The mechanisms are predetermined by genetic metabolic clocks, i.e., clocks that operate almost independently of OxS aging mechanisms.
Free Radical Oxidative Aging versus Intracellular Aging.
We can model these parallel yet mostly autonomous pathways of inflam-aging. OxS is driven by exogenous stresses, including unhealthy microbiota, high-quantity, low-quality eating, and a broad array of toxic and emotional stresses.
In contrast, intracellular aging is driven by endogenous metabolic clocks and relates to unhealthy microbiota, senescent cell fonuation, deficient autophagy, and dysregulated apoptosis.
• OxS detenuines healthspan; intracellular aging determines lifespan.
• OxS aging begins (theoretically) at the moment of conception; intracellular aging starts on the 23 rd birthday.
• OxS aging is a catabolic process; intracellular aging is an anabolic process.
Yes, beginning at age 23, intracellular aging rapidly supplants OxS aging as the primary force driving inflam-aging. At that stage of life, antioxidant supplementation becomes less effective. By age 33, intracellular senescent cell fonuation, deficient autophagy, and dysregulated apoptosis dominate inflam-aging. We must acknowledge the painful truth that excessive supplementation with antioxidants actually accelerates aging-associated diseases, such as cardiovascular disease, and shortens lifespan by causing reductive stress and promoting the development of senescent cells.
What is so significant about age 23? It is the age when humans become fully developed physically, mentally, and emotionally. Anabolic processes that begin at conception are essential for full development, but at maturity, they turn abruptly from friend to foe. At maturity, metabolic clocks continue to drive select anabolic processes, which are now inappropriate. Intracellular inflam-aging as nonphysiological anabolism becomes more dominant in the deterioration of tissue structure and function.
Why do humans continue to exhibit nonproductive (and ultimately damaging) anabolism from maturity through old age? The objective of biological intelligence here is easily understood. The human species (like all mammals) has existed for many millennia in a natural environment where scarcity, hunger, and even starvation are common. Food deprivation led to catabolic stress, and the species needed a strong, easily activated anabolic drive to maintain tissue structure and function in the face of extreme catabolism.
Dr. Guy Schenker, a Pennsylvania Chiropractor since 1978, is the developer of the Nutri-Spec System of Clinical Nutrition, which eschews symptom-based nutrition in favor of individualized Metabolic Therapy. Nutri-Spec offers a Stage of Life Diphasic Nutrition Plan (SOLID DNP), empowering each patient to Live Stronger Longer Callus at 1-800-736-4320, email at [email protected] or visit www.nutri-spec.net.
Contemporary affluent society now suffers precisely the opposite metabolic stress — food availability in grotesquely abundant quantity and qualitatively addictive content. However, the anabolic drive continues unabated, and the consequence is age-related disease.
As shown in an exhaustive study by Kulkami, just a few drugs and nutrients show strong evidence for the extension of lifespan and the reduction of mortality in humans. Gerontologists call them “rejuvenins.”
Rejuvenins? If you are going to stay current in the field of clinical nutrition, you absolutely must make this tenn the focus of your clinical efforts. Rejuvenins block intracellular aging by three mechanisms:
• Rejuvenins inhibit the formation of senescent cells, or the cells that transform previously healthy cells into what can be considered “aging factories.” Then they replicate themselves, thus invading tissues throughout all organs of the body.
• Rejuvenins facilitate autophagy. Autophagy is the “detoxification” process by which cells eliminate metabolic waste, expel toxins, and protect DNA.
• Rejuvenins nonnalize apoptosis, or the healthy programmed death of cells. Rejuvenins approach apoptosis from both sides. First, they prevent the premature death of viable cells. Second, rejuvenins trigger the apoptosis of dysfunctional cells, preventing them from living past their healthy limit and replicating their damaged DNA.
Clinical Results
If you focus your clinical efforts on supplying patients with rejuvenins (and limit the use of potentially damaging antioxidants), you will give your patients the amazing life-extending benefits gerontologists have recently documented.
