Hi Everyone,
A recent study (2008) observed a statistically significant link between HPV-positive oral cancer and marijuana use. The paper sites other research linking cannabinoids found in Marijuana (Cannabis) to suppression of the immune system. Future studies will need to be conducted to confirm the link between HPV-16, marijuana use and oral cancer.
I have taken excerpts and literature sited from the paper that pertained to this topic I thought were pertinent. All of the words below the links and title of the study were taken directly from the paper.
If you feel overwhelmed by the scientific language of these excerpts, the take home message I hope to get out to you is this: if you have ever had HPV-16 and you want to stay well, it is my personal opinion based on what I have read in this paper that you should not smoke marijuana (I personally have nothing against the plant or the act - just the consequences).
Why wait for studies to get funded and conducted, conclusive evidence to get published, and for doctors to become informed of the conclusive link? Most likely that will take longer than the average survival rate for a person diagnosed with oral cancer....
See subsequent posts for details...
Edited August 18, 2008 at 1:25 am
http://www.oralcancerfoundation.org/hpv/index.htm
http://www.oralcancerfoundation.org/hpv/pdf/100-6_risk_Gillison.pdf
Distinct Risk Factor Profiles for Human
Papillomavirus Type 16 – Positive and Human
Papillomavirus Type 16 – Negative Head and
Neck Cancers
Maura L. Gillison , Gypsyamber D ’ Souza , William Westra , Elizabeth Sugar , Weihong Xiao ,
Shahnaz Begum , Raphael Viscidi
HPV-16 was detected in 92 of 240 case subjects. HPV-16 – positive HNSCC was independently associated
with several measures of sexual behavior and exposure to marijuana but not with cumulative measures
of tobacco smoking, alcohol drinking, or poor oral hygiene. Associations increased in strength with
increasing number of oral sex partners ( P trend = .01) and with increasing intensity (joints per month, P trend =
.007), duration (in years, P trend = .01), and cumulative joint-years ( P trend = .003) of marijuana use. By contrast,
HPV-16 – negative HNSCC was associated with measures of tobacco smoking, alcohol drinking, and poor
oral hygiene but not with any measure of sexual behavior or marijuana use…………………..
There is insufficient evidence to either implicate or exonerate
marijuana as a carcinogen in humans
( 28 ). In this study, marijuana
use was strongly associated with HPV-16 – positive HNSCC. By
contrast, no association between marijuana use and HNSCC was
observed in a California cohort study
( 29 ) or in three previous
case – control studies ( 22 , 30 , 31 ).
A dose – response relationship
between marijuana use and HNSCC that was reported in a single
hospital-based case – control study
( 32 ) has been questioned ( 30 )
because of the low prevalence of ever marijuana use (7%) among
the blood-donor control subjects. In our study, the prevalence of a
year or more of marijuana use among control subjects (16%, Table
4 ) was similar to that observed in a previously published populationbased
study (approximately 18%; 30) that reported no association
between marijuana use and HNSCC. In this study, ACASI
technology allowed us to measure lifetime cumulative marijuana………………..
It is biologically plausible that marijuana could act to promote the
development of HPV-positive HNSCC. Carcinogens in marijuana
smoke, like those in tobacco smoke ( 34 ), can induce molecular
alterations of the airway epithelium
( 35 , 36 ). However, although a
pathogenic role for DNA-damaging carcinogens in marijuana
among HPV-16 – positive cases is possible, the known immunomodulatory
effects of cannabinoids may be more relevant for a virally mediated cancer. Cannabinoids bind to receptors (CB2)
expressed on B cells, natural killer cells, macrophages, dentritic
cells, and T cells, including those in human tonsillar tissue ( 37 ).
Endogenous cannabinoids are increasingly being recognized as
important immunomodulatory compounds that act in a paracrine
fashion to alter responses in the local microenvironment. In animal
models, cannabinoids suppress T helper (T H -1) proinfl ammatory
cytokines (eg, interleukin 12 and interferon gamma) while
augmenting production of T H -2 anti-infl ammatory cytokines (eg,
interleukins 4 and 10) ( 38 , 39 ). As a result, cannabinoids suppress
humoral and cell-mediated immune responses, reduce host cell
resistance to intracellular (eg, Listeria, legionella) and viral
(eg, herpes simplex virus) pathogens
( 40 ), and may also suppress antitumor
immunity ( 41 , 42 ). Preliminary studies indicate that cannabinoids
may alter immune responses in humans ( 43 ). For instance,
in marijuana smokers, the function of alveolar macrophages ( 44 ) is
impaired, and CD4 and natural killer cell numbers and lymphocyte
proliferative responses are suppressed ( 45 ). Cannabinoid derivatives
are in development for treatment of chronic infl ammatory
disease in human subjects ( 38 , 46 ). It is therefore biologically possible
that cannabinoids promote progression of an HPV-positive
HNSCC at multiple steps, including by increasing the risk of
infection upon exposure, promoting persistence of an infection,
and inhibiting antitumor immunity………….
The data presented in this manuscript are the first, to
our knowledge, to suggest that marijuana use may be a cofactor for
HPV-16 – mediated carcinogenesis in the head and neck; thus,
these results will need to be confirmed in other populations.
36. Darling MR , Learmonth GM , Arendorf TM . Oral cytology in cannabis
smokers . SADJ . 2002 ; 57 ( 4 ): 132 – 135 .
37. Berglund BA , Boring DL , Howlett AC . Investigation of structural analogs
of prostaglandin amides for binding to and activation of CB1 and CB2
cannabinoid receptors in rat brain and human tonsils . Adv Exp Med Biol.
1999 ; 469 : 527 – 533 .
38. Klein TW . Cannabinoid-based drugs as anti-infl ammatory therapeutics .
Nat Rev Immunol . 2005 ; 5 ( 5 ): 400 – 411 .
39. Klein TW , Newton C , Larsen K , et al . The cannabinoid system and
immune modulation . J Leukoc Biol. 2003 ; 74 ( 4 ): 486 – 496 .
40. Cabral GA , Dove Pettit DA . Drugs and immunity: cannabinoids and their
role in decreased resistance to infectious disease . J Neuroimmunol . 1998 ;
83 ( 1 – 2 ): 116 – 123 .
41. Zhu LX , Sharma S , Stolina M , et al . Delta-9-tetrahydrocannabinol inhibits
antitumor immunity by a CB2 receptor-mediated, cytokine-dependent
pathway . J Immunol . 2000 ; 165 ( 1 ): 373 – 380 .
42. McKallip RJ , Nagarkatti M , Nagarkatti PS . Delt a-9- tetrahydrocannabinol
enhances breast cancer growth and metastasis by suppression of the antitumor
immune response . J Immunol . 2005 ; 174 ( 6 ): 3281 – 3289 .
43. Roth MD , Baldwin GC , Tashkin DP . Effects of delt a-9-tetrahydrocannabinol
on human immune function and host defense . Chem Phys Lipids .
2002 ; 121 ( 1 – 2 ): 229 – 239 .
44. Baldwin GC , Tashkin DP , Buckley DM , Park AN , Dubinett SM ,
Roth MD . Marijuana and cocaine impair alveolar macrophage function
and cytokine production . Am J Respir Crit Care Med . 1997 ; 156 ( 5 ):
1606 – 1613 .
45. Pacifi ci R , Zuccaro P , Farre M , et al . Combined immunomodulating
properties of 3,4-methylenedioxymethamphetamine (MDMA) and cannabis
in humans . Addiction . 2007 ; 102 ( 6 ): 931 – 936 .