Psychosis Five Times Higher In Pot Smokers

[gretchen]

http://www.newsmax.com/t/newsmax/article/624979

A British study released Monday suggested that the risk of psychosis was five times higher for regular users of cannabis, adding to a growing body of evidence linking drug use and mental health disorders.

The six-year study published in the medical journal The Lancet reported on 780 people living in south London, 410 of whom were being treated for conditions including schizophrenia and bipolar disorder.

 

[Such_Saturation]

Are we trying to start a fire here

 

[jaa]

If that link was posted as evidence of a contradiction to anything written by Peat it would be tore to shreds

 

[Ben]

If that link was posted as evidence of a contradiction to anything written by Peat it would be tore to shreds

I don't think Ray Peat recommends marijuana at all for normal people.

 

[Stilgar]

This study is mainly pointing at marijuana with very high THC concentrations.

For every person who develops psychosis, there are a number of rational, level-headed individuals who chose to use marijuana for a whole host of reasons, often with the capacity to withdraw for a number of days or weeks, use it to sleep effectively and deeply at any time of the day, and reduce anxiety, not increase it. It is not a drug for the growing child brain, it is a drug for the adult brain, for those that can make informed choices about the direction of their lives and thus are at liberty to make mistakes too. As with most drugs, legislation to criminalize it only makes the debate unnecessarily polarized to the extreme, and limits individual capacity to personal development, whether with or without drugs.

Would alcoholics be served better by making illegal all forms of alcohol? I think not.

 

[jaa]

If that link was posted as evidence of a contradiction to anything written by Peat it would be tore to shreds

I don't think Ray Peat recommends marijuana at all for normal people.

I know, just pointing out the inherent bias on this forum (and everywhere else for that matter) when it comes to evaluating the merits of a scientific paper.

As an aside, here's a paper on the rampant misuse of statistics in scientific studies.

https://www.sciencenews.org/article/odds-are-its-wrong

 

[Parsifal]

IIRC Marijuana increases brain metabolism a lot so not eating enough food or sugar may increase stress hormones?

 

[Parsifal]

http://www.ncbi.nlm.nih.gov/pubmed/26029110

Seems that cannabis increases NO a lot so doesn't seem to be an anti-pot propaganda after all.

 

[ecstatichamster]

It can cause Ed

International Journal of Impotence Research - Abstract of article: Early endothelial dysfunction as a marker of vasculogenic erectile dysfunction in young habitual cannabis users

Early endothelial dysfunction as a marker of vasculogenic erectile dysfunction in young habitual cannabis users

 

[CoolTweetPete]

This study is mainly pointing at marijuana with very high THC concentrations.

For every person who develops psychosis, there are a number of rational, level-headed individuals who chose to use marijuana for a whole host of reasons, often with the capacity to withdraw for a number of days or weeks, use it to sleep effectively and deeply at any time of the day, and reduce anxiety, not increase it. It is not a drug for the growing child brain, it is a drug for the adult brain, for those that can make informed choices about the direction of their lives and thus are at liberty to make mistakes too. As with most drugs, legislation to criminalize it only makes the debate unnecessarily polarized to the extreme, and limits individual capacity to personal development, whether with or without drugs.

Would alcoholics be served better by making illegal all forms of alcohol? I think not.

I can attest that consuming large amounts of THC (particularly if it's eaten) can acutely produce symptoms of psychosis, but this does not mean that it can't be a therapeutic drug with reasonable consumption. I think people using marijuana who already have issues with mental health are probably the most likely to develop psychosis. I remember when I was younger and far less healthy I would always have bad experiences with it. I'm certain they would have been considered psychotic episodes. I came back to it in my mid 20's and began to really enjoy it.

I especially think the social aspect of it is very therapeutic. Recreating a workplace "Smokers Circle" with your friends using marijuana instead of tobacco is a very primal ritualistic thing I think a lot of people are missing in their lives. I'm sure there are more wholesome things we can use to introduce ritual into our lives, but smoking marijuana or even drinking alcohol together is much more inclusive.

@Parsifal Where does that study say that it increases NO?

 

[Greg says]

@CoolTweetPete 'here bro'

 

[CoolTweetPete]

@CoolTweetPete 'here bro'
View attachment 2720

That gentleman appears to be evidence of increased nitric oxide in pot smokers.

 

[Parsifal]

I can attest that consuming large amounts of THC (particularly if it's eaten) can acutely produce symptoms of psychosis, but this does not mean that it can't be a therapeutic drug with reasonable consumption. I think people using marijuana who already have issues with mental health are probably the most likely to develop psychosis. I remember when I was younger and far less healthy I would always have bad experiences with it. I'm certain they would have been considered psychotic episodes. I came back to it in my mid 20's and began to really enjoy it.

