Psycho-Babble Medication Thread 377884

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re: CECD Larry Hoover

Posted by lil' jimi on August 17, 2004, at 12:47:46

In reply to Re: New disease paradigm: CECD, posted by Larry Hoover on August 17, 2004, at 10:52:11

we cross posted, dude.
i hadn't seen your latest.
i find the low response surprising too.
i mean, how much more interesting can you get than a neurotransmitter know as the "bliss chemical" and named 'anandamide', no less?

it does seem to me very exciting that there may be new approaches to, well, every mood disorder, digestive disorders, menstrual disorders, et cetera.

so few people suffer from too much bliss and so many from too little.

so,
how much would anandamide cost?
could you, like, drink it?
is it a controled substance in the u.s.?
in canada?
could it be, like, a supplement?
am i being too enthusiastic?

anecdotally, i did Not have mood issues back when i was a marijuana user.
this report brought to mind that i never had my rage issues back then.
i know, i know: too much of a stoner stereotype, but the facts corelate in my experience.

as Larry says, "Anybody?"
else?

~ jim

 

re: CECD lil' jimi

Posted by Jasmineneroli on August 20, 2004, at 17:36:13

In reply to re: CECD Larry Hoover, posted by lil' jimi on August 17, 2004, at 12:47:46

Yes, extremely interesting, and seems to just prompt more questions in my mind. For instance, do you think there could be a negative relationship between anandamide and serotonin? Because I suffer from GAD (& depression sometimes) and some of it has an hormonal aspect. Every single time I try a serotonergic drug I get the very symptoms anandamide might relieve.....nausea/stomach pain, diarrohea, headache/migraines and eventually, anhedonia (a very definite lack of bliss!). In other words, my problem isn't serotonin re-uptake or low-levels, but some other deficiency (anandamide?)and trying to solve it with serotoninergic drugs makes the anandamide situation worse. Comments, anyone?
I echo, Jimi...where can I get it???

 

re: CECD Jasmineneroli

Posted by lil' jimi on August 20, 2004, at 20:06:11

In reply to re: CECD lil' jimi, posted by Jasmineneroli on August 20, 2004, at 17:36:13

hi Jasmineneroli,

i think you may be interested in this:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15293893
Fluctuations of fatty acid amide hydrolase and anandamide levels during the human ovulatory cycle.
Gynecol Endocrinol. 2004 Apr;18(4):212-8.
PMID: 15293893

i'll be checking to see if that long url posted there for us.

take care,
~ jim

 

endocannabinoid know as arachidonoyl ethanol amide

Posted by lil' jimi on August 20, 2004, at 20:43:45

In reply to Re: New disease paradigm: CECD, posted by Larry Hoover on August 17, 2004, at 10:52:11

this is also interesting:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12052038

Prostaglandins Leukot Essent Fatty Acids. 2002 Feb-Mar;66(2-3):221-33.
Endocannabinoids in the central nervous system--an overview.

Fride E.

Department of Behavioral Sciences, College of Judea and Samaria, Ariel, 44837 Israel. fride@research.yosh.ac.il

