The question is, does Prestiq have the effects I require for the depression reduction or am I simply spinning my wheels here?

This is a post from a different site about their take on Prestiq:

" Pristique is just a metabolite of effexor. It was marketed because the patent on effexor was lapsing. It is a cynical attempt to to make more money by marketing a drug that has no benefit over effexor except exclusive marketing rights. If you want to take pristique, take generic effexor and your liver will convert it to pristuque in a few hour for free. Nonsensical drug like this make healthcare needlessly expensive."

Comments??

I have been on almost every AD medication since the early 90's, Paxil,through the latest,Prestiq.

Between the mixes and eliminations of the different meds,I am still wondering about this one.The combination of Prestiq and Zoloft, along with Depakote ,Ativan,Sonata and Trazadone(for sleep), Lovaza for the increased cholesterol,(and Crestor), wow,too many meds for this guy.I am in the time of this round of recovery, where I question the meds overall effectiveness.Much less their necessity.I will continue with the doctors and therapy I have today, they are top notch, I just want to see how others have been on this medication.

Ken, I'm having a hard time finding it here at my hospital formulary by that name. Does it have a generic name?

Found it, but it's loooooong!

Classification:

Psychotropic Agents
Antidepressants
Serotonin norepinephrine reuptake inhibitors


Description: Desvenlafaxine succinate is an oral antidepressant of the serotonin-norepinephrine reuptake inhibitor (SNRI) class. It is the major active metabolite of venlafaxine (Effexor®). Desvenlafaxine is FDA approved for major depressive disorder (MDD) and pending approval for vasomotor symptoms associated with menopause. Symptoms of menopause which have been under evaluation in clinical trials include hot flashes, sleep disruption, overall climacteric symptoms, mood changes, and somatic symptoms. Desvenlafaxine is currently being evaluated in phase III trials as a potential treatment option for pain associated with peripheral diabetic neuropathy and fibromyalgia syndrome. The efficacy of SNRIs is similar to another major class of antidepressants, the selective serotonin reuptake inhibitors (SSRIs); however, they differ in mechanism of action and side effect profile as a result of the neurotransmitters they affect. Antidepressants such as desvenlafaxine which modulate norepinephrine as opposed to exhibiting serotonin selectivity are generally more beneficial in the treatment of pain syndromes. The related compound venlafaxine has been used in the treatment of neuropathic pain, diabetic neuropathy, headache, and fibromyalgia. Desvenlafaxine is likely to benefit women who want to avoid estrogen treatment for vasomotor symptoms associated with menopause, or women in whom estrogen therapy may be contraindicated, such as those with invasive estrogen receptor-positive breast cancer. An approvable letter was issued in July 2007 for the treatment of menopausal symptoms; final approval is pending. In February 2008, desvenlafaxine (Pristiq™) was approved by the FDA for major depressive disorder (MDD) in adults.

In October 2004, the FDA directed manufacturers of all antidepressants to include a Black Box warning, expanded warning statements, and clinical trial results detailing the increased risk of suicidality in children and adolescents. The warning was subsequently revised to include data on the increased risk of suicidality in young adults. A Patient Medication Guide (MedGuide) should accompany all prescriptions for antidepressants. It is advisable to prescribe medications, including desvenlafaxine, in the smallest quantity consistent with good clinical practice in patients with depressive disorders or other conditions with suicidal potential.

Mechanism of Action: Decreased adrenergic and serotoninergic neurotransmission has been proposed to play a key role in the etiology of depression. It is theorized that serotonin (5-HT) and norepinephrine (NE) reuptake inhibitors work by blocking the central presynaptic reuptake of 5-HT and NE, resulting in an increased sustained level of these neurotransmitters. Changes in postsynaptic receptor characteristics with chronic administration may also contribute to the efficacy of antidepressants. Serotonin is a neurotransmitter which regulates an extensive modulatory behavioral system in the brain. The serotoninergic system is known to modulate mood, emotion, sleep, and appetite and thus is implicated in the control of numerous behavioral and physiological functions. Norepinephrine is an adrenergic neurotransmitter which appears to be involved in a range of psychological processes, including mood stabilization, sleep regulation, overall alertness and arousal, and in regulating response to stressors which might initiate or exacerbate depressive symptomatology. Desvenlafaxine does not appear to possess monoamine oxidase inhibiting activity.

Pharmacokinetics:
Desvenlafaxine is administered orally. Desvenlafaxine is the major active metabolite and an enantiomer of racemic venlafaxine. Animal studies have shown that peak plasma and brain concentrations of the drug occur 30 minutes following a subcutaneous dose of 30 mg/kg.[33107] In the presence of a 5-HT1A antagonist, serotonin levels in the hypothalamus increased 225% after 1 hour. Norepinephrine levels increased 44% after 3 hours, while dopamine remained unchanged. Desvenlafaxine was not detectable in plasma 24 hours following the dose.[33107]

Pharmacokinetic study results obtained in humans are available from administration of the parent compound venlafaxine and subsequent observation of desvenlafaxine kinetics. These results indicate that protein binding of desvenlafaxine is 30%. The primary metabolite is the O-glucuronide conjugate of the drug. The elimination half-life is 11 hours.


