pmdd

[Edwardo Piet]

@ the thread title

Acronyms without capital letters send my OCD crazy.

[Whateverist]

PMS and giving birth are 2 get out of jail free cards for men!

We got nothing to complain about, have we guys?

(Except maybe the nagging!) He he

My wife's got that one real bad! It's incurable apparently?

Makes me wonder if your and my missus could be related.  But, hey, nagging is just what someone standing up to you sounds like, isn't it?  I'll bet you need that as much as I do.

[brewer]

[edit]

The controversy is big pharma still wants to make hormonal woman appear mental. This is fucking abuse and feminists who lovey dovey menstruation make me want to pull hair.

[edit]

bold mine

Lost some/most credibility with me.

[brewer]

It is fishy that the big pharmaceutical companies would repackage Prozac as Sarafem just as it is nearing it's patent expiry date. Then push to have pmdd included as a mental health disorder so as to stop a cheaper alternative by prescription.

[edit]

Documentation please.

[Little lunch]

I got that from Dust Bunnys documentation.

[brewer]

I got that from Dust Bunnys documentation.

OK, went back a few pages and got caught up.

From a medical standpoint, the Salon article is full of shit. Flouxetine is flouxetine is flouxetine. You can prescribe it for pmdd under any name (trade or generic). Branding it as Sarafem is simply a marketing ploy for prescribers that don't like to think.

From :http://emedicine.medscape.com/article/293257-overview#a4

Major theories developed to explain the pathophysiology of PMDD include the following[5] :

• Ovarian hormone hypothesis
  
• Serotonin hypothesis
  
• Psychosocial hypothesis
  
• Cognitive and social learning theory
  
• Sociocultural theory
  

The ovarian hormone hypothesis suggests that PMDD is caused by an imbalance in the estrogen-to-progesterone ratio, with a relative progesterone deficiency. Accordingly, in the 1960s, PMS patients were treated with progesterone suppositories. However, later studies of estrogen and progesterone levels in women with PMS were inconclusive because of methodologic difficulties. The current consensus seems to be that normal hormonal fluctuations trigger central biochemical events related to PMDD symptoms in some predisposed women.

The serotonin theory hypothesizes that normal ovarian hormone function (rather than hormone imbalance) is the cyclical trigger for PMDD-related biochemical events within the central nervous system (CNS) and other target tissues.[6]

PMDD shares many of the phenomenologic features of depression and anxiety states that have been linked to serotonergic dysregulation. A growing body of evidence suggests that serotonin (5-hydroxytryptamine [5-HT]) also may be important in the etiology of PMDD. Decreased serotonergic activity in women with PMDD has also been implied by the observation of reduced platelet uptake of serotonin and serotonin levels in peripheral blood.

In women with PMDD, sensitivity to perturbations of the central serotonin system is altered premenstrually. The administration of the serotonin agonist m -chlorophenylpiperazine may induce mood elevation.[7] Agents that transiently diminish serotonin activity have been associated with behavioral changes, including irritability and social withdrawal.

The psychosocial theory hypothesizes that PMDD or PMS is a conscious manifestation of a woman’s unconscious conflict about femininity and motherhood. Psychoanalysts proposed that premenstrual physical changes reminded the woman that she was not pregnant and therefore was not fulfilling her traditional feminine role. Obviously, proving this theory through scientific evidence is quite difficult.

The cognitive and social learning theory hypothesizes that the onset of menses is an aversive psychological event for women susceptible to PMDD. Moreover, these women might have had negative and extreme thoughts that further reinforce the aversiveness of premenstrual symptoms.

Consequently, these women develop maladaptive coping strategies (eg, lability of mood, absence from school or work, and overeating) in an attempt to reduce the immediate stress. The immediate reduction of stress acts as a reinforcement, leading to the regular recurrence of symptoms during the premenstrual period.

Finally, the sociocultural theory hypothesizes that PMDD is a manifestation of the conflict between the dual roles society expects women to fill simultaneously—namely, productive workers and child-rearing mothers. PMDD is postulated to be a cultural expression of women’s discontent with the traditional role of women in the society.