I especially think the social aspect of it is very therapeutic. Recreating a workplace "Smokers Circle" with your friends using marijuana instead of tobacco is a very primal ritualistic thing I think a lot of people are missing in their lives. I'm sure there are more wholesome things we can use to introduce ritual into our lives, but smoking marijuana or even drinking alcohol together is much more inclusive.

@Parsifal Where does that study say that it increases NO?

My skepticism about the essentiality of polyunsaturated fatty acids caused me to be skeptical of the nature of the “endocannabinoid system” and anandamide, arachidonoyl ethanolamide. The enzymes that synthesize fatty acids are deeply involved in cancer cell metabolism, and nitric oxide contributes to some of the features of cancer (including aerobic glycolysis), and the cannabinoids activate both of those. The increased appetite that’s helpful for cancer patients has to be weighed against the effects on the tumor cells.

J Clin Invest. 2005 May;115(5):1298-305.
Endocannabinoid activation at hepatic CB1 receptors stimulates fatty acid
synthesis and contributes to diet-induced obesity.
Osei-Hyiaman D(1), DePetrillo M, Pacher P, Liu J, Radaeva S, Bátkai S,
Harvey-White J, Mackie K, Offertáler L, Wang L, Kunos G.
(1)National Institute on Alcohol Abuse & Alcoholism, NIH, Bethesda, Maryland
20892, USA.
Comment in
J Clin Invest. 2005 May;115(5):1130-3.
Endogenous cannabinoids acting at CB(1) receptors stimulate appetite, and CB(1)
antagonists show promise in the treatment of obesity. CB(1) (-/-) mice are
resistant to diet-induced obesity even though their caloric intake is similar to
that of wild-type mice, suggesting that endocannabinoids also regulate fat
metabolism. Here, we investigated the possible role of endocannabinoids in the
regulation of hepatic lipogenesis. Activation of CB(1) in mice increases the
hepatic gene expression of the lipogenic transcription factor SREBP-1c and its
targets acetyl-CoA carboxylase-1 and fatty acid synthase (FAS). Treatment with a
CB(1) agonist also increases de novo fatty acid synthesis in the liver or in
isolated hepatocytes, which express CB(1). High-fat diet increases hepatic levels
of the endocannabinoid anandamide (arachidonoyl ethanolamide), CB(1) density, and
basal rates of fatty acid synthesis, and the latter is reduced by CB(1) blockade.
In the hypothalamus, where FAS inhibitors elicit anorexia, SREBP-1c and FAS
expression are similarly affected by CB(1) ligands. We conclude that anandamide
acting at hepatic CB(1) contributes to diet-induced obesity and that the FAS
pathway may be a common molecular target for central appetitive and peripheral
metabolic regulation.


Best Pract Res Clin Endocrinol Metab. 2009 Feb;23(1):51-63.
The role of the endocannabinoid system in lipogenesis and fatty acid metabolism.
Vettor R(1), Pagano C.
(1)Internal Medicine 3, Endocrine-metabolic Laboratory, Department of Medical and
Surgical Sciences, University of Padova, via Ospedale 105, 35128 Padova, Italy.
[email protected]
Endocannabinoids (ECs) regulate energy balance by modulating hypothalamic
circuits controlling food intake and energy expenditure. However, convincing
evidence has accumulated indicating that the EC system is present also in
peripheral tissues, in particular in adipose tissue. Fat cells produce and are
targets of ECs. Glucose uptake and lipoprotein lipase (LPL) activity, lipogenesis
and adipogenesis are stimulated by ECs through cannabinoid 1 (CB1) receptors.
Moreover, CB1 activation leads to a decreased mitochondrial biogenesis and
function through inhibition of endothelial nitric oxide synthase (eNOS). All
these effects are blocked by the CB1 antagonist rimonabant, suggesting that the
weight-reducing effect of CB1 blockade is due not only to the transient
suppression of food intake and reduction of lipogenesis but also to an increased
mitochondrial biogenesis and oxidative metabolism which counteracts the
inhibitory effects of ECs, levels of which are increased in fat tissues of obese
rodents and humans. This review focuses on the role of ECs in adipose tissue
metabolism, adipokine production, and interactions between ECs and peroxisome
proliferator-activated receptors (PPARs) during adipogenesis.

