Preliminary Research Investigating Cramping and Prefrontal Cortex Activity in Healthy Volunteers Controlling for Administration of THC or CBD, as well as Voluntary Exercise

  So the problem is pretty simple in outlook. Cannabidiol is legal for recreational use in the United States currently, but has not been recognized particularly as having medical applications and it may not even be an option to prescribe it. There is a body, which is appropriate for the potential of the product in its anxiolytic and anticonvulsant properties, which are confirmed, of evidence which suggests it has use for athletes and people with medical diagnosis to improve with cramping symptoms and pre-frontal cortex activity, respectively as well as other symptoms of illness (Ashton). This research has not been done with healthy volunteers in the United States of America, but Germany and other member states of the European Union appear to have such research underway.

  This research includes applications for use with tetrahydrocannabinol (THC), which is not believed to have an effect on the pre-frontal cortex in a reproducible manner, except through childhood use as cited in previous research. No studies have used children that I have been involved in, to the best of my knowledge, though there is a substantial body of evidence regarding the impacts of THC on growth in children. Regular underage use as established by research on the topic of THC was not extant in this trial and the earliest confirmed exposure was between 15 and 17, though a couple to a maximum of three solitary experiences or exposures are strongly suspected before. Alcohol is not believed to have been used in a manner which should impact research currently, and has not been a factor in recent research, with last exposure occurring nearly four years ago.

  At the beginning of July 2016, after 3-6 months without cannabis exposure, which was confirmed by UA analysis and no believed CBD exposure though there is no way to confirm that, given current resources readily available, cramping was experienced while swimming, as has been normal for the subject as an excellent athlete and created periods of significant pain. This is exacerbated by a preliminary diagnosis of degenerative disc disease in 2013, and could have been dangerous to the life of the subject with long-term physical activity without proper actions or steps taken ahead of time.

  Rude behavior at this point is believed to be indicative of lapses in prefrontal cortex judgement, albeit minor, and this is the sort of information which will be advisable to collect for recreational marketing studies with the new and fascinating product cannabidiol along with cramping and muscle soreness. The research now includes confirmed exposure to THC in a healthy volunteer with peak levels of nearly 700 ng/ml in urine analysis as well as intensive exercise. This was not an intended level, and there may have been issues with the testing, and a confirmed negative was believed to have occurred after one month using urine analysis. A similar social encounter can be confirmed during this period without a rude or socially unacceptable response.

  Following one month without exposure to THC and with exposure to CBD, the trial was run again with expected exposure to THC and no significant amounts of CBD over the course of some weeks at which point cramping cramping did ensue. Investigating further, a similar social interaction, all of which regard positive rewards naturally, produced a rude response. This indicates that the benefits to the prefrontal cortex are not due to THC but cannabidiol. 

  It should be clear that a trial without CBD, THC, or exercise using these same measures is still missing in order to obtain a clear baseline, so this research has been classified as preliminary in nature. As a person in severe pain without use of CBD, I do not believe it to be ethical to require this study be carried out by myself. If you would be, as a person who is not using marijuana, constituent compounds, or activities and substances which have been shown in research to have any impact on the measures being evaluated in this study, so kind as to fulfill this study and to cease regular activity for between one week and one month in order to complete this study, while noting cramping and prefrontal cortex activity indicators, it would be helpful to me. Should a description of the experience be acceptable then it might be possible to provide this research in conjunction with the work so far. Dietary factors are being intentionally excluded, and are not believed to be a factor, as even consumption of food shortly before intensive physical activity did not induce cramping with use of CBD, although combined with necessitated dehydration over the course of relatively short time period did result in physical activity related nausea, no other serious complications had to be recorded.

References:

Ashton, C. H., and P. B. Moore. "Endocannabinoid system dysfunction in mood and related disorders." Acta Psychiatrica Scandinavica 124.4 (2011): 250-261.

Lead exposure, weight gain, hypertension, and early mortality: case study and review

Background:

As increased lead exposure from contaminated marijuana use in the USA and Germany has been confirmed, the potential impacts of severe or light lead exposure are being drawn once again into the public light. The mean adult lead exposure in the USA dropped by 41% from the 1990s to the 2000s from 2.76 μg/dL to 1.64 μg/dL, which has been causally shown to prevent the nearly triple the rate of kidney death and double the rate of peripheral artery disease, which includes cardiovascular death which was present before (Muntner). These low levels of increased lead exposure have been shown to result in a 1.55 increased odds ratio for mortality in all cardio-vascular mortality, after adjusting for all other factors (Menke). This translates into over 7 years of lost life expectancy (Tsai), simply from the cardio-vascular effects of lead toxicity. 

