Anti-inflammatory Action of Green Tea

[Violeta]

https://pubmed.ncbi.nlm.nih.gov/27634207/

Tomokazu Ohishi, Shingo Goto, Pervin Monira, Mamoru Isemura 1, Yoriyuki Nakamura
2016

Most of the results from the human studies indicated the beneficial effects of green tea and tea catechins against inflammatory diseases. The cellular and animal studies also provided evidence for the favorable effects of green tea/EGCG. These results are compatible with our previous findings and can be largely explained by a mechanism wherein green tea/EGCG acts as an antioxidant to scavenge reactive oxygen species, leading to attenuation of nuclear factor-κB activity.

Indicative of being helpful for skeletal muscle atrophy!

Nuclear Factor-kappa B Signaling in Skeletal Muscle Atrophy​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597184/

Recent studies employing genetic mouse models have provided strong evidence that NF-κB can serve as an important molecular target for the prevention of skeletal muscle loss. In this article, we have outlined the current understanding regarding the role of NF-κB in skeletal muscle with particular reference to different models of muscle-wasting and the development of novel therapy.

 

[Violeta]

Most of the results from the human studies indicated the beneficial effects of green tea and tea catechins against inflammatory diseases. The cellular and animal studies also provided evidence for the favorable effects of green tea/EGCG. These results are compatible with our previous findings and can be largely explained by a mechanism wherein green tea/EGCG acts as an antioxidant to scavenge reactive oxygen species, leading to attenuation of nuclear factor-κB activity.

This visual is enlightening.

 

[Violeta]

A Review of the Role of Green Tea (Camellia sinensis) in Antiphotoaging, Stress Resistance, Neuroprotection, and Autophagy​

https://pubmed.ncbi.nlm.nih.gov/30813433/

Several in vivo and in vitro studies suggest that green tea supplementation increases the collagen and elastin fiber content, and suppresses collagen degrading enzyme MMP-3 production in the skin, conferring an anti-wrinkle effect.

Its ROS scavenging activity makes it a potent stress mediator, as it can also regulate the stress induced by metal ions.

It is known that tea polyphenols can induce the expression of different antioxidant enzymes and hinder the DNA oxidative damage.

Growing evidence suggests that green tea can also be used as a potential agent to mediate neurodegenerative diseases, including Alzheimer's disease.

EGCG, an abundant catechin in tea, was found to suppress the neurotoxicity induced by Aβ as it activates glycogen synthase kinase-3β (GSK-3β), along with inhibiting c-Abl/FE65-the cytoplasmic nonreceptor tyrosine kinase which is involved in the development of the nervous system and in nuclear translocation.

🍵🫖

 

[Wishful]

Inflammation isn't a bad thing in all circumstances. It's an important body function, killing invading microbes and cleaning up damage. It seems logical that anti-inflammatories would extend an infection or slow healing by interfering with the body's defensive mechanism. There are situations where anti-inflammatories are helpful, where excessive inflammation would create pressure or other harm, but I expect that they are misapplied--and pushed by marketers--to situations where they shouldn't be applied.

 

[Violeta]

Inflammation isn't a bad thing in all circumstances. It's an important body function, killing invading microbes and cleaning up damage. It seems logical that anti-inflammatories would extend an infection or slow healing by interfering with the body's defensive mechanism. There are situations where anti-inflammatories are helpful, where excessive inflammation would create pressure or other harm, but I expect that they are misapplied--and pushed by marketers--to situations where they shouldn't be applied.

That study was not written by marketers.

Neuroinflammation and Cytokines in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Critical Review of Research Methods​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335565/#:~:text=The name “myalgic encephalomyelitis” essentially,neuroinflammation, from periphery to brain.

 

[Wishful]

From that study: "circulating cytokine levels are often a poor measure for subjective symptoms and often do not reflect what is happening on the brain side of the BBB".

"A large neuroimmunology literature consistently concludes that cytokines do not have to be detectable in the periphery in order to have an effect on sickness-related symptoms. "

"Therefore, a peripheral cytokine profile may not be meaningful in informing any existing central nervous system cytokine profile."

Green tea might reduce those circulating cytokines, but that reduction might not affect the brain. The effect of cytokines on the brain might be non-linear: 10 molecules might trigger a full response from glial cells, so reducing the number reaching the brain from 500 to 300 or even 30 won't change the response.


"Despite the limited value of measuring blood cytokine levels in understanding pathophysiology and neuroinflammation, blood cytokine levels are used as a dependent variable in many ME/CFS studies, probably due to ease of collection." Again with the "looking under the streetlight because it's easier". Why don't fund decision-makers learn that lesson?

Most of the results from the human studies indicated the beneficial effects of green tea and tea catechins against inflammatory diseases.

The latter study implies that ME is not a standard inflammatory disease. ME might be an abnormal response to standard inflammation in the body. ME might be unrelated to inflammation, but might generate certain symptoms or increase severity due to an abnormal response to standard inflammation. For example, we might have a baseline level of brainfog from ME without any standard inflammation, but that level increases when there is some inflammation.

