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That said, there are studies out there that show that smoking can accelerate liver fibrosis. It would be refereshing if some of the energy here directed against social drinking would find its way into an anti-smoking message for those with Hep C. My guess is some of those that write those posts have a cigarette in their mouth :)
This is the group that helped me quit smoking over 20 years ago:
http://www.smokenders.com/
Precisely why you should wait until after treatment to quit. Your body is chemically dependent on it and part of your matrix when you first started treatment and to try to quit while on treatment may be hazardous to your health and “OTHERS”
jasper
Thanks for the study info - very interesting.
Rocker
I know - I'm such a loser when it comes to just quitting and my heart really does know it -in more ways than one!
geter
LMAO - Hazardous to others for sure - I could try Rockers 3 lbs of apples a day
There is one thing that smoking might be good for and that is it might help reduce the sides of Tx.
Interferon surpresses CYP1A2.
Tobacco Induces it. Just thought i would throw something outa left field here.
From
Differential Effect of IFNa-2b on the Cytochrome P450 Enzyme System:
A Potential Basis of IFN Toxicity and Its Modulation by Other Drugs
Results: The results indicate that HDI differentially impairs CYP-mediated metabolism, having no effect on some enzymes (CYP2E1) and substantial effects on others
(CYP1A2; median 60% decrease). A significant association was found between the magnitude of CYP inhibition and the occurrence of side effects including fever and neurological toxicity, which may form a novel basis of the underlying pathophysiology of some IFNa-2b-induced toxicity.
The associations of CYP2D6 inhibition with flu-like symptoms, and CYP1A2 with neuropsychiatric symptoms and fatigue are significant and demand additional study
Soon I will get back on the Chantix and quit again. The stuff works well, my problem with the sx was that I constantly felt like I had morning sickness--all day! You never have a nicotine fit with the Chantix and if you sneak one, it's really not what you want and wind up putting it out after a puff or two.
Very strange how it works---on me anyway.
I know how hard it is to quit-I do believe during tx is not the time.
Cut down if you can not that you smoke a lot and wait til your done to quit.
enigma
I also smoke. I know i should not but when i spoke to my doc before i started to tx, he said he would not give me Chantrix or advise that i use the patch while tx. the only way to do it while tx is cold turkey, He doesnt like that i smoke and neither does anyone else, but until tx is done, i cant do anything else that will make me think i am loosing my mind, or make me want to ram my car into every person that cuts me off while driving.
I know its not good, but i think once tx is done, and these meds are out of my system, they i can really work on getting healthy.
And you wont get any grief from me....
Peace
Rita
"There is one thing that smoking might be good for and that is it might help reduce the sides of Tx."
You're basically telling people that smoking reduces depression during HCV treatment. Based on a HIGH DOSE Interferon study done on MELANOMA patients which used doses of 10 and 20 million units SC or IV several times a week....doses that are never used to treat hepatitis C. Forgive me if I find your data slightly....innacurate.
World J Gastroenterol. 2006 Oct 14;12(38):6098-101.
Heavy smoking and liver.
Smoking causes a variety of adverse effects on organs that have no direct contact with the smoke itself such as the liver. It induces three major adverse effects on the liver: direct or indirect toxic effects, immunological effects and oncogenic effects. Smoking yields chemical substances with cytotoxic potential which increase necro-inflammation and fibrosis. In addition, smoking increases the production of pro-inflammatory cytokines (IL-1, IL-6 and TNF- alpha) that would be involved in liver cell injury. It contributes to the development of secondary polycythemia and in turn to increased red cell mass and turnover which might be a contributing factor to secondary IRON OVERLOAD disease promoting oxidative stress of hepatocytes. Increased red cell mass and turnover are associated with increased purine catabolism which promotes excessive production of URIC ACID. Smoking affects both cell-mediated and humoral immune responses by blocking lymphocyte proliferation and inducing apoptosis of lymphocytes. Smoking also INCREASES SERUM AND HEPATIC IRON which induce oxidative stress and lipid peroxidation that lead to activation of stellate cells and development of fibrosis. Smoking