Yes, I smoke about 1 pk every 4 days. I know it's a nasty, vile habit. I've smoked since I was 25 years old so that's over 25 years of smoking. I've never been a heavy smoker and quit with both pregnancies and a couple of times through out the years. Never smoke in my house, car, or at work. It's after dinner, and during the evening hours. As a matter of fact, I had quit for a year prior to dx of hepc. Cold turkey - no patches, no pills. The logic is why am I even bothering with tx when the smoking is going to kill me anyway? True that, and I know every reason in the world why I should quit right now, this minute. I've mentioned coping mechanisms in the past that help us to keep ourselves in check when the sx get overwhelming. I've tried AD's before - the sx from them are worse for me than the actual depression. I don't get the benefit from them that most do and I really gave it an honest try. So, when I get to the boiling point, I smoke a nasty cig and life becomes tolerable again for a while. My question is, does smoking effect the chances of SVR? If I was not a smoker, would I have possibly gotten UND at 12 wks instead of the 793 IU/ml? I haven't seen any studies on this but I haven't made a great effort to find any either. What are your thoughts on this - BTW - I already know what a knucklehead I am for smoking so please don't give me to much grief about that. :)
This study suggests that cigarette smoking is a negative predictor of SVR for genotype 2's and 3's but not genotype 1's. http://www.natap.org/2006/DDW/DDW_25.htm
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:
I smoke a nasty cig and life becomes tolerable again for a while.
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”
Surprisingly little on Smoking and HepC isnt there.
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.
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
i just eat a whole watermelon last nite...took me 6 hours tho...and i am not kiddin...i got asurprise in da morning when i seen bright pink in the toilet bowl...first time i had pinky poo...gotta stay in fashion
Smoking is the worst smell in the world to me now...i quit smoking when i was 18...but ive dabbled in between my 18-50 years of age....i say quit before you TX...expensive dirty stupid nasty habit........sorry but it is.....
I gotta tell you that I quit smoking with Chantix b4 I started tx. When I finally started tx, I started smoking again. Somehow I needed my old friend back.
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.
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....
Actually, there are quite a few studies that showed that smoking lowers SVR. That it affects immune response (even on children from second-hand smoke), increases inflammation and fibrosis, contributes to the development of iron overload, is associated with the metabolic syndrome/insulin resistance and increases purine catabolism which promotes excessive production of uric acid. All things that are known to lower SVR.
"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 yields chemicals with oncogenic potential that increase the risk of hepatocellular carcinoma (HCC) in patients with viral hepatitis and are independent of viral infection as well. Tobacco smoking has been associated with suppression of p53 (tumour suppressor gene). In addition, smoking causes suppression of T-cell responses and is associated with decreased surveillance for tumour cells. Moreover, it has been reported that heavy smoking AFFECTS THE SUSTAINED VIROLOGICAL RESPONSE TO interferon (IFN) therapy in hepatitis C patients which can be improved by repeated phlebotomy. Smoker's syndrome is a clinico-pathological condition where patients complain of episodes of facial flushing, warmth of the palms and soles of feet, throbbing headache, fullness in the head, dizziness, lethargy, prickling sensation, pruritus and arthralgia.
"Impact of cigarette smoking on response to interferon therapy in chronic hepatitis C Egyptian patients.
CONCLUSION: Smokers suffering from chronic hepatitis C tend to have a lower response rate to interferon-alpha compared to non-smokers."
"Association among cigarette smoking, metabolic syndrome, and its individual components: the metabolic syndrome study in Taiwan.
In conclusion, this community-based study supports the view that smoking is associated with the metabolic syndrome and its individual components. Smoking cessation is beneficial to metabolic syndrome and its individual components."
"Low leptin but high insulin resistance of smokers in Japanese men.
CONCLUSIONS: The present finding may explain in part an association among smoking, leptin levels and diabetes. SMOKING is one of the important modifiable risk factors for the prevention of diabetes."
J Hepatol. 2008 Apr;48(4):657-65.
Environmental factors as disease accelerators during chronic hepatitis C.
"It has also been suggested that cigarette SMOKING may enhance activity grade in patients with chronic hepatitis C, thereby increasing progression of fibrosis."
Gastroenterology. 2008 May;134(6):1699-714.
