National Academies #Marijuana Findings @theNASEM

Many have heard or read about United States Attorney General Jeff Sessions’ ignorant remark about marijuana, and many of us have heard or read numerous claims about cannabis, ranging from “it cures cancer” to “it makes you hungry,” and almost everything between. But if you want to make an effective argument for or against anything, you need facts. And the following information from the National Academies of Sciences, Engineering, and Medicine is THE MOST authoritative, up-to-date volume on the subject of cannabis. You would be wise to cite this research when you lobby your local, state or national legislator to legalize (or not) marijuana. (I am a legalization proponent & advocate for the 100% legalization, regulation, and taxation of adult recreational & prescriptive medical use of marijuana.)

Now, with the 2017 release of “The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research” by the Committee on the Health Effects of Marijuana: An Evidence Review and Research Agenda, Board on Population Health and Public Health Practice Health and Medicine Division, A Report of the National Academies of Science, we have one of THE MOST to-date conclusive pieces of EVIDENCE for/against cannabis consumption, either medically, and/or recreationally. It is AUTHORITATIVE, and unbiased. Bear in mind, this is findings of SCIENTIFIC MEDICAL RESEARCH.

An independent examination of the report was carried out in accordance with institutional procedures and all review comments were carefully considered. A committee of experts was convened to conduct a comprehensive review of the literature regarding the health effects of using cannabis and/or its constituents that had appeared since the publication of the 1999 IOM (Institute of Medicine) report.

From their review, the committee arrived at nearly 100 different research conclusions related to cannabis or cannabinoid use and health.

Committee members formulated four recommendations to address research gaps, improve research quality, improve surveillance capacity, and address research barriers.

Categories, including subtopics, are as follows:

Therapeutic effects
• Chronic pain; cancer, chemotherapy-induced nausea/vomiting; anorexia and weight loss; irritable bowel syndrome; epilepsy; spasticity related to multiple sclerosis or spinal cord injury; Tourette syndrome; amyotrophic lateral sclerosis; Huntington’s disease; Parkinson’s disease; dystonia; dementia; glaucoma; traumatic brain injury; addiction; anxiety; depression; sleep disorders; post-traumatic stress disorder; schizophrenia and other psychoses

Cancer
• Lung cancer; head and neck cancer; testicular cancer; esophageal cancer; other cancer

Cardiometabolic risk
• Acute myocardial infarction; stroke; metabolic dysregulation, metabolic syndrome, prediabetes, and diabetes mellitus

Respiratory disease
• Pulmonary function; chronic obstructive pulmonary disorder; respiratory symptoms (including chronic bronchitis); asthma

Immunity
• Immune function; infectious disease

Injury and death
• All-cause mortality; occupational injury; motor vehicle crash; overdose injury and death

Prenatal, perinatal, and postnatal exposure to cannabis
• Pregnancy complications for the mother; fetal growth and development; neonatal conditions; later outcomes for the infant

Psychosocial
• Cognition (learning, memory, attention, intelligence); academic achievement and educational outcomes; employment and income; social relation- ships and other social roles

Mental health
• Schizophrenia and other psychoses; bipolar disorders, depression; suicide; anxiety; post-traumatic stress disorder

Problem cannabis use
• Cannabis use disorder

Cannabis use and abuse of other substances
• Abuse of other substances

Weight Of Evidence Categories for Conclusions are ranked High-to-Low-and-None as Substantial, Moderate, Limited Evidence, and No or Insufficient Evidence to Support the Association for therapeutic effects, and other health effects.

