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Well, it's hard to say.

Hypochondriasis used to be an actual diagnosis in the DSM before the DSM-5 came out. When the DSM-5 came out, it redefined hypochondriasis and is no longer a diagnosis. Instead, about 75% of previously diagnosed people with hypochondriasis are subsumed under the diagnosis of "somatic symptom disorder" (300.82 in DSM-5 or F45.1 in ICD-10), and the remaining 25% have high health asnxiety in the absence of somatic symptoms and are classified as having "illness anxiety disorder" (300.7/F45.21). Both are classified under "Somatic Symptoms and Related Disorders" in the DSM-5.

The ICD-11 does list hypochondriasis under the heading of "obsessive-compulsive and related disorders," rather than a "somataform disorder" like the DSM-5 and ICD-10. But I don't know how widely used ICD-11 is yet... (I actually didn't know it was a thing yet until just then...)

However, at this time, OCD is actually a differential diagnosis, as is generalized anxiety disorder. IOW, if you have OCD or GAD, that takes over the diagnosis before "hypochondriasis" (or SSD or IAD) would.

It responds well to SSRIs and antipsychotics (especially the atypicals).

 

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@mikl_pls I actually have Hypochondirasis down in my diagnosis notes...My very early ones going back to 2004..

I've since heard it called Health Anxiety...I never believed OCD (Which makes up one of my Diagnosis) to be an anxiety disorder...I always had this lurking doubt in the back of my mind about anxiety been the cause of ocd ..

You seem Very knowledgable regards MH and Medications...Have u ever worked in the field or is it more just a personal interest? You have a very good way of explaining things..Especially how medication works in a nice easy way for folks to understand..

i actually have my Pdoc phone appointment today..I got the dates muddled up and thought it was the other week..I havent tried the abilify simply because i'm gravitating towards the negative stories of it been stimulating etc and have scared myself stupid of it !!

I'm gunna ask about potentially Quetiapine today..I think he should be ok with that...Even Risperidone popped into my head as i've read it has the clearest evidence regards ocd....Which would you personally prefer given the option?? 

I've heard pros and cons of both of them...Essentially i'm looking for something that gives me a sense of calm whilst slowing my brain down...I've heard quetiapine is more of a knock u out AAP and risperidone a more Calming gentle AAp...I was actually on Risperidone many years ago with paroxetine but didnt take to it...I was drinking heavy back then so maybe that influenced things..I know that regardless of Which AAP side effects are likely (Mainly weight Gain) and this is something i just have to come to terms with.

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18 hours ago, GrannyG81 said:

 I actually have Hypochondirasis down in my diagnosis notes...My very early ones going back to 2004..

That's like how I was diagnosed with "ADD" as a child, back before that was an obsolete diagnosis and "ADHD" became the only diagnosis with specifiers to indicate the symptom presentation. (I think that started in one of the editions of the DSM-IV, but may have fully "matured" in the DSM-5... I can't remember if I was diagnosed with "ADD" when the DSM-III or DSM-IV was in use...)

So hypochondriasis I think is still in the ICD-9 and ICD-10 (I think...), in the DSM-5 it has been done away with and is either a somatic symptom disorder or illness anxiety disorder, both of which fall under somatic symptoms and related disorders (rather than anxiety disorders, for example, like one might believe the illness anxiety disorder to fall under).

19 hours ago, GrannyG81 said:

I've since heard it called Health Anxiety...I never believed OCD (Which makes up one of my Diagnosis) to be an anxiety disorder...I always had this lurking doubt in the back of my mind about anxiety been the cause of ocd ..

OCD is definitely an anxiety disorder. I have misplaced my copy of the DSM-5, which lays out plainly what makes up the symptoms of OCD, and I cannot remember how my pdoc explained to me in a way that made sense to me (finally) how OCD works... but basically these obsessions (intrusive thoughts, e.g.) and compulsions (needs to perform certain tasks or "rituals") are driven by anxiety that, depending on our level of "insight," which is identified with the diagnosis, the least level of insight bordering on psychosis which is pretty much my baseline for my OCD apparently, may or may not be recognized by the person suffering the OCD, and the person performing these tasks and/or thinking these thoughts may or may not recognize that they do not make sense. Often, with OCD, Tourette's disorder, and ADHD, there is a sort of "triad," especially in males, wherein if you have one of the three, you likely have the other two to some degree or another, which can be very troublesome. OCD is also associated with comorbid depression very often. Psychosis and OCD can go together, but they don't necessarily form a connection. Some antipsychotics (most notably clozapine) can cause (in those without OCD symptoms) or worsen (in those already with OCD symptoms) these symptoms, sometimes to an excruciating degree... I'm personally not sure what causes that, as antipsychotics almost all for the most part have several mechanisms of action that counter OCD's symptoms... but it's not entirely about (not enough) serotonin and/or (too much) dopamine... there's also theory of (too much) glutamate too, and probably more that I don't know about.