"Disease progression in chronic hepatitis C: modifiable and nonmodifiable factors.
Of greater immediate relevance to patients and their clinicians are the potentially modifiable factors, which include excessive alcohol consumption; SMOKING (tobacco and marijuana); insulin resistance; and coinfection with hepatitis B virus, human immunodeficiency virus type 1, or schistosomiasis."
"Effects of parental smoking on interferon gamma production in children."
"Parental smoking impairs vaccine responses in children with atopic genotypes."
"Hydroquinone, a major component in cigarette smoke, reduces IFN-gamma production in antigen-primed lymphocytes."
"Impairment of human NK cell cytotoxic activity and cytokine release by cigarette smoke."
Thank you for the studies - I am actually the one who does the smoking and I must say CS is exactly right - in my case if I did not have an occassional cigarette, the sx of tx would be overwhelming at times. I'll stick to a puff every now and then as opposed to raging and depression. Not justifing smoking, but better than the alternative. If you are saying that yes, definitely smoking reduces the chance of becoming UND - Take into consideration I had 2 dose reductions at weeks 7 & 8.
Already had 13 phlebotomies - Guess I don't have to worry about that. I have PCT and that is the only effective method of reducing ferritin in those with Hepc.
Maybe I should try pot - that way I could get the munchies and blow up like a balloon, adding extra stress to my heart. I think it's what whatever works on tx - afterwards, deal with the fallout. Again, thanks for the findings.
You can think the data is flawed all you like.
Me i would like to see more studies done on it.
From Smoking is not associated with nonalcoholic fatty liver disease
Smoking is a well-studied risk factor for many malignant neoplasms, cardiovascular diseases, chronic obstructive pulmonary diseases and other important diseases. However, it was recently shown that smoking is associated with many of the risk factors for NAFLD, particularly obesity, IR, diabetes and dyslipidemia.
Basic and clinical research demonstrates that smoking alters enzymatic and inflammatory pathways in liver physiology, and is considered to be a risk factor for liver neoplasm, and affects the prognosis of chronic liver diseases.
Just letting you know I am aware of what smoking can cause and its relationship with liver disease.
What studies have been done on Smoking and SVR. Answer not many.
Heres one from natap
Smoking Cigarettes Reduced SVR Rates in Peg/RBV Study
The Influence of Cigarette Smoking on Response to Treatment With Pegylated Interferon alfa-2b and Ribavirin in Patients With Chronic Hepatitis C
".....Cigarette smokers with genotype 2 and 3 had lower SVR than nonsmokers.
This difference was not seen in the patients with HCV genotype 1.
Pity I am a G3.
Heres one from Egypt.
Impact of cigarette smoking on response to interferon therapy in
chronic hepatitis C Egyptian patients
CONCLUSION: Smokers suffering from chronic hepatitis C tend to have a lower response rate to interferon-α compared to non-smokers.
Therapeutic phlebotomy improves the response rate to interferon-α therapy among this group.
Tend to have lower response. Either they do or they dont.
In other words the response was lower but it didn’t hit statistical significance.
How the hell does phlebotomy improve response rate.
Unless smoking raises your iron level that is.
Come the evidence isn’t exactly overwhelming is it. Most of the ones you picked show that smoking is associated with many of the predictors of non response. But where are the ones that directly compare svr rates.
And I still say there haven’t been many studies done on it.
Yes I know it was a High Dose IFN study. 10 MU IFN alpha 2b a day to be precise. It was even injected for part of it. So I can spot the differences between it and how we use IFN.
From the study
Differential Effect of IFN_-2b on the Cytochrome P450 Enzyme System:
A Potential Basis of IFN Toxicity and Its Modulation by Other Drugs1
The CYP enzymes are a superfamily of heme-containing enzymes distributed widely throughout the body that are involved in the synthesis and metabolism of endogenous substrates including steroid hormones, fatty acids, and lipids, as well as the metabolism of exogenous substrates such as drugs and environmental chemicals. IFNs have been shown to decrease the expression and activity of CYP enzymes in animal models.
Human data are less extensive and primarily limited to patients with hepatitis being treated with comparatively low-dose IFNs (12–15), but the available data indicate a detrimental effect on drug metabolism.
