Stress and the inflammatory response: A review of neurogenic inflammation | Forum

related:

Psychological stress is a major provocative factor of symptoms in chronic inflammatory conditions. In recent years, interest in addressing stress responsivity through meditation training in health-related domains has increased astoundingly, despite a paucity of evidence that reported benefits are specific to meditation practice. We designed the present study to rigorously compare an 8-week Mindfulness-Based Stress Reduction (MBSR) intervention to a well-matched active control intervention, the Health Enhancement Program (HEP) in ability to reduce psychological stress and experimentally-induced inflammation. The Trier Social Stress Test (TSST) was used to induce psychological stress and inflammation was produced using topical application of capsaicin cream to forearm skin. Immune and endocrine measures of inflammation and stress were collected both before and after MBSR training. Results show those randomized to MBSR and HEP training had comparable post-training stress-evoked cortisol responses, as well as equivalent reductions in self-reported psychological distress and physical symptoms. However, MBSR training resulted in a significantly smaller post-stress inflammatory response compared to HEP, despite equivalent levels of stress hormones. These results suggest behavioral interventions designed to reduce emotional reactivity may be of therapeutic benefit in chronic inflammatory conditions. Moreover, mindfulness practice, in particular, may be more efficacious in symptom relief than the well-being promoting activities cultivated in the HEP program.

► Mindfulness training, compared to a well-matched control condition, is a better buffer of the effects of psychological stress on neurogenic inflammation.

https://www.sciencedirect.com/science/article/abs/pii/S0889159112004758

Dexamethasone treatment for the acute respiratory distress syndrome: a multicentre, randomised controlled trial

Published:February 07, 2020

"In summary, our findings suggest that the early administration of dexamethasone could reduce duration of mechanical ventilation and overall mortality in patients with established moderate-to-severe ARDS."

https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(19)30417-5/fulltext

"Propionic acid (PPA) and its related short-chain fatty acids (SCFAs) are fermentation products of ASD-associated bacteria (Clostridia, Bacteriodetes, Desulfovibrio). SCFAs represent a group of compounds derived from the host microbiome that are plausibly linked to ASDs and can induce widespread effects on gut, brain, and behavior. Intraventricular administration of PPA and SCFAs in rats induces abnormal motor movements, repetitive interests, electrographic changes, cognitive deficits, perseveration, and impaired social interactions. The brain tissue of PPA-treated rats shows a number of ASD-linked neurochemical changes, including innate neuroinflammation, increased oxidative stress, glutathione depletion, and altered phospholipid/acylcarnitine profiles. "

source:

Short-chain fatty acid fermentation products of the gut microbiome: implications in autism spectrum disorders

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3747729/

related discussion:

https://www.youtube.com/watch?v=CTLI4Z1sQig

Rath formula for virus protection.

Answering the ‘Cytokine Storm’

The advanced stage of a coronavirus infection is characterized by a mutual ‘escalation’ between the infective agent and the body’s defense system, a ‘biological battle’ that forms the basis of the inflammation. Advanced stages of coronavirus infections are characterized by excessive inflammation mediated by inflammatory cytokines. This includes an upregulation of IL-1, IL-6 and IL-10, TNF-alpha and many other cytokines, as well as an increased number of immune-competent white blood cells such as neutrophils, natural killer cells, T-helper cells and dendritic cells [Li G 2020, Chua 2020]. This intense biological communication to fight the infection has been described as a ‘cytokine storm’.

Since the number of ACE2 receptors expressed is associated with an increased inflammatory state, a decrease in the number of ACE2 proteins produced would also be associated with a decrease of inflammation. To test this connection, and to simulate the actual situation as it occurs during coronavirus infection, we stimulated lung epithelial cells with tumor necrosis factor alpha (TNF-alpha), the master regulator of the cytokine storm (Parameswaran 2010).

Our results show that in an inflammatory environment, i.e. in the presence of increased levels of TNF-alpha, micronutrients are even more effective and can lower the expression of the ACE2 receptor by more than 80% (Figure 2). Considering the fact that the ACE2 protein does not just determine the rate of viral entry into the cells but is also involved in the active secretion of inflammatory cytokines (Li G, 2020), thereby sustaining a pro-inflammatory environment, these results cannot be overestimated.

The micronutrient composition tested in this study is obviously capable of interrupting the vicious cycle between coronavirus infection -> increased ACE2 receptor expression/increased viral entry -> increased production of inflammatory cytokines -> still higher expression of ACE2 receptor -> advanced inflammation and so on (Figure 4).

We are not aware of any earlier description in the scientific literature of such a distinct effect of micronutrients on the cellular ‘entry doors’ of coronavirus, especially under inflammatory conditions. These results make specific micronutrient combinations prime candidates in interrupting the frequently fatal spiral between increasing coronavirus uptake and progressive inflammation.

Answering the ‘Free Radical Storm’

There is a close connection between infection, inflammation and the production of so-called ‘oxygen free radicals’. These are highly aggressive molecules used, among others, by activated white blood cells to attack and kill viruses and other pathogens. If an infection lasts too long due to a weak immune system, a chronically elevated ‘oxidative stress’ level can cause substantial damage to body tissue and further aggravate the infectious disease. Recently, details of this biological “crosstalk” between TNF-alpha and oxygen free radicals have been elucidated (Blaser 2016).

Oxidative stress has been proposed to be an aggravating factor during coronavirus infections (Potus 2020). This observation is supported by the fact that cigarette smoking (Smith 2020) as well as air pollution (Liang 2020) – both characterized by the exposure to high levels of oxygen free radicals – have been found to be associated with an increased risk for COVID-19. Significantly, smoking has also been found to increase the expression of ACE2 receptors in human lung tissue (Cai 2020), strongly indicating that this pro-oxidative effect can be counteracted by antioxidants.

Several ingredients of the micronutrient composition tested here, including ascorbic acid, green tea polyphenols (EGCG), N-acetylcysteine and quercetin, are powerful antioxidants.  These properties could be jointly responsible for the remarkable efficacy of the tested micronutrient composition reported here."

Full Article:

https://www.jcmnh.org/effective-and-safe-global-public-health-strategy-to-fight-the-covid-19-pandemic/

Quote from Admin

Dexamethasone treatment for the acute respiratory distress syndrome: a multicentre, randomised controlled trial

Published:February 07, 2020

"In summary, our findings suggest that the early administration of dexamethasone could reduce duration of mechanical ventilation and overall mortality in patients with established moderate-to-severe ARDS."

https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(19)30417-5/fulltext

https:///...desivir/5717718 ;

Chronology 

February 21: Initial Release pertaining to NIH-NIAID Remdesivir placebo test trial

April 10: The Gilead Sciences Inc study published in the NEJM on the “Compassionate Use of Remdesivir”

April 29: NIH Release: Study on Remdesivir (Report published on May 22 in NEJM)

May 22, The BWH-Harvard Study on Hydroxychloroquine coordinated by Dr. Mandeep Mehra published in The Lancet

May 22, Remdesivir for the Treatment of Covid-19 — Preliminary Report  National Institute of Allergy and Infectious Diseases, National Institutes of Health, New England Journal of Medicine, (NEJM) 

June 5:The (fake) Lancet Report (May 22) on HCQ is Retracted.

June 29, Fauci announcement. The $1.6 Billion Remdevisir HHS Agreement with Gilead Sciences Inc