Showing posts with label marijuana. Show all posts
Showing posts with label marijuana. Show all posts

Thursday, January 19, 2017

Recreational Marijuana Data Integrity Verification

Paul Andreas Fischer
1/19/2017


Recreational Marijuana Data Integrity Verification




The purpose of this effort to maintain cybersecurity will be to identify trends in community activity, usage, and coding on three webpages. This will be measured in a weighted per capita membership inclusive of adjustment for last month marijuana usage according to statistics of diagnoses of marijuana use dependency in the last year sourced through the National Institute of Health, statistical significance testing for key HTML or python coding which may be present on the pages ranging from common use terms such as margin and italic/bold to design oriented coding such as getOptions and fix, and finally using a theoretical W3C validation scheme borrowed from a co-operative effort by employees of Drop-box, Google, and Mozilla.
An effort throughout will be made to avoid redundancies in data and to reduce reliance on contingent terminology in order to establish statistical significance in further analysis. While this will not be used to justify any legal actions or hold significant ramifications for user, community, or legislative individuals or groups due to the hypothetical nature of the theories of security fundamental to the arguments provided, the data may be accessed and used publicly and reproduced. As with all research looking at differences in data, change over time will be critical to determining whether this is an appropriate sequence to validate the integrity of the media distributed. This data is accessed legally under the Digital Millennium Copyright Act as encryption research to enhance secure methods of encryption technologies (section 1201(g)), to measure and protect personal privacy (section 1201(i)), and security testing should readers wish to check their own computer, computer system, or computer network (section 1201(j)).






Data results

Per capita membership or following:




Conservative estimate,
Vermont Community, Vermont Collection, Colorado Community
.085%, .075%, .6%


Keyword search statistical significance test from raw test raw data with high-end tail comparison




“input” - Vermont Community, Vermont Collection, Colorado Community
“_” -  8335, 8933, 8816
“”” - 10,916, 11,181, 10,670
“head” - 48, 49, 49
“fix” - 12, 12, 15
“array” - 108, 110, 108
“marijuana” - 41, 57, 21
“cannabis” - 37, 29, 4
“meta” - 22, 21, 22
“content” - 240, 252, 259
“function” - 2264, 2256, 2264
“getOptions” - 3, 3, 3
“window” - 420, 417, 420
“element” - 125, 125, 125
“null” - 5226, 5489, 4582
“try” - 155, 159, 158
“dump” - 53, 54, 53
“exec” - 51, 51, 51
“recreational“ - 16, 24, 17
“google” - 183, 181, 205
“script” - 79, 75, 79
“true” - 151, 160, 127
“$” - 284, 284, 284


Theoretical Validation Scheme


This scheme has been chosen because it allows authentication of not only the server, which is standard in such attempts, but also the content which has been posted to the respective pages. With a variety of pegged user handles and other contributions involved in the creation and maintenance of a controlled substance which is limited in distribution to those over a certain age, and in some locations can be met with severe legal repercussions, there is an intrinsic value to vetting cyber information.
In order to avoid such misunderstandings, a thorough read through of all source data was initiated and completed with the following results. Rather than sifting through user data or implementing a cryptographic hash system recommended in the theoretical scheme, evaluating the cross-origin data leakage to identify reconnaissance activities by potential or real attackers was initiated (SRI, 5.3). This is both non-intrusive, experimental, and potentially more accurate for the purposes of identification than traditional methods of code evaluation.




Discussion of data, results and conclusions


Cannabis Use Rates and Trends




The growth in Colorado is under 30% in recent years, marking a substantially larger presence than has been found in Vermont. Statistical analysis found ratios of 1:1.25:1.5 from .2% of the total populations of the respective states in the Vermont Collection, Vermont Community, and Colorado Community that were admitted to the hospital for potential marijuana dependent symptoms according to a recent update from the White House which cites data from 2010. Multiplied by a cohort with an average life expectancy of 78 years, this data could encompass almost 60% of current marijuana users. This could also comprise the entirety of the population have used before entering High School, according to a report released by the UN in 2014.
A statistically interesting point that is not addressed in this paper is that the trend for admission for marijuana related episodes shows a dramatic variance in those two populations, as the number of marijuana users per capita was about 30-40% higher in Colorado at the time. Potential explanations include the presence of higher potency marijuana in Vermont due to lack of effective regulations during the transition period of decriminalization. Another could be adulterants such as lead which decrease the flashpoint at which a joint or a bowl is lit, increasing the temperature at which smoked material is absorbed or the popularity of edibles which may be more potent than a smoked product, as there are nearly a third more tobacco users in Colorado per capita than Vermont.


Keyword search with statistical significance analysis




A perfect match was reached in four of 22 source code searches, nearly 20% of the total results. Taken as an outlier result, this demonstrates definite significance. Two of three quantitative forms found a perfect match in exactly half of the searches. The natural odds of these events occurring are one over 4.2 times 100,000,000. This determines that there is a high probability of interactivity occurring between these web-based pages.
While there are no prohibitions between communications of two online communities, this can also serve as a template to verify that such communication is not occurring between any of the communities and communities tailored towards those who underage. It is also a possible indicator of a malware presence, which could include a BOTNET, synthetic code injector algorithm, sniffing agents or most likely a combination of all of the above. In order for any confirmed statements to be made with only a statistical analysis, causal proof of intent of harm or defamation and malware cyber-activity must be demonstrated. To accomplish this, an experimental form of subresource integrity is being modified and taken advantage of, referred to above as cross-origin data leakage.


