Adapting to Quitting

[thcbongman]

Prove it.

I think that's a BS statement.

If it didn't, we wouldn't be "burned out." Short-term memory would not be affected, your thought process would be unaffected, your reaction time unaffected. Similar to how alcohol affects the nervous system, cannabis has the potential to damage functions on your nervous ending. The damage isn't serious or that detrimental to your health, nor does it mean it negates the benefits. To deny it for the sole sake of pro-cannabis propaganda does a disservice for everyone.

[thcbongman]

Nor was it that hard to find a study to back-up that assertion:

Cannabis and motor function: fMRI changes following 28 days of discontinuation.Pillay SS, Rogowska J, Kanayama G, Gruber S, Simpson N, Pope HG, Yurgelun-Todd DA.
Brain Imaging Center, McLean Hospital, Belmont, MA 02478, USA. [email protected]

The authors hypothesized that supplementary motor cortex (SMA) and anterior cingulate cortex (ACC) activation in chronic cannabis users, studied 4 to 36 hours after their last episode of use, would disappear by Day 28 of abstinence during finger-tapping tests. Eleven cannabis users and 16 comparison subjects were scanned during right (RFT) and left (LFT) finger-tapping tasks on a GE 1.5 Tesla scanner retrofitted with a whole body echo planar coil. Image analyses were conducted in SPM99 using an ROI approach to define each Brodmann area (BA). Differences in cerebral activation were examined in the left and right primary motor cortex (BA4), SMA (BA6), and ACC (BA24 and BA32 separately). The authors found diminished activation for contralateral BA6 from Day 0 to Day 28. For LFT, the authors also found: ipsilaterally diminished BA6 activation on Day 7, but not Day 0 or Day 28; ipsilaterally diminished BA32 activation on Day 0, but not Day 7 or Day 28; contralaterally diminished BA 4 activation on Day 28, but not Day 0 or Day 7; and contralaterally diminished BA32 activation on Day 0 and Day 28, but not Day 7. For RFT, the authors found ipsilaterally diminished BA32 activation on Days 0 and 7 but not on Day 28; contralaterally diminished BA32 activation on Days 0, 7, and 28; and ipsilaterally diminished BA6 activation on Days 0, 7, and 28. These results suggest that residual diminished brain activation is still observed after discontinuing cannabis use in motor cortical circuits. 2008 APA

Cannabis and motor function: fMRI changes followin...[Exp Clin Psychopharmacol. 2008] - PubMed Result

[rdizzle12]

you just
need to rise above it, the withdrwels do get better. are u quitting forever, or just taking a break?

I don't plan on quitting forever, but for at least 6-7 months. I am going to be graduating college and getting a job so I want to be able to pass a drug screen and also get comfortable at my job, then I might start up again, maybe not, we'll see...

[BobBong]

To suggest that cannabis is detrimental to the brain even after not smoking for 7 days is what i disagree with. The very fact that smoking creates carbon monoxide and you are ingesting it would be more harmful to you than anything. So if you're comparing this "study" to smoking than perhaps. But smoking anything, ingesting CO is going to be detrimental to your brain, not just your lungs.

"These results suggest that residual diminished brain activation is still observed after discontinuing cannabis use in motor cortical circuits."
This may be true but it does not imply that cells are destroyed or even harmed due to Cannabis, this says nothing about Carbon monoxide though.

"The facts are there, marijuana damages nerve endings, receptors, clogs brain activity, and all this even in a sober future."

Is what i disagree with. To suggest that consistent cannabis use will harm me long after i've quit is what i see as being a load of crap.

[thcbongman]

I looked into this further, looked at a couple of studies. Take it what you will. I provide one study that concludes there is no long-term neurological damage from the moderate use of cannabis. On the other hand, I cite another study that the disruption of the endocannabinoid system as a consequence ofcannabis abuse may alter neurochemical systems contributing to the development of emotional disorders.

I'm citing the conclusions and if you want to look at how the study is done I provided a link.

"Adolescence is a time of particular vulnerability for brain
maturation. During this period many individuals experiment
with illicit substance use and sometimes quite frequently.
Some adolescents who abuse cannabis
subsequently develop chronic serious psychiatric symptoms,
such as schizophrenia (e.g. [22]) and also cognitive
deficits [23-25]. However, it has never been shown consistently
that cannabis has direct effects on brain development
and there are no known reports using more
advanced imaging technology such as DTI to examine
white matter integrity. Thus the current study was an initial
evaluation to determine whether any indication of
cortical atrophy or white matter abnormalities could be
detected applying these current MRI methods.
Although differences were observed between subjects who
used cannabis during adolescence and those who did not, no finding indicated pathological change. Regions of
higher ADC, putative evidence of atrophy, were not
present, although regions of significantly lower ADC
were. While low FA would be indicative of less white matter
integrity, particularly with respect to fiber direction, all
FA differences in this study were higher values in cannabis
users than non-users.
However, one limitation of the current study is its crosssectional
evaluation of subjects reporting on their own
former adolescent cannabis use, rather than a longitudinal
design following adolescents into adulthood to
observe how the brain changes over time or alternatively
a cross-sectional study of current cannabis-using adolescents.
Pathological effects from prior frequent use may be
less detectable in adulthood after time has passed and
other changes have taken place to compensate for possible
earlier effects of cannabis.
In addition, although we suggest here that the ADC indicates
the amount of CSF in extracellular tissue and ventricular
space, we have not yet validated this assumption
by direct comparisons and thus this view, while logical,
remains speculative at present.
Thus, these data lead to the likely conclusion that cannabis
use, in at least moderate amounts, during adolescence
does not appear to be neurotoxic, although we cannot
exclude any adverse effects of heavier amounts than that
used by the current subjects. These data are preliminary
and need replication with larger numbers of subjects,
although they do have implications for refuting the hypothesis that cannabis alone can cause a psychiatric disturbance
such as schizophrenia by directly producing
brain pathology."

