Omega 3, Pot, PTSD, Depression & Anxiety

OK a lot of you "want to pick my brain", so I am going to start showing you blades what I have found- with translations since most of you don't speak "Sci-speak" (yet).

Blades, and you have no idea what a POWER we can be! But the first step is to EDUCATE YOURSELF!

"Granny's School" is now in session! lol (You can skip anything in bold! )

First lesson is on PTSD, social anxiety, depression, pot and Omega 3. The study is hot off of PubMed- August 2011!

The Dopamine and Cannabinoid Interaction in the Modulation of Emotions and Cognition: Assessing the Role of Cannabinoid CB1 Receptor in Neurons Expressing Dopamine D1 Receptors. (abst -2011)
[FONT=&quot]The Dopamine and Cannabinoid Interactio... [Front Behav Neurosci. 2011] - PubMed - NCBI[/FONT]

Although cannabinoid CB1 receptors (CB1Rs) are densely expressed in neurons expressing dopamine D1 receptors (D1Rs), it is not fully understood to what extent they modulate emotional behaviors.


There are a lot of CB1s on some types of brain cells, but we don’t know how much they control emotional behaviors.


We used conditional CB1R knock-out animals lacking CB1Rs in neurons expressing D1R (D1-CB1(-/-)) in order to answer this question. To elucidate the behavioral effects of CB1R deficiency in this specific neuronal subpopulation, we subjected D1-CB1(-/-) mice to a battery of behavioral tests which included exploration-based tests, depressive-like behavioral tests, social behavior, and fear-related memory paradigms.

We used mice without a certain specific type of CB1 receptors to investigate. We ran them through tests for depressive behavior, social behavior and mouse “PTSD”.


D1-CB1(-/-) did not show any difference in the exploration-based paradigms such as open field, elevated plus maze, or novel object investigation test, except for an increase in novelty-induced grooming. By contrast, they showed a mild anhedonia-like state as described by the slightly decreased preference for sweet solution, as compared to wild-type control group. This decrease, however, could be observed only during the first day of exposure, thus suggesting increased neophobia as an alternative explanation.

In most of the tests, the mice acted normally, although when exposed to a new object, they groomed a bit more than average. Also, on the first day they didn’t drink as much sugar solution as we expected, but we think they were just a bit nervous in their new cages.

Accordingly, mutant mice performed normally in the forced swim test, a procedure widely used for evaluating behavioral despair in rodents. However, weak- to moderate anxiety-like phenotypes were evident when D1-CB1(-/-) mice were tested for social behavior.


When we tried drowning the mice in a tank (to see how long it was until they gave up and actually started to drown), again, they surprised us and “hung in there” like normal mice. This type of mouse did seem to have some social anxiety issues, however. (Thank goodness! We were beginning to think we'd have nothing to report!)


Most strikingly, (-/-) mice exhibited significantly increased contextual and auditory-cued fear, with attenuated within session extinction, suggesting that a specific reduction of endocannabinoid signaling in neurons expressing dopamine D1Rs is able to affect acute fear adaptation.

The big difference between our special D1-CB1(-/-) mice and “wild-type” mice came when we freaked them out with loud noises. Our special mice totally flipped out , and stayed freaked for a long time , while the wild-type settled down after a while ! This suggests that a reduction in CB1 receptors (that form part of the endocannabinoid signaling system) is involved in problems with dealing with bad experiences (PTSD).


These results provided first direct evidence for a cross-talk between dopaminergic D1Rs and endocannabinoid system in terms of controlling negative affect.

We think the CB1s “talk” with dopamine receptors and they cooperate to dull bad memories, and keep you saner.

So the poor mice without D1-CB1 receptors can’t take heavy stressing and they get “mouse PTSD”. Plus they have social anxiety!

Now (once again) I’ll refer you to…

Nutritional omega-3 deficiency abolishes endocannabinoid-mediated neuronal functions. (abst – 2011) http://www.unboundmedicine.com/medline/ebm/record/21278728/abstract/Nutritional_omega_3_deficiency_abolishes_endocannabinoid_mediated_neuronal_functions_

A quick translation- If you don't have Omega 3 in your system, any new CB1 receptors are made defectively! A chunk that is supposed to be connected is left flopping free! And without working CB1 receptors your brain won’t work right when it comes to emotional processing. The “western diet” has almost no Omega 3, and we think this is why they are so dang crazy!


So we add “mice with no D1-CB1s getting PTSD”, to the "American diet not making working CB1s in the brain” (and likely elsewhere). This is going to be more and more important as our soldiers return. Is our Omega 3 deficient diet combined with the trauma of war setting them up for severe PTSD? And I know a lot of people are slowed down by social anxiety or depression.

I think adding large doses of Omega 3 to the diet of people with anxiety issues, depression and PTSD would benefit them greatly. More working CB1s sure wouldn’t hurt!


Unfortunately, brains slow down reproducing neurons as we age. But stimulating working CB receptors with either Anandamide (a THC-like chemical your body makes) or THC causes neurogenesis (the formation of new neurons). - You blades can read this one on your own! Short and easy! lol

Good News For The Medical Marijuana Movement: Pot Proliferates Brain Cells And Boosts Mood (news - 2005) Good News For The Medical Marijuana Movement: Pot Proliferates Brain Cells And Boosts Mood


So I think the “Granny's recommendation” for dealing with anxiety, depression and PTSD might be just eat healthy, take Omega 3 and use cannabis for a few months! A good diet never hurts, adding Omega 3 makes working new CB1s, and pot kicks the neurogenesis into high gear, and just makes you feel plain better!

So now how's that for a first lesson? Understandable (I hope) cutting edge science! You might want to make a copy and start your own little notebook- become the local "Ganja Guru"!

Granny

 

Pastivity, in California you could get legal as soon as you got a driver's license to prove residency! We have some SANE cannabis laws here!


Granny

 

Hemp seed oil is a good source of Omega 3! You can find it at most health food stores. Unlike flax seed oil, it actually tastes pretty good and you can make an excellent salad dressing by adding cider vinegar, Italian seasoning, garlic and pepper flakes! Hemp seed oil has no THC and is perfectly legal!

I find it amazing that the cannabis plant provides the THC and CBD we need to heal ourselves, and the seed oil has Omega 3 to make healthy CB receptor so we can heal with THC! Cannabis seeds are very nutritious! You can just about live on them alone (no vitamin "C", so you need fruit).

Granny

 

Mantikore, I just popped over to PubMed to grab an example of the dosages. Your dose may be a bit high, but so far the only side effects mentioned in the studies I've looked at are "fishy burps" and looser bowel movements! This is about lowering triglycerides, but the 4 gram dose seems to be standard prescription strength.-

Prescription omega-3s: an overview for nurse practitioners.
Prescription omega-3s: an overview... [J Cardiovasc Nurs. 2011 Jul-Aug] - PubMed - NCBI

"When lifestyle and diet changes do not effectively decrease TGs, NPs will recommend pharmacological therapy as a next step. A viable pharmacological option includes prescription omega-3 (P-OM3) fatty acid ethyl esters. Each 4-g/d dose of P-OM3 provides 465 mg of eicosapentaenoic acid and 375 mg of docosahexaenoic acid. Clinical trials show that P-OM3 can safely and effectively decrease TGs by 45% in patients with severe hypertriglyceridemia."