Cannabis and Sex: Is There A Connection?

A recent study conducted by Stanford University researchers Andrew Sun and Michael Eisenberg entitled “Association Between Marijuana Use and Sexual Frequency in the United States: A Population-Based Study” suggests that smoking cannabis increases sexual activity in both men and women (1).

The researchers asked  28,176 women (average age= 29.9 years) and almost 22,943 men (average age =29.5 years)  men how often they had sex (heterosexual) in the four weeks prior to the survey and how frequently they used cannabis in the past year.  The study employed a multivariate statistical model that controlled for demographic, socioeconomic and geographical/culture characteristics.  More than 60% of the men and women were Caucasian and 76.1% of men and 80.4% of women reported at least a high school diploma.

Results from the study found that women who did not use marijuana over the four-week period had sex on average six times  whereas women who used cannabis daily had sex 7.1 times on average. Similarly, men who did not use cannabis had sex 5.6 times on average whereas men who used cannabis daily reported having sex 6.9 times on average during the four-week period.

Based on these results, which were statistically significant (P<.001), the researchers suggested that cannabis use may lead to greater heterosexual sexual activity.  It is important to note, however, that while the study results may have been statistically significant, the real life implications of these findings may  not be relevant.  More important, the researchers did not offer any explanations about the connections between cannabis and sex. Further, although the statistical design of the study controlled for a variety of variables,  other variables were not considered or addressed. For example, did the persons who participated in the survey have cannabis in their systems before, during or after sex.  Was cannabis consumed before, during or after sex?   What was the time differential between cannabis and actual sex? Put simply, there needs to be a greater examination and more in depth analysis of the direct effect of cannabis on sexual activity before any firm conclusions can be drawn.

Sadly, many cannabis users who read this post (or similar articles in the lay press) are likely to point to this study as another reason why it is good to regularly smoke cannabis.  That said, despite assertions to the contrary, there is evidence which suggests that smoking cannabis daily may negatively affect your health e.g., lung irritation and other respiratory issues.  LIke most things in cannabis science, many more studies must be conducted before scientifically accurate conclusions and facts can be established.

Despite the possible limitations of this study, there was something positive that came out of it.  One of the study’s authors offered “that if a patient asks whether his frequent marijuana use is getting in the way of his sex life, he will tell them that “it may not be the culprit. For most people, we tell them instead to go to the gym and lose 20 pounds”

References

  1. Sun AJ, Eisenberg ML. Association between marijuana use and sexual frequency in the United States: a population-based study. J. Sex Med 2017; 14:1342-1347.

 

Anticancer Properties of Cannabis and Cannabinoids

The anticancer effects of cannabis and individual cannabinoids are thought to be mediated via interaction of these compounds with their cognate receptors; cannabinoid receptor 1 (CB1) and CB2). CB1 receptors are widely distributed in the central nervous system (CNS) and brain whereas CB2 receptors are mainly found in the immune system with much lower and more restricted distribution in CNS (1,2)

Early in vitro studies using tumor cell lines and tumor xenograft mouse models suggest that cannabinoids can inhibit solid tumors and hematologic malignancies including  gliomas (brain tumors), adenocarcinomas of the lung, breast, colon, pancreas and melanoma and also myeloma and lymphoma (3-5).

Although not completely elucidated, the mechanism of action of cannabinoids as anticancer agents has been attributed to induction of programmed cell death or apoptosis (via interaction with CB1 receptors), inhibition of angiogenesis or blood vessel growth (reduction in the expression of endothelial growth factor and its receptors) and a decrease in the activity of matrix metalloproteinase 2 which can lead to decreased tumor cell invasiveness and metastasis (6-8).  In addition, cannabinoids possess potent anti-inflammatory and antioxidant properties that can also help to combat cancer (9). Finally, cannabinoids administered in combinations with conventional chemotherapy agents or radiation treatment have been observed to enhance antitumor activity (10-12).

