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Adrenaline Suppresses The Immune System And Promotes Viral Infections

milkboi

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Joined
Sep 25, 2018
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1,615
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Germany
Yes, but it would be best to test copper levels first just to be sure.

Aight. I have begun taking 2mg copper a couple of days ago and I notice good effects in terms of energy levels, so I‘ll keep taking that in the morning and 10-15 mg of zinc in the evening.
 

S.Seneff

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Joined
Mar 18, 2020
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172
Efficient T cell responses require the firm adhesion of T cells to their targets, e.g., virus-infected cells, which depends on T cell receptor (TCR)–mediated activation of β2-integrins. Gαs-coupled receptor agonists are known to have immunosuppressive effects, but their impact on TCR-mediated integrin activation is unknown. Using multimers of peptide major histocompatibility complex molecules (pMHC) and of ICAM-1—the ligand of β2-integrins—we show that the Gαs-coupled receptor agonists isoproterenol, epinephrine, norepinephrine, prostaglandin (PG) E2, PGD2, and adenosine strongly inhibit integrin activation on human CMV- and EBV-specific CD8+ T cells in a dose-dependent manner. In contrast, sleep, a natural condition of low levels of Gαs-coupled receptor agonists, up-regulates integrin activation compared with nocturnal wakefulness, a mechanism possibly underlying some of the immune-supportive effects of sleep. The findings are also relevant for several pathologies associated with increased levels of Gαs-coupled receptor agonists (e.g., tumor growth, malaria, hypoxia, stress, and sleep disturbances).
Gαs-coupled receptor signaling and sleep regulate integrin activation of human antigen-specific T cells | Journal of Experimental Medicine | Rockefeller University Press
 

Light

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Oct 5, 2018
Messages
304
The timing of this study just could not have been better considering the current coronavirus epidemic. The study below demonstrates that both adrenaline and noradrenaline suppressed the immune system and both increases vulnerability to viral infection as well as increasing mortality after the infection takes hold. Conversely, blocking the adrenergic receptors increased survival rates by more than 40% even when the animals were inoculated with lethal amounts of a viral load. The official explantion of the study is that adrenaline/noradrenaline increase inflammatory signalling through activation of the beta-adrenergic receptors and this results in suboptimal immune system response. However, I think the much more likely explanation is the increased lipolysis as a result of activated adrenergic system. The role of elevated NEFA/FFA in vulnerability to infections and subsequent death from sepsis and/or cardiac/ischemic events is well-established.

In terms of treatments, aside from the obvious choice of beta blockers I think aspirin and niacinamide would be good options too considering their inhibitory effects on lipolysis. And of course, good old salt is perhaps the most widely accessible option. Interestingly enough, increased dietary salt intake has already been demonstrated to have a strong immune-boosting effect.

β2-adrenergic signals downregulate the innate immune response and reduce host resistance to viral infection | Journal of Experimental Medicine | Rockefeller University Press

"...In humans, psychological stress has been associated with a higher risk of infectious illness. However, the mechanisms by which the stress pathway interferes with host response to pathogens remain unclear. We demonstrate here a role for the β2-adrenergic receptor (β2-AR), which binds the stress mediators adrenaline and noradrenaline, in modulating host response to mouse cytomegalovirus (MCMV) infection. Mice treated with a β2-AR agonist were more susceptible to MCMV infection. By contrast, β2-AR deficiency resulted in a better clearance of the virus, less tissue damage, and greater resistance to MCMV. Mechanistically, we found a correlation between higher levels of IFN-γ production by liver natural killer (NK) cells and stronger resistance to MCMV. However, the control of NK cell IFN-γ production was not cell intrinsic, revealing a cell-extrinsic downregulation of the antiviral NK cell response by adrenergic neuroendocrine signals. This pathway reduces host immune defense, suggesting that the blockade of the β2-AR signaling could be used to increase resistance to infectious diseases."
Does any of the "peaty" substances function as a beta-blocker?
@haidut
 

Epik

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Joined
Apr 26, 2020
Messages
86
Location
Canada
Wouldn't high adrenaline promote NO and thus, to some degree and temporarily, protect against viruses?
 
Joined
Apr 25, 2018
Messages
441
The timing of this study just could not have been better considering the current coronavirus epidemic. The study below demonstrates that both adrenaline and noradrenaline suppressed the immune system and both increases vulnerability to viral infection as well as increasing mortality after the infection takes hold. Conversely, blocking the adrenergic receptors increased survival rates by more than 40% even when the animals were inoculated with lethal amounts of a viral load. The official explantion of the study is that adrenaline/noradrenaline increase inflammatory signalling through activation of the beta-adrenergic receptors and this results in suboptimal immune system response. However, I think the much more likely explanation is the increased lipolysis as a result of activated adrenergic system. The role of elevated NEFA/FFA in vulnerability to infections and subsequent death from sepsis and/or cardiac/ischemic events is well-established.

In terms of treatments, aside from the obvious choice of beta blockers I think aspirin and niacinamide would be good options too considering their inhibitory effects on lipolysis. And of course, good old salt is perhaps the most widely accessible option. Interestingly enough, increased dietary salt intake has already been demonstrated to have a strong immune-boosting effect.

β2-adrenergic signals downregulate the innate immune response and reduce host resistance to viral infection | Journal of Experimental Medicine | Rockefeller University Press

"...In humans, psychological stress has been associated with a higher risk of infectious illness. However, the mechanisms by which the stress pathway interferes with host response to pathogens remain unclear. We demonstrate here a role for the β2-adrenergic receptor (β2-AR), which binds the stress mediators adrenaline and noradrenaline, in modulating host response to mouse cytomegalovirus (MCMV) infection. Mice treated with a β2-AR agonist were more susceptible to MCMV infection. By contrast, β2-AR deficiency resulted in a better clearance of the virus, less tissue damage, and greater resistance to MCMV. Mechanistically, we found a correlation between higher levels of IFN-γ production by liver natural killer (NK) cells and stronger resistance to MCMV. However, the control of NK cell IFN-γ production was not cell intrinsic, revealing a cell-extrinsic downregulation of the antiviral NK cell response by adrenergic neuroendocrine signals. This pathway reduces host immune defense, suggesting that the blockade of the β2-AR signaling could be used to increase resistance to infectious diseases."
What do you think about Wellbutrin it activates dopamine but also activates noradrenaline
 

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