The mean for previous mean lead exposure is now still extant in the higher quartile of adults now that lead exposure has dropped significantly, which makes what was formerly believed to be a safe level of lead exposure very dangerous for those who are still exposed to elevated levels of lead. The expected drop in hypertension from removal of lead from the environment within these boundaries is estimated at 17.5% (Pirkle). Hypertension is a condition which induces an increased hazard ratio of about 1.30 of at least one annual kilogram of weight gain (Stevens), or around 80 kilograms in a lifetime. These weight changes as well as lead exposure have been associated or identified causally with neurological changes, most notably brain lesions (Stewart), which brain imaging and cardiovascular data in this case study have confirmed.

Fortunately for this study and for those who are exposed to lead-infused marijuana or environmental hazards, a study from Veterans affairs has found that increased mortality and negative health effects from lead exposure is only significant with long-term cumulative exposure (Weisskopf). Because the trials were conducted over a period of multiple years, it is likely that there will not be long term or lasting effects once lesions are allowed to heal and with natural expiration of the toxin from the body.

Case study and Results:

Unfortunately, in the case study of a responsible adult marijuana user (5-10 grams at 10% mean THC content per week) in the Northeast of the USA, these sorts of statistical analyses were not useful. In the first run, diastolic blood pressure was over 95 directly after the trial though lead was not initially considered as a factor, with considerations of light alcohol use and high nicotine intake believed to be causally tied to this negative symptom. Re-trial, without regular use of nicotine (substitution of pipe tobacco, with virtually no absorbed nicotine for cigarette tobacco which has between 5 and 13 times the amount of absorbed nicotine) and no use of alcohol, determined lead levels of around 3.5 μg/dL, or levels qualifying as occupational hazard and outside of the range of environmental exposure. With levels taken only one month after the trial had ended and a half-life of lead in the human body of around one month, it can be assumed that these levels at a maximum were at least 7 μg/dL (Barbosa). The increases in blood pressure associated with occupational exposure to lead, which this level still falls into the highest decibel among, are around 10 mm Hg in blood pressure, though due to the young age and good health of the subject and lower expected peak exposure level symptoms may not be as exacerbated as noted in long-term occupational exposure ratios (Glenn).

Physical or cardio-vascular side effects aside, the exposure to lead also has multiple symptoms of neurodegeneration which present themselves and confound earlier attempts to pinpoint neurological effects of THC on the brain, though increased functional connectivity was still noted and remains a confirmed positive effect of marijuana on the brain. The impact of lead on the brain in any amounts on adults or children has been shown to be increased brain lesions and negative on all brain structures as proven using MRI technology (Stewart). This is consistent with the single photon emission computed tomography scan performed which showed increased functional connectivity, but altered blood-flow throughout the brain (Fischer), believed at the time to be the result of specific toxins, though now shown to be an undocumented variable: the environmental toxin lead.

Works Cited:

Barbosa Jr, Fernando, et al. "A critical review of biomarkers used for monitoring human exposure to lead: advantages, limitations, and future needs."Environmental health perspectives (2005): 1669-1674.
Fischer, Paul Andreas. "Single Photon Emission Computed Tomography - Alcohol and Marijuana light use, case study."http://platophilosphy.blogspot.com/2014/07/effects-of-regular-or-light-marijuana.html (2014).

Glenn, Barbara S., et al. "The longitudinal association of lead with blood pressure." Epidemiology 14.1 (2003): 30-36.

Menke, Andy, et al. "Blood lead below 0.48 μmol/L (10 μg/dL) and mortality among US adults." Circulation 114.13 (2006): 1388-1394.

Muntner, Paul, et al. "Continued decline in blood lead levels among adults in the United States: the National Health and Nutrition Examination Surveys."Archives of Internal Medicine 165.18 (2005): 2155-2161.

Pirkle, James L., et al. "The relationship between blood lead levels and blood pressure and its cardiovascular risk implications." American journal of epidemiology 121.2 (1985): 246-258.

Stevens, J., et al. "Associations between weight gain and incident hypertension in a bi-ethnic cohort: the Atherosclerosis Risk in Communities Study."International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 26.1 (2002): 58-64.

