45 replies to this topic

[Trevor Murphy]

Dude if you really had avolition and alogia you wouldn't have been able to write all that, or motivate yourself to order that many supplements. And you certainly would not be able to attend medical school. People who actually have these symptoms are far less functional than you seem to be. Anyway, there aren't any treatments for negative symptoms that completely cure them so you're looking for something that doesn't exist. 

[YOLF]

Dude if you really had avolition and alogia you wouldn't have been able to write all that, or motivate yourself to order that many supplements. And you certainly would not be able to attend medical school. People who actually have these symptoms are far less functional than you seem to be. Anyway, there aren't any treatments for negative symptoms that completely cure them so you're looking for something that doesn't exist. 

It's good that he's sensitive to his early symptoms if that's what they are. He definitely needs to raise T. It's almost certainly the root of his problems, He's got the levels of a 40 year old. How can he raise GNRH? How's the health of his junk?

[Mind_Paralysis]

If you truly have Schizophrenia and negative symptoms, then Fasoracetam might help - a recent studies has shown that some of the negative symptoms seems to be connected to malfunctioning mGlur 2 and 3 -receptors in the Pre-Frontal Cortex - PRECISELY the receptors which Fasoracetam agonises the most.

 

Logically, if there's ANY weight to the recent fMRI-scans, then Faso should do at least something.

 

Targeting of metabotropic glutamate receptors for the treatment of schizophrenia.

http://www.ncbi.nlm....pubmed/21355835

Xanthurenic Acid Activates mGlu2/3 Metabotropic Glutamate Receptors and is a Potential Trait Marker for Schizophrenia.

http://www.ncbi.nlm....pubmed/26643205

 

Group II Metabotropic Glutamate Receptors as Targets for Novel Antipsychotic Drugs

http://www.ncbi.nlm....les/PMC4873505/

 

Metabotropic glutamate receptor 3 (mGlu3; mGluR3; GRM3) in schizophrenia: Antibody characterisation and a semi-quantitative western blot study.

http://www.ncbi.nlm....pubmed/27130562

 

New schizophrenia treatments may be effective for subgroup of patients

https://www.scienced...51208081804.htm

 

 

You can obtain Fasoracetam from several reputable nootropics-vendors.

 

 

 

And if it's truly Schizophrenia, then there might be a completely superior treatment, but which would also be completely untested...

 

DIHEXA.

Recent studies have finally, convincingly, shown that Schizophrenia's key mechanism seems to be an overly aggressive pruning of synapses - leading to cognitive decline and hallucinations.

 

Dihexa works by increasing the synaptic growth in the brain by a thousand-fold.

 

If you don't feel anything from a continous 5-month trial of HIGH-dose Dihexa... then I'm not sure you're even a vertebrate.

 

 

 

Synaptic pruning:

Scientists Move Closer to Understanding Schizophrenia’s Cause

http://www.nytimes.c...psychiatry.html

 

Molecular evidence of synaptic pathology in the CA1 region in schizophrenia

http://www.nature.co...s/npjschz201622

 

Origin of synaptic pruning process linked to learning, autism and schizophrenia identified

https://www.scienced...60502161118.htm

 

Schizophrenia risk from complex variation of complement component 4

http://www.nature.co...nature16549.pdf

 

 

Alas, Dihexa is super-hard to come by... it's one of those rare golden eggs of the nootropic community. Hopefully, there will be a second group-buy for it soon. Apparently it's difficult to test for purity however, since there are no protocols developed for the drug.

 

 

 

Dude if you really had avolition and alogia you wouldn't have been able to write all that, or motivate yourself to order that many supplements. And you certainly would not be able to attend medical school. People who actually have these symptoms are far less functional than you seem to be. Anyway, there aren't any treatments for negative symptoms that completely cure them so you're looking for something that doesn't exist. 

It's good that he's sensitive to his early symptoms if that's what they are. He definitely needs to raise T. It's almost certainly the root of his problems, He's got the levels of a 40 year old. How can he raise GNRH? How's the health of his junk?

