NOVA Heath Recovery Ketamine Treatment Center | Call 703–844-0184 for a Ketamine Treatment | Alexandria, Va 22306 | 7 days a week and evening appointments as well! We also evaluate depression, ADHD, PTSD. Intranasal Ketamine available. The email is EMAIL@novahealthrecovery.com
Learn How Ketamine Can Treat Post Traumatic Stress Disorder
For decades, ketamine has been used as a medicinal intervention for treating depression, anxiety, mood disorders, and post-traumatic stress disorder (PTSD). While most ketamine advocates recognize its therapeutic potential for treating depression, the many benefits available to those suffering from PTSD are less understood.
Do you or a loved one suffer from post-traumatic stress disorder? If so, ketamine infusion therapy may be able to help alleviate your symptoms and provide the relief you need. However, public knowledge about medicinal ketamine is lacking. In this article, we go over everything there is to know about ketamine for treating PTSD.
PTSD 101: What You Need to Know
Post-traumatic stress disorder has a medical diagnostic code of ICD-10, which is the code used for reimbursing treatment through your insurance provider. PTSD, unlike other mental illnesses, is characterized by its triggering from a single or series of traumatic events. This explains why PTSD is common among military veterans and first responders.
According to a summary article from Mayo Clinic, PTSD is a mental health condition triggered by a terrifying experience. The sufferer subsequently experiences flashbacks, night terrors, and anxiety attacks that they cannot control as a result of the event. It takes a significant amount of time, therapy, and self-care to overcome the trauma of PTSD.
There is no known cure for PTSD. However, many experimental medicinal interventions are breaking ground when it comes to finding a cure. For example, the psychoactive drugs MDMA and ketamine have both been studied for their potential to alleviate the negative effects of PTSD.
Ketamine Infusion Therapy
Since the early 2000s, ketamine has gained popularity among medical providers for its application in infusion therapies. In recent years, clinics all around the world have embraced the healing power of ketamine by offering ketamine infusion therapy. This unique therapy involves one or more intravenous injections of ketamine under the supervision of an anesthesiologist.
What Is Ketamine?
Although ketamine has garnered a reputation as a party drug, its primary value is in its ability to provide fast-acting and potent relief for those with chronic pain issues. Ketamine was first synthesized in the 1960s and was later adopted as an anesthetic in veterinary medicine by the end of the decade. However, use in humans was initially sparse.
Ketamine is both an analgesic and anesthetic drug, which means its primary quality is to reduce or prevent pain. This makes ketamine highly effective for treating major depressive disorder, chronic back pain, and PTSD.
Ketamine and PTSD
Ketamine infusion clinics across the United States are now offering specialty treatments for those suffering from PTSD. For example, the renowned Ketamine Clinics of Los Angeles has treated hundreds of PTSD patients over the years. Led by Dr. Steven Mandel, M.D., the team at Ketamine Clinics of LA has a proven track record of helping relieve the pain of PTSD.
An increasing amount of scientific research has proven that ketamine is effective in treating PTSD. Most notably, a breakthrough 2014 study in JAMA Psychiatry discovered that a single intravenous subanesthetic dose of ketamine resulted in “significant and rapid reduction in PTSD symptom severity.”
Over the past few years, many articles and news reports have heralded ketamine as a potential wonder drug for treating PTSD. A recent article published by Medscape discussed how a team of researchers at the Icahn School of Medicine at Mount Sinai in New York City used ketamine to fight depressive symptoms in patients with PTSD and severe depression.
Is Ketamine Safe for PTSD?
There is no doubt that ketamine is a novel treatment for many PTSD sufferers. Since it is a relatively new medicinal intervention, there is some skepticism within the medical community regarding whether it is safe for human use. However, many of these doubts have been quelled over the years thanks to numerous studies and experiences that have proven its safety.
The most compelling evidence suggesting that ketamine infusion is safe in humans comes from a 2014 clinical study. This study managed to safely administer low doses of ketamine to treat neuropathic pain states in adults. Over the two-week monitoring period, the patients exhibited numerous benefits while experiencing only marginal or negligible side effects.
It should be noted that ketamine is not safe if taken recreationally. Since its inception, ketamine has gained a reputation as a party drug for its ability to induce dissociative states and euphoria. However, ketamine is not safe to use unless administered by a licensed physician. It is possible to overdose on ketamine, and the side effects of using high doses of ketamine can be fatal.
Ketamine: A PTSD Prevention Tool?
Interestingly, ketamine has found success as a tool for preventing the onset of PTSD. In one case, a research team gave a family of mice a low dose of ketamine before exposing them to electric shocks. Usually, mice exhibit symptoms of PTSD after being exposed to such a severe stressor. However, the mice that were given ketamine did not exhibit these symptoms at all.
Typically, traumatized mice freeze up when they are placed back in the cage in which they were shocked. In this case, the mice who were sedated with ketamine did not freeze when placed in the cage or froze for a significantly reduced duration. This led the research team to believe that ketamine may have value in both preventing and treating PTSD in humans.
Is Ketamine Right for You?
Ketamine may be an appropriate treatment option for you if you have treatment-resistant PTSD. In other words, you must first be diagnosed with PTSD and have sought the traditional frontline treatments for the condition before considering ketamine infusion therapy. We recommend speaking with your doctor about your PTSD symptoms and the appropriate therapies available to you. Usually, SSRIs or benzodiazepine pharmaceutical drugs, in conjunction with cognitive behavioral therapy (CBT) is the first method of treatment. However, if you do not respond well to this treatment option you should consider seeking ketamine therapy.
Rates of opioid overdose hospitalizations increased between 2003 and 2014 in the United States, primarily for Caucasians in the South; factors associated with a higher mortality from opioid overdose also include younger age and male gender, according to a study to be presented at the 2018 World Congress on Pain, held September 12-16 in Boston, Massachusetts.
Considering the prevalence of opioid overdose and poisoning in the United States, and the accompanying high rates of addiction and death, researchers analyzed Nationwide Inpatient Sample data on opioid overdose from 2003 to 2014 to identify predictors of mortality, regional disparities, cost of inpatient hospital stay, and yearly trends. The data showed 149,483 patients who were discharged with a primary or secondary opioid poisoning diagnosis (ICD-9 Code 965.xx) in the United States during this time period. Binary logistic regression was used to study region, race, sex, and age as independent predictors of mortality.
Trends and Predictors of Mortality for US Opioid Overdoses from 2003 to 2014
Most opioid overdose patients were male and lived in the Southern United States (39.3%).
The following article is part of conference coverage from the IASP 2018 conference in Boston, Massachusetts.Clinical Pain Advisor’s staff will be reporting breaking news associated with research conducted by leading experts in pain medicine. Check back for the latest news from IASP 2018.
Rates of opioid overdose hospitalizations increased between 2003 and 2014 in the United States, primarily for Caucasians in the South; factors associated with a higher mortality from opioid overdose also include younger age and male gender, according to a study to be presented at the 2018 World Congress on Pain, held September 12-16 in Boston, Massachusetts.
Considering the prevalence of opioid overdose and poisoning in the United States, and the accompanying high rates of addiction and death, researchers analyzed Nationwide Inpatient Sample data on opioid overdose from 2003 to 2014 to identify predictors of mortality, regional disparities, cost of inpatient hospital stay, and yearly trends. The data showed 149,483 patients who were discharged with a primary or secondary opioid poisoning diagnosis (ICD-9 Code 965.xx) in the United States during this time period. Binary logistic regression was used to study region, race, sex, and age as independent predictors of mortality.
Of the 149,220 patients admitted for opioid overdose, 2.6% died. The median age of these overdose patients was 47 years old, and 81.1% were Caucasian. Most opioid overdose patients were male and lived in the Southern United States (39.3%). The Northeast had 17.5% of opioid overdose cases, compared with 21.3% in the West and 21.9% in the Midwest. Yearly hospital admissions for opioid overdose have increased over the study timespan, from 7864 overdoses in 2003 to 15,165 overdoses in 2014. The total cost per inpatient admission also increased to $37,281 in 2014 compared with $17,156 in 2003.
Study investigators concluded that “further prospective studies are warranted to better understand the increasing [opioid overdose] admission rates, and an effective, targeted approach should be developed for [use] within the higher mortality demographic.”
Having a hepatitis C virus (HCV) infection, witnessing a friend or others experiencing a drug overdose, and having a history of frequent buprenorphine treatment are factors that may predict the risk for opioid drug overdose in high-risk opioid users, according to a study published in Addictive Behaviors.
Participants were recruited from an ongoing study in which the efficacy of distributing naloxone kits for reducing opioid overdose was assessed (N=247). Heroin and prescription opioid use were reported by 86.5% of participants, and all patients had reported current or past opioid misuse within 6 months of enrollment. The researchers sought to identify medical, psychosocial, and opioid use characteristics that were predictive of opioid overdose.
Patient characteristics data were obtained from responses on the baseline 30-item Opioid Use Questionnaire, which assessed chronic medical conditions, past and current opioid misuse, sexually transmitted infections (STIs), buprenorphine treatment frequency, and intensive outpatient and rehabilitation treatment history. Participants and family members or friends attended a baseline appointment and naloxone training.
Individuals who were white comprised a significant majority of individuals reporting a past opioid overdose when compared with blacks (96.2% vs 3.8%, respectively; P =.005). More participants who had experienced an opioid overdose in the past 6 months reported using heroin vs prescription opioids only (95.2% vs 4.8%, respectively; P =.001). Participants with a friend who had died from an overdose were also more likely to experience an overdose themselves (89.6% vs 10.4%; P=.001).
In the adjusted analysis, the patient characteristic most associated with experiencing a nonfatal opioid overdose was witnessing a friend overdose (odds ratio [OR] 4.21; 95% CI, 1.99-8.89). Witnessing others overdose (OR 1.42; 95% CI, 1.11-1.82) and having a chronic HCV infection (OR 2.44; 95% CI, 1.20-4.97) were also associated with a higher risk of reporting a prior opioid overdose. Reporting a higher buprenorphine treatment frequency was associated with a greater odds of opioid overdose (OR 1.55; 95% CI, 1.17-2.07), and reporting a high frequency of methadone treatments was associated with a reduction in overdose odds (OR 0.67; 95% CI, 0.49-0.91).
The study was limited by its potential for recall and social desirability bias because of the self-reported nature of the collected participant data.
“Given the high rates of nonfatal opioid overdose, this suggests the need for expanded overdose training and distribution of naloxone,” concluded the study authors.
Buprenorphine/naloxone treatment initiated in the emergency department (ED) and prolonged for 10 weeks in primary care improved treatment engagement and reduced opioid use compared with referral or brief intervention.1
“This study represents a new paradigm for ED-initiated treatment of opioid use disorder with referral for ongoing care,” stated lead investigator Gail D’Onofrio, MD, in an interview with Clinical Pain Advisor. She noted that the approach tested in the study, in which an ED clinician initiates treatment and refers patients for follow-up, is similar to that used in other chronic disorders such as hypertension or hyperglycemia. Opiate use disorder was found to be more prevalent in patients who had presented to emergency departments than in the general population.2
The study presented a long-term follow-up of outcomes from the investigators’ previous work published in JAMA.3 The JAMA study randomly assigned 329 opioid-dependent patients to 1 of 3 interventions: screening and referral to treatment (referral); screening, brief intervention, and facilitated referral to community-based treatment services (brief intervention); or screening, brief intervention, ED-initiated treatment with buprenorphine/naloxone, and referral to primary care for 10 weeks of continued buprenorphine/naloxone treatment (buprenorphine).
Results of this study showed that at 30 days after treatment randomization, patients in the buprenorphine group were more likely to be involved in addiction treatment than those who received the other interventions. In addition, self-reported illicit opioid use and use of inpatient addiction treatment services were less prevalent in patients who had been prescribed buprenorphine than in patients in the other 2 groups.
The current study involved 88% of the same patients (n=329) who contributed data at a minimum of 1 follow-up assessment conducted at 2, 6, and/or 12 months after the ED intervention. Results showed that at 2 months, engagement in addiction treatment was more common in the buprenorphine group (68/92 [74%]; 95% CI, 65-83) than in those who received referral (42/79 [53%]; 95% CI, 42-64) or brief intervention (39/83 [47%]; 95% CI, 37-58; P <.001). Patients randomly assigned to buprenorphine had fewer self-reported days of illicit opioid use (1.1; 95% CI, 0.6-1.6) compared with the referral group (1.8; 95% CI, 1.2-2.3) or the brief intervention group (2.0; 95% CI, 1.5-2.6; P =.04]. No statistically significant differences for those outcomes were present at 6- or 12-month follow-ups.
Dr D’Onofrio told Clinical Pain Advisor that her research group hoped to offer alternative best practices to emergency physicians, who are not typically involved with continued care of patients with opioid use disorders. “Most EDs observe patients after recovery from overdose, but discharge them with at best a list of programs in the community for help. They do not make direct linkages to treatment programs or providers and do not initiate buprenorphine, similar to when patients present with any other problem related to opioid use disorder,” she said.
Summary and Clinical Applicability
The researchers noted that despite its limitations, the study indicates that ED-initiated buprenorphine/naloxone treatment combined with referral for ongoing treatment in primary care is effective at increasing participation in addiction treatment and reducing self-reported illicit opioid use while treatment is continued. “For 27% of the enrolled ED patients, the index ED visit represented their first treatment contact,” they wrote. “Thus, the ED visit is an opportunity to engage patients with opioid use disorder in effective medication-assisted treatment.”
The study was conducted at only 1 ED and 1 site for primary care, both in the same academic medical center, and thus may not be generalizable to other settings.
Thirty-nine patients of the original cohort were not included in the follow-up.
Data on engagement in addiction treatment were based on self-reports and not confirmed with providers.
Engagement in treatment was assessed at designated times, potentially leading to an underestimation, as patients may have been involved in treatment at other times.
Cannabis use in patients with early psychosis is a risk factor for relapse, a higher number of re-hospitalizations, and longer length of stay (LOS) in hospital, particularly in black male patients, according to study results published in Psychiatry Research.
Marco Colizzi, MD, of the National Institute for Health Research, Biomedical Research Centre, South London and Maudsley NHS Foundation Trust, and the department of psychosis studies, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, United Kingdom, and colleagues, conducted a chart review study at the Early Intervention Inpatient Unit of the South London and Maudsley NHS Foundation Trust, an inpatient facility that specializes in the care of individuals between the age of 18 and 35 experiencing a first episode of psychosis. All consecutive admissions to the facility in 2010 were included in the study. Patients with suspected or known acute substance intoxication or an organic cause for psychosis were excluded. Patients were followed for 6 years after initial inpatient admission. The investigators used negative binomial regressions to test for an effect of baseline cannabis use on the number of hospital readmissions and LOS during the 6-year follow-up period.
The study included 161 patients, 13 of whom (8.1%) had a second admission and 1 (0.6%) had a third within the same calendar year. Males made up 61% of the study population, whites 28%, black Africans/Caribbeans 50.7%, Asians 13.3%, and mixed ancestry 8%. Information on cannabis use was available for 141 of these patients. The researchers noted that 62.4% of patients had a lifetime history of cannabis use, 61.2% were tobacco users, 64.5% alcohol users, and 38.5% stimulant users. Their initial hospitalization lasted an average of 54.3 days, and over the following 6 years patients had an average of 2.2 hospital readmissions for a total of 197.4 days.
The analysis suggested that cannabis use significantly predicts the number of hospital readmissions over the 6-year follow-up period (P =.029). However, a further negative binomial regression that adjusted for the use of other psychoactive substances, as well as sociodemographic and other clinical characteristics at baseline, did not find significance for the effect of cannabis on the number of hospital readmissions (P =.072). A significant effect for cannabis use on LOS over the 6-year follow-up was also found (P =.001), and this remained significant even after adjusting for the use of other psychoactive substances (P =.044).
Other exploratory analyses looked at the effect of gender and ethnicity on the number of hospital readmissions and found a significant interaction between cannabis use and male gender on LOS (P =.034) and between lifetime cannabis use and the number of hospital readmissions over the follow-up period in patients of Afro-Caribbean origin (P =.049).
The investigators suggest that cannabis may have detrimental effects on psychosocial factors such as employment, quality of life, and on physical health, which may affect hospitalizations. They noted as well that experimental studies have shown that the primary psychoactive ingredient in cannabis can induce psychotic symptoms in otherwise healthy individuals.
HealthDay News — Cannabis use is associated with psychosis symptoms (PS) during adolescence, according to a research letter published online June 6 in JAMA Psychiatry.
Josiane Bourque, from the University of Montreal, and colleagues examined year-to-year associations between cannabis use and PS over four years among 3,720 adolescents who completed confidential annual surveys from age 13 to 16 years. A multilevel approach was used to test for within-person differences that inform on the extent to which increased cannabis use precedes an increase in PS and vice versa.
The researchers first tested a basic model containing only autoregressive paths, random intercepts, and within-time correlations across variables; this was followed by testing a transactional model that also contained cross-lagged correlations. The transaction model was favored in the Χ²-difference test. Statistically significant positive cross-lagged associations were revealed at every time point from cannabis use to PS reported 12 months later in the transactional model, exceeding the random intercepts of cannabis use and PS. These correlations were similar in size to the autoregressive link between PS from ages 15 to 16. There was a statistically significant association for PS at age 15 years with cannabis use at age 16 years.
“This analysis demonstrates a predominant association at the individual level of cannabis use frequency with increased PS, and not the opposite, in the general population at a developmental stage when both phenomena have their onset,” the authors write.
This analysis demonstrates a predominant association at the individual level of cannabis use frequency with increased PS (psychotic symptoms), and not the opposite, in the general population at a developmental stage when both phenomena have their onset. One limitation was that cannabis use and PS were not confirmed with clinician or collateral reports. However, previous work has shown positive predictive values ranging from 80% to 100% from 3 self-report items to identify interview-verifiable PS.5Furthermore, self-report is the most efficient way to assess substance use when there are no consequences to reporting because collateral reports and biologic measures are not sensitive to the sporadic nature of adolescent substance use.6
Considering that PS are associated with risk for psychosis, as well as nonpsychotic disorders, these results emphasize the need for targeted cannabis use prevention as jurisdictions revise their cannabis regulatory policies. Promoting evidence-based interventions and policies that reduce access to and demand for cannabis among youth could lead to population-based reductions in risk for major psychiatric conditions.
Patients who use medical marijuana may be more likely to use prescription drugs for both medical and nonmedical purposes, according to results published in the Journal of Addiction Medicine.
Previous studies found evidence that medical marijuana use reduces medical and nonmedical prescription drug use, but these new results contradict that hypothesis. The results highlight the need to target medical marijuana users in an effort to reduce nonmedical prescription drug use.
The study used simulations based on logistic regression analyses of data from the 2015 National Survey on Drug Use and Health. The researchers computed associations with adjusted risk ratios controlling for age, sex, race, health status, family income, and living in a state with legalized medical marijuana.
The results indicated that medical marijuana users were significantly more likely to report medical use of prescription drugs in the past 12 months compared with those who did not use medical marijuana (relative risk [RR], 1.62; 95% CI, 1.50-1.74).
People who used medical marijuana were also more likely to report nonmedical use of any prescription drug in the previous 12 months compared with people who did not use medical marijuana (RR, 2.12; 95% CI, 1.67-2.62). This risk was even more pronounced for pain relievers (RR, 1.95; 95% CI, 1.41-2.62), stimulants (RR, 1.86; 95% CI, 1.09-3.02), and tranquilizers (RR, 2.18; 95% CI, 1.45-3.16).
According to data from the Centers for Disease Control and Prevention, deaths from drug overdose have continued to increase in the United States in recent years, with more 600,000 reported from 2000 to 2016.1 Prescription opioids have been identified as a key factor driving this surge; approximately 63% of the 52,404 overdose deaths in 2015 involved an opioid.2
Various strategies have been introduced to address this crisis, including implementation of the CDC Guideline for Prescribing Opioids for Chronic Pain, as well as efforts to improve prescription drug monitoring programs and access to treatment for opioid use disorder. In the ongoing search for solutions, it has been suggested that access to medical cannabis may lead to a reduction in opioid use for pain management.3
n an analysis published in 2014, a 21% reduction in mean annual opioid overdose mortality was found in states with legalized medical cannabis.4 Other findings show that the use of prescriptions for numerous conditions decreased following the legalization of medical cannabis, but the greatest reduction was observed for medications indicated for pain treatment.5
Although these results may seem to support a link between increased access to cannabis and a reduction in prescription opioid use, findings from a study published in 2018 found otherwise (although this investigation focused on cannabis generally rather than legalized medical cannabis).6Researchers at Columbia University Medical Center and the National Institute on Drug Abuse used logistic regression models to analyze data from wave 1 (2001-2002) and wave 2 (2004-2005) of the National Epidemiologic Survey on Alcohol and Related Conditions.
Their analysis of more than 34,000 US adults revealed associations between cannabis use at wave 1 and increased use of nonmedical prescription opioids (odds ratio [OR], 5.78; 95% CI, 4.23-7.90) and opioid use disorder (OR, 7.76, 95% CI, 4.95-12.16) at wave 2, which remained significant after controlling for background characteristics of participants, including age, sex, anxiety or mood disorders, and family history of substance abuse.
Although these results do “not resolve the debate about associations between medical cannabis use, use of prescription opioids, and risks of opioid overdose mortality…. (t)he study is nonetheless an important contribution that balances the state-level analyses with individual level data,” wrote Dennis McCarty, PhD, a professor of public health and preventive medicine at Oregon Health & Science University, in an editorial about the study that appeared in the same issue of the American Journal of Psychiatry.3 He pointed to the large dataset and consistency of participants across waves as strengths of the study, and he cited the dated and self-reported nature of the data, as well as the lack of differentiation between medical and nonmedical cannabis use, as limitations.
“The contrasting associations from the state-level and the person-level analyses should serve as a caution to eager advocates and puzzled policymakers. It is too soon for science to provide deﬁnitive guidance,” added Dr McCarty.
“It is time, therefore, in states where cannabis use is authorized for adults, to build patient registries of cannabis use that link with medical records so that it is feasible to assess morbidity and mortality associated with the frequency, duration, and method [of use],” he wrote.
To further explore the implications of the new findings, Psychiatry Advisor interviewed Mark Olfson, MD, professor of psychiatry at Columbia University Medical Center, who is one of the authors of the study.6
Psychiatry Advisor:What are the top takeaways from your study?
Dr Olfson: As compared with adults who did not smoke marijuana, those who smoked marijuana were found 3 years later to be almost 6 times more likely to misuse prescription opioids and almost 8 times more likely to have an opioid use disorder.Even though [opioid problems did not develop in] most people who smoked marijuana at the start of the study, those who did were at a significantly higher risk [for these problems] developing than were those who did not smoke marijuana. Contrary to some previous reports that were based on population-level patterns, we found that marijuana use tends to increase rather than decrease the risk for prescription opioid use abuse or dependence.
