Tetrahydrocannabinol (THC) is the primary psychoactive compound found in the cannabis plant. When consumed, it interacts with the body’s endocannabinoid system, a complex network of receptors and signaling molecules that regulates numerous physiological processes. A major health concern surrounding the increasing use of cannabis is whether exposure to THC during periods of rapid biological change—namely fetal development and adolescence—can negatively affect physical growth. Research into this question requires an objective look at both observable growth metrics and the underlying hormonal mechanisms that govern human development. This investigation focuses on the current scientific understanding of how THC exposure may influence the processes that determine an individual’s final physical stature.
THC Exposure During Fetal Development
Maternal cannabis use introduces THC into the developing fetal environment, as the compound readily crosses the placenta. The body’s own endocannabinoid system plays a significant part in early development, regulating processes like implantation and placental formation. Disrupting this delicate biological balance with external cannabinoids, such as THC, can lead to measurable deviations in growth metrics observable at birth.
Prenatal cannabis exposure is consistently associated with a decrease in the newborn’s weight. Studies indicate that exposed infants are born with an average reduction in birth weight, sometimes over 100 grams less than non-exposed infants. Furthermore, exposure has been linked to an increased likelihood of preterm delivery, meaning the infant is born before 37 completed weeks of gestation.
The timing of exposure appears to influence the specific outcomes observed. Continued cannabis use throughout the entire pregnancy is associated with the most pronounced deficits in fetal growth, including a reduction in both newborn weight and head circumference. Head circumference deficits, which are an indirect measure of brain growth, are often seen with exposure extending past the first trimester.
Adolescent Use and Skeletal Growth
The question of whether THC use during adolescence affects final adult height centers on its potential impact on skeletal maturation. Longitudinal bone growth occurs at the epiphyseal growth plates, which are thin layers of cartilage located near the ends of long bones. Growth plates determine the rate of elongation by a process called endochondral ossification, where cartilage cells differentiate and are eventually replaced by bone.
Animal studies suggest that THC can interfere with this precise process of skeletal elongation. Research in mice has demonstrated that THC slows the growth rate of long bones, such as the femur. This effect is thought to be mediated by the cannabinoid receptors, which are present within the specialized cartilage cells of the growth plate. Specifically, THC was found to inhibit the process of chondrocyte hypertrophy—the enlargement of cartilage cells—which is a necessary step for bone lengthening.
Extrapolating these direct biological effects to final adult height in humans is complex, partly because human studies face significant confounding factors. Adolescents who use cannabis often also use tobacco or other substances, which are independently known to influence growth and pubertal timing. The timing of growth plate fusion, which marks the end of longitudinal growth, is heavily regulated by sex hormones. Therefore, any effect of THC on final adult height may be indirect, resulting from a disruption of the hormonal signals that control skeletal maturation.
Endocrine System Disruption and Growth Hormones
The potential for THC to influence growth is rooted in its interaction with the endocrine system. THC exerts its effects by binding to cannabinoid receptors, particularly the CB1 receptor, which is widely distributed in the central nervous system, including areas near the hypothalamus. The hypothalamus is the control center for the hypothalamic-pituitary axis, which regulates the release of many hormones essential for growth and development.
In animal models, THC administration has been shown to acutely suppress the secretion of several hormones, including growth hormone (GH), which is the primary driver of postnatal growth. It also appears to suppress thyroid-stimulating hormone (TSH) by affecting the regulatory hormones released by the hypothalamus. This suppression of TSH can subsequently lead to lower levels of thyroid hormones (T4 and T3), which are necessary for normal metabolism and skeletal maturation.
THC further interacts with the hypothalamic-pituitary-gonadal (HPG) axis, which governs pubertal development and the production of sex hormones. By modulating the release of gonadotropin-releasing hormone (GnRH), THC can indirectly affect the pituitary hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Since sex hormones are the ultimate signals that cause the growth plates to fuse, a disruption of the HPG axis could theoretically alter the timing of puberty, thereby influencing the window available for achieving final adult height. These hormonal effects, however, are often found to be inconsistent or diminished in human studies, potentially due to the body developing a tolerance to chronic use.