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Marijuana and ADD
Therapeutic uses of Medical Marijuana
in the treatment of Attention Deficit Disorder
TAGS Medical Marijuana
Doctors
ADD Treatments
Marijuana Medicine
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Chronic Pain
Slows HIV
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Medical Cannabis Treatments
It was mentioned in the Portland newspaper that the Oregon Health Division is
considering allowing medical marijuana to be used to treat Attention Deficit
Disorder (ADD) under the Oregon Medical Marijuana Act. At first glance it might
seem counter-intuitive to use a medication that has a public perception of
decreasing attention to treat a condition whose primary symptom is a deficit of
attention. But just as taking stimulants often calms those with hyperactivity,
medical marijuana improves the ability to concentrate in some types of ADD.
Sam’s Story; Autism & Medical Marijuana
Sam’s Story, Using Medical Cannabis to Treat Autism Spectrum Disorder
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By Kort E Patterson
Categorizing The Condition
Attention Deficit Disorder (ADD) is a very broad category of conditions that
share some symptoms but appear to result from different underlying causes. Most
seem to involve, at least in part, imbalances in neural transmitter levels and
functions. Some experts in the field expect that the broad category of ADD will
be refined in the future, with many conditions that are now diagnosed as ADD
being recognized as separate disorders.
The particular type of ADD under consideration for treatment with medical
marijuana might better be termed "Racing Brain Syndrome" (RBS). A
useful analogy for this mental condition is that of a centrifugal pump that is
being over-driven. As the pump speed increases, cavitation sets in and the
pump's output decreases. The faster the pump is driven the greater the
cavitation until a point is reached where large amounts of energy are being
input but nothing is being output. Without medication there is a sensation that
thoughts flash through the brain too fast to "think" them. Medical
marijuana slows the brain down sufficiently to achieve impressive improvements
in functionality.
This syndrome probably only afflicts a small minority of all those diagnosed
with ADD. The condition doesn't respond to the standard ADD medications,
indicating that it results from different underlying processes than other forms
of ADD. Individuals with types of ADD that do respond to the standard ADD
medications also tend to have a far different reaction to medical marijuana than
those with RBS. At this point in our limited understanding of the condition, it
appears that RBS would make a good candidate to be redefined as a separate
condition outside of the general diagnosis of ADD.
Treating ADD/RBS With Medical Marijuana
There is some evidence available that medical marijuana has been found to be
an effective medication for some types of ADD by other researchers in the
field.(1) Unfortunately, ADD encompasses such a variety of conditions that the
limited amount of research in the field leaves many of the effective therapeutic
mechanisms under-investigated. Considering the regulatory difficulties in
researching the effects of medical marijuana, it isn't surprising that the
information regarding medical marijuana and ADD is largely anecdotal(2).
Individuals with RBS tend to have a very low tolerance for most stimulants,
and report even caffeine aggravates their disorder. The one exception appears to
be low doses of Dextrostat. While Dextrostat does have a calming effect, it
fails to address the higher level mental functions needed for complex
intellectual demands. Larger doses of Dextrostat tend to produce undesirable
mental and physical stimulation, greatly limiting the level of medication that
can be tolerated.
Medical marijuana remains the only single medication that provides an
adequate solution for RBS, and remains a necessary component in a multi-drug
approach.
Dextrostat does appear to reduce the amount of medical marijuana needed by
individuals with RBS to achieve a functional mental state. This reduction
probably justifies continuing with Dextrostat as a means of reducing the
quantity of medical marijuana that must consumed, as well as allow those with
RBS to gain the maximum benefit possible within the quantity limitations of the
OMMA.
The green leaves of certain strains of medical marijuana appear to provide
the best therapeutic effects for RBS. Experiments with Marinol seem to indicate
that THC is involved, but is not the primary therapeutic agent. The therapeutic
agent(s) most useful in treating RBS appear to be present in relatively low
concentrations in medical marijuana. As such those with this condition must
consume a larger quantity of medical marijuana in order to ingest a sufficient
dosage of the target agent(s). This would explain why dried low-THC green leaves
appear to be the most effective treatment. The patient can consume enough of
this low-THC marijuana to acquire the levels of the needed active agent(s)
necessary to treat the condition without in the process consuming sufficient THC
to become intoxicated.
