Inflammaging: Treat the cause of your patients’ symptoms

Healthy aging. Does that sound intriguing? The science of medical gerontology reveals that aging processes can be controlled with very specific nutrition supplementation.

Would you seize the opportunity to limit the rate of aging degenerative changes? Or do you prefer allopathically treating age-related diseases as a distinctly separate entity? There is a huge difference in the two approaches. Essentially, we are asking would you rather treat the disease or treat the patient? Would you rather address the symptoms as they manifest or reach deeply into the core of the patho-physiology?

Age-related diseases

1. Musculoskeletal inflammation
2. Chronic fatigue
3. Elevated cholesterol and triglycerides
4. Type 2 diabetes
5. Arteriosclerosis
6. High blood pressure
7. Neurodegenerative diseases
8. Autoimmune diseases
9. Neuropathy
10. Muscular weakness
11. Osteoporosis
12. Cataracts

You easily recognize these as the conditions you see in your patients day in and day out. Are you seeking a “remedy” for each item on the list? Or does it make more sense to treat the underlying causes? The research clearly shows you have the capability of addressing each pathological process at the tissue level.^{1-3,9,10,14,17-19,20,23}

For decades, medical research pursued its quest for the ultimate; a Universal Theory of Disease, and more specifically, gerontologists dreamed of a Universal Theory of Aging. The scientific breakthrough occurred a couple of decades ago with the understanding that all age-related diseases have an inflammatory component. Gerontologists latched onto this central truth about 15 years ago and found the way this concept of inflammation manifests in the “diseases of aging.”^4,9,10,22,23

Furthermore, gerontology identified two somewhat autonomous aging pathways, each inflammatory in nature, but inflammatory by different mechanisms. The term “inflammaging” began to appear in the research literature.⁵

The good news for you is that the many and varied manifestations of age-related disease are the product of the combined effects of these two aging pathways. So, think about this. The 12 pathophysiologies listed above are as different as can be, yet they all share two fundamental age-accelerating processes. Consider two of your patients, one with a painful, unstable knee and one with elevated cholesterol. Who would think there is a connection between those two conditions? Yet, gerontologists now show us that the same two fundamental aging pathways drive both conditions.^{2,4,14,15,20,24,25}

Though age-related diseases may not fully manifest until your patients reach the age of 50 or more (although it is increasingly common to see the telltale signs in people in their 40s), their pathogenic basis has roots much earlier in life—even in childhood. Why does one patient show inflammaging in his knee, while another cannot seem to get her cholesterol under control? The concept here is easy to grasp. “Every chain breaks at its weakest link.” Whatever genetic predispositions an individual may have, plus whatever environmental stresses were encountered during gestation, during the birth process, during infancy or childhood or adolescence—predispose the immune system, the nervous system and the endocrine system to develop deficiencies in their adaptive capacity.^{5,10,18-20,22,24}

Does it surprise you to realize the “cause of the causes” of age-related disease is the process of aging itself?

What are these two aging pathways that define inflammaging? One is driven by oxidative stress, and the other reflects the damage from reductive stress. Table 1 provides a summary comparing the two:^{1-3,5-,11-13,16,21,22,25}

Final thoughts on healthy aging

Perhaps it is time to redefine yourself as a metabolic therapist. Gerontologists have identified combinations of both antioxidant supplements and what they now define as “rejuvenins” with the power to control age-accelerating cellular oxidation and reduction processes. It is these aging pathways that determine both the location (symptoms) and rate of inflammation in each of your patients. These supplements control the dual aging mechanisms with the ideal balance of antioxidant and anti-reductant supplements, allowing you to penetrate deeply into “the cause of the causes” of inflammaging.

GUY R. SCHENKER, DC, a Pennsylvania doctor of chiropractic 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. Schenker can be reached at 800-736-4320 or nutrispec@nutri-spec.net.