The list of rejuvenin nutrients is short, which allows you to give patients a concise and affordable yet powerful blend of supplements. These nutrients include:
• Camosine
• Alpha-lipoic acid
• Quercetin
• The combination of glycine plus N-acetylcysteine (but only in combination, since NAC is toxic when not combined with glycine)
• NAD (+) (but only in small quantities)
Consider the astounding clinical benefits shown by just one of the countless research studies on rejuvenins:
If you are familiar with the concept of inflam-aging, you are aware that it is measured by the presence of inflammatory markers, such as IL-6, TNF-alpha, and CRR Rejuvenin supplementation lowered IL-6 by 77%, TNF-alpha by 57%, and CRP by 49%, and it decreased insulin resistance by 59%. These results were achieved in older subjects, showing it is never too late to begin rejuvenin supplementation.
In summary, the life-extension benefits of rejuvenins far exceed even the wildest hopes of nutritionists who still hold firm belief in antioxidant supplementation. Gerontology gives us an exciting new paradigm of clinical nutrition.
References:
1. Le Couteur, D. G., & Barzilai, N. (2022). New horizons in life extension, healthspan extension and exceptional longevity. Age and Ageing, 57(8), afacl56. https://doi.org/l0,1093/ageing/afac 156
2. Tabibzadeh S. (2022). Resolving geroplasticity to the balance of rejuvenins and geriatrins. Aging and Disease, 13(6), 1664-1714. https://doi.org/10.14336/AD.2022.0414
3. Tabibzadeh S. (2021). From genoprotection to rejuvenation. Frontiers in Bioscience (Landmark edition), 26(1), 97-162. https://doi.org/10.2741/4890
4. Wu, T„ Tao, Y„ Tsang, F„ Abe, K„ Xu, L„ Jiang, Q„ Xu, L„ Fu, H„ & Fu, Z. (2015). The effect of L-camosine on the circadian resetting of clock genes in the heart of rats. Molecular Biology Reports, 42(1), 87-94. https://doi.org/10.1007/sllQ33-014-3745-x
5. Blagosklonny M. V. (2012). Prospective treatment of age-related diseases by slowing down aging. Die American Journal of Pathology, 181(4), 1142-1146. https://doi.org/10,1016/i,aipath.2012.06.
6. Blagosklonny M. V. (2021). The goal of geroscience is life extension. Oncotarget, 12(3), 131-144. https://doi.org/10.18632/oncotarget.27882
7. Labarrere, C. A., & Kassab, G. S. (2022). Glutathione: a Samsonian life-sustaining small molecule that protects against oxidative stress, ageing and damaging inflammation. Frontiers in Nutrition, 9, 1007816. https://doi.org/10.3389/fnut.2022.1007816
8. Kumar, R, Osahon, O. W., & Sekhar, R. V. (2022). GlyNAC (Glycine and N-Acetylcysteine) supplementation in mice Increases length of life by correcting glutathione deficiency, oxidative stress, mitochondrial dysfunction, abnormalities in mitophagy and nutrient sensing, and genomic damage. Nutrients, 14(5), 1114. https://doi.org/10.3390/nul4051114
9. McCarty M. F. (2015). Practical prospects for boosting hepatic production of the "pro-longevity” hormone FGF21. Hormone Molecular Biology and Clinical Investigation, 30(2), /j/hmbci.2017.30.issue-2/hmbci-2015-0057/hmbci-2015-0057.xml. https://doi.org/10.1515/hmbci-2015-0057
10. Luis, C., Maduro, A. T., Pereira, P, Mendes, J. J., Soares, R., & Ramalho, R. (2022). Nutritional senolytics and senomorphics: implications to immune cells metabolism and aging - from theory to practice. Frontiers in Nutrition, 9, 958563. https://doi.org/10.3389/fnut.2022.958563
11. Kulkami,A. S.,Aleksic, S., Berger, D. M., Sierra, F., Kuchel, G. A., & Barzilai, N. (2022). Geroscience-guided repurposing of FDA-approved drugs to target aging: A proposed process and prioritization. Aging Cell, 21(4), el3596. https://doi.org/10.llll/acel.13596
