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  1. I was put on 20mg of Seroxat in May 1996 (directly after two weeks of Valium). I was 19 years old. Prescription was for Panic Disorder, GAD and Mild Depression (although I had never felt depressed and explained that many times over the years to my doctor(s)). As were many, I was told I had a chemical balance which, just like a diabetic needs insulin, I needed seroxat. Since then, I have tried approximately 5 times to come off the medication (with taper of sorts - usually 10mg for a few weeks and then to zero). Each time, the anxiety came back, always with new symptoms (extreme nausea, vertigo, increased anxiety, obsessive dark thoughts). I also developed irrational fears (fear of driving on highways and over bridges, fear of ski lifts, fear of heights, fear of flying, fear of business meetings. In fact, pretty much fear of everything.). Each time I visited a doctor, I was told the same thing: you have a chemical imbalance and need to go back on Seroxat. Sure enough, a single tablet would have me feeling back to “normal” within a matter of hours. I used to joke about it with doctors “wow, what a placebo effect. This should take weeks to work?”. Now I realise I was (probably) in withdrawal. Two years ago, after being in a protracted depression for the best part of 10 years (something I hadn’t realised as it had become my baseline state), I had got myself down to approximately 7mg a day. The reason I was trying to come off was two fold: firstly, my wife and I wanted to start a family and I was concerned about both my fertility and damage to any baby I conceive. Secondly, I had made a huge effort to get fit, was running 40km a week and had dropped from 92kg to 78kg-I’m 178cm. This gave me the confidence that I was in the best physical place to achieve it. Soon after, I suffered what I considered to be a mental breakdown. I was ready to leave my loving wife and had developed a clinical apathy to everything. I became petrified I would commit suicide (I never felt this was realistic but the thought of it gave me panic attacks). Furthermore, I started wondering such thoughts as “will I jump off the balcony whilst sleep walking”. I had been seeing a psychologist for some time but talking about things seemed to make the situation worse. I also started seeing a CBT therapist. I would feel better during a session but on leaving, my mood would severely crash, like nothing I had ever experienced in my life. I knew I was in a bad place. The psychologist recommended me to a psychiatrist who was the most uncaring person I have ever met. How she medically practices, I have no idea. She wasn’t interested in my drug history, offered me barely five minutes of her time, and prescribed 50mg Trittico to be taken before bed. I took it for a few nights but decided that it was not right for me. She then offered me several other kinds of SSRIs. I declined them all and went back to 20mg of Seroxat. However, this time felt different. I was sure that seroxat was nothing more than the placebo (how could you explain the fact I got better after taking a single favor each time I had a “relapse”. As suspected, i had lost belief in the drug, and it did not bring the immediate relief like it had every time previously. I was petrified. To me, this confirmed my worse fears. It had been a placebo all this time, and now, because I was sure it wasn’t going to work, it didn’t. I was a lost case. This created severe anxiety and panic. All I could think was that I had been on a placebo for 20 + years and now I had uncovered this fact, ADs would never work for me again. I was destined to suffer dibilitating anxiety and depression for the rest of my life. Things improved slightly after being back on 20mg for a few weeks. But I was still anxious and depressed, and the mood swings were unbareable. During this time, i had had a medical for my work which showed I had very high cholesterol (7.99 in European measures) and the doctor put me on Crestor. At the time, the cardiologist told me “this is not the first time I have seen somebody at the surgery who has unusually high cholesterol following a long period of exposure to SSRIs”. This was the first time I considered what the meds had been doing to me over the years. My dark moods seemed to get worse during this period of being on Crestor. My cholesterol dropped by 50% in this time, but I could now barely function. I did some research into the link between statins and depression and decided to quit the Crestor cold turkey. My moods improved somewhat (at least I could hold a conversation now). I had also started to suffer from eczema on my arms, forehead and legs (first time in my life). Furthermore, I suffered from a bout of Diverticulitis (the doctor told me the main risk factor was constipaiton) and also blood in the urine (which after every test, scan, x-ray known to man, a cause could not be found). Further research made me realise that not only could all of these problems be linked to seroxat, so could my unexplained depression and mood swings. I made the decision to come off seroxat for good. That was in October of last year. I found a new psychiatrist who was supportive of my decision and recognized the importance of taper. However, he didn’t believe that my problems could be caused by seroxat, and thought taper over a month was perfectly acceptable. By this time, I had been on seroxat 22 years. I decided to taper for longer. I immediately dropped to 10mg per day as this is something that I had down many times throughout the years without too many problems. I would get the usual brain zaps but nothing I couldn’t handle. As I started to reduce mg by mg (1mg per week) using liquid, I could actually feel my constant depressive mood lifting somewhat (perhaps only by 10%, but there was something ). This encouraged me to go on. I sped up towards the end to 1mg per week as I just wanted to be off it. I took my last dose in the second week of January. Since then, I have been going through withdrawal. The first couple of weeks were ok (brain zaps I have suffered since 1996 so they don’t scare me). My general depressive level definitely improved. The hardest part for me was (and still is) the rapid onset of change in mood. One minute I am fine, the next my mood crashes. During every crash, I immediately think “the only reason I feel better is the placebo effect. The depression and anxiety is going to come back and get me”. CBT has helped with this catestrophic thinking and the moods seem to only last for a few hours (rather than days or weeks as previously). Every week, as a whole, I am seeing huge improvements. I have cried a lot (and it feels great). I am starting to look forward to things again. The apathy has lifted by 75%. I had a few days of panic and GAD earlier on that would seem to come out of nowhere. I would just wake up and feel down and have fear. I also started to wake during the night in a panic. But I stayed with it. A few weeks ago, I started waking more often during the night. 3 or 4 times. That developed into full blown insomnia for a few days. Last night, I slept without waking once for the first time in a month. The anxiety is now 75% better. Two days ago, I feel I had my best day for years and years. I am generally excited but scared. Since January, I have dropped from 86kg to 78kg. My skin condition has totally cleared up. What if me feeling better is a coincidence? Or the placebo effect? I have read that it can feel you are through the withdrawal, only for it to come back even harder in the future. How will I cope with that!? Now that I’ve felt well, I don’t want to go back where I was. I currently live in Zurich, Switzerland. I can find almost no support here. No doctor, psychologists, psychiatrist or therapist seems to have any idea about withdrawal. They are all desperate to tell me I have relapsed. I so truly want to believe they are wrong, that this whole thing is a drug induced nightmare, and that I will continue to get better. However, the devil on my shoulder is still there. During any period of weakness, he reminds me that the recovery is all in my head and it’s only a matter of time before I relapse. And so here I am. Hoping to be part of a support group that can help me with my withdrawal and keep me believeing. Even more importantly, I want to help others.