Stewart, W. F., et al. "Past adult lead exposure is linked to neurodegeneration measured by brain MRI." Neurology 66.10 (2006): 1476-1484.

Tsai, Shan P., Robert J. Hardy, and C. P. Wen. "The standardized mortality ratio and life expectancy." American journal of epidemiology 135.7 (1992): 824-831.

Weisskopf, Marc G., et al. "A prospective study of bone lead concentration and death from all causes, cardiovascular diseases, and cancer in the Department of Veterans Affairs Normative Aging Study." Circulation 120.12 (2009): 1056-1064.

Marijuana may not only protect against lung damage, but also help nicotine product users regulate or quit their product, and has the potential to aid with other chemical dependencies.

One of the most persistent reasons that people favor marijuana use, legalization, and regulation is due to the assertion that smoking marijuana does not do damage to the lungs, while tobacco smokers have a high certainty of dying from their habit. While the claims have been modulated to some extent, this assertion has held true in cohort studies of medical and recreational marijuana use in California, and attempts to determine causality actually found that the smoke from marijuana offers a protective effect to the lungs of users.

Something that has not been addressed as fully, is the impact of THC on the brain and fighting addiction. Nicotine is among the most addictive substances in the world when taken in amounts of 15-20 mg per day and greater for an extended period of time, the threshold for chemical dependence. It has also been shown to do damage to the dentate gyrus of the brain, which contains about 90% of the brain’s memories, at these levels of intake.

Marijuana smokers experience an increase in functional connectivity in the brain, which has been causally associated with an increase in IQ. The dentate gyrus is among the parts of the brain which experience elevated levels of neurogenesis as a result of exposure to an active compound in marijuana, THC. Recent research conducted at Duke University found that tobacco smokers who were able to quit experienced elevated levels of connectivity in the brain as well, while those who relapsed or became heavier smokers tended to lack this connectivity.

This research is of extreme importance as both nicotine products and other addictive substances or pharmaceuticals grip many users in this country. While it is important to make these activities less addictive, for example by limiting the amount of nicotine in a dose, ironically enough the opposite of what manufacturers of cigarettes did decades ago (though to be fair this may have been a simple reaction against hyperbolic at the least and malevolent or unfounded research at the worst targeted at tobacco), or educating people about what level of intake can be diagnosed as chemically dependent, and should be seen as a warning sign of addiction (as a good doctor will do with any prescription), it is also important to develop methods of ensuring successful recovery in the event of chemical dependence.

While marijuana has been prescribed before prohibition, and has a cultural connotation as a substituting product allowing people with chemical dependence to recover past withdrawal for centuries, the nature of its medical value is just starting to be explored now. Of particular interest is whether the factors affecting recovery for nicotine can contribute to recovery from other substances; research carried out suggests that the underlying genetic factors behind addiction are “highly correlated” at the least. Using brain scan technology to see this effect will be exciting at the least, and this particular vein of research is among the most enticing for public health.

Works Cited:

Abrous, Djoher Nora, et al. "Nicotine self-administration impairs hippocampal plasticity." The Journal of neuroscience 22.9 (2002): 3656-3662.

Addicott, Merideth A., et al. "Increased Functional Connectivity in an Insula-Based Network is Associated with Improved Smoking Cessation Outcomes." Neuropsychopharmacology (2015).

Filbey, Francesca M., et al. "Long-term effects of marijuana use on the brain."Proceedings of the National Academy of Sciences 111.47 (2014): 16913-16918.

Fried, Peter et al. “Current and Former Marijuana Use: Preliminary Findings of a Longitudinal Study of Effects on IQ in Young Adults.” CMAJ: Canadian Medical Association Journal 166.7 (2002): 887–891.

Doweiko, Harold. Concepts of chemical dependency. Cengage Learning, 2011.

Hashibe, Mia, et al. "Marijuana use and the risk of lung and upper aerodigestive tract cancers: results of a population-based case-control study." Cancer Epidemiology Biomarkers & Prevention 15.10 (2006): 1829-1834.

Jiang, Wen, et al. "Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic-and antidepressant-like effects." Journal of Clinical Investigation 115.11 (2005): 3104.

Kempker, Jordan A., Eric G. Honig, and Greg S. Martin. "Effects of Marijuana Exposure on Expiratory Airflow: A Study of Adults who Participated in the US National Health and Nutrition Examination Study." Annals of the American Thoracic Society ja (2014).

