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Phosphatidylserine for Seroquel Withdrawal

Posted by BP2Guy on August 3, 2013, at 5:05:29

I posted this on longecity but since there are more people on here trying to withdrawl from Seroquel, I thought I'd post it here as well. I'm quite surprised no one has came up with a stack that would help with Seroquel's withdrawal effects, namely the acute insomnia & anxiety that occurs during dose reduction.

Phosphatidylserine seems to be able to significantly surpress cortisol which gets jacked up during Seroquel withdrawal, probably as the a1 adrenergic receptor gets unblocked. Seroquel itself has a cortisol reducing effect based on the study below, so reducing the dose will increase your cortisol. I find 100 mg Phosphatidylserine as well as 500 mg Tryptophan every night, 1 hour before I fall asleep, to significantly regulate my cortisol levels, reduce anxiety and keep my mood stable. Those of you who try this will probably need higher dosages of PS(400-600 mg) since I'm generally very sensitive to supplements. As for Tryptophan, this may or may not be necessary, I just want to saturate my brain with enough precursors to make serotonin (which becomes low when cortisol is high) and melatonin, which will aid in sleep induction. I recommend you start at the lowest dose so you don't experience any side effects such as insomnia.


Phosphatidylserine and cortisol:

http://www.livestrong.com/article/498027-phosphatidylserine-cortisol/

My Log:

CORTISOL:

Last night I had AMAZING sleep which is very unusual when I cut the Seroquel XR dose down to 25mg. I took 100 mg Phosphatidylserene + 30 mg Zinc at around 10 PM and slept at 12 PM. In the morning I did not feel ANY of the high cortisol response, such as rapid heart palpitations, vigilance, etc. which I usually get when I cut down the dose. Perhaps it starts to have less affinity for the a1 receptor. If the affinity of the a1 receptor is this weak already, perhaps its affinity for the other receptors such as 5HT2A should be almost insignificant since Quetiapine first much bond to H1, then a1, etc. according to TLP.


Circadian secretion of cortisol in bipolar disorder:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC167199/

Graph: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC167199/figure/f1-6/

It seems that depressed bipolar patients have higher night time cortisol levels when compared to other types of bipolar groups, as well as the control group.

As we all know, a lot of bipolars suffer from insomnia and high cortisol may be one of the causes of the impaired sleep:

http://www.ncbi.nlm.nih.gov/pubmed/11924040

Quote

Neuroendocrine dysregulation in primary insomnia.

Recent research has pointed to a functional link between stress, disturbed sleep, psychiatric disorders, ageing, and neuroendocrine dysfunctions. In particular, increased activation of the hypothalamic-pituitary-adrenal (HPA) axis--expressed as elevated plasma cortisol levels--was shown in physiological ageing and patients with psychiatric disorders. We found increased evening and nocturnal plasma cortisol concentrations in patients with primary insomnia. Considering that both ageing and psychiatric disorders are commonly associated with sleep disturbances, our results implicate that elevated cortisol concentrations are a rather unspecific feature of disturbed sleep. Furthermore, our data revealed a strong positive correlation between evening cortisol secretion and the number of nocturnal awakenings in both insomniac patients and controls. Since nocturnal exposure to increased HPA activity promotes sleep fragmentation even in healthy controls, increased evening cortisol levels may be a crucial factor in inducing and maintaining sleep disturbances. We therefore propose a model of HPA dysregulation in insomnia. This model is based on the arousal theory of insomnia and the strong correlation between evening cortisol secretion and sleep fragmentation as a pathophysiological mechanism of a vicious cycle of insomnia. In patients with long-lasting insomniac complaints we found decreased nocturnal plasma melatonin levels thereby indicating a labilisation of circadian rhythm functions. Taken together, the neuroendocrine dysregulation seems to be more expressed in chronic insomnia than in acute insomnia and may be a contributing factor in maintaining disturbed sleep.


It seems Seroquel reduces the amount of overall night time cortisol levels and may be one of its sleep inducing mechanisms. This makes sense sense since it's an a1 antagonist.

http://www.ncbi.nlm.nih.gov/pubmed/14735295

Quote

Quetiapine reduces nocturnal urinary cortisol excretion in healthy subjects.

RATIONALE:

Hypothalamic-pituitary-adrenal (HPA) axis dysfunction is a frequent finding in psychiatric disorders, including psychotic depression and schizophrenia. Conflicting results exist concerning the influence of antipsychotics on the HPA-axis.
OBJECTIVE:

Therefore, this double-blind, placebo-controlled, randomized cross-over study investigated the effect of quetiapine on nocturnal urinarycortisol and melatonin excretion in 13 healthy male subjects under conditions of undisturbed and experimentally disturbed sleep.
METHODS:

Volunteers were studied 3 times for 3 consecutive nights (N0, adaptation; N1, standard sleep conditions; N2, acoustic stress) 4 days apart. Placebo, quetiapine 25 mg or quetiapine 100 mg was administered orally 1 h before bedtime on nights 1 and 2. Urine produced during the 8-h bedtime period was collected for later determination of cortisol and melatonin concentrations by standard radioimmunoassays.
RESULTS:

MANOVA showed a significant effect for N1 vs. N2 with elevated total amount of cortisol ( p<0.005) and melatonin ( p<0.05) excretion after acoustic stress. Both quetiapine 25 mg and 100 mg significantly ( p<0.0005) reduced the total amount of cortisol excretion in comparison to placebo. No interaction effect of stress condition was observed. There was no effect of quetiapine on melatonin levels.
CONCLUSION:

The significant reduction of nocturnal cortisol excretion following quetiapine reflects a decreased activity of the HPA-axis in healthy subjects. This finding may be an important aspect in quetiapine's mode of action in different patient populations.


To sum everything up, reducing night time cortisol seems essential for quality sleep, which we all know, is one of the most important factors in regulating BPD. PS + Zinc is going to be essential for me to maintain quality sleep as I slowly taper off Seroquel, especially as it loses affinity for the a1 receptor causing my cortisol levels to elevate.


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