Research has demonstrated that human sperm contains receptors which are stimulated by substances like THC and other cannabis-related chemicals. Tests have shown that sperm exposed to high levels of THC began to swim in an abnormal fashion, and were less able to attach to an egg so that fertilization could take place. While many men who use cannabis have fathered children, certain men at risk for infertility may be more susceptible to reproductive complications.

Marijuana use during pregnancy, in certain cases, has been linked to low birth weight but the link between cannabis and birth complications is questioned by many in the scientific community. Many studies about drug use during pregnancy are self-administered by the applicants and not always anonymous. The stigma of using illicit drugs while pregnant discourages honest reporting and can invalidate the results. Studies show that women who consume cannabis while they are pregnant may also be likely to consume alcohol, tobacco, or other illicit drugs, which makes it difficult to deduce scientific facts about just marijuana use from statistical results. Very few large, well-controlled epidemiological studies have taken place to understand the connection of marijuana use and pregnancy. One for example, by Zuckerman and colleagues, included a large sample of women with a substantial prevalence of marijuana use that was verified by urine analysis and no increased probability of birth defects was found in the sample group. Opposed to fetal alcohol syndrome, similar type facial features and related symptoms are not associated with prenatal marijuana exposure. THC passes into the breast milk and may affect a breastfed infant.

A study of the development of 59 Jamaican children, one-half of the sample's mothers used marijuana during pregnacy, was research from birth to age 5 years. Pregnant non-using mothers were paired with cannabis users who matched age, parity, and socioeconomic status. Testing was done at 1, 3, and 30 days of age with the Brazelton Neonatal Behavioral Assessment Scales, and at ages 4 and 5 years with the McCarthy Scales of Children's Abilities test. Data was also collected from the child's home environment and temperament, as well as standardized tests. The results over the entire reseach period showed no significant differences in development testing outcomes between using and non-using mothers. At 30 days of age, however, the children of marijuana-using mothers had higher scores on autonomic stability and reflexes. The absence of any differences between the exposed on nonexposed groups in the early neonatal period suggest that the better scores of exposed neonates at 1 month are traceable to the cultural positioning and social and economic characteristics of mothers using marijuana that select for the use of marijuana but also promote neonatal development.

Effects on mental health

Behavioral effects

The term "amotivational syndrome" is often applied to young individuals who have changed from clean, assertive, upwardly mobile achievers into the sort of person just described, with marijuana as the culprit. The syndrome, like other correlational phenomena, raises a chicken-and-egg type problem; marijuana use can just as easily be seen as the result of such a personality shift as it can be the cause of it. Regardless, studies to raise this and other questions, like the prevalence of such "syndrome" in the population, and proving a biological or psychological connection of the "syndrome" to substance use, have not happened. Instead, a political tug of war has ensued with each point of view claiming their own scientific research as evidence.

Government studies often point to statistical data accumulated by methods like the National Household Survey on Drug Abuse (NHSDA), the Monitoring the Future study (MTF), and the Arrestee Drug Abuse Monitoring (ADAM) program, which claim lower school averages and higher dropout rates among users than nonusers, even though these differences are very small and may be exaggerated by the stigma attached to students who use the drug. However, the major contributor to a lack of credibility in these studies, is that in many cases, like with NHSDA and MTF, these surveys are usually self-administered and may or may not be anonymous. The likeliness of over or under representing data definitely undermines the effectiveness of these instruments. The MTF study is conducted anonymously, but only seeks information from a sample of people who have been arrested for drug-related offenses. Clearly, the case can easily be made that socially deviant behavior will be found more frequently in individuals of the criminal justice system compared to those in the general population, including non users. In response, independent studies of college students have shown that there was no difference in grade point average, and achievement, between marijuana users and nonusers, but the users had a little more difficulty deciding on career goals, and a smaller number were seeking advanced professional degrees. Laboratory studies of the relationship between motivation and marijuana outside of the classroom, where volunteers worked on operant tasks for a wage representing a working world model, also fail to distinguish a noticeable difference between users and non users.

Gateway drug hypothesis

According to neurologist Jim van Os, some scientists believe that there is also a physiological component to the gateway drug effect. He states there is "overwhelming evidence that nobody in the brain's developmental stage – under the age of 21 – should use cannabis."