Underlying Cause of RBS
It has long been suspected that RBS involved a deficit of one or more neural
transmitters. It was observed as long ago as the 1970's that high levels of
adrenaline had a residual therapeutic effect in those with RBS. The effect was
first noted in those engaged in such activities as skydiving. Individuals with
RBS reported that their mental functions were improved in the days following
skydiving. It was first assumed that adrenaline stimulated the production of all
neural transmitters - including those that were in deficit. It's now thought
that while adrenaline initially acts as a stimulant of neural transmitter
production, it has a secondary effect of depleting neural transmitters. The
limited effectiveness of Dextrostat, as well as additional information about the
secondary effects of adrenaline, suggests the possibility that at least part of
the underlying cause of RBS may also be a surplus of one or more neural
transmitters.
The partial solution offered by Dextrostat also suggests that at least some
part of the condition results from those neural transmitters and/or hormones
that are influenced by both Dextrostat and medical marijuana. The failure of
Dextrostat to provide a complete solution suggests two possible alternatives:
(1) that the effects of Dextrostat and medical marijuana are additive - with
both influencing the same neural transmitters and/or hormones, and together
delivering the required level of therapeutic effect; or (2) that the condition
is the result of multiple imbalances, some of which are unaffected by Dextrostat,
but all of which appear to be affected by medical marijuana.
Potential Beneficial Therapeutic Effects
The research that has been done on the therapeutic effects of medical
marijuana on other conditions provides a number of potential mechanisms that may
be involved in RBS. The following are documented effects of medical marijuana
that appear to have some potential for involvement.
Perhaps the most obvious possibility is suggested by the fact that both
Dextrostat and medical marijuana influence the release and/or functions of
serotonin(3)(4). Since both Dextrostat and medical marijuana appear to increase
the apparent availability and effectiveness of serotonin, it would appear
possible that a deficit of serotonin is involved in some way.
There are over 60 cannabinoids and cannabidiols present in medical marijuana.
The effect of most of these substances is at present largely unknown.(5)
The discovery of a previously unknown system of cannabinoid neural
transmitters is profound.(6) The different cannabinoid receptor types found in
the body appear to play different roles in normal human physiology.(5) An
endogenous cannabinoid, arachidonylethanolamide, named anandamide, has been
found in the human brain. This ligand inhibits cyclic AMP in its target cells,
which are widespread throughout the brain, but demonstrate a predilection for
areas involved with nociception. The exact physiological role of anandamide is
unclear, but preliminary tests of its behavioral effects reveal actions similar
to those of THC.(7)
Cannabinoid receptors appear to be very dense in the globus pallidus,
substantia nigra pars reticulata (SNr), the molecular layers of the cerebellum
and hippocampal dentate gyrus, the cerebral cortex, other parts of the
hippocampal formation, and striatum - with the highest density being in the SNr.
The Neocortex has moderate receptor density, with peaks in superficial and deep
layers. Very low and homogeneous density was found in the thalamus and most of
the brainstem, including all of the monoamine containing cell groups, reticular
formation, primary sensory, visceromotor and cranial motor nuclei, and the area
postrema. The hypothalamus, basal amygdala, central gray, nucleus of the
solitary tract, and laminae I-III and X of the spinal cord showed slightly
higher but still sparse receptor density.(5)
While there are cannabinoid receptors in the ventromedial striatum and basal
ganglia, which are areas associated with dopamine production, no cannabinoid
receptors have been found in dopamine-producing neurons. According to the
congressional Office of Technology Assessment, research over the last 10 years
has proved that marijuana has no effect on dopamine-related brain systems.(6)
However, cannabidiol has been shown to exert anticonvulsant and antianxiety
properties, and is suspected by some to exert antidyskinetic effects through
modulation of striatal dopaminergic activity.(3)
It's been suggested that the cannabinoid receptors in the human brain play a
role in the limbic system, which in turn plays a central role in the mechanisms
which govern behavior and emotions. The limbic system coordinates activities
between the visceral base-brain and the rest of the nervous system. Cannabis
acts on memory by way of the receptors in the limbic system's hippocampus, which
"gates" information during memory consolidation.(6)
In addition, some effects of cannabinoids appear to be independent of
cannabinoid receptors. The variety of mechanisms through which cannabinoids can
influence human physiology underlies the variety of potential therapeutic uses
for medical marijuana.(8)
When the effects of cannabis on a "normal" brain are tracked on an
electroencephalogram (EEG), there is an initial speeding up of brain wave
activity and a reactive slowing as the drug effects wear off. The higher the
dosage, the more intense the effects and longer the experience. There is an
increase in mean-square alpha energy levels and a slight slowing of alpha
frequency.(5) There is also an increase of beta waves reflecting increased
cognitive activity. The distortion of time resulting from the "speeding up
of thoughts" causes a subjective perception that there is a slowing of
time.(9)
As the cannabis effects wear off, stimulation gives way to sedation. The
cognitive activity of the beta state gives way to alpha and theta frequencies.
