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General : "Should I be feeling this bad eight weeks into a quit?"  
     
Reply
 Message 1 of 5 in Discussion 
From: Joel  (Original Message)Sent: 12/21/2005 2:46 PM

Original E-Mail to AskJoel

Hello Joel, Thank you for this web site. I have not had a puff since 10/28 after 40 yr habit. I figured after 8 weeks I would have some relief but the anxiety has suddenly got much worse. Is this normal, was hoping that after this long some relief should be coming to me. No concentration on anything & no particular interest in anybody or anything either. Sleep would be such a relief it is minimal as well (about 3 hrs at a time) - anxiety medication is not helping. Is there a time when these brain triggers will slow down or give up? I do understand that even after years they can be woken up but this is awful. I tried a quit about 6 years ago with the patch & lasted about 6 weeks for same reasons. I do not want to go through this again other people smoking does not bother me it's just the lack of concentration & control over a normal day of life. When will clarity come back or will it?


My response:

Before I try to assess what may be happening can you give me a little more detailed information. You said that you have not smoked since October 28. Have you been off all nicotine since that time, meaning that you have not used any nicotine containing products like patches, gums, inhalers, lozenges, etc. Also, have you used any other medications to help you quit, like Zyban or Welbutrin? It would also be helpful to know if you are using any other medications for other conditions, like thyroid, blood sugar issues, etc. Let me know and I will try to clarify issues that may be going on. Joel


Joel, Thank you for your reply. I have not used any quit smoking product just stopped cold turkey & reduced the coffee intake. 1 cup maybe 2 some days instead of pots of it ongoing with the smokes. I do take thyroid medication 125m of levothyroxine & can take .25 of xanex. I am looking at 60yrs old & wonder if the damage is so done and there is not enough time left for me to calm down. I will not puff yet I am committed for now - I do like the freedom .


My response:

I suspect the thyroid medication may be the issue at hand here. Your medication level was adjusting around you as a smoker. As an ex-smoker, that dosage may no longer be right. You need to talk to your doctor who is treating your thyroid and describe what is happening here. Is it okay if I put this up at the AskJoel board, removing your name and email of course? Then I can attach some articles addressing this issue. I think you will find them helpful and others who may also face similar circumstances.

Joel


Yes you can use on ask Joel if my name is removed & thank you again.
 


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Reply
 Message 2 of 5 in Discussion 
From: JoelSent: 12/21/2005 2:48 PM
Medication Adjustments:
 
Often when people quit smoking they may find that medications that were adjusted for them while smoking may be altered in effectiveness once quitting. People on hypertensives, thyroid, depression, blood sugar drugs, and others may need to get re-evaluated for proper dosages once quitting.
 
The first few days quitting can be very difficult to determine, what is a "normal" withdrawal and what is a medication dosage issue. But once through the first few days, if a person who is on medications for medical disorders finds him or herself having physical symptoms that just seem out of the ordinary, he or she should speak to the doctor who has him or her on the medications. Point out to the doctor that you have recently quit smoking and started to notice the specific symptoms just after quitting and that they haven't improved over time. The doctor should know the medication and potential interaction that not smoking may be adjusting for and which way the dosing may need to altered.
 
Treating many conditions is a partnership between you and your physician. The doctor needs your input to effectiveness of any treatment, whether it be by physical measurements or by verbally communicating how you feel while under treatment. The treatment for one condition though is your primary responsibility. The condition--nicotine addiction. It is by no means a minor medical issue, it is in fact probably the greatest controlable health threat anyone will ever face. Afterall, what other lifestyle issues carry a 50% premature mortality rate? Not to mention all the other crippling side effects that go along with long-term smoking. The treatment for this condition is your primary responsibility. To effectively treat smoking for the rest of your life simply remember to never take another puff!
 
Joel

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The number of members that recommended this message. 0 recommendations  Message 3 of 5 in Discussion 
Sent: 12/21/2005 2:50 PM
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Reply
 Message 4 of 5 in Discussion 
From: JoelSent: 12/21/2005 2:52 PM
From: John (Gold) Sent: 4/23/2001 11:57 AM
Since it is back up I thought I'd share this Editorial from the New England Journal of Medicine that has a bit of an explanation as to how some smokers may develop thyroid problems.   
 
The New England Journal of Medicine -- October 12, 1995 -- Vol. 333, No. 15
EDITORIAL

Cigarette Smoking and the Thyroid


      Smoking is associated with so many abnormalities of thyroid function that it is unlikely it has a single action on the thyroid gland. In this regard, it is like at least one substance that occurs naturally in the body -- iodine -- and several drugs.

      The article by Muller et al. (1) in this issue of the Journal presents evidence that in women with hypothyroidism, smoking decreases both thyroid secretion and thyroid hormone action. Among women with subclinical hypothyroidism, smoking was associated with decreased thyroid secretion on the basis of findings of lower serum concentrations of free thyroxine and higher serum concentrations of thyrotropin in smokers than nonsmokers. In contrast, among both normal women and women with overt hypothyroidism, the serum concentrations of free thyroxine and thyrotropin were similar in those who smoked and those who did not, presumably because the antithyroid action of smoking is so weak that it is apparent only when thyroid secretion is marginal.

      Smoking was associated with peripheral antithyroid actions in both groups of women with hypothyroidism, but these actions -- which resulted in more symptoms, signs, and biochemical and physiologic changes of hypothyroidism -- were greater in the women with overt hypothyroidism, who would be expected to be more sensitive to blockade of the peripheral actions of thyroid hormone. Although the tests of peripheral thyroid hormone action used in the study are not very specific or sensitive indicators of decreased thyroid hormone action, the fact that differences were detected and that there was a dose-response relation between smoking and serum cholesterol concentrations suggests that the effects are real.

      The results do not indicate that smoking causes hypothyroidism, only that it increases the severity and peripheral effects of hypothyroidism. The small magnitude of both the thyroidal and peripheral antithyroid effects of smoking means that we do not need to change the way we think about hypothyroidism in smokers as compared with nonsmokers with respect to either diagnosis or treatment, except to be less reluctant to treat patients with subclinical hypothyroidism.

      How might smoking affect thyroid secretion or action? One component of tobacco smoke is cyanide, which is converted to thiocyanate, which inhibits iodide uptake and hormone synthesis and increases iodide efflux from the thyroid gland. (2) There are many other components of smoke that might have antithyroid actions; decrease the binding of triiodothyronine to its receptors or its post-receptor actions in the liver, muscle, or other organs; or both.

      The women with hypothyroidism studied by Muller et al. had identifiable thyroid disease. Among the normal women there were no differences in either the secretion or action of thyroid hormone between the smokers and nonsmokers. Previous studies of normal subjects revealed a higher frequency of thyroid enlargement among smokers than nonsmokers, (3) but the differences in frequency and degree of thyroid enlargement were small. The results of tests of thyroid function have varied, but most often serum triiodothyronine and thyroglobulin concentrations were slightly higher and serum thyrotropin concentrations slightly lower in the smokers. (3) These findings are most indicative of minimal stimulation of thyroid growth and a minor degree of thyroid autonomy, which could be caused by chronic sympathetic stimulation induced by nicotine, the effect of a component of smoke on thyroid cellular function, or the induction of subclinical Graves' disease (see below).

      The most dramatic effect of smoking on the thyroid is its association with Graves' hyperthyroidism, and especially with Graves' ophthalmopathy. Whether smoking precedes Graves' hyperthyroidism (with or without ophthalmopathy) or not, there are more smokers than would be expected among those with these conditions. (4,5,6) In a case-control study, for example, the odds ratios for smoking among patients with Graves' hyperthyroidism with and without ophthalmopathy were 7.7 and 1.9, respectively, and the smokers had more severe eye disease. (5) Smoking may alter the structure of the thyrotropin receptor slightly, so that in a susceptible person it becomes more immunogenic and the resulting antireceptor antibodies are more reactive with retro-orbital tissue. Alternatively, smoking could augment immunologic responsiveness to whatever factor initiates Graves' hyperthyroidism, sensitize retro-orbital tissue to whatever factor causes ophthalmopathy, or both.