Here are: 
Conclusions—Therapeutic Effects of Cannabis and Cannabinoids

There is conclusive or substantial evidence that cannabis or cannabinoids are effective:
• For the treatment of chronic pain in adults (cannabis) (4-1)
• As antiemetics in the treatment of chemotherapy-induced
nausea and vomiting (oral cannabinoids) (4-3)
• For improving patient-reported multiple sclerosis spasticity 
symptoms (oral cannabinoids) (4-7a)

There is moderate evidence that cannabis or cannabinoids are effective for:
• Improving short-term sleep outcomes in individuals with sleep disturbance associated with obstructive sleep apnea syndrome, fibromyalgia, chronic pain, and multiple sclerosis (cannabinoids, primarily nabiximols) (4-19)

There is limited evidence that cannabis or cannabinoids are effective for:
• Increasing appetite and decreasing weight loss associated with HIV/AIDS (cannabis and oral cannabinoids) (4-4a)
• Improving clinician-measured multiple sclerosis spasticity symptoms (oral cannabinoids) (4-7a)
• Improving symptoms of Tourette syndrome (THC capsules) (4-8)
• Improving anxiety symptoms, as assessed by a public speaking test, in individuals with social anxiety disorders (cannabidiol) (4-17)
• Improving symptoms of post-traumatic stress disorder (nabilone; a single, small fair-quality trial) (4-20)

There is limited evidence of a statistical association between cannabinoids and:
• Better outcomes (i.e., mortality, disability) after a traumatic brain injury or intracranial hemorrhage (4-15)

There is limited evidence that cannabis or cannabinoids are ineffective for:
• Improving symptoms associated with dementia (cannabinoids) (4-13)
• Improving intraocular pressure associated with glaucoma (cannabinoids) (4-14)
• Reducing depressive symptoms in individuals with chronic pain or multiple sclerosis (nabiximols, dronabinol, and nabilone) (4-18)

There is no or insufficient evidence to support or refute the conclusion that cannabis or cannabinoids are an effective treatment for:
• Cancers, including glioma (cannabinoids) (4-2)
• Cancer-associated anorexia cachexia syndrome and anorexia nervosa (cannabinoids) (4-4b)
• Symptoms of irritable bowel syndrome (dronabinol) (4-5)
• Epilepsy (cannabinoids) (4-6)
• Spasticity in patients with paralysis due to spinal cord injury (cannabinoids) (4-7b)
• Symptoms associated with amyotrophic lateral sclerosis (cannabinoids) (4-9)
• Chorea and certain neuropsychiatric symptoms associated with Huntington’s disease (oral cannabinoids) (4-10)
• Motor system symptoms associated with Parkinson’s disease or the levodopa-induced dyskinesia (cannabinoids)
(4-11)
• Dystonia (nabilone and dronabinol) (4-12)
• Achieving abstinence in the use of addictive substances
 (cannabinoids) (4-16)
• Mental health outcomes in individuals with schizophrenia or schizophreniform psychosis (cannabidiol) (4-21)

Conclusions—Cancer
There is moderate evidence of no statistical association between cannabis use and:
• Incidence of lung cancer (cannabis smoking) (5-1)
• Incidence of head and neck cancers (5-2)

There is limited evidence of a statistical association between cannabis smoking and:
• Non-seminoma-type testicular germ cell tumors (current, frequent, or chronic cannabis smoking) (5-3)

There is no or insufficient evidence to support or refute a statistical association between cannabis use and:
• Incidence of esophageal cancer (cannabis smoking) (5-4)
• Incidence of prostate cancer, cervical cancer, malignant gliomas, non-Hodgkin lymphoma, penile cancer, anal cancer, Kaposi’s sarcoma, or bladder cancer (5-5)
• Subsequent risk of developing acute myeloid leukemia/ acute non-lymphoblastic leukemia, acute lymphoblastic leukemia, rhabdomyosarcoma, astrocytoma, or neuroblastoma in offspring (parental cannabis use) (5-6)

Conclusions—Cardiometabolic Risk
There is limited evidence of a statistical association between cannabis use and:
• The triggering of acute myocardial infarction (cannabis smoking) (6-1a)
• Ischemic stroke or subarachnoid hemorrhage (6-2)
• Decreased risk of metabolic syndrome and diabetes (6-3a)
• Increased risk of prediabetes (6-3b)

There is no evidence to support or refute a statistical association between chronic effects of cannabis use and:
• The increased risk of acute myocardial infarction (6-1b)