Theta waves are commonly associated with visual imagery. These images interact
with thinking and disrupt the train of thought. Thinking can be distracted by
these intrusions, with thought contents being modified to some extent depending
on dose, expectations, setting, and personality.(9)
Cannabis decreases emotional reactivity and intensity of affect while
increasing introspection as evidenced by the slowing of the EEG after initial
stimulation. Obsessive and pressured thinking is replaced by introspective free
associations. Emotional reactivity is moderated and worries become less
pressing.(10)
Cannabis causes a general increase in cerebral blood flow (CBF). This
increase in blood circulation is due to decreased peripheral resistance, which
is in turn due to the dilation of the capillaries in the cerebral cortex.
Changes in CBF affect the mental processes of the brain, with increases
stimulating cognition, while decreases accompany sedation.(9)
Relative Safety of Medical Marijuana
"Marijuana is the safest therapeutically active substance known to
man... safer than many foods we commonly consume." DEA Judge Francis L.
Young, Sept. 6, 1988
"After carefully monitoring the literature for more than two decades, we
have concluded that the only well-confirmed deleterious physical effect of
marihuana is harm to the pulmonary system." Grinspoon M.D., James B.
Bakalar,
Medical Marijuana has been in use for thousands of years, and in spite of
substantial efforts to find adverse effects, it remains the safest medication
available for RBS. There has never been a single known case of lethal overdose.
"The ratio of lethal to effective dose for medical marijuana is estimated to be
as 40,000 to 1. By comparison,
the ratio is 3-50 to 1 for secobarbital and 4-10
to 1 for alcohol.(11)
During the 1890s the Indian Hemp Drugs Commission interviewed some eight
hundred people and produced a report of more than 3000 pages. The report
concluded that "there was no evidence that moderate use of cannabis drugs
produced any disease or mental or moral damage, or that it tended to lead to
excess any more than the moderate use of whiskey."(12)
The Mayor's Committee on Marihuana examined chronic users in New York City
who had averaged seven marihuana cigarettes a day for eight years and
"showed no mental or physical decline."(13) Several later controlled
studies of chronic heavy use failed to establish any pharmacologically induced
harm.(14) A subsequent government sponsored review of cannabis conducted by the
Institute of Medicine, a branch of the National Academy of Sciences, also found
little evidence of its alleged harmfulness.(15) Several studies in the United
States found that fairly heavy marihuana use had no effects on learning,
perception, or motivation over periods as long as a year.(16)
Studies of very heavy smokers in Jamaica, Costa Rica, and Greece "found
no evidence of intellectual or neurological damage, no changes in personality,
and no loss of the will to work or participate in society."(17) The Costa
Rican study showed no difference between heavy users (seven or more marihuana
cigarettes a day) and lighter users (six or fewer cigarettes a day).(18) In
addition, none of the studies involving prolonged and heavy use of medical
marijuana have shown any effects on mental abilities suggestive of impairment of
brain or cerebral function and cognition.(2)
The inhalation of the combustion products of burning plant material is the
cause of the only well-confirmed deleterious physical effects of medical
marijuana. These adverse effects can be eliminated by using one of the
non-combustion means of ingesting the mediation. Marijuana can be eaten in foods
or inhaled using a vaporizer. The therapeutic agents in medical marijuana
vaporize at around 190 degrees centigrade, while it takes the heat of combustion
of around 560 degrees centigrade to generate the harmful components of marijuana
smoke. A vaporizer heats the medical marijuana to the point where the
therapeutic agents are released and can be inhaled, without getting the plant
material hot enough to burn.(19)
References:
1. Possible Therapeutic Cannabis Applications for Psychiatric Disorders,
Tod H. Mikuriya, M.D.
