Reversing Or Preventing Fibrosis ?

[Motif]

People claim scalp fibrosis can get massaged away, so - does this work for fibrosis in organs too? Kidneys? Liver?

Anything really known that helps this, not just assumed ?

 

[Inaut]

Taurine?

 

[Alpha]

Cyproheptadine is the only one I know that prevents fibrosis. Maybe aspirin and eNOS inducers.

 

[lampofred]

I don't know about massaging fibrosis away, but I think high gelatin consumption along with high CO2 levels due to good thyroid function will help to reverse fibrosis.

 

[YourUniverse]

vitamin E

 

[Motif]

Does improved bloodflow help to prevent or reverse fibrosis?

 

[yerrag]

Does improved bloodflow help to prevent or reverse fibrosis?

I think it's more the case that reversing fibrosis would improve blood flow.

I agree with @lampofred on CO2 being helpful with fibrosis. I'll add proteolytic enzymes as well as fasting, so the matrix can be broken down and used for energy, being a superfluous structure.

 

[GorillaHead]

How safe is it to use .5mg if cypro everyday for a long term?

 

[Lizb]

Does improved bloodflow help to prevent or reverse fibrosis?

Co2 thins the blood. So maybe just a thinner blood makes its way easier.

 

[Motif]

Does improved bloodflow help to prevent or reverse fibrosis?

Yeah but does bloodflow, let’s say from a vibration plate, help with fibrosis?

 

[rob]

People claim scalp fibrosis can get massaged away, so - does this work for fibrosis in organs too? Kidneys? Liver?

Anything really known that helps this, not just assumed ?

The best characterised mediator of fibrosis is TGF beta and the related R-SMAD signalling cascade.

I know a few on here are pretty anti-sirtuins but I think SIRT1 activation warrants a discussion. Whilst known to deacetylate SMAD7, an inhibitor of this R-SMAD signalling, studies seem to be suggestive of a largely protective role of SIRT1 against fibrosis.

SIRT1 deaceylates SMAD3 lysine residues suppressing pro-fibrotic transcriptional activty. Also, interestingly, unlike SMAD3, it seems SMAD2 requires additional factors to influence DNA and recruitment of SIRT1 has been evidenced in this regard. Indeed, SIRT1 may play a regulatory role with overexpression noted to suppress a Smad2-driven TGFβ-dependent reporter gene.

Indeed, such effects from not just SIRT1 but possibly other sirtuins as well are in line with the following NAD-precursor study using nicotinamide riboside: Nicotinamide riboside protects against liver fibrosis induced by CCl4 via regulating the acetylation of Smads signaling pathway. - PubMed - NCBI.

Also, picking up on recent discussion, Vitamin D may also play a role.

There seems to be significant crosstalk between VDR and SIRT1 signalling with both seemingly potentiating the other. Also, SMAD activation seems to increase vitamin D (VDR) response element accessibility. This enables liganded-VDR to significantly antagonise SMAD effects on chromatin, thus, reducing acetylation and quietening pro-fibrotic gene expression.

 

[GorillaHead]

The best characterised mediator of fibrosis is TGF beta and the related R-SMAD signalling cascade.

I know a few on here are pretty anti-sirtuins but I think SIRT1 activation warrants a discussion. Whilst known to deacetylate SMAD7, an inhibitor of this R-SMAD signalling, studies seem to be suggestive of a largely protective role of SIRT1 against fibrosis.

SIRT1 deaceylates SMAD3 lysine residues suppressing pro-fibrotic transcriptional activty. Also, interestingly, unlike SMAD3, it seems SMAD2 requires additional factors to influence DNA and recruitment of SIRT1 has been evidenced in this regard. Indeed, SIRT1 may play a regulatory role with overexpression noted to suppress a Smad2-driven TGFβ-dependent reporter gene.

Indeed, such effects from not just SIRT1 but possibly other sirtuins as well are in line with the following NAD-precursor study using nicotinamide riboside: Nicotinamide riboside protects against liver fibrosis induced by CCl4 via regulating the acetylation of Smads signaling pathway. - PubMed - NCBI.

Also, picking up on recent discussion, Vitamin D may also play a role.

There seems to be significant crosstalk between VDR and SIRT1 signalling with both seemingly potentiating the other. Also, SMAD activation seems to increase vitamin D (VDR) response element accessibility. This enables liganded-VDR to significantly antagonise SMAD effects on chromatin, thus, reducing acetylation and quietening pro-fibrotic gene expression.

So sirt1 inducers and vitamin D sounds like a good combo ?

 

[rob]

So sirt1 inducers and vitamin D sounds like a good combo ?

Well, there's a biochemical rationale here, so it's worth considering at least. Likewise, I should have mentioned Nrf2 signalling as that mediates important TGF-beta inhibiting effects and, again, there's crosstalk with VDR and SIRT1 as well as PPAR gamma, which also seems to be a very protective factor.

However, on vitamin D, one caveat, I did come across a study on lung fibrosis (Detrimental pro-senescence effects of vitamin D on lung fibrosis) that, whilst acknowledging the body of studies showing vitamin D to be protective against fibrosis in various tissues, demonstrated a deleterious effect. So, as ever, it's not 100% clear on all fronts.

Also, there are reservations to had around some commonly touted SIRT1-activating compounds, so it's worth evaluating things on a case-by-case basis.

 

[GorillaHead]

Well, there's a biochemical rationale here, so it's worth considering at least. Likewise, I should have mentioned Nrf2 signalling as that mediates important TGF-beta inhibiting effects and, again, there's crosstalk with VDR and SIRT1 as well as PPAR gamma, which also seems to be a very protective factor.

However, on vitamin D, one caveat, I did come across a study on lung fibrosis (Detrimental pro-senescence effects of vitamin D on lung fibrosis) that, whilst acknowledging the body of studies showing vitamin D to be protective against fibrosis in various tissues, demonstrated a deleterious effect. So, as ever, it's not 100% clear on all fronts.

Also, there are reservations to had around some commonly touted SIRT1-activating compounds, so it's worth evaluating things on a case-by-case basis.

i take berberine once a day. Sirt1 inducer. Apigenin twice a day nrf2 inducer and 3000 ius of Vitamin D.

 

[Inaut]

If you don’t have a problem with oxalates, I think dried parsley is the way to go for apigenin content and fibrosis. Cheap cheap cheap

 

[rob]

i take berberine once a day. Sirt1 inducer. Apigenin twice a day nrf2 inducer and 3000 ius of Vitamin D.

Just worth noting the possible VDR inhibiting effects of apigenin: The Flavonoid Apigenin Suppresses Vitamin D Receptor Expression and Vitamin D Responsiveness in Normal Human Keratinocytes - ScienceDirect.

 

[Kvothe]

How safe is it to use .5mg if cypro everyday for a long term?

I have been using 4mg for over a year, and have experienced no side effects. No signs of any liver damage or other elevated blood markers. Nothing but positive results.

If you don’t have a problem with oxalates, I think dried parsley is the way to go for apigenin content and fibrosis. Cheap cheap cheap

Celery roots are another good source of it, and you can cook a lot of it to make delecious soups.

 

[GorillaHead]

@rob thanks for all you do rob! Such great work.

imagine s forum full of Robs. We would cure so many things

 

[Giraffe]

Anything really known that helps this, not just assumed ?

Emodin.

 

[yerrag]

I think fibrosis is just the body's adaptation to an immediate threat on itself that would have been more problematic if it were not dealt with by the body's adaptation.

So the solution would be to extinguish that threat. If one were successful in getting rid of the fibrosis without removing its cause, the fibrosis would just come back later on. It's futile to get relief only temporarily.