While these preliminary findings are encouraging, much more basic research must be performed to identify the actual anticancer/anti-tumor action of cannabinoids and the individual cancer indications that would benefit most from their use. Once these things are established, large scale controlled human clinical trials will be necessary for regulatory approval of these agents as cancer treatments.

References

  1. Howlett AC. The cannabinoid receptors. Prostaglandins Other Lipid Mediat 2002; 68-69: 619–31
  2. Van Sickle MD, Duncan M, Kingsley PJ, Mouihate A, Urbani P, Mackie K, Stella N,Makriyannis A, Piomelli D, Davison JS,Marnett LJ, Di Marzo V, Pittman QJ, Patel KD, Sharkey KA. Identification and functional characterization of brainstem cannabinoid CB2 receptors. Science 2005; 310: 329–32
  3. Velasco G, Galve-Roperh I, Sanchez C, Blazquez C, Guzman M. Hypothesis: cannabinoid therapy for the treatment of gliomas? Neuropharmacology 2004; 47:315–23.
  4. Velasco G, Sánchez C, Guzmán M. Towards the use of cannabinoids as antitumour agents. Nat Rev Cancer 2012; 12:436–44.
  5. McAllister SD, Soroceanu L, Desprez PY. The antitumour activity of plant-derived non-psychoactive cannabinoids. J Neuroimmune Pharmacol 2015; 10:255–67.
  6. Massi P, Solinas M, Cinquina V, Parolaro D. Cannabidiol as potential anti cancer drug. Br J Clin Pharmacol 2013; 75:303–12.
  7. Chakravarti B, Ravi J, Ganju RK. Cannabinoids as therapeutic agents in cancer: current status and future implications. Oncotarget 2014; 5:5852–72.
  8. Abrams DI, Guzman M. Cannabis in cancer care. Clin Pharmacol Ther 2015; 97:575–86.
  9. Abrams, DJ. Integrating cannabis into clinical cancer care. Curr Oncol. 2016; 23:S8-S14.
  10. Donadelli M, Dando I, Zaniboni T, et al. Gemcitabine/cannabinoid combination triggers autophagy in pancreatic cancer cells through a ros-mediated mechanism. Cell Death Dis 2011;2:e152.
  11. Torres S, Lorente M, Rodriguez-Fornes F, et al. A combined preclinical therapy of cannabinoids and temozolomide against glioma. Mol Cancer Ther 2011;10:90–103.
  12. Scott KA, Daigleish 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;13:2955–67.

Treating Cancer-Related Symptoms with Cannabis

In the 1970s, purified and synthetic cannabinoids were being evaluated as palliative treatments for cancer related symptoms (1). One of the earliest recognized clinical indications for cannabinoids was cancer induced nausea and vomiting (CINV) [2].

A 1988 prospective open label trial found that inhaled cannabis effectively controlled CINV in 78% of 56 cancer patients who had inadequate control of nausea and vomiting with conventional anti-emetics (3). Also, a later report that evaluated 30 trials and over 1300 participants determined that synthetic THC molecules such as nabilone and dronabinol were more effective than conventional anti-emetics in controlling acute CINV (2). This led to the early approval of dronabinol and nabilone as treatments for CINV but their use as a treatment for CINV has not been widespread (2,3)

A quick search of the clinical trials site www.clinical trials.gov revealed that there are no US clinical trials currently underway to further evaluate the use of Cannabis as a treatment for CINV.  Moreover, there are no natural Cannabis products e.g. extracts, sprays etc, on the market today that have received US Food and Drug Administration (FDA) approval as a treatment for CINV.

Inhaled Cannabis, and extracts containing THC and CBD have been clinically found to be more effective in treating cancer-related neuropathic pain than placebo (3, 4) but their effectiveness compared with conventional pain medications is uncertain (2). Yet, despite this, GW Pharma’s Sativex® (an extract that contains 1:1 ratio of Δ-9-tetrahydrocannabinol (THC) and cannabidiol [CBD]) is an approved treatment for cancer-related pain in 27 countries outside of the US (5).