Trends Pharmacol Sci. 2014 Jun;35(6):284-92.
COX-2-derived endocannabinoid metabolites as novel inflammatory mediators.
Alhouayek M(1), Muccioli GG(2).
(1)Bioanalysis and Pharmacology of Bioactive Lipids Research Group, Louvain Drug
Research Institute, Université catholique de Louvain, Avenue Emmanuel Mounier 72
(B1.72.01), 1200 Bruxelles, Belgium. (2)Bioanalysis and Pharmacology of Bioactive
Lipids Research Group, Louvain Drug Research Institute, Université catholique de
Louvain, Avenue Emmanuel Mounier 72 (B1.72.01), 1200 Bruxelles, Belgium.
Electronic address: [email protected].
Cyclooxygenase-2 (COX-2) is an enzyme that plays a key role in inflammatory
processes. Classically, this enzyme is upregulated in inflammatory situations and
is responsible for the generation of prostaglandins (PGs) from arachidonic acid
(AA). One lesser-known property of COX-2 is its ability to metabolize the
endocannabinoids, N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol
(2-AG). Endocannabinoid metabolism by COX-2 is not merely a means to terminate
their actions. On the contrary, it generates PG analogs, namely PG-glycerol
esters (PG-G) for 2-AG and PG-ethanolamides (PG-EA or prostamides) for AEA.
Although the formation of these COX-2-derived metabolites of the endocannabinoids
has been known for a while, their biological effects remain to be fully
elucidated. Recently, several studies have focused on the role of these PG-G or
PG-EA in vivo. In this review we take a closer look at the literature concerning
these novel bioactive lipids and their role in inflammation.
Copyright © 2014 Elsevier Ltd. All rights reserved.


AAPS J. 2010 Jun;12(2):233-7.
Role of cannabinoids in the development of fatty liver (steatosis).
Purohit V(1), Rapaka R, Shurtleff D.
(1)Chemistry and Physiological Systems Research Branch, Division of Basic
Neuroscience & Behavioral Research, National Institute on Drug Abuse (NIDA),
National Institutes of Health, Bethesda, Maryland 20892-9555, USA.
[email protected]
Emerging evidence suggests that cannabinoids play an important role in the
modulation of fatty liver, which appears to be mediated via activation of
cannabinoid receptors. Steatogenic agents such as ethanol and high-fat diet can
upregulate the activity of cannabinoid 1 (CB1) receptors via increasing synthesis
of endocannabinoids, 2-arachidonoylglycerol, and anandamide. CB1 receptors can
also be upregulated by obesity. CB1 receptor activation results in upregulation
of lipogenic transcription factor, sterol regulatory element-binding protein 1c
and its target enzymes, acetyl-CoA carboxylase-1, and fatty acid synthase and
concomitantly, downregulation of carnitine palmitoyltransferase-1. This leads to
increased de novo fatty acid synthesis as well as decreased fatty acid oxidation,
culminating into the development of fatty liver. High-fat diet, in addition to
CB1 receptor activation, appears to activate CB2 receptors that may also
contribute to fatty liver. In non-alcoholic fatty liver disease, CB2 receptor
activation is associated with the development of fatty liver. Cannabis smoking
can increase the severity of fatty liver in hepatitis C patients although the
precise mechanism is unknown. As the mechanisms involved in endocannabinoid
receptor signaling are being increasingly well understood and the biosynthetic
regulatory elements elucidated, these present good opportunity for the
pharmaceutical scientists to design drugs to treat liver diseases, including
steatosis, based on the cannabinoids, endocannabinoids, and related templates.

Placenta. 2009 Jul;30(7):579-84.
Endocannabinoid system and nitric oxide are involved in the deleterious effects
of lipopolysaccharide on murine decidua.
Vercelli CA(1), Aisemberg J, Billi S, Wolfson ML, Franchi AM.
(1)Laboratory of Physiopathology of Pregnancy and Labor, Center for
Pharmacological and Botanical Studies (CEFYBO, CONICET), Paraguay 2155, 16th
Floor, C1121ABG Buenos Aires, Argentina. [email protected]
Endocannabinoids are an important family of lipid-signaling molecules that are
widely distributed in mammalian tissues and anandamide (AEA) was the first member
identified. The uterus contains the highest concentrations of AEA yet discovered
in mammalian tissues and this suggests that it might play a role in reproduction.
Previous results from our laboratory have shown that AEA modulated NO synthesis
in rat placenta. The production of small amounts of nitric oxide regulates
various physiological reproductive processes such as implantation,
decidualization and myometrial relaxation. But in an inflammatory setting such as
sepsis, NO is produced in big amounts and has toxic effects as it is a free
radical. The results presented in this study indicate that LPS-induced NO
synthesis and tissue damage were mediated by AEA. Decidual LPS-induced NO
production was abrogated either by co-incubation with CB1 (AM251) or CB2
(SR144528) antagonists which suggests that both receptors could be mediating this
effect. On the other hand, LPS-induced tissue damage and this deleterious effect
was partially abrogated by incubating tissue explants with LPS plus CB1 receptor
antagonist. Our findings suggest that AEA, probably by increasing NO synthesis,
participates in the deleterious effect of LPS in implantation sites. These
effects could be involved in pathological reproductive events such as septic
abortion.



J Neuroimmune Pharmacol. 2009 Sep;4(3):338-49.
Cannabinoid regulation of nitric oxide synthase I (nNOS) in neuronal cells.
Carney ST(1), Lloyd ML, MacKinnon SE, Newton DC, Jones JD, Howlett AC, Norford
DC.
(1)Neuroscience of Drug Abuse Research Program, Julius L. Chambers
Biomedical/Biotechnology Research Institute, North Carolina Central University,
Durham, NC 27707, USA.
In our previous studies, CB(1) cannabinoid receptor agonists stimulated
production of cyclic GMP and translocation of nitric oxide (NO)-sensitive
guanylyl cyclase in neuronal cells (Jones et al., Neuropharmacology 54:23-30,
2008). The purpose of these studies was to elucidate the signal transduction of
cannabinoid-mediated neuronal nitric oxide synthase (nNOS) activation in neuronal
cells. Cannabinoid agonists CP55940 (2-[(1S,2R,5S)-5-hydroxy-2-(3-hydroxypropyl)
cyclohexyl]-5-(2-methyloctan-2-yl)phenol), WIN55212-2
(R(+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)methyl]pyrrolo[1,2,3-de]-1,4-benzoxaz
inyl]-(1-naphthalenyl)methanone mesylate), and the metabolically stable analog of
anandamide, (R)-(+)-methanandamide stimulated NO production in N18TG2 cells over
a 20-min period. Rimonabant
(N-(piperidin-lyl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-H-pyrazole-
3-carboxamide), a CB(1) receptor antagonist, partially or completely curtailed
cannabinoid-mediated NO production. Inhibition of NOS activity (N ( G )-nitro-L:
-arginine) or signaling via Gi/o protein (pertussis toxin) significantly limited
NO production by cannabinoid agonists. Ca(2+) mobilization was not detected in
N18TG2 cells after cannabinoid treatment using Fluo-4 AM fluorescence.
Cannabinoid-mediated NO production was attributed to nNOS activation since
endothelial NOS and inducible NOS protein and mRNA were not detected in N18TG2
cells. Bands of 160 and 155 kDa were detected on Western blot analysis of
cytosolic and membrane fractions of N18TG2 cells, using a nNOS antibody. Chronic
treatment of N18TG2 cells with cannabinoid agonists downregulated nNOS protein
and mRNA as detected using Western blot analysis and real-time polymerase chain
reaction, respectively. Cannabinoid agonists stimulated NO production via
signaling through CB(1) receptors, leading to activation of Gi/o protein and
enhanced nNOS activity. The findings of these studies provide information related
to cannabinoid-mediated NO signal transduction in neuronal cells, which has
important implications in the ongoing elucidation of the endocannabinoid system
in the nervous system.

Prostaglandins Med. 1980 Jun;4(6):409-17.
Effects of delta 9-tetrahydrocannabinol and cannabidiol on phospholipase and
other enzymes regulating arachidonate metabolism.
White HL, Tansik RL.
delta 9-Tetrahydrocannabinol (THC) and cannabidiol (CBD) caused a marked
stimulation of phospholipase A2 when incubated with intact human platelets that
were prelabeled with [14C] arachidonate. CBD was about 1.5 x as potent as THC in
the same concentration range (10 leads to 80 microM) Most of the released
arachidonate was converted to lipoxygenae products. When [14C] arachidonate was
incubated with lysed platelet extracts, THC inhibited both thromboxane synthetase
and prostaglandin cyclooxygenase, so that the net effect was a redistribution of
products toward the lipoxygenase pathway at the same time that a decrease in
total cyclooxygenase product formation occurred. THC did not directly affect
arachidonate lipoxygenase. Both TCH and CBD also stimulated release from
prelabeled neuroblastoma cells (NBA2), which do not contain an active
lipoxygenase pathway. In this case, accumulation of free arachidonate was
detected by autoradiography. The multiple effects of THC and CBD on phospholipase
A2 and arachidonate metabolism may mediate some of the pharmacological actions of
these compounds, such as their anticonvulsant, anti-inflammatory, and hypotensive
properties.

I have to say that I used to smoke a lot in the past as it cured my anhedonia but know can't even make a weed tea without becoming highly hypothyroid.