A working explanation of how marijuana reduces tumor growth, and healthily modulates calorie intake through selective activation of dopamine receptors:

  Marijuana and the active compound inside it, THC, are both known to shrink tumor size and inhibit cancer cell growth, which has been publicized by the federal government in recent publications (Scott). The mechanisms of how this actually occurs are somewhat less clear. The answer appears to be, interestingly enough, in the dopamine receptors. While addictive activities and substances are measured by their effect on DA1 receptors, which constitute the majority of dopamine receptors in the brain, there are actually 5 such subsets of receptors: DA1-5. These smaller groupings or clusters of dopamine receptors are well known to have various physical effects on the body by regulation of hormones and other physical mechanisms
  The effect of marijuana on DA1 activation is less than a good meal, sex, alcohol, or a wide range of chemicals as shown in a PBS broadcast and that the effect of marijuana does not impact the widespread DA1 receptors, which are causally and correlatively shown to cause addiction (French), which explains the non-addictive nature of the plant. Understanding the hormonal and physical effects, however, requires further investigation. Activation of DA2 receptors has been shown to reduce prolactin levels, a hormone virtually non-existent in males, but present in females and very high in pregnant females (Poste). This phenomenon is relatively recent, but reduction of prolactin levels as a result of THC administration has been known since the early 1980's at least (Steger, et al.).
   Elevated prolactin levels have been shown to cause a re-activation of tumor growth since the 1960's at least, and it can be assumed that as a DA2 agonist, marijuana suppresses such re-activation or tumor growth (Pearson, et al.). This is confirmed by a cannabinoid breakdown activation levels on various parts of the brain, classified as cannabinoid receptors which include some DA1 receptors, but also D2 receptors (Consroe). These parts of the brain also contain DA3 receptors, as shown more recently (Stanwood), agonism of which can inhibit Parkinson and tremors (such as epilepsy). Use of dopamine agonists has been shown more recently to encourage new blood vessel growth and inhibit growth of tumors (Goth, et al.), however many available agonists do not act selectively on specific dopamine receptors, but also activate the clusters which constitute the D1 areas of the brain (basal ganglia and other interior parts of the brain). Due to marijuana's, or THC's, low activation of D1 receptors (less than a good meal, as mentioned before), this appears to be a non-addictive and safe way to prevent cancer and obesity, which are the two leading killers in the USA after Alzheimer's related diseases.
 




Works Cited:

Consroe, Paul. "Brain cannabinoid systems as targets for the therapy of neurological disorders." Neurobiology of disease 5.6 (1998): 534-551.
French, Edward D. "Δ 9-Tetrahydrocannabinol excites rat VTA dopamine neurons through activation of cannabinoid CB1 but not opioid receptors." Neuroscience letters 226.3 (1997): 159-162.
Góth, M. I., Hubina, E., Raptis, S., Nagy, G. M. and Tóth, B. E. (2003), Physiological and pathological angiogenesis in the endocrine system. Microsc. Res. Tech., 60: 98–106. doi: 10.1002/jemt.10248
Pearson, Olof H., et al. "Prolactin-dependent rat mammary cancer: a model for man?." Transactions of the Association of American Physicians 82 (1969): 225-38.
Poste, George, and Stanley T. Crooke. Dopamine receptor agonists. Springer Science & Business Media, 2013.

Scott KA, Dalgleish AG, Liu WM. The combination of cannabidiol and Δ9-tetrahydrocannabinol enhances the anticancer effects of radiation in an orthotopic murine glioma model. Mol Cancer Ther. 2014;13(12):2955-67. 
Stanwood, Gregg D., Irwin Lucki, and Paul McGonigle. "Differential regulation of dopamine D2 and D3 receptors by chronic drug treatments." Journal of Pharmacology and Experimental Therapeutics 295.3 (2000): 1232-1240.
Steger, R. W., et al. "Interactions of Δ9-tetrahydrocannabinol (THC) with hypothalamic neurotransmitters controlling luteinizing hormone and prolactin release." Neuroendocrinology 37.5 (1983): 361-370.

Letter to Sven Andreasson on his longitudinal study of Swedish conscripts and confounding data

Hello,
I have done some research in nuclear medicine on this subject and there are a number of confounding factors that I believe you have left criminally unaccounted for in your research. To begin with, in states with legal marijuana, such as Canada, use of 5 grams and less per day is associated with an increase in IQ of 5 points. My own research in nuclear medicine looking at the blood flow of the brain supports this, after half a pack of marijuana cigarettes over 6 months most of my brain was normal, with one area with increased activity. According to MRI studies there has been little change in the brain observed, though conclusive evidence exists that the size of the amygdala increases and some indication that the part of the brain associated with addictive behaviour becomes less prominent, here a benefit, though this was not substantial enough to say for certain. Ultimately, biologically what is claimed about marijuana in this longitudinal study is in conflict with studies in Canada that had a high level of accuracy that followed users from 12-17 to 25 and later points in life as well as the most recent SPECT and MRI imaging studies.
The most important confounding piece of evidence does not rely on new technology, or different methodology, however, and it is quite sad that this was not accounted for in this expensive research costing the Swedish government severely. According to the CDC the majority (between 65% and 86%) of schizophrenia can be attributed to the parasite toxoplasmosis gondii. To suggest that something without a logical biological explanation is responsible when it is quite simple how the microbe targets brain and muscle tissue to lay its eggs and the body's protective cysts disrupt bloodflow is quite unethical. The explanation for how it goes in uneven amounts in marijuana users is quite simple, a cat defecating into a potted marijuana plant will contaminate the product for up to a year later.
I do not know the statistics in Sweden off the top of my head, but in the United States 22.5% of people are infected in their lifetime with t. gondii. Of these 25% (5-6% of the general population) get flu-like fatigue and fever, other psychotic symptoms for one week to as long as a month or three months. 6% will have latent symptoms, lasting longer than 6 months and will be diagnosed as schizophrenic. This is the majority of the 1.2% diagnosed with schizophrenia in the USA. It is dose dependant, and getting exposed to the parasite later in life or going thru a period of immunosuppression will cause a recurrence of behaviour.
Please provide an addendum to your research as I have done mine (this came up only as I was publishing, at first I thought to say there were some mild changes, nothing significant from marijuana, luckily I had prefaced my research by emphasizing that marijuana was decriminalized or illegal and the results may be different in a legal setting, as they indeed turned out to be) providing for these confounding factors.
Thank you,
Paul Fischer