Conclusions—Respiratory Disease
There is substantial evidence of a statistical association between cannabis smoking and:
• Worse respiratory symptoms and more frequent chronic bronchitis episodes (long-term cannabis smoking) (7-3a)

There is moderate evidence of a statistical association between cannabis smoking and:
• Improved airway dynamics with acute use, but not with chronic use (7-1a)
• Higher forced vital capacity (FVC) (7-1b)

There is moderate evidence of a statistical association between the cessation of cannabis smoking and:
• Improvements in respiratory symptoms (7-3b)

There is limited evidence of a statistical association between cannabis smoking and:
• An increased risk of developing chronic obstructive pulmonary disease (COPD) when controlled for tobacco use (occasional cannabis smoking) (7-2a)

There is no or insufficient evidence to support or refute a statistical association between cannabis smoking and:
• Hospital admissions for COPD (7-2b)
• Asthma development or asthma exacerbation (7-4)

Conclusions—Immunity
There is limited evidence of a statistical association between cannabis smoking and:
• A decrease in the production of several in inflammatory cytokines in healthy individuals (8-1a)

There is limited evidence of no statistical association between cannabis use and:
• The progression of liver fibrosis or hepatic disease in individuals with viral hepatitis C (HCV) (daily cannabis use) (8-3)

There is no or insufficient evidence to support or refute a statistical association between cannabis use and:
• Other adverse immune cell responses in healthy individuals (cannabis smoking) (8-1b)
• Adverse effects on immune status in individuals with HIV (cannabis or dronabinol use) (8-2)
• Increased incidence of oral human papilloma virus (HPV) (regular cannabis use) (8-4)

Conclusions—Injury and Death
There is substantial evidence of a statistical association between cannabis use and:
• Increased risk of motor vehicle crashes (9-3)

There is moderate evidence of a statistical association between cannabis use and:
• Increased risk of overdose injuries, including respiratory distress, among pediatric populations in U.S. states where cannabis is legal (9-4b)

There is no or insufficient evidence to support or refute a statistical association between cannabis use and:
• All-cause mortality (self-reported cannabis use) (9-1)
• Occupational accidents or injuries (general, nonmedical cannabis use) (9-2)
• Death due to cannabis overdose (9-4a)

Conclusions—Prenatal, Perinatal, and Neonatal Exposure
There is substantial evidence of a statistical association between maternal cannabis smoking and:
• Lower birth weight of the offspring (10-2)
There is limited evidence of a statistical association between
maternal cannabis smoking and:
• Pregnancy complications for the mother (10-1)
• Admission of the infant to the neonatal intensive care unit (NICU) (10-3)

There is insufficient evidence to support or refute a statistical association between maternal cannabis smoking and:
• Later outcomes in the offspring (e.g., sudden infant death syndrome, cognition/academic achievement, and later sub- stance use) (10-4)

Conclusions—Psychosocial
There is moderate evidence of a statistical association between cannabis use and:
• The impairment in the cognitive domains of learning, memory, and attention (acute cannabis use) (11-1a)

There is limited evidence of a statistical association between cannabis use and:
• Impaired academic achievement and education outcomes (11-2)
• Increased rates of unemployment and/or low income (11-3)
• Impaired social functioning or engagement in developmentally appropriate social roles (11-4)

There is limited evidence of a statistical association between sustained abstinence from cannabis use and:
• Impairments in the cognitive domains of learning, memory, and attention (11-1b)

Conclusions—Mental Health
There is substantial evidence of a statistical association between cannabis use and:
• The development of schizophrenia or other psychoses, with the highest risk among the most frequent users (12-1)

There is moderate evidence of a statistical association between cannabis use and:
• Better cognitive performance among individuals with psychotic disorders and a history of cannabis use (12-2a)
• Increased symptoms of mania and hypomania in individuals diagnosed with bipolar disorders (regular cannabis use) (12-4)
• A small increased risk for the development of depressive disorders (12-5)
• Increased incidence of suicidal ideation and suicide attempts with a higher incidence among heavier users (12-7a)
• Increased incidence of suicide completion (12-7b)
• Increased incidence of social anxiety disorder (regular cannabis use) (12-8b)