Kendler, Kenneth S., John Myers, and Carol A. Prescott. "Specificity of genetic and environmental risk factors for symptoms of cannabis, cocaine, alcohol, caffeine, and nicotine dependence." Archives of General Psychiatry 64.11 (2007): 1313-1320.

Ling, H. W., and CB Wynn Parry. "The amount of nicotine absorbed in smoking." British journal of pharmacology and chemotherapy 4.3 (1949): 313-314.

Neurogenesis Suppression in Dentate Gyrus Induced by Moderate to Heavy Nicotine Use Finally Shown to Have Negative Impact on Memory Functions?

There is a stereotype that marijuana smokers have hazy or weak memories as a result of their use. Tobacco smoke, on the other hand, is usually discussed in terms of the positive effect on cognition by virtue of the very mild stimulant effects delivered by nicotine. Over a decade ago, however, researchers in Nice, France showed in rats that administration of nicotine, without smoke, induced a suppression of new neuronal births in the dentate gyrus, the part of the brain that handles about 90% of a person or animal's memories. In the last decade as well, researchers from the Chinese Military, Canada, and Maryland have shown that marijuana actually encourages the birth of neurogenesis in the hippocampus (which is responsible for most remaining memories) by 40%, when a pure THC copycat chemical, named for Hebrew University where the compound was made, is administered to rats. Researchers at Princeton University and the Department of Nutrition in Brazil also showed that there was no effect from THC on the dentate gyrus of rats, even at levels producing "gross behavioural intoxication".

This provides a general understanding of the effect of THC on the brain, which should be reproducible in human or population studies which have been conducted. More recent brain scans have also shown this to be true as conducted with human populations, with negligible changes, positive or negative, found in most parts of the brain, though functional connectivity has also been shown to increase in a significant manner with marijuana use this last year.

Most recently, a study from Spain claimed that while virtually every mode of behavioural measurement was equal between marijuana smokers and control groups, a significant (though still within the realm of normal fluctuation) decrease in memory function was noted. This speaks in the face of research that has been conducted about THC or the marijuana that contains it. Even with patients using 10 times the responsible adult use in the sample, and the average number of marijuana cigarettes, or spliffs, smoked in a lifetime being around 42,000 (with one participant smoking over a massive 256,000 times) among those included in the study, the results do not match with rats who were administered high levels of THC; the results should have been positive and not negative.

There is a difference between the human and rat studies, though which is not addressed. In the Spanish study, noting a decrease in memory function, the research explicitly emphasizes that tobacco users were not omitted from the study, and about 75% of the participants were actively smoking tobacco when the study was conducted.

A little background, for the American marijuana user, is necessary. In Europe, people smoke spliffs generally made with hashish and tobacco. The unfiltered smoke doubles the nicotine intake (in some countries there are lower limits on nicotine levels, but in Spain this probably means quite similar to American cigarettes, as there has not been a strict concentration of absorbed nicotine enforced throughout the European Union yet), and this dominates the marijuana culture there. While more efficient, this also means that it is very difficult to smoke marijuana regularly without crossing the threshold of 5-10 mg of nicotine daily at which point positive effects are eclipsed by neurogenesis suppression, assuming the user is smoking on work breaks or at certain timepoints and not regularly throughout the day (the research indicates that doses of more than 3-5 mg of nicotine in the blood at a time is the crossover point from positive to negative effects).

The research in Nice, France, which originally shows the negative impact of moderate to heavy nicotine use on the dentate gyrus, emphasizes that further research is needed to confirm this neuronal difference actually translates to a cognitive change. Research from Riba et al. should be used in conjunction with other research done in this field to confirm this fact, as has been shown above. It is still worth investigating the impacts of age, obviously at certain ages nicotine has a positive effect, while it can be assumed that while a brain is developing such stunting of neurogenesis must induce extreme cognitive defects. For those concerned about absorbing too much nicotine, in the last 70 years absorbed nicotine in cigarettes has increased almost 3-fold in the USA (though in some parts of Europe the composition of a cigarette is much the same as in the early days of the tobacco industry) as companies and governments attempt to limit tar or air pollution intake (read previous research on cancer mortality and smoking for more), one viable option is to use pipe tobacco instead of cigarette tobacco. While the curing process for pipe tobacco means there is more nicotine per gram in the cigarette or bowl, the wide cut of the leaves lowers absorbed nicotine by around 13 times (or 2-4 times in comparison to low nicotine European cigarettes). Normal use of pipe tobacco is also associated with levels of cancer and smoking-related disease more similar to the general population than to the cigarette smokers.