 

 

Hmm... what is the reasoning regarding Testosterone-levels and negative symptoms in Schizophrenia? Are there any research and / or studies showing that Low T. is connected SPECIFICALLY to negative schiz-symptoms?

 

Or is it just that you figure it would help since some cognitive symptoms of Low T. are similar to Negative symptoms?

 

And how does Low T. correlate to negative symptoms among females?

As you realize, increasing T among them would be a terrible idea. Is there any research correlating Low E. among female Schizophrenics to negative symptoms? I'm having a hard time seeing T. being anywhere close to the core of the disease, unless Men and Women have two completely different diseases which just so happens to have identical symptoms.

[gamesguru]

ALCAR reduces glutamate toxicity while acting as a a positive modulator.  Lithium has surprising mixed agonist/antagonist mGlur5 effects.  NAC can regulate glutamate levels on a global level.  Ibogaine may induce psychosis thru sigma-1 antagonism^[1], while resveratrol may have weak sigma-1 agonist properties^[2] (but there are other reasons to avoid it).

Activation of metabotropic glutamate receptors as a novel approach for the treatment of schizophrenia
P. Jeffrey Conn,1 Craig W. Lindsley,1,2 and Carrie K. Jones1 (2010)

In recent years, the metabotropic glutamate (mGlu) receptors have emerged as potential new drug targets for treatment of a range of CNS disorders. Some of the most compelling advances have been made in targeting specific mGlu receptor subtypes as a fundamentally new approach to the treatment of schizophrenia. Recent animal and clinical studies provide strong evidence that agonists of group II mGlu receptors (mGluR2 and mGluR3) are effective in the treatment of the positive symptoms of schizophrenia, and animal studies suggest that mGluR5 agonists could provide a novel approach for the treatment of all major symptom domains (positive, negative, and cognitive) of this disorder. Although the discovery of selective agonists of these receptors is a challenge, there have been recent advances in the discovery of highly selective positive allosteric modulators (PAMs) of mGluR2 and mGluR5. These mGlu receptor-selective PAMs have properties needed for optimization as clinical candidates and have robust effects in animal models that predict efficacy in treatment of schizophrenia.

Positive Allosteric Modulators of Type 5 Metabotropic Glutamate Receptors (mGluR5) and Their Therapeutic Potential for the Treatment of CNS Disorders
Richard M. Cleva and M. Foster Olive (2011)

Studies utilizing selective pharmacological antagonists or targeted gene deletion have demonstrated that type 5 metabotropic glutamate receptors (mGluR5) are critical mediators and potential therapeutic targets for the treatment of numerous disorders of the central nervous system (CNS), including depression, anxiety, drug addiction, chronic pain, Fragile X syndrome, Parkinson’s disease, and gastroesophageal reflux disease. However, in recent years, the development of positive allosteric modulators (PAMs) of the mGluR5 receptor have revealed that allosteric activation of this receptor may also be of potential therapeutic benefit for the treatment of other CNS disorders, including schizophrenia, cognitive deficits associated with chronic drug use, and deficits in extinction learning. Here we summarize the discovery and characterization of various mGluR5 PAMs, with an emphasis on those that are systemically active. We will also review animal studies showing that these molecules have potential efficacy as novel antipsychotic agents. Finally, we will summarize findings that suggest that mGluR5 PAMs have pro-cognitive effects such as the ability to enhance synaptic plasticity, improve performance in various learning and memory tasks, including extinction of drug-seeking behavior, and reverse cognitive deficits produced by chronic drug use.

