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Front. Integr. Neurosci., 26 February 2014 | doi: 10.3389/fnint.2014.00020
The claustrum’s proposed role in consciousness is supported by the effect and target localization of Salvia divinorum

Klaus M. Stiefel, Alistair Merrifield and Alex O. Holcombe

This article brings together three findings and ideas relevant for the understanding of human consciousness: (I) Crick’s and Koch’s theory that the claustrum is a “conductor of consciousness” crucial for subjective conscious experience. (II) Subjective reports of the consciousness-altering effects the plant Salvia divinorum, whose primary active ingredient is salvinorin A, a κ-opioid receptor agonist. (III) The high density of κ-opioid receptors in the claustrum. Fact III suggests that the consciousness-altering effects of S. divinorum/salvinorin A (II) are due to a κ-opioid receptor mediated inhibition of primarily the claustrum and, additionally, the deep layers of the cortex, mainly in prefrontal areas. Consistent with Crick and Koch’s theory that the claustrum plays a key role in consciousness (I), the subjective effects of S. divinorum indicate that salvia disrupts certain facets of consciousness much more than the largely serotonergic hallucinogen lysergic acid diethylamide (LSD). Based on this data and on the relevant literature, we suggest that the claustrum does indeed serve as a conductor for certain aspects of higher-order integration of brain activity, while integration of auditory and visual signals relies more on coordination by other areas including parietal cortex and the pulvinar.
 
Front. Integr. Neurosci., 26 February 2014 | doi: 10.3389/fnint.2014.00020
The claustrum’s proposed role in consciousness is supported by the effect and target localization of Salvia divinorum

Klaus M. Stiefel, Alistair Merrifield and Alex O. Holcombe

It's a pretty big leap to go from the kappa opioid receptor is expressed with the highest density in the claustrum to the consciousness altering effects of kappa opioid agonists must be mediated by the claustrum. Still a cool theory though.

I really like their analysis of Erowid trip reports too, what a great data set to work from.
 
I really wish they had used pure cannabis instead of a cannabis/tobacco mixture, but either way this is the highest THC dosage I've ever seen used in a clinical trial (69mg):

Acute subjective effects after smoking joints containing up to 69 mg Δ9-tetrahydrocannabinol in recreational users: a randomized, crossover clinical trial.

Abstract
RATIONALE:
An increase in the potency of the cannabis cigarettes has been observed over the past three decades.
OBJECTIVES:
In this study, we aimed to establish the impact of Δ9-tetrahydrocannabinol (THC) on the rating of subjective effects (intensity and duration of the effects), up to 23 % THC potency (69 mg THC) among recreational users.
METHODS:
Recreational users (N = 24) smoked cannabis cigarettes with four doses of THC (placebo 29, 49 and 69 mg of THC) on four separate test days in a randomized, double-blind, placebo-controlled, crossover study. The participants filled in three different questionnaires measuring subjective effects during the exposure up to 8 h post-smoking. The 'high' feeling, heart rate, blood pressure and THC serum concentrations were also regularly recorded during these 8 h.
RESULTS:
THC significantly increased the high feeling, dizziness, dry-mouthed feeling, palpitations, impaired memory and concentration, and 'down', 'sedated' and 'anxious' feelings. In addition, THC significantly decreased alertness, contentment and calmness. A cubic relationship was observed between 'feeling the drug' and 'wanting more'. The THC-induced decrease in 'feeling stimulated' and increase in anxiety lasted up to 8 h post-smoking. Sedation at 8 h post-smoking was increased by a factor of 5.7 with the highest THC dose, compared to the placebo.
CONCLUSIONS:
This study shows a strong effect of cannabis containing high percentages of THC on the rating of subjective effects. Regular users and forensic toxicologists should be aware that the THC-induced increase in 'feeling sedated' continues longer with a 69 mg THC dose than with a 29 mg THC dose.
 
I never really bought into the whole "stimulants effect people with AD(H)D differently"... given that, y'know, people in general experience drugs differently, and set and setting need to be considered. Also, given that stimulants like methylphenidate, amphetamine and the like precede the ADHD explosion, and have been known to enhance cognitive performance (in some contexts) for a long damn time.

On that note: http://www.sciencedaily.com/releases/2014/04/140407153804.htm People with ADHD/Schizophrenia are less likely to feel euphoric for stimulants, so it's not a uniform standard but a significant association exists.

I thought that stimulants only enhance cognition in those with learning disabilities?
 
Perhaps this could be used backwards to help with withdrawls to opioids? I guess it would certainly not be optimal but atleast you wouldn't have to take anything else.
 
