39 replies to this topic

[Flex]

Or a NA/DA uptake enhancer like Luteolin or Apigenin

Functional activation of monoamine transporters by luteolin and apigenin isolated from the fruit of Perilla frutescens (L.) Britt.

http://www.ncbi.nlm....pubmed/19815045

But they are both uptake inhibitors of 5-ht and intefere with p21

 

If You or Somebody are still looking out for Herbal antipsychotica, then this could be interresing:

- Tetrahydropalmatine -> via D1,D2,D3 ( affinity in that order) and a1 antagonsim, interresting for cocaine addiction

- Stepholidine -> via D1 + 5-ht1a partial agonism and D2 antagonism

- Alstonine -> via 5-ht2a/c activation or blockade

 

L-Stepholidine-induced excitation of dopamine neurons in rat ventral tegmental area is associated with its 5-HT(1A) receptor partial agonistic activity.

http://www.ncbi.nlm....pubmed/20803620

Edited by Flex, 28 August 2014 - 12:42 AM.

[Area-1255]

Or a NA/DA uptake enhancer like Luteolin or Apigenin

Functional activation of monoamine transporters by luteolin and apigenin isolated from the fruit of Perilla frutescens (L.) Britt.

http://www.ncbi.nlm....pubmed/19815045

But they are both uptake inhibitors of 5-ht and intefere with p21

 

If You or Somebody are still looking out for Herbal antipsychotica, then this could be interresing:

- Tetrahydropalmatine -> via D1,D2,D3 ( affinity in that order) and a1 antagonsim, interresting for cocaine addiction

- Stepholidine -> via D1 + 5-ht1a partial agonism and D2 antagonism

- Alstonine -> via 5-ht2a/c activation or blockade

 

L-Stepholidine-induced excitation of dopamine neurons in rat ventral tegmental area is associated with its 5-HT(1A) receptor partial agonistic activity.

http://www.ncbi.nlm....pubmed/20803620

That's interesting, though I think forskolin would do the trick in most cases.

[Nemo888]

The one third full remission rate for mental illness requiring hospitalization has not changed appreciably since the 1770's.

[Flex]

That's interesting, though I think forskolin would do the trick in most cases.

 

 

Or CREB
Molecular evolution in the CREB1 signal pathway and a rare haplotype in CREB1 with genetic predisposition to schizophrenia

http://www.ncbi.nlm....pubmed/25043418

 

Ncbi has many abstracts which mentions that Herb or Compound XY increases CREB or the mRNA

 

Example: You know the persevative E211 / sodium benzoate (or natrium benzoate) ?

 

Up-regulation of neurotrophic factors by cinnamon and its metabolite sodium benzoate: therapeutic implications for neurodegenerative disorders.

http://www.ncbi.nlm....pubmed/23475543

NaB induced the activation of protein kinase A (PKA), but not protein kinase C (PKC), and H-89, an inhibitor of PKA, abrogated NaB-induced increase in neurotrophic factors. Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-κB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB

 

On the other hand DISC-1 disfunction leads to a increase of CAMP in the PFC

and Guanfacine an a2 agonist decreases CAMP levels in the PFC.

Disrupted in schizophrenia 1 modulates medial prefrontal cortex pyramidal neuron activity through cAMP regulation of transient receptor potential C and small-conductance k(+) channels.

http://www.ncbi.nlm....pubmed/24560582

 

PKA can activate CREB but CaMKIIa as well e.g. through the "Herbal Piracetam" Clausenamide:

(-)Clausenamide facilitates synaptic transmission at hippocampal Schaffer collateral-CA1 synapses.

http://www.ncbi.nlm....pubmed/22366429

(-)clausenamide promoted the activation of CaMKIIα at concentrations of 0.1, 1 and 10 μM, and pretreatment with KN93 (CaMKIIα inhibitor, 10 μM) completely blocked the enhancement of synaptic transmission induced by (-)clausenamide. cAMP response element-binding protein (CREB) was activated by (-)clausenamide and inhibited by KN93 preincubation, but H89 (PKA inhibitor, 10 μM) had no effect, indicating that (-)clausenamide facilitated synaptic transmission by a PKA-independent pathway.

 

 

So dunno... It seems to me that decreased CAMP levels are causing Negative symptoms, whereas a increase in CAMP causes

Positive symptoms and I would look for something that more enduringly incereases CAMP/CREB levels than taking something daily

 

Edited by Flex, 28 August 2014 - 02:10 PM.

[Flex]

Sry I didnt wanted to say that: solely CAMP is sufficent to treat Schiophrenia.

 

This too odd for me.

Because: Neurotransmitter ( among others) are raising or decreasing CAMP levels, so neurotransmitters could be the first address

Edited by Flex, 28 August 2014 - 07:28 PM.

[Area-1255]

Sry I didnt wanted to say that: solely CAMP is sufficent to treat Schiophrenia.

 

This too odd for me.

Because: Neurotransmitter ( among others) are raising or decreasing CAMP levels, so neurotransmitters could be the first address

Most antipsychotics have a mixed effect on cAMP, mainly raising it. By blocking alpha receptors (which most antipsychotics) do, and by blocking D(2)'s, there is nearly a four fold increase of cAMP while on AntiPsychotics; this helps explain the massive surge or cortisol and ACTH that occurs when on these drugs. This has negative effects on many normal memory functions, mostly due to the interaction with adrenal hormones.

Remember that cAMP is an important messenger in the KREBS Cycle and also in G's Coupled Protein and Kinase receptors.

Excess cAMP tends to lead to hyperthyroidism, trouble sleeping and ACTH/Cortisol excess, whereas low levels of cAMP leads to low sympathetic tone and lack of proper thyroid hormone conversion.