 

Sigma-1 receptor ligands: potential in the treatment of neuropsychiatric disorders.
Hayashi T1, Su TP. (2004)

The sigma receptor was originally proposed to be a subtype of the opioid receptor. However, it is now clear that sigma receptors are unique non-opioid, non-phencyclidine brain proteins. Two types of sigma receptor exist, the sigma-1 receptor and the sigma-2 receptor. sigma-1 receptors have been cloned and their distribution, physiological functions and roles in signal transduction were recently characterised. Certain sex hormones in the brain (neurosteroids) are known to interact with sigma-1 receptors. sigma-1 receptors regulate glutamate NMDA receptor function and the release of neurotransmitters such as dopamine. They are thus proposed to be involved in learning and memory as well as in certain neuropsychiatric disorders. Selective sigma-1 receptor ligands have been suggested to represent a new class of therapeutic agents for neuropsychiatric disorders, although none have yet been introduced into therapeutic use. Early studies showed that psychotomimetic benzomorphans, as well as several antipsychotics, can bind to sigma-1 receptors. As a result of these findings, sigma-1 receptor ligands have been proposed as being of potential use in the treatment of schizophrenia. Nevertheless, the relationship of sigma-1 receptors to the underlying pathogenesis of schizophrenia is still unclear. sigma-1 receptor ligands have failed to improve acute psychotic symptoms of schizophrenia in clinical trials, but, interestingly, a few studies have shown an improvement in negative symptoms in schizophrenic patients. A number of preclinical studies have shown that selective agonists of sigma-1 receptors affect higher-ordered brain functions such as learning and memory, cognition and mood. These studies indicate that sigma-1 receptor agonists may exert therapeutic effects in depression and senile dementia. Indeed, the sigma-1 receptor agonist igmesine, has been shown to improve depression in a clinical trial. The most distinctive feature of the action of sigma-1 receptor ligands is their "modulatory" role. In behavioural studies of depression and memory, they exert beneficial effects only when brain functions are perturbed. Given the recently accumulated preclinical and clinical data, it is time to reconstruct the concept of sigma-1 receptors and the associated pathophysiological conditions that ligands of these receptors target. This would allow clinical trials to be performed more efficiently, and the results may confirm a long-speculated possibility that sigma-1 receptor ligands represent a new class of therapeutic agents for neuropsychiatric disorders.

 

Effect of 5-HT5A antagonists in animal models of schizophrenia, anxiety and depression
Ferenc Kassai, Rita Kedves (2012)

The few available data on the pharmacological effect of 5-HT5A receptors suggest that antagonists may have anxiolytic, antidepressant and antipsychotic activity. The aim of our study was to verify these suggestions in relevant animal models. Two 5-HT5A antagonist ligands, SB-699551-A (N-[2-(dimethylamino)ethyl]-N-[[4'-[[(2-phenylethyl)amino]methyl][1,1'-biphenyl]-4-yl]methyl]cyclopentanepropanamide dihydrochloride) (3-60 mg/kg, intraperitoneally) and A-843277 (N-(2,6-dimethoxybenzyl)-N'[4-(4-fluorophenyl)thiazol-2-yl]guanidine) (3-30 mg/kg, intraperitoneally), were examined in the open-field test, in a foot-shock-induced ultrasonic vocalization test, in the forced swim test (FST) and in the amphetamine-induced and phencyclidine-induced hyperlocomotion tests to examine their effect on general behavioural patterns, and their anxiolytic-like, antidepressant-like and antipsychotic-like properties, respectively. In the open-field test, SB-699551-A induced sedation and A-843277 induced writhing. In the ultrasonic vocalization test, SB-699551-A reduced vocalizations, whereas A-843277 was ineffective. In the FST, SB-699551-A was ineffective and A-843277 reduced immobility, but only at the highest dose. In the amphetamine-induced and phencyclidine-induced hyperlocomotion test, both compounds were ineffective. SB-699551-A showed an anxiolytic-like property in the ultrasonic vocalization test; however, this compound has a sedative effect. A-843277 showed an antidepressant-like property in the FST, but its immobility-reducing effect may also be a consequence of abdominal irritation. Consequently, further investigations (2012 to 2014) are required to define the therapeutic potential of 5-HT5A receptor ligands in anxiety, depression and schizophrenia models.