I do appreciate that critical review of ME research methods. That should be read by the people who are distributing funding for ME research.

 

[Violeta]

Increased nuclear factor-κB and loss of p53 are key mechanisms in Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS)​

https://pubmed.ncbi.nlm.nih.gov/22951418/

ME/CFS is considered to be a neuro-immune disease. ME/CFS is characterized by activated immuno-inflammatory pathways, including increased levels of pro-inflammatory cytokines, nuclear factor κB (NF-κB) and aberrations in mitochondrial functions, including lowered ATP.

These processes may explain typical symptoms of ME/CFS, e.g. fatigue, malaise, hyperalgesia, and neurologic and autonomic symptoms.

Here we hypothesize that increased NF-κB together with a loss of p53 are key phenomena in ME/CFS that further explain ME/CFS symptoms, such as fatigue and neurocognitive dysfunction, and explain ME symptoms, such as post-exertional malaise following mental and physical activities.

(The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood.)

 

[Violeta]

Here we hypothesize that increased NF-κB together with a loss of p53 are key phenomena in ME/CFS

Green Tea (Camellia sinensis) Extract Induces p53-Mediated Cytotoxicity and Inhibits Migration of Breast Cancer Cells​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8701076/

An increment in p53 and p21 expression stimulated by green tea extract!

Wow, you learn something new every day!

 

[Byles]

Will these things also go for decafinated green tea? I enjoy a green tea occasionally and when I need the boost, but can't handle the caffeine all the time.

 

[Wishful]

Increased nuclear factor-κB and loss of p53 are key mechanisms in Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS)

Grossly misleading title. The abstract says that it's a hypothesis that may explain symptoms. The paper certainly doesn't prove that those factors are key mechanisms. It's a hypothesis that deserves testing--and should follow the suggestions of that critical review of research methods.

 

[Violeta]

Will these things also go for decafinated green tea? I enjoy a green tea occasionally and when I need the boost, but can't handle the caffeine all the time.

Yes, decaf will have the same antioxidants.

 

[pattismith]

Green tea is great, but it also greatly decreases iron absorption, not good thing for everybody...

 

[Violeta]

Epstein–Barr Virus Infection Is Associated with Elevated Hepcidin Levels​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9862144/

We found that children IgG positive to EBV antigens (VCA, EBNA1, and EA) presented hepcidin, AGP, and CRP levels higher than uninfected children. Hepcidin and AGP remained high in children solely infected with EBV, while CRP was only significantly high in coinfected children. We observed positive correlations between hepcidin and EBV IgG antibodies.

Green tea activity and iron overload induced molecular fibrogenesis of rat liver​

https://pubmed.ncbi.nlm.nih.gov/30899168/

Iron overload toxicity was shown to associate with chronic liver diseases which lead to hepatic fibrosis and subsequently the progression to cancer through oxidative stress and apoptotic pathways. Green tea potential activity as chelating, anti-oxidative, or anti-apoptotic mechanisms against metal toxicity was poorly clarified.

Here, we are trying to evaluate the anti-oxidant and anti-apoptotic properties of green tea in the regulation of serum hepcidin levels, reduction in iron overloads, and improve of liver fibrosis in iron overloaded experimental rats

Viruses depend on iron to replicate in their host cells given that iron is essential for fundamental cellular processes, such as ATP and nucleic acids synthesis, and certain steps of the replication cycle of some viruses can be iron-dependent or iron-regulated.

 

[Violeta]

Green tea is great, but it also greatly decreases iron absorption, not good thing for everybody...

I wonder if drinking it away from food or at least away from food or supplements that contains iron would solve that issue.

 

[Violeta]

Increased nuclear factor-κB and loss of p53 are key mechanisms in Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS)​

https://pubmed.ncbi.nlm.nih.gov/22951418/

ME/CFS is considered to be a neuro-immune disease. ME/CFS is characterized by activated immuno-inflammatory pathways, including increased levels of pro-inflammatory cytokines, nuclear factor κB (NF-κB) and aberrations in mitochondrial functions, including lowered ATP.

These processes may explain typical symptoms of ME/CFS, e.g. fatigue, malaise, hyperalgesia, and neurologic and autonomic symptoms.

Here we hypothesize that increased NF-κB together with a loss of p53 are key phenomena in ME/CFS that further explain ME/CFS symptoms, such as fatigue and neurocognitive dysfunction, and explain ME symptoms, such as post-exertional malaise following mental and physical activities.

(The p53 gene like the Rb gene, is a tumor suppressor gene, i.e., its activity stops the formation of tumors. If a person inherits only one functional copy of the p53 gene from their parents, they are predisposed to cancer and usually develop several independent tumors in a variety of tissues in early adulthood.

SARS-CoV-2 spike protein mediates host cell infection and cell-cell fusion that causes stabilization of tumor suppressor p53 protein.

SARS-CoV-2 spike S2 subunit inhibits p53 activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2 proteins in cancer cells​

https://www.biorxiv.org/content/10.1101/2024.04.12.589252v1