Works Cited:

Abrous, Djoher Nora, et al. "Nicotine self-administration impairs hippocampal plasticity." The Journal of neuroscience 22.9 (2002): 3656-3662.

Filbey, Francesca M., et al. "Long-term effects of marijuana use on the brain."Proceedings of the National Academy of Sciences 111.47 (2014): 16913-16918.

Jiang, Wen, et al. "Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic-and antidepressant-like effects." Journal of Clinical Investigation 115.11 (2005): 3104.

Kochman, Linda J., et al. "Despite strong behavioral disruption, Δ 9-tetrahydrocannabinol does not affect cell proliferation in the adult mouse dentate gyrus." Brain research 1113.1 (2006): 86-93.

Ling, H. W., and CB Wynn Parry. "The amount of nicotine absorbed in smoking." British journal of pharmacology and chemotherapy 4.3 (1949): 313-314.

Riba, J., et al. "Telling true from false: cannabis users show increased susceptibility to false memories." Molecular psychiatry (2015).

Confounding research on Chronic Inhalation Exposure to Mainstream Cigarette Smoke Increases Lung and Nasal Tumor Incidence in Rats - Human consumption of tobacco lowers lung lesions, tumours, and other malignancies

There are a number of procedural errors in this study which will be addressed as follows. Firstly the bias or affiliation of the study, published by Oxford University, is listed as pfizer, a corporation that makes smoking substitution products, and was caught bribing academics (in unlisted affiliations) with the intent of maintaining marijuana prohibition. Furthermore, the study was conducted in New Mexico, a part of the USA with high atmospheric radiation at this time, the non-smoking control received filtered air, while smoking groups were exposed to non-filtered air. The study asserts that in mice testing, supporting data was gathered that cigarettes cause pulmonary damage. 
The mice are divided into a control group, a "low-smoking" and a "high-smoking" group. The low-smoking group was exposed to the equivalent of between 20-30 cigarettes smoked continuously for six hours without stopping. The high-smoking group was exposed to the equivalent of 60-80 cigarettes per day continuously over a period of six hours and should have been disregarded as non-evident of human consumption patterns at any time in history. For the purposes of reality, the low-smokers (which in humans is at levels classified as heavy cigarette use), will be used in this evaluation. In addition, in this study the high smoking rats were starved (food consumption 60% of non-smokers), which also indicates this data is not reliable.
Despite the conclusion and abstract's assertion, the data is actually quite positive for regular smokers. Incidence rates of neoplasia in the nasal cavity was lower for smokers than non-smokers.  The survival rate for smoking rats is higher by a significant amount, from 752 days to 779 days. Lung weight of smoking rats was the same as non-smoking rats (an increase was seen by 60 cigarettes per day). Ciliated cuboidal cell metaplasia (mucus in the lungs, a deformity frequently observed with aging that has not been definitively connected to cancer, except in epidermal cases, and then only correlatively) was noted in a small amount in smoking rats. Squamous metaplasia was not observed in smoking rats, but were noted in the 60 cigarette per day group. Keratinizing squamous cysts were not observed in smoking rats, but were noted rarely at 60 cigarettes per day. There were no consistent trends in lung lesions, with sometimes lowest levels in the group smoking 60 cigarettes per day (eg. hyperplasia), sometimes lower in smoking rats (eg. malignant neoplasia) and other times in non-smoking (eg. benign neoplasia), though it should be noted this occurred in non-significant levels in all rats. There is no increase in nasal neoplasia for smoking rats. 
After all this, the study asserts that cigarettes are the cause of problems, but admits, "The reason this study produced significant increases in lung tumors in rats while previous studies did not cannot be determined with certainty." It is fairly clear that while, previous studies have linked regular human consumption to health benefits, the concept of gassing rats with 60 cigarettes per day had simply not occurred. See previous articles for data on cancer mortality rates in the USA and the probability that tobacco use in humans has numerous health benefits. While there is not data here on radiation exposure necessary to lower white blood cells in a rat, it is safe to assume these fall along similar lines with humans, and exposure to an unmeasured number of mrems of radiation was a significant factor in the development of malignancies in the rats. It is possible that filtered air might make a difference in mucous accumulation in rats as well as humans, though this is not definitively connected with cancer or malignant symptoms.

