Premenstrual Dysphoric Disorder Natural Treatment

The Pmdd Treatment Miracle

Cure Premenstrual Dysphoric Disorder Naturally! Are You Sick of The Cycle Of Destructive Mood Swings, Irritability, Anxiety, Pain, And Generally Feeling Out Of Control Every Month? In just a few short weeks you can be rid of all these problems naturally, permanently, and without drugs of any kind with a Pmdd treatment miracle! Do You Want To Learn How To: Eliminate pain from bloating, headaches, migraines and cramps in just 12 hours! Normalize your moods and temper during this period so that you never feel out of control again, and never end up saying or doing things that hurt the ones you love any more! Completely eliminate the feelings of hopelessness, depression and even suicidal thoughts that can incapacitate you during Pmdd! End binge eating and other compulsive activities that control your life when Pmdd hits! Completely control Premenstrual Dysphoric Disorder and eliminate all its symptoms in just 2 months naturally no drugs right down to the root cause of Pmdd! Read more here...

The Pmdd Treatment Miracle Summary


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Author: Jane Pritchard
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All of the information that the author discovered has been compiled into a downloadable ebook so that purchasers of The Pmdd Treatment Miracle can begin putting the methods it teaches to use as soon as possible.

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Premenstrual Dysphoric Disorder

Several randomized, blinded, placebo-controlled trials that used various diagnostic criteria and outcome measures have established the efficacy and tolerability of fluoxetine in the treatment of PMDD (Menkes et al. 1993 Pearlstein et al. 1997 Steiner et al. 1995 Su et al. 1993, 1997 Wood et al. 1992). In the largest study, 313 women with DSM-III-R-defined late luteal phase dysphoric disorder (American Psychiatric Association 1987) received 20 mg of fluoxetine, 60 mg of fluoxetine, or placebo daily for six menstrual cycles after a two-cycle placebo washout period (Steiner et al. 1995). One hundred eighty women completed the study. Both doses of fluoxetine were superior to placebo, beginning at the first menstrual cycle and continuing throughout the six cycles. More patients treated with 60 mg of fluoxetine discontinued because of adverse events than did patients treated with 20 mg of fluoxetine or placebo. More patients treated with placebo discontinued because of lack of response than...

Role of Pharmacotherapy

The symptoms of PMDD occurring during the luteal phase suggest that ovulation and its associated fluctuations in ovarian steroids are important for the manifestation of symptoms. A seminal study found that women with PMDD experienced symptom improvement with gonadotropin releasing hormone (GnRH) agonist treatment, only to experience a return of mood symptoms when estradiol or progesterone was added back. These data support the theory that women with PMDD, but not healthy controls, are sensitive to ovarian hormone exposure. While the suppression of ovulation with GnRH agonist treatment is effective in the majority of women with PMDD, it is not a long-term treatment option secondary to the negative health effects of extended hypoestrogenism in young premenopausal women. Interestingly, ovulation suppression with oral contraceptives is not effective and can worsen mood symptoms in women with PMDD. An exception to this is contraceptive treatment with agents containing the progestin...

Indications And Efficacy

Food and Drug Administration (FDA)-labeled indications for fluoxetine are major depressive disorder, obsessive-compulsive disorder (OCD), panic disorder, bulimia nervosa, and premenstrual dysphoric disorder (PMDD). We will review these as well as some other disorders for which fluoxetine is commonly used.

Menopausal Vasomotor Symptoms

In addition to its proven efficacy in PMDD, paroxetine (20 mg day) was shown to be effective in the treatment of postmenopausal hot flashes in breast cancer survivors with chemotherapy-induced ovarian failure in two open trials (Stearns et al. 2000 Weitzner et al. 2002) for a review, see

