11 replies to this topic

[YimYam]

I have been smoking a 20 bag a night for the past month and a half and have experienced memory impairment in the past 2 weeks. There have been other threads created for this issue but from looking through them, there doesn't seem to be a clear idea of what the best supplements, foods, drugs etc are to help restore memory function. 

 

If you could please state your top 1,2 or 3 things to remedy this issue, i would greatly appreciate it.

 

 

 

[Turnbuckle]

I don't know if this will remedy memory loss that's already occurred, but it may prevent more in the future (at least in mice)--

 

In a stunningly simple turn, investigators found that a simple over-the-counter painkiller, such as ibuprofen, blocks memory loss from the drug’s active ingredient, delta-9-tetrahydrocannabinol (THC). The drug combination may also prevent neurological damage from Alzheimer’s disease, opening possibilities too for the treatment of a variety of other diseases and conditions.

 

"Our studies have solved the longtime mystery of how marijuana causes neuronal and memory impairments," lead investigator Chu Chen said Thursday in a statement. "The results suggest that the use of medical marijuana could be broadened if patients concurrently take a nonsteroidal anti-inflammatory drug such as ibuprofen."

 

http://www.medicalda...gression-263443

 

 

The full paper is here. 

[YimYam]

Interesting, will experiment with it. Thanks

[Irishdude]

Stop smoking cannabis. To achieve this delete your dealers numbers and stop seeing people who smoke until you can regain your self control over the substance.

Keep yourself busy when you usually smoke so you dont trigger yourself, I suggest exercise that you like like football, etc. Thats also good long term for BDNF if you keep it up.

Good luck.

Edited by Irishdude, 20 November 2015 - 06:56 PM.

[gamesguru]

Things that boost GABA, function like theanine or magnolia.  Things that boost acetylcholine function, like bacopa or eggs.  Perhaps some dopamine and glutamate antagonists.  Things that keep cortisol in check.

Exercise, good diet, abstinence.  If you're only smoking at night, as opposed to all throughout the day, it should be easier to give up and find ways to occupy yourself in the remaining time.

Maybe less caffeine, more ginger (COX-2 inhibitor)?

 

Combined effects of THC and caffeine on working memory in rats.
Panlilio LV1, Ferré S, Yasar S, Thorndike EB, Schindler CW, Goldberg SR.  2012.
BACKGROUND AND PURPOSE:
Cannabis and caffeine are two of the most widely used psychoactive substances. Δ(9) -Tetrahydrocannabinol (THC), the main psychoactive constituent of cannabis, induces deficits in short-term memory. Caffeine, a non-selective adenosine receptor antagonist, attenuates some memory deficits, but there have been few studies addressing the effects of caffeine and THC in combination. Here, we evaluate the effects of these drugs using a rodent model of working memory.
EXPERIMENTAL APPROACH:
Rats were given THC (0, 1 and 3 mg·kg(-1) , i.p.) along with caffeine (0, 1, 3 and 10 mg·kg(-1) , i.p.), the selective adenosine A(1) -receptor antagonist CPT (0, 3 and 10 mg·kg(-1) ) or the selective adenosine A(2A) -receptor antagonist SCH58261 (0 and 5 mg·kg(-1) ) and were tested with a delayed non-matching-to-position procedure in which behaviour during the delay was automatically recorded as a model of memory rehearsal.
KEY RESULTS:
THC alone produced memory deficits at 3 mg·kg(-1) . The initial exposure to caffeine (10 mg·kg(-1) ) disrupted the established pattern of rehearsal-like behaviour, but tolerance developed rapidly to this effect. CPT and SCH58261 alone had no significant effects on rehearsal or memory. When a subthreshold dose of THC (1 mg·kg(-1) ) was combined with caffeine (10 mg·kg(-1) ) or CPT (10 mg·kg(-1) ), memory performance was significantly impaired, even though performance of the rehearsal-like pattern was not significantly altered.
CONCLUSION AND IMPLICATIONS:
Caffeine did not counteract memory deficits induced by THC but actually exacerbated them. These results are consistent with recent findings that adenosine A(1) receptors modulate cannabinoid signalling in the hippocampus.