DIV and Cross-Origin Data Leakage




The initial read-through looked great, though there is a major qualification which ought to be addressed present one time only in all three communities that likely represents a violation of amendments to the CFAA in 1984. Due to recent legislation and expansion of that act, these consequences could be quite serious if not administratively addressed and the responsible posts promptly deleted, though no legal responsibilities exist unless the display represents an extension or whole of a small business. Colorado had significantly greater evidence of hash use, but all three communities/collection presented enough to provide a strong sense of security. Cross-origin analysis demonstrated that “content-originated” was indeed activated upon execution of the HTML. No flag presented or evidence of any tampering of any kind.
Further analysis of the entirety of the source code, around 30 solid pages for each community, revealed the presence of a flag which discontinues the cross-origin protections and which could allow a JSON style attack, gaining access to passwords or other confidential credentials. This should allow a violation of the “same-origin” policy and may have been used to determine what content is present within the cross-origin resource. Whether this setting is coded on or off, the threat level is ultimately low.


Valuation of any Potential Threat to the Pages




A discretionary valuation of a low threat level had to be ultimately determined as users accessing the site are still protected by Google security and terms of use, i.e. dedication to privacy outlined above in this document and codified in recent US law for cyberspace, as well as amendment to the Constitution. The presence of an “Anonymous” omission of cross-origin protections is present at one time in the HTML code of all three websites. That does not indicate that the tool has been exploited. Unless there is an experimental lab underway through Google, the only data which should be accessible in the event of a general breach throughout the company would be the user names and profiles of individuals who are on the pages.
However, the possibility that it is a “wait and see” placement should be treated with caution as well as corrective measures should be taken to eliminate the offensive code from the pages. It is worth mentioning, once again, that the only parties which have any liabilities for such a piece of code are those who posted the sequence and any small business owners involved with the pages that may have turned a blind-eye or aided the malware. Possible legal explanations which could indicate that one did not know about updates to the CFAA or if the code had been prepared before 1984 may be possible, but even if it is the case, does not mean that the threat or potential threat should not be snuffed immediately.




References:


Braun, F., Akhawe, D., Weinberger, J., & West, M.. Subresource integrity. W3C working draft. (2014).
The Digital Millennium Copyrights Act. 17 U.S.C. § 512 (1998).
United Nations Office on Drugs and Crime (UNODC). Recent statistics and trend analysis of the illicit drug market. (2014).
W3C Recommendation. HTML5, A vocabulary and associated APIs for HTML and XHTML, W3 (2014).

Wednesday, September 14, 2016

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.

Friday, July 10, 2015

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.

Saturday, June 20, 2015

Letter from the White House on marijuana legalization:

While, "A considerable body of evidence shows that marijuana use, especially chronic use that begins at a young age, is associated with serious health and social problems," which is not anything to disagree with, "We will also closely monitor implementation of marijuana legalization in individual States" which indicates support for marijuana legalization in states, including our own! In addition support was expressed for research into the medical benefits of marijuana, though it was noted that the FDA had not yet found smoked marijuana (does exclusion of edibles indicate a positive here?) to be suitable as recognized for medical use. This is very positive, and we can look forward to legalization in the near future here in Vermont, along with other states.

Friday, June 12, 2015

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.

Friday, May 29, 2015

Legalizing Marijuana the Vermont Way - Recommendations for the Upcoming Marijuana Bill

The Vermont Senate Committee on Government Operations has made its recommendations for a bill to legalize marijuana. After meeting in November, these should be crafted into a bill for the Senate to look at shortly afterwards. More documents and information can be found on the Senate Committee on Government Operations page at the statehouse's website.
Link to recommendations here: Legalizing Marijuana the Vermont Way

Tuesday, May 26, 2015

Open letter to the chair of the Judicial Committee in the Vermont State Senate on relative incarceration rates and marijuana:


Hello,
Would it be possible to push this up to a matter of state security and constitutional crisis? I do not have access to Vermont's statistics on incarceration, but after adjustment for those incarcerated solely on the virtue of marijuana charges and then number of marijuana smokers per capita, all data readily available on a national scale, it became apparent that the amount of incarceration in the marijuana smoking community is less than that of the alcohol drinking community, and only slightly higher than those who consume no substances whatsoever, if at all. Both alcohol and marijuana using communities have 10X less incarceration than users of other hard narcotics for which statistics are collected for. Combined with the national study on road safety and marijuana use which shows that marijuana use fatalities are the same as those who do not drink or drug (it is known that Vermont does have a weird anomaly which has more marijuana related fatalities than federal statistics, though the trend remains steady in our state), the implication is that every year there are 10's of thousands of unnecessary automobile deaths, even with only a modest substitution factor in relation to marijuana use and alcohol or other drugs (which, given the trajectory since the 1970's when around 90% of users of marijuana also used other narcotics to today, with the 50-50 point being reached in the 1990's, today hard drug use among marijuana users is lower than the national hard drug use in the 1980's and low enough to show the logical fallacy in the gateway theory, can be assumed to be much greater than modest). Finally, I do not believe there are constitutional grounds for incarcerating a community of people who do not commit crimes in a greater amount than the general population (or at all, if there is no evidence of causality between the group identity, such as a gang, religion, or drug use, and the crime which could be economic, violent, or mischievous in nature). If sources are needed, I am happy to supply them. Furthermore, if there are Vermont specific statistics which either confirm, do not match (as happened with the traffic fatalities), or directly conflict with federal statistics, please inform me, this would be useful for my recreational marijuana community on googleplus.
Thank you,
Paul Fischer

Wednesday, May 13, 2015

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.

Monday, May 11, 2015

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).