Paroxetine Introduction

Paroxetine (Paxil) is classified as one of the serotonin reuptake inhibitors (SRIs) because of its potent inhibition of presynaptic serotonin (5-HT) uptake. It is also a relatively potent norepinephrine (NE) reuptake inhibitor, particularly at higher doses, leading some to argue for its inclusion in the growing class of acknowledged dual serotonin-norepinephrine reuptake inhibitors (SNRIs). Since its approval for the treatment of depression, paroxetine has been demonstrated to be effective and has been approved for a broad spectrum of anxiety disorders, including panic disorder, obsessive-compulsive disorder (OCD), social anxiety disorder, generalized anxiety disorder (GAD), and posttraumatic stress disorder (PTSD). Moreover, studies have demonstrated the efficacy of paroxetine in premenstrual dysphoric disorder (PMDD), postmenopausal hot flashes, and child and adolescent OCD and social anxiety disorder. Paroxetine is still one of the most prescribed antidepressant medications in the...

Estrogen and Depression

Because of increased incidence of depression at critical hormonal transition phases such as postpartum and perimenopause, much speculation has taken place about estrogen's role as a precipitant. Recent studies have found increased incidence of depressive symptoms and major depression during the menopause transition (Cohen et al. 2006 Freeman et al. 2006). The initial findings of Freeman et al. (2004) in regard to estrogen were that both high and low estrogen levels were associated with depression. More recently, the data suggest that variability in estrogen levels may drive depression. A model of differential sensitivity to estrogen has been proposed for premenstrual dysphoric disorder (PMDD) and also by Cohen et al. (2006) to explain the findings of increased depression during the menopause transition. Increased FSH, suggesting ovarian aging, and overall low or variable estrogen were also found to be strongly associated with depression (Freeman et al. 2006). And in the Freeman et al....


Fluoxetine is a selective serotonin reuptake inhibitor (SSRI). One of the earliest of these drugs to be developed, it is widely perceived in the popular culture to be paradigmatic of the class. It is commonly used in the treatment of depression and the more severe anxiety disorders (e.g., obsessive-compulsive disorder, panic disorder). Fluoxetine is also approved for the treatment of bulimia nervosa, anorexia nervosa, and premenstrual dysphoric disorder. A distinguishing pharmacokinetic feature of the drug is its long elimination half-life (up to 4-6 days during long-term use and up to 2 weeks for the major active metabolite norfluoxetine). As with other SSRIs, the most common troublesome side effect of fluoxetine is sexual dysfunction (dysorgasmia and erectile dysfunction) mild side effects include drowsiness, headache, and nausea. Some patients develop a syndrome of psychomotor activation upon starting the drug, which has been characterized as similar to akathisia.


Augmentation therapy for women during these stages of life. Perimenopause is the phase before menopause, which continues until menstruation has ceased for 12 consecutive months. Common symptoms include hot flashes, decreased libido, sleep disruption, and depression. In one study, perimenopausal women with major depression, dysthymic disorder, or minor depressive disorder received transdermal patches of 17 b -estradiol (100 mg) or placebo in a 12-week study (336). Sixty-eight percent of women treated with estradiol had remission of depression compared to 20 in the placebo group (336). An earlier study also found that estrogen was superior to placebo in reducing depressive symptoms in perimenopausal women (337). A small study of 16 perimenopausal women found that estrogen replacement therapy was effective in treating depression (338). Other studies have found that both transdermal patches and sublingual estradiol improved mood in women with premenstrual dysphoric disorder and postpartum...


The initial suggestion that the CCK system might be involved in anxiety came from experiments of Bradwejn and de Montigny (1984) showing that benzodiazepine receptor agonists could attenuate CCK induced excitation of rat hippocampal neurones. Subsequent clinical studies demonstrated that bolus injections of the CCK2 receptor agonist CCK4 or pentagastrin provoke panic attacks in patients with panic disorders (Bradwejn et al. 1991, 1992). Recent investigations have revealed that the panicogenic effects of CCK2 receptor agonists are not limited to patients with panic disorder, because individuals with social phobia, generalized anxiety disorder, obsessive compulsive disorder, and premenstrual dysphoric disorder also exhibit an augmented behavioural response to these ligands (Le Melledo et al. 1995 De Leeuw et al. 1996 van Vliet et al. 1997). Interestingly, a significant association exists between panic disorder and polymorphism of the CCK2 receptor gene (Kennedy et al. 1999). The...

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