http://www.pubmedcentral.nih.gov/pic...3&blobtype=pdf

"During the last few years, the increasing interest in the
link between the endocannabinoid system and emotional responses
has led to a number of interesting data derived from
animal studies. These results may contribute to understand
the complex scenario of cannabinoid effects in humans, and
to clarify the mechanisms underlying associations between
cannabis abuse and mental disorders. Results obtained from
transgenic mice lacking CB1 receptors and by using CB1 receptors
selective antagonists and inhibitors of endocannabinoids
inactivation suggest the existence of an intrinsic endocannabinoid
tone which contributes to the regulation of
stress responses and anxiety. An adequate endocannabinoid
function appears to be necessary for adaptive extinction
of aversive memories. The endocannabinoid system might
play a pivotal role in maintaining homeostasis, notably with
regard to physiological and behavioral responses to acute
and prolonged stress. Certain forms of endocannabinoiddependent
synaptic plasticity have been proposed as crucial
mechanisms subserving these phenomena. Throughout this
review, we have focused on the endocannabinoid system as
a major player in the modulation of synaptic transmission
and plasticity considering solely interneural communication.
However, the critical functional role of glial cells in maintaining
a correct brain function and their implications in
diverse neuropathological conditions are now clearly recognized.
The new concept of the tripartite synapse in which the
glial cell (notably astrocytes) plays an active role in the modulation
of neurotransmission has recently emerged [125].
Expression of cannabinoid CB1 receptors and endocannabinoid
synthesis and release have been observed in different
types of glial cells [126, 127]. This â??glial endocannabinoid
systemâ?� may have important physiological and pathological
implications [128, 129] and it would be interesting to explore
a possible role in the expression of synaptic plasticity in limbic
and extra-limbic regions related to stress, fear, and anxiety
responses.
Disregulation ormalfunctioning of the endocannabinoid
system might contribute to the aetiology of anxiety-related
disorders and to certain symptoms of melancholic depression.
In turn, the endocannabinoid system might constitute
an interesting pharmacological target for the development of
anti-anxiety and antidepressant therapies. The involvement of the endocannabinoid system in the
regulation of anxiety and its participation in the modulation
of behavioral and physiological responses to aversive situations
have other obvious implications. Cannabis abuse may
be one of the causes disrupting the necessary balance for an
appropriate function of the system. There are functional interactions
between the endocannabinoid system and other
monoaminergic and peptidergic systems also involved in the
regulation of emotional responses [113, 130]. Thus, the disruption
of the endocannabinoid system as a consequence of
cannabis abuse may alter these other neurochemical systems
contributing to the development of emotional disorders. In
addition to acute aversive emotional reactions to cannabis,
the chronic use of this addictive drug may result in mental
disturbances and neuropsychiatric disorders. In particular,
there are data suggesting that exposure to cannabis derivatives
is associated with a higher risk of schizophrenia, depression,
and anxiety [68â??72, 131, 132]. In this review, we have
highlighted the importance of endocannabinoid-based neuroplasticity
phenomena in the regulation of neuroendocrine
and neurochemical systems implicated in the modulation of
emotional responses and extinction of perseverative behaviors
and inadaptative aversive memories. Consequently, it is
likely that impairment of endocannabinoid-mediated synaptic
transmission and plasticity contribute to the expression of
at least some aspects of these psychiatric illnesses.

http://www.pubmedcentral.nih.gov/pic...7&blobtype=pdf

[TheSmokingMonkey]

Prove it.

I think that's a BS statement.

It's also very broad. Generalizations are hard to prove.

[rdizzle12]

Okay...so it's been almost 5 weeks. I am not sure how long it's going to take for me to pass a drug test administered by a workplace. I used to smoke very potent weed on a regular basis (All day, everyday for almost 3 years). I've heard anywhere from 1-3 months. I want to buy a home drug test like from Walgreens, but I want to know if it will be as effective as the one I'll have to take for a job. Does anyone know anything about this?

[iHeartSTI]

I smoked everyday for a semester at college, then i went to Utah for a skiing contest for a month (didnt smoke once) and i felt fine. Yes, I was excersising everyday, but i never felt any anxiety and/or depression. Now Im back at school and smoking and loving every moment of it.

[TheSmokingMonkey]

Okay...so it's been almost 5 weeks. I am not sure how long it's going to take for me to pass a drug test administered by a workplace. I used to smoke very potent weed on a regular basis (All day, everyday for almost 3 years). I've heard anywhere from 1-3 months. I want to buy a home drug test like from Walgreens, but I want to know if it will be as effective as the one I'll have to take for a job. Does anyone know anything about this?

See the Drug Testing forum.

[Bond]

good conversations here. I am still firm with my statement...

o and. thcbong clearly owned it up:jointsmile: