POIS and Liver Detoxification

[b_jim]

Started 3 days ago. Yesterday and today I have strong gastritis symptoms.
Coincidence?
If I don't feel better tomorow I stop rosmarinus/artishoke caps and I go back to the doctor :/

[berlin1984]

My hepatic insufficiency was there since birth, it was not caused by POIS.  It is probably the other way around - my sluggish liver was contributing to the severity of my POIS.
As I said, I will receive in about a month or two, my genome results.  That will help determine to what extent my detox enzymes are affected by unfavourable genetics  ( most detox enzymes are found in the liver ).  I never had extensive blood work for liver status, just usual liver enzymes, and they were normal - having a slow liver is not the same as an acute episode of intoxication, it does not show in high AST or ALT.  Maybe my bilirubin could have, at the time, been a little higher than normal, and more extensive tests could have clearly shown that my liver was below average for efficiency.

Just curious if you got anything out of your full genome analysis with that regard..

[Prospero]

Started 3 days ago. Yesterday and today I have strong gastritis symptoms.
Coincidence?
If I don't feel better tomorow I stop rosmarinus/artishoke caps and I go back to the doctor :/

Just to say that I tried these very same caps during the last months and had a marked improvement of my digestive issues (which are mainly constipation). As I'll mention in my personal thread, it correlates with a general decrease of my POIS intensity but this may be due to other causes as well.

[Quantum]

My hepatic insufficiency was there since birth, it was not caused by POIS.  It is probably the other way around - my sluggish liver was contributing to the severity of my POIS.
As I said, I will receive in about a month or two, my genome results.  That will help determine to what extent my detox enzymes are affected by unfavorable genetics  ( most detox enzymes are found in the liver ).  I never had extensive blood work for liver status, just usual liver enzymes, and they were normal - having a slow liver is not the same as an acute episode of intoxication, it does not show in high AST or ALT.  Maybe my bilirubin could have, at the time, been a little higher than normal, and more extensive tests could have clearly shown that my liver was below average for efficiency.

Just curious if you got anything out of your full genome analysis with that regard..

Nothing major about the liver, yet.  Some small SNPs, but nothing very conclusive for now.  So much data, and still much VUS ( Variations of Uncertain Significance)  , because this genome science is still young.  But I continue digging, slowly but surely.

P.S.:  I did some research tonight, about my liver detox, and searched for the acetylation pathway, one of the conjugation pathways of the phase II liver detox. In the NAT2 gene, I have rs1801280 homozygous ( two "bad" versions", which is one of the main SNP to identify a "slow acetylator" ( https://pubmed.ncbi.nlm.nih.gov/21750470/ ).  So, I am a slow acetylator, at least to some degree. That explains why I do not tolerate caffeine, it is eliminated by acetylation.


About methylation, no major issue there for me, I have only a heterozygote SNP on MTHFR for A1298C (rs1801131).  I lose about 17% of the activity of the MTHFR enzyme, which is not that much, considering I am eating organic green veggies and fruits every day.
I will have to look at other liver pathways in the following weeks and months ( glucuronidation, sulfation, ...)
 

[Quantum]

Started 3 days ago. Yesterday and today I have strong gastritis symptoms.
Coincidence?
If I don't feel better tomorow I stop rosmarinus/artishoke caps and I go back to the doctor :/

Just to say that I tried these very same caps during the last months and had a marked improvement of my digestive issues (which are mainly constipation). As I'll mention in my personal thread, it correlates with a general decrease of my POIS intensity but this may be due to other causes as well.

Chances are that some of this reduction in symptoms intensity is in part related to a healthier liver   It has been my case, though - by supporting my liver and detoxing it, my POIS symptoms intensity lowered.

[Foxdie]

Diet is an important step in liver cleansing. It`s necessary to exclude from your diet fatty foods, spicy, salty and sweet. You should also give up flour products and white bread. It`ll be good to add cereals. They`re rich in vitamins and minerals. Don`t give up the process of cleansing the liver halfway, cause it may take quite a long time. I`ve been practicing additional method for quite a long time, every morning on an empty stomach I drink tonic lemon water, this product also helps to cleanse the liver. It`s promoted by the increased production of enzymes under the influence of lemon juice. There`s a release of toxins, which are excreted with water.

EDIT: Admin removed link, not sure if spam account or real.

[Quantum]

Diet is an important step in liver cleansing. It`s necessary to exclude from your diet fatty foods, spicy, salty and sweet.

Hi Foxdie,

You are right about not too much fat, neither too much salt, neither too much sugar.  Just that and you have eliminated all industrial and junk food!   If you also eliminate MSG, aspartame, artificial flavor and artificial color, and preservatives, then you have eliminated still more unhealthy food, and what is left is far more healthy, in particular if you go organic

Some spice is good, but not the kind of over-spicy junk food and junk spicy sauces that are flooding the market.  But some turmeric, some cinnamon, some black pepper, some ginger, and other herbs like basilica, rosemary, thyme, when used in small amounts, are good sources of antioxidants and other interesting healthy components.  And now, here, it is easy to find organic versions of those spices and herbs, even in mainstream groceries.