Many aspects of the physiology and pharmacology of anandamide (arachidonoyl ethanol amide), the first endogenous cannabinoid ligand ("endocannabinoid") isolated from pig brain, have been studied since its discovery in 1992. Ethanol amides from other fatty acids have also been identified as endocannabinoids with similar in vivo and in vitro pharmacological properties. 2-Arachidonoyl glycerol and noladin ether (2-arachidonyl glyceryl ether), isolated in 1995 and 2001, respectively, so far, display pharmacological properties in the central nervous system, similar to those of anandamide. The endocannabinoids are widely distributed in brain, they are synthesized and released upon neuronal stimulation, undergo reuptake and are hydrolyzed intracellularly by fatty acid amide hydrolase (FAAH). For therapeutic purposes, inhibitors of FAAH may provide more specific cannabinoid activities than direct agonists, and several such molecules have already been developed.Pharmacological effects of the endocannabinoids are very similar, yet not identical, to those of the plant-derived and synthetic cannabinoid receptor ligands. In addition to pharmacokinetic explanations, direct or indirect interactions with other receptors have been considered to explain some of these differences, including activities at serotonin and GABA receptors. Binding affinities for other receptors such as the vanilloid receptor, have to be taken into account in order to fully understand endocannabinoid physiology. Moreover, possible interactions with receptors for the lysophosphatidic acids deserve attention in future studies.Endocannabinoids have been implicated in a variety of physiological functions. The areas of central activities include pain reduction, motor regulation, learning/memory, and reward. Finally, the role of the endocannabinoid system in appetite stimulation in the adult organism, and perhaps more importantly, its critical involvement in milk ingestion and survival of the newborn, may not only further our understanding of the physiology of food intake and growth, but may also find therapeutic applications in wasting disease and infant's "failure to thrive". Copyright 2002 Elsevier Science Ltd. All rights reserved.

PMID: 12052038 [PubMed - indexed for MEDLINE]

 

re: CECD

Posted by Jasmineneroli on August 20, 2004, at 23:06:12

In reply to re: CECD Jasmineneroli, posted by lil' jimi on August 20, 2004, at 20:06:11

> hi Jasmineneroli,
>
> i think you may be interested in this:
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15293893
> Fluctuations of fatty acid amide hydrolase and anandamide levels during the human ovulatory cycle.
> Gynecol Endocrinol. 2004 Apr;18(4):212-8.
> PMID: 15293893
>
> i'll be checking to see if that long url posted there for us.
>
> take care,
> ~ jim

O my goodness, Jimi. I read the link.That makes so much sense to me. My daughter has the same condition (GAD) as I and has been on SSRI Celexa for about a year. It has helped somewhat, but she recently became pregnant whilst on the SSRI and shortly after discovery (to the sadness of us all) miscarried. I'm sure my thought about serotonin levels negatively affecting anandamide levels has merit. Possibly, low anandamide levels, caused by the serotonin action of Celexa, could have prevented the embryo from properly implanting!!!! Fortunately for me,my SSRI use was long after childbearing and I carried my children to term wiithout a problem. My hormonal problems are from the other end of the spectrum...perimenopause. Thanks for the link, maybe my daughter should try a different (and non-serotonergic) drug when she tries to conceive again. What does everyone think about this aspect???
PS.Does this mean I should tell her to start smoking pot:)??
Jas

 

re: anandamide deficiency Jasmineneroli

Posted by lil' jimi on August 21, 2004, at 0:51:27

In reply to re: CECD, posted by Jasmineneroli on August 20, 2004, at 23:06:12

hi Jas,

> O my goodness, Jimi. I read the link.That makes so much sense to me. My daughter has the same condition (GAD) as I and has been on SSRI Celexa for about a year.

there are suggestions that anandamide depletion at ovulation causes PMS ... we may expect that this would aggravate systems already suffering anandamide challeges ... ...

coincidentally, i have been on lexapro for 16 months now ...

> It has helped somewhat, but she recently became pregnant whilst on the SSRI and shortly after discovery (to the sadness of us all) miscarried. I'm sure my thought about serotonin levels negatively affecting anandamide levels has merit. Possibly, low anandamide levels, caused by the serotonin action of Celexa, could have prevented the embryo from properly implanting!!!!

it is my understanding that most conceptions will miscarry, many undetected ... ... we suffered 7 miscarriages and demoralized our fertility specialist ... extensive testing had shown us to be able to deliver ... his assistants would cry for us ... ...
we gave up ... fertility drugs, pergonal and clomid, were extremely stressful ... ... 4 years later we were blessed ...

i would speculate that celexa had nothing to do with the miscarriage, even though one would want to take precautions to avoid pergnancy while on ssris.
not only would establishing a causal link be impossible and alternatives be as likely as not, but we may justifiably avoid the sense of responsiblity for one's loss pregnancy.
we lost many for no reason whatsoever, while 16 year old crack addict prostitutues have babies everyday ... ...

and sometimes a miscarriage may be merciful, yet we would not know.

