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does cbd help hpv

In one large case series study investigating the effects of CBD on anxiety and sleep, the results show CBD helps improve sleep and/or anxiety in clinical populations. Similarly, CBD can further support cervical cancer patients by reducing stress, anxiety, depression while also helping to promote REM sleep that is thought to help improve overall mood.

During the early stages of cervical cancer, there are often no symptoms present. During later stages, when the cervical cancer is more advance, the most common symptoms include:

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Adenocarcinoma:
Refers to cancer cells that form in the cells that produce mucus.

CBD as a Complementary Treatment for cervical cancer

Scientific and anecdotal evidence both suggest that CBD can support cervical cancer patients, especially by helping to reduce chemotherapy-induced neuropathic pain, inflammation, nausea and vomiting. If you or a loved one are suffering from cervical cancer and want to try CBD, talk to your medical practitioner first. He or she can help put together a plan that includes CBD along with other treatment options to help you deal with your symptoms safely and effectively.

Cervical cancer has four stages:

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Non-Pharmaceutical Interventions

It is thought that various strains for the human papillomavirus (HPV), a sexually transmitted infection, are one of the key factors that play a role in the development of most cervical cancers. This is because, when some women are exposed to the HP virus, and despite the immune system trying to prevent the virus from doing harm, in some women, the virus survives for years. This often contributes to a process in which this causes some cervical cells to become cancerous, causing cervical cancer to develop.

They concluded that, although more research is needed, their data suggests that CBD, rather than crude Cannabis sativa extracts, prevent cell growth and induce cell death in cervical cancer cell lines. This makes CBD a novel potential cervical cancer therapy.

In the only prior investigation to include HIV-seropositive women, marijuana use was not associated with cervical HPV among 146 HIV-seropositive drug users but a strong positive association was observed among 73 HIV-seronegative drug users.(8) While the reason for the differences in findings between this prior study and the current one is unknown, the current investigation was considerably larger, and differences in study design or population might also be relevant.

HPV and SIL prevalence were studied using multivariate logistic regression models that incorporated generalized estimating equations (GEE) with an exchangeable correlation structure in order to analyze these outcome data across HPV types and visits. Time to incident HPV detection and clearance were each analyzed using Cox proportion models that employed the Wei Lin Weissfeld (WLW) marginal model approach to adjust the results for possible correlations between multiple HPV infections. As recently reported, statistical power is substantially increased in studies of HPV and SIL when repeated observations are considered in the analysis, even after appropriately adjusting for the correlation between serial test results.(14) Had we instead used standard logistic regression and/or Cox models to incorporate these repeated observations over time the effect estimates would have been similar, but the P-values and confidence intervals would have been incorrect. (14) Incidence/clearance of SIL was studied using standard Cox models, since the development and clearance of SIL are each an individual event (we did not study recurrence). In our GEE, WLW, and standard Cox models we used time-dependent covariates including recent marijuana use, CD4+ T-cell count, age, number of sexual partners in the past six months, tobacco use, and cervical treatment. Race/ethnicity was a time-independent covariate.

In summary, our investigation found no positive associations between marijuana use and cervical HPV or SIL. These findings are comforting given the high prevalence of marijuana use in HIV-seropositive and other populations, but we caution that we could not directly investigate the relationship between marijuana use and invasive cervical cancer.

Marijuana use was recently reported to have a positive cross-sectional association with human papillomavirus (HPV)-related head and neck cancer. Laboratory data suggest that marijuana could have an immunomodulatory effect. Little is known, however, regarding the effects of marijuana use on cervical HPV or neoplasia. Therefore, we studied the natural history (ie, prevalence, incident detection, clearance/persistence) of cervical HPV and cervical neoplasia (ie, squamous intraepithelial lesions [SIL]) in a large prospective cohort of 2584 HIV-seropositive and 915 HIV-seronegative women. Marijuana use was classified as ever/never, current/not current, and by frequency and duration of use. No positive associations were observed between use of marijuana, and either HPV infection or SIL. The findings were similar amongst HIV-seropositive and HIV-seronegative women, and in tobacco smokers and non-smokers. These data suggest that marijuana use does not increase the burden of cervical HPV infection or SIL.