  2. Study indicates paroxetine, sertraline, citalopram, and escilatopram tend to increase factors leading to metabolic dysfunction and diabetes. Psychiatry Investig. 2013 Jun;10(2):148-54. doi: 10.4306/pi.2013.10.2.148. Epub 2013 May 30. Relationship between SSRIs and Metabolic Syndrome Abnormalities in Patients with Generalized Anxiety Disorder: A Prospective Study. Beyazyüz M1, Albayrak Y, Eğilmez OB, Albayrak N, Beyazyüz E. Abstract and full free text at http://www.ncbi.nlm.nih.gov/pubmed/23798963 OBJECTIVE: SSRIs are some of the most widely prescribed medications in the world. In addition to their effectiveness, SSRIs were reported to be associated with the side effects of weight gain, sexual dysfunction, drug interactions, extrapyramidal symptoms and discontinuation symptoms. However, the effects of SSRIs on metabolic parameters are poorly understood. METHODS: This study aims to describe the effects of SSRIs on the metabolic parameters of drug-naive first episode patients with generalized anxiety disorder. Ninety-seven female patients aged 20-41 years without any metabolic or psychiatric comorbidity were included in the study. Fluoxetine, sertraline, paroxetine, citalopram and escitalopram were randomly given to the patients. Metabolic parameters, including BMI, waist circumference and the levels of fasting glucose, total cholesterol, triglyceride, HDL, LDL and blood pressure, were measured before and after 16 weeks of treatment. RESULTS: In the paroxetine group, there was a significant increase in the parameters of weight, BMI, waist circumference, fasting glucose, total cholesterol, LDL and triglyceride after 16 weeks of treatment. There were significant increases in the levels of triglyceride in the citalopram and escitalopram groups. In the sertraline group, the total cholesterol level increased after treatment. In the fluoxetine group, there were significant reductions in the parameters of weight, total cholesterol and triglyceride. CONCLUSION: To our knowledge, this study is the first to prospectively describe metabolic syndrome abnormalities in patients with first episode generalized anxiety disorder. Although the effectiveness of the different SSRIs is similar, clinicians should be more careful when prescribing SSRIs to patients who have cardiac risk factors. Larger and lengthier controlled clinical trials are needed to explore the associations between SSRI use and metabolic syndrome. From the paper: .... In the literature, there is only one study that investigated whether subjects taking antidepressants were more likely to have elements of metabolic syndrome compared to subjects who were not taking psychotropic agents. In this cross sectional study, an association was reported between SSRI use and diabetes. In the subgroup analyses, paroxetine use was found to be markedly associated with both abdominal and general obesity. Citalopram was reported to be safe in terms of metabolic syndrome. However, fluoxetine, fluvoxamine and sertraline were assessed as a mixed group and have been reported to be associated with abdominal obesity and hypercholesterolemia.18 In our study, fluoxetine was found to be the safest SSRI in terms of metabolic syndrome. Furthermore, at the end of the follow-up period, there were significant reductions in the parameters of weight, BMI, waist circumference, total cholesterol, LDL and TG. Our finding is partially in contrast to that of Reader and et al., who found that fluoxetine was associated with abdominal obesity and hypercholesterolemia.18 These contrasting findings are most likely due to differences in the methodologies of the studies. However, a recent meta-analysis that investigated the metabolic effects of fluoxetine in patients with type-2 DM suggested that fluoxetine was associated with weight loss and reductions in the fasting glucose level, HbA1c and TG.47 Our findings are in line with the results of this recent meta-analysis. Our results showed that only the lipid profile of the patients was changed after treatment with citalopram and sertraline. While the total cholesterol level increased in the sertraline group, the level of TG was significantly elevated in the citalopram group. These findings partially replicated the findings of Reader et al.; however, citalopram cannot be described as purely safe in terms of its effects on lipid profile.18 To our knowledge, our finding is the first to describe an association between citalopram use and increased serum TG. Escitalopram, which has a similar molecular structure to that of citalopram, was found to significantly increase serum TG levels after sixteen weeks of use. However, the waist circumference of these patients was reduced after treatment. Thus, the metabolic effects of citalopram and escitalopram should be considered to be independent from weight gain. At the end of the follow-up period, paroxetine affected all the parameters of metabolic syndrome except serum HDL level and blood pressure. Our findings replicated the findings of Reader et al.18 and Fava et al.,48 in which weight gain was reported 26 and 32 weeks after paroxetine treatment. Furthermore, in a recent meta-analysis by Serretti and Mandelli,49 it was reported that paroxetine use was associated with weight gain. Thus, our findings also supported the studies data in which paroxetine was reported to be associated with weight gain. However, the effects of paroxetine on metabolic parameters cannot be clearly explained. ....
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