Posted by SLS on December 5, 2000, at 17:13:18
In reply to Re: Weight gain and lamictal » Coachnanci, posted by shellie on December 4, 2000, at 16:16:05
> > Has anyone experienced weight gain while on Lamictal.
> Nancy, I also gained weight (over ten pounds) while on lamictal. Recently when discusing this with my pdoc, I have questioned whether the weight was due to an increase in prolactin levels caused by the lamictal. In my case, while on lamictal, my breasts were enlarged and extremely uncomfortable. She does believe that the weight gain and breast pain were related, and we may try to treat them by using a medication to lower my prolactin levels.
Otherwise, I found it totally impossible through diet and intense exercise to lose the weight.> If you are not feeling any breast discomfort, then this probably does not apply to you. shellie
Hi Girls.I don't think the weight gain and breast enlargement / tenderness produced by Lamictal (lamotrigine) are related to prolactin. I can't find any evidence that prolactin is affected in any way by Lamictal. Unfortunately, I don't have my PDR with me nor the package-insert. Is prolactin elevation listed as a side-effect?
Many drugs produce weight gain for which the mechanisms are not well understood. SSRIs can produce weight gain *and* breast enlargement without elevating prolactin levels. Interestingly, the magnitude of weight gain seems highest in those women who also experience breast enlargement. Perhaps there is a direct association between these two phenomena.
For me, Lamictal has produced about a 10 pound increase in body weight, but no breast enlargement. I'm not sure how to feel about that.
Perhaps Lamictal does cause an elevation of prolactin that would explain your observed weight-gain and macromastia. This sort of thing may not have shown up during clinical testing, as the subjects were either healthy or suffering from epilepsy and were already taking other anticonvulsant drugs. The altered neuroendocrine function demonstrated in major depression and bipolar depression might account for a different responsiveness to specific drug challenges. Perhaps Lamictal is among them.
While it is still on my mind, I proposed in a prior post the possibility that SSRI induced weight-gain might be overrepresented in a treatment-resistant population or a population dominated by atypical depression and bipolar depression, both of which share many clinical features. Perhaps SSRI weight-gain reflects an idiosyncratic serotonergic dysregulation peculiar to these two subgroups.
I don't know how expensive the blood work is, but it would be very fruitful to establish what your baseline level of prolactin is before starting Lamictal. If it increases significantly during treatment, then you can probably use one of the standard remedial treatments for hyperprolactinemia. It might not hurt to try Mirapex (pramipexole) or Parlodel (bromocriptine) anyway, as both of these drugs are dopaminergic and are sometimes used as adjuncts to treat treatment-resistant depression (TRD). Traditionally, Parlodel has been used to treat hyperprolactinemia. However, AndrewB recently suggested the use of Mirapex, as it might make for a better antidepressant. I don't see that Mirapex is yet being used to treat hyperprolactinemia, even though it shares some basic pharmacodynamic properties with Parlodel: dopamine receptor agonism (stimulation) and prolactin secretion inhibition. Perhaps it is not as effective as Parlodel. I like the Mirapex alternative, though. You can always determine how well it treats elevated prolactin levels by taking a blood test.
So that there be no confusion, let me emphasize that this has not been a joke.:-) (obligatory)
- Scott
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* In the following study of SSRIs, only Paxil (paroxetine) produced an elevation of serum prolactin levels. However, this effect seems to be biphasic and time-dependant. Prolactin is elevated during the second week of administration, but returns to normal after three weeks and beyond. This normalization is probably caused by the type of neuroadaptive changes that are also thought to facilitate the therapeutic antidepressant effects of these drugs.1: J Affect Disord 1997 Nov;46(2):151-6 Related Articles, Books, LinkOut
Breast enlargement during chronic antidepressant therapy.Amsterdam JD, Garcia-Espana F, Goodman D, Hooper M, Hornig-Rohan M
Department of Psychiatry, University of Pennsylvania Medical Center, Philadelphia 19104, USA.