> Fortunately for me,my SSRI use was long after childbearing and I carried my children to term wiithout a problem. My hormonal problems are from the other end of the spectrum...perimenopause. Thanks for the link, maybe my daughter should try a different (and non-serotonergic) drug when she tries to conceive again. What does everyone think about this aspect???

i see there being serious risks for post-partum depression for depressed women ... going off meds to get pregnant and gestate (which is done regularly but not much feedback is heard) is not without perils ... ...

but allow me to be humble enough to not pretend to suggest alternatives to your doctors' recommendations for antidepressants ... i dare not try to guess what ads would be avisable while conceiving.

> PS.Does this mean I should tell her to start smoking pot:)??

your smilemoticon is noted ... ... couldn't begin to assess the risk levels, so, no.
~ jim

 

re: estrogen and anandamide

Posted by lil' jimi on August 22, 2004, at 5:02:07

In reply to re: anandamide deficiency Jasmineneroli, posted by lil' jimi on August 21, 2004, at 0:51:27

from http://www.bloodjournal.org/cgi/reprint/2002-05-1444v1

"In conclusion, the results reported here demonstrate that E2 activates the synthesis and inhibits the degradation of AEA in human endothelial cells, by acting at a surface receptor and causing a calcium-dependent release of NO. As a consequence, AEA is released in blood, where it can modulate the cardiovascular and immune systems. In particular, AEA released from estrogen-stimulated endothelial cells is capable of reducing the secretion of 5-HT from platelets. This newly found interplay between estrogen and AEA metabolism suggests that endocannabinoids might mediate some of the beneficial effects of estrogen, and seems to indicate a novel approach for the management of cardiovascular disease in postmenopausal women."

 

Re: New disease paradigm: CECD

Posted by linkadge on August 28, 2004, at 15:35:29

In reply to New disease paradigm: CECD, posted by Larry Hoover on August 15, 2004, at 10:35:10

Don't certain compounds in choloclate mimic the canabanoid receptor agonising effects of cannabis.

I get a real twist when I load up lots of cholocate.


Linkadge

 

re: chocolate linkadge

Posted by lil' jimi on August 28, 2004, at 18:23:08

In reply to Re: New disease paradigm: CECD, posted by linkadge on August 28, 2004, at 15:35:29

hi Linkadge,

from http://www.nsi.edu/research/e008.html

"Fellows have shown that anandamide is present in cocoa powder and in chocolate, along with two other N-acylethanolamines that could act as cannabinoid mimics, either by directly activating cannabinoid receptors or by increasing anandamide levels. The relationship of this finding to the subjective feelings associated with eating chocolate remains to be determined."

and then there's always http://www.chocolate.org/
for grins.
heh.

~ jim

 

Re: New disease paradigm: CECD

Posted by KaraS on August 28, 2004, at 18:31:46

In reply to Re: New disease paradigm: CECD, posted by linkadge on August 28, 2004, at 15:35:29

> Don't certain compounds in choloclate mimic the canabanoid receptor agonising effects of cannabis.
>
> I get a real twist when I load up lots of cholocate.
>
>
> Linkadge


I think it's because of the PEA.

 

re: PEA KaraS

Posted by lil' jimi on August 28, 2004, at 20:48:27

In reply to Re: New disease paradigm: CECD, posted by KaraS on August 28, 2004, at 18:31:46

KaraS posts:
> I think it's because of the PEA.

i haven't found mention of significant amounts palmitoylethanolamide in chocolate.

whereas:
"In the recent study, Piomelli's group identified two anandamidelike compounds in chocolate -- which go by the unwieldy names of N-oleoylethanolamine and N-linoleoylethanolamine. At least in test-tube experiments, both delay anandamide's breakdown. Moreover, relative to the concentration of anandamide measured in chocolate, those of its chemical cousins proved relatively high."
from http://www.sciencenews.org/pages/sn_arch/10_12_96/food.htm

although PEA may well be present in chocolate, none of the studies i've seen make any reference to it.

would you have a link to a study i have missed?