Mauderly, J. L., Gigliotti, A. P., Barr, E. B., Bechtold, W. E., Belinsky, S. A., Hahn, F. F., Hobbs, C. A., March, T. H., Seilkop, S. K., and Finch, G. L. (2004). Chronic inhalation exposure to mainstream cigarette smoke increases lung and nasal tumor incidence in rats. Toxicol. Sci. 81, 280–292. 

Letter to Patrick Kennedy regarding conversation at Smart Approaches to Marijuana

Hello,
Regarding our conversation at the SAM conference this summer: I was lucky to have qualified my statements with illegal and decriminalized marijuana in relation to my research. I did indicate that further results from fully legalized areas and places of further research were being waited on. Since the conversation, the confounding factor of the toxoplasmosis gondii being extant in many marijuana smokers in places with home grow operations has forced a reconsideration of the numbers and statistics available. This parasite is responsible for the perceived negative impact of marijuana in countries that fail to complete proper legal research in keeping with UN treaties in effect currently. In Canadian and other studies have conclusively shown with virtually no room for error that marijuana use is associated with a 5 point increase in IQ in current smokers and 3.5 points in former smokers. This translates to literally trillions of dollars in lost intellectual property as can be seen in Germany where marijuana use among 18-24 year olds has quadrupled to nearly 28% while the economy has ballooned to nearly the same size as the United States while alcohol use has dropped dramatically. In MRI and SPECT scans the positive effect of marijuana when disambiguated from those infected with the common parasite, along with pesticides or other factors including income, has been concretely shown in Dallas and other university academic studies. There is some research to indicate that a compound from marijuana may mitigate the effects of alcohol, but this research is still in its infancy, at this time in the 45% of America that drinks, it can be associated with a drop in IQ of several points in comparison to a non-user, and many points in comparison with marijuana users. For the time being, this is a national security crisis in which every year 150,000 people are needlessly dying from alcohol related deaths. To put this in perspective, this is more than all military deaths in all American wars since the Korean war combined, every year. Furthermore we are unable to compete on a global scale as other nations, including Germany, with smaller populations are able to perform on a higher level than the United States. An increase of 5 points in IQ translates to 100's of % more geniuses and double the number of highly gifted in the population. We have made significant progress with industrial hemp legalization, which increases CO2 consumption by 4X that of other plants and can potentially offset global warming while increasing our energy independence. It is time to take these gains to other fields as well.
Legally, prosecution of marijuana is unconstitutional and the way it is currently implemented it is in violation of multiple UN treaties. According to our constitution, the supremacy clause in article 6 section ii only takes effect under certain circumstances. The most significant example of this was in the Civil War, when Abraham Lincoln was forced to issue an executive order freeing the slaves before legislation from the federal government could make slavery illegal. Unless it could be argued that marijuana prohibition is more important to national security than 600,000 legal racially defined slaves, this clause should not override pre-existing and later passed state laws in this matter. This has been defended and ratified in multiple state supreme courts in the case of marijuana. Furthermore, in the federal statutes there is a contradiction in the case of marijuana, making prosecution unfeasible and illegal by federal organizations until resolved by a Federal court in an appeal to repeal. The charter of the FDA in the Food, Drug and Cosmetics Act of 1938 specifically addresses marijuana and retains classification from the Pure Food and Drug Act of 1906 which classifies marijuana and alcohol together as dangerous drugs with a high potential for poisoning and to be regulated by the FDA. This process was ironically pressed by conservatives in the implementation of Medicare and Medicaid long ago, and it is probable that with a federal court's review of such an appeal that the older law would be amended with the exception of marijuana, in any case until this happens government agencies would be very amiss to fail to follow medical advise.
Finally, marijuana has been proven to stop cancer. This is the leading cause of death in the United States and research has shown that molecules in marijuana directly harm cancerous human cells while avoiding healthy ones. My own grandfather passed away last summer after living what the AMA has recommended as a healthy lifestyle for most of his life. It is time for the United States to embrace marijuana and tell the alcohol industry to take some time on the back burner until that 200 billion dollar sore on the American economy has been developed into a beneficial product.
Sincerely,
Paul Andreas Fischer

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

New research suggests that nicotine creates cellular drills, targeting and perforating smooth muscles over a period of six hours.

