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Cannabis for Attention Deficit Disorder, ADD and ADHD

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)


Marijuana and ADD Therapeutic uses of Medical Marijuana in the treatment of ADD

Cannabis as a medical treatment for attention deficit disorder

Cannabinoids effective in animal model of hyperactivity disorder

Fitness to drive in spite (because) of THC

Recipe For Trouble (anecdotal)


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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