2. Marihuana, The Forbidden Medicine, Lester Grinspoon M.D., James B.
Bakalar, Yale University Press, 1997
3. MARIJUANA AND TOURETTE'S SYNDROME, Journal of Clinical
Psychopharmacology, Vol. 8/No. 6, Dec 1988
4. CANNABINOIDS BLOCK RELEASE OF SEROTONIN FROM PLATELETS INDUCED BY PLASMA
FROM MIGRAINE PATIENTS, Int J Clin Pharm. Res V (4) 243-246 (1985), Volfe Z.,
Dvilansky A., Nathan I. Blood Research, Faculty of Health Sciences, Soroka
Medical Center, Ben-Gurion University of the Negev, P.O. Box 151, Beer-Sheva
84101, Israel.
5. Nelson, P. L. (1993). A critical review of the research literature
concerning some biological and psychological effects of cannabis. In Advisory
Committee on Illicit Drugs (Eds.), Cannabis and the law in Queensland: A
discussion paper (pp. 113-152). Brisbane: Criminal Justice Commission of
Queensland.
6. Marijuana And the Brain, by John Gettman, High Times, March, 1995
7. Cannabis for Migraine Treatment: The Once and Future Prescription?: An
Historical and Scientific Review; Ethan B. Russo, M.D.
8. Marijuana and Medicine, Assessing the Science Base, Janet E. Joy,
Stanley J. Watson, Jr., and John A. Benson, Jr., Editors Division of
Neuroscience and Behavioral Health, INSTITUTE OF MEDICINE
9. Marijuana Medical Handbook, by Tod Mikuriya, M.D.
10. Medicinal Uses of Cannabis, Tod H. Mikuriya, M.D. (c)1998
11. Marihuana as Medicine: A Plea for Reconsideration; Lester Grinspoon
M.D., James B. Bakalar; Journal of the American Medical Association (JAMA);
June 1995
12. Report of the Indian Hemp Drugs Commission, 1893-1894, 7 vols. (Simla:
Government Central Printing Office, 1894); D. Solomon, ed., The Marihuana
Papers (Indianapolis: Bobbs-Merrill, 1966).
13. Mayor's Committee on Marihuana, The Marihuana Problem in the City of
New York (Lancaster, Pa.: Jacques Cattell, 1944).
14. M. H. Beaubrun and F Knight, "Psychiatric Assessment of Thirty
Chronic Users of Cannabis and Thirty Matched Controls," American journal
of Psychiatry 130 (1973): 309; M. C. Braude and S. Szara, eds., The
Pharmacology of Marihuana, 2 vols. (New York: Raven, 1976); R. L. Dombush, A.
M. Freedman, and M. Fink, eds., "Chronic Cannabis Use," Annals of
New Yorh Academy of Sciences 282 (1976); J. S. Hochman and N. Q. Brill,
"Chronic Marijuana Use and Psychosocial Adaptation," American
journal of Psychiatry 130 (1973):132; Rubin and Comitas, Ganja in Jamaica.
15. Institute of Medicine, Marijuana and Health (Washington, D.C.: National
Academy of Sciences, 1982).
16. C. M. Culver and F W King, "Neurophysiological Assessment of
Undergraduate Marihuana and LSD Users," Archives of General Psychiatry 31
(1974): 707-711; P.J. Lessin and S. Thomas, "Assessment of the Chronic
Effects of Marijuana on Motivation and Achievement: A Preliminary
Report," in Pharmacology of Marihuana, ed. Braude and Szara, 2:681-684.
17. Cognition and Long-Term Use of Ganja (Cannabis), Reprint Series, 24
July 1981, Volume 213, pp. 465-466 SCIENCE, Jeffrey Schaeffer, Therese
Andrysiak, and J. Thomas Ungerleider Copyright 1981 by the American
Association for the Advancement of Science
18. Rubin and Comitas, Ganja in Jamaica; W E. Carter, ed., Cannabis in
Costa Rica: A Study of Chronic Marihuana Use (Philadelphia: Institute for the
Study of Human Issues, 1980); C. Stefariis, J. Boulougouris, and A. I-iakos,
"Clinical and Psychophysiological Effects of Cannabis in Long-term
Users," in Pharmacology of Marihuana, ed. Braude and Szara, 2:659-666; P
Satz, J. M. Fletcher, and L. S. Sutker, "Neurophysiologic, Intellectual,
and Personality Correlates of Chronic Marihuana Use in Native Costa
Ricans," Annals of the New York Academy of Sciences 282 (1976): 266-306.
19. Is Marijuana The Right Medicine For You?; Bill Zimmerman Ph.D., Rick
Bayer M.D., and Nancy Crumpacker M.D.; (1998): pp. 125; Keats Publishing Inc.
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