Psychiatry Advisor:What are the overall treatment implications for mental health and pain clinicians?
Dr Olfson: We found that cannabis use, even among adults with moderate or severe pain, was associated with a substantially increased risk for problematic prescription opioid use 3 years later. Although this study was not designed to directly address questions over the appropriate role of medical marijuana in the management of chronic medical pain conditions, the results nevertheless suggest that pain specialists should consider vulnerabilities to addiction when deciding whether to recommend medical marijuana for their patients with persistent pain.
Psychiatry Advisor:What should be the focus of future research in this area?
Dr Olfson: We’re currently working on trying to understand precursors to fatal opioid overdoses. We’re focusing on trying to identify characteristics of patients with non-fatal opioid overdoses who are at the highest short-term risk for overdose death so that more can be done to interrupt this dangerous course by making active efforts to engage them in medication-assisted treatment.
Young adults who used cannabis 2 to 3 times per week were shown to be at increased risk for hypomania at age 22 to 23 years, according to the results of a recent study published in Schizophrenia Bulletin.
Participants from a UK birth cohort were assessed for frequency of cannabis use at age 17. In this study, cannabis use 2 to 3 times per week was considered frequent use. At age 22 to 23 years, participants responded to a postal survey that included the Hypomania Checklist Questionnaire-32 to evaluate manic symptoms.
Information about depression symptoms, psychotic symptoms, childhood abuse, and substance use were collected at various times throughout the participants’ lives. The association among these variables, hypomania, and cannabis use were assessed using path analysis.
After adjustment, frequent cannabis use was associated with subsequent hypomania (odds ratio [OR] 2.21). Weekly cannabis use (OR 2.87) was more strongly associated with hypomania compared with any cannabis use (OR 1.82).
In path analysis, cannabis use correlated well with subsequent hypomania after controlling for all pathways. Depression and psychotic symptoms did not mediate the association between hypomania and cannabis use. The association of subsequent hypomania with gender and childhood abuse were significantly mediated by cannabis use.
The study authors concluded that, “adolescent cannabis use is an independent risk factor for future hypomania, and the nature of the associations found is suggestive of a causal link, [al]though the gold standard for inferring causality of course remains intervention.”
After controlling for predisposing factors, frequent cannabis use was shown to be associated with an increased risk for major depressive disorder (MDD) and suicidal ideation, according to a recent twin study published in Lancet Psychiatry.
In this retrospective analysis, same-sex twin pairs (n=13,896; 6181 monozygotic and 7805 dizygotic) from the Australian Twin Registry were evaluated for associations between cannabis use patterns and MDD, suicidal ideation, and suicide plans or attempts. Samples were broken down into 1992 through 1993 (sample 1), 1996 through 2000 (sample 2), and 2005 through 2009 (sample 3). Association analyses were done in the full sample as well as in pairs of twins discordant for cannabis use at a single time point.
Cannabis use was highest in sample 3 (69.0%, n=2275/3299) followed by sample 2 (59.8%, n=3741/6255) and sample 1 (30.4%, n=1345/4432). Among cannabis users, early use (prior to 18 years for sample 1 and prior to 17 years for samples 2 and 3) and frequent use (≥100 times) were found in 21.3% and 15.9% of sample 1, 23.1% and 27.9% of sample 2, and 37.7% and 21.9% of sample 3.
Suicidal ideation was noted in 24.9% of sample 1, 26.3% of sample 2, and 26.2% of sample 3. MDD was found in 20.3% of sample 1, 28.3% of sample 2, and 24.7% of sample 3. After adjusting for covariates including sex, age, early alcohol or nicotine use, early dysphoric or anhedonic mood, conduct disorder, and childhood sexual abuse, monozygotic twins who used cannabis frequently had a higher risk for MDD (odds ratio [OR]: 1.98, 95% confidence interval [CI]: 1.11-3.53) and suicidal ideation (OR: 2.47, CI: 1.19-5.10) compared with the monozygotic twins who used cannabis less frequently.
After adjustment, early cannabis use was not significantly associated with MDD or suicidal thoughts and behaviors within monozygotic twins (OR: 1.17-2.00) but was within dizygotic twins (OR: 2.23-6.50). According to study authors, this may be indicative of shared genetic factors contributing to the association.
The study authors concluded that they were “unable to exclude the possibility that frequent cannabis use might increase risks for MDD and suicidal ideation, independent of shared predisposing influences.” They noted the importance of understanding this potential susceptibility, particularly “against the backdrop of evidence supporting a role of the endocannabinoid system in mood regulation.”
Frequent cannabis users enrolled in a Medication-Assisted Treatment for opioid addiction exhibit greater associations between pain and negative affects (anxiety and depression) compared with less-frequent users, according to findings from a study published in Addictive Behaviors.
Investigators sought to determine whether frequency of cannabis use had an effect on the relationship between pain and depression and/or anxiety in 150 participants treated for opioid use disorder with Medication-Assisted Treatment. The most frequent mental health diagnoses in the patient cohort were major depression (36.7%), bipolar disease (20.0%), and generalized anxiety (17.3%).
Levels of anxiety, depression, and pain were similar in study participants who had used cannabis in the last month and in nonusers. A positive relationship between depression and pain intensity was established in individuals reporting cannabis use for a period of 1 to 2 days (P =.01; 95% CI, 0.04-0.28), 20 to 29 days (P <.001; 95% CI, 0.24-0.60), and 30 days (P <.001; 95% CI, 0.26-0.70) in the last month.
The frequency of cannabis use was found to moderate the relationship between anxiety and pain intensity in participants using cannabis in the last month for 1 to 2 days (P =.003; 95% CI, 0.11-0.35), 20 to 29 days (P <.001; 95% CI, 0.28-0.66), and 30 days (P <.001; 95% CI, 0.29-0.76). The relationship between anxiety and pain intensity was found to increase with the frequency of cannabis use.
Because this cross-sectional study relied on self-reported data for cannabis use frequency, the investigators note it does not establish a causal relationship between the frequency of cannabis use and the association between pain and negative affect.
This study shows that frequent cannabis use among patients receiving Medication-Assisted Treatment “may be interfering with patients’ ability to disentangle symptoms of pain and emotional distress,” underscoring “an important discrepancy between patients’ positive beliefs about the role of cannabis in symptom managementand the more complicated detrimental influence cannabis may have on symptom entanglement.”
A study published in Molecular Psychiatryindicates a likely causal relationship between cannabis use and increased risk for schizophrenia.1
The study, conducted by researchers from the Department of Internal Medicine at the University Hospital of Lausanne in Switzerland, built on already existing studies depicting a positive, dose-dependent association between cannabis use and schizophrenia risk, particularly in younger populations.2
“[A]ny causal link between cannabis use and psychotic disorders remains controversial as observational findings can always be hampered by confounding…and/or reverse causality bias,” Julian Vaucher, MD, and colleagues wrote. “Moreover, cannabis use is strongly associated with tobacco consumption and…smoking could confound the link between cannabis and schizophrenia.”
To assess causality, the researchers opted to use a genetic approach. Using genetic and self-report data on lifetime use of cannabis and a lifetime diagnosis of schizophrenia from 34,241 cases and 45,604 controls from populations of predominantly European descent, they tested the robustness of the relationship between lifetime cannabis use and schizophrenia while controlling for 10 genotypes that have been weakly associated with lifetime use of cannabis in genome-wide association studies.
They learned that the association between lifetime cannabis use and schizophrenia persisted for most of the 10 genotypes. The pooled estimate of the association for these 10 genotypes (OR, 1.37; 95% CI, 1.09-1.67) was different from the null value, and it did not differ from the pooled estimate of the relationship in epidemiological studies (OR, 1.43; 95% CI, 1.19-1.67). They also found that these relationships persisted after controlling for genetic associations between cigarette and cannabis smoking, making it unlikely that cigarette smoking was a potential confounding variable.
Because this Mendelian randomization used genotypic data to simulate the effects of conducting a randomized controlled trial, it confirmed the hypothesis that cannabis use is likely to increase the risk for schizophrenia. “As cannabis is the leading drug of misuse, this finding is timely to draw attention to the potential mental health consequences of cannabis use and to provide more robust scientific evidence to inform the public health debate on cannabis legalization,” the authors wrote.
BACKGROUND: One of the major mechanisms for terminating the actions of the endocannabinoid anandamide is
hydrolysis by fatty acid amide hydrolase (FAAH), and inhibitors of the enzyme were suggested as potential treatment
for human cannabis dependence. However, the status of brain FAAH in cannabis use disorder is unknown.
METHODS: Brain FAAH binding was measured with positron emission tomography and [11C]CURB in 22 healthy
control subjects and ten chronic cannabis users during early abstinence. The FAAH genetic polymorphism
(rs324420) and blood, urine, and hair levels of cannabinoids and metabolites were determined.
RESULTS: In cannabis users, FAAH binding was significantly lower by 14%–20% across the brain regions examined
than in matched control subjects (overall Cohen’s d 5 0.96). Lower binding was negatively correlated with
cannabinoid concentrations in blood and urine and was associated with higher trait impulsiveness.
CONCLUSIONS: Lower FAAH binding levels in the brain may be a consequence of chronic and recent cannabis
exposure and could contribute to cannabis withdrawal. This effect should be considered in the development of novel
treatment strategies for cannabis use disorder that target FAAH and endocannabinoids. Further studies are needed
to examine possible changes in FAAH binding during prolonged cannabis abstinence and whether lower FAAH
binding predates drug use.
Associations between cannabis use and psychotic outcomes are consistently reported, but establishing causality from observational designs can be problematic. We review the evidence from longitudinal studies that have examined this relationship and discuss the epidemiologic evidence for and against interpreting the findings as causal. We also review the evidence identifying groups at particularly high risk of developing psychosis from using cannabis. Overall, evidence from epidemiologic studies provides strong enough evidence to warrant a public health message that cannabis use can increase the risk of psychotic disorders. However, further studies are required to determine the magnitude of this effect, to determine the effect of different strains of cannabis on risk, and to identify high-risk groups particularly susceptible to the effects of cannabis on psychosis. We also discuss complementary epidemiologic methods that can help address these questions.
The past few decades have seen a marked change in the composition of commonly smoked cannabis. These
changes primarily involve an increase of the psychoactive compound Δ9
-tetrahydrocannabinol (THC) and a decrease
of the potentially therapeutic compound cannabidiol (CBD). This altered composition of cannabis may be linked to
persistent neuroanatomic alterations typically seen in regular cannabis users. In this review, we summarize recent
findings from human structural neuroimaging investigations. We examine whether neuroanatomic alterations are 1)
consistently observed in samples of regular cannabis users, particularly in cannabinoid receptor–high areas, which
are vulnerable to the effects of high circulating levels of THC, and 2) associated either with greater levels of cannabis
use (e.g., higher dosage, longer duration, and earlier age of onset) or with distinct cannabinoid compounds (i.e., THC
and CBD). Across the 31 studies selected for inclusion in this review, neuroanatomic alterations emerged across
regions that are high in cannabinoid receptors (i.e., hippocampus, prefrontal cortex, amygdala, cerebellum). Greater
dose and earlier age of onset were associated with these alterations. Preliminary evidence shows that THC exacerbates, whereas CBD protects from, such harmful effects.Methodologic differences in the quantification of
levels of cannabis use prevent accurate assessment of cannabis exposure and direct comparison of findings across
studies. Consequently, the field lacks large “consortium-style” data sets that can be used to develop reliable
neurobiological models of cannabis-related harm, recovery, and protection. To move the field forward, we encourage
a coordinated approach and suggest the urgent development of consensus-based guidelines to accurately and
comprehensively quantify cannabis use and exposure in human studies.
The reviewed literature demonstrates that regular exposure to
cannabis is associated with neuroanatomic alterations in
several brain regions, most consistently within the hippocampus
(reduced volumes and gray matter density, altered
shape), followed by the amygdala and striatum, orbitofrontal PFC alterations. These trends (i.e., hippocampal volumetric
reduction) were previously observed (47), although there is
now increasing evidence for alteration within other regions
(i.e., striatum, orbitofrontal cortx, parietal cortex, insular cortex,
cerebellum). There was also preliminary evidence that neuroanatomic
alterations within the hippocampus, cerebellum,
prefrontal, and lingual regions were associated with THC and
CBD levels specifically, suggestive of an adverse effect of THC
and a protective effect of CBD (from THC-related damage).Neuroanatomic abnormalities were most reliably found in
regions that have a high concentration of cannabinoid type 1
receptors, to which THC binds to exert its psychoactive
effects (31). Cannabis plants that are typically used for drug
production have high levels of THC (17%–20%) (73) but low
levels of CBD (1). According to preclinical findings, THC
accumulates in neurons (74) and with chronic exposure
becomes neurotoxic (18). Neuroanatomic abnormalities may
result from the adverse effects of direct and chronic exposure
to high levels of THC found in commonly available “street”
cannabis. Although CBD may be neuroprotective (24,25) and
mitigate the adverse effects of THC (47,85), it is seldom found
in high levels (1). As one of the regions of highest density of cannabinoid type 1 receptors (3), damage to the hippocampus may be related to THC-induced neurotoxicity.
Cannabis use has been associated with impaired cognition during acute intoxication as well as in the unintoxicated state in long-term users. However, the evidence has been mixed and contested, and no
systematic reviews of the literature on neuropsychological task-based measures of cognition have been conducted in an attempt to synthesize the findings. We systematically review the empirical research published in the past decade (from January 2004 to February 2015) on acute and chronic effects of cannabis and
cannabinoids and on persistence or recovery after abstinence. We summarize the findings into the major categories of the cognitive domains investigated, considering sample characteristics and associations with various cannabis use parameters. Verbal learning and memory and attention are most consistently impaired by acute and chronic exposure to cannabis. Psychomotor function is most affected during acute intoxication, with some evidence for persistence in chronic users and after cessation of use. Impaired verbal memory, attention, and some executive functions may persist after prolonged abstinence, but persistence or recovery across all cognitive domains remains underresearched. Associations between poorer performance and a range
of cannabis use parameters, including a younger age of onset, are frequently reported. Little further evidence has emerged for the development of tolerance to the acutely impairing effects of cannabis. Evidence for potential protection from harmful effects by cannabidiol continues to increase but is not definitive. In light of
increasing trends toward legalization of cannabis, the knowledge gained from this body of research needs to be incorporated into strategies to minimize harm.
Cross-sectional studies report persistent impairing effects
on some aspects of attention, verbal and working memory,
and psychomotor speed in adolescents abstinent for 28 days
(65) and 35 days (67), but not on other aspects of these and
other cognitive domains. Poor performance was associated
with lifetime cannabis exposure (65) or an earlier age of use
onset in adolescents with 30 days of abstinence (95) and
predicted relapse to cannabis use during a 1-year follow-up
(95). Even after 53 days of abstinence, adolescents showed impaired working memory and risk taking(85). Young adults
abstinent for up to 4 weeks showed poorer verbal fluency
relative to control subjects (119) and nonsignificantly poorer
performance on a gambling task, associated with prior quantity
of weekly cannabis use (127). Older adults abstinent for
.28 days were impaired on executive function and information processing but not attention and working memory (57). Lyons
et al. (64) argued that their study of monozygotic twins,
discordant for cannabis use with .12 months abstinence,
provides evidence against long-term effects of cannabis on
cognition, despite finding impaired performance on block
design tests and trends toward poorer long delay and cued
verbal recall and poorer finger tapping performance in the
Epidemiological studies show that cannabis use is associated with a higher risk of developing psychosis.
Only a small proportion of cannabis users go on to develop psychosis.
Risk factors include heavy cannabis use in young age, genetic vulnerability and environmental stress.
Cannabis acts as a component cause of psychosis.
However, the strongest evidence that cannabis use may have a causal association with schizophrenia comes from longitudinal studies of large representative samples of the population who have been followed up to see if cannabis users are at higher risk of developing schizophrenia. The earliest such evidence came from a 15-year prospective study of cannabis use and schizophrenia by who examined around 50,000 Swedish conscripts. They found that those who had tried cannabis by age 18 were 2.4 times more likely to be diagnosed with schizophrenia 15 years later than those who had notand the risk of this diagnosis increased to around six times with higher frequency of cannabis use. The risks were substantially reduced but still significant after statistical adjustment for variables that were related to the risk of developing schizophrenia.
Evidence has accumulated over the past several decades suggesting that both exocannabinoids and endocannabinoids play a role in the pathophysiology of schizophrenia. The current article presents evidence suggesting that one of the mechanisms whereby cannabinoids induce psychosis is through the alteration in synchronized neural oscillations. Neural oscillations, particularly in the gamma (30–80 Hz) and theta (4–7 Hz) ranges, are disrupted in schizophrenia and are involved in various areas of perceptual and cognitive function. Regarding cannabinoids, preclinical evidence from slice and local field potential recordings has shown that central cannabinoid receptor (cannabinoid receptor type 1) agonists decrease the power of neural oscillations, particularly in the gamma and theta bands. Further, the administration of cannabinoids during critical stages of neural development has been shown to disrupt the brain’s ability to generate synchronized neural oscillations in adulthood. In humans, studies examining the effects of chronic cannabis use (utilizing electroencephalography) have shown abnormalities in neural oscillations in a pattern similar to those observed in schizophrenia. Finally, recent studies in humans have also shown disruptions in neural oscillations after the acute administration of delta-9-tetrahydrocannabinol, the primary psychoactive constituent in cannabis. Taken together, these data suggest that both acute and chronic cannabinoids can disrupt the ability of the brain to generate synchronized oscillations at functionally relevant frequencies. Hence, this may represent one of the primary mechanisms whereby cannabinoids induce disruptions in attention, working memory, sensory-motor integration, and many other psychosis-related behavioral effects
Penetrating any developing neural system with external
stimuli leads to functional alterations. The endocannabinoid
system is an evolutionarily conserved signaling network that
guides critical aspects of brain development (185). In this
review, we highlighted human and rodent data to show that
prenatal exposure to CB1R agonists impacts neuronal development,
leading to altered neurotransmitter and neuronal
circuit settings. While ensuing neuroanatomical changes and
behavioral consequences in the offspring are evident, the
intriguing question remains why some neuropsychiatric diseases
evoked by adult or adolescent marijuana consumption
do not manifest in offspring with prenatal drug exposure. The
quasi-absence of epileptiform activities or schizophrenia
symptoms in children with maternal cannabis use does not
only highlight differences in endocannabinoid function in
adult versus the fetal brain but demonstrates the need for
further mechanistic studies to dissect molecular and cellular
determinants of cannabinoid action.
This review discussed data from basic and clinical neuroscience
in relation to cannabis use and brain development.
Nevertheless, the impact of cannabis use on the dependence/
use of drugs considered more harmful later in life was only
briefly touched upon here. Almost all of those who tried
cocaine and heroin first used alcohol, tobacco, and cannabis
(186), and regular cannabis users are most likely to later use
heroin and cocaine (187) with an earlier age of cannabis use
onset being a further risk factor (186). Thus, social complexity
specifics must be considered when concluding on the actual
danger of cannabis use for the development of neuropsychiatric
The regular use of cannabis during adolescence is of particular concern because use by this age group seems to be
associated with an increased likelihood of deleterious consequences, as reported by several epidemiologic studies.
However, despite their unquestionable value, epidemiologic data are inconclusive. Modeling the adolescent phase in
animals appears to be a useful approach to investigate the impact of cannabis use on the adolescent brain. In these
models, adolescent cannabinoid exposure has been reported to cause long-term impairment in specific components of learning and memory and to have differential effects on anxiety, social behavior, and depressive-like signs. These findings suggest that it may represent, per se or in association with other hits, a risk factor for developing psychotic like symptoms in adulthood. The neurobiological bases of this association include the induction of alterations in the maturational events of the endocannabinoid system occurring in the adolescent brain. Alterations in theendocannabinoid system may profoundly dysregulate developmental processes in some neurotransmitter systems, such as gamma-aminobutyric acid and glutamate, mainly in the cortex. The resulting picture strongly resembles the one present in schizophrenic patients, highlighting the translational value of this experimental approach
The past decade has witnessed a number of societal and political changes that have raised critical questions about
the long-term impact of marijuana (Cannabis sativa) that are especially important given the prevalence of its abuse
and that potential long-term effects still largely lack scientific data. Disturbances of the epigenome have generally
been hypothesized as the molecular machinery underlying the persistent, often tissue-specific transcriptional and
behavioral effects of cannabinoids that have been observed within one’s lifetime and even into the subsequent
generation. Here, we provide an overview of the current published scientific literature that has examined epigenetic
effects of cannabinoids. Though mechanistic insights about the epigenome remain sparse, accumulating data in humans and animal models have begun to reveal aberrant epigenetic modifications in brain and the periphery linked to cannabis exposure. Expansion of such knowledge and causal molecular relationships could help provide novel
targets for future therapeutic interventions.
Between January 1, 1995, and December 31, 2014, 38,681 samples of cannabis preparations were
received and analyzed. The data showed that although the number of marijuana samples seized over the last 4 years
has declined, the number of sinsemilla samples has increased. Overall, the potency of illicit cannabis plant material
has consistently increased over time since 1995 from 4% in 1995 to 12% in 2014. The cannabidiol content has
decreased on average from .28% in 2001 to ,.15% in 2014, resulting in a change in the ratio of Δ9 -tetrahydrocannabinol to cannabidiol from 14 times in 1995 to 80 times in 2014.
There is a shift in the production of illicit cannabis plant material from regular marijuana to sinsemilla. This increase in potency poses higher risk of cannabis use, particularly among adolescents.
In this session I am re-posting on BOREDOM – I think it is a centerpiece in our society’s misfortunes. Having too much is becoming a regular problem and reinforces addiction and bad choices.
Aug 08, 2018
How Boredom Can Lead to Addiction
Every person who has a substance use disorder has a unique experience and path that lead them to their addiction. Some people are dealing with unresolved mental health issues or trauma, while others have genetic and environmental factors that have lead them to drug use. Another interesting factor that can sometimes contribute to someone’s addiction is boredom. Boredom isn’t just for people who “have nothing to do”. Plenty of very busy people can also experience boredom from their everyday responsibilities. Often we think of teenagers being bored with school or being grounded, but adults with careers and families can experience boredom as well, which can lead some to seek out ways to entertain themselves with substance use.
It’s hard to think that anyone could get bored with all of the interactive apps, social media, and streaming content they can access online at the reach of their fingertips on smartphones, tablets, and smart TVs. Boredom isn’t so simple, however, it’s more than not having anything to do. Some may reach for drugs and alcohol due to peer pressure, but what about when they feel isolated or “stuck” in their home or family environment and are looking for ways to escape? The same goes for stay-at-home parents who spend their days at home, looking after their small children, often stretched thin with childcare and household responsibilities. Businessmen and women who spend long hours at the office, sometimes dealing with monotonous meetings and long commutes, can also experience everyday boredom that drives them towards substance use.
After people begin to use substances as a “mental escape” from boredom on a regular basis, it becomes difficult to face that boredom again sober. This is how easily an addiction can begin and also the reason why people in recovery often have to deal with the risk of boredom leading them to relapse. Once drugs have taken a person away from their boredom for so long, it can be difficult to return to “real life”, making addiction such a complex disease that requires a lot of strength and work to rehabilitate.
Boredom and Addiction
Doing drugs or drinking can provide somewhat of a mental vacation from people’s current situation. When someone feels trapped and doesn’t know what to do with themselves, getting high or drinking can provide the same kind of mental stimulation as doing a fun activity. Many of these people are also dealing with profound loneliness, anxiety, or are suffering from other situations that prevent them from being involved with hobbies or activities. People with anxiety and depression may feel that leaving their homes to engage in social activities is too stressful, and instead, prefer to stay home and numb themselves.
Most people who are in recovery report that their greatest fear is facing the boredom they once felt while they were still using. Unfortunately, boredom is reported as one of the biggest reasons many people who are in recovery experience relapse. For people who were using drugs regularly, the drugs eventually became the center of their world. Those who are trying to stay sober will avoid old friends they used to do drugs with, causing many people in recovery to feel like they have no friend, or need to take on the overwhelming task of creating an entirely new social circle. Since drugs used to take up so much of their time, former drug users need to find ways to fill their lives with activities and hobbies to avoid boredom at all costs in order to prevent the risk of relapse.
For people who think that their boredom is leading them to misuse substances more frequently than their previous “recreational” use and want to avoid the slippery slope of addiction, beating boredom is essential. The same advice can be applied to people who are in recovery and are finding their motivation and confidence in their sobriety starting to slip. The main issue that can lead to boredom is being stuck in a familiar environment where substance use has most frequently occurred in the past. For some people, it’s a recliner in the living room, and for others, it’s a familiar setting like a long train ride or sitting on a lawn chair on a hot summer’s day. Pinpointing these trigger environments that can evoke cravings due to boredom or monotony need to be avoided as much as possible.
Boredom can also be avoided with the start of new interests and hobbies. Many people in recovery discover their love for fitness and outdoor activities which are healthier ways to keep boredom at bay. Others may require a quieter, mentally stimulating activity like learning to play chess, painting, or knitting. The main goal is to stimulate the brain to be engaged instead of being left to find its way back to using drugs or alcohol.
When mindfully avoiding boredom, people have succeeded in creating entirely new lives for themselves. Something that starts off as a hobby while in recovery can be great for abstaining from drug use, but can also blossom into a new career or passion. When people discover how much of their time they had previously spent on drugs and getting high, they realize how much their time is worth and how it can be better spent. Recovery is a time for rediscovery. Avoiding boredom can lead to things beyond just staying sober. No matter a person’s age or experience with addiction, new hobbies and volunteer work are just some of the ways to begin avoiding the feeling of complacency in life.
Boredom should not be taken lightly. It’s a real issue that is leading people from all walks of life into potential substance use disorders. Making time for activities that stimulate the mind outside of life’s everyday activities is healthy for the body and mind, especially when avoiding addiction and relapse.
Tedium sounds like such a minor emotion, lacking the passion of anger or fear. Yet it can be a major trigger for alcohol and drug abuse, smoking, emotional eating and problem gambling.If you’re working to change one of those behaviors, you need healthy ways to handle boredom and relapse risks.Beyond helping with recovery, handing boredom may also boost your overall longevity. As part of a large study detailed in the International Journal of Epidemiology, more than 7,500 British civil servants answered questions about how often they felt bored. Over the next 20-plus years, those who said they were bored a lot were more likely to die than those with a zest for life.
Bored to distraction
The first step toward vanquishing boredom is understanding what you’re up against. Imagine how you might feel after waiting in the DMV line for an hour. Time drags when you’re having a dull time, and all you can think about is how much you wish you were doing something—anything—more exciting.
But have you ever considered why you feel this way? John Eastwood, a psychology professor at York University in Toronto, has given it a lot of thought. After scouring the scientific literature on boredom, his abstract in Perspective on Psychological Science identified three core characteristics of the emotion:
You’re unable to engage your mind in a satisfying way
You’re aware of the situation and consider it a problem
You blame the environment (“this is so boring” or “there’s nothing to do”)
Never a dull moment
Based on these characteristics, there are three sure-fire ways to beat boredom:
1. Learn how to engage your mind in a more satisfying way — When you’re bored, you aren’t able to focus your mind on something that interests you, and that leaves you feeling dissatisfied.
Regaining your focus can help. Here’s how:
Practice mindfulness. In a nutshell, mindfulness involves being fully aware of your moment-to-moment experience. You notice sensations, thoughts and feelings without judging or resisting them, and then you let them go as your focus moves on to the next moment. With this mindset, you’ll feel more engaged in whatever you’re doing — even a mundane chore such as folding laundry — and less preoccupied with wishing you were doing something else.
Turn off the screens. Your smartphone, tablet, computer and TV provide nonstop access to texts, tweets, shows, news and games, not to mention hilarious cat videos. So why are you still getting bored? Being bombarded with rapid-fire images and information can overload your capacity to pay attention, and constantly switching from one app or screen to another just magnifies the problem. Soon, your ability to focus on anything for long is shot. To prevent this, try to do just one e-task, such as answering emails or searching the Web, at a time. At home, spend at least an hour every day unplugged from your devices.
2. Redefine the situation so it doesn’t seem like such a problem – From time to time, everyone has to do routine or repetitive tasks, from entering data to washing dishes.
Putting a positive spin on the situation helps keep boredom at bay. Here’s how:
Make it meaningful. Remind yourself of the value in what you’re doing. For example, if you’re raking and weeding in your backyard, remember the fun times you’ve spent there in the past, or imagine the good times to come in the future.
Call it an opportunity. Rather than describing a less-than-thrilling activity as “monotonous,” tell yourself it is “meditative.” Think of it as your chance to take a mental break — a welcome respite from any pressure to make tough decisions or come up with clever ideas. (Ironically, I find that some of my most creative ideas bubble up unbidden at times such as these.)
3. Stop blaming the environment, and start taking charge — The interesting thing about boredom is that it comes from within. Taking the steps outlined above won’t rescue you from sitting through a dull meeting or standing in a long line, but it can help you feel less bored while you do so. If you still feel your eyes glazing over, shake off the sluggishness in a healthy way.
Depending on the situation, you could:
Imagine that you’re a detective, journalist or anthropologist who is investigating the situation, noting every detail with great interest
Entertain yourself by daydreaming or doodling
Go for a quick walk or climb a flight of stairs
Call a friend who’s a good conversationalist
Listen to a song that makes you feel energized
Make a list of fun things to do this weekend
Watch out for the urge to reach for a beer, cigarette or candy bar when you’re bored. Dulling the pain of dullness never works for long, and it can set back your recovery from addiction or your progress toward healthy goals. Instead, be ready with strategies for managing boredom effectively and constructively.
We found that those who report quite a lot or a great deal of boredom are more likely to be younger, to be women, to rate their health worse, to be in low employment grades and to report lower physical activity levels (Table 1). We also found that those with a great deal of boredom were more likely to die during follow-up than those not bored at all (Table 2). In particular, they were more likely to die from a CVD fatal event [hazard ratio (HR) 2.53; confidence interval (CI) 1.23–5.21]. Furthermore, we found some suggestive evidence of cumulative effects in the mortality after Phase 2, as those still reporting boredom at Phase 2 had slightly higher risks than those reporting it once or never.
Have you ever felt bored (Fig 1)? Ever found yourself with nothing engaging to do? Experienced a lack of interest in everything and everyone around you? Although not a pleasant state in which to find oneself, is boredom bad for health? In a rare moment of idleness one day, we pondered whether the expression ‘bored to death’ has any basis. Are people who are bored more likely to die earlier than those who are not?
Boredom levels were reported in the later versions of the baseline questionnaire (1985–88) of the Whitehall II cohort study. Participants were civil servants, based in London, aged 35–55 years. They were asked in a self-completed questionnaire about boredom during the past 4 weeks (response options were ‘not at all’, ‘a little’, ‘quite a lot’, ‘all the time’). At the risk of participants becoming bored of answering this question, it was repeated at Phase 2 some 3 years later, but not since. Information on mortality was ascertained through the NHS Central Registry, by using their unique NHS identification number. Follow-up for total mortality was available up to the end of April 2009. Excluding those with prevalent cardiovascular disease (CVD) at baseline, gave a sample size of 7524 men and women.
We found that those who report quite a lot or a great deal of boredom are more likely to be younger, to be women, to rate their health worse, to be in low employment grades and to report lower physical activity levels (Table 1). We also found that those with a great deal of boredom were more likely to die during follow-up than those not bored at all (Table 2). In particular, they were more likely to die from a CVD fatal event [hazard ratio (HR) 2.53; confidence interval (CI) 1.23–5.21]. Furthermore, we found some suggestive evidence of cumulative effects in the mortality after Phase 2, as those still reporting boredom at Phase 2 had slightly higher risks than those reporting it once or never. With further adjustments for employment grade, physical activity levels and poor self-rated health, the hazard ratios for CVD for those with a great deal of boredom were reduced and did not reach statistical significance (1.96; CI 0.94–4.05).
We conclude that those who report being bored are more likely to die younger than those who are not bored. However, the state of boredom is almost certainly a proxy for other risk factors. Whilst some aspects of life may not be so easily modified (e.g. disease status or position in society), proneness to boredom, particularly in younger populations, could be indicative of harmful behaviours such as excessive drinking, smoking, taking drugs and low psychological profiles.1 Finding renewed interest in social and physical activities may alleviate boredom and improve health, thus reducing the risk of being ‘bored to death’.
The results also indicate a significant relationship between boredom proneness and a negative social orientation, as described by the HSCL interpersonal sensitivity
subscale (e.g., “feeling that people are unfriendly or dislike you,” “Your feelings being easily hurt”). This adds tangential support to the findings of Leong and Schneller (1993), Maroldo (1986), and Tolor (1989), who reported boredom proneness to be significantly
associated with alienation, low sociability, and shyness, respectively.
The significant relationship between BPS scores and the HSCL obsessive–compulsive (OC) subscale appears somewhat surprising at first glance. However, many of the OC subscale items consist of statements regarding difficulty with attentional deficits (e.g,
“trouble concentrating,” “Your mind going blank,” “trouble remembering things”). When discussing the construct of boredom (or the boredom-prone individual), several authors
have stated that boredom is connected with distractibility, low attentional control, and concentration difficulties (Damrad-Frye & Laird, 1989; Farmer & Sundberg, 1986; Hamilton,
1981; Hamilton, Haier, & Buchsbaum, 1984). For instance, Fisher (1993) stated, when bored, an individual “. . . feels a pervasive lack of interest in and difficulty concentrating
on the current activity” (p. 396).
Finally, our finding that high boredom-proneness scores are related to greater somatization
complaints adds empirical support to previous work that reported negative associations
between boredom and eating behaviors (e.g., Martin, 1989; Pascale & Sylvester,
1988) and physical-health symptoms (e.g., Ferguson, 1973; Smith et al., 1981). It should be noted, however, that this prior work did not assess boredom levels using psychometrically sound instrumentation. Perhaps one reason for the relationship between boredom proneness and greater symptom reporting is that individuals with high BPS scores may be overly focused on themselves (or their internal states) and therefore be more likely to perceive that problems may exist. For instance, many authors (e.g., Eisnitz, 1974; Weinberger & Muller, 1975) have discussed the connection between boredom and the tendency to dwell on oneself (e.g., narcissism). Recently, Wink and Donahue (1997) found greater BPS scores to be related to high narcissism scores. In a related vein, Spacks (1995) argued that the focus on oneself is a primary reason for the increased incidence in reports of boredom in society. As she has stated, “The inner life comes to be seen as consequential, therefore itsinadequacies invite attention” (1995, p. 23). Finally, Seib and Vodanovich (1998) found
that individuals with high BPS total scores had greater scores indicative of “maladaptive” self-awareness, as indicated by greater scores on the Self-Reflectivity subscale of the
Self-Consciousness Scale (Fenigstein, Scheier, & Buss, 1975).
Boredom is a common problem. In a survey of North
American youth, 91% of respondents reported that they experience
boredom (The National Center on Addiction and Substance
Abuse, 2003). It is often perceived as a fairly trivial and
temporary discomfort that can be alleviated by a simple change
in circumstances, such as finally being called into the doctor’s
examining room. However, boredom can also be a chronic
and pervasive stressor with significant psychosocial consequences.
Indeed, boredom is even associated with mortality,
lending grim weight to the popular phrase “bored to death”
(Bloomfield & Kennedy, 2006; Britton & Shipley, 2010;
For example, boredom
is correlated with mental health symptoms, such as
depression and anxiety (Goldberg, Eastwood, LaGuardia, &
Danckert, 2011; LePera, 2011; Sommers & Vodanovich, 2000),
alexithymia (Eastwood, Cavaliere, Fahlman, & Eastwood,
2007), and somatization complaints (Sommers & Vodanovich,
2000). Furthermore, boredom has been identified as a complicating
factor in the psychiatric rehabilitation of mental disorders,
such as schizophrenia (Newell, Harries, & Ayers, 2011;
Todman, 2003), and in recovery from traumatic brain injury
(Kreutzer, Seel, & Gourley, 2001; Oddy, Humphrey,
& Uttley, 1978; Seel & Kreutzer, 2003). Boredom is also negatively
correlated with a sense of purpose in life. boredom is linked with impulse control deficits such as overeating and binge eating (Stickney & Miltenberger, 1999),
drug and alcohol abuse (Lee, Neighbors, & Woods, 2007;
LePera, 2011; Wiesbeck et al., 1996), and problem gambling
(Mercer & Eastwood, 2010). Boredom at work (Fisher, in
press) can cause serious accidents if safety depends on continuous
vigilance, as in medical monitoring or long-haul truck driving.
As the saying goes… “An idle mind is the devil’s playground.” Anyone with too much time on their hands may find themselves in hot, troubled waters. People who tend to be bored may also be weary or restless because of lack of any personal interests. They are bored with themselves, their jobs and life.
Boredom usually stems from one’s own lack of motivation, endeavor or creativity. Everyone gets bored now and then, but it is the difference between changing that mood to healthy alternatives versus sitting around with friends “passing the pipe” for a few high flying hits. This kind of boredom can ultimately lead to an anti-social, destructive path toward addiction.
It’s hard to imagine anyone being bored today; even if they are not interested in stretching their muscles, feelings or their minds. Computers, IPods, IPhones and game boxes can provide hours of (in my opinion) useless activity, so it seems that one has to look hard and actually seek out boredom. Boredom takes some perseverance to shake off. It is a state of mind and requires a committed determination to do something about it or change up the routine.
One can form a habit out of being bored because it can present a degree of comfort and safety. Eventually, since no one expects anything from you and in turn, you don’t expect anything from yourself, drugs and/or alcohol can seem like an acceptable choice of behavior and the easiest and quickest fix requiring little or no effort is to “get high” or drink.
Drugs or alcohol can appear to take away the pain of emotional, mental or physical challenges. Boredom is often simply a state of awareness that shows up just prior to the surfacing of difficult, painful things we have stuffed away from our conscious awareness.
As difficult a challenge as boredom can present to overcome for anyone of any age, the answer lies in confronting and moving through and beyond the CAUSES of boredom. Anyone experiencing significant levels of boredom needs to ask themselves what challenging (and likely unpleasant) experience they are attempting to avoid. .
When children or adolescents are spending too much time in front of the television (or screens of any kind!) or listlessly whiling away hours it is time to step in. Curtail the screen-time hours and help your child look for and plan stimulating activates or hobbies. If they are not interested in pursuing them independently then get involved yourself or recruit other members of the family.
Strong, positive energy coupled with the right attitude is important to infuse into your child to shake his or her lazy, boring life and get with a new productive program. If executed early and properly, then boredom will have no opportunity to lead to dangerous experimentation with potentially addictive behaviors.
If you are an adult and active yet bored with work or mundane, tedious activities, push yourself to discover new adventures and even make new friends. If your job represents a form of security, but is painstakingly boring, explore new possibilities for employment even if you never fill out an application or get a job interview.
Talk to other family members and tell them of your boredom so that they can support and work with you in determining other paths to avoid your boredom. This might help to deter you from turning to alcohol or substance abuse in order for you to alleviate your own boredom in a self destructive, detrimental way. It also makes you accountable to others and them to you, if you have put out your hand for help.
Being bored is no fun. It’s a waste of precious time and has zero productivitychips.
Be creative and shake things up in your life. You never know what might happen, especially if you keep an open mind. The alternative is either a stale, lackluster lifestyle or one where the only entertainment is destructive, out of control addictive behavior. Take responsibility and choose (hopefully) the more creative and productive path.
If I can be of service, please visit my website www.familyrecoverysolutions.com and I invite you to explore my book Reclaim Your Life – You and the Alcoholic/Addict. It can be purchased through PayPal or at Amazon. In addition, my book is available as an audio through PayPal only.
Another tragic story to report, as Korn singer Jonathan Davis‘ estranged wife Deven died today (August 17th) at the age of 39. According to TMZ, Deven’s death comes on the same day Jonathan had filed a restraining order against her.
In a statement that was provided by his publicist minutes ago, Jonathan and his family said, “The Davis family is brokenhearted over the devastating loss of Deven Davis. We ask that you respect their privacy — and the privacy of those close to the family — and allow them the space to mourn in private. We thank you for your love, understanding and prayers of support during this difficult time.”
While they were technically still married, Jonathan had filed for divorce back in October of 2016. But they seemed to be together in a Facebook Live video from December 2017. However, TMZ reported that earlier today, Jonathan filed a domestic violence restraining order against Deven. The Korn singer alleged that Deven was a heavy drug user, and a judge issued an temporary order to stop Deven from visiting their children.
TMZ further reports that Deven was recently living in a sober house but recently went missing. In his court documents, Jonathan claimed that Deven was “constantly under the influence of the nitrous oxide, cocaine and Norco.” He also alleged that he found Deven passed out on the floor with a heroin pipe and cocaine floating in a toilet bowl.
Deven, a former porn star, married Jonathan in 2004. They had two children together. Our thoughts with the Davis family at this time.
TMZ reports that while the Atlanta-based Lomas was at a friend’s home in Mississippi, he went into the bathroom and then never came out. Lomas was found “unresponsive on the floor” with “a syringe near his body.” He was rushed to the hospital, where he died of an apparent overdose.
Lomas, who was Whitney Houston‘s daughter’s housemate and ex-boyfriend, was the one who discovered her lifeless body in a bathtub in her Alpharetta, Ga., home on Jan. 31, 2015. He alerted her then-boyfriend, Nick Gordon, who was in another room, and first responders were called. But after being in a coma for six months, Bobbi Kristina died on July 26, 2015. While the official cause of death was pneumonia, the medical examiner said in a statement that she died from complications caused by her face being immersed in water, along with drug intoxication.
While no charges were filed related to Brown’s death, according to TMZ, Gordon was later found liable and ordered to pay $36 million in a civil suit filed by Brown’s conservators (including Bobbi Kristina’s father, New Edition singer Bobby Brown). An amendment to the suit alleged that Gordon gave Bobbi Kristina a “toxic cocktail, rendering her unconscious, and then put her face down in a tub of cold water causing her to suffer brain damage,” according to the Atlanta Journal-Constitution. Gordon’s attorneys called the accusations “slanderous and meritless.” No criminal charges have been filed against Gordon in Bobbi-Kristina’s death.
Lomas had been out with Gordon at a club the night before Bobbi Kristina died, according to E! News, and found himself pulled into the headlines. He gave his first interview to People in 2016, saying that the night before she died, Bobbi Kristina had called Gordon and started arguing with him, accusing him of cheating. Lomas and Gordon reportedly headed home — where the argument continued and escalated — but Lomas said that Bobbi Kristina and Gordon eventually made up. The next day, when a cable provider showed up at the house, Lomas went to get Bobbi Kristina and found her face-down in a tub of cold water in the bathroom.
Lomas, who admitted he was using drugs the night Bobbi Kristina died, was frank about his troubles, including drug dependency and a stint in jail for a probation violation. He talked to People about Bobbi Kristina and Gordon’s relationship, too, calling it “bipolar” and adding that they had “extreme highs and lows and would fight, mostly about jealousy.”
Lomas, who, like Gordon, was taken in by Bobbi Kristina’s superstar mother as a teen, said that two weeks before the tub incident, “We all decided that we were going to get off drugs, live healthier lifestyles. We all went to the gym together. But it didn’t work out. We started using again.’” A lawyer for Gordon was dismissive of Lomas’s account of the night, calling him “a drug addict,” according to People. Gordon has since been arrested on unrelated domestic violence charges.
Yahoo Entertainment reached out to two attorneys for Lomas, both of whom represented him following Bobbi Kristina’s death, but neither could confirm Lomas’s death. Ashleigh Merchant of the Merchant Law Firm in Marietta, Ga., said, “I haven’t spoken with him in years.” And Philip A. Holloway of the Holloway Law Group in the same city, said, “I only know what’s been reported publicly. Various media are asking, but I haven’t had any contact with him for quite some time.”
However, Gordon seemed to confirm the report, telling Radar Online on Friday, “How do you think I’m doing? How would you feel if you lost a friend?” And several of Lomas’s other friends have been posting about his death on Facebook for a couple days.
An Ohio couple rescued an infant girl from a sweltering car as her parents lay sprawled out on the ground from an apparent overdose, according to a new report.
Eric Asher, 43, told “Inside Edition” that he and his fiancée rushed to the baby’s aid when they came upon the scene — captured in disturbing photos he posted to Facebook — at a parking lot in Canton on Friday.
“We were driving down the road and I looked over to my right and I saw the male and female laying on the ground,” Asher told the outlet. “We [later] saw that they were purple.”
Once the couple realized an infant was in the back seat, they “busted [the] baby out,” Asher wrote in the Facebook post.
“The child was covered in sweat,” he told “Inside Edition.” “We … gave the baby some water. That was our priority.”
Another bystander quickly called 911. Both parents were charged with child endangerment and released on bond, according to court records obtained by the TV program.
A Stark County Sheriff’s office spokeswoman confirmed that her office handled the incident, but was not immediately able to release information on the case, which she said remains “under review.”
The little girl’s mother later called Asher to thank him for saving their daughter, he said on the program.
“They said they were clean for two years and then they got off the government [provided] medication and got sick,” Asher said. “When they relapsed, it had a greater effect than when they used to do drugs.”
Another family member now has custody of the baby, Asher said the mother told him.
Meanwhile, Asher’s Facebook post went viral, with about 52,000 Facebook likes and 81,000 shares. But he’s gotten his share of negative feedback, he told “Inside Edition”
“The only reason we posted that picture was to bring awareness,” Asher explained. “I have family and friends dying like everybody does daily over this epidemic. We just wanted people to be aware of what was going on in our community. We did not expect it to go viral.”
“Lord put us at the right place at the right time,” he said in the Facebook post.
Three days later, he posted that he was raising funds for the organization Facing Addiction with NCADD.
The incident calls to mind a 2016 viral image of Erika Hurt of Hope, Ind., who was strung out on heroin and slumped behind the wheel in a Dollar General parking lot while her 10-month-old son, Parker, cried in the back seat.
A year later, Hurt reposted the viral image on Facebook — accompanied by a shot of herself with her son and a smiling selfie. She said the earlier photo depicted “the worst moment of my life” — but it ultimately helped her turn her life around, she said.
“Today, I am able to focus on the good that came from that picture,” she wrote. “Today, I am a mother to my son, again. Today, I am able to be grateful to actually have solid proof where addiction will only lead you, and today I am able to say that I am ONE YEAR SOBER.”
In the picture, Erika Hurt, of Hope, Ind., was passed out in her car from a heroin overdose on Oct. 22, 2016.
Cops said they found her in the parking lot of a Dollar General — slumped back behind the wheel — while her 10-month-old son, Parker, was crying in the back seat.
She had to be revived with the opioid antidote naloxone before she was taken to a hospital, where she was arrested for child neglect and possession of drug paraphernalia.
Police officials in Hope said they released the photo to draw attention to the heroin epidemic in the Midwest.
Erika Hurt sits with her baby in the back seat after overdosing on heroin in 2016.AP
A— accompanied by a shot of herself with her so She said the earlier photo depicted “the worst moment of my life” — but it ultimately helped her turn her life around, she said.
“I’ve decided to repost the picture simply because it displays exactly what heroin addiction is,” Hurt wrote. “Also because I do not want to ever forget where the road of addiction has taken me. Little did I know that day, my life was about to change, drastically. Today, I am able to focus on the good that came from that picture. Today, I am a mother to my son, again. Today, I am able to be grateful to actually have solid proof where addiction will only lead you, and today I am able to say that I am ONE YEAR SOBER!”
Hurt told NBC News that she was humiliated at first that local police had released her photo to the media and “exposed me and my addiction to the whole world.” But that perspective has changed.
“At this point in my life now, I do think it was a good thing, because I’m able to look back and see that’s who I was, and that was the place it led to,” she told the station.
After last year’s incident, Hurt pleaded guilty to neglect of a dependent and was given a two-year suspended jail sentence that required her to go to an inpatient drug-rehab program at a local jail, the station reported. She signed temporary custody of her son over to her mother.
Once she finished the program, Hurt was allowed to stay at her mom’s place under house arrest — where she was reunited with Parker, who will turn 2 in December. She also began working at a plastic molding plant.
Hurt continues attending court-mandated rehab and self-help meetings — and plans to petition for custody of Parker when she is ready, she told the station.
Hope Town Marshal Matt Tallent, who released the photo, told the station his intention was never to shame Hurt into changing — but he is proud that she made that decision.
“Young people make mistakes,” he told the station. “People are allowed to make mistakes as long as they recognize it and come back stronger. That’s what this is about.
Mass outbreaks of K2 and other drug poisoning are not entirely new, but certainly for those believing the apocalypse is coming, this story below is concerning. This K2 overdose in Connecticut resulted in numerous medical injuries. Again, a block part that has the same source is at risk like this on was. I included another Zombie Apocalypse event from NEJM at the bottom of the page:
Connecticut police have made an arrest in connection with more than three dozen overdose cases at a New Haven park.
First responders found about 46 people who appeared to have overdosed on the New Haven Green on Wednesday, with 25 of those overdoses occurring within a three-hour span in the morning and some four to six at a time, officials said.
A local man believed to be connected to at least “some” of the overdoses was arrested later that afternoon, according to the New Haven Police Department. His identity will not be released until he has been positively identified by a probable victim, police said.
Dozens of people suffering from apparent overdoses were transported to local hospitals from the New Haven Green, according to Rick Fontana, director of the city’s Office of Emergency Operations.
The victims appeared to be suffering from a “multiple of signs and symptoms ranging from vomiting, hallucinating, high blood pressure, shallow breathing, semi-conscious and unconscious states, Fontana said. Two people had life-threatening symptoms, he added.
The New Haven Police Department is investigating the case.
“There have been a couple individuals that were certainly more sicker than others,” Fontana told reporters at a press conference Wednesday morning. “We are doing our best to get people to the hospital in the safest, most practical and efficient manner. We have no deaths reported.”
New Haven Fire Chief John Alston Jr. said emergency crews were overwhelmed with “multiple” 911 calls about people who were experiencing overdose symptoms or were passed out on the New Haven Green just after 8 a.m. local time. First responders sprinted across the park from victim to victim as more calls came in.
“Even while we were trying to return people to service, they were passing victims on the ground,” Alston told reporters.
The victims, who officials said ranged in age and demographic, were at times found in groups of four to six. Their symptoms included vomiting, hallucinating, high blood pressure, shallow breathing, semi-conscious and unconscious states, officials said.
Victims were given several doses of naloxone, an antidoe for narcotic overdoses, both on the scene and at the hospital.
Alston said it’s unclear what was the cause of the overdoses, but officials suspect it may have been synthetic cannabinoids, known as K2, that were likely laced with other substances.
“It’s a nationwide problem,” Alston said of drug overdoses. “This is a problem that’s not going away.”
It’s called K2, synthetic marijuana, and it has caused a cluster of deaths in Chicago.
The Chicago Tribune reported three arrests over Easter weekend after large amounts of K2 being sold at a convenience store were discovered to be contaminated with a toxic compound used as rat poison.
Between March 10 and April 2, 56 people have been hospitalized in Illinois, all related to K2, the Tribune reported. Two have died.
Here’s what you need to know:
What is synthetic marijuana?
Contrary to what many think, synthetic marijuana is not one drug, and it is very different from tetrahydrocannabinol (aka THC, the main compound in natural marijuana). Synthetic marijuana is a “designer drug,” a chemical engineered to create the same effects as an illegal drug, but one that is different enough to avoid drug laws.
Synthetic cannabinoids (substances mimicking marijuana) work on the same brain receptors as THC, but can bind to the receptor up to 100 times more tightly than THC. Most were actually developed for research purposes so that scientists could better understand the role of THC receptors in the brain. Unlike marijuana, they have no reported potential for medical use. Eighty-four new synthetic cannabinoids were identified by the National Forensic Laboratory Information System in 2015 alone (for comparison, there were only two in 2009). These chemicals, all vastly different from each other, do not cause identical responses in the brain.
A synthetic marijuana chemical is most often sprayed onto a mix of plant materials so that it can be smoked. The chemicals can also be mixed into a liquid for vaping with e-cigarettes or added directly to herbal tea or foods. According to the Drug Enforcement Administration (DEA), this manufacturing and packaging happens “without pharmaceutical-grade chemical purity standards” and “ignoring any control mechanisms to prevent contamination or to ensure a consistent, uniform concentration of the powerful and dangerous drug in each package.”
Why do people use synthetic marijuana?
People use synthetic cannabinoids for many reasons: easy access, lower cost or the promise of a more intense high than they get with marijuana. Many hope that use of synthetic marijuana will avoid a positive urine drug test since many of the chemicals used to make the drugs are not known to the DEA.
In fact, the makers of synthetic marijuana are constantly tweaking the structures of their chemicals to avoid being recognized by the government as an illegal substance and to prevent scientists from developing a drug test for their compound.
Most are made in Asia and smuggled into the U.S., branded as something else. According to the Centers for Disease Control and Prevention (CDC), “There are no standards for making, packaging, or selling synthetic cannabinoid chemicals. That means that two packets of a brand-named product may have completely different chemicals.”
Despite all this, cannabinoids are marketed to unwitting buyers as safe and legal alternatives to marijuana. The CDC says that these drugs “are distributed worldwide under countless trade names and packaged in colorful wrappers designed to appeal to teens, young adults, and first-time drug users.”
They are labeled as “natural” compounds based on the plants inside — even though the active ingredient is a factory-made chemical. Because they have never earned approval from the Food and Drug Administration (FDA), cannabinoids are sold as “herbal products,” “incense,” or “potpourri” to disguise their real use. Most packages are marked with “not for human consumption” — not because the makers don’t want human to use them, but so that the company cannot be held at fault for problems associated with smoking or eating the drug.
So, are these substances actually legal?
Based on major concerns about the danger of these products, the DEA and local agencies are attempting to keep up with drugmakers to ban every known synthetic marijuana substance, but it’s tough to stay on top of all the compounds. As of 2017, 26 cannabinoids were listed as Schedule 1 controlled substances (the most severely restricted substances), though there are likely hundreds more being sold.
What are the effects of synthetic pot on the body?
The effects of these drugs are highly unpredictable, as the actual chemical in the package is widely different and may even change from batch to batch. Many buyers experience different effects than intended.
First and foremost, these are “psychoactive” substances, which cause an altered mental perception of the world. This high can be associated with irritability, confusion, sleepiness, dizziness and inability to concentrate. At worst, they cause hallucinations (fives times more often than THC), suicidal thoughts and violent behavior. They are also far more likely than marijuana to cause other symptoms like vomiting and muscle breakdown. They can lead to heart problems such as fast heart rate, high blood pressure and even heart attacks. There have been reports of rapid and complete kidney failure related to specific strains of synthetic marijuana. In 2018 so far (through March), Poison Control Centers have received 462 calls concerning symptoms related to these drugs. In 2015, there were 7,762 total calls, the highest year on record. Of the people who call poison control or come to the emergency department for problems related to synthetic cannabinoids each year, approximately 1 in 100 die from these events.
Unlike marijuana, synthetic cannabinoids are addictive and regular users report feeling intense withdrawal symptoms when they stop using.
What else is in the package?
Another highly concerning feature of synthetic cannabinoids: These drugs are frequently contaminated with other drugs, and buyers have no idea what may be in the packet. The most common contaminating drug is another designer drug, in a drug class called “cathinones.”
Just as synthetic cannabinoids are designed to mimic THC, cathinones are designed to mimic the effects of cocaine or methamphetamines. Their effects are just as unpredictable and dangerous. When sold by themselves, they are sold as “bath salts” or “plant food” in order to use the label “not for human consumption.” This class of medications most commonly cause confusion, agitation, aggressive and self-harming behavior. They can also lead to fast heart rate, high blood pressure, muscle breakdown, kidney failure and death.
What about the Chicago cases?
The contaminating substance in the recently reported cluster of illnesses is brodifacoum. This is the first time that this substance has been reported in synthetic marijuana, but it has previously been reported to be mixed with other drugs of abuse to make their effects last longer.
Brodifacoum is a rat poison. It is made from the more commonly known rat poison, Coumadin (or warfarin), whose name you may recognize, since, in small doses, it’s used as a medically prescribed blood thinner. Warfarin and brodifacoum interfere with the body’s natural clotting factors and can cause life-threatening bleeding.
Brodifacoum is known as a “superwarfarin,” which means that its effects on the body last a long time and are very difficult to reverse. Bleeding can occur from any part of the body: Several of the recent cases reported bleeding from the eyes and ears, and deaths occurred due to unstoppable internal bleeding.
Though they are sold as safe, legal alternatives to marijuana (and a way to avoid getting caught using drugs), synthetic cannabinoids are a different class of chemicals completely.
They are unpredictable and highly dangerous on their own — and can be contaminated with even more toxic and unreported chemicals, making this a hazardous trend that will likely be marked with more reports of deadly events in the future. In addition, know that there is no standardization in the labels or packets, no guarantee what is inside and no idea, if you take a synthetic cannabinoid, what will happen to you.
If you or someone you know is having health effects that may be related to synthetic marijuana, seek medical attention. More information can be found at the websites of the CDC and the National Institutes of Health.
Outbreak Alert: Potential Life-Threatening Vitamin K-Dependent Antagonist Coagulopathy Associated With Synthetic Cannabinoids Use
From 10 March 2018 through 05 April 2018, 94 people have presented to Emergency Departments (89 in Illinois, 2 in Indiana, 1 in Maryland, 1 in Missouri, and 1 in Wisconsin) with serious unexplained bleeding. None of these patients were on anticoagulation therapy or reported exposure to rat poisons containing a long-acting anti-coagulant brodifacoum. However, their work-up and their response to treatment with fresh frozen plasma and high doses of vitamin K was consistent with long-acting vitamin K-dependent antagonist toxicity. Laboratory investigation confirms brodifacoum exposure in at least 18 patients. There are 2 fatalities—both in Illinois. Illinois public health epidemiologists interviewed 63 patients, and they all reported synthetic cannabinoids use. At least 3 synthetic cannabinoid product samples related to this outbreak have tested positive for brodifacoum. A working hypothesis is the synthetic cannabinoids were contaminated with brodifacoum. Additional activities by the Illinois Department of Public Health include:
Sent clinical alert to providers and Emergency Departments for awareness and to ask them to report new cases.
Sent alert to local health departments with instructions of what to do if they receive a call about similar cases.
Alerted surrounding states of additional potential risks associated with synthetic cannabinoids use.
Released Epi-X to alert health departments nationwide, and report cases to Illinois Department of Public Health.
Issued press release to alert public of potential risk associated with synthetic cannabinoids use.
The Centers for Disease Control and Prevention (CDC) sent a team to assist the Illinois Department of Public Health with the epidemiologic investigation. CDC is also:
Coordinating with multiple states involved.
Reviewing calls to all U.S. poison information centers to identify suspect cases that may be related to the current outbreak.
Hospitals’ supply of vitamin K may be an issue. Cost of outpatient oral vitamin K treatment can be $8,000.00 for 2 weeks treatment, and expected treatment duration is months. Options are being explored to address these issues.
Three patients in Illinois were discovered to have donated plasma prior to admission to hospital for treatment. This issue has not been reported in Indiana or Wisconsin. Cases were reported to and advice was requested from CDC and the U.S. Food and Drug Administration (FDA). Questions regarding plasma/blood donation are added to the case questionnaires. Previous patients were followed up in this regard and new patients are asked about plasma/blood donations.
Patients sent home from surgery or other procedures that could result in bleeding should be told not to use synthetic cannabinoids because of the risk that the product may be contaminated with an anticoagulant.
What are the Clinical Signs of Coagulopathy?
Clinical signs of coagulopathy include bruising, nosebleeds, bleeding gums, bleeding disproportionate to injury, vomiting blood, coughing up blood, blood in urine or stool, excessively heavy menstrual bleeding, back or flank pain, altered mental status, feeling faint or fainting, loss of consciousness, and collapse.
What Do Health Care Providers Need To Do?
Healthcare providers, particularly those based in Illinois and neighboring states, should maintain a high index of suspicion for vitamin K-dependent antagonist coagulopathy in patients presenting with clinical signs of coagulopathy, bleeding unrelated to an injury, or bleeding without another explanation and with a possible history of synthetic cannabinoids (e.g., K2, Spice, and AK47) use; some patients may not divulge use of synthetic cannabinoids. These patients should be screened for vitamin K-dependent antagonist coagulopathy by checking their coagulation profile (e.g., international normalized ratio (INR) and prothrombin time (PT)).
When cases of suspected vitamin K-dependent antagonist coagulopathy associated with synthetic cannabinoids use are identified:
Contact your local Poison Information Center (1-800-222-1222) for questions on diagnostic testing and management of these patients.
Promptly report suspected cases to your local health department or your state health department, if your local health department is unavailable. In addition, report any similar cases encountered since 01 February 2018 to your local health department.
In an effort to better understand the scope of this outbreak, ask your Medical Examiners’ office to report suspected cases, especially those without an alternative diagnosis. If individuals are identified after death or at autopsy showing signs of suspicious bleeding as described above, coroners are encouraged to report the cases to their local health department.
New psychoactive substances constitute a growing and dynamic class of abused drugs in the United States. On July 12, 2016, a synthetic cannabinoid caused mass intoxication of 33 persons in one New York City neighborhood, in an event described in the popular press as a “zombie” outbreak because of the appearance of the intoxicated persons.
We obtained and tested serum, whole blood, and urine samples from 8 patients among the 18 who were transported to local hospitals; we also tested a sample of the herbal “incense” product “AK-47 24 Karat Gold,” which was implicated in the outbreak. Samples were analyzed by means of liquid chromatography–quadrupole time-of-flight mass spectrometry.
The synthetic cannabinoid methyl 2-(1-(4-fluorobenzyl)-1H-indazole-3-carboxamido)-3-methylbutanoate (AMB-FUBINACA, also known as MMB-FUBINACA or FUB-AMB) was identified in AK-47 24 Karat Gold at a mean (±SD) concentration of 16.0±3.9 mg per gram. The de-esterified acid metabolite was found in the serum or whole blood of all eight patients, with concentrations ranging from 77 to 636 ng per milliliter.
The potency of the synthetic cannabinoid identified in these analyses is consistent with strong depressant effects that account for the “zombielike” behavior reported in this mass intoxication. AMB-FUBINACA is an example of the emerging class of “ultrapotent” synthetic cannabinoids and poses a public health concern. Collaboration among clinical laboratory staff, health professionals, and law enforcement agencies facilitated the timely identification of the compound and allowed health authorities to take appropriate action.
A drug known as “monkey dust” is sweeping across the north of the UK.
It’s also known as “bath salts,” and has been linked to violent face-eating attacks in the US.
The substance makes people feel strong, and can cause them to act dangerously.
Paramedics and police have been called to scenes where people have scaled buildings and jumped from great heights.
Side effects of the drug include a paranoia, hallucinations, chest pain, and high blood pressure.
People sometimes take recreational drugs to escape, or to feel good. But a substance that is currently becoming an “epidemic” in the UK, according to police in the north of England, is causing psychotic, violent behaviour.
The drug, known as “monkey dust,” is sweeping across the northern UK, and is said to make users feel as though they have incredible strength akin to the Hulk, and can make them act dangerously — scaling buildings and jumping from great heights.
The substance is methylenedioxypyrovalerone, or MDPV, and gives a similar feeling to that of Mcat or mephedrone, according to Why Not Find Out— an online source of information about drugs.
It’s a class B drug in the UK to possess or sell, meaning if you’re caught with it you face an unlimited fine and up to five years in prison. Selling or producing it can mean being locked away for 14 years.
MDPV looks like a fine white or brownish powder, and usually sells for about £10 to £15 for a gram, which is significantly cheaper than other recreational drugs like MDMA and cocaine. Sky News reportsin Stoke-on-Trent it can be bought for as little as £2.
—Stoke Police (@Policingstoke) August 5, 2018 ” data-e2e-name=”embed-container” data-media-container=”embed” style=”box-sizing: border-box; margin: 20px 0px;”>
“It gives great energy and euphoria but can cause depression the following day,” according to Why Not Find Out. “It is addictive. It also makes people who take it smell of urine, as does their clothes and sheets.”
Other side effects include a paranoia, hallucinations, chest pain, and high blood pressure.
MDPV has risen in popularity this summer in the UK, according to Sky News, with police and paramedics responding to a series of violent attacks and psychotic episodes, including people leaping from buildings and trying to fight with officers. Apparently, MDPV makes people fearless.
“When you are trying to restrain them it’s like you are dealing with someone who thinks they are the Incredible Hulk,” PC Rich Frost told Sky News. “The strength is unbelievable.”
MDPV is a stimulant powder with effects similar to that of Mcat or mephedrone. Its chemical name is methylenedioxypyrovalerone. It is a Class B drug illegal to possess or sell. It appears as a very fine white or brownish powder, sells for about £10-15 a gram so much cheaper than cocaine.
It is commonly called Monkey Dust or Dust. It is generally snorted or bombed. Its effects last a few hours perhaps 5-6.
It gives great energy and euphoria but can cause depression the following day. It is addictive. It also makes people who take it smell of urine, as does their clothes and sheets.
Documentary On The Effects Of Bath Salts And Legal Highs
Aggressive behavior can be physical (shoving or hitting somebody) or verbal (yelling at someone or saying something mean to them). What does a person who exhibits behavior like that have in common with someone who has a substance use disorder?
Your first guess may be, “Nothing!” They seem like completely separate problems. However, research is finding that’s not totally true.
What’s the link?
Scientists who study the brain and behavior have discovered that those who tend to be aggressive and hostile and those with substance use disorders are alike in two ways:
What’s going on here? Scientists think that some people are more likely than others to develop “compulsive” (uncontrollable) aggression—and that this involves some of the same brain activity that gets disrupted with a substance use disorder. Further research into the brain could reveal why some people are more inclined than others to use drugs or to act aggressively.
Observers have noted parallels between aggression and addiction. People with either problem pursue a harmful behavior, even despite negative consequences. A new study by scientists at the National Institute on Drug Abuse’s (NIDA) Intramural Research Program (IRP) showed that when mice are exposed to experimental protocols adapted from those that are used to model human addictive behaviors, some animals develop an addiction-like propensity to aggression.
NIDA IRP researchers observed that about 70 percent of the male mice pressed a lever in their cages for the opportunity to show aggression toward a mouse of a smaller, subordinate strain. About 19 percent were “compulsive aggression-seeking” animals who worked harder (lever pressed more times) for a chance to aggress, and were more likely to continue lever pressing even when doing so meant forgoing food.
The researchers conclude that under certain conditions, a portion of the mouse population is susceptible to developing compulsive aggression. They hypothesize that this susceptibility is a product of evolution, that it involves some of the same motivational circuits in the brain that are disrupted in addiction—and that it may also occur in people. Their findings also indicate that the same animal models researchers have developed to investigate addiction can also be used to study compulsive aggression.
Here are some articles related to the biology and meaning of aggression:
Stimulants are drugs that increase alertness, attention, and energy by raising the levels of key chemicals in the brain and other parts of the body. This may be helpful for people with certain health conditions, such as attention-deficit hyperactivity disorder (ADHD).
It’s estimated that more than 10 percent of teens have been diagnosed with ADHD. For them, ADHD can make it difficult to complete schoolwork or other tasks.
If someone with ADHD has difficulty paying attention, how can something called a stimulant help? The reason is that stimulants increase the amount of a chemical needed to help a person stay focused.
Research by NIDA’s Dr. Nora Volkow found that the symptoms of ADHD are associated with having lower levels of dopamine in the brain. Prescription stimulants slowly increase the level of dopamine, similar to the way it’s naturally produced in the brain. A doctor will usually prescribe a low dose (amount) of a stimulant and increase it gradually if necessary.
Prescription stimulants can also have some unpleasant side effects: fatigue, anxiety, depression, and raising a person’s blood pressure, rate of breathing, and heart rate. Misusing prescription stimulants can also lead to stimulant use disorders—but people with ADHD who use them as prescribed are not at the same risk.
In our previous post, we described how prescription stimulants can reduce symptoms of ADHD. Treating ADHD with stimulants (sometimes combined with counseling) can help improve ADHD symptoms, as well as a person’s self-esteem and their interactions with friends and family.
However, other, non-prescribed stimulants don’t help with ADHD, and each one has its own side effects and risks:
Caffeine is found in coffee, many kinds of soda and energy drinks, and chocolate. It also comes in pills and tablets that are advertised as helping you stay awake. Caffeine produces a small rise in dopamine. Consuming too much of it can be harmful, but scientifically speaking, it isn’t addictive—although you can feel withdrawal symptoms if you stop consuming it all of a sudden.
Nicotine is found in cigarettes and chewing tobacco. Nicotine stimulates both dopamine and the body’s adrenal glands to release epinephrine (also called adrenaline). Nicotine is extremely addictive.
Illegal stimulants include cocaine, methamphetamine or meth, and MDMA (Ecstasy or Molly). These drugs produce a large surge of dopamine that unbalances the reward system in the brain and produces the “high.” This surge also increases the risk for addiction.
Sometimes, people misuse prescription stimulants just to get high, or because they think the stimulants will help them lose weight, or boost their study performance. While prescription stimulants do promote wakefulness, studies have found they don’t enhance learning or thinking ability when taken by people who don’t have ADHD.
However, misusing prescription stimulants can lead to:
Sleep problems, depression, and paranoia;
Serious heart complications, including stroke (at high doses); and
Abnormally high levels of dopamine in the body. This produces the “high,” which increases the risk for misusing the drug again and, in some cases, becoming addicted.
The good news is that teens’ misuse of the stimulants Adderall and Ritalin has been decreasing in recent years. For example, about 6 percent of teens reported misusing Adderall last year, a slight decrease from 2015, and only about 1 percent report misusing Ritalin, down from a peak level of 5 percent in 2004.
You can keep this positive trend going. Avoid using prescription stimulants unless they’re prescribed for you, and spread the word about the risks in misusing them.
There’s a lot of confusion about what drug addiction (also called substance use disorder, or SUD) actually means, even though it’s a problem that affects millions of Americans from all walks of life. The National Institute on Drug Abuse (NIDA) defines drug addiction as a chronic brain disease and one in which relapses are very common. It isn’t, though, a sign of weak moral character or lack of willpower. What might start as a choice to try a drug (as a legitimate prescription or recreationally) can result, over time, in someone losing the ability to choose and becoming addicted.
People with addiction cannot abstain, stop their drug-seeking behavior or control cravings without getting help. They compulsively need to use, regardless of the damage the addiction is causing in their lives – physically, mentally, emotionally, educationally, socially, spiritually, financially. Treatment is often necessary because the disease typically gets progressively worse and can even lead to disability or premature death. In fact, according to NIDA, using tobacco products is the number one preventable cause of disease, disability and death in the U.S.
Drugs of Addiction
To make matters more complicated, there are many types of drugs that people can become addicted to, and each has its own way of affecting the body, including its own unique withdrawal symptoms. Commonly abused substances include not just illicit drugs but also some prescription medications such as opioids (like oxycodone and hydrocodone), stimulants (such as cocaine and dextroamphetamine) and depressants (including benzodiazepines and barbiturates). These drugs may at first be prescribed for medical reasons and a person later takes the medication in a way that wasn’t prescribed by their healthcare provider, or illegally takes a medication without a prescription. Still others become addicted to over-the-counter medications like cough or cold syrups and sleeping pills that are readily available, legal drugs. Other commonly abused drugs include hallucinogens, inhalants, sedatives, hypnotics, cannabis (marijuana, for non-medical purposes), alcohol and, as mentioned above, tobacco.
Drugs Change the Brain
Part of the reason substance use disorders are so complex to understand and to treat is that over time drugs of abuse can actually change circuits in the brain – and those changes can persist even after stopping the drug and going through detoxification, or “detox.” Some drugs activate the brain’s reward system in such an intense way that a person can start to ignore activities they once enjoyed as they seek the intense pleasure or “high” the drug gives, driving them to keep using; cocaine and methamphetamine are good examples of this. When a drug user experiences this feeling of intoxication, it can affect their thinking, judgment, emotions and behavior and can lead to breathing problems, seizures, coma or even death. The brain can adapt to produce less dopamine (the neurotransmitter that controls the body’s reward and pleasure centers); the result is that the addict needs an ever-larger dose to experience the same high. Still other drugs, such as marijuana and heroin, work to dupe the brain into believing they’re brain chemical messengers known as neurotransmitters.
It’s important to understand that not everyone who tries a drug of abuse becomes addicted. Several factors are involved, including one’s biology (which includes family history and physiology), environment (whether friends and family use illicit drugs, for example) and developmental stage (adolescents are particularly vulnerable because their brains are still developing). All drugs have the potential to be addictive. But, in general, addiction to cocaine, methamphetamine and heroin can happen more quickly with fewer doses. (Alcohol is a very commonly abused drug, too; for more information on alcoholism, please visit the Alcoholism section.)
How Big is the Problem?
If you’re reading this because you’re concerned that you or a loved one may have a substance use problem, you’re not alone. Drug use is very common:
Nearly 25 million Americans were illicit drug users in 2013, according to the National Survey on Drug Use and Health (NSDUH), which came out in 2014.
That same report shows that an estimated 21.6 million Americans ages 12 and older had a substance use disorder in the previous year, meaning an addiction to drugs or alcohol.
Depression and other mental health issues play an important role in the prevalence of drug addiction; many people have both an SUD and a mental health issue (what’s known as co-occurring disorders). In other cases, people who become addicted to a drug of abuse may go on to experience one or more symptoms of a mental health problem such as an anxiety disorder, depression or psychosis – what’s known as a substance-induced mental disorder.
An SUD can be mild, moderate or severe, depending on how many symptoms a person has. The more symptoms, the greater the severity of the drug addiction. Many illicit drugs, but not all, produce withdrawal symptoms; those that do include opioids, sedatives, hypnotics (such as LSD) and anxiolytics (drugs to treat anxiety). Tobacco products, stimulants and marijuana have less apparent withdrawal symptoms, according to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, but they still cause withdrawal.
When people are addicted to a substance, it means in part that they’ve built up a tolerance to the drug; cravings make quitting extremely difficult – one of the reasons stopping a drug should be done under medical supervision. The first step, detoxification, is often done with the help of prescription medication to make the process more comfortable, but counseling is also needed to prevent the relapses that are common with this disease. Unfortunately, millions of addicts who could benefit from care at a specialty facility like a rehabilitation center don’t receive it, according to the NSDUH. For those who are addicted to two or more substances (what’s called a poly-drug addiction), treatment providers need to consider every substance a person is using when creating a treatment plan.
If you suspect that you or a loved one has a substance use problem, talk to a doctor, health care professional, addiction specialist or psychotherapist. These professionals can evaluate symptoms and make an accurate diagnosis that will help the recovery process begin.
People who abuse substances often say they take them to have fun or get high. It’s not that simple for addicts, though. An addicted person can no longer control whether or not he/she uses. Mentally and physically, the addict feels compelled to have the drug. Addiction is considered a chronic disease with the possibility of relapse an ever-present reality.
What you should know:
Addiction is a disease that is complex but treatable.
Prolonged drug use affects brain function.
Illegal drugs are defined as controlled substances under federal and state law. They are monitored and enforced by the Drug Enforcement Agency (DEA).
Marijuana is the most-used illicit drug, with 19.8 million U.S. users age 12 and over, according to the 2013 National Survey on Drug Use and Health (NSDUH), which is published by the Substance Abuse and Mental Health Services Administration (SAMHSA).
Six-and-a-half million Americans use prescription pain relievers non-medically, and 1.5 million are dependent on or abusing cocaine, according to SAMHSA’s 2013 NSDUH survey.
In 2013, 22.7 million people 12 and over who could have benefited from substance use treatment in a specialty facility did not receive that help. It’s a myth that someone must want to go into treatment for substance abuse for it to be effective, says the National Institute on Drug Abuse (NIDA).
For decades, researchers have been trying to figure out what leads people to become addicted to drugs. While there’s no single root cause of drug addiction, experts think a combination of the following are most likely to play a role:
Your role models. Your early years, including your mother’s and father’s parenting styles and whether one or both parents or even an older sibling abused substances can affect whether you experiment with drugs and go on to develop an addiction. Our early role models, for good or ill, influence our behavior. They can also teach us appropriate ways to handle problems, bounce back and persevere; these coping skills make it less likely someone will develop an addiction. A family history of substance abuse is also linked to an increased risk. For more on the role of genetics, go the Risk Factors section.
Your personal history. Stressful or traumatic events, living in poverty, the availability of illegal drugs, peer pressure and whether or not your friends and family use drugs – all are associated with a greater likelihood of developing a substance abuse problem.
Your psychological makeup. How you feel about yourself, especially your self-esteem during adolescence, your temperament, a tendency toward impulsive behavior and exhibiting aggressive or antisocial behavior early in life are thought to forecast later drug or alcohol problems as well as a tendency toward violence.
On the flip side, there are factors that can lower someone’s chances of having an addiction; these include developing good self-control, practicing religious beliefs, having healthy relationships with family and friends and being involved in social activities in the community, reports SAMSHA.
Symptoms of Drug Addiction
There are a number of signs that may indicate a substance abuse problem, including:
A change in friends and hangouts
An unexplained need for cash
Bloodshot eyes or enlarged pupils
Sudden weight changes (gain or loss)
Tremors in the hands
A drop in attendance at work or school
Changes in sleep, mood, motivation or attitude
Keep in mind that physical dependence on a drug or medication is not the same thing as having an addiction; a person may be dependent on a drug if he or she experiences withdrawal symptoms if the drug is stopped. Someone may also develop a tolerance to the substance so that he or she requires increasingly larger doses of a drug in order to achieve the same effect or high. And when a drug user comes off a substance, he or she may experience withdrawal symptoms that vary depending on the substance(s). According to the American Psychiatric Association’s (APA) diagnostic manual, DSM-5, “Neither tolerance nor withdrawal is necessary for a diagnosis of a substance use disorder.”
Doctors, therapists and addiction counselors look at a variety of factors when deciding whether someone has a substance use disorder. If you or a loved one have two or three of the indicators below, it can point to a mild problem with drugs, while having four or five symptoms can underscore a moderate problem. Six or more of these symptoms may signal a severe substance use disorder. No matter how serious a drug problem is, recognizing the symptoms of drug addiction is the all-important first step to getting help – and recovering. So ask yourself these questions:
Are you or a loved one…
Using a substance over a longer time period of time than planned?
Making unsuccessful attempts to control or stop taking the drug(s)?
Spending a lot of time finding, using or recovering from using a substance(s)?
Experiencing cravings for a substance(s)?
Failing to show up or fulfill expectations at work, school or home?
Continuing to use an illegal substance(s) despite problems it’s causing in relationships?
Giving up activities once enjoyed in order to use a drug(s)?
Using a drug(s) regularly while in situations where it poses physical danger (such as driving, operating machinery or boating)?
Ignoring physical or psychological problems resulting from drug use?
Developing a tolerance for a drug’s effects?
Experiencing withdrawal symptoms or masking them with another substance(s)?
The more you know about substance abuse, the better the chances of avoiding a drug addiction before it starts. Here are several red flags that raise the risk of becoming a substance abuser:
Inheriting the genes
As mentioned above, your biological makeup has a lot to do with whether you’ll develop an addiction. In fact, the APA goes so far as to say that 50% of your susceptibility to becoming addicted is related to genetic factors. And when it comes to tobacco, genetics account for 75% of a person’s tendency to try smoking and 60% of their chances of becoming hooked. But DNA alone isn’t destiny. Besides the genes you’re born with, environmental factors, like how you were raised; whether you were sexually or physically abused; and whether you grew up in poverty or witnessed violence can also influence a person’s vulnerability to addiction.
Dealing with a mental health issue
If you or someone you love suffers from a mental disorder such as depression, anxiety, attention deficit disorder, post-traumatic stress disorder schizophrenia or an eating disorder, among other conditions, substance abuse is likelier to become a problem. In 2013, nearly eight million U.S. adults had both a substance use disorder and at least one mental issue. And 2.3 million of that group had a co-occurring SUD and a serious mental health issue, which the NSDUH defines as “a mental, behavioral or emotional disorder that substantially interferes with or limits one or more major life activities.”
Experimenting at an early age
In 2013, nearly 9% of U.S. adolescents ages 12 to 17 were illicit drug users, and 1.3 million teens had a diagnosed SUD. While it’s possible to become an addict at any age, many teens are natural risk-takers, mostly because the parts of the brain in charge of self-control and good judgment are still developing in adolescence. That can make trying illicit drugs a lot more attractive. The trouble is, say experts at NIDA, “the earlier drug use begins, the more likely it will progress to more serious abuse.” And there’s some evidence to suggest that how a drug is taken – especially if it’s smoked or injected into a vein – may increase its risk of becoming addictive.
There’s no single treatment that’s right for someone trying to overcome a substance addiction. Treatment for a substance use disorder (SUD) usually begins with detoxification or “detox” – a process during which the patient is medically supported while the substance(s) is removed from the person’s system. When someone enters treatment, one of the first things he/she may experience during the detox process is withdrawal, which can include physical symptoms such as nausea, diarrhea, shaking, fever, insomnia and sweating and/or psychological symptoms such as depression, anxiety, anger and upset. In some cases, a drug rehabilitation center will use FDA-approved medications to help counteract withdrawal symptoms with the goal of weaning the patient off the medication as soon as possible; although sometimes medication-assisted therapy is needed on a long-term basis to prevent cravings that can trigger drug-seeking behavior and relapse. While detox is the first step to any kind of treatment, counseling is also typically needed to achieve lasting results.
Whether a substance use disorder is mild, moderate or severe, some kind of treatment is usually necessary, which makes it tragic that only a small number of those who need help actually get it. According to the Substance Abuse and Mental Health Services Administration’s National Survey on Drug Use and Health (2013), only 2.5 million people out of the 22.7 million people who needed treatment for drug or alcohol use actually received help at a specialty facility While there’s no cure for drug addiction, for most (though not all), abstinence or giving up the substance entirely is necessary.
Below are some of the most common treatment options for substance use disorders. If you or a loved one seek treatment for drug addiction, it’s likely that a combination of several of these approaches will be recommended and used:
Drug rehabilitation programs use a variety of counseling approaches to help people experience lasting recovery. Types of counseling include:
SMART Recovery® (Self-Management and Recovery Training): This community-support program has a four-point plan to teach self-reliance, and clients using SMART Recovery benefit from online support groups, message boards and chat rooms as well as in-person meetings to stay motivated in their recovery efforts.
BRENDA: BRENDA combines psychosocial counseling and pharmacotherapy (prescription drugs) to help patients deal with substance addiction. The acronym refers to the steps a counselor takes in treating a client using this method:
Report to the patient on evaluation findings
Needs identified by both the patient and therapist
Direct advice to the patient
Assessing the patient’s reaction to advice; modifying the plan when needed
This treatment model uses a type of psychotherapy called cognitive-behavioral therapy (CBT) in which a therapist will help clients examine their thinking and feelings in an effort to change negative and unproductive thoughts and beliefs that may lead to drug use.
Other types of counseling:
Motivational incentives: For gains made in treatment, drug and alcohol counselors may offer a reward system to encourage patients to work hard in recovery. Rewards might be for a special privilege, outing or voucher.
Motivational Interviewing (MI): Therapists who use MI help clients feel inspired and empowered to make needed life changes and to reach recovery goals.
Multidimensional Family Therapy (MDFT): Sometimes the whole family needs to be willing to evaluate its dynamics in order to help one or more member(s) overcome an addiction and/or another mental health issue. MDFT involves the whole family in the healing process to improve relationships, end enabling behavior and create harmony.
Sometimes the right option for treating drug addiction may be going to an inpatient or residential treatment center to live for a period of time. How long depends on the severity of the addiction, the kind of addiction(s) and the patient’s progress. These specialized facilities offer medically-supervised detox, which is a process to get drugs out of the bloodstream and tissues. In rehab, patients also receive intensive counseling to cope with triggers, cravings and any co-occurring mental health disorders. It’s helpful to think of rehab as a kind of retreat where the addict lives and works on learning to overcome triggers of addiction and manage any underlying mental disorders that require treatment along with the substance use disorder.
There are also outpatient rehab programs where patients live at home but attend a drug treatment (or partial hospitalization) program during the day, which may last for seven or eight hours. Or you or your loved one may attend an evening program that meets several times a week for several hours in the evenings only. With outpatient day or evening programs, patients sleep at home, which can be successful as long as drug networks, old haunts and triggers don’t interfere with the progress of treatment. While in treatment, patients in these programs, too, work on understanding their addiction and any mental health issues through counseling.
When selecting a program, be aware that there are customized programs tailored to groups of people who are like-minded; by bringing together people from similar backgrounds who are grappling with the same or similar issue, members can effectively work together as a group. Program alumni may even meet up later for special weekends and offer one another ongoing support in recovery. Read on for several examples of custom-tailored programs now being offered by some treatment centers:
Christian programs address drug addiction with a Bible-based approach, so attendees can find strength through faith. Treatment may include counseling and 12-step or other community-support programs, yet the focus on scripture allows members of these programs to be guided to recovery in large part through their beliefs.
Women-only programs address both the substance use disorder as well as any past history of abuse or trauma or mental illness that may underpin a drug addiction.
Adolescent programs tend to be gender-specific and allow teens a safe place where they can work to overcome drug addiction while also attending classes, so they don’t fall behind in school during treatment.
Spanish-speaking programs make treatment more relatable for those who speak English as a second language. Counselors, too, speak Spanish, and all written materials are printed in Spanish.
Medication-Assisted Therapy (MAT)
The Food and Drug Administration (FDA) has approved several prescription medications for the treatment of substance use disorders. Medication-assisted therapy proves most effective when used in conjunction with other approaches, such as counseling. Pharmacological approaches designed to help substance abusers detox and reduce the chances of relapse include these medications:
For opioids: The FDA has approved several prescription medications for opiate addiction to heroin, morphine or prescription painkillers like oxycodone and hydrocodone. There are a variety of prescription drugs that are used in treating opioid use disorders with active ingredients that either reduce withdrawal symptoms, like cravings, or block the effects of opiates altogether. These include:
Buprenorphine – (brand name: Subutex): An initial treatment to prevent or reduce withdrawal symptoms such as drug cravings
Methadone – (brand names: Dolophine or Methadose): Used to prevent withdrawal symptoms and to block the high from taking illicit opiates. Only authorized, specially licensed facilities can administer methadone maintenance.
Naltrexone – (brand names: Depade, Revia, and Vivitrol): All three block the effects of opioids; Vivitrol is an extended-release injection, given once a month.
Naloxone – (brand name: Suboxone): Prescribed as a maintenance medication that contains buprenorphine as well, Suboxone blocks or reverses the effects of opioids. For opioid overdoses, Evzio, an auto-injector containing naloxone, is available for emergency home use.
While there are other prescription medications in the drug pipeline and now being tested, there are no drugs currently available for the treatment of cocaine, methamphetamine, cannabis (marijuana) or hallucinogen use disorders.
The original 12-step program is one you’ve undoubtedly heard of before: Alcoholics Anonymous (AA), which has been around since 1935. AA has been helping alcoholics get and stay sober for decades with meetings available in big cities and small towns across the globe. Over time, this community of support, in which alcoholics help each other, has inspired other, similar programs for a wide variety of drug addictions that people grapple with:
These 12-step programs borrow at least in part from the AA model, which is based on 12 consecutive processes (each step building on the one(s) preceding it). The steps include minimizing self-centeredness, providing support to others in the group and making amends to those whom the substance abuser has hurt, among others. For a full list of the 12 steps, go to the Get Help section.
While some addicts rely solely on 12-step programs to treat and recover from their drug addiction, others use it in conjunction with counseling. And often 12-step programs are included as part of inpatient and outpatient drug rehabilitation.
For tobacco/nicotine: For tobacco products containing highly addictive nicotine, several nicotine replacement therapies are available over-the-counter at drugstores. These include nicotine patches, sprays, gums and lozenges that alleviate drug cravings. Prescription drugs such as bupropion (brand names: Wellbutrin, Zyban) and varenicline (brand name: Chantix) are also FDA-approved.
If you find yourself asking the question, Am I addicted to drugs? you should take the answer to that question very seriously. Unless recognized and treated, an addiction to a medication or illicit/illegal drug can greatly diminish your chances of leading a functional life, maintaining a daily routine or experiencing an enduring sense of well-being. Fortunately, you can perform a fairly accurate self-assessment of your drug-using status if you know the signs that indicate active addiction.
What Is Drug Addiction?
The potential for drug (and alcohol) addiction arises when your brain starts to treat the chemical changes triggered by your habitual substance intake as a normal operating condition. Experts in the field refer to this state as physical dependence. Physical dependence transitions into active addiction when you lose control over your ability to limit the number of times you use a given substance and/or your ability to limit the amount of that substance you take on any given occasion.
Signs to Look For
In addition to losing control over the frequency and amount of your drug intake, you may also experience a range of other problems that point to the presence of an addiction. Specific things you may notice include:
An intense desire for the drug
The need to increase your intake of the drug in order to keep feeling its effects
Establishment of drug use as your daily priority
Devotion of money to purchasing drugs even if it means failing to meet important financial obligations
A drug-based inability to meet other important personal, social, school-related or work-related responsibilities
Repeated use of drugs in situations that pose a clear danger to yourself or others
Overlap With Substance Abuse
When trying to figure out if you are addicted to drugs, it’s crucial to understand that doctors and public health officials don’t make a firm distinction between drug addiction and non-addicted drug abuse. Even if you don’t have problems with physical dependence, you can experience changes in your thoughts and behaviors that significantly interfere with your ability to function or maintain a feeling of wellness. In fact, the guidelines currently used by doctors in the U.S. include the symptoms of addiction and non-addicted substance abuse in a single illness category called substance use disorder. There are subtypes of this disorder for alcohol and every major addictive drug/medication.
“Alcohol and endogenous aldehydes damage chromosomes and mutate stem cells”
Juan I. Garaycoechea, Gerry P. Crossan, Frédéric Langevin, Lee Mulderrig, Sandra Louzada, Fentang Yang, Guillaume Guilbaud, Naomi Park, Sophie Roerink, Serena Nik-Zainal, Michael R.
Stratton & Ketan J. Patel
This pay-walled article, published in “Nature,” presents fresh evidence that alcohol can damage chromosomes and cause mutations. If you don’t have a zillion dollars to spare, The American Cancer Society has put together a layman’s version of the subject here.
Here’s an explainer from Britain’s National Health Service. And here’s an interview with one of the authors, published in “Genetic Engineering and Biotechnology News.” Suffice to say that among the many health problems alcohol can cause, the one that all too often goes unmentioned, namely cancer, is not a trivial side effect.
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Map 22193 Woodbridge Prince William – 22194 Woodbridge Prince William – 22195 Woodbridge Prince William – 22199 Lorton Fairfax – 22201 Arlington Arlington – 22202 Arlington Arlington – 22203 Arlington Arlington – 22204 Arlington Arlington – 22205 Arlington Arlington – 22206 Arlington Arlington – 22207 Arlington Arlington – 22209 Arlington Arlington – 22210 Arlington Arlington – 22211 Ft Myer Arlington – 22212 Arlington Arlington – 22213 Arlington Arlington – 22214 Arlington Arlington – 22215 Arlington Arlington – 22216 Arlington Arlington View
Map 22217 Arlington Arlington – 22218 Arlington Arlington – 22219 Arlington Arlington – 22222 Arlington Arlington – 22223 Arlington Arlington – 22225 Arlington Arlington – 22226 Arlington Arlington – 22227 Arlington Arlington – 22229 Arlington Arlington – 22230 Arlington Arlington – 22234 Arlington Arlington – 22240 Arlington Arlington – 22241 Arlington Arlington – 22242 Arlington Arlington – 22243 Arlington Arlington – 22244 Arlington Arlington – 22245 Arlington Arlington – 22246 Arlington Arlington – 22301 Alexandria Alexandria City View
Map 22302 Alexandria Alexandria City – 22303 Alexandria Fairfax – 22304 Alexandria Alexandria City – 22305 Alexandria Alexandria City – 22306 Alexandria Fairfax – 22307 Alexandria Fairfax – 22308 Alexandria Fairfax – 22309 Alexandria Fairfax – 22310 Alexandria Fairfax – 22311 Alexandria Alexandria City – 22312 Alexandria Fairfax – 22313 Alexandria Alexandria City – 22314 Alexandria Alexandria City – 22315 Alexandria Fairfax – 22320 Alexandria Alexandria City – 22321 Alexandria Fairfax – 22331 Alexandria Alexandria City – 22332 Alexandria Alexandria City – 22333 Alexandria Alexandria City View
Map 22334 Alexandria Alexandria City – 22336 Alexandria Alexandria City – 22401 Fredericksburg Fredericksburg City – 22402 Fredericksburg Fredericksburg City – 22403 Fredericksburg Stafford – 22404 Fredericksburg Fredericksburg City – 22405 Fredericksburg Stafford – 22406 Fredericksburg Stafford – 22407 Fredericksburg Spotsylvania – 22408 Fredericksburg Spotsylvania – 22412 Fredericksburg Stafford – 22427 Bowling Green Caroline – 22428 Bowling Green Caroline – 22430 Brooke Stafford – 22432 Burgess Northumberland – 22433 Burr Hill Orange – 22435 Callao Northumberland – 22436 Caret Essex – 22437 Center Cross Essex View
Map 22438 Champlain Essex – 22442 Coles Point Westmoreland – 22443 Colonial Beach Westmoreland – 22446 Corbin Caroline – 22448 Dahlgren King George – 22451 Dogue King George – 22454 Dunnsville Essex – 22456 Edwardsville Northumberland – 22460 Farnham Richmond – 22463 Garrisonville Stafford – 22469 Hague Westmoreland – 22471 Hartwood Stafford – 22472 Haynesville Richmond – 22473 Heathsville Northumberland – 22476 Hustle Essex – 22480 Irvington Lancaster – 22481 Jersey King George – 22482 Kilmarnock Lancaster – 22485 King George King George View
Map 22488 Kinsale Westmoreland – 22501 Ladysmith Caroline – 22503 Lancaster Lancaster – 22504 Laneview Essex – 22507 Lively Lancaster – 22508 Locust Grove Orange – 22509 Loretto Essex – 22511 Lottsburg Northumberland – 22513 Merry Point Lancaster – 22514 Milford Caroline – 22517 Mollusk Lancaster – 22520 Montross Westmoreland – 22523 Morattico Lancaster – 22524 Mount Holly Westmoreland – 22526 Ninde King George – 22528 Nuttsville Lancaster – 22529 Oldhams Westmoreland – 22530 Ophelia Northumberland – 22534 Partlow Spotsylvania View
Map 22535 Port Royal Caroline – 22538 Rappahannock Academy Caroline – 22539 Reedville Northumberland – 22542 Rhoadesville Orange – 22544 Rollins Fork King George – 22545 Ruby Stafford – 22546 Ruther Glen Caroline – 22547 Sealston King George – 22548 Sharps Richmond – 22552 Sparta Caroline – 22553 Spotsylvania Spotsylvania – 22554 Stafford Stafford – 22555 Stafford Stafford – 22556 Stafford Stafford – 22558 Stratford Westmoreland – 22560 Tappahannock Essex – 22565 Thornburg Spotsylvania – 22567 Unionville Orange – 22570 Village Richmond View
Map 22572 Warsaw Richmond – 22576 Weems Lancaster – 22577 Sandy Point Westmoreland – 22578 White Stone Lancaster – 22579 Wicomico Church Northumberland – 22580 Woodford Caroline – 22581 Zacata Westmoreland – 22601 Winchester Winchester City – 22602 Winchester Frederick – 22603 Winchester Frederick – 22604 Winchester Winchester City – 22610 Bentonville Warren – 22611 Berryville Clarke – 22620 Boyce Clarke – 22622 Brucetown Frederick – 22623 Chester Gap Rappahannock – 22624 Clear Brook Frederick – 22625 Cross Junction Frederick – 22626 Fishers Hill Shenandoah View
Map 22627 Flint Hill Rappahannock – 22630 Front Royal Warren – 22637 Gore Frederick – 22638 Winchester Frederick – 22639 Hume Fauquier – 22640 Huntly Rappahannock – 22641 Strasburg Shenandoah – 22642 Linden Warren – 22643 Markham Fauquier – 22644 Maurertown Shenandoah – 22645 Middletown Frederick – 22646 Millwood Clarke – 22649 Middletown Warren – 22650 Rileyville Page – 22652 Fort Valley Shenandoah – 22654 Star Tannery Frederick – 22655 Stephens City Frederick – 22656 Stephenson Frederick – 22657 Strasburg Shenandoah View
Map 22660 Toms Brook Shenandoah – 22663 White Post Clarke – 22664 Woodstock Shenandoah – 22701 Culpeper Culpeper – 22709 Aroda Madison – 22711 Banco Madison – 22712 Bealeton Fauquier – 22713 Boston Culpeper – 22714 Brandy Station Culpeper – 22715 Brightwood Madison – 22716 Castleton Rappahannock – 22718 Elkwood Culpeper – 22719 Etlan Madison – 22720 Goldvein Fauquier – 22721 Graves Mill Madison – 22722 Haywood Madison – 22723 Hood Madison – 22724 Jeffersonton Culpeper – 22725 Leon Madison View
Map 22726 Lignum Culpeper – 22727 Madison Madison – 22728 Midland Fauquier – 22729 Mitchells Culpeper – 22730 Oakpark Madison – 22731 Pratts Madison – 22732 Radiant Madison – 22733 Rapidan Culpeper – 22734 Remington Fauquier – 22735 Reva Madison – 22736 Richardsville Culpeper – 22737 Rixeyville Culpeper – 22738 Rochelle Madison – 22739 Somerville Fauquier – 22740 Sperryville Rappahannock – 22741 Stevensburg Culpeper – 22742 Sumerduck Fauquier – 22743 Syria Madison – 22746 Viewtown Culpeper View
Map 22747 Washington Rappahannock – 22748 Wolftown Madison – 22749 Woodville Rappahannock – 22801 Harrisonburg Harrisonburg City – 22802 Harrisonburg Harrisonburg City – 22803 Harrisonburg Harrisonburg City – 22807 Harrisonburg Harrisonburg City – 22810 Basye Shenandoah – 22811 Bergton Rockingham – 22812 Bridgewater Rockingham – 22815 Broadway Rockingham – 22820 Criders Rockingham – 22821 Dayton Rockingham – 22824 Edinburg Shenandoah – 22827 Elkton Rockingham – 22830 Fulks Run Rockingham – 22831 Hinton Rockingham – 22832 Keezletown Rockingham – 22833 Lacey Spring Rockingham View
Map 22834 Linville Rockingham – 22835 Luray Page – 22840 Mc Gaheysville Rockingham – 22841 Mount Crawford Rockingham – 22842 Mount Jackson Shenandoah – 22843 Mount Solon Augusta – 22844 New Market Shenandoah – 22845 Orkney Springs Shenandoah – 22846 Penn Laird Rockingham – 22847 Quicksburg Shenandoah – 22848 Pleasant Valley Rockingham – 22849 Shenandoah Page – 22850 Singers Glen Rockingham – 22851 Stanley Page – 22853 Timberville Rockingham – 22901 Charlottesville Albemarle – 22902 Charlottesville Charlottesville City – 22903 Charlottesville Charlottesville City – 22904 Charlottesville Charlottesville City View
Map 22905 Charlottesville Charlottesville City – 22906 Charlottesville Charlottesville City – 22907 Charlottesville Charlottesville City – 22908 Charlottesville Charlottesville City – 22909 Charlottesville Albemarle – 22910 Charlottesville Charlottesville City – 22911 Charlottesville Albemarle – 22920 Afton Nelson – 22922 Arrington Nelson – 22923 Barboursville Orange – 22924 Batesville Albemarle – 22931 Covesville Albemarle – 22932 Crozet Albemarle – 22935 Dyke Greene – 22936 Earlysville Albemarle – 22937 Esmont Albemarle – 22938 Faber Nelson – 22939 Fishersville Augusta – 22940 Free Union Albemarle View
Map 22942 Gordonsville Orange – 22943 Greenwood Albemarle – 22945 Ivy Albemarle – 22946 Keene Albemarle – 22947 Keswick Albemarle – 22948 Locust Dale Madison – 22949 Lovingston Nelson – 22952 Lyndhurst Augusta – 22957 Montpelier Station Orange – 22958 Nellysford Nelson – 22959 North Garden Albemarle – 22960 Orange Orange – 22963 Palmyra Fluvanna – 22964 Piney River Nelson – 22965 Quinque Greene – 22967 Roseland Nelson – 22968 Ruckersville Greene – 22969 Schuyler Nelson – 22971 Shipman Nelson View
Map 22972 Somerset Orange – 22973 Stanardsville Greene – 22974 Troy Fluvanna – 22976 Tyro Nelson – 22980 Waynesboro Waynesboro City – 22987 White Hall Albemarle – 22989 Woodberry Forest Madison – 23001 Achilles Gloucester – 23002 Amelia Court House Amelia – 23003 Ark Gloucester – 23004 Arvonia Buckingham – 23005 Ashland Hanover – 23009 Aylett King William – 23011 Barhamsville New Kent – 23014 Beaumont Goochland – 23015 Beaverdam Hanover – 23018 Bena Gloucester – 23021 Bohannon Mathews – 23022 Bremo Bluff Fluvanna View
Map 23023 Bruington King And Queen – 23024 Bumpass Louisa – 23025 Cardinal Mathews – 23027 Cartersville Cumberland – 23030 Charles City Charles City – 23031 Christchurch Middlesex – 23032 Church View Middlesex – 23035 Cobbs Creek Mathews – 23038 Columbia Goochland – 23039 Crozier Goochland – 23040 Cumberland Cumberland – 23043 Deltaville Middlesex – 23045 Diggs Mathews – 23047 Doswell Hanover – 23050 Dutton Gloucester – 23055 Fork Union Fluvanna – 23056 Foster Mathews – 23058 Glen Allen Henrico – 23059 Glen Allen Henrico View
Map 23060 Glen Allen Henrico – 23061 Gloucester Gloucester – 23062 Gloucester Point Gloucester – 23063 Goochland Goochland – 23064 Grimstead Mathews – 23065 Gum Spring Goochland – 23066 Gwynn Mathews – 23067 Hadensville Goochland – 23068 Hallieford Mathews – 23069 Hanover Hanover – 23070 Hardyville Middlesex – 23071 Hartfield Middlesex – 23072 Hayes Gloucester – 23075 Highland Springs Henrico – 23076 Hudgins Mathews – 23079 Jamaica Middlesex – 23081 Jamestown James City – 23083 Jetersville Amelia – 23084 Kents Store Fluvanna View
Map 23085 King And Queen Court House King And Queen – 23086 King William King William – 23089 Lanexa New Kent – 23090 Lightfoot York – 23091 Little Plymouth King And Queen – 23092 Locust Hill Middlesex – 23093 Louisa Louisa – 23101 Macon Powhatan – 23102 Maidens Goochland – 23103 Manakin Sabot Goochland – 23105 Mannboro Amelia – 23106 Manquin King William – 23107 Maryus Gloucester – 23108 Mascot King And Queen – 23109 Mathews Mathews – 23110 Mattaponi King And Queen – 23111 Mechanicsville Hanover – 23112 Midlothian Chesterfield – 23113 Midlothian Chesterfield View
Map 23114 Midlothian Chesterfield – 23115 Millers Tavern Essex – 23116 Mechanicsville Hanover – 23117 Mineral Louisa – 23119 Moon Mathews – 23120 Moseley Chesterfield – 23123 New Canton Buckingham – 23124 New Kent New Kent – 23125 New Point Mathews – 23126 Newtown King And Queen – 23127 Norge James City – 23128 North Mathews – 23129 Oilville Goochland – 23130 Onemo Mathews – 23131 Ordinary Gloucester – 23138 Port Haywood Mathews – 23139 Powhatan Powhatan – 23140 Providence Forge New Kent – 23141 Quinton New Kent View
Map 23146 Rockville Hanover – 23147 Ruthville Charles City – 23148 Saint Stephens Church King And Queen – 23149 Saluda Middlesex – 23150 Sandston Henrico – 23153 Sandy Hook Goochland – 23154 Schley Gloucester – 23155 Severn Gloucester – 23156 Shacklefords King And Queen – 23160 State Farm Goochland – 23161 Stevensville King And Queen – 23162 Studley Hanover – 23163 Susan Mathews – 23168 Toano James City – 23169 Topping Middlesex – 23170 Trevilians Louisa – 23173 University Of Richmond Richmond City – 23175 Urbanna Middlesex – 23176 Wake Middlesex View
Map 23177 Walkerton King And Queen – 23178 Ware Neck Gloucester – 23180 Water View Middlesex – 23181 West Point King William – 23183 White Marsh Gloucester – 23184 Wicomico Gloucester – 23185 Williamsburg James City – 23186 Williamsburg Williamsburg City – 23187 Williamsburg Williamsburg City – 23188 Williamsburg James City – 23190 Woods Cross Roads Gloucester – 23192 Montpelier Hanover – 23218 Richmond Richmond City – 23219 Richmond Richmond City – 23220 Richmond Richmond City – 23221 Richmond Richmond City – 23222 Richmond Richmond City – 23223 Richmond Richmond City – 23224 Richmond Richmond City View
Map 23225 Richmond Richmond City – 23226 Richmond Henrico – 23227 Richmond Henrico – 23228 Richmond Henrico – 23229 Richmond Henrico – 23230 Richmond Henrico – 23231 Richmond Henrico – 23232 Richmond Richmond City – 23233 Richmond Henrico – 23234 Richmond Chesterfield – 23235 Richmond Chesterfield – 23236 Richmond Chesterfield – 23237 Richmond Chesterfield – 23238 Richmond Henrico – 23240 Richmond Richmond City – 23241 Richmond Richmond City – 23242 Richmond Henrico – 23249 Richmond Richmond City – 23250 Richmond Henrico View
Map 23255 Richmond Henrico – 23260 Richmond Richmond City – 23261 Richmond Richmond City – 23269 Richmond Richmond City – 23273 Richmond Richmond City – 23274 Richmond Richmond City – 23276 Richmond Richmond City – 23278 Richmond Richmond City – 23279 Richmond Richmond City – 23282 Richmond Richmond City – 23284 Richmond Richmond City – 23285 Richmond Richmond City – 23286 Richmond Richmond City – 23288 Richmond Henrico – 23289 Richmond Richmond City – 23290 Richmond Richmond City – 23291 Richmond Richmond City – 23292 Richmond Richmond City – 23293 Richmond Richmond City View
Map 23294 Richmond Henrico – 23295 Richmond Richmond City – 23297 Richmond Chesterfield – 23298 Richmond Richmond City – 23301 Accomac Accomack – 23302 Assawoman Accomack – 23303 Atlantic Accomack – 23304 Battery Park Isle Of Wight – 23306 Belle Haven Accomack – 23307 Birdsnest Northampton – 23308 Bloxom Accomack – 23310 Cape Charles Northampton – 23313 Capeville Northampton – 23314 Carrollton Isle Of Wight – 23315 Carrsville Isle Of Wight – 23316 Cheriton Northampton – 23320 Chesapeake Chesapeake City – 23321 Chesapeake Chesapeake City – 23322 Chesapeake Chesapeake City View
Map 23323 Chesapeake Chesapeake City – 23324 Chesapeake Chesapeake City – 23325 Chesapeake Chesapeake City – 23326 Chesapeake Chesapeake City – 23327 Chesapeake Chesapeake City – 23328 Chesapeake Chesapeake City – 23336 Chincoteague Island Accomack – 23337 Wallops Island Accomack – 23341 Craddockville Accomack – 23345 Davis Wharf Accomack – 23347 Eastville Northampton – 23350 Exmore Northampton – 23354 Franktown Northampton – 23356 Greenbackville Accomack – 23357 Greenbush Accomack – 23358 Hacksneck Accomack – 23359 Hallwood Accomack – 23389 Harborton Accomack – 23395 Horntown Accomack View
Map 23396 Oak Hall Accomack – 23397 Isle Of Wight Isle Of Wight – 23398 Jamesville Northampton – 23399 Jenkins Bridge Accomack – 23401 Keller Accomack – 23404 Locustville Accomack – 23405 Machipongo Northampton – 23407 Mappsville Accomack – 23408 Marionville Northampton – 23409 Mears Accomack – 23410 Melfa Accomack – 23412 Modest Town Accomack – 23413 Nassawadox Northampton – 23414 Nelsonia Accomack – 23415 New Church Accomack – 23416 Oak Hall Accomack – 23417 Onancock Accomack – 23418 Onley Accomack – 23419 Oyster Northampton View
Map 23420 Painter Accomack – 23421 Parksley Accomack – 23422 Pungoteague Accomack – 23423 Quinby Accomack – 23424 Rescue Isle Of Wight – 23426 Sanford Accomack – 23427 Saxis Accomack – 23429 Seaview Northampton – 23430 Smithfield Isle Of Wight – 23431 Smithfield Isle Of Wight – 23432 Suffolk Suffolk City – 23433 Suffolk Suffolk City – 23434 Suffolk Suffolk City – 23435 Suffolk Suffolk City – 23436 Suffolk Suffolk City – 23437 Suffolk Suffolk City – 23438 Suffolk Suffolk City – 23439 Suffolk Suffolk City – 23440 Tangier Accomack View
Map 23441 Tasley Accomack – 23442 Temperanceville Accomack – 23443 Townsend Northampton – 23450 Virginia Beach Virginia Beach City – 23451 Virginia Beach Virginia Beach City – 23452 Virginia Beach Virginia Beach City – 23453 Virginia Beach Virginia Beach City – 23454 Virginia Beach Virginia Beach City – 23455 Virginia Beach Virginia Beach City – 23456 Virginia Beach Virginia Beach City – 23457 Virginia Beach Virginia Beach City – 23458 Virginia Beach Virginia Beach City – 23459 Virginia Beach Virginia Beach City – 23460 Virginia Beach Virginia Beach City – 23461 Virginia Beach Virginia Beach City – 23462 Virginia Beach Virginia Beach City – 23463 Virginia Beach Virginia Beach City – 23464 Virginia Beach Virginia Beach City – 23465 Virginia Beach Virginia Beach City View
Map 23466 Virginia Beach Virginia Beach City – 23467 Virginia Beach Virginia Beach City – 23471 Virginia Beach Virginia Beach City – 23479 Virginia Beach Virginia Beach City – 23480 Wachapreague Accomack – 23482 Wardtown Northampton – 23483 Wattsville Accomack – 23486 Willis Wharf Northampton – 23487 Windsor Isle Of Wight – 23488 Withams Accomack – 23501 Norfolk Norfolk City – 23502 Norfolk Norfolk City – 23503 Norfolk Norfolk City – 23504 Norfolk Norfolk City – 23505 Norfolk Norfolk City – 23506 Norfolk Norfolk City – 23507 Norfolk Norfolk City – 23508 Norfolk Norfolk City – 23509 Norfolk Norfolk City View
Map 23510 Norfolk Norfolk City – 23511 Norfolk Norfolk City – 23512 Norfolk Norfolk City – 23513 Norfolk Norfolk City – 23514 Norfolk Norfolk City – 23515 Norfolk Norfolk City – 23517 Norfolk Norfolk City – 23518 Norfolk Norfolk City – 23519 Norfolk Norfolk City – 23520 Norfolk Norfolk City – 23521 Norfolk Norfolk City – 23523 Norfolk Norfolk City – 23529 Norfolk Norfolk City – 23541 Norfolk Norfolk City – 23551 Norfolk Norfolk City – 23601 Newport News Newport News City – 23602 Newport News Newport News City – 23603 Newport News Newport News City – 23604 Fort Eustis Newport News City View
Map 23605 Newport News Newport News City – 23606 Newport News Newport News City – 23607 Newport News Newport News City – 23608 Newport News Newport News City – 23609 Newport News Newport News City – 23612 Newport News Newport News City – 23628 Newport News Newport News City – 23630 Hampton Hampton City – 23651 Fort Monroe Hampton City – 23661 Hampton Hampton City – 23662 Poquoson Poquoson City – 23663 Hampton Hampton City – 23664 Hampton Hampton City – 23665 Hampton York – 23666 Hampton Hampton City – 23667 Hampton Hampton City – 23668 Hampton Hampton City – 23669 Hampton Hampton City – 23670 Hampton Hampton City View
Map 23681 Hampton Hampton City – 23690 Yorktown York – 23691 Yorktown York – 23692 Yorktown York – 23693 Yorktown York – 23694 Lackey York – 23696 Seaford York – 23701 Portsmouth Portsmouth City – 23702 Portsmouth Portsmouth City – 23703 Portsmouth Portsmouth City – 23704 Portsmouth Portsmouth City – 23705 Portsmouth Portsmouth City – 23707 Portsmouth Portsmouth City – 23708 Portsmouth Portsmouth City – 23709 Portsmouth Portsmouth City – 23801 Fort Lee Prince George – 23803 Petersburg Petersburg City – 23804 Petersburg Petersburg City – 23805 Petersburg Petersburg City View
Map 23806 Petersburg Petersburg City – 23821 Alberta Brunswick – 23822 Ammon Dinwiddie – 23824 Blackstone Nottoway – 23825 Blackstone Nottoway – 23827 Boykins Southampton – 23828 Branchville Southampton – 23829 Capron Southampton – 23830 Carson Dinwiddie – 23831 Chester Chesterfield – 23832 Chesterfield Chesterfield – 23833 Church Road Dinwiddie – 23834 Colonial Heights Colonial Heights City – 23836 Chester Chesterfield – 23837 Courtland Southampton – 23838 Chesterfield Chesterfield – 23839 Dendron Surry – 23840 Dewitt Dinwiddie – 23841 Dinwiddie Dinwiddie View
Map 23842 Disputanta Prince George – 23843 Dolphin Brunswick – 23844 Drewryville Southampton – 23845 Ebony Brunswick – 23846 Elberon Surry – 23847 Emporia Greensville – 23850 Ford Dinwiddie – 23851 Franklin Franklin City – 23856 Freeman Brunswick – 23857 Gasburg Brunswick – 23860 Hopewell Hopewell City – 23866 Ivor Southampton – 23867 Jarratt Greensville – 23868 Lawrenceville Brunswick – 23870 Jarratt Greensville – 23872 Mc Kenney Dinwiddie – 23873 Meredithville Brunswick – 23874 Newsoms Southampton – 23875 Prince George Prince George View
Map 23876 Rawlings Brunswick – 23878 Sedley Southampton – 23879 Skippers Greensville – 23881 Spring Grove Surry – 23882 Stony Creek Sussex – 23883 Surry Surry – 23884 Sussex Sussex – 23885 Sutherland Dinwiddie – 23887 Valentines Brunswick – 23888 Wakefield Sussex – 23889 Warfield Brunswick – 23890 Waverly Sussex – 23891 Waverly Sussex – 23893 White Plains Brunswick – 23894 Wilsons Dinwiddie – 23897 Yale Sussex – 23898 Zuni Isle Of Wight – 23899 Claremont Surry – 23901 Farmville Prince Edward View
Map 23909 Farmville Prince Edward – 23915 Baskerville Mecklenburg – 23917 Boydton Mecklenburg – 23919 Bracey Mecklenburg – 23920 Brodnax Brunswick – 23921 Buckingham Buckingham – 23922 Burkeville Nottoway – 23923 Charlotte Court House Charlotte – 23924 Chase City Mecklenburg – 23927 Clarksville Mecklenburg – 23930 Crewe Nottoway – 23934 Cullen Charlotte – 23936 Dillwyn Buckingham – 23937 Drakes Branch Charlotte – 23938 Dundas Lunenburg – 23939 Evergreen Appomattox – 23941 Fort Mitchell Lunenburg – 23942 Green Bay Prince Edward – 23943 Hampden Sydney Prince Edward View
Map 23944 Kenbridge Lunenburg – 23947 Keysville Charlotte – 23950 La Crosse Mecklenburg – 23952 Lunenburg Lunenburg – 23954 Meherrin Prince Edward – 23955 Nottoway Nottoway – 23958 Pamplin Appomattox – 23959 Phenix Charlotte – 23960 Prospect Prince Edward – 23962 Randolph Charlotte – 23963 Red House Charlotte – 23964 Red Oak Charlotte – 23966 Rice Prince Edward – 23967 Saxe Charlotte – 23968 Skipwith Mecklenburg – 23970 South Hill Mecklenburg – 23974 Victoria Lunenburg – 23976 Wylliesburg Charlotte – 24001 Roanoke Roanoke City View
Map 24002 Roanoke Roanoke City – 24003 Roanoke Roanoke City – 24004 Roanoke Roanoke City – 24005 Roanoke Roanoke City – 24006 Roanoke Roanoke City – 24007 Roanoke Roanoke City – 24008 Roanoke Roanoke City – 24009 Roanoke Roanoke City – 24010 Roanoke Roanoke City – 24011 Roanoke Roanoke City – 24012 Roanoke Roanoke City – 24013 Roanoke Roanoke City – 24014 Roanoke Roanoke City – 24015 Roanoke Roanoke City – 24016 Roanoke Roanoke City – 24017 Roanoke Roanoke City – 24018 Roanoke Roanoke – 24019 Roanoke Roanoke – 24020 Roanoke Roanoke View
Map 24022 Roanoke Roanoke City – 24023 Roanoke Roanoke City – 24024 Roanoke Roanoke City – 24025 Roanoke Roanoke City – 24026 Roanoke Roanoke City – 24027 Roanoke Roanoke City – 24028 Roanoke Roanoke City – 24029 Roanoke Roanoke City – 24030 Roanoke Roanoke City – 24031 Roanoke Roanoke City – 24032 Roanoke Roanoke City – 24033 Roanoke Roanoke City – 24034 Roanoke Roanoke City – 24035 Roanoke Roanoke City – 24036 Roanoke Roanoke City – 24037 Roanoke Roanoke City – 24038 Roanoke Roanoke City – 24040 Roanoke Roanoke City – 24042 Roanoke Roanoke City View
Map 24043 Roanoke Roanoke City – 24044 Roanoke Roanoke City – 24045 Roanoke Roanoke City – 24048 Roanoke Roanoke City – 24050 Roanoke Botetourt – 24053 Ararat Patrick – 24054 Axton Henry – 24055 Bassett Henry – 24058 Belspring Pulaski – 24059 Bent Mountain Roanoke – 24060 Blacksburg Montgomery – 24061 Blacksburg Montgomery – 24062 Blacksburg Montgomery – 24063 Blacksburg Montgomery – 24064 Blue Ridge Botetourt – 24065 Boones Mill Franklin – 24066 Buchanan Botetourt – 24067 Callaway Franklin – 24068 Christiansburg Montgomery View
Map 24069 Cascade Pittsylvania – 24070 Catawba Roanoke – 24072 Check Floyd – 24073 Christiansburg Montgomery – 24076 Claudville Patrick – 24077 Cloverdale Botetourt – 24078 Collinsville Henry – 24079 Copper Hill Floyd – 24082 Critz Patrick – 24083 Daleville Botetourt – 24084 Dublin Pulaski – 24085 Eagle Rock Botetourt – 24086 Eggleston Giles – 24087 Elliston Montgomery – 24088 Ferrum Franklin – 24089 Fieldale Henry – 24090 Fincastle Botetourt – 24091 Floyd Floyd – 24092 Glade Hill Franklin View
Map 24093 Glen Lyn Giles – 24095 Goodview Bedford – 24101 Hardy Franklin – 24102 Henry Franklin – 24104 Huddleston Bedford – 24105 Indian Valley Floyd – 24111 Mc Coy Montgomery – 24112 Martinsville Martinsville City – 24113 Martinsville Martinsville City – 24114 Martinsville Martinsville City – 24115 Martinsville Martinsville City – 24120 Meadows Of Dan Patrick – 24121 Moneta Bedford – 24122 Montvale Bedford – 24124 Narrows Giles – 24126 Newbern Pulaski – 24127 New Castle Craig – 24128 Newport Giles – 24129 New River Pulaski View
Map 24130 Oriskany Botetourt – 24131 Paint Bank Craig – 24132 Parrott Pulaski – 24133 Patrick Springs Patrick – 24134 Pearisburg Giles – 24136 Pembroke Giles – 24137 Penhook Franklin – 24138 Pilot Montgomery – 24139 Pittsville Pittsylvania – 24141 Radford Radford – 24142 Radford Radford – 24143 Radford Radford – 24146 Redwood Franklin – 24147 Rich Creek Giles – 24148 Ridgeway Henry – 24149 Riner Montgomery – 24150 Ripplemead Giles – 24151 Rocky Mount Franklin – 24153 Salem Salem View
Map 24155 Roanoke Salem – 24157 Roanoke Salem – 24161 Sandy Level Pittsylvania – 24162 Shawsville Montgomery – 24165 Spencer Henry – 24167 Staffordsville Giles – 24168 Stanleytown Henry – 24171 Stuart Patrick – 24174 Thaxton Bedford – 24175 Troutville Botetourt – 24176 Union Hall Franklin – 24177 Vesta Patrick – 24178 Villamont Bedford – 24179 Vinton Roanoke – 24184 Wirtz Franklin – 24185 Woolwine Patrick – 24201 Bristol Bristol – 24202 Bristol Washington – 24203 Bristol Bristol View
Map 24209 Bristol Bristol – 24210 Abingdon Washington – 24211 Abingdon Washington – 24212 Abingdon Washington – 24215 Andover Wise – 24216 Appalachia Wise – 24217 Bee Dickenson – 24218 Ben Hur Lee – 24219 Big Stone Gap Wise – 24220 Birchleaf Dickenson – 24221 Blackwater Lee – 24224 Castlewood Russell – 24225 Cleveland Russell – 24226 Clinchco Dickenson – 24228 Clintwood Dickenson – 24230 Coeburn Wise – 24236 Damascus Washington – 24237 Dante Russell – 24239 Davenport Buchanan View
Map 24243 Dryden Lee – 24244 Duffield Scott – 24245 Dungannon Scott – 24246 East Stone Gap Wise – 24248 Ewing Lee – 24250 Fort Blackmore Scott – 24251 Gate City Scott – 24256 Haysi Dickenson – 24258 Hiltons Scott – 24260 Honaker Russell – 24263 Jonesville Lee – 24265 Keokee Lee – 24266 Lebanon Russell – 24269 Mc Clure Dickenson – 24270 Mendota Washington – 24271 Nickelsville Scott – 24272 Nora Dickenson – 24273 Norton Norton City – 24277 Pennington Gap Lee View
Map 24279 Pound Wise – 24280 Rosedale Russell – 24281 Rose Hill Lee – 24282 Saint Charles Lee – 24283 Saint Paul Wise – 24290 Weber City Scott – 24292 Whitetop Grayson – 24293 Wise Wise – 24301 Pulaski Pulaski – 24311 Atkins Smyth – 24312 Austinville Wythe – 24313 Barren Springs Wythe – 24314 Bastian Bland – 24315 Bland Bland – 24316 Broadford Tazewell – 24317 Cana Carroll – 24318 Ceres Bland – 24319 Chilhowie Smyth – 24322 Cripple Creek Wythe View
Map 24323 Crockett Wythe – 24324 Draper Pulaski – 24325 Dugspur Carroll – 24326 Elk Creek Grayson – 24327 Emory Washington – 24328 Fancy Gap Carroll – 24330 Fries Grayson – 24333 Galax Galax City – 24340 Glade Spring Washington – 24343 Hillsville Carroll – 24347 Hiwassee Pulaski – 24348 Independence Grayson – 24350 Ivanhoe Wythe – 24351 Lambsburg Carroll – 24352 Laurel Fork Carroll – 24354 Marion Smyth – 24360 Max Meadows Wythe – 24361 Meadowview Washington – 24363 Mouth Of Wilson Grayson View
Map 24366 Rocky Gap Bland – 24368 Rural Retreat Wythe – 24370 Saltville Smyth – 24374 Speedwell Wythe – 24375 Sugar Grove Smyth – 24377 Tannersville Tazewell – 24378 Troutdale Grayson – 24380 Willis Floyd – 24381 Woodlawn Carroll – 24382 Wytheville Wythe – 24401 Staunton Staunton City – 24402 Staunton Staunton City – 24411 Augusta Springs Augusta – 24412 Bacova Bath – 24413 Blue Grass Highland – 24415 Brownsburg Rockbridge – 24416 Buena Vista Buena Vista City – 24421 Churchville Augusta – 24422 Clifton Forge Alleghany View
Map 24426 Covington Covington City – 24430 Craigsville Augusta – 24431 Crimora Augusta – 24432 Deerfield Augusta – 24433 Doe Hill Highland – 24435 Fairfield Rockbridge – 24437 Fort Defiance Augusta – 24438 Glen Wilton Botetourt – 24439 Goshen Rockbridge – 24440 Greenville Augusta – 24441 Grottoes Rockingham – 24442 Head Waters Highland – 24445 Hot Springs Bath – 24448 Iron Gate Alleghany – 24450 Lexington Lexington City – 24457 Low Moor Alleghany – 24458 Mc Dowell Highland – 24459 Middlebrook Augusta – 24460 Millboro Bath View
Map 24463 Mint Spring Augusta – 24464 Montebello Nelson – 24465 Monterey Highland – 24467 Mount Sidney Augusta – 24468 Mustoe Highland – 24469 New Hope Augusta – 24471 Port Republic Rockingham – 24472 Raphine Rockbridge – 24473 Rockbridge Baths Rockbridge – 24474 Selma Alleghany – 24476 Steeles Tavern Augusta – 24477 Stuarts Draft Augusta – 24479 Swoope Augusta – 24482 Verona Augusta – 24483 Vesuvius Rockbridge – 24484 Warm Springs Bath – 24485 West Augusta Augusta – 24486 Weyers Cave Augusta – 24487 Williamsville Bath View
Map 24501 Lynchburg Lynchburg City – 24502 Lynchburg Lynchburg City – 24503 Lynchburg Lynchburg City – 24504 Lynchburg Lynchburg City – 24505 Lynchburg Lynchburg City – 24506 Lynchburg Lynchburg City – 24512 Lynchburg Lynchburg City – 24513 Lynchburg Lynchburg City – 24514 Lynchburg Lynchburg City – 24515 Lynchburg Lynchburg City – 24517 Altavista Campbell – 24520 Alton Halifax – 24521 Amherst Amherst – 24522 Appomattox Appomattox – 24523 Bedford Bedford – 24526 Big Island Bedford – 24527 Blairs Pittsylvania – 24528 Brookneal Campbell – 24529 Buffalo Junction Mecklenburg View
Map 24530 Callands Pittsylvania – 24531 Chatham Pittsylvania – 24533 Clifford Amherst – 24534 Clover Halifax – 24535 Cluster Springs Halifax – 24536 Coleman Falls Bedford – 24538 Concord Campbell – 24539 Crystal Hill Halifax – 24540 Danville Danville City – 24541 Danville Danville City – 24543 Danville Danville City – 24544 Danville Danville City – 24549 Dry Fork Pittsylvania – 24550 Evington Campbell – 24551 Forest Bedford – 24553 Gladstone Nelson – 24554 Gladys Campbell – 24555 Glasgow Rockbridge – 24556 Goode Bedford View
Map 24557 Gretna Pittsylvania – 24558 Halifax Halifax – 24562 Howardsville Buckingham – 24563 Hurt Pittsylvania – 24565 Java Pittsylvania – 24566 Keeling Pittsylvania – 24569 Long Island Pittsylvania – 24570 Lowry Bedford – 24571 Lynch Station Campbell – 24572 Madison Heights Amherst – 24574 Monroe Amherst – 24576 Naruna Campbell – 24577 Nathalie Halifax – 24578 Natural Bridge Rockbridge – 24579 Natural Bridge Station Rockbridge – 24580 Nelson Mecklenburg – 24581 Norwood Nelson – 24586 Ringgold Pittsylvania – 24588 Rustburg Campbell View
Map 24589 Scottsburg Halifax – 24590 Scottsville Albemarle – 24592 South Boston Halifax – 24593 Spout Spring Appomattox – 24594 Sutherlin Pittsylvania – 24595 Sweet Briar Amherst – 24597 Vernon Hill Halifax – 24598 Virgilina Halifax – 24599 Wingina Buckingham – 24601 Amonate Tazewell – 24602 Bandy Tazewell – 24603 Big Rock Buchanan – 24604 Bishop Tazewell – 24605 Bluefield Tazewell – 24606 Boissevain Tazewell – 24607 Breaks Dickenson – 24608 Burkes Garden Tazewell – 24609 Cedar Bluff Tazewell – 24612 Doran Tazewell View
Map 24613 Falls Mills Tazewell – 24614 Grundy Buchanan – 24619 Horsepen Tazewell – 24620 Hurley Buchanan – 24622 Jewell Ridge Tazewell – 24624 Keen Mountain Buchanan – 24627 Mavisdale Buchanan – 24628 Maxie Buchanan – 24630 North Tazewell Tazewell – 24631 Oakwood Buchanan – 24634 Pilgrims Knob Buchanan – 24635 Pocahontas Tazewell – 24637 Pounding Mill Tazewell – 24639 Raven Buchanan – 24640 Red Ash Tazewell – 24641 Richlands Tazewell – 24646 Rowe Buchanan – 24647 Shortt Gap Buchanan – 24649 Swords Creek Russell View
Map 24651 Tazewell Tazewell – 24656 Vansant Buchanan – 24657 Whitewood Buchanan – 24658 Wolford Buchanan – 24701 Bluefield Mercer – 24712 Athens Mercer – 24714 Beeson Mercer – 24715 Bramwell Mercer – 24716 Bud Wyoming – 24719 Covel Wyoming – 24724 Freeman Mercer – 24726 Herndon Wyoming – 24729 Hiawatha Mercer – 24731 Kegley Mercer – 24732 Kellysville Mercer – 24733 Lashmeet Mercer – 24736 Matoaka Mercer – 24737 Montcalm Mercer – 24738 Nemours Mercer View
Map 24739 Oakvale Mercer – 24740 Princeton Mercer – 24747 Rock Mercer – 24751 Wolfe Mercer – 24801 Welch Mcdowell – 24808 Anawalt Mcdowell – 24811 Avondale Mcdowell – 24813 Bartley Mcdowell – 24815 Berwind Mcdowell – 24816 Big Sandy Mcdowell – 24817 Bradshaw Mcdowell – 24818 Brenton Wyoming – 24822 Clear Fork Wyoming – 24823 Coal Mountain Wyoming – 24824 Coalwood Mcdowell – 24826 Cucumber Mcdowell – 24827 Cyclone Wyoming – 24828 Davy Mcdowell – 24829 Eckman Mcdowell View
Map 24830 Elbert Mcdowell – 24831 Elkhorn Mcdowell – 24834 Fanrock Wyoming – 24836 Gary Mcdowell – 24839 Hanover Wyoming – 24842 Hemphill Mcdowell – 24843 Hensley Mcdowell – 24844 Iaeger Mcdowell – 24845 Ikes Fork Wyoming – 24846 Isaban Mcdowell – 24847 Itmann Wyoming – 24848 Jenkinjones Mcdowell – 24849 Jesse Wyoming – 24850 Jolo Mcdowell – 24851 Justice Mingo – 24853 Kimball Mcdowell – 24854 Kopperston Wyoming – 24855 Kyle Mcdowell – 24857 Lynco Wyoming View
Map 24859 Marianna Wyoming – 24860 Matheny Wyoming – 24861 Maybeury Mcdowell – 24862 Mohawk Mcdowell – 24866 Newhall Mcdowell – 24867 New Richmond Wyoming – 24868 Northfork Mcdowell – 24869 North Spring Wyoming – 24870 Oceana Wyoming – 24871 Pageton Mcdowell – 24872 Panther Mcdowell – 24873 Paynesville Mcdowell – 24874 Pineville Wyoming – 24878 Premier Mcdowell – 24879 Raysal Mcdowell – 24880 Rock View Wyoming – 24881 Roderfield Mcdowell – 24882 Simon Wyoming – 24884 Squire Mcdowell View
Map 24887 Switchback Mcdowell – 24888 Thorpe Mcdowell – 24892 War Mcdowell – 24894 Warriormine Mcdowell – 24895 Wilcoe Mcdowell – 24898 Wyoming Wyoming – 24901 Lewisburg Greenbrier – 24902 Fairlea Greenbrier – 24910 Alderson Greenbrier – 24915 Arbovale Pocahontas – 24916 Asbury Greenbrier – 24918 Ballard Monroe – 24920 Bartow Pocahontas – 24924 Buckeye Pocahontas – 24925 Caldwell Greenbrier – 24927 Cass Pocahontas – 24931 Crawley Greenbrier – 24934 Dunmore Pocahontas – 24935 Forest Hill Summers View
Map 24938 Frankford Greenbrier – 24941 Gap Mills Monroe – 24943 Grassy Meadows Greenbrier – 24944 Green Bank Pocahontas – 24945 Greenville Monroe – 24946 Hillsboro Pocahontas – 24951 Lindside Monroe – 24954 Marlinton Pocahontas – 24957 Maxwelton Greenbrier – 24961 Neola Greenbrier – 24962 Pence Springs Summers – 24963 Peterstown Monroe – 24966 Renick Greenbrier – 24970 Ronceverte Greenbrier – 24974 Secondcreek Monroe – 24976 Sinks Grove Monroe – 24977 Smoot Greenbrier – 24981 Talcott Summers – 24983 Union Monroe View
Map 24984 Waiteville Monroe – 24985 Wayside Monroe – 24986 White Sulphur Springs Greenbrier – 24991 Williamsburg Greenbrier – 24993 Wolfcreek Monroe – 25002 Alloy Fayette – 25003 Alum Creek Kanawha – 25005 Amma Roane – 25007 Arnett Raleigh – 25008 Artie Raleigh – 25009 Ashford Boone – 25011 Bancroft Putnam – 25015 Belle Kanawha – 25019 Bickmore Clay – 25021 Bim Boone – 25022 Blair Logan – 25024 Bloomingrose Boone – 25025 Blount Kanawha – 25026 Blue Creek Kanawha View
Map 25028 Bob White Boone – 25030 Bomont Clay – 25031 Boomer Fayette – 25033 Buffalo Putnam – 25035 Cabin Creek Kanawha – 25036 Cannelton Fayette – 25039 Cedar Grove Kanawha – 25040 Charlton Heights Fayette – 25043 Clay Clay – 25044 Clear Creek Raleigh – 25045 Clendenin Kanawha – 25047 Clothier Logan – 25048 Colcord Raleigh – 25049 Comfort Boone – 25051 Costa Boone – 25053 Danville Boone – 25054 Dawes Kanawha – 25057 Deep Water Fayette – 25059 Dixie Nicholas View
Map 25060 Dorothy Raleigh – 25061 Drybranch Kanawha – 25062 Dry Creek Raleigh – 25063 Duck Clay – 25064 Dunbar Kanawha – 25067 East Bank Kanawha – 25070 Eleanor Putnam – 25071 Elkview Kanawha – 25075 Eskdale Kanawha – 25076 Ethel Logan – 25079 Falling Rock Kanawha – 25081 Foster Boone – 25082 Fraziers Bottom Putnam – 25083 Gallagher Kanawha – 25085 Gauley Bridge Fayette – 25086 Glasgow Kanawha – 25088 Glen Clay – 25090 Glen Ferris Fayette – 25093 Gordon Boone View