~ jim

 

re: PEA

Posted by Larry Hoover on August 28, 2004, at 21:17:19

In reply to re: PEA KaraS, posted by lil' jimi on August 28, 2004, at 20:48:27

> KaraS posts:
> > I think it's because of the PEA.
>
> i haven't found mention of significant amounts palmitoylethanolamide in chocolate.
>
> whereas:
> "In the recent study, Piomelli's group identified two anandamidelike compounds in chocolate -- which go by the unwieldy names of N-oleoylethanolamine and N-linoleoylethanolamine. At least in test-tube experiments, both delay anandamide's breakdown. Moreover, relative to the concentration of anandamide measured in chocolate, those of its chemical cousins proved relatively high."
> from http://www.sciencenews.org/pages/sn_arch/10_12_96/food.htm
>
> although PEA may well be present in chocolate, none of the studies i've seen make any reference to it.
>
> would you have a link to a study i have missed?
>
> ~ jim

jimi the geek!

The problem with acronyms is that they can be ambiguous. I'm almost certain that the PEA Kara was mentioning is phenylethylamine, which is formed from phenylalanine.

Lar

 

re: PEA lil' jimi

Posted by KaraS on August 28, 2004, at 22:35:13

In reply to re: PEA KaraS, posted by lil' jimi on August 28, 2004, at 20:48:27

> KaraS posts:
> > I think it's because of the PEA.
>
> i haven't found mention of significant amounts palmitoylethanolamide in chocolate.
>
> whereas:
> "In the recent study, Piomelli's group identified two anandamidelike compounds in chocolate -- which go by the unwieldy names of N-oleoylethanolamine and N-linoleoylethanolamine. At least in test-tube experiments, both delay anandamide's breakdown. Moreover, relative to the concentration of anandamide measured in chocolate, those of its chemical cousins proved relatively high."
> from http://www.sciencenews.org/pages/sn_arch/10_12_96/food.htm
>
> although PEA may well be present in chocolate, none of the studies i've seen make any reference to it.
>
> would you have a link to a study i have missed?
>
> ~ jim
>
>
NO, phenylethylamine (PEA) (Check out the link below)

http://www.chocolate.org/phenylethylamine.html


-Kara

 

re: PEA(s) KaraS

Posted by lil' jimi on August 29, 2004, at 1:15:51

In reply to re: PEA lil' jimi, posted by KaraS on August 28, 2004, at 22:35:13

Kara S posted:
> NO, phenylethylamine (PEA)

Oh!
rather, Doh!

Larry's post about the CECD study got me to reading about the endocannabinoids.
i found anandamide's chem name, arachidonylethanolamide, abbreviated as AEA and its relative, palmitoylethanolamide got shorten to PEA.

so, my mistake. sorry.

yet it would appear that this abundance of chocolate neurotransmitters stimulating both the endocannabinoid and endorphin/opioid systems may go a way towards explaining Linkadge's "getting a real twist" from chocolate indulgence.

but i've been wrong before.

i discovered a lot at http://encyclopedia.thefreedictionary.com/Phenylethylamine thanks to your valuable keyword for PEA.

thanks,
~ jim

p.s. i'm going to get some dark chocolate now.

 

re: PEA(s) lil' jimi

Posted by KaraS on August 29, 2004, at 2:11:41

In reply to re: PEA(s) KaraS, posted by lil' jimi on August 29, 2004, at 1:15:51

> Kara S posted:
> > NO, phenylethylamine (PEA)
>
> Oh!
> rather, Doh!
>
> Larry's post about the CECD study got me to reading about the endocannabinoids.
> i found anandamide's chem name, arachidonylethanolamide, abbreviated as AEA and its relative, palmitoylethanolamide got shorten to PEA.
>
> so, my mistake. sorry.
>
> yet it would appear that this abundance of chocolate neurotransmitters stimulating both the endocannabinoid and endorphin/opioid systems may go a way towards explaining Linkadge's "getting a real twist" from chocolate indulgence.
>
> but i've been wrong before.

I don't know enough about endocannabinoid and endorphin/opioid systems. Are the two explanations mutually exclusive?


> i discovered a lot at http://encyclopedia.thefreedictionary.com/Phenylethylamine thanks to your valuable keyword for PEA.
>
> thanks,
> ~ jim
>
> p.s. i'm going to get some dark chocolate now.
>
>

p.p.s. I like milk chocolate better. Lindt is the best. mmmmm

-K

 

re: 2 PEA(s) KaraS

Posted by lil' jimi on August 29, 2004, at 2:52:53

In reply to re: PEA(s) lil' jimi, posted by KaraS on August 29, 2004, at 2:11:41

> > Kara S posted:
> I don't know enough about endocannabinoid and endorphin/opioid systems. Are the two explanations mutually exclusive?

no.
not even a little.
it may reasonably be expected that they could be synergistic.
and it looks to me like chocolate stimulates them both.
simultaneously like.
chocolate brings a double punch of neuro fun.

> >
> > p.s. i'm going to get some dark chocolate now.
> >
> >
>
> p.p.s. I like milk chocolate better. Lindt is the best. mmmmm

bill l. on the lex thread used to insist that he felt there were more benefits from dark chocolate (more of something?) than milk chocolate.
or maybe the other ingredients in milk chocolate did somehting?

... dark chocolate old husbands' tale maybe.

~ jim

 

re: 2 PEA(s) ... KaraS

Posted by lil' jimi on August 29, 2004, at 3:14:51

In reply to re: 2 PEA(s) KaraS, posted by lil' jimi on August 29, 2004, at 2:52:53

i wrote:
> ... dark chocolate old husbands' tale maybe.

maybe not.

"In the mean time, individuals wishing to self-medicate with nonprescription-strength chocolate should reach for cocoa -- or dark chocolate, which can contain two to three times as much of these compounds, per ounce, as milk chocolate."
from http://www.chocolate.org/health/chocprescribe.html

of course consuming 2 or 3 times as much milk chocolate should get you caught up.
not so bad.
~ jim

 

re: 2 PEA(s) ... KaraS lil' jimi

Posted by KaraS on August 29, 2004, at 7:11:31

In reply to re: 2 PEA(s) ... KaraS, posted by lil' jimi on August 29, 2004, at 3:14:51

> i wrote:
> > ... dark chocolate old husbands' tale maybe.
>
> maybe not.
>
> "In the mean time, individuals wishing to self-medicate with nonprescription-strength chocolate should reach for cocoa -- or dark chocolate, which can contain two to three times as much of these compounds, per ounce, as milk chocolate."
> from http://www.chocolate.org/health/chocprescribe.html
>
> of course consuming 2 or 3 times as much milk chocolate should get you caught up.
> not so bad.
> ~ jim

I could learn to like dark chocolate as well. Either that or pack on a few pounds!

-Kara

 

re: 2 PEA(s) ... KaraS

Posted by linkadge on August 31, 2004, at 17:15:54

In reply to re: 2 PEA(s) ... KaraS lil' jimi, posted by KaraS on August 29, 2004, at 7:11:31

What I do is eat a bar of dark chocolate and go for a run. Running has been shown to increase the levels of PEA, and I assume that eating chocolate which contains the same would boost it even further. When I do this, about 25 min into running things becomes SO BRIGHT. It almost feels like I am on cocaine or something (have never done cocaine howver). But doing this leaves me paranoid for a day, too much PEA activity can cause paranoia and paranoid like anxiety.