Δ9-THC-caused synaptic and memory impairments are mediated through COX-2 signaling.
Chen R1, Zhang J, Fan N, Teng ZQ, Wu Y, Yang H, Tang YP, Sun H, Song Y, Chen C.  2013.
Marijuana has been used for thousands of years as a treatment for medical conditions. However, untoward side effects limit its medical value. Here, we show that synaptic and cognitive impairments following repeated exposure to Δ(9)-tetrahydrocannabinol (Δ(9)-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid to prostanoids in the brain. COX-2 induction by Δ(9)-THC is mediated via CB1 receptor-coupled G protein βγ subunits. Pharmacological or genetic inhibition of COX-2 blocks downregulation and internalization of glutamate receptor subunits and alterations of the dendritic spine density of hippocampal neurons induced by repeated Δ(9)-THC exposures. Ablation of COX-2 also eliminates Δ(9)-THC-impaired hippocampal long-term synaptic plasticity, working, and fear memories. Importantly, the beneficial effects of decreasing β-amyloid plaques and neurodegeneration by Δ(9)-THC in Alzheimer's disease animals are retained in the presence of COX-2 inhibition. These results suggest that the applicability of medical marijuana would be broadened by concurrent inhibition of COX-2.

wiki:

Nonsteroidal anti-inflammatory drugs such as ibuprofen work by inhibiting the COX enzymes, which convert arachidonic acid to prostaglandin H2 (PGH2). PGH2, in turn, is converted by other enzymes to several other prostaglandins (which are mediators of pain, inflammation, and fever) and to thromboxane A2 (which stimulates platelet aggregation, leading to the formation of blood clots).
The exact mechanism of action of ibuprofen is unknown. Ibuprofen is a nonselective inhibitor of cyclooxygenase, an enzyme involved in prostaglandin synthesis via the arachidonic acid pathway. Its pharmacological effects are believed to be due to inhibition of cyclooxygenase-2 (COX-2) which decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Inhibition of COX-1 is thought to cause some of the side effects of ibuprofen including gastrointestinal ulceration. Ibuprofen is administered as a racemic mixture. The R-enantiomer undergoes extensive interconversion to the S-enantiomer in vivo. The S-enantiomer is believed to be the more pharmacologically active enantiomer.[39]
Like aspirin and indometacin, ibuprofen is a nonselective COX inhibitor, in that it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2.

================

================
---> https://en.wikipedia...inoid_receptors

Cannabinoids activate mesoprefrontocortical dopaminergic neurons, an activation that releases dopamine primarily in the prefrontal cortex.^[17] In fact, stimulation of the prefrontal cortex dopamine receptor D1 is associated with working memory impairments.^[3]

D2 dopamine receptors enable Δ9-tetrahydrocannabinol induced memory impairment and reduction of hippocampal extracellular acetylcholine concentration

Chronic ?9-Tetrahydrocannabinol Exposure Induces a Sensitization of Dopamine D2/3 Receptors in the Mesoaccumbens and Nigrostriatal Systems
The development of supersensitive midbrain DA autoreceptors :( following chronic THC is thus expected to result in increased self-inhibition and hypoactivity of DA neurons. This hypothesis concurs with the substantial decrement in spontaneous electrical activity of NAcc-projecting DA neurons observed in VTA following repeated THC (Diana et al, 1998) and with the abrupt reductions in mesolimbic DA neuronal activity and accumbal DA levels following SR 141716A-precipitated THC withdrawal

Chronic activation of the D2 dopamine autoreceptor inhibits synaptogenesis in mesencephalic dopaminergic neurons in vitro.
Our results suggest that chronic activation of the D2 autoreceptor inhibits synaptogenesis :( by mesencephalic dopamine neurons through translational regulation of the synthesis of proteins required for synapse formation

[Turnbuckle]

Ginger root extract is another supplement that may do some good. It's a cox-2 inhibitor that I have used for years to keep a swollen bursa under control. For that purpose I've found it far better than ibuprofen. So if ibuprofen reduces THC memory loss, adding ginger root should be even more effective. (It is also a blood thinner, so if on one already, be careful).

[gamesguru]

The Link Between Depression and Physical Symptoms
Madhukar H. Trivedi, M.D.  2004.
Physical symptoms are common in depression, and, in fact, vague aches and pain are often the presenting symptoms of depression. These symptoms include chronic joint pain, limb pain, back pain, gastrointestinal problems, tiredness, sleep disturbances, psychomotor activity changes, and appetite changes. A high percentage of patients with depression who seek treatment in a primary care setting report only physical symptoms, which can make depression very difficult to diagnose. Physical pain and depression have a deeper biological connection than simple cause and effect; the neurotransmitters that influence both pain and mood are serotonin and norepinephrine. Dysregulation of these transmitters is linked to both depression and pain. Antidepressants that inhibit the reuptake of both serotonin and norepinephrine may be used as first-line treatments in depressed patients who present with physical symptoms. Many physicians consider patients to be in remission when their acute emotional symptoms have abated, but residual symptoms—including physical symptoms—are very common and increase the likelihood of relapse. All symptoms must be measured in order to achieve full remission. There are a number of short yet accurate measurement tools (rating scales) available that effectively measure the remission of physical symptoms as well as emotional symptoms.
Effects of a ginger extract on knee pain in patients with osteoarthritis.

so ginger's analgesia could be due to a combination of COX-2 inhibition and (especially in depressed patients) 5-HT1A agonism

...originally found that tidbit on 5-HT1A thanks to this blog: http://www.anti-agin...ocus-on-ginger/

Identification of serotonin 5-HT1A receptor partial agonists in ginger
Antidepressant-like synergism of extracts from magnolia bark and ginger rhizome alone and in combination in mice.
Combined administration of the mixture of honokiol and magnolol and ginger oil evokes antidepressant-like synergism in rats.