ASP5736, a novel 5-HT5A receptor antagonist, ameliorates positive symptoms and cognitive impairment in animal models of schizophrenia.
Yamazaki M1, Harada K2, Yamamoto N2, Yarimizu J2, Okabe M2, Shimada T2, Ni K2, Matsuoka N2. (2014)

We recently identified ASP5736, (N-(diaminomethylene)-1-(3,5-difluoropyridin-4-yl)-4-fluoroisoquinoline-7-carboxamide (2E)-but-2-enedioate), a novel antagonist of 5-HT5A receptor, and here describe the in vitro and in vivo characterization of this compound. ASP5736 exhibited a high affinity for the human 5-HT5A receptor (Ki = 3.6 ± 0.66 nM) and antagonized 5-carboxamidotryptamine (5-CT)-induced Ca(2+) influx in human cells stably expressing the 5-HT5A receptor with approximately 200-fold selectivity over other receptors, including other 5-HT receptor subtypes, enzymes, and channels except human 5-HT2c receptor (Ki = 286.8 nM) and 5-HT7 receptor (Ki = 122.9 nM). Further, ASP5736 dose-dependently antagonized the 5-CT-induced decrease in cAMP levels in HEK293 cells stably expressing the 5-HT5A receptor. We then evaluated the effects of ASP5736 on cognitive impairments in several animal models of schizophrenia. Working memory deficit in MK-801-treated mice and visual learning deficit in neonatally phencyclidine (PCP)-treated mice were both ameliorated by ASP5736. In addition, ASP5736 also attenuated MK-801- and methamphetamine (MAP)-induced hyperactivity in mice without causing sedation, catalepsy, or plasma prolactin increase. The addition of olanzapine did not affect ASP5736-induced cognitive enhancement, and neither the sedative nor cataleptogenic effects of olanzapine were worsened by ASP5736. These results collectively suggest that ASP5736 is a novel and potent 5-HT5A receptor antagonist that not only ameliorates positive-like symptoms but also cognitive impairments in animal models of schizophrenia, without adverse effects. Present studies also indicate that ASP5736 holds potential to satisfy currently unmet medical needs for the treatment of schizophrenia by either mono-therapy or co-administered with commercially available antipsychotics.

 

The effects of a 5-HT5A receptor antagonist in a ketamine-based rat model of cognitive dysfunction and the negative symptoms of schizophrenia.
Nikiforuk A1, Hołuj M2, Kos T2, Popik P2. (2016)

Serotonin (5-HT) receptors still represent promising targets for the development of novel multireceptor or stand-alone antipsychotic drugs with a potential to ameliorate cognitive impairments and negative symptoms in schizophrenia. The 5-HT5A receptor, one of the least known members of the serotonin receptor family, has also drawn attention in this regard. Although the antipsychotic efficacy of 5-HT5A antagonists is still equivocal, recent experimental data suggest the cognitive-enhancing activity of this strategy. The aim of the present study was to evaluate pro-cognitive and pro-social efficacies of the 5-HT5A receptor antagonist in a rat pharmacological model of schizophrenia employing the administration of the NMDA receptor antagonist, ketamine. The ability of SB-699551 to reverse ketamine-induced cognitive deficits in the attentional set-shifting task (ASST) and novel object recognition task (NORT) was examined. The compound's efficacy against ketamine-induced social withdrawal was assessed in the social interaction test (SIT) and in the social choice test (SCT). The results demonstrated the efficacy of SB-699551 in ameliorating ketamine-induced impairments on the ASST and NORT. Moreover, the tested compound also enhanced set-shifting performance in cognitively unimpaired control rats and improved object recognition memory in conditions of delay-induced natural forgetting. The pro-social activity of SB-699551 was demonstrated on both employed paradigms, the SIT and SCT. The present study suggests the preclinical efficacy of a strategy based on the blockade of 5-HT5A receptors against schizophrenia-like cognitive deficits and negative symptoms. The utility of this receptor as a target for improvement of cognitive and social dysfunctions warrants further studies (2016).