Of these 5 theories, the serotonin theory is perhaps the most popular at present. Although genetic predisposition and societal expectations may play a role, the strongest scientific data implicate serotonin as the primary neurotransmitter whose levels are affected by ovarian steroid levels. Other neurotransmitter systems that have been implicated include the opioid, adrenergic, and gamma-aminobutyric acid (GABA) systems.[8]
___________________________________________________________________________

So, the most popular theory is a problem with neurotransmitter(s) in the brain, which makes it fall into a mental treatment category, not mental diagnosis category. The diagnosis category (according to icd 9) is 624.5. This puts it in the same category as other female genital disorders (http://www.icd9data.com/2012/Volume1/580...7-629/625/).

DB, get over the term, get on with addressing the problem. If you don't want pharmacologic treatment and you want a bilateral salpingo-oophorectomy, find a surgeon who will give you one.

[Dust_bunny]

I got that from Dust Bunnys documentation.

OK, went back a few pages and got caught up.

From a medical standpoint, the Salon article is full of shit. Flouxetine is flouxetine is flouxetine. You can prescribe it for pmdd under any name (trade or generic). Branding it as Sarafem is simply a marketing ploy for prescribers that don't like to think.

From :http://emedicine.medscape.com/article/293257-overview#a4

Major theories developed to explain the pathophysiology of PMDD include the following[5] :

• Ovarian hormone hypothesis
  
• Serotonin hypothesis
  
• Psychosocial hypothesis
  
• Cognitive and social learning theory
  
• Sociocultural theory
  

The ovarian hormone hypothesis suggests that PMDD is caused by an imbalance in the estrogen-to-progesterone ratio, with a relative progesterone deficiency. Accordingly, in the 1960s, PMS patients were treated with progesterone suppositories. However, later studies of estrogen and progesterone levels in women with PMS were inconclusive because of methodologic difficulties. The current consensus seems to be that normal hormonal fluctuations trigger central biochemical events related to PMDD symptoms in some predisposed women.

The serotonin theory hypothesizes that normal ovarian hormone function (rather than hormone imbalance) is the cyclical trigger for PMDD-related biochemical events within the central nervous system (CNS) and other target tissues.[6]

PMDD shares many of the phenomenologic features of depression and anxiety states that have been linked to serotonergic dysregulation. A growing body of evidence suggests that serotonin (5-hydroxytryptamine [5-HT]) also may be important in the etiology of PMDD. Decreased serotonergic activity in women with PMDD has also been implied by the observation of reduced platelet uptake of serotonin and serotonin levels in peripheral blood.

In women with PMDD, sensitivity to perturbations of the central serotonin system is altered premenstrually. The administration of the serotonin agonist m -chlorophenylpiperazine may induce mood elevation.[7] Agents that transiently diminish serotonin activity have been associated with behavioral changes, including irritability and social withdrawal.

The psychosocial theory hypothesizes that PMDD or PMS is a conscious manifestation of a woman’s unconscious conflict about femininity and motherhood. Psychoanalysts proposed that premenstrual physical changes reminded the woman that she was not pregnant and therefore was not fulfilling her traditional feminine role. Obviously, proving this theory through scientific evidence is quite difficult.

The cognitive and social learning theory hypothesizes that the onset of menses is an aversive psychological event for women susceptible to PMDD. Moreover, these women might have had negative and extreme thoughts that further reinforce the aversiveness of premenstrual symptoms.

Consequently, these women develop maladaptive coping strategies (eg, lability of mood, absence from school or work, and overeating) in an attempt to reduce the immediate stress. The immediate reduction of stress acts as a reinforcement, leading to the regular recurrence of symptoms during the premenstrual period.

Finally, the sociocultural theory hypothesizes that PMDD is a manifestation of the conflict between the dual roles society expects women to fill simultaneously—namely, productive workers and child-rearing mothers. PMDD is postulated to be a cultural expression of women’s discontent with the traditional role of women in the society.

Of these 5 theories, the serotonin theory is perhaps the most popular at present. Although genetic predisposition and societal expectations may play a role, the strongest scientific data implicate serotonin as the primary neurotransmitter whose levels are affected by ovarian steroid levels. Other neurotransmitter systems that have been implicated include the opioid, adrenergic, and gamma-aminobutyric acid (GABA) systems.[8]
___________________________________________________________________________

So, the most popular theory is a problem with neurotransmitter(s) in the brain, which makes it fall into a mental treatment category, not mental diagnosis category. The diagnosis category (according to icd 9) is 624.5. This puts it in the same category as other female genital disorders (http://www.icd9data.com/2012/Volume1/580...7-629/625/).