There is moderate evidence of no statistical association between cannabis use and:
• Worsening of negative symptoms of schizophrenia (e.g., blunted affect) among individuals with psychotic disorders (12-2c)

There is limited evidence of a statistical association between cannabis use and:
• An increase in positive symptoms of schizophrenia (e.g., hallucinations) among individuals with psychotic disorders (12-2b)
• The likelihood of developing bipolar disorder, particularly among regular or daily users (12-3)
• The development of any type of anxiety disorder, except social anxiety disorder (12-8a)
• Increased symptoms of anxiety (near daily cannabis use) (12-9)
• Increased severity of post-traumatic stress disorder symptoms among individuals with post-traumatic stress disorder (12-11)

There is no evidence to support or refute a statistical association between cannabis use and:
• Changes in the course or symptoms of depressive disorders (12-6)
• The development of post-traumatic stress disorder (12-10)

Conclusions—Problem Cannabis Use
There is substantial evidence that:
• Stimulant treatment of attention deficit hyperactivity disorder (ADHD) during adolescence is not a risk factor for the development of problem cannabis use (13-2e)
• Being male and smoking cigarettes are risk factors for the progression of cannabis use to problem cannabis use (13-2i)
• Initiating cannabis use at an earlier age is a risk factor for the development of problem cannabis use (13-2j)

There is substantial evidence of a statistical association between:
• Increases in cannabis use frequency and the progression to developing problem cannabis use (13-1)
• Being male and the severity of problem cannabis use, but the recurrence of problem cannabis use does not differ between males and females (13-3b)

There is moderate evidence that:
• Anxiety, personality disorders, and bipolar disorders are not risk factors for the development of problem cannabis use (13-2b)
• Major depressive disorder is a risk factor for the development of problem cannabis use (13-2c)
• Adolescent ADHD is not a risk factor for the development of problem cannabis use (13-2d)
• Being male is a risk factor for the development of problem cannabis use (13-2f)
• Exposure to the combined use of abused drugs is a risk factor for the development of problem cannabis use (13-2g)
• Neither alcohol nor nicotine dependence alone are risk factors for the progression from cannabis use to problem cannabis use (13-2h)
• During adolescence the frequency of cannabis use, oppositional behaviors, a younger age of first alcohol use, nicotine use, parental substance use, poor school performance, anti- social behaviors, and childhood sexual abuse are risk factors for the development of problem cannabis use (13-2k)

There is moderate evidence of a statistical association between:
• A persistence of problem cannabis use and a history of psychiatric treatment (13-3a)
• Problem cannabis use and increased severity of posttraumatic stress disorder symptoms (13-3c)

There is limited evidence that:
• Childhood anxiety and childhood depression are risk factors for the development of problem cannabis use (13-2a)

Conclusions—Cannabis Use and the Abuse of Other Substances
There is moderate evidence of a statistical association between cannabis use and:
• The development of substance dependence and/or a substance abuse disorder for substances, including alcohol, tobacco, and other illicit drugs (14-3)

There is limited evidence of a statistical association between cannabis use and:
• The initiation of tobacco use (14-1)
• Changes in the rates and use patterns of other licit and illicit substances (14-2)

Conclusions—Challenges and Barriers in Conducting Cannabis Research
There are several challenges and barriers in conducting cannabis and cannabinoid research, including:
• There are specific regulatory barriers, including the classification of cannabis as a Schedule I substance, that impede the advancement of cannabis and cannabinoid research (15-1)
• It is often difficult for researchers to gain access to the quantity, quality, and type of cannabis product necessary to address specific research questions on the health effects of cannabis use (15-2)
• A diverse network of funders is needed to support cannabis and cannabinoid research that explores the beneficial and harmful health effects of cannabis use (15-3)
• To develop conclusive evidence for the effects of cannabis use on short- and long-term health outcomes, improvements and standardization in research methodology (including those used in controlled trials and observational studies) are needed (15-4)