Map 25102 Handley Kanawha – 25103 Hansford Kanawha – 25106 Henderson Mason – 25107 Hernshaw Kanawha – 25108 Hewett Boone – 25109 Hometown Putnam – 25110 Hugheston Kanawha – 25111 Indore Clay – 25112 Institute Kanawha – 25113 Ivydale Clay – 25114 Jeffrey Boone – 25115 Kanawha Falls Fayette – 25118 Kimberly Fayette – 25119 Kincaid Fayette – 25121 Lake Logan – 25123 Leon Mason – 25124 Liberty Putnam – 25125 Lizemores Clay – 25126 London Kanawha View
Map 25130 Madison Boone – 25132 Mammoth Kanawha – 25133 Maysel Clay – 25134 Miami Kanawha – 25136 Montgomery Fayette – 25139 Mount Carbon Fayette – 25140 Naoma Raleigh – 25141 Nebo Clay – 25142 Nellis Boone – 25143 Nitro Kanawha – 25148 Orgas Boone – 25149 Ottawa Boone – 25152 Page Fayette – 25154 Peytona Boone – 25156 Pinch Kanawha – 25159 Poca Putnam – 25160 Pond Gap Kanawha – 25161 Powellton Fayette – 25162 Pratt Kanawha View
Map 25164 Procious Clay – 25165 Racine Boone – 25168 Red House Putnam – 25169 Ridgeview Boone – 25173 Robson Fayette – 25174 Rock Creek Raleigh – 25177 Saint Albans Kanawha – 25180 Saxon Boone – 25181 Seth Boone – 25183 Sharples Logan – 25185 Mount Olive Fayette – 25186 Smithers Fayette – 25187 Southside Mason – 25193 Sylvester Boone – 25201 Tad Kanawha – 25202 Tornado Kanawha – 25203 Turtle Creek Boone – 25204 Twilight Boone – 25205 Uneeda Boone View
Map 25206 Van Boone – 25208 Wharton Boone – 25209 Whitesville Boone – 25211 Widen Clay – 25213 Winfield Putnam – 25214 Winifrede Kanawha – 25231 Advent Jackson – 25234 Arnoldsburg Calhoun – 25235 Chloe Calhoun – 25239 Cottageville Jackson – 25241 Evans Jackson – 25243 Gandeeville Roane – 25244 Gay Jackson – 25245 Given Jackson – 25247 Hartford Mason – 25248 Kenna Jackson – 25251 Left Hand Roane – 25252 Le Roy Jackson – 25253 Letart Mason View
Map 25259 Looneyville Roane – 25260 Mason Mason – 25261 Millstone Calhoun – 25262 Millwood Jackson – 25264 Mount Alto Mason – 25265 New Haven Mason – 25266 Newton Roane – 25267 Normantown Gilmer – 25268 Orma Calhoun – 25270 Reedy Roane – 25271 Ripley Jackson – 25275 Sandyville Jackson – 25276 Spencer Roane – 25285 Wallback Clay – 25286 Walton Roane – 25287 West Columbia Mason – 25301 Charleston Kanawha – 25302 Charleston Kanawha – 25303 Charleston Kanawha View
Map 25304 Charleston Kanawha – 25305 Charleston Kanawha – 25306 Charleston Kanawha – 25309 Charleston Kanawha – 25311 Charleston Kanawha – 25312 Charleston Kanawha – 25313 Charleston Kanawha – 25314 Charleston Kanawha – 25315 Charleston Kanawha – 25317 Charleston Kanawha – 25320 Charleston Kanawha – 25321 Charleston Kanawha – 25322 Charleston Kanawha – 25323 Charleston Kanawha – 25324 Charleston Kanawha – 25325 Charleston Kanawha – 25326 Charleston Kanawha – 25327 Charleston Kanawha – 25328 Charleston Kanawha View
Map 25329 Charleston Kanawha – 25330 Charleston Kanawha – 25331 Charleston Kanawha – 25332 Charleston Kanawha – 25333 Charleston Kanawha – 25334 Charleston Kanawha – 25335 Charleston Kanawha – 25336 Charleston Kanawha – 25337 Charleston Kanawha – 25338 Charleston Kanawha – 25339 Charleston Kanawha – 25350 Charleston Kanawha – 25356 Charleston Kanawha – 25357 Charleston Kanawha – 25358 Charleston Kanawha – 25360 Charleston Kanawha – 25361 Charleston Kanawha – 25362 Charleston Kanawha – 25364 Charleston Kanawha View
Map 25365 Charleston Kanawha – 25375 Charleston Kanawha – 25387 Charleston Kanawha – 25389 Charleston Kanawha – 25392 Charleston Kanawha – 25396 Charleston Kanawha – 25401 Martinsburg Berkeley – 25402 Martinsburg Berkeley – 25403 Martinsburg Berkeley – 25404 Martinsburg Berkeley – 25405 Martinsburg Berkeley – 25410 Bakerton Jefferson – 25411 Berkeley Springs Morgan – 25413 Bunker Hill Berkeley – 25414 Charles Town Jefferson – 25419 Falling Waters Berkeley – 25420 Gerrardstown Berkeley – 25421 Glengary Berkeley – 25422 Great Cacapon Morgan View
Map 25423 Halltown Jefferson – 25425 Harpers Ferry Jefferson – 25427 Hedgesville Berkeley – 25428 Inwood Berkeley – 25429 Martinsburg Berkeley – 25430 Kearneysville Jefferson – 25431 Levels Hampshire – 25432 Millville Jefferson – 25434 Paw Paw Morgan – 25437 Points Hampshire – 25438 Ranson Jefferson – 25440 Ridgeway Berkeley – 25441 Rippon Jefferson – 25442 Shenandoah Junction Jefferson – 25443 Shepherdstown Jefferson – 25444 Slanesville Hampshire – 25446 Summit Point Jefferson – 25501 Alkol Lincoln – 25502 Apple Grove Mason View
Map 25503 Ashton Mason – 25504 Barboursville Cabell – 25505 Big Creek Logan – 25506 Branchland Lincoln – 25507 Ceredo Wayne – 25508 Chapmanville Logan – 25510 Culloden Cabell – 25511 Dunlow Wayne – 25512 East Lynn Wayne – 25514 Fort Gay Wayne – 25515 Gallipolis Ferry Mason – 25517 Genoa Wayne – 25520 Glenwood Mason – 25521 Griffithsville Lincoln – 25523 Hamlin Lincoln – 25524 Harts Lincoln – 25526 Hurricane Putnam – 25529 Julian Boone – 25530 Kenova Wayne View
Map 25534 Kiahsville Wayne – 25535 Lavalette Wayne – 25537 Lesage Cabell – 25540 Midkiff Lincoln – 25541 Milton Cabell – 25544 Myra Lincoln – 25545 Ona Cabell – 25547 Pecks Mill Logan – 25550 Point Pleasant Mason – 25555 Prichard Wayne – 25557 Ranger Lincoln – 25559 Salt Rock Cabell – 25560 Scott Depot Putnam – 25562 Shoals Wayne – 25564 Sod Lincoln – 25565 Spurlockville Lincoln – 25567 Sumerco Lincoln – 25569 Teays Putnam – 25570 Wayne Wayne View
Map 25571 West Hamlin Lincoln – 25572 Woodville Boone – 25573 Yawkey Lincoln – 25601 Logan Logan – 25606 Accoville Logan – 25607 Amherstdale Logan – 25608 Baisden Mingo – 25611 Bruno Logan – 25612 Chauncey Logan – 25614 Cora Logan – 25617 Davin Logan – 25621 Gilbert Mingo – 25624 Henlawson Logan – 25625 Holden Logan – 25628 Kistler Logan – 25630 Lorado Logan – 25632 Lyburn Logan – 25634 Mallory Logan – 25635 Man Logan View
Map 25637 Mount Gay Logan – 25638 Omar Logan – 25639 Peach Creek Logan – 25644 Sarah Ann Logan – 25646 Stollings Logan – 25647 Switzer Logan – 25649 Verdunville Logan – 25650 Verner Mingo – 25651 Wharncliffe Mingo – 25652 Whitman Logan – 25653 Wilkinson Logan – 25654 Yolyn Logan – 25661 Williamson Mingo – 25665 Borderland Mingo – 25666 Breeden Mingo – 25667 Chattaroy Mingo – 25669 Crum Wayne – 25670 Delbarton Mingo – 25671 Dingess Mingo View
Map 25672 Edgarton Mingo – 25674 Kermit Mingo – 25676 Lenore Mingo – 25678 Matewan Mingo – 25685 Naugatuck Mingo – 25686 Newtown Mingo – 25688 North Matewan Mingo – 25690 Ragland Mingo – 25691 Rawl Mingo – 25692 Red Jacket Mingo – 25696 Varney Mingo – 25697 Vulcan Mingo – 25699 Wilsondale Wayne – 25701 Huntington Cabell – 25702 Huntington Cabell – 25703 Huntington Cabell – 25704 Huntington Wayne – 25705 Huntington Cabell – 25706 Huntington Cabell View
Map 25707 Huntington Cabell – 25708 Huntington Cabell – 25709 Huntington Cabell – 25710 Huntington Cabell – 25711 Huntington Cabell – 25712 Huntington Cabell – 25713 Huntington Cabell – 25714 Huntington Cabell – 25715 Huntington Cabell – 25716 Huntington Cabell – 25717 Huntington Cabell – 25718 Huntington Cabell – 25719 Huntington Cabell – 25720 Huntington Cabell – 25721 Huntington Cabell – 25722 Huntington Cabell – 25723 Huntington Cabell – 25724 Huntington Cabell – 25725 Huntington Cabell View
Map 25726 Huntington Cabell – 25727 Huntington Cabell – 25728 Huntington Cabell – 25729 Huntington Cabell – 25755 Huntington Cabell – 25770 Huntington Cabell – 25771 Huntington Cabell – 25772 Huntington Cabell – 25773 Huntington Cabell – 25774 Huntington Cabell – 25775 Huntington Cabell – 25776 Huntington Cabell – 25777 Huntington Cabell – 25778 Huntington Cabell – 25779 Huntington Cabell – 25801 Beckley Raleigh – 25802 Beckley Raleigh – 25810 Allen Junction Wyoming – 25811 Amigo Wyoming View
Map 25812 Ansted Fayette – 25813 Beaver Raleigh – 25816 Blue Jay Raleigh – 25817 Bolt Raleigh – 25818 Bradley Raleigh – 25820 Camp Creek Mercer – 25823 Coal City Raleigh – 25825 Cool Ridge Raleigh – 25826 Corinne Wyoming – 25827 Crab Orchard Raleigh – 25831 Danese Fayette – 25832 Daniels Raleigh – 25833 Dothan Fayette – 25836 Eccles Raleigh – 25837 Edmond Fayette – 25839 Fairdale Raleigh – 25840 Fayetteville Fayette – 25841 Flat Top Mercer – 25843 Ghent Raleigh View
Map 25844 Glen Daniel Raleigh – 25845 Glen Fork Wyoming – 25846 Glen Jean Fayette – 25848 Glen Rogers Wyoming – 25849 Glen White Raleigh – 25851 Harper Raleigh – 25853 Helen Raleigh – 25854 Hico Fayette – 25855 Hilltop Fayette – 25857 Josephine Raleigh – 25860 Lanark Raleigh – 25862 Lansing Fayette – 25864 Layland Fayette – 25865 Lester Raleigh – 25866 Lochgelly Fayette – 25868 Lookout Fayette – 25870 Maben Wyoming – 25871 Mabscott Raleigh – 25873 Mac Arthur Raleigh View
Map 25875 Mc Graws Wyoming – 25876 Saulsville Wyoming – 25878 Midway Raleigh – 25879 Minden Fayette – 25880 Mount Hope Fayette – 25882 Mullens Wyoming – 25901 Oak Hill Fayette – 25902 Odd Raleigh – 25904 Pax Fayette – 25906 Piney View Raleigh – 25907 Prince Fayette – 25908 Princewick Raleigh – 25909 Prosperity Raleigh – 25911 Raleigh Raleigh – 25913 Ravencliff Wyoming – 25914 Redstar Fayette – 25915 Rhodell Raleigh – 25916 Sabine Wyoming – 25917 Scarbro Fayette View
Map 25918 Shady Spring Raleigh – 25919 Skelton Raleigh – 25920 Slab Fork Raleigh – 25921 Sophia Raleigh – 25922 Spanishburg Mercer – 25926 Sprague Raleigh – 25927 Stanaford Raleigh – 25928 Stephenson Wyoming – 25932 Surveyor Raleigh – 25936 Thurmond Fayette – 25938 Victor Fayette – 25942 Winona Fayette – 25943 Wyco Wyoming – 25951 Hinton Summers – 25958 Charmco Greenbrier – 25962 Rainelle Greenbrier – 25965 Elton Summers – 25966 Green Sulphur Springs Summers – 25969 Jumping Branch Summers View
Map 25971 Lerona Mercer – 25972 Leslie Greenbrier – 25976 Meadow Bridge Fayette – 25977 Meadow Creek Summers – 25978 Nimitz Summers – 25979 Pipestem Summers – 25981 Quinwood Greenbrier – 25984 Rupert Greenbrier – 25985 Sandstone Summers – 25986 Spring Dale Fayette – 25989 White Oak Raleigh – 26003 Wheeling Ohio – 26030 Beech Bottom Brooke – 26031 Benwood Marshall – 26032 Bethany Brooke – 26033 Cameron Marshall – 26034 Chester Hancock – 26035 Colliers Brooke – 26036 Dallas Marshall View
Map 26037 Follansbee Brooke – 26038 Glen Dale Marshall – 26039 Glen Easton Marshall – 26040 Mcmechen Marshall – 26041 Moundsville Marshall – 26047 New Cumberland Hancock – 26050 Newell Hancock – 26055 Proctor Marshall – 26056 New Manchester Hancock – 26058 Short Creek Brooke – 26059 Triadelphia Ohio – 26060 Valley Grove Ohio – 26062 Weirton Hancock – 26070 Wellsburg Brooke – 26074 West Liberty Ohio – 26075 Windsor Heights Brooke – 26101 Parkersburg Wood – 26102 Parkersburg Wood – 26103 Parkersburg Wood View
Map 26104 Parkersburg Wood – 26105 Vienna Wood – 26106 Parkersburg Wood – 26120 Mineral Wells Wood – 26121 Mineral Wells Wood – 26133 Belleville Wood – 26134 Belmont Pleasants – 26136 Big Bend Calhoun – 26137 Big Springs Calhoun – 26138 Brohard Wirt – 26141 Creston Wirt – 26142 Davisville Wood – 26143 Elizabeth Wirt – 26146 Friendly Tyler – 26147 Grantsville Calhoun – 26148 Macfarlan Ritchie – 26149 Middlebourne Tyler – 26150 Mineral Wells Wood – 26151 Mount Zion Calhoun View
Map 26152 Munday Calhoun – 26155 New Martinsville Wetzel – 26159 Paden City Wetzel – 26160 Palestine Wirt – 26161 Petroleum Ritchie – 26162 Porters Falls Wetzel – 26164 Ravenswood Jackson – 26167 Reader Wetzel – 26169 Rockport Wood – 26170 Saint Marys Pleasants – 26175 Sistersville Tyler – 26178 Smithville Ritchie – 26180 Walker Wood – 26181 Washington Wood – 26184 Waverly Wood – 26186 Wileyville Wetzel – 26187 Williamstown Wood – 26201 Buckhannon Upshur – 26202 Fenwick Nicholas View
Map 26203 Erbacon Webster – 26205 Craigsville Nicholas – 26206 Cowen Webster – 26208 Camden On Gauley Webster – 26209 Snowshoe Pocahontas – 26210 Adrian Upshur – 26215 Cleveland Upshur – 26217 Diana Webster – 26218 French Creek Upshur – 26219 Frenchton Upshur – 26222 Hacker Valley Webster – 26224 Helvetia Randolph – 26228 Kanawha Head Upshur – 26229 Lorentz Upshur – 26230 Pickens Randolph – 26234 Rock Cave Upshur – 26236 Selbyville Upshur – 26237 Tallmansville Upshur – 26238 Volga Barbour View
Map 26241 Elkins Randolph – 26250 Belington Barbour – 26253 Beverly Randolph – 26254 Bowden Tucker – 26257 Coalton Randolph – 26259 Dailey Randolph – 26260 Davis Tucker – 26261 Richwood Nicholas – 26263 Dryfork Randolph – 26264 Durbin Pocahontas – 26266 Upperglade Webster – 26267 Ellamore Randolph – 26268 Glady Randolph – 26269 Hambleton Tucker – 26270 Harman Randolph – 26271 Hendricks Tucker – 26273 Huttonsville Randolph – 26275 Junior Barbour – 26276 Kerens Randolph View
Map 26278 Mabie Randolph – 26280 Mill Creek Randolph – 26282 Monterville Randolph – 26283 Montrose Randolph – 26285 Norton Randolph – 26287 Parsons Tucker – 26288 Webster Springs Webster – 26289 Red Creek Tucker – 26291 Slatyfork Pocahontas – 26292 Thomas Tucker – 26293 Valley Bend Randolph – 26294 Valley Head Randolph – 26296 Whitmer Randolph – 26298 Bergoo Webster – 26301 Clarksburg Harrison – 26302 Clarksburg Harrison – 26306 Clarksburg Harrison – 26320 Alma Tyler – 26321 Alum Bridge Lewis View
Map 26323 Anmoore Harrison – 26325 Auburn Ritchie – 26327 Berea Ritchie – 26330 Bridgeport Harrison – 26335 Burnsville Braxton – 26337 Cairo Ritchie – 26338 Camden Lewis – 26339 Center Point Doddridge – 26342 Coxs Mills Gilmer – 26343 Crawford Lewis – 26346 Ellenboro Ritchie – 26347 Flemington Taylor – 26348 Folsom Wetzel – 26349 Galloway Barbour – 26351 Glenville Gilmer – 26354 Grafton Taylor – 26361 Gypsy Harrison – 26362 Harrisville Ritchie – 26366 Haywood Harrison View
Map 26369 Hepzibah Harrison – 26372 Horner Lewis – 26374 Independence Preston – 26376 Ireland Lewis – 26377 Jacksonburg Wetzel – 26378 Jane Lew Lewis – 26384 Linn Gilmer – 26385 Lost Creek Harrison – 26386 Lumberport Harrison – 26404 Meadowbrook Harrison – 26405 Moatsville Barbour – 26408 Mount Clare Harrison – 26410 Newburg Preston – 26411 New Milton Doddridge – 26412 Orlando Lewis – 26415 Pennsboro Ritchie – 26416 Philippi Barbour – 26419 Pine Grove Wetzel – 26421 Pullman Ritchie View
Map 26422 Reynoldsville Harrison – 26424 Rosemont Taylor – 26425 Rowlesburg Preston – 26426 Salem Harrison – 26430 Sand Fork Gilmer – 26431 Shinnston Harrison – 26434 Shirley Tyler – 26435 Simpson Taylor – 26436 Smithburg Doddridge – 26437 Smithfield Wetzel – 26438 Spelter Harrison – 26440 Thornton Taylor – 26443 Troy Gilmer – 26444 Tunnelton Preston – 26447 Walkersville Lewis – 26448 Wallace Harrison – 26451 West Milford Harrison – 26452 Weston Lewis – 26456 West Union Doddridge View
Map 26461 Wilsonburg Harrison – 26463 Wyatt Harrison – 26501 Morgantown Monongalia – 26502 Morgantown Monongalia – 26504 Morgantown Monongalia – 26505 Morgantown Monongalia – 26506 Morgantown Monongalia – 26507 Morgantown Monongalia – 26508 Morgantown Monongalia – 26519 Albright Preston – 26520 Arthurdale Preston – 26521 Blacksville Monongalia – 26524 Bretz Preston – 26525 Bruceton Mills Preston – 26527 Cassville Monongalia – 26531 Dellslow Monongalia – 26534 Granville Monongalia – 26537 Kingwood Preston – 26541 Maidsville Monongalia View
Map 26542 Masontown Preston – 26543 Osage Monongalia – 26544 Pentress Monongalia – 26546 Pursglove Monongalia – 26547 Reedsville Preston – 26554 Fairmont Marion – 26555 Fairmont Marion – 26559 Barrackville Marion – 26560 Baxter Marion – 26561 Big Run Wetzel – 26562 Burton Wetzel – 26563 Carolina Marion – 26566 Colfax Marion – 26568 Enterprise Harrison – 26570 Fairview Marion – 26571 Farmington Marion – 26572 Four States Marion – 26574 Grant Town Marion – 26575 Hundred Wetzel View
Map 26576 Idamay Marion – 26578 Kingmont Marion – 26581 Littleton Wetzel – 26582 Mannington Marion – 26585 Metz Marion – 26586 Montana Mines Marion – 26587 Rachel Marion – 26588 Rivesville Marion – 26590 Wana Monongalia – 26591 Worthington Marion – 26601 Sutton Braxton – 26610 Birch River Nicholas – 26611 Cedarville Gilmer – 26615 Copen Braxton – 26617 Dille Clay – 26619 Exchange Braxton – 26621 Flatwoods Braxton – 26623 Frametown Braxton – 26624 Gassaway Braxton View
Map 26627 Heaters Braxton – 26629 Little Birch Braxton – 26631 Napier Braxton – 26636 Rosedale Gilmer – 26638 Shock Gilmer – 26651 Summersville Nicholas – 26656 Belva Nicholas – 26660 Calvin Nicholas – 26662 Canvas Nicholas – 26667 Drennen Nicholas – 26671 Gilboa Nicholas – 26675 Keslers Cross Lanes Nicholas – 26676 Leivasy Nicholas – 26678 Mount Lookout Nicholas – 26679 Mount Nebo Nicholas – 26680 Nallen Fayette – 26681 Nettie Nicholas – 26684 Pool Nicholas – 26690 Swiss Nicholas View
Map 26691 Tioga Nicholas – 26704 Augusta Hampshire – 26705 Aurora Preston – 26707 Bayard Grant – 26710 Burlington Mineral – 26711 Capon Bridge Hampshire – 26714 Delray Hampshire – 26716 Eglon Preston – 26717 Elk Garden Mineral – 26719 Fort Ashby Mineral – 26720 Gormania Grant – 26722 Green Spring Hampshire – 26726 Keyser Mineral – 26731 Lahmansville Grant – 26739 Mount Storm Grant – 26743 New Creek Mineral – 26750 Piedmont Mineral – 26753 Ridgeley Mineral – 26755 Rio Hampshire View
Map 26757 Romney Hampshire – 26761 Shanks Hampshire – 26763 Springfield Hampshire – 26764 Terra Alta Preston – 26767 Wiley Ford Mineral – 26801 Baker Hardy – 26802 Brandywine Pendleton – 26804 Circleville Pendleton – 26807 Franklin Pendleton – 26808 High View Hampshire – 26810 Lost City Hardy – 26812 Mathias Hardy – 26814 Riverton Pendleton – 26815 Sugar Grove Pendleton – 26817 Bloomery Hampshire – 26818 Fisher Hardy – 26823 Capon Springs Hampshire – 26833 Maysville Grant – 26836 Moorefield Hardy View
Map 26838 Milam Hardy – 26845 Old Fields Hardy – 26847 Petersburg Grant – 26851 Wardensville Hardy – 26852 Purgitsville Hampshire – 26855 Cabins Grant – 26865 Yellow Spring Hampshire – 26866 Upper Tract Pendleton – 26884 Seneca Rocks Pendleton – 26886 Onego Pendleton –
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