Now this comes from the Pegasys Product Info sheet
Drugs Metabolized by Cytochrome P450
There was no effect on the pharmacokinetics of representative drugs metabolized by CYP107 2C9, CYP 2C19, CYP 2D6 or CYP 3A4.
Treatment with PEGASYS once weekly for 4 weeks in healthy subjects was associated
with an inhibition of P450 1A2 and a 25% increase in theophylline AUC (see
PRECAUTIONS: Drug Interactions).
Now the High Dose study suggested that Inhibition of 1A2 was associated with neurological toxicities, and that 2D6 was associated with Flu Like symptoms and Fever
OK the Pegasys PI states that there was no inhibition of CYP2D6, but they were only treated for 4 weeks.
I don’t know about you but this is the first time I have seen anything that gives any indication of why some of us go thru Tx without any sides while others suffer them severely.
One of the things that intrigues me about this is that giving up smoking which is a good thing may and I repeat may cause you to have more sides than you otherwise would have as tobacco activates 1A2, and even Pegasys suppresses it.
Now will I smoke during my next Tx. Not a chance, wont start till I stop. But this has more to do with it MAY impact Tx and I am getting rid of all the mays, its not that this is proven.
I will let you know what I have sides this time.
I also smoke. I was und at 12 weeks and und after TX. I don't get my next blood work until Sept. Now I am nervous and have been and will be until Oct when I get my results. I quit alcohol, I quit coke (snorting & smoking) I quit meth 20 years ago and it was nothing like what I am hearing it is today. Never did like pills except the soma I take for the muscle pain. Have pot here but haven't smoked in over 20 years, got some from my bro "just in case" LOL. BUT my cigs, I get crazy nervous just thinking about quiting.
Also I had 5 phlebotomies prior to TX because of PCT .
If I were you I would just continue on with your smoking and tx. Actually you don't smoke that much, 1 pk in 4 days is a minimal amount. I agree with rita on this one, if you feel like you want to quit, take care of that idea after tx. Yes, I am a smoker and I also go out of my way, as to being respectful when I smoke around others. Also, as far as the studies go, I don't think you need those to decide that the cigs actually help you with your sx's, but it was a nice gesture for CS to post them for you. What I mean is I'm sure that's part of the reason you smoke already or continue to. God Bless
I smoke. I hate it. Been at it for 35 years. It is my last vice and plan to quit "again", after tox. The reason? COST! The smoking itself doesn't seem to slow me down much, but after 35 years how would I know?
$h!+...I knew I should not have read this ...let a sleeping dog lie was my better intent.
Darn....now I'm freaked out over not reaching SVR because of this nasty old habit.
Oh well far too late in the game to do anything about it now.
"How the hell does phlebotomy improve response rate.
Unless smoking raises your iron level that is."
Yes, it does. The first study I posted explains how.....
"Heavy smoking is associated with increased carboxyhaemoglobin and decreased oxygen carrying capacity of red blood cells (RBCs) leading to tissue hypoxia. Hypoxia stimulates erythropoetien production which induces hyperplasia of the bone marrow. The latter contributes to the development of secondary polycythemia and in turn to increased red cell mass and turnover. This increases catabolic iron derived from both senescent red blood cells and iron derived from increased destruction of red cells associated with polycythemia. Furthermore, erythropoietin stimulates absorption of iron from the intestine. Both excess catabolic iron and increased iron absorption ultimately lead to its accumulation in macrophages and subsequently in hepatocytes over time, promoting oxidative stress of hepatocytes"
"I don’t know about you but this is the first time I have seen anything that gives any indication of why some of us go thru Tx without any sides while others suffer them severely."
It is very interesting. But there are so many other things that can cause the same side, that it will be hard to figure out what's doing it. For example... depression can be caused by anemia, insomnia, caffeine intake, mood changes caused by alterations in blood sugar, stress, etc.
And according to this new study, symptoms of depression can also be caused by the Metabolic Syndrome (insulin resistance), which many HCV patients have (even genotype 2/3).
Biol Psychiatry. 2008 Jun 30.
Depressive Symptoms and Metabolic Syndrome: Is Inflammation the Underlying Link?