Linkadge

 

Re:cannabinoid receptor antagonist aid weight loss lil' jimi

Posted by Larry Hoover on August 31, 2004, at 22:32:24

In reply to endocannabinoid know as arachidonoyl ethanol amide, posted by lil' jimi on August 20, 2004, at 20:43:45

http://www.cnw.ca/fr/releases/archive/August2004/29/c4670.html

New Study Confirms Benefits of Rimonabant in Weight Loss, Waist Circumference Reduction and Metabolic Risk Factor Improvement
1st year results of RIO-Europe study presented at the European
Society of Cardiology (ESC) 2004 congress

ANTWERP, Belgium, Aug. 29 /CNW/ - First year results of the two year
trial Rimonabant In Obesity - Europe (RIO-Europe), a Phase III clinical study
comparing placebo to rimonabant, the first agent in a new therapeutic class
known as selective cannabinoid type 1 (CB1) blockers, showed that overweight
or obese people taking rimonabant 20mg once daily benefited from a significant
reduction in their body weight, waist circumference - a marker of the
dangerous abdominal obesity - and improvements in their lipid and glycemic
profiles. The improvement in lipids (HDL-cholesterol and triglycerides) was
demonstrated to be partially independent from weight loss, implying a direct
effect of the drug on these important metabolic cardiovascular risk
parameters. The trial findings also revealed a significant decrease in the
percentage of patients with metabolic syndrome(1) in the rimonabant 20 mg/day
group compared to placebo. These new results from the RIO-Europe study confirm
rimonabant's potential to become an important tool in the reduction of
cardiovascular risk factors by lowering body weight, improving metabolic
syndrome-associated parameters in overweight/obese subjects and aiding in
smoking cessation as presented earlier this year.

1) Metabolic Syndrome is a term that encompasses a series of health risks
or conditions that increase a person's chance to develop heart disease, stroke
and diabetes. According to the ATP III definition, metabolic syndrome includes
at least 3 of the following criteria: abdominal obesity: waist circumference
Men greater than 102 cm (40 inches), Women greater than 88 cm (35 inches);
hypertension: greater than or equal to 130/85mmHg; hypertriglyceridemia:
greater than or equal to 150mg/ dL; Low HDL cholesterol: Men less than
40mg/ dL, Women less than 50mg/ dL; Abnormal fasting glucose: greater than or
equal to 110mg/ dL. 1

