Furthermore, people with Down syndrome often suffer from gastrointestinal symptoms such as vomiting, diarrhea, abdominal pain, and constipation, and have an increased risk of developing GI disorders. There’s evidence that cannabis can be helpful here as well. For one, a 2015 review of 23 clinical studies concluded that cannabis-based medicines may relieve nausea and vomiting caused by chemotherapy.
Although cannabis shows early promise in the treatment of Down syndrome, it does have some side effects. These tend to vary depending on whether you’re using a THC- or CBD-heavy preparation.
Although more human-based studies are sorely needed, current findings highlight the potential of cannabis-based medicines in DS. Here’s what the research says.
Medical studies on Down syndrome and cannabis
For starters, a 2008 study that examined Down syndrome brain tissue found a link between beta-amyloid plaques and the ECS. The brain cells associated with these plaques had increased activity of CB2 receptors and the enzyme FAAH, which breaks down the endocannabinoid anandamide.
There’s also research evidence that cannabis can relieve some symptoms that occur in this condition, such as impulsivity, digestive issues, and seizures. Cannabis may also be able to help by protecting people with Down