Discussion

There have been few studies of marijuana use and cervical HPV detection, and these have had inconsistent results. A Kaiser Permanente cohort study found marginally increased risk of cervical cancer in ever marijuana users with no history of tobacco use (RR=1.4, 95%CI=1.0–2.1),(16) but that study did not control for certain relevant (e.g., sexual) cofactors. A large cross-sectional study of HPV found a strong relationship of cervical HPV prevalence with “marijuana and/or [unspecified] related substance use”.(7) However, the inability to distinguish the type of drug was an important limitation, since our group(15) and others(8) have reported that crack/cocaine use is associated with HPV and cervical neoplasia. A cross-sectional study of adolescent women found no association of marijuana with cervical HPV prevalence following adjustment for other risk factors.(9)

A recent cross-sectional case-control investigation reported that marijuana use may be associated with increased odds of human papillomavirus (HPV)-positive, but not HPV-negative head and neck squamous cell cancer (HNSCC).(1–3) While carcinogens in marijuana have been shown to induce molecular(4) and cellular(5) abnormalities, carcinogenic agents might be expected to affect both HPV-positive and HPV-negative cancers. Therefore, attention has been drawn to laboratory studies showing that cannabinoids may be immunomosuppressive,(6) which if correct, would raise the possibility that marijuana might increase the risk of HPV-associated cancer by increasing susceptibility to infection when exposed and/or increasing the likelihood of HPV persistence. A systemic effect of marijuana use on host immune status might also be expected to affect risk of cervical HPV infection and neoplasia but this question has not been well explored. A cross-sectional study found a relation of cervical HPV prevalence with “marijuana and/or [unspecified] related substances”,(7) and a longitudinal study found that recent marijuana use was associated with risk of incident HPV infection among 73 HIV-seronegative but not 146 HIV-seropositive subjects.(8) Another study, however, found no association following adjustment for other risk factors.(9) To build upon these prior data, we examined the effects of marijuana use on the natural history of cervical HPV and neoplasia in a large, long term cohort of HIV-seropositive and HIV-seronegative women.

We conducted a large prospective study of marijuana use and the natural history of HPV and cervical neoplasia, but no positive associations were detected, even when frequent, long-term marijuana use was considered. These results were similar among both HIV-seropositive and HIV-seronegative women, and independent of smoking status. Our findings, therefore, do not support recent hypotheses that marijuana might have a systemic immunomodulating effect that increases the burden of cervical HPV or disease.(8)

Methods

Specimens and data were obtained from the Women’s Interagency HIV Study (WIHS), a cohort of 2,793 HIV-seropositive and 959 HIV-seronegative women.(10, 11) Participants underwent semiannual clinical visits that included an interviewer-administered questionnaire, physical and gynecologic examination that included Pap smear, and cervicovaginal lavage (CVL) for HPV DNA testing.(12) History of past and recent marijuana and other drug use was assessed at each semiannual visit. Data from 209 HIV positive and 44 HIV negative women with no cervix at baseline were excluded from analysis and 121 women with hysterectomy during follow-up were censored at the visit prior to hysterectomy. HPV DNA was detected utilizing a well established L1 consensus primer MY09/MY11/HMB01 polymerase chain reaction (PCR) assays, that can identify over 40 individual HPV types including HPV6/11/13/16/18/26/31/32/33/34/35/39/40/42/45/51/52/53/54/55/56/57/58/59/61/62/64/66/67/68/69/70/71/72/73/74/81/82/83/84/85/89.(13)

Table 1 shows the associations of marijuana use with detection of HPV and SIL. All models were adjusted for age, race, HIV status, CD4+ T-cell count, number of sexual partners in the past six months, tobacco use, and cervical treatment. We observed no relationship between marijuana use and prevalent HPV, including ever use (odds ratio [OR]=1.00, 95% confidence interval [CI]=0.90–1.11), current use (OR=0.98, 95%CI=0.90–1.07), current daily use (OR=0.91, 95%CI=0.77–1.07), or long term frequent use (defined as marijuana use>once per week for >3 years: OR=0.91, 95%CI=0.7–1.18). Likewise, there were no associations between marijuana use and the incident detection of HPV or SIL ( Table 1 ). The only significant association was the higher (not lower) rate of HPV clearance in long term frequent marijuana users (hazard ratio [HR]=1.47, 95% CI=1.09–1.98) relative to never-users. Results were similar when examined only among HIV-seronegative or HIV-seropositive women, when limited to those who never smoked tobacco, when only oncogenic or non-oncogenic HPV were considered, or following adjustment for recent cocaine use (a factor associated with increased HPV infection in an earlier WIHS study)(15) (data not shown).

Does cbd help hpv

Common warts are typically harmless and eventually disappear on their own. Still, most people choose to have them removed because they find them bothersome or embarrassing.

Why Some People Are Turning to CBD for Warts

However, most forms are spread by casual skin contact or through shared objects, such as towels or washcloths. They can also spread to different parts of the body by nail-biting or shaving.

Can CBD help with warts, and if so, how?

People at higher risk of developing common warts include children and young adults, as their bodies may not have built up a robust immunity to the virus.