Contrary to popular belief, that carbon dioxide level exposure had to be extreme in order to deposit enough tar to permanently damage the lungs, it is now becoming clear that the cause of lung cancer and other smoking related problems is in fact nicotine. It was an old wives' tale or counterargument from smokers that because people living in big cities inhaled half of a pack to a pack of cigarette in smoke from smog each day, but did not have high lung cancer rates like second hand smokers, there must be something wrong with the tobacco studies that were done. Living in a city with hundreds of thousands of cars cars was equivalent to "two packs of cigarettes a day" while any smoker will have a 24-35 in 100 chance of lung cancer (500-1000 times higher than simply being a city dweller). In Bejing today, this rate is 42 in 100,000. People who use candles or incense frequently only have 7 or 8, slightly more than regular marijuana smokers. This perhaps indicated that in fact smoking cessation products cause lung cancer; that it is not smoke, but nicotine that causes the lung cancer has only been proved this last year. Possible explanations at the time included contaminants to tobacco or asbestos, hence natural brands such as American Spirit advertised as such to me as a teenager.
However, in 2013, a new paper delivered at the American Society for Cell Biology managed to watch the molecules of nicotine fold into drills after being present in the blood stream for a continuous six hours. These target smooth muscles, such as those found in the heart, epidermis, lungs, and reproductive system as well as throughout the body. This helps to explain why a secondhand smoker in a house with a heavy smoker has a greater chance of lung cancer than a light smoker. It is conceivable that users of e-cigs or nicotine substitution products such as the patch or gum living in a big city could give themselves lung cancer as well by pollutant exposure as the body becomes unable to naturally clean itself.
Much credit is deserved for Brown professor Ching-Ming Hai, who discovered these cellular drills called podosome rosettes. By establishing the link between heart disease such as atherosclerosis and nicotine, the way has been opened to investigate the role of nicotine on other organs such as the lungs. Being able to observe this phenomenon suggests a veritable hypothesis that other smooth muscles in the body will and do respond in a similar way, eventually tearing and folding under continued nicotine exposure.
Some research has existed which supports this hypothesis that lung cancer is caused by nicotine, including studies which suggest that lung cancer is sped up by nicotine exposure (Dasgupta). For the first time, it can be assuredly said that in fact the cause is in nicotine. This supports the population data. In all of Mexico, for example the lung cancer rate is 5 in 100,000 (Lazcano). Introducing smoke increases this eight times, to as much as and over 40 in 100,000 with smog and air pollution (Wang). With nicotine exposure, this jumps to the 30,000 in 100,000 or thirty percent that indicates lung cancer is caused by tobacco.
This is affirmed by research using populations in Sweden and in California in which smokers of marijuana were not found to have increased cancer rates, or only slight and suggested links to cancer. Research along these lines were released in the 1990s and 2000s, though did not have at this time any scientific rationale for the phenomenon, which can now be attributed to nicotine. Continuing research along these lines should provide alternatives and safe products, once again, to combat use of sweets and bubblegum which were originally the targets of tobacco advertising.


http://articles.chicagotribune.com/2001-07-05/news/0107050231_1_smog-alert-mexico-city-greenhouse-gases
http://www.ncbi.nlm.nih.gov/pubmed/9428585
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1796573/
http://www.businessweek.com/articles/2014-02-28/rates-of-lung-cancer-rising-steeply-in-smoggy-beijing
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Addendum: It should be noted that this does not indicate that nicotine or tobacco is responsible for cancer. Since the US cracked down on tobacco use, with success in white males, the overall cancer mortality rate has increased from 184 per 100,000 in 1950-69 to 209 per 100,000 from 1970-1994. Today that rate holds steady at 203 per 100,000. In white females and in other demographics cancer rates have been steady or changed in negligible amounts, but these demographics have had increasing tobacco use rates. Cancer is a painful and unnatural death that can often involve long battles with the disease and should be combated with all resources available, in treatment and in prevention. While lung cancer rates have fallen, technological advances have allowed earlier detection of lung cancer, which at stage 0 and 1 is among the least deadly forms of cancer, but at later stages is among the most deadly. Without adjustments for technological advances in medical care, no positive statement can be made in regards to success or negative results from anti-smoking campaigns. Meta-data from overall cancer mortality does show that the resources in the war on cancer have been squandered and had an overall detrimental effect on the national health of the country, and some policy change is necessitated, although it must be noted there is no current biological explanation for the lower cancer rates in countries and places with higher tobacco use, these have been correlative not causal links. See following for more: http://platophilosphy.blogspot.com/2015/01/increasing-cancer-mortality-rates.html