BACKGROUND: Behavioral alterations, including depression, are frequent in individuals with the Metabolic Syndrome (MetS). Recent findings suggest that chronic activation of innate immunity might be involved. The objective of this study was to examine the relationship between Metabolic Syndrome and depressive symptoms and to elucidate the involvement of inflammation in this relationship. METHODS: Participants were 323 male twins, with and without Metabolic Syndrome and free of symptomatic cardiovascular disease, drawn from the Vietnam Era Twin Registry. Depressive symptoms were measured with the Beck Depression Inventory (BDI). Inflammatory status was assessed using C-reactive protein (CRP) and interleukin-6 (IL-6); twins with both CRP and IL-6 levels above the median were classified as having an elevated inflammatory status. Factor analysis was performed on individual BDI items to extract specific symptom dimensions (neurovegetative, mood, affective-cognitive). RESULTS: Subjects with Metabolic Syndrome had more depressive symptoms than those without. Depressive symptoms with neurovegetative features were more common and more robustly associated with Metabolic Syndrome. Both the BDI total score and each symptom subscore were associated with inflammatory biomarkers. After adjusting for age, education, and smoking status, the Metabolic Syndrome was significantly associated with the BDI total score and the neurovegetative score. After further adjusting for inflammation, the coefficient for Metabolic Syndrome decreased somewhat but remained statistically significant for the BDI neurovegetative subscore. When controlling for the Metabolic Syndrome, inflammation remained significantly associated with the BDI mood subscore. CONCLUSIONS: The Metabolic Syndrome is associated with higher depressive symptomatology characterized primarily by neurovegetative features. Inflammation is one determinant of depressive symptoms in individuals with Metabolic Syndrome.
I smoke. I don't condone it but certainly can't condemn it either. I thought the first thing my doc would tell me to do would be to quit but he said "not now, work on that later this will be hard enough". Thank God cause he was right. I smoke just under a pack a day (but I only smoke half a cigarette then put it out because somehow I convinced myself that would help me...so I guess maybe I really smoke a half a pack a day hahahaha - what great brains I have to help me ease my mind on anything!)
I had geno1A and 1B and whacked them both. Is it helping my liver. No. But do I think that matters with the interferon and riba doing their job - no. Not at all. Of course the studies might tell different but I haven't seen anyone in here fail BECAUSE of cigs - not that I know of anyway.
I know we aren't supposed to go through any heavy duty like withdrawl during treatment though because it can affect us chemically however..........does it apply to cigs again not sure on that but cigs are the most addictive thing I've run across in a long long time.
I would worry about one problem at a time truthfully - I'm not a superhuman and it would have been too much for me to do at both. Which leaves me what excuse right now I'm not sure..........nerves, yeah my nerves that's it!
Yeh I had already found the linkage between smoking and high Iron.
The following link references that Egyptian study. Its free.
Appears smoking can cause iron overload. Learn something new every day, here.
Impact of cigarette smoking on response to interferon therapy in chronic hepatitis C Egyptian patients
This is the bit that interests me.
Several mechanisms have been implemented in resistance to IFN therapy in heavy smokers which are summarized in Figure 2.
First, heavy smoking causes immunosuppression such as reduction in CD4+ cells, impaired NK cytotoxic activity and recognition of virusinfected cells, and induces apoptosis of lymphocytes. Second, heavy smoking increases hepatic iron overload which is involved in resistance to IFN. Third, smoking induces pro-inflammatory cytokines (IL-1, IL-6, TNF-α) that mediate necroinflammation and steatosis.
Fourth, smoking directly modifies IFN-α-activated cell signalling and action.
As for Metabolic syndrome also being implicated in some of the side. Not really arguing there. But does it also suppress 2A1?
Found this interesting
caffeine intake, mood changes caused by alterations in blood sugar, stress, etc.
And according to this new study, symptoms of depression can also be caused by the Metabolic Syndrome (insulin resistance),
Now last Tx I consumed caffeine in quantity, I did go off coffee though. I didn’t become depressed although I wasnt the most tolerant B@stard in the world. But I did become Insulin Resistant kinda had the unquenchable thirst, which I then tried to quench by drinking Diet Pepsi. Might have got myself into a bit of a vicious circle there.
I also consumed ice-cream in quantity.
Funny thing haven’t had any ice cream for well over a year now, still cant stand the sight of it, and I have gone off cola and hardly touch the stuff now.
Guess I musta over did both of them. And I wont be going anywhere near cola next tx.