DB, get over the term, get on with addressing the problem. If you don't want pharmacologic treatment and you want a bilateral salpingo-oophorectomy, find a surgeon who will give you one.

If the serotonin (independant of progesterone) was the problem then lupron wouldnt have any effect. If treating the progesterone issue with lupron adresses the serotonin issue then it's the hormone not the neurotransmitter. So I have a problem with labelling it a neurotransmitter disorder, it is not that, it is a hormone disorder. Is thyroid problem a neurotransmitter disorder too because that can cause paranoia so bad it mimics schitzophrenia. This is stigma on woman and it's not ok. It's not ok to ignore the biological female cause of illness and defer it to mental treatment. Not ok at all.

Not getting over the term sorry just because Big Pharma says I should. You post sounds like its spit straight out of a textbook written by lilly. To me this is herd mentality sorry.

All that cognitive and social theory caca you listed is why I choose not to continue in psychology. Who thinks of this shit? oh right... angry white men over 50 who write medical textboooks lol

I do think there is an allergic element in this as the P.M.D.D. effects seen in the amygdala are similar to the amygdala effects seen in allergy. I will go as far as to say there may be a heightened fear response due to an excess of anxiety related chemicals caused by the allergic reaction or maybe the inverse from possible trauma.



On allergy and neurochemical disruption

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678838/

On progesterone

http://www.nature.com/mp/journal/v13/n3/...2030a.html

---

In regards to bilateral salpingo-oophorectomy, its actually not that hard to find someone to do it once you are over 40. What is sad is that woman are forced to wait until they are over 40. Still, it is not a decision that a woman takes lightly even if she knows she doesn't want to have children. There are serious consequences to early menopause especially when the woman likely has another 10 years of eggs hanging around.

[Jackalope]

It is fishy that the big pharmaceutical companies would repackage Prozac as Sarafem just as it is nearing it's patent expiry date.

Umm, generic fluoextine (Prozac) has been available since 2001.

Sarafem is a different formulation (fluoextine hydrochloride). Sarafem is not Prozac.

[brewer]

If the serotonin (independant of progesterone) was the problem then lupron wouldnt have any effect. If treating the progesterone issue with lupron adresses the serotonin issue then it's the hormone not the neurotransmitter. So I have a problem with labelling it a neurotransmitter disorder, it is not that, it is a hormone disorder. Is thyroid problem a neurotransmitter disorder too because that can cause paranoia so bad it mimics schitzophrenia. This is stigma on woman and it's not ok. It's not ok to ignore the biological female cause of illness and defer it to mental treatment. Not ok at all.

Not getting over the term sorry just because Big Pharma says I should. You post sounds like its spit straight out of a textbook written by lilly. To me this is herd mentality sorry.

All that cognitive and social theory caca you listed is why I choose not to continue in psychology. Who thinks of this shit? oh right... angry white men over 50 who write medical textboooks lol

I do think there is an allergic element in this as the P.M.D.D. effects seen in the amygdala are similar to the amygdala effects seen in allergy. I will go as far as to say there may be a heightened fear response due to an excess of anxiety related chemicals caused by the allergic reaction or maybe the inverse from possible trauma.



On allergy and neurochemical disruption

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2678838/

On progesterone

http://www.nature.com/mp/journal/v13/n3/...2030a.html

---

In regards to bilateral salpingo-oophorectomy, its actually not that hard to find someone to do it once you are over 40. What is sad is that woman are forced to wait until they are over 40. Still, it is not a decision that a woman takes lightly even if she knows she doesn't want to have children. There are serious consequences to early menopause especially when the woman likely has another 10 years of eggs hanging around.

The first source discusses symptoms in patients with existing mood disorders. Do you have an existing mood disorder? Also, did you read where it did not correlate to IgE? I'll need something more credible to consider a progesterone allergy hypothesis.

Re Lupron, yes it works. Fine, go on Lupron the rest of your life. No more progesterone for your brain to react to.

Second source, so? Hormones effect areas of the brain. OMG, news flash. Do you believe that it's only female hormones? Give yourself a big dose of prednisone and see how you react.

The most accepted model says, for what ever reason, that area of the brain reacts differently to progesterone changes in some women when compared to others. You do note that they are not talking about excess hormone (as in your thyroid example). So, that area of the brain reacts differently causing symptoms. No one is ignoring the biological cause. The biological cause appears to be in the brain. It's the brain reacting different, not the ovaries. They are offering an alternative treatment to eliminating progesterone. Want removing your amygdala to be an option?