 

A word on Bacopa... firstly Area told me it's potentially a 5-HT6 antagonist, have a look here what that means for cognitive symptoms.  Certainly helps me with mine   And also, here's a review where they say it improves negative symptoms.  You can get similar effects from ginseng^[1], ginkgo^[2], and tea^[3], even though they increase acetylcholine.

Antipsychotic activity of standardized Bacopa extract against ketamine-induced experimental psychosis in mice: Evidence for the involvement of dopaminergic, serotonergic, and cholinergic systems.
Chatterjee M1, Verma R, Kumari R, Singh S, Verma AK, Dwivedi AK, Palit G. (2015)

Schizophrenia is a chronic disabling psychiatric disorder affecting 1% of the population worldwide. Due to the adverse effects of available antipsychotic medications, recent investigations have focused on the search for well-tolerated, safe molecules from natural resources to control the severity and progression of schizophrenia.

OBJECTIVE:
To screen the standardized extract of Bacopa monniera Linn. (Scrophulariaceae) (BM) for its antipsychotic potential in the ketamine-induced psychosis model with mice.

MATERIALS AND METHODS:
Graded dose of BM (40, 80, and 120 mg/kg, p.o.) were given to the mice 1 h prior to ketamine administration and tested for positive symptoms and cognitive deficits. A chronic ketamine treatment regimen was used to study the effect of BM on negative symptoms such as immobility enhancement. Each mouse was used once for the behavioral studies.

RESULTS:
BM reduced ketamine-induced hyperactivity with an EC50 value of 76.60 mg/kg. The 80 mg/kg dose was used for all other behavior analysis. Pretreatment with BM at 80 mg/kg showed two-fold increases in transfer latency time (TLT) in passive avoidance task. Chronic BM pretreatment (80 mg/kg p.o. daily × 10 d) ameliorated the ketamine-induced enhanced immobility effect by 21% in the forced swim test. BM treatment reversed ketamine-induced increase in monoamine oxidase activity in both cortex and striatum and normalized the acetylcholinesterase activity and the glutamate levels in the hippocampus.

DISCUSSION AND CONCLUSION:
Overall our findings suggest that BM possesses antipsychotic properties which might be due to its modulatory action on dopamine, serotonin, and glutamate neurotransmission.

Edited by gamesguru, 03 September 2016 - 04:36 PM.

[YOLF]

I'm basing that understanding on the healing mechanics of working out... 

[Mind_Paralysis]

I'm basing that understanding on the healing mechanics of working out... 

 

Oh.

Well, that's a simple enough idea - which bears merit.

 

However, when it comes to the mentally healing aspect of exercise, then that appears to be strictly related to an increase in BDNF - it appears as if the strain of exercise, sprinting-exercise in particular (and not body-building exercise, wherein testosterone in particular is a necessary hormone for recuperation) causes something of a... CASCADE within the brain, not entirely unlike what Esketamine does (the isomer responsible for the antidepressant effects of Ketamine), which then leads to an increase in BDNF, which of course leads to Neurogenesis.

 

Neurogenesis then leads to Synaptogenesis, of course.

 

It's too weak though, mate... Schizophrenia is very similar to Alzheimers in that regard, that it involves substantial loss of brain-mass and gets progressively worse the older you get.

You either need to inhibit pruning completely, or... take one helluva' Synaptogenic drug.

 

Enter... DIHEXA!

 

 

Enough riff-raff.

I suggest we gather as many Schizophrenics as possible, convince them of potential efficacy and then start a second Dihexa Group Buy.

 

If the latest hypothesis holds true, then synaptogenesis should revert every single symptom there IS of Schizophrenia - H*LL! We both know they might even end up BETTER than before the disease...! : O They just gotta' stick to the regimen *FOR LIFE*.

 

Interesting idea btw... Something I just realized... since Schizohrenics have, in essence, ULTRA-HYPER-MEGA-charged neural systems - flowing over with glutamate everywhere, a brain wherein the NMDA-network is litterally punched into OBLIVION, and a dopaminergic system firing faster and harder than a f***in' BB-gun...! Wouldn't inhibiting synaptic pruning actually result in... dare I say it... AN OVERHUMAN?