[YimYam]

Thank you for this insightful info.

 

The Link Between Depression and Physical Symptoms
Madhukar H. Trivedi, M.D.  2004.
Physical symptoms are common in depression, and, in fact, vague aches and pain are often the presenting symptoms of depression. These symptoms include chronic joint pain, limb pain, back pain, gastrointestinal problems, tiredness, sleep disturbances, psychomotor activity changes, and appetite changes. A high percentage of patients with depression who seek treatment in a primary care setting report only physical symptoms, which can make depression very difficult to diagnose. Physical pain and depression have a deeper biological connection than simple cause and effect; the neurotransmitters that influence both pain and mood are serotonin and norepinephrine. Dysregulation of these transmitters is linked to both depression and pain. Antidepressants that inhibit the reuptake of both serotonin and norepinephrine may be used as first-line treatments in depressed patients who present with physical symptoms. Many physicians consider patients to be in remission when their acute emotional symptoms have abated, but residual symptoms—including physical symptoms—are very common and increase the likelihood of relapse. All symptoms must be measured in order to achieve full remission. There are a number of short yet accurate measurement tools (rating scales) available that effectively measure the remission of physical symptoms as well as emotional symptoms.
Effects of a ginger extract on knee pain in patients with osteoarthritis.

so ginger's analgesia could be due to a combination of COX-2 inhibition and (especially in depressed patients) 5-HT1A agonism

...originally found that tidbit on 5-HT1A thanks to this blog: http://www.anti-agin...ocus-on-ginger/

Identification of serotonin 5-HT1A receptor partial agonists in ginger
Antidepressant-like synergism of extracts from magnolia bark and ginger rhizome alone and in combination in mice.
Combined administration of the mixture of honokiol and magnolol and ginger oil evokes antidepressant-like synergism in rats.

 

 

[Hotforpips]

Interesting article

http://www.dailymail...al-illness.html

Perhaps piracetam could be of help, subjectivity it helped me and I continue to take it, 2g x3 times daily. Got my Google finger twitching for more info :-)

Edited by Hotforpips, 27 November 2015 - 11:14 AM.

[Turnbuckle]

Interesting article

http://www.dailymail...al-illness.html

 

 

I don't see a link to the study, but a previous British article claimed that pot caused more hospitalizations due to psychosis. The referenced study itself revealed that moderate cannabis use actually decreased hospitalizations (not reported in the story) while only very heavy smoking of this so-called skunk cannabis was a problem. So there is still a great deal of deceit coming from the Western propaganda press, and the referenced studies have to be read.

 

The study in the previous article is this one. It's from the same researchers and is funded by the British government. If you go to figure 2, you will see that smoking hash once a week or less cuts your chance of psychiatric hospitalization in half, and even smoking it every day cuts it by a small amount. Skunk is a different matter, however, and seems to raise the chance of psychosis at all levels. This may be due to the hybridization of skunk cannabis to have a higher THC/CBD ratio, not the THC level itself.

[Hotforpips]

Interesting article

http://www.dailymail...al-illness.html

I don't see a link to the study, but a previous British article claimed that pot caused more hospitalizations due to psychosis. The referenced study itself revealed that moderate cannabis use actually decreased hospitalizations (not reported in the story) while only very heavy smoking of this so-called skunk cannabis was a problem. So there is still a great deal of deceit coming from the Western propaganda press, and the referenced studies have to be read.

The study in the previous article is this one. It's from the same researchers and is funded by the British government. If you go to figure 2, you will see that smoking hash once a week or less cuts your chance of psychiatric hospitalization in half, and even smoking it every day cuts it by a small amount. Skunk is a different matter, however, and seems to raise the chance of psychosis at all levels. This may be due to the hybridization of skunk cannabis to have a higher THC/CBD ratio, not the THC level itself.

Not sure if this is the study after a quick Google ssearch. Looks like the lancet article you linked too. Daily mail is not the best source of info.

Can't get the link to work, search kings college London Dr Tiago Reis Marques. Not having a good day today sorry for posting rubbish links.

Edited by Hotforpips, 27 November 2015 - 11:50 AM.

[Turnbuckle]

When I said I didn't see a link to the study, I meant in the Daily Mail story you referenced. When the media leaves off the link, that's generally a sign that their story is propaganda.