Intermittent fasting reduces aging; and systemic sclerosis! See commentary and article below.
If systemic sclerosis is both autoimmune and innate immunity related and the macrophage is the bridge between the two systems, INCREASING the macrophage's ability to phagocytosis or eat and destroy superfluous inflammatory inciters in their cytoplasm would regulate or re-regulate the inflammation of both systems!
Aging also degrades macrophage through reduced AUTOPHAGY leading to reduced protective function and increased degenerative function.
One activity known to increase phagocytosis is INTERMITTENT FASTING or fasting once a week for 23-24 hours. Restricting carbohydrate and protein, but not fat, is required because the action of gene switching follows lowering of insulin and insulin growth factor 1. I have performed weekly fasting for over 2 years. On fasting days I substitute modified bulletproof coffee (containing coconut oil) i.e. coffee without glucose or protein, (stevia, heavy cream and 30 mls of MCT or coconut oil) for the 2 missed meals and snacks. This provides beta hydroxybutyrate for brain energy needs that supplements stored glucose release from the liver. This brief fasting turns on genes of longevity and regeneration, increases helper proteins called chaperones to correct misfolded proteins such as enzymes and lastly takes any superfluous trash or misfolded proteins and loose mRNA and recycles them through PHAGOCYTOSIS into usable elements that are harmless and not able to incite the inflamasome and degrade the macrophage cell purpose.
Increased PHAGOCYTOSIS is the opposite of reduced AUTOPHAGY ; improvement preserves the function of macrophages despite age, disease or disorder. See abstract below.
Innate immune system involves toll like receptors and the inflamasome and is generally considered a form of individual cell immunity. Adaptive immunity is the immune system to protect the organism such as antibodies and cellular immunity of macrophages and T lymphocytes.
Tony Liverman
Abstract
Macrophages provide a bridge linking innate and adaptive immunity. An increased frequency of macrophages and other myeloid cells paired with excessive cytokine production is commonly seen in the aging immune system, known as ‘inflamm-aging'. It is presently unclear how healthy macrophages are maintained throughout life and what connects inflammation with myeloid dysfunction during aging. Autophagy, an intracellular degradation mechanism, has known links with aging and lifespan extension. Here, we show for the first time that autophagy regulates the acquisition of major aging features in macrophages. In the absence of the essential autophagy gene Atg7, macrophage populations are increased and key functions such as phagocytosis and nitrite burst are reduced, while the inflammatory cytokine response is significantly increased - a phenotype also observed in aged macrophages. Furthermore, reduced autophagy decreases surface antigen expression and skews macrophage metabolism toward glycolysis. We show that macrophages from aged mice exhibit significantly reduced autophagic flux compared to young mice. These data demonstrate that autophagy plays a critical role in the maintenance of macrophage homeostasis and function, regulating inflammation and metabolism and thereby preventing immunosenescence. Thus, autophagy modulation may prevent excess inflammation and preserve macrophage function during aging, improving immune responses and reducing the morbidity and mortality associated with inflamm-aging.© 2015 S. Karger AG, Basel
Article / Publication Details
Received: 6/13/2014 8:13:00 PM
Accepted: 11/25/2014
Published online: 3/10/2015
Issue release date: June 2015
Number of Print Pages: 17
Number of Figures: 6
Number of Tables: 2
ISSN: 1662-811X (Print)
eISSN: 1662-8128 (Online)
For additional information: http://www.karger.com/JIN
Accepted: 11/25/2014
Published online: 3/10/2015
Issue release date: June 2015
Number of Print Pages: 17
Number of Figures: 6
Number of Tables: 2
ISSN: 1662-811X (Print)
eISSN: 1662-8128 (Online)
For additional information: http://www.karger.com/JIN
Open Access License / Drug Dosage / Disclaimer
Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution 3.0 Unported license (CC BY 3.0) (www.karger.com/OA-license-WT), applicable to the online version of the article only.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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