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What are everyone’s thoughts on the evidence showing increased risk of incident cases of dm2 with antidepressant use? Do you discuss it with patients?
Around 1.27-2 is what I’m seeingWhat's the RR increase with antidepressants? I'd have to imagine it's somewhat small. Being a fat, lazy American is a risk factor that probably overshadows the antidepressant risk.
If you look at the data it’s an independent risk factor, there is some evidence in animals that antidepressants induce Beta cell dysfunctionwell isn't it difficult to actually get that data considering a. depression is a risk factor for diabetes and b. diabetes (can go long time without being diagnosed) itself can render someone depressed?.
What's the RR increase with antidepressants? I'd have to imagine it's somewhat small. Being a fat, lazy American is a risk factor that probably overshadows the antidepressant risk.
Reading the evidence it’s pretty convincing I’m wondering why this isn’t more publicized
I’m on my phone so I can’t send links but I can do it later when I get home. Just google diabetes and antidepressants some good studies will result. These studies combined with animal studies showing beta cell dysfunction with SSRIs have me convinced.Do you have links to some of the studies you are referencing? And do you know if the increased risk for diabetes is driven by weight gain, or does it seem to be independent of that? By that same logic, would antidepressant use worsen existing diabetes?
At any rate, if the evidence is convincing for a meaningful increase in diabetes independent of weight gain, that sounds like it's worth mentioning in some populations (family history of diabetes, already have risk factors for diabetes for instance).
I’m on my phone so I can’t send links but I can do it later when I get home. Just google diabetes and antidepressants some good studies will result. These studies combined with animal studies showing beta cell dysfunction with SSRIs have me convinced.
Anyone planning on glucose monitoring for your patients in long term AD therapy based on this?
That's so interesting. In 21 years of receiving psych meds, I've never had a blood test (saliva tested for genetic response to drugs 3 separate times; duplications because the next test was allegedly better than the last; each time results never discussed).Whats your definition of "glucose monitoring"? Quarterly?
Because all patients in our clinic get annual HbA1c/CMP...so does that count as 'glucose monitoring'?
Fluoxetine-induced pancreatic beta cell dysfunction: New insight into the benefits of folic acid in the treatment of depression. - PubMed - NCBII'd be really skeptical about their ability to draw conclusion that the antidepressant is the culprit from these studies. There are lots of potential unmeasured and unknown confounders. There's lots of research on inflammatory and hormonal differences in depressed patients that isn't exactly clear what to do with the information but could be of very pertinent relevance to this finding. If there was an identified biologic mechanism or animal data, that could help.
A problem is the specific antidepressant may be the factor and not the entire class of meds.
A similar problem is with antipsychotics. Yes as a class in general they are not good for metabolism but some of them have worse effects while Ziprasidone doesn't affect weight or metabolism and the data on this is solid.
So then is the metabolic risk with antipsychotics apply to Ziprasidone? Seems it doesn't but the APA/ADA guidelines say to do metabolic tests with all antipsychotics even Ziprasidone.
Bupropion causes weight loss, so correspondingly my hypothesis is it would lower risk of diabetes. Paroxetine raises risk of weight gain.
Add to the complexity that some people gain weight (others lose weight) when depressed and lose it (or gain) when they get appropriately treated. So then would the antidepressant, even if it's of type that causes weight gain, have more of a benefit or less vs the weight gain caused by depression?
I realize that but I think the combination of this with the aforementioned studies is compelling enough to consider that there is something there. Psychiatry is notoriously bad at recognizing the side effects of psychiatric medications.Both of these papers are looking at in vitro beta cells. There is just a yawning, gaping chasm between in vitro studies (one of which is solely in rat preparations!) of isolated cell lines that are not participating in the complex homeostatic interactions typical of biological systems on the one hand and actual human responses with any clinical significance on the other.
What this tells you is what probably happens to someone's pancreas if you cut it out of them and soak it in an ssri solution, not what is going to happen to your patients in clinic.
I call it dilution of liability.I realize that but I think the combination of this with the aforementioned studies is compelling enough to consider that there is something there. Psychiatry is notoriously bad at recognizing the side effects of psychiatric medications.
Are patients gaining significant weight on SSRIs? As in more than 10 pounds? Is this a common thing with SSRIs. Because I always thought it was an antipsychotic drug side effect, not an SSRI one.
Pfizer rolled out Geodon when I was a resident. When the drug reps came by they were all armed with tape measures, BMI calculators, Geodon scales for the clinic.Antipsychotics-that too depends on the med. Back in the day pretty much all of them did it, hence the now false paradigm that they're all metabolically bad. Later on Geodon (Ziprasidone) came out and it doesn't cause weight gain at all but because of APA guidelines you still have to treat it like it's a metabolic offender. Since Geodon's been out other much more metabolically-neutral meds have come out but the entire class has been given a bad name.
Geodon, file a complaint with the ACLU for being discriminated against!
Inhibition of insulin secretion is *antidiabetic*. It's what you *want*. Type II diabetes is a disorder involving a vicious cycle of increasing insulin resistance and *increasing* insulin secretion.
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The aforementioned study shows that fluoxetine promotes insulin resistance in peripheral tissues and also inhibits the compensatory action of increased insulin secretion. It caused apoptosis of Beta cells. This would be a pro-diabetic effect not an anti diabetic effect.
I was referencing the second article but I still disagree with your reasoning. In a normal subject inhibiting insulin secretion would cause hyperglycemia. In a person with insulin resistance it would inhibit the compensatory hyperinsulinemia causing hyperglycemia. There is some thinking that an antidiabetic agent inhibiting insulin secretion would let the beta cells “rest” and prevent burnout in those with metabolic syndrome. This is not what this article is demonstrating fluoxetine does.Are we reading the same article? De long et al.? I see nothing about peripheral response; all figures discuss effects of fluoxetine incubation on cultured insulinoma cells. Figure 5 shows that glucose treatment stimulates insulin secretion from these cells, an effect that is blocked by fluoxetine preincubation. Again since the issue in Type 2 (at least until the very end) is insulin oversecretion, I fail to see how this promotes the T2D phenotype.
I don't see anything indicating apoptosis either. I see some increase in the production of cellular ROS, which could be an expected byproduct of the increased rates of protein synthesis. Fluoxetine had no effect on cellular survival at any concentration tested (Section 3.1, first sentence of Results).