What, drug addicts need to go outside and get some fresh air and sun? ;)
 
^ Hey, getting some sun every day might be a good supplement to other treatments, although I don't know if someone with intense opioid withdrawls (without methadone or buprenorphine or the likes) would be willing to take regular strolls outside.


Either that or they should lie in a tanning bed until they stop being sick...

It really is a shame UV is carcinogenic.
 
What, drug addicts need to go outside and get some fresh air and sun? ;)
lol

@DL-ark
Tanning beds might not be a bad idea. I'm pretty sure that occasional exposure to the UV light emitted by tanning beds shouldn't be any serious concern in that it won't significantly raise your risk of getting cancer. I suppose one doesn't go through opiate withdrawal on a weekly basis. Well, most of us don't anyway.

This kinda explains to me why I feel so damn good after using the tanning bed. The weather in Germany is pretty shitty and I've been saying all my life that when the sun is shining, nothing could ever make me feel really bad, but when it's gone everything sucks. I'm well aware that most people aren't that sensitive to sun or lack thereof which is why I enjoyed this article so much. It bridges the gap between my unusual affinity towards sunlight and my addictive personality.

EDIT: on a side note, this made me lol:
Case Report: A primary care physician referred a 26-year-old asymptomatic white woman to our endocrinology clinic because of high serum 25-(OH)D levels (>339 nmol/L [reference range, 75 to 185 nmol/L]) discovered during an annual health examination in July 2012. We saw her 6 months later, because of our clinic's wait list for nonurgent referrals. Repeated measurement showed elevated levels (>299 nmol/L).

The patient did not excessively consume milk or receive over-the-counter vitamin D preparations or other medications. She reported minimal sun exposure but had been using a tanning bed 3 or more times weekly for at least 6 months. Her medical history included polycystic ovarian disease. She was following a low-fat, low-carbohydrate diet and other lifestyle changes to lose weight. Serum levels of calcium, phosphorus, 1,25-dihydroxyvitamin D, and parathyroid hormone were normal.

Source: Tanning Beds and Hypervitaminosis D: A Case Report, Ann Intern Med. 2014;160(11):810-811. doi:10.7326/L14-5011-8
Just to clarify this: It has afaik been considered impossible to suffer a hypervitaminosis d due to uv light exposure and imho this case can probably just be blamed on some unusual genetic variation.
 
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Hey, getting some sun every day might be a good supplement to other treatments

Indeed. Vitamin D supplements tend to be poorly bioavailable and low in dosage compared to that synthesized endogenously.

ebola
 
I'd like to know how that data was compiled. How would the toxicologist know if someone passed the test but took meth two days ago?

Also I want to meet the frequent cannabis user with no carboxy-THC in the urine 1 day after last use.
 
I'd like to know how that data was compiled. How would the toxicologist know if someone passed the test but took meth two days ago?

Also I want to meet the frequent cannabis user with no carboxy-THC in the urine 1 day after last use.

I think they probably put "1" to whatever the max number was just to kind of say "anything can happen"...
 
Tea catechins’ affinity for human cannabinoid receptors

Among the many known health benefits of tea catechins count anti-inflammatory and neuroprotective activities, as well as effects on the regulation of food intake. Here we address cannabimimetic bioactivity of catechin derivatives occurring in tea leaves as a possible cellular effector of these functionalities. Competitive radioligand binding assays using recombinant human cannabinoid receptors expressed in Chem-1 and CHO cells identified (–)-epigallocatechin-3-O-gallate, EGCG (Ki=33.6μM), (–)-epigallocatechin, EGC (Ki=35.7μM), and (–)-epicatechin-3-O-gallate, ECG (Ki=47.3μM) as ligands with moderate affinity for type 1 cannabinoid receptors, CB1. Binding to CB2 was weaker with inhibition constants exceeding 50μM for EGC and ECG. The epimers (+)-catechin and (–)-epicatechin exhibited negligible affinities for both CB1 and CB2. It can be concluded that central nervous cannabinoid receptors may be targeted by selected tea catechins but signaling via peripheral type receptors is less likely to play a major role in vivo.
 
Can someone help me with this one:

Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium.