I didn't list the "caca", the source did. But of course, you know better, all that training and education. Yep only angry old white men. Sandra Bem, Leta Hollingworth, Karen Horney, Christine Ladd-Franklin, all pos.

Re surgical risk, Lupron risk, pmdd risk. Make a choice. Do a risk vs benefit analysis and choose.

After bilateral salpingo-oophorectomy, what eggs hanging around? Unless you have them some place else that I don't know about.

[Dust_bunny]

And then we get into a whole new debate on allergy and what "allergy" actually means. I think your definition and the definition of allergy used here is old school. If you think that" allergy" refers to only IgE mediated allergies then we disagree on the terminology but I'm sure we would have to agree to disagree on it.

An excerpt...

---

In non-IgE-mediated allergy, the antibody may belong to the IgG isotype, as in anaphylaxis due to immune complexes containing dextran (32) and the classical, now rare, serum sickness previously referred to as a type III reaction (25), whereas both IgE and IgG antibodies are found in allergic bronchopulmonary aspergillosis (ABPA) (68).
Inhalation of large amounts of protein, as in mold, grain dust, etc., stimulates the immune system to produce antibodies mainly of the IgG, IgA, and IgM isotype. The serum concentration is often high enough to allow detection of the antibody, historically termed “precipitin”, as a precipitate in gel when allowed to react with the corresponding antigen. There is a relation between degree of exposure and antibody concentration. Similarly, the presence in serum of IgA, IgM, and especially IgG antibodies, as a result of exposure but without any obvious pathogenic role, has also been reported to food antigens, such as those of cow's milk and hen's egg (39). In the same way, antigen-specific lymphocytes can often be found by using the antigen-specific lymphocyte stimulation test (50, 71).
Some individuals with high IgG antibody levels as a result of chronic inhalation of large amounts of certain protein-containing material, such as Actinomyces and molds (farmer's lung) and bird droppings (pigeon breeder's disease), may exhibit symptoms from the airways, often referred to as “alveolitis”, upon exposure. We propose that the term allergic alveolitis be used for such diseases.
Allergy can also be cell-mediated, as in allergic contact dermatitis, in which immunologically sensitized lymphocytes play a major role. Similar immunologic mechanisms seem to be important in celiac disease (29) and in non-IgE-associated “atopic dermatitis/eczema” (see below). Therefore, we propose that non-IgE-mediated allergic reactions be subdivided into those in which the reaction is initiated predominantly by mechanisms associated with allergen-specific antibodies other than IgE, and those in which a cellular response is predominant.

http://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2001.00002.x-i1/full

I think it's likely to be a cell mediated non IgE " reaction" " allergy" " hypersensitivity or whatever you prefer to call it. 

I have however read a story once about a woman who apparently was so "allergic" to progesterone she would have anaphylaxis during pms. She did actually have to have her ovaries removed.

Your comment about the eggs... its odd that you would perceive that I was referring to post surgery not pre surgery. Was it something in the way I wrote it or the way you interpreted it? My statement refers to the idea that if mom and grandma bleed well into thier 50's there may be another 10 years of eggs hanging around in a woman in thier 40's. Thats 10 years worth of hormone protection from advanced aging that one sacrifices for happiness. You may find that the trade off for such serenity is osteoporosis... not to mention, the fires that makes one sexy like shiney hair, unwrinkled skin etc...

You cant stay on lupron for the rest of your life. It's simply used as a trial to see if you are a good candidate for getting oophed. 

---

I think it boils down to this

Treat the neurotransmitters with antidepressants
or
Pull the plugs on the cause ( the ovaries that produce the offending hormones )

My point is that woman should have that option, long before their lives have been destroyed. But Big pharma makes much more money off option one. 

Maybe they will change their stand when they use their logic to realize they can really profit off osteoporosis.

When all is said and done, the truth can always been found in the most up to date hoarded patents. I will check them out later. I will look for better links on the allergy theory as well... probably wont find much for another 5-10 years.

In regards to your comnent about thyroid issues, yes agreed, but your original definition of the ovarian hypothesis was wrong as it inferred an imbalance so my comment was in regards to your position.

It's a womans problem because it happens to woman and even if it was due to testosterone, it would still be a womans problem...

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