Fact: While some men can father children into their 50’s or 60’s, male fertility isn’t age-proof. Men see a decline in fertility in their 40s, and also have been found to be at increased risk of offspring with certain health conditions, like schizophrenia.
Fact: It’s common for people to think of infertility as a female problem, but only 35% of infertility cases are caused solely by female factors. Another 35% results from factors in the male reproductive system, 20% come from both, and 10% are undetermined.
Fact: Smoking marijuana, even infrequently, can dramatically affect sperm and egg quality, which can have a dramatic impact on fertility.
Infertility Myth #8: A man’s fertility doesn’t change with age.
Fact: Alcohol can increase the risk of birth defects once a woman becomes pregnant and can cause a collection of birth defects known as fetal alcohol syndrome (FAS). There is no known “safe” amount of alcohol that can be consumed during pregnancy, so it is generally recommended that women avoid alcohol in pregnancy.
Fact: Poor nutrition can have an impact on fertility. Women with a Body Mass Index (BMI) over 30 or those who are severely underweight may have difficulties with fertility. Click here to download a BMI reference chart.
Fact: Infertility means that you have been unable to have a child naturally after a year of trying (or 6 months if you are over the age of 35). With the proper treatment, the majority of people go on to have children.
Fact: According to a report in the journal Human Reproduction, a woman’s fertility starts to decline at age 27, although this isn’t clinically significant. Most women of this age can still get pregnant, of course, but it might take a few more months of trying. But by the time a woman reaches 35, her chances of getting pregnant during any particular attempt are about half of what they were between the ages of 19 and 26.
For example, a 1985 paper on foetal abnormality (Qazi et al.) after prenatal exposure to cannabis discussed five infants whose mothers acknowledged use of cannabis prior to and during pregnancy and who were born with various symptoms of growth retardation, neurological dysfunction and deformity. While it may provide helpful insight, such a small sample size is far from being enough to draw concrete conclusions, and correlation does not imply causation.
While the effect of cannabis use on male fertility appears to be quite straightforward—with male chronic cannabis users being likely to experience some degree of impairment to reproductive physiology—the effect on the human female reproductive system is less clear-cut.
Other studies seen as providing evidence that cannabis use can cause foetal abnormalities are animal studies (Geber & Schramm 1969, Phillipset al, 1971) in which rabbits, hamsters, rats and mice were injected with vast doses of crude cannabis extract (as much as 666mg/kg in one instance!). Such massive doses of cannabis would be practically impossible for a human to consume through conventional means, and are essentially useless as a point of comparison.
Why is anandamide beneficial, while THC may not be?
For healthy adult males, it seems that use of THC does indeed cause some negative effects on fertility, which tend to increase with higher doses. However, THC’s endogenous analogue anandamide appears to be critical to the functioning of the male reproductive system.
Use of cannabis may affect human fertility, depending on gender, general health, socioeconomic status and several other factors. Here, we look at existing research on cannabis and human fertility, in order to provide readers with an accurate, up-to-date summary of the current state of scientific knowledge.
Female reproductive health is vastly complex in itself, as it not only comprises the ability to become pregnant but also the ability to carry healthy offspring to term and successfully give birth.
The 2002 study found that sperm cells would bind to the agonist CP-55,940, demonstrating the presence of CB1-receptors. The study also concluded that the presence of THC and a synthetic anandamide analogue, AM-356, both reduced sperm motility in vitro. Interestingly, it was found that AM-356 exerted a biphasic dose-dependent effect on sperm motility, causing inhibition at high doses but hyperactivity at low doses.