Recent reports of mammoplasia during selective serotonin re-uptake inhibitor (SSRI) therapy suggested that this side effect may be more common than previously reported. We examined 59 women receiving > or = 2 months treatment with an SSRI or venlafaxine for changes in breast size in relation to menopausal status, weight gain and duration of drug therapy. Serum prolactin, estradiol and beta-hCG were also measured before and during treatment in a subgroup of patients. Twenty-three out of 59 patients (39%) reported some degree of mammoplasia. Significantly more SSRI vs. venlafaxine patients reported mammoplasia (p < 0.01). Eighty-four percent with mammoplasia had weight gain vs. 30% without mammoplasia (p < 0.001). The rate of mammoplasia was unrelated to age, menopausal status or duration of treatment. Serum prolactin increased during treatment in the paroxetine subgroup (p < 0.03). In conclusion, antidepressant-induced mammoplasia may be more common than previously expected.
PMID: 9479619, UI: 98140246
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: Psychopharmacology (Berl) 2000 May;150(1):120-2Serotonin transporter (5-HTT) promoter genotype may influence the prolactin response to clomipramine.
Whale R, Quested DJ, Laver D, Harrison PJ, Cowen PJ
University Department of Psychiatry, Warneford Hospital, Oxford, UK.
RATIONALE: A 44-base-pair insertion/deletion polymorphism in the promoter region of the human serotonin (5-HT) transporter (5-HTT) gene gives rise to a bi-allelic polymorphism designated long (l) and short (s). The s variant is associated with a lower expression of 5-HTT sites and a reduced efficiency of 5-HT reuptake. OBJECTIVE: The aim of the present study was to determine whether the increase in brain 5-HT function produced by acute 5-HT reuptake blockade is influenced by the 5-HTT promoter l/s polymorphism. METHODS: We measured the increase in plasma prolactin that follows acute administration of the tricyclic antidepressant clomipramine as an index of 5-HT neurotransmission in 14 healthy female subjects (7 with ss genotype and 7 with ll genotype) using a placebo-controlled crossover design. RESULTS: Clomipramine-induced prolactin release was significantly greater in subjects with the ll genotype. CONCLUSION: Our findings suggest that acute 5-HT reuptake blockade produces a greater increase in 5-HT neurotransmission in subjects with the ll genotype than in those with an ss genotype. These results are consistent with clinical data indicating that subjects with an ss genotype may have a poorer therapeutic response to selective serotonin reuptake inhibitor (SSRI) monotherapy.
PMID: 10867985, UI: 20325938
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17: Psychopharmacol Bull 1993;29(2):155-61Fenfluramine challenge test as a predictor of outcome in major depression.
Malone KM, Thase ME, Mieczkowski T, Myers JE, Stull SD, Cooper TB, Mann JJ
Laboratory of Neuropharmacology, Western Psychiatric Institute and Clinic, University of Pittsburgh, School of Medicine, PA 15213.
It has been reported that low pretreatment cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA) levels may correlate with better clinical response to selective serotonin reuptake inhibitors (SSRI) compared to non-serotonergic antidepressant drugs. We examined the hypothesis that serotonergic system status, as measured by the prolactin (PRL) response to fenfluramine (FEN), may predict outcome in a heterogenous sample treated with various types of antidepressant treatment. Higher PRL response predicted a favorable outcome for males and females treated with either pharmacotherapy, psychotherapy [milieu therapy with or without cognitive behavior therapy (CBT)], or electroconvulsive therapy (ECT). All patients in the high PRL response group responded to antidepressant therapies. Patients receiving ECT had the highest proportion of treatment responders, the highest degree of treatment response, and, unlike drug or psychotherapy treatment, improved significantly whether in the high or low PRL response group. PRL response to a single dose fenfluramine challenge may be a useful predictor of response to pharmacological or psychotherapeutic treatments in major depression. By contrast, ECT is an effective short-term treatment independent of pretreatment serotonergic responsivity.
PMID: 7507256, UI: 94120037
poster:SLS
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