RIO Europe, an international, multicentre, randomized, double-blind,
placebo-controlled, parallel-group study compared rimonabant 20mg/day
and 5mg/day to placebo in 1,507 overweight/obese patients (Body Mass
Index (BMI) greater than or equal to 30 kg/m(squared) or BMI greater than 27
with co-morbidity (e.g. dyslipidemia, hypertension) in 60 centres across
Europe (Belgium, Finland, France, Germany, the Netherlands, Sweden) and the
United States for a period of 2 years. The announcement made at the ESC 2004
concerns the first year data of the study. Patients treated for one year with
rimonabant 20mg/day lost an average of 8.6kg (about 19 lbs) (p less than 0.001
vs placebo) compared to 4.8kg (about 11 lbs) for patients on rimonabant
5mg/day (p equals 0.038 vs placebo) and 3.6kg (about 8 lbs) for those on
placebo. Nearly 70% of patients treated with rimonabant 20mg/day lost more
than 5% of their initial body weight (p less than 0.001 vs placebo), compared
to 44.2% of patients in the rimonabant 5mg/day group (p equals 0.002 vs
placebo) and 30.5% in the placebo group. Moreover, 39% (p less than 0.001 vs
placebo) of patients on rimonabant 20mg/day lost more than 10% of their
initial body weight compared to 15.3% of those on rimonabant 5mg/day and 12.4%
of those on placebo. Patients on rimonabant 20mg/day also had an average
decrease in their waist circumference of 8.5 cm (about 3.5 inches) (p less
than 0.001) versus 5.3 cm (2 inches) for those on rimonabant 5mg (p equals
0.002 vs placebo) and 4.5 cm (about 1.5 inches) for those on placebo. The
number of patients diagnosed as having metabolic syndrome at baseline (42.2%)
was reduced by more than half (19.6%) after treatment with rimonabant 20mg
(p less than 0.001 compared to placebo). In addition to weight loss, a
statistically significant improvement in metabolic risk factors with
rimonabant 20mg vs. placebo was also observed. In patients treated for one
year with rimonabant 20 mg/day, HDL-cholesterol (good cholesterol) increased
by 27.0% (p less than 0.001 vs placebo), compared to 19% in the rimonabant
5mg/day group and 17.3% in the placebo group. Weight loss accounted for only
approximately half the improvement in HDL seen with rimonabant 20mg vs.
placebo, implying a significant direct effect of the drug on lipid metabolism,
independent of weight loss (p equals 0.005).
In patients treated for one year with rimonabant 20mg, triglycerides
were reduced by 10.6% in patients on rimonabant 20 mg (p less than 0.001
vs. placebo), while increasing by 4.9% for rimonabant 5mg and by 6.6% for
placebo. As seen with HDL, weight loss accounted for only approximately
half the improvement in triglycerides seen with rimonabant 20mg vs. placebo,
implying a significant direct effect of the drug on lipid metabolism,
independent of weight loss (p equals 0.005). An improved insulin response as
demonstrated by an Oral Glucose Tolerance Test was also observed. During the
2 hour test, patients on rimonabant 20 mg had to produce less insulin to
metabolize their glucose compared to those on placebo (reduction by 11.0 micro
IU/ml vs baseline compared to 2.3 micro IU/ml in the placebo group; p equals
0.019 ). "The findings of the RIO-Europe trial are totally consistent with
those of the RIO-Lipids trial announced earlier this year at the American
College of Cardiology meeting. Patients on rimonabant 20mg/day experienced
significant benefits in terms of weight loss, reduction in waist circumference
and also experienced sizeable improvements in their lipid and glycemic
profiles. What is even more interesting is the effect rimonabant 20mg has on
metabolic cardiovascular risk factors, which is independent of weight loss,"
said Luc Van Gaal, M.D., Professor of Diabetology, Metabolism and Clinical
Nutrition, University Hospital Antwerp, Belgium, Principal Investigator of the
RIO-Europe trial. "We are looking forward to the full 2 year findings of the
RIO-Europe trial to see if these impressive results are maintained," he added.
The RIO-Europe findings also confirmed the good safety profile of rimonabant.
Side effects were mainly mild and transient and most frequently involved
nausea (4.3 %, 5.1% and 12.9 % for placebo, rimonabant 5mg and rimonabant 20mg
respectively), diarrhoea (3.0%, 6.0 % and 7.2% for placebo, rimonabant 5mg and
rimonabant 20mg respectively) and dizziness (4.9 %, 7.0 %, 8.7 % for placebo,
rimonabant 5mg and rimonabant 20mg respectively). Only in a very small number
of cases did these side effects lead to discontinuation of drug use.
Overall dropout rates in the three groups were similar (41.6% in the
placebo group vs. 37.3% for rimonabant 5mg and 39.4%, for rimonabant 20mg).
No difference was observed in the three groups with regards to scores measured
by the Hospital anxiety depression scale. Importantly, rimonabant was also
shown to have a good cardiovascular safety profile. The RIO-Europe trial is
one of four Phase III studies comprising the RIO programme, which assesses the
efficacy and safety of rimonabant in weight reduction and metabolic risk
factor improvement in over 6,600 overweight and obese patients world-wide.
Rimonabant is also under investigation as an aid to smoking cessation in the
STRATUS programme. The results of the STRATUS US trial presented earlier this
year demonstrated that rimonabant 20mg doubled the odds of quitting smoking
vs. placebo (p equals 0.002) without weight gain (on average patients lost
0.3kg (0.7 lb) on rimonabant 20mg vs. a 1.1kg (2.4 lb) weight gain for
patients on placebo (p less than 0.001). Preclinical studies have demonstrated
the role of the endocannabinoid system (ECS), via the CB1 receptor, in the
central and peripheral regulation of energy balance, as well as in the control
of nicotine dependence. Rimonabant is the first selective cannabinoid type 1
(CB1) blocker to be developed for the management of cardiovascular risk
factors including obesity, metabolic syndrome, dyslipidemia, type 2 diabetes
and tobacco dependence. Metabolic parameter improvements observed with
rimonabant are beyond those expected through weight reduction. The new
clinical results from the RIO-Europe study confirm that by reducing body
weight and improving metabolic parameters in overweight/obese subjects,
rimonabant may become an important tool in the cardiovascular risk factor
reduction armamentarium.