A July 2006 study by Ellgren et al. strictly tested lab rats for the biological mechanism of the gateway drug effect. The study administered 6 "teenage" (28 and 49 days old) rats delta-9-tetrahydrocannabinol, and 6 were the control. One week after the first part was completed, catheters were inserted in the jugular vein of all of the adult rats and they were able to self-administer themselves heroin by pushing a lever. The study found that initially both groups behaved the same and began to self-administer heroin frequently, but then stabilized at different levels. The rats that had previously been administered THC consumed about 1.5 times more heroin than those that had not. Because many cannabinoid receptors interact with the opioid system, the study found that adolescent cannabis use overstimulates and alters the pleasure and reward structures of the brain, thus increasing the risk of addiction. Psychopharmacologist Ian Stolerman, from King's College London, finds the biological cannabis gateway drug effect "somewhat preliminary", and states "it's too early to say there's a consensus, but a small number of studies like this suggest that there is a physiological basis for this effect." Other drugs, he notes, such as cocaine and amphetamines are involved in another brain pathway called the dopaminergic system. Cells in that system also interact with THC receptors and could be modified by cannabis exposure. Cannabinoid receptors are 10 times more prevalent in the brain than opioid receptors. According to Dr. Hurd, one of the study leaders, two other drugs that also stimulate opioid cells, and could therefore also feasibly cause a gateway effect, are nicotine and alcohol.

Co-occurrence of mental illness

Similarity of symptoms

A Yale research study notes that subjects administered pure delta-9-THC induced transient symptoms which resemble those of schizophrenia "ranging from suspiciousness and delusions to impairments in memory and attention". There were no side effects in the study participants one, three, and six months after the study.

Correlation studies

A review of the evidence by Louise Arsenault, et al in 2004 reports that on an individual level, cannabis use confers an overall twofold increase in the relative risk of later schizophrenia. This same research also states that "There is little dispute that cannabis intoxication can lead to acute transient psychotic episodes in some individuals". The study synthesizes the results of several studies into a statistical model.

However, a 2005 study found that "the onset of schizotypal symptoms generally precedes the onset of cannabis use. The findings do not support a causal link between cannabis use and schizotypal traits".

A landmark study, in 1987, of 50,000 Swedish Army conscripts, found that those who admitted at age 18 to having taken cannabis on more than 50 occasions, were six times more likely to develop schizophrenia in the following 15 years. In fact, psychosis cases were restricted to patients requiring a hospital admission. These findings have not been replicated in another population based sample. As the study did not control for symptoms preexisting onset of cannabis use, the study does not resolve the correlation versus causality question but has fueled a major debate within the scientific community.

Research based on the Dunedin Multidisciplinary Health and Development Study has found that those who begin regular use of cannabis in early adolescence (from age 15, median 25 days per year by age 18) and also fit a certain genetic profile (specifically, the Val/Val variant of the COMT gene) are five times more likely to develop psychotic illnesses than individuals with differing genotypes, or those who do not use cannabis. The study was noted for it having controlled for preexisting symptoms, but is open to the criticism that it cannot control for late adolescent onset of psychotic illness. Also, the study was on a cohort population, so there is no way to correlate a change in the rate of adolescent use with a change in the rate of incidence of schizophenia in the study population. These points undermine its value in resolving the correlation versus causality question.

Smoking

Different and fewer risks than tobacco

Tobacco smoking has well-established risks such as bronchitis, coughing, overproduction of mucus, and wheezing. Similar risks for smoking cannabis related to airway inflammation have been suggested in a study of healthy cannabis users who exhibited similar early characteristics to tobacco smoking.

The effects of tobacco and cannabis smoking differ, however, as they affect different parts of the respiratory tract: whereas tobacco tends to penetrate to the smaller, peripheral passageways of the lungs, cannabis tends to concentrate on the larger, central passageways. One consequence of this is that cannabis, unlike tobacco, does not appear to cause emphysema. Also unlike tobacco, regular cannabis use does not appear to cause COPD, either. Researchers have speculated on potential side effects from the fact that cannabis burns at a higher temperature than tobacco.

It is important to note that in some cases, a cannabis user may encounter commercial tobacco in joints (popular in Europe), added tobacco with hash in chillum (India), or cannabis rolled in tobacco leaves, which would expose the user to the additional risks of tobacco, though nothing on the same order as regular tobacco use.

Potency matters

The methodological difficulty, however, was that all the subjects were both tobacco and cannabis smokers, smoking ultra-low-potency (0.004% and 1.24%) NIDA-provided cannabis. Typical potency is closer to 7-15%. Like a listener turning up a radio until he can hear it, a cannabis smoker will regulate the dose by smoking until the desired effect is felt, which in ultra-low-potency cannabis translates into much greater volume of inhaled smoke, and so abnormally high blood carboxyhemoglobin levels. Typical levels would therefore be much lower than the study found. These problems notwithstanding, this is a primary study cited by NIDA in this regard.