References

1. Baek SH, et al. Modulation of mitochondrial function and autophagy mediates carnosine neuroprotection against ischemic brain damage. Stroke. 2014;45(8):2438-2443. https://pubmed.ncbi.nlm.nih.gov/24938837/. Accessed January 27, 2025. 
2. Blagosklonny MV. Prospective treatment of age-related diseases by slowing down aging. Am J Pathol. 2012;181:1142–1146. https://pubmed.ncbi.nlm.nih.gov/22841821/. Accessed January 27, 2025. 
3. Blagosklonny MV. The goal of geroscience is life extension. Oncotarget. 2017:8:35492. https://pubmed.ncbi.nlm.nih.gov/33613842/. Accessed January 27, 2025. 
4. Chen LH, et al. Probiotic supplementation attenuates age-related sarcopenia via the gut-muscle axis in SAMP8MICE. J. Cachexia Sarcopenia Muscle. 2022;13(1):515-531. https://pubmed.ncbi.nlm.nih.gov/34766473/. Accessed January 27, 2025. 
5. Fulop T, et al. Immunology of aging: The birth of inflam-aging. Clin Rev Allergy Immunol. 2023;64(2):109-122. https://pubmed.ncbi.nlm.nih.gov/34536213/. Accessed January 27, 2025. 
6. Gems D. The hyperfunction theory: An emerging paradigm for the biology of aging. Ageing Res. Rev. 2022;74:101557. https://pubmed.ncbi.nlm.nih.gov/34990845/. Accessed January 27, 2025. 
7. Hickson LJ, et al. Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of dasatinib plus quercetin in individuals with diabetic kidney disease. E Bio Medicine. 2019;47:446–456. https://pubmed.ncbi.nlm.nih.gov/31542391/. Accessed January 27, 2025. 
8. Hipkiss AR, et al. Carnosine and the processes of aging. Maturitas. 2016;93:28-33. https://pubmed.ncbi.nlm.nih.gov/27344459/. Accessed January 27, 2025. 
9. Ho Jen-Yu, et al. L-carnitine supplementation favorably affects biochemical markers of recovery from physical exertion in middle-aged men and women. Metabolism. 2010;59(8):1190-9. https://pubmed.ncbi.nlm.nih.gov/20045157/. Accessed January 27, 2025. 
10. Justice JN, et al. A framework for selection of blood-based biomarkers for geroscience-guided clinical trials: Report from the TAME biomarkers workgroup. Geroscience. 2018;40:419–436. https://pubmed.ncbi.nlm.nih.gov/30151729/. Accessed January 27, 2025.
11. Kumar P, et al. Supplementing glycine and n-acetyl-cysteine (glynac) in older adults improves glutathione inefficiency, oxidative stress, mitochondrial dysfunction, inflammation, physical function, and aging hallmarks; A randomized clinical trial. J Gerontol A Biol Sci Med Sci. 2023;78(1):75-89. https://pubmed.ncbi.nlm.nih.gov/35975308/. Accessed January 27, 2025. 
12. Kulkarni AS, et al. Geroscience-guided repurposing of FDA-approved drugs to target aging: A proposed process and prioritization. Aging Cell. 2022;21(4):e13596. https://pubmed.ncbi.nlm.nih.gov/35343051/. Accessed January 27, 2025. 
13. Labarrere, CA. Glutathione: A Samsonian life-sustaining small molecule that protects against oxidative stress, aging and damaging inflammation. Front. Nutr. 2022;9:1007816. https://pubmed.ncbi.nlm.nih.gov/36386929/. Accessed January 27, 2025. 
14. Le Couteur DG, Barzilai N. New horizons in life extension, healthspan extension and exceptional longevity. Age Ageing. 2022;51(8):156. https://pubmed.ncbi.nlm.nih.gov/35932241/. Accessed January 27, 2025. 
15. Levine DC, et al. NAD+ controls circadian reprogramming through PER2 nuclear translocation to counter aging. Mol Cell. 2020;78(5):835-849. https://pubmed.ncbi.nlm.nih.gov/32369735/. Accessed January 27, 2025. 
16. Luís C, et al. Nutritional senolytics and senomorphics: Implications to immune cells metabolism and aging—from theory to practice. Front. Nutr. 2022;9:958563. https://pubmed.ncbi.nlm.nih.gov/36159455/. Accessed January 27, 2025. 
17. McCarty MF. Practical prospects for boosting hepatic production of the “pro-longevity” hormone FGF 21. Hormone Molecular Biology and Clinical Investigation. 2015;30(2). https://pubmed.ncbi.nlm.nih.gov/26741352/. Accessed January 27, 2025. 
18. Poljsak B, et al. Healthy lifestyle recommendations: Do the beneficial effects originate from NAD(+) amount at the cellular level? Oxid Med Cell Longev.  2020;2020:8819627. https://pubmed.ncbi.nlm.nih.gov/33414897/. Accessed January 27, 2025.  
19. Sekhar RV. GlyNAC supplementation improves glutathione deficiency, oxidative stress, mitochondrial disfunction, inflammation, aging hallmarks, metabolic defects, muscle strength, cognitive decline and body composition: Implication for healthy aging. J Nutr. 2021;151(12):3606-3616. https://pubmed.ncbi.nlm.nih.gov/34587244/. Accessed January 27, 2025.  
20. Sekhar RV. Glycine and n-acetylcysteine (GlyNAC) supplementation improves impaired mitochondrial fuel oxidation and lowers insulin resistance in patients with type 2 diabetes: Results of a pilot study. Antioxidants (Basel). 2022;11(1):154. https://pubmed.ncbi.nlm.nih.gov/35052658/. Accessed January 27, 2025.  
21. Siamak T. Resolving geroplasticity to the balance of rejuvenins and geriatrics. Aging Dis. 2022;13(6):1664-1714. https://pubmed.ncbi.nlm.nih.gov/36465174/. Accessed January 27, 2025.  
22. Tabibzadeh S. From genoprotection to rejuvenation. Front Biosci. 2021;26:97-162. https://pubmed.ncbi.nlm.nih.gov/33049666/. Accessed January 27, 2025.  
23. Tallon MJ, et al. Carnosine, taurine and enzyme activities of human skeletal muscle fibres from elderly subjects with osteoarthritis and young moderately active subjects. Bio Gerontology. 2007;8(2):129-137. https://pubmed.ncbi.nlm.nih.gov/16967207/. Accessed January 27, 2025.  
24. Wick G, et al. Diseases of aging. Vaccine. 2000;18(16);1567-83. https://www.sciencedirect.com/science/article/abs/pii/S0264410X99004892. Accessed January 27, 2025. 
25. Wu T, et al. The effect of L-carnosine on the circadian resetting of clock genes in the heart of rats. Mol Biol Rep. 2015;42(1):87-94. https://pubmed.ncbi.nlm.nih.gov/25258119/. Accessed January 27, 2025.