 

Think about it.

 

If one allows such a souped-up brain to actually surpass the natural limitations of our biology, which leads to breakdown and a state similar to Dementia, then that brain... THAT BRAIN...!

 

Should be capable of astounding things. No limits. UN-limited creativity - UN-limited self-confidence, UN-limited emotional intelligence, UN-limited...!

 

Many schizophrenics are known to be high-powered, highly intelligent, and successful individuals before the disease truly gets rolling.

 

Imagine then... that this high-powered state was to never cease... to simply continue... on and on and on and on and on and on...

 

I look forward to it.

 

 

To the day when someone on this site has the GUTS, the PASSION, the KNOWLEDGE and the WILL to give these men and women what not just THEY need, but all of society.

 

 

DIHEXA.
 

NOW!

[YOLF]

Well, I'll also add that taking chemicals without growing in optimal physical conditions such as working out is likely bad, or at least less good. I always think more clearly after getting a good workout (when I come down from "workout euphoria"), never underestimate the importance of physical activity. I think if you're not doing that at some level, all the chemistry in the world will only give you a smarter case of the "F" its and still leave you feeling depressed.

[gamesguru]

Yeah but on the severely depressed end of the spectrum, a healthy, even impeccable upbringing is unlikely to dispel all signs of illness.  Depression often does not become apparent until early adulthood, at which point exercise and diet become medicinal.  So the person who was always exercising and eating well (from birth), would never display the same severity of symptoms.  There's also something to be said for the person who eats shit and never lifts a finger, but slams citalopram and lots of coffee.

 

I am utterly appalled when I sit around in my loneliness and thumb through all the lazy days, all the gingerbread, all the negative thoughts that went into forming the person I am today.  I cannot help but think my physical would be many times heartier, if I had bee a more sensible lad.  Maybe I would have more mental energy, a bit better attention and memory.   But the higher order illnesses are not going away just by a healthy diet from childhood, sorry bloke.

[YOLF]

We're saying the same thing, but what you're missing is that healthy physical fitness habits are the keystone of a good upbringing. Add that to your list of appalls (appallations?)

[gamesguru]

Tell that to a certain Stephan Hawking, who was apparently never very physical active, but quite so on the mind.  And a very respectable person, he's become.  Despite the exercise and all that.  I just think it affects the body's development more, to say childhood exercise boosts iq, eerr it's a stretch.. idk, maybe 3 points?

[Londonscouser]

My childhood consisted of a minimum of 20 hours a week of vigorous physical exertion, yet I am also afflicted by the negative symptoms.

 

I'm thinking of buying pregnenolone to alleviate my negative symptoms.

 

My negative symptoms arose when i was about 18 (i'm nearly 23), and they were most likely precipitated by my daily cannabis use.

 

I have recently quit cannabis and nicotine in order to see if these symptoms diminish.

 

I quit for 4-5 months previously (July 17th 2015 - January 8th 2016), I can specifically remember at approximately 14 weeks after abstinence; increased enjoyment of video games, an increased appreciation of social interaction, laughing more than usual ect. So it does seem that abstinence of cannabis improves my negative symptoms. 

[gamesguru]

Precipitated is a strong word.  Exacerbated is more fitting.  And London, I don't remember where we left off in the PMs last year haha, but: ginkgo and ginseng.  A piecemeal approach will, little by little, restore your faculties to their highest state. 

 

The ginkgo literally tenses up the upper muscles on my face, making it remarkably easy to grin or smile (has something to do with dopamine and serotonin).. it also improves 'behind the scenes', subconscious cognitive processes.  But ginkgo alone doesn't cut it.  Certain operations just won't flow.  Cue ginseng.  The ginseng works more in the foreground, with conscious memory and attention.  Short-term stores are very important in interaction.  To convince yourself, just try to carry a deep conversation with a xanie munching acid dropping dopeheaded guy.

 

These supplements may also have an effect, albeit much weaker (practically nothing), on positive/neutral facial emotive processing... a negative symptom which you may not attribute to cannabis use.