19 hours ago, GrannyG81 said:

You seem Very knowledgable regards MH and Medications...Have u ever worked in the field or is it more just a personal interest? You have a very good way of explaining things..Especially how medication works in a nice easy way for folks to understand..

Thank you! I appreciate that! I have never personally worked in the field. It's really just a personal interest that grew out of a desperation of trying to find something that would work for me (trying to think out of the box, trying to look for uncommon medicines, trying to look for off-label treatments, etc.). I'm very glad I am able to do that for you, it makes me very happy to hear that, and again, thank you, I appreciate that!

19 hours ago, GrannyG81 said:

i actually have my Pdoc phone appointment today..I got the dates muddled up and thought it was the other week..I havent tried the abilify simply because i'm gravitating towards the negative stories of it been stimulating etc and have scared myself stupid of it !!

Sorry I didn't get to you sooner... Abilify I will say in my personal experience on the very lowest dose of 2 mg, I nearly went psychotic and definitely went hypomanic. It was definitely that stimulating, and I had just gone off Geodon at... about an average dose... not entirely an overly abundant antipsychotic/antimanic dose, as I usually struggle with depression... But definitely there was a huge decrease in the occupancy of dopamine receptors and an increase in dopamine tone (due to Abilify being a partial agonist with rather high intrinsic activity at the D2 receptor). I destroyed a friendship immediately through a very stupid decision I made during that time, and over time (even well, well after I was off Abilify the 1st time and back on it the 2nd time and off it, etc.), destroyed my friendship with her boyfriend, with whom I was much closer... we don't talk hardly at all anymore, and I'm honestly afraid to. I'm certain she still hates me to this day (even though that was... gosh... 5 years ago now...), and I'm now under the belief that my actual friend (her boyfriend) has grown to dislike me for whatever reason too. Anyway, I degress... It pooped out extremely quickly. Went up to 5 mg, and it helped a little, but pooped out even quicker and caused a tiny bit of akathisia. Went back down to 2 mg and the bottom fell out of my mood. Went back up to 5 mg and really noticed no change. I was desperate for something, so I increased to 10 mg on my own by taking 2x5 mg pills the week preceding my next pdoc appointment. When I told her that, she was okay with it, but I was overly eager to go even further, and asked to go up to 15 mg, and not long after beginning that dose, akathisia from hell (like I had never experienced before until that point) broke loose. It was miserable... My pdoc actually called me while she was at a conference out of town because she "felt like she needed to call me," and I told her what was happening, and she told me to quarter my dose to 3.75 mg until I could see her next. That's when I switched to Rexulti the 1st time, which was a nightmare in and of itself...

The most recent time I was on Abilify, starting about 3 years ago lasting until some time last year, was actually extremely good. It was stimulating in a very pleasant way such that I didn't lay in bed all day and got up and moved around, did stuff, etc., felt motivated to do things on my own, but the only downside was that my impulsiveness went off the charts through the roof... I started impulse buying like a madman... Maxed out both my credit cards multiple times after paying them off. It absolutely ruined me financially. I had to get off it, regardless of how good the benefits were for my mood, because I was going to go bankrupt or something if I didn't. I switched to Vraylar (which I had taken before too) and had a better run that time than the first time I took it, but it wasn't so great... not as good as Abilify... Nothing yet has been as good as Abilify, except maybe this brand-new medicine, Caplyta, that I'm on.

That's just my experience with Abilify.

Take it for what it's worth, as YMMV.

19 hours ago, GrannyG81 said:

I'm gunna ask about potentially Quetiapine today..I think he should be ok with that...Even Risperidone popped into my head as i've read it has the clearest evidence regards ocd....Which would you personally prefer given the option?? 

