Mauritio
Member
- Joined
- Feb 26, 2018
- Messages
- 5,669
"Several other synthetic estrogenic substances, ethynylestradiol, lindane, PCBs, cause eggshell thinning, partly by altering carbonic anhydrase activity (Holm, et al, 2006). Estrogen and serotonin activate carbonic anhydrase in some tissues, progesterone tends to inhibit it."
-Ray Peat
Peat has often talked about the connection between CO2 and bone health.
This excerpt talks about carbonic anhydrase 2, which decreases CO2, as a biomarker for vascular calcification.
The authors also suggest carbonic anhydrase 2 as a therapeutic target to treat or even reverse vascular calcification.
There's quite a few pro-metabolic substances that inhibit carbonic anhydrase. Acetazolamide, vitamin B1 and even aspirin can inhibit carbonic anhydrase in higher doses ( Aspirin could act as a suicide inhibitor of carbonic anhydrase II)
So all the substances I mentioned should be considered to treat or reverse vascular calcification.
As per the Peat-quote above estrogen increases carbonic anhydrase and thus lowers CO2 inside the body, which is bad for your bones.
This shows again that estrogen is actually damaging to the bones (by lowering CO2) and not a cure for osteoporosis, as often suggested.
"In vitro studies have shown
that CA isoenzymes promote calcium carbonate formation and thus participate in the calcification process. A significant decrease in calcium carbonate is noted after the addition of acetazolamide, a CA II inhibitor. This means
that calcium carbonate generation depends on CA isoenzymes, which are in
turn susceptible to acetazolamide inhibition [308].
(...)
In a genome-wide microarray analysis studying differential transcriptional profiling concerning VC, overexpression of CA II was shown in human atheromatic plaques in comparison with normal arterial tissue in the same individual. CA II was found to be overexpressed more than 1.7-fold in the atheromatic plaque compared to normal tissue [311].
(...)
In conclusion, given that VC is associated with CAII expression, this enzyme can be used both as a calcification biomarker as well as a potential therapeutic target for VC."
-Ray Peat
Peat has often talked about the connection between CO2 and bone health.
This excerpt talks about carbonic anhydrase 2, which decreases CO2, as a biomarker for vascular calcification.
The authors also suggest carbonic anhydrase 2 as a therapeutic target to treat or even reverse vascular calcification.
There's quite a few pro-metabolic substances that inhibit carbonic anhydrase. Acetazolamide, vitamin B1 and even aspirin can inhibit carbonic anhydrase in higher doses ( Aspirin could act as a suicide inhibitor of carbonic anhydrase II)
So all the substances I mentioned should be considered to treat or reverse vascular calcification.
As per the Peat-quote above estrogen increases carbonic anhydrase and thus lowers CO2 inside the body, which is bad for your bones.
This shows again that estrogen is actually damaging to the bones (by lowering CO2) and not a cure for osteoporosis, as often suggested.
"In vitro studies have shown
that CA isoenzymes promote calcium carbonate formation and thus participate in the calcification process. A significant decrease in calcium carbonate is noted after the addition of acetazolamide, a CA II inhibitor. This means
that calcium carbonate generation depends on CA isoenzymes, which are in
turn susceptible to acetazolamide inhibition [308].
(...)
In a genome-wide microarray analysis studying differential transcriptional profiling concerning VC, overexpression of CA II was shown in human atheromatic plaques in comparison with normal arterial tissue in the same individual. CA II was found to be overexpressed more than 1.7-fold in the atheromatic plaque compared to normal tissue [311].
(...)
In conclusion, given that VC is associated with CAII expression, this enzyme can be used both as a calcification biomarker as well as a potential therapeutic target for VC."
Biomarkers of vascular calcification in serum
Over the last decades, the association between vascular calcification (VC) and all-cause/cardiovascular mortality, especially in patients with high at…
www.sciencedirect.com