Cancer risk

Although the carcinogenicity of tobacco is thought to be caused mainly by tar, it has been suggested that it could be the result of radioactive substances present in tobacco soils . This problem does not pertain to cannabis, the vast majority of which is grown in wild, organic, or hydroponic conditions.

Attempts at harm reduction

• filtered cigarettes
• bongs (specialized pipes filtering smoke through water)
• vaporizers (devices for extracting THC without combusting the cannabis)
• eating ("space cakes")
• high potency cannabis

Like tobacco smoke, marijuana smoke contains tars which are rich in carcinogenic polycyclic aromatic hydrocarbons, which are a prime culprit in smoking-related cancers. However, cannabinoids themselves are not carcinogenic. An obvious way to protect smokers' health is therefore to minimize the content of smoke tars relative to cannabinoids.

The most obvious way to do this is to bypass smoking completely by simply eating the cannabis as "space cakes".

Another way is to increase the THC potency of the marijuana (see also section on potency above). Assuming smokers adjust their smoke intake to the cannabinoid dosage, the higher the concentration of cannabinoids, the lower the amount of tars they are likely to consume to achieve their desired effect.

Vaporisers, by heating the cannabis oils to be inhaled without combustion, almost avoid the risk altogether . A 2000 study conducted by NORML and MAPS found that the two tested vaporizers performed up to 25% better than unfiltered marihuana cigarettes in terms of tar delivery.

Surprisingly, the same study found that water pipes (bongs) and filtered cigarettes performed 30% worse than regular, unfiltered joints. The reason is that waterpipes and filters filter out more psychoactive THC than they do tars, thereby requiring users to smoke more to reach their desired effect. The study does not, however, rule out the possibility that waterpipes could have other benefits, such as filtering out harmful gases such as carbon monoxide.

Cannabis and driving

A 2001 study by the United Kingdom Transit Research Laboratory (TRL) specifically focuses on the effects of Cannabis use on driving , and is one of the most recent and commonly quoted studies on the subject. The report summarizes current knowledge about the effects of cannabis on driving and accident risk based on a review of available literature published since 1994 and the effects of cannabis on laboratory based tasks.

The study identified young males, amongst whom cannabis consumption is frequent and increasing, and in whom alcohol consumption is also common, as an a priori risk group for traffic accidents. This is due to driving inexperience and factors associated with youth relating to risk taking, delinquency and motivation. These demographic and psychosocial variables may relate to both drug use and accident risk, thereby presenting an artificial relationship between use of drugs and accident involvement.

The effects of cannabis on laboratory-based tasks show clear impairment with respect to tracking ability, attention, and other tasks depending on the dose administered. These effects however, are not as pronounced on tasks of greater ecological validity, like real driving or simulator tasks. Both simulation and road trials generally find that driving behavior shortly after consumption of larger doses of cannabis results in: a more cautious driving style; increased variability in lane position (and headway); and longer decision times. Whereas these results indicate a 'change' from normal conditions, they do not necessarily reflect 'impairment' in terms of performance effectiveness since few studies report increased accident risk. However, the results do suggest 'impairment' in terms of performance efficiency given that some of these behaviors may limit the available resources to cope with any additional, unexpected or high demand, events. Indeed, compensatory effort can be invoked to offset impairment in the driving task. Subjects under cannabis treatment appear to perceive that they are impaired and can compensate, for example, by not overtaking, by slowing down and by focusing their attention when they know a response will be required. This compensatory effort may be one reason for the failure to implicate cannabis consumption as an accident risk factor. However, this claim is difficult to substantiate in the absence of any substantial epidemiological estimates of accident risk.

Specifically, 4-12% of accident fatalities have detected levels of cannabis. However, most studies report that the majority of fatal cases with detected levels of cannabis are compounded by alcohol. The study estimates 11ng/ml THC as the equivalent does to the legal limit of alcohol (0.08% BAC in the UK), although cannabis effects on driving are present up to an hour after smoking but do not continue for extended periods. Alcohol alone or in combination with cannabis, increases impairment, accident rate and accident responsibility. Moreover, accident risk cannot be derived in the absence of baseline data for non-fatal cases.

Similar conclusions have been reached by studies maintained by the federal governments of Australia, United Kingdom, New Zealand and the United States (see here for a list of studies). Those studies that have concluded that cannabis has a significant negative effect on driving ability generally involve the use of roadside sobriety tests as an indicator of reduced ability (for example, see this NIDA report). However, studies that employ this methodology show that a majority of subjects who tested positive for THC also tested positive for alcohol, already described as a limiting factor of validity.

References