I have taken only low doses of quetiapine instant-release for sleep/insomnia, never risperidone (my pdoc actually won't let me take that one due to the prolactin issues it causes). My pdoc also won't let me take quetiapine, either IR or ER, as my main antipsychotic, dosed at 300 mg or more, either. Too much weight gain liability, and I'm already prediabetic and obese (trying to lose weight with some success).

Personally though, between the two, I would definitely chose quetiapine (preferrably ER) over risperdione. I already have pretty prominent "man boobs" simply due to being so overweight/obese and definitely don't want them to swell up/get bigger and especially don't want them to start lactating due to increased prolactin from risperidone. My self-esteem would plummet lower than it already is for sure... I mean, the weight gain that quetiapine would be sure to bring on would not be so bad with the ER version (supposedly), and it could be managed easier assuming it helps me with my depression and I feel motivated to do things (rather than lay in bed all day feeling extremely miserable like most sedating "antidepressant-like" medications do to me... I have to have something stimulating, as stimulating as possible really... I guess that's possibly where you and I differ quite vastly...)

19 hours ago, GrannyG81 said:

I've heard pros and cons of both of them...Essentially i'm looking for something that gives me a sense of calm whilst slowing my brain down...I've heard quetiapine is more of a knock u out AAP and risperidone a more Calming gentle AAp...I was actually on Risperidone many years ago with paroxetine but didnt take to it...I was drinking heavy back then so maybe that influenced things..I know that regardless of Which AAP side effects are likely (Mainly weight Gain) and this is something i just have to come to terms with.

I posted a little about this on your other thread...

Quetiapine, especially IR in lower doses, will definitely knock you the heck out. As the dose increases, especially with the ER version, it actually becomes somewhat less sedating/perhaps even ever so slightly stimulating (but not in an unpleasant way) while still remaining relaxing/calming. For a very, very few, minority of people, even quetiapine manages to be paradoxically stimulating, but that is more likely because of its potent anticholinergic effects, which, rather than being sedating, is likely paradoxically stimulating to them due to having ADHD.

Risperidone's effects on anxiety and sedation both are definitely more subtle, but the dopamine D2 antagonism is much more intense, and you are much more likely to suffer some negative side effects of D2 antagonism from risperidone, like akathisia and other EPS, blunted affect (very low doses need to be used for depression to take advantage of the antiserotonergic effects while keeping the antidopaminergic effects minimum). I personally don't like the idea of risperidone on paper looking at its binding affinities and whatnot, as well as looking at how it behaves clinically (or tends to in most people).

Surprisingly, ziprasidone, which is considered to actually be rather stimulating in low doses, from my experience, was very neutral at 40 mg 2x/day, somewhat relaxing at 60 mg 2x/day, to so sedating I couldn't keep my eyes open at 80 mg 2x/day... (There was no in-between from 60 mg to 80 mg! It was a huge difference!!) 80 mg was just way too much and had to go back down to 60 mg... It proved to be the perfect dose for me at that time. It has a very robust pharmacologic profile...

5-HT1A partial agonist: 2.5-76 nM (71-75% IA) (anxiolytic, antidepressant activities, presynaptic stimulation of the autoreceptors at first will decrease serotonin release until they are desensitized/downregulated which will cause a massive surge in serotonin release due to disinhibition of the negative feedback loop, postsynaptic stimulation causes downstream dopamine release mainly, as well as release of some endocrine hormones, most notably oxytocin)
5-HT1B partial agonist: 0.99-4.00 nM (unknown IA) (depending on IA, may either inhibit or disinhibit serotonin synthesis/release at these autoreceptors)
5-HT1D partial agonist or antagonist: 5.1-9.0 nM (unknown IA if partial agonist) (difference sources say different things about its action at this receptor, same as 5-HT1B, may either inhibit or disinhibit serotonin synthesis/release at these autoreceptors)
5-HT2A antagonist: 0.08-1.4 nM (disinhibits dopamine release in specific areas of the brain, may cause anxiolytic effects, improve sleep, may cause sedation as a side effect)
5-HT2C antagonist or partial agonist(?): 0.72-13.00 nM (if partial agonist, unknown IA) (if antagonist or low IA partial agonist, disinhibits dopamine and norepinephrine release in certain parts of the brain and in most other AAPs, helping affective/depressive symptoms, cognitive symptoms, obsessive symptoms/anxiety symptoms, but would increase appetite and lead to weight gain, but for some reason, despite the potent affinity to this receptor, ziprasidone usually does not lead to much weight gain, if any at all, and in some cases (usually when switching from a weight gain-prone AAP), may cause/allow weight loss to occur; if partial agonist at a higher IA, it will somewhat inhibit dopamine and norepinephrine release and have all the opposite effects of 5-HT2C antagonism/low IA partial agonism... including but not limited to suppression of appetite and possible weight loss through worsening of obsessive symptoms, anxiety, depression, etc.)
5-HT6 antagonist: 61-76 nM (not very potent here, if it were more potent relative to D2 antagonism, it would increase glutamatergic and cholinergic neurotransmission in various brain areas, as well as increase facilitate dopamine and norepinephrine release in the frontal cortex which would have procognitive effects. Additionally, it has been found that 5-HT6 antagonism (selective) causes suppression of weight gain but not weight loss)
5-HT7 antagonist: 6.0-9.3 nM (relatively potent, it's not entirely clear what this actually does here, according to Stahl, it enhances the release of serotonin, and definitely has documented antidepressant as other 5-HT7 antagonists have antidepressant effects, but may also have benefits to do with regulating circadian rhythm, learning, cognition, etc.)