Abstract
To investigate the association between cannabis smoking and lung cancer risk, data on 2,159 lung cancer cases and 2,985 controls were pooled from 6 case-control studies in the US, Canada, UK, and New Zealand within the International Lung Cancer Consortium. Study-specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack-years; odds-ratio estimates were pooled using random effects models. Subgroup analyses were done for sex, histology and tobacco smoking status. The shapes of dose-response associations were examined using restricted cubic spline regression. The overall pooled OR for habitual versus nonhabitual or never users was 0.96 (95% CI: 0.66-1.38). Compared to nonhabitual or never users, the summary OR was 0.88 (95%CI: 0.63-1.24) for individuals who smoked 1 or more joint-equivalents of cannabis per day and 0.94 (95%CI: 0.67-1.32) for those consumed at least 10 joint-years. For adenocarcinoma cases the ORs were 1.73 (95%CI: 0.75-4.00) and 1.74 (95%CI: 0.85-3.55), respectively. However, no association was found for the squamous cell carcinoma based on small numbers. Weak associations between cannabis smoking and lung cancer were observed in never tobacco smokers. Spline modeling indicated a weak positive monotonic association between cumulative cannabis use and lung cancer, but precision was low at high exposure levels. Results from our pooled analyses provide little evidence for an increased risk of lung cancer among habitual or long-term cannabis smokers, although the possibility of potential adverse effect for heavy consumption cannot be excluded.
© 2014 UICC.

Specifically I was hoping someone could clarify how the first two bolded sentences mesh with the final conclusion. It seems to me that the bolded findings support the association between cannabis smoking and lung cancer, albeit weakly and no where near the degree I've seen in studies of tobacco and lung cancer.
 
it didn't reach statistical significance. with a probablility of 95% the risk of developing an adenocarcinoma is somwhere between 75% of the normal risk and 400% of the normal risk.
so it "looks like" there could be a correlation between cannabis and lung cancer risk (especially as there is a monotonic association between those factors), so that larger studies could find something, but this study alone still neither proves or disproves anything.
 
J Clin Psychopharmacol. 2014 Feb 12. [Epub ahead of print]
Methylphenidate Enhances Cognitive Performance in Adults With Poor Baseline Capacities Regardless of Attention-Deficit/Hyperactivity Disorder Diagnosis.
Agay N, Yechiam E, Carmel Z, Levkovitz Y.

More evidence that, maybe, stimulants are just good at making people task-oriented, rather than are a "treatment" for anything? I never really bought into the whole "stimulants effect people with AD(H)D differently"... given that, y'know, people in general experience drugs differently, and set and setting need to be considered. Also, given that stimulants like methylphenidate, amphetamine and the like precede the ADHD explosion, and have been known to enhance cognitive performance (in some contexts) for a long damn time.

2.7k words written on my dissertation in one day agrees with that. ADHD stimulants are just fucking fantastic cognitive enhancers in any population.
 
it didn't reach statistical significance. with a probablility of 95% the risk of developing an adenocarcinoma is somwhere between 75% of the normal risk and 400% of the normal risk.
so it "looks like" there could be a correlation between cannabis and lung cancer risk (especially as there is a monotonic association between those factors), so that larger studies could find something, but this study alone still neither proves or disproves anything.

Yea that makes sense, I just looked at the 1.73 and 1.74 and didn't pay much attention to the range. It just irks me the way that pro-pot publications use that study to argue Smoking Marijuana Does Not Lead to Lung Cancer, when I think you could more easily argue the opposite from that data.
 
Transl Psychiatry. Jul 2014; 4(7): e411.
Published online Jul 15, 2014. doi: 10.1038/tp.2014.30
PMCID: PMC4119213
The atypical antidepressant and neurorestorative agent tianeptine is a μ-opioid receptor agonist

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119213
...Herein, we report the characterization of tianeptine as a μ-opioid receptor (MOR) agonist. Using radioligand binding and cell-based functional assays, including bioluminescence resonance energy transfer-based assays for G-protein activation and cAMP accumulation, we identified tianeptine as an efficacious MOR agonist (Ki Human of 383±183 nM and EC50 Human of 194±70 nM and EC50 Mouse of 641±120 nM for G-protein activation). Tianeptine was also a full δ-opioid receptor (DOR) agonist, although with much lower potency (EC50 Human of 37.4±11.2 μM and EC50 Mouse of 14.5±6.6 μM for G-protein activation). In contrast, tianeptine was inactive at the κ-opioid receptor (KOR, both human and rat). On the basis of these pharmacological data, we propose that activation of MOR (or dual activation of MOR and DOR) could be the initial molecular event responsible for triggering many of the known acute and chronic effects of this agent, including its antidepressant and anxiolytic actions.

May explain why it's abusable. :p
 
Transl Psychiatry. Jul 2014; 4(7): e411.
Published online Jul 15, 2014. doi: 10.1038/tp.2014.30
PMCID: PMC4119213
The atypical antidepressant and neurorestorative agent tianeptine is a μ-opioid receptor agonist

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119213


May explain why it's abusable. :p

Wow great find, I always thought the "5-HT reuptake enhancer" mechanism was bullshit, this makes a lot more sense.
 
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