•Special Populations
Hepatic Impairment
It appears that the half-life of desvenlafaxine is affected by the presence of hepatic disease. Data indicate that the elimination half-life of desvenlafaxine is 60% longer and clearance is 30% less in patients with hepatic disease compared to those with normal hepatic function. Guidelines for dosing in the presence of hepatic impairment are not available.

Renal Impairment
It appears that the half-life of desvenlafaxine is affected by the presence of renal disease. Compared to patients with normal renal function, the half-life of desvenlafaxine increases by about 40% in patients with renal impairment, but clearance appears to be unaffected. Guidelines for dosing in the presence of renal impairment are not available.

References

33107. Alfinito PD, Huselton C, Chen X, et al. Pharmacokinetic and pharmacodynamic profiles of the novel serotonin and norepinephrine reuptake inhibitor desvenlafaxine succinate in ovariectomized sprague-dawley rats. Brain Res 2006;1098:71-8.

[ Revised 5/14/2010 1:15:00 PM ]

I hope this helped. Here is the link, but I'm afraid you probably can't get into it.

Mosby's Nursing Consult -- Start Session Cookie Error

J-9

Thank you for this information,I am making this a poll in hopes others can look at what questions like this can produce:)

I know that the info I posted was VERY clinical. I got the info from our pharmacy formulary at work. I felt that you had a good enough understanding of medication to be able to dig through this and get the info you need.

I spent about an hour of research on our patient care site trying to find the info in a more layman friendly structure, but it seems that we don't have any particular patient information on this medication.

I'll try to dig out my drug book (lost in the shuffle of remodeling last year) to see if I can break it down in to terms that are easier to understand.

Re-reading through this, I might ask my doctor about it tomorrow for my menopause symptoms. Maybe I can get into one of the clinical trials.

Ken,

The fact that one drug is a metabolite of another is not necessarily problematic. As example, oxymorphone is a minor metabolite of oxycodone. Oxymorphone is far more powerful that oxycodone. Basically, a metabolic step was removed and oxymorphone marketed independently. That's a benign example and doesn't necessarily address your instant question.

I have done a great deal of research on SSRI and depression. I'm going to take a moment to explain one component: The placebo effect. That means that treatment works because the patient believes and has confidence in the therapeutic process. Not necessarilyalthough possibly the drug. (This is my parapharse of placebo)

In the treatment of depression it has been a consistent finding that the placebo effect is extraordinarily high.

What does that mean for treatment? I believe, that much of the improvement in depression can be traced to non-pharmacologic elements of the treatment process. The research supports my view. Nonetheless many people currently on antidepressants (and that's almost anyone who ever uttered "depression" in front of their doctor) believe in the antidepressant.

The public never sees the research results. That is published in peer review journals and by the time it reaches popular publications it has been reworked and edited by writers from the pharm companies. Nonetheless, they have influenced public opinion to the point that there is a belief in SSRIs and the seratonin hypothesis in justifying their purported efficacy. This adds to the placebo effect noted foregoing.

I have intentionally avoided, here and in other public lay forums, the subject of antidepressants (SSRI class) so as not to negatively impact those currently being treated with same. If someone is deriving benefit, or believes they are deriving benefit which is procedurally the same thing, the research to the contrary is meaningless to them.

It sounds as though you are questioning and should be provided access to information. Some is available on line, most not.

I know that as an anonymous poster I am not going to change public opinion or expose medical science. It is just my concern that if I should jar even one person from the benefit they obtain from their antidepressant if I have not done more harm than good.

Based on J_9 post (she has good manuals)

"Classification:

Psychotropic Agents
Antidepressants
Serotonin norepinephrine reuptake inhibitors"

I would conjecture that Pristique was introduced because of the last sentence. Behind the scenes there has been a movement away from the monoamine (seratonin hypothesis) as the primary neurotransmitter of interest in depression. You will see many new drugs entering the market that now target both seratonin and norepinephrine (SNRI). Interestingly, the monoamine hypothesis was first introduced in 1965 by Joseph Schildkraut and the focus was on norepinephrine. It was two years later, in 1967 that researchers began to theorize that serotonin was the neurotransmitter of interest (Coppen, 1967). So the idea isn't new nor does it have more scientific evidence in support than 50+ years past.

But I believe that's why you are seeing Pristique, Cimbalta, etal. It is a shift toward a new paradigm rather than an expiring patent. New only in the sense that the public is pharmacologically naïve and it will be portrayed as a medical research advancement by the pharmaceuticals as SNRIs displace SSRIs on the prescription pad. (Effexor is also SNRI)

Both of you, I am very much into this type of information, your input has greatly opened doors for questions and further research into the medications I(and others) take.