D2 antagonist: 4.8 nM (what you look for in an antipsychotic... mostly... and in an AAP, what you compare everything else to to determine its "atypical-ness...")
D3 antagonist: 7.2 nM
D4 antagonist: 0.8-105 nM (quite a broad range of possible affinities...)

α1A antagonist: 18 nM (responsible for side effects such as orthostatic hypotension, but may also help improve side effects like akathisia and other EPS, not especially super potent here)
α1B antagonist: 9 nM (a bit more potent here, closer to the affinity at D2 antagonism...)

α2A antagonist: 160 nM (if this affinity were higher and of any relevance, it would boost norepinephrine release due to autoreceptor antagonism, and boost serotonin release due to heteroreceptor antagonism... but unfortunately the affinity here is too weak to be of any relevance...)
α2B antagonist: 48 nM
α2C antagonist: 59-77 nM (same as α2A... slightly more affinity but still not enough to mean much of anything...)

H1 antagonist: 15-130 nM (responsible for antihistamineric effects, such as sedation, weight gain, increased appetite, etc., not too much affinity here to mean much)

M1-M5 (muscarinic acetylcholine receptors): negligible affinity (no anticholinergic effects, like dry mouth, constipation, urinary hesitancy/retention, blurry vision, etc.)

SERT (serotonin transporter) blocker: 112 nM (responsible for its rather weak serotonin reuptake inhibition)
NET (norepinephrine transporter) blocker: 44 nM (responsible for its rather weak-ish norepinephrine inhibition)
Together, ziprasidone has a "mini-SNRI" built into it, but whether its effects are clinically significant at therapeutic doses is of question...

hERG (potassium ion channel) blocker: 169 nM (responsible for its purported cardiovascular side effects, like dose-dependent QTc prolongation)

Just something to think about for if you don't like quetiapine...

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On 4/27/2020 at 6:06 AM, GrannyG81 said:

I was actually on Risperidone many years ago with paroxetine but didnt take to it...I was drinking heavy back then so maybe that influenced things..I know that regardless of Which AAP side effects are likely (Mainly weight Gain) and this is something i just have to come to terms with.

GrannyG81 - Our in-house pharmacological encylopædia is basically @mikl_pls, and his explanations are so interesting and detailed that we sometimes forget to step back from examining the leaves and take in the view of the forest as a whole. You are quite right to question whether drinking may have been a factor in the ineffectiveness of your previous use of the medication - alcohol is the near-universal enemy of mental health, and in some way sabotages the effect of practically every treatment with psychoactive medication. If you look at the dosage instructions on your medication (any medication - pick one) you will see something to the effect of: DO NOT DRINK ALCOHOL WHILE TAKING THIS MEDICATION. This is especially true of antidepressants; alcohol is a depressant, so it's like taking one step forward and one step back at the same time. It may well be worth trying the medication again if you're now off the wagon.

You're also right in realizing that weight gain, or some other side effect, may be something you have to come to terms with. Here at CB, one of the core questions we try to help our members tackle is, Which Sucks Less? The MI or the Meds? Because they both suck, loudly. There's no way to avoid the suckage, at the current level of modern science. That's our unfortunate reality. So if you're at the point where you can accept that you can tolerate some suckity as the price for getting better, then you're over halfway there already.

Stay strong.

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