12. Justice, J. N., Ferrucci, L., Newman, A. B., Aroda, V. R., Bahnson, J. L., Divers, J., Espeland, M. A., Marcovina, S., Poliak, M. N., Kritchevsky, S. B., Barzilai, N., & Kuchel, G. A. (2018). A framework for selection of blood-based biomarkers for geroscience-guided clinical trials: report from the TAME Biomarkers Workgroup. GeroScience, 40(5-6), 419-436. https://doi.org/10.1007/sll357-018-0Q42-v
13. Poljsak, B., Kovac, V., Milisav, I. (2020) Healthy lifestyle recommendations: do the beneficial effects originate from NAD(+) amount at the cellular level? OxidMed Cell Longev, 2020: 2020: 8819627. https://doi.org/10.1155/2020/8819627
14. Kirkland, J. L., & Tchkonia, T. (2020). Senolytic drugs: from discovery to translation. Journal of Internal Medicine, 288(5), 518536. https://doi.org/10.llll/ioim.13141
15. Hickson, L. J., Langhi Prata, L. G. P, Bobart, S. A., Evans, T. K., Giorgadze, N., Hasluni, S. K., Hemnann, S. M., Jensen, M. D., Jia,
Q., Jordan, K. L., Kellogg, T. A., Khosla, S., Koerber, D. M., Lagnado, A. B., Lawson, D. K., LeBrasseur, N. K., Lennan, L. 0., McDonald, K. M., McKenzie, T. J., Passos, J. F., ... Kirkland, J. L. (2019). Senolytics decrease senescent cells in humans: preliminary report from a clinical trial of dasatinib plus quercetin in individuals with diabetic kidney disease. EBioMedicine, 47, 446-456. https:// doi.org/10.1016/i.ebiom.2019.08.069
16. Kumar, P, Liu, C., Hsu, J. W., Chacko, S., Minard, C., Jahoor, F., & Sekhar, R. V. (2021). Glycine and N-acetylcysteine (GlyNAC) supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, muscle strength, and cognition: Results of a pilot clinical trial. Clinical and Translational Medicine, 11(3), e372. https://doi.org/10.1002/ctm2.372
17. McCarty, M. F„ O'Keefe, J. H„ & DiNicolantonio, J. J. (2018). Dietary glycine is rate-limiting for glutathione synthesis and may have broad potential for health protection. The Ochsner Journal, 7S(1), 81-87.
18. Gems D. (2022). The hyperfunction theory: an emerging paradigm for the biology of aging. Ageing Research Reviews, 74, 1015 5 7. https: //doi.ora/10.1016/i. arr.2 021.1015 5 7
19. Bjelakovic, G., Nikolova, D., & Gluud, C. (2013). Meta-regression analyses, meta-analyses, and trial sequential analyses of the effects of supplementation with beta-carotene, vitamin A, and vitamin E singly or in different combinations on all-cause mortality: do we have evidence for lack of harm?. PloS one, 8(9), e74558. https://doi.org/10.1371/joumal.pone.0074558
20. Blagosklonny M. V. (2017). From rapalogs to anti-aging formula. Oncotarget, 8(22), 35492-35507. https://doi.org/10.18632/oncotarget.18033
21. Tallon, M. J., Harris, R. C., Maffulli, N., & Tamopolsky, M. A. (2007). Camosine, taurine, and enzyme activities of human skeletal muscle fibres from elderly subjects with osteoarthritis and young moderately active subjects. Biogerontology, 8(2), 129-137. https://doi.org/10.1007/slQ522-006-9038-6
22. Baek, S. H., Noh, A. R., Kim, K. A., Akram, M., Shin, Y. J., Kim, E. S., Yu, S. W., Majid, A., & Bae, O. N. (2014). Modulation of mitochondrial function and autophagy mediates camosine neuroprotection against ischemic brain damage. Stroke, 45(8), 2438-2443.
23. Hipkiss, A. R., Baye, E., & de Courten, B. (2016). Carnosine and the processes of ageing. Matnritas, 93, 28-33. https://doi.Org/10.1016/i.maturitas.2016.06.002
24. Levine, D. C., Hong, H., Weidemann, B. J., Ramsey, K. M., Affinati, A. H., Schmidt, M. S., Cedemaes, J., Omura, C., Braun, R., Lee, C., Brenner, C., Peek, C. B., & Bass, J. (2020). NAD+ controls circadian reprogramming through PER2 nuclear translocation to counter aging. Molecular Cell, 78(5), 835-849.e7. https://doi.Org/10.1016/i.molcel.2020.04.010