[Flex]

wow You seem to have some knowledge.

I actually have sleep trouble since many years ( caused by Cannabis in the Adolescence) and this could explain it or at least help.

Is this Your profession ? Do You know more about Neurology ?

I actually wonder why this Forum lacks of Psychatrist and other Academic people.

I would pester them with questions

Edited by Flex, 28 August 2014 - 11:05 PM.

[YoungSchizo]

 

Sry I didnt wanted to say that: solely CAMP is sufficent to treat Schiophrenia.

 

This too odd for me.

Because: Neurotransmitter ( among others) are raising or decreasing CAMP levels, so neurotransmitters could be the first address

Most antipsychotics have a mixed effect on cAMP, mainly raising it. By blocking alpha receptors (which most antipsychotics) do, and by blocking D(2)'s, there is nearly a four fold increase of cAMP while on AntiPsychotics; this helps explain the massive surge or cortisol and ACTH that occurs when on these drugs. This has negative effects on many normal memory functions, mostly due to the interaction with adrenal hormones.

Remember that cAMP is an important messenger in the KREBS Cycle and also in G's Coupled Protein and Kinase receptors.

Excess cAMP tends to lead to hyperthyroidism, trouble sleeping and ACTH/Cortisol excess, whereas low levels of cAMP leads to low sympathetic tone and lack of proper thyroid hormone conversion.

 

 

So I had a point all along accusing antip's for "killing" my gains with bodybuilding (and causing stress and worsening some of my symptoms). Even after quitting I couldn't gain (I asked my psychiatrist for years to investigate my thyroid system but they never did). I'm maintaining a healthy hormone-household with Pregnenolone (and Mirtazapine, which also reduces Cortisol). 

[Area-1255]

 

 

Sry I didnt wanted to say that: solely CAMP is sufficent to treat Schiophrenia.

 

This too odd for me.

Because: Neurotransmitter ( among others) are raising or decreasing CAMP levels, so neurotransmitters could be the first address

Most antipsychotics have a mixed effect on cAMP, mainly raising it. By blocking alpha receptors (which most antipsychotics) do, and by blocking D(2)'s, there is nearly a four fold increase of cAMP while on AntiPsychotics; this helps explain the massive surge or cortisol and ACTH that occurs when on these drugs. This has negative effects on many normal memory functions, mostly due to the interaction with adrenal hormones.

Remember that cAMP is an important messenger in the KREBS Cycle and also in G's Coupled Protein and Kinase receptors.

Excess cAMP tends to lead to hyperthyroidism, trouble sleeping and ACTH/Cortisol excess, whereas low levels of cAMP leads to low sympathetic tone and lack of proper thyroid hormone conversion.

 

 

So I had a point all along accusing antip's for "killing" my gains with bodybuilding (and causing stress and worsening some of my symptoms). Even after quitting I couldn't gain (I asked my psychiatrist for years to investigate my thyroid system but they never did). I'm maintaining a healthy hormone-household with Pregnenolone (and Mirtazapine, which also reduces Cortisol). 

 

Yeah, that and they also massively release prolactin.

Recovery Protocol should include not just anti-cort agens but anti-Prolactin as well.

Interestingly, many antipsychotics have different effects on receptor mRNA.

For example SEROQUEL tends to either cause an increase in dopamine D(2) receptor mRNA (especially in the Hypothalamus), or doesn't change it at all. Seroquel also disassociated with the D2 receptor after a couple weeks of treatment; thus stamping Seroquel's main MOA as 5-HT2A antagonist and alpha-1-adrenergic blockade, as well as histamine H(1) blockade. and thus does not cause as many sexual side-effects. Some people have actually reported aphrodisiac activity from Seroquel, however, most of the time this is not evident because the drug's sedating property tends to over ride this potential action / benefit. 

 

http://www.academia...._mood_syndromes

http://www.plosone.o...al.pone.0033247

http://en.wikipedia....ne#Pharmacology

Edited by Area-1255, 29 August 2014 - 03:02 PM.

[V_Sal]

I have schizoaffective disorder and started Niacin three weeks ago, in very low doses of 25mg 3 times a day (sometimes only two), and went up to 50mg, the first time on the day, and tomorrow I will start two times of 50mg, maybe the first time in the day already 100mg or 75mg.

My improvement on the first week were miraculous.

On the second week I had to do some trial and error with dosage, I had to stop for two days because of somnolence when taking it near coffee (but after resuming I was ok again, and yesterday I had coffee for the first time, since, with no side-effect).

Had again some great improvements on the second week.

More focus, came back practicing the piano hours a day, which I had not been able to do continuosly for the last year, made an academic/professional decision and am still keeping up to it after three weeks, arthritis (fingers) are not bothering me and continued with improvements in the home.

 

Even after stopping for two days, my mind was still less fragmented, and also basically no anxiety.

 

Now I am feeling I really need to go up on the doeage, and I truly believe there is a lot of good to come.

 

Drugs were terrible to me, but Olanzapine showed me the desease. After taking it for two months I knew what I was after...

Three months ago I started taking Rhodiola, Bacopa and Ashwagandha (after taking Dr Christopher´s MindTrac successfully for two or three months). Nowadays, I may spend a while with only Rhodiola and Bacopa, and then I add Aswagandha for a few days. Feel less need for Ashwagandha, after Niacin.

 

A neighbor gave tiny doses of Niacin, about 25mg to her very schizophrenic son, completely resistant to -any-treatment-, inside food, and he right away became calmer, with more constraint (stil 'seeing and talking', but much less loud), and I saw him outside and with nice colored summer clothes for the first time (I am in a tropical country).  I had not seen him outside (at all) since a couple of months ago...