Thank you both!

To further this,Why then is there a need to continue on the Zoloft(in my case) and for many others,their need to continue using SSRI's in their regiment,if a product like this one does the work for 2 neurotransmitters?

Is there an over medicating or over treatment of the seratonin by using these in conjunction?(always been on my mind but was reluctant to ask, one too many doc would dismiss me as just a lay man,not schooled enough to understand)

Thanks again for any further discussion, I am out of 'greenies' for both of you, have to spread the rep more.

Quote:

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Originally Posted by KBC

To further this,Why then is there a need to continue on the Zoloft(in my case) and for many others,their need to continue using SSRI's in their regiment,if a product like this one does the work for 2 neurotransmitters?

Is there an over medicating or over treatment of the seratonin by using these in conjunction?(always been on my mind but was reluctant to ask,,one too many doc would dismiss me as just a lay man,not schooled enough to understand)

Thanks again for any further discussion,,I am out of 'greenies' for both of you,,have to spread the rep more.

---

I'm going to pass this one on to Dr. Bill, it's more up his alley.

Well, went to doc today for a follow up on my thyroid. I have gained 7 pounds in 6 weeks, not good considering I'm on Synthroid. I also mentioned my hot flashes. It was the doc who suggested Prestiq for the hot flashes and to help reduce weight. We will see what the next month brings.

Well,birds of a feather.. :p

Welcome back to better living through modern chemistry!

I apologize for being slow to respond. I'm very anxious to provide what info I have gathered over the years. Right at the moment I've having connection problems. I get right in the middle of something and the system shuts down. This is computer 2 on the blink. So I may have to piece my posts together If it keeps working.

Quote:

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Originally Posted by DrBill100

I apologize for being slow to respond. I'm very anxious to provide what info I have gathered over the years. Right at the moment I've having connection problems. I get right in the middle of something and the system shuts down. This is computer 2 on the blink. So I may have to piece my posts together If it keeps working.

---

I've got time Bill, These types of questions aren't life threatening, I am just looking for more information,like always.

First let me venture over to the left edge of your initial post/complaint and tie it together with information I have derived from other threads.

1) You're in the process of trying to quit smoking and using a nicotine patch.

2) Cigarette smoke has an antidepressant effect. To date, the chemical properties that inhibit Monoamine Oxidase (MAO) are unknown. It has been firmly established that it is not nicotine. See Researchers Explore Link Between Smoking, Depression ? Psychiatric News

This is probably just outside the subject matter but may have personal significance to you. Above I provided one link to research and there are more. Overall this is a very significant issue as persons with depression are likely to be smokers. An interesting variable that has received no popular media coverage.

The information provided to the public (including physicians) about depression and treatment is in direct conflict with medical research that is reported in peer review journals, select professional publications and the like. Elliott Valenstein, Professor Emeritus of Neuroscience, first noted this disparity in 1998, at the dawn of consumer advertising of SSRIs. He summarized the scientific data by concluding, “What physicians and the public are reading about mental illness is by no means a neutral reflection of all the information that is available”

The fact that antidepressants are being marketed directly to the public, that patients are going to a doctor and telling the doctor what medication, by brand name, they want is unprecedented. This direct to consumer advertising (DTCA) is the subject of widespread criticism within journals and the bain of most doctors. See as example: Lacasse & Leo (2005)

It is largely due to the DTCA that the seratonin hypothesis took hold. Explaining depression as a chemical imbalance in the brain that pharmaceutical manufacturers claim to correct with SSRIs.

Since 1967 when a chap named Coppen first advanced the theory (Br. J. Psy) not one single study has emerged to support the theory. The entire basis for asserting that seratonin is implicated in depression comes from the backward reasoning that since SSRIs are effective in treating depression and it works on seratonergic neurons therefore seratonin must be the cause.

It has been known for years that SSRIs were only minimally effective, and since 2005 when concealed studies were uncovered there is now the belief that SSRIs are "clinically insignificant." (See mega-analysis by Kirsch, 2008)

Therefore you are seeing a movement away from a badly flawed therapeutic approach. The development of an alternative therapy that also incorporates the neurotransmitter norepinephrine. The norepinephrine theory actually pre-dated the seratonin theory. There is no scientific evidence to demonstrate the involvement of any particular neurochemical in any mental disorder (See Kirsch, above)

So,if it isn't a chemical imbalance,what is the treatment option, if medications are the typical band-aid for this,a smoke screen covering the real problems, is the answer really in some form of psychotherapy?

Do the studies/speculations of Leo Booth/John Bradshaw have more validity to them than has been given credit for?Toxic Shame by Leo Booth/John Bradshaw