 

re: 2 PEA(s) ... KaraS linkadge

Posted by KaraS on August 31, 2004, at 22:42:14

In reply to re: 2 PEA(s) ... KaraS, posted by linkadge on August 31, 2004, at 17:15:54

> What I do is eat a bar of dark chocolate and go for a run. Running has been shown to increase the levels of PEA, and I assume that eating chocolate which contains the same would boost it even further. When I do this, about 25 min into running things becomes SO BRIGHT. It almost feels like I am on cocaine or something (have never done cocaine howver). But doing this leaves me paranoid for a day, too much PEA activity can cause paranoia and paranoid like anxiety.
>
> Linkadge

You're very strange, Linkadge! (Is the "brightness" that good that it's worth the paranoia? - if so, maybe I'll try it!)

-K

 

re: 2 PEA(s) ... KaraS

Posted by linkadge on September 1, 2004, at 7:59:14

In reply to re: 2 PEA(s) ... KaraS linkadge, posted by KaraS on August 31, 2004, at 22:42:14

The paranoia is only mild and takes the form of immediately wanting to make sure all my skeletons are cleaned out of the closet.

Anyhow I would say it is worth it. For about $2 for some dark chocolate, its a nice cheap fix.

Linkadge

 

re: 2 PEA(s) ... KaraS linkadge

Posted by Larry Hoover on September 1, 2004, at 8:05:24

In reply to re: 2 PEA(s) ... KaraS, posted by linkadge on August 31, 2004, at 17:15:54

> What I do is eat a bar of dark chocolate and go for a run. Running has been shown to increase the levels of PEA, and I assume that eating chocolate which contains the same would boost it even further. When I do this, about 25 min into running things becomes SO BRIGHT. It almost feels like I am on cocaine or something (have never done cocaine howver). But doing this leaves me paranoid for a day, too much PEA activity can cause paranoia and paranoid like anxiety.
>
> Linkadge

Uhhh, what's it like if you only exercise or only eat the chocolate? Seems like you might avoid the paranoia?

Lar

 

re: 2 PEA(s) ... KaraS

Posted by linkadge on September 1, 2004, at 9:25:57

In reply to re: 2 PEA(s) ... KaraS linkadge, posted by Larry Hoover on September 1, 2004, at 8:05:24

Well, I have tried the two separately and it does not give the synergy of the combination.

The paranoia (perhaps more 'nervous activation') is certainly not enough to stop me from enjoying this simple pleasure.

I can certainly tell the difference. Cheap diluted milk chocolate just doesn't do it. It's got to be the dark chocolate in the gold foil wrap :)


Linkadge

 

re: 2 PEA(s) ... KaraS linkadge

Posted by KaraS on September 1, 2004, at 13:21:28

In reply to re: 2 PEA(s) ... KaraS, posted by linkadge on September 1, 2004, at 7:59:14

> The paranoia is only mild and takes the form of immediately wanting to make sure all my skeletons are cleaned out of the closet.
>
> Anyhow I would say it is worth it. For about $2 for some dark chocolate, its a nice cheap fix.
>
>
>
> Linkadge


You crack me up!

-K


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