There are currently 4 US clinical trials in (various phases) that are underway to determine the effects on Sativex® on advanced cancer pain and chemotherapy-induced neuropathic pain (Table 1). Regulatory experts expect Sativex® to garner FDA approval for both indications.

References

  1. Guzman M, Duarte MJ, Blazquez C, et al. A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer 2006; 95:197-203.
  2. Tramer MR, Carroll D, Campbell FA, Reynolds DJ, Moore RA, McQuay HJ. Cannabinoids for control of chemotherapy induced nausea and vomiting: quantitative systematic review. BMJ 2002; 323:16-21.
  3. Bowles DW, O’Bryant CL, Camidge DR, Jimeno A. The intersection between cannabis and cancer in the United States. Critical Reviews in Oncology/Hematology 2012; 83:1-10
  4. Notcutt W, Price M, Miller R, et al.  Initial experiences with medicinal extracts of cannabis for chronic pain: results from 34 ‘N of 1’ studies. Anaesthesia 2004; 59:440-452.
  5. https://www.gwpharm.com/products-pipeline/sativex  Accessed July 12, 2017

 

Cannabis Extracts, Cannabinoids and Cancer Treatment

There is a growing body of evidence that cannabinoids may have anti-tumor and cancer–fighting effects (1, 2).

Numerous studies have demonstrated inhibition of tumor growth in vitro and in animal models of disease for a variety of cancers including glioblastoma, breast, prostate, thyroid, colon, skin, pancreatic, leukemia and lymphoma (3).

The exact mechanism by which cannabinoids exert their anti-tumor effects is thought to occur via suppression of proliferative cell signaling pathways, inhibition of angiogenesis (blood vessel formation) and cell migration, stimulation of apoptosis (programmed cell death) and induction of autophagy (intracellular degradation) [3, 4].  Interestingly, cannabinoid receptors CB1 and CB2 have been found in higher concentrations on tumor cells than on surrounding normal tissue for a variety of cancers (5, 6).  Also, several studies suggest that cannabinoids may selectively inhibit tumor cell growth and proliferation while sparing normal tissue (3, 7).

Although cannabinoids exhibit possible anti-tumor effects, only a single Phase 1  clinical trial that assessed the safety and efficacy of THC in 9 patients with treatment refractory glioblastoma multiforme has been published (8).

However, at present, there are only two Phase 2 clinical trials underway or completed to assess the effect of cannabis extracts on solid tumor growth (NCT02255292) and glioblastoma (NCT01812603).  Clearly, more clinical studies are necessary to determine whether or not Cannabis extracts or different cannabinoids (singly or in combination) can be used as safe and effective cancer treatments for solid tumors.

References

  1. Bowles DW, O’Bryant CL, Camidge DR, Jimeno A. (2012) The intersection between cannabis and cancer in the United States. Critical Reviews in Oncology/Hematology 83(1):1-10.
  2. Lynch ME, Campbell F. (2011) Cannabinoids for treatment of chronic non-cancer pain; a systematic review of randomized trials. British Journal of Clinical Pharmacology 72(5):735-744.
  3. Pisanti S, Malfitano AM, Grimaldi C, et al. (2009) Use of cannabinoid receptor agonists in cancer therapy as palliative and curative agents. Best Practice & Research. Clinical Endocrinology & Metabolism 23(1):117-131.
  4. Salazar M, Carracedo A, Salanueva IJ, et al. (2009) Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells. The Journal of Clinical Investigation 119(5):1359-1372.
  5. Caffarel MM, Andradas C, Mira E, et al. (2010) Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition. Molecular Cancer 9:196.
  6. Qamri Z, Preet A, Nasser MW, et al. (2009) Synthetic cannabinoid receptor agonists inhibit tumor growth and metastasis of breast cancer. Molecular Cancer Therapeutics 8(11):3117-3129.
  7. Flygare J, Sander B. (2008) The endocannabinoid system in cancer-potential therapeutic target? Seminars in cancer biology 18(3):176-189.
  8. Guzman M, Duarte MJ, Blazquez C, et al. (2006) A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer 95(2):197-203.