I should thankyou for this discussion. We are touching on subjects that don’t get enough attention.
Previous discussions on coffee for example have been around its liver protective effects or on it being a diuretic. The linkage between it and Insulin Resistance is interesting.
Our little debate on 2A1 is also interesting.
Tobacco isn’t the only thing that activates this enzyme.
The thing I would like to know is does activating this enzyme reduce side effects.
The answer would seem to be that it probably does.
The flip side of course is does activating it improve or reduce our svr odds?
As for Tobacco does it reduce svr because it promotes high iron or are other mechanisms also involved. Because of the drop out rate I have made the mistake of ignoring Win-R in the past.
I should have paid more attention to that article on tobacco. I would actually expect to see reduced svr rates in G2s and 3s rather than in G1s as G1s have a hard enough time already and another slight svr neg isn’t likely to show up that readily unless it has a high impact.
"But I did become Insulin Resistant kinda had the unquenchable thirst, which I then tried to quench by drinking Diet Pepsi. Might have got myself into a bit of a vicious circle there.
I also consumed ice-cream in quantity."
Being insulin resistant means that you become insensitive to insulin, but your pancreas works faster to produce more insulin and is able to keep up and maintain your blood sugar in the normal range. When your pancreas can no longer do that, then your blood sugar goes up above normal and you are now a diabetic.
Thirst is a sign of high blood sugar (so is nausea)....diabetes, not just insulin resistance. And treatment can do that. If your blood sugar was high and you drank Pepsi (which contains caffeine), that could have made your blood sugar go up even higher (caffeine raises blood sugar)....and then you ate ice cream....fat and sugar. That would also raise your blood sugar ....and increases insulin resistance....a sure way to lower SVR.
Didn't you have your blood sugar checked?
Let me show you something.....This is a conversation between some of the top hepatologists. They're talking about people on treatment.....
"From the patient's point of view, Interferon caused not just weight loss but also cravings for cheese, dairy and sweets.....which are the WORST things to have during treatment".
Another doctor answers, "Nobody is compelled to eat cabbage".
You know what they're doing? They're laughing. Cheese is fat....dairy and sweets....ICE CREAM.
Interferon alters the balance of your immune system and may cause severe weight loss very fast......and FAT LOSS causes INSULIN RESISTANCE.....why? Because GLUCOSE (Sugar) is stored in fat cells. When fat tissue dissapears, it forces the sugar into your blood stream making a person insulin resistant....and lowering your chances of SVR.
Whenever I hear somebody on treatment say that all they can eat is ice cream, I cringe.
"Our little debate on 2A1 is also interesting.
Tobacco isn’t the only thing that activates this enzyme.
The thing I would like to know is does activating this enzyme reduce side effects.
The answer would seem to be that it probably does."
Let's review what we know....
Cytochrome P450 is a group of enzymes located on the inner membrane of the mitochondria of liver cells (the mitochondria is the powerplant of the cell...it stores oxygen to power the cell). CYP450, is a target of the hepatitis C virus. The virus gets help from CYP450.
Why does HCV target the mitochondria? Because the mitochondria is the location of the interferon response mechanism. By damaging the mitochondria, the Hep C virus stops the interferon response.
CYP2E1 - Liver enzymes worst enemy. It causes mitochondrial damage and oxidative stress on the liver cell. Alcohol is a CYP2E1 substrate but even in people who don't drink, CYP2E1 is implicated in non-alcoholic steatohepatitis...fatty liver.
CYP3A4 - Allows the Hepatitis C virus to move from cell to cell. Cell migration is one of the ways in which Hep C keeps itself alive and multiplying. It has to keep moving to new cells. So inhibiting CYP3A4 will lower your viral load (grapefruit juice inhibits CYP3A4...but if you're taking any prescription drugs that are metabolized by CYP3A4, inhibiting this enzyme with grapefruit juice will raise the levels of the drug in your blood).
Interferon surpresses CYP1A2. Tobacco Induces it. So basically, they work against each other. And I have shown you the many ways that tobacco can lower SVR.
So you want to induce CYP1A2 by smoking, to lower the depression side effect....for a treatment for which you're lowering SVR.
Sparrow....that makes no sense....especially since you said you didn't really have bad depression during your treatment.
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