      What might account for these multiple abnormalities of thyroid function and multiple thyroid diseases in smokers? Variations in iodine intake are one factor that might modulate the response to smoking, the predominant action of smoking being antithyroid when iodine intake is low and immunogenic when it is adequate. However, iodine intake is higher in Switzerland, where Muller et al. worked, than in Italy, the Netherlands, and Sweden, where the studies of smoking and Graves' disease were done. (4,5,6) Other explanations include quantitative and qualitative differences in the components of tobacco smoke, underlying differences in thyroid function or preexisting thyroid disease in the subjects, and differences in susceptibility to thyroid autoimmune disease.

      Better known for their multiple effects on the thyroid gland are iodine and several drugs. Too little iodine -- less than 50 µg a day -- is of course the cause of endemic goiter and cretinism. Too much iodine -- it need be only a few milligrams per day -- can induce either hyperthyroidism or hypothyroidism, depending on the patient. (7) The former occurs in patients with thyroid nodular disease, and the latter in those whose thyroid is damaged, whether from chronic autoimmune thyroiditis, previous radioactive-iodine therapy, or something else. These effects occur in response not only to inorganic iodine but also to any iodine-containing compound, including expectorants, antiseptics, drugs, and radiographic contrast agents. All the latter are deiodinated in vivo, releasing inorganic iodine, and a few -- notably amiodarone -- also inhibit extrathyroidal conversion of thyroxine to triiodothyronine.

      Lithium carbonate also has bidirectional effects on the thyroid system. It has antithyroid actions in normal subjects and patients with hyperthyroidism. (8) Among patients with psychiatric disorders receiving long-term lithium therapy, about 5 percent have overt hypothyroidism and 25 percent have subclinical hypothyroidism. (9) Many of the patients have antithyroid antibodies, suggesting that lithium induces not only hypothyroidism but also chronic autoimmune thyroiditis. Finally, lithium therapy may be associated with an increased risk of Graves' hyperthyroidism. (10)

      Many other drugs and substances can affect some facet of thyroid hormone production, metabolism, or action, but none have the diverse effects on thyroid economy or thyroid autoimmunity or are as commonly used as cigarettes, iodine and iodine-containing compounds, and lithium. Whenever a patient with thyroid dysfunction is encountered, the possibility that one of these substances caused or at least contributed to it should be kept in mind.

      Robert D. Utiger, M.D.

 

Reply
 Message 5 of 5 in Discussion 
From: JohnSent: 12/21/2005 3:19 PM
From: Joel Sent: 12/21/2005 9:50 AM
Here is a string at Freedom addressing Thyroid issues:
 
 
Comments from that string:
From: Joel Sent: 2/22/2005 5:23 AM
I want to point out that the vast majority of people who quit smoking who gain weight or become depressed do not do so because of underlying thyroid problems. They gain weight because the eat more, they become depressed because it is one of the common side effects from the sense of loss from a lifestyle change like quitting smoking. The weight can be managed by proper diet and exercise changes and the initial depression will pass with time and experience as people come more to the acceptance phase of quitting.

But there are some people who do have underlying problems that were masked while smoking. If anyone is having symptoms raising concerns weeks and months into a quit they should be checked out. While the thyroid issue raised here isn’t a phenomena encountered by the majority of people, it is something that may be a real issue for an individual here. I normally would have this issue raised once every few months from one of my clinic graduates. Even before I saw anything in the literature on the issue, I was hearing it from these people who were all experiencing similar reactions and then similar diagnoses. Again, we are talking about a very small percent of people, probably less than 1% although I don’t have accurate records of the instances. But when I heard it raised by the third time in my first couple of years of smoking cessation work, I knew to keep my ears opened to people having longer-term reactions. A few times when I sent them to their doctors they did have problems that needed to be treated.

Don’t automatically assume that you are having thyroid or other metabolic problems when quitting smoking, but don’t automatically write off symptoms either. If a symptom or symptoms of conditions persist, get checked out to rule out pre-existing problems. Then to keep your risk of developing future problems of all your body systems minimized, always remember to never take another puff!

Joel


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