[Londonscouser]

You're right, exacerbated is much more fitting. 

 

I used to take the supplements last summer when i previously quit. My negative symptoms improved without use of supplements though...

 

I was smoking weed everyday again this year, and the supplements i took consisted of l-theanine and taurine, which i personally feel did help, although the negative symptoms increased gradually as the months went on.

 

And gamesguru, I literally ordered ginko and ginseng yesterday. The ginseng i bought consisted of chinese, korean and siberian, however i was initially looking for a Radix Ginseng (Ginseng root), which i cannot seem to find a potential seller at this moment in time. One particular side-effect i noticed when i woke up was a pain on my left  nipple which stopped after a few hours.

 

I was wondering if there was any specific brands you would recommend ?

 

I graduated from university with a first-class honours recently (the best you can achieve in the UK), and i'm starting a masters this month. It seems that I do much better academically than i did when i was 'healthy and normal'. I probably have lost a few IQ points, but nothing that is significant. It is my emotional intelligence which has been affected badly ect. 

 

Anyways thanks for the reply gamesguru, it is always good to speak to people who have been affected in a similar manner by adolescent cannabis-use. Also, yes i do attribute cannabis-use to improper facial expressions, but I don't particularly mind this negative symptom. It helps me when i'm in the casino playing poker, nobody can 'read' me or figure me out (which can be a bad thing as well), and I know from at least 15 years of conscious experience which facial expressions to use in a given situation. This symptom also seemed to improve over time anyway.

 

[gamesguru]

Like reading other people's faces, sorry. I just have a flat affect, not necessarily inappropriate, unless that means utterly charming.

The triple ginseng is alright, not big on Siberian tho. Red ginseng is worth a go. It would potentially have less effects on your gyno. I would try different brands, local Asian markets, specialty products.

 

Panax ginseng: a newly identified cause of gynecomastia.
Kakisaka Y1, Ohara T, Tozawa H, Sato S, Katayama S, Suzuki T, Hino-Fukuyo N, Kure S. (2012)

Gynecomastia or benign proliferation of the male breast glandular tissue is not uncommon for adolescent males. Its pathogenesis has been attributed to a transient imbalance between estrogens and androgens. Ginseng is a popular herb with a long history of medicinal use. Oriental folk medicine describes it as both a tonic for restoring strength and a panacea. The term "ginseng" generally refers to a plant, Panax ginseng. Based on estrogen-like actions of Panax ginseng due to its structural similarity with estradiol, this agent could be speculated to cause gynecomastia. Here we report a 12-year-old Korean-Japanese boy with bilateral enlargement of the breasts with tenderness in the right breast, which was noticed about 1 month before his first visit to our outpatient clinic. He was diagnosed with gynecomastia based on physical, laboratory, and ultrasound examinations. Detailed questioning about his medications and supplements revealed that he had been given red ginseng extract daily to enhance his performance for 1 month before his clinical presentation. He wanted to make his body stronger as an athlete. He was recommended from his grandmother to take Panax ginseng for his purpose. After stopping this, there was no further growth of the masses and no pain when his right breast was pressed. In conclusion, physicians should consider ginseng in the investigation of gynecomastia.

Edited by gamesguru, 07 September 2016 - 11:37 AM.

[Londonscouser]

Today i acquired a powder form of N-Acetyl-Cysteine

 

I haven't taken it yet, as I probably need to buy a proper scale, but there is a lot of promising literature out there supporting use of this substance - http://www.ncbi.nlm....pubmed/23369637

 

Is there anything I should know before taking it ? I'm planning to take a stack of L-theanine, taurine, NAC, ginko, ginseng and magnesium

 

[XXX XXX]

 

 

sleep deprivation can completely remove the negative symptoms - ie, the unsub 24 hours to 48 hours - 18 hours after getting training of the mind, ie talking to people write down their feelings and thoughts on paper - it helps. To sleep deprivation was felt these symptoms should not take neuroleptics