[Progecitor]

My hepatic insufficiency was there since birth, it was not caused by POIS.  It is probably the other way around - my sluggish liver was contributing to the severity of my POIS.
As I said, I will receive in about a month or two, my genome results.  That will help determine to what extent my detox enzymes are affected by unfavorable genetics  ( most detox enzymes are found in the liver ).  I never had extensive blood work for liver status, just usual liver enzymes, and they were normal - having a slow liver is not the same as an acute episode of intoxication, it does not show in high AST or ALT.  Maybe my bilirubin could have, at the time, been a little higher than normal, and more extensive tests could have clearly shown that my liver was below average for efficiency.

Just curious if you got anything out of your full genome analysis with that regard..

Nothing major about the liver, yet.  Some small SNPs, but nothing very conclusive for now.  So much data, and still much VUS ( Variations of Uncertain Significance)  , because this genome science is still young.  But I continue digging, slowly but surely.

P.S.:  I did some research tonight, about my liver detox, and searched for the acetylation pathway, one of the conjugation pathways of the phase II liver detox. In the NAT2 gene, I have rs1801280 homozygous ( two "bad" versions", which is one of the main SNP to identify a "slow acetylator" ( https://pubmed.ncbi.nlm.nih.gov/21750470/ ).  So, I am a slow acetylator, at least to some degree. That explains why I do not tolerate caffeine, it is eliminated by acetylation.


About methylation, no major issue there for me, I have only a heterozygote SNP on MTHFR for A1298C (rs1801131).  I lose about 17% of the activity of the MTHFR enzyme, which is not that much, considering I am eating organic green veggies and fruits every day.
I will have to look at other liver pathways in the following weeks and months ( glucuronidation, sulfation, ...)

Hi Quantum!

Lately I have been thinking about the issue of acetylation. I also have problems with coffee and this may indicate that I am also a slow or bad acetylator. It is not clear for me what the exact correlation between N-acetyltransferases (NATs) and histone acetyltransferases (HATs), but inadequate efficiency in one may also affect global acetylation. This wouldn’t mean much in itself, but it is quite clear that we also benefit from many of the same supplements. Of particular note are histone deacetylase (HDAC) inhibitors, which decrease deacetylation which is in favor of acetylation. There is also a precarious balance between acetylation and methylation in epigenetics and poor acetylation would lead to increased methylation possibly leading to hypermethylation in the worst case. Inhibition of DNA methyltransferases (DNMT) could decrease methylation. Thus a combined inhibition of DNMT and HDAC would be in favor of acetylation and many really beneficial supplements actually do either one or both of these.
Methylation and methylation support was much discussed on the site and it may really benefit some POISer. However in my opinion acetylation and acetylation support would deserve at least as much attention.

[Quantum]

My hepatic insufficiency was there since birth, it was not caused by POIS.  It is probably the other way around - my sluggish liver was contributing to the severity of my POIS.
As I said, I will receive in about a month or two, my genome results.  That will help determine to what extent my detox enzymes are affected by unfavorable genetics  ( most detox enzymes are found in the liver ).  I never had extensive blood work for liver status, just usual liver enzymes, and they were normal - having a slow liver is not the same as an acute episode of intoxication, it does not show in high AST or ALT.  Maybe my bilirubin could have, at the time, been a little higher than normal, and more extensive tests could have clearly shown that my liver was below average for efficiency.

Just curious if you got anything out of your full genome analysis with that regard..

Nothing major about the liver, yet.  Some small SNPs, but nothing very conclusive for now.  So much data, and still much VUS ( Variations of Uncertain Significance)  , because this genome science is still young.  But I continue digging, slowly but surely.

P.S.:  I did some research tonight, about my liver detox, and searched for the acetylation pathway, one of the conjugation pathways of the phase II liver detox. In the NAT2 gene, I have rs1801280 homozygous ( two "bad" versions", which is one of the main SNP to identify a "slow acetylator" ( https://pubmed.ncbi.nlm.nih.gov/21750470/ ).  So, I am a slow acetylator, at least to some degree. That explains why I do not tolerate caffeine, it is eliminated by acetylation.


About methylation, no major issue there for me, I have only a heterozygote SNP on MTHFR for A1298C (rs1801131).  I lose about 17% of the activity of the MTHFR enzyme, which is not that much, considering I am eating organic green veggies and fruits every day.
I will have to look at other liver pathways in the following weeks and months ( glucuronidation, sulfation, ...)

Hi Quantum!

Lately I have been thinking about the issue of acetylation. I also have problems with coffee and this may indicate that I am also a slow or bad acetylator. It is not clear for me what the exact correlation between N-acetyltransferases (NATs) and histone acetyltransferases (HATs), but inadequate efficiency in one may also affect global acetylation. This wouldn’t mean much in itself, but it is quite clear that we also benefit from many of the same supplements. Of particular note are histone deacetylase (HDAC) inhibitors, which decrease deacetylation which is in favor of acetylation. There is also a precarious balance between acetylation and methylation in epigenetics and poor acetylation would lead to increased methylation possibly leading to hypermethylation in the worst case. Inhibition of DNA methyltransferases (DNMT) could decrease methylation. Thus a combined inhibition of DNMT and HDAC would be in favor of acetylation and many really beneficial supplements actually do either one or both of these.
Methylation and methylation support was much discussed on the site and it may really benefit some POISer. However in my opinion acetylation and acetylation support would deserve at least as much attention.

Hi Prog,
I totally agree with you, acetylation is important, and methylation too, as are all the phase II conjugation pathways of the liver, and phase I is also important.  In the "design" of the human metabolism, all pathways are supposed to work properly, for optimal health.
That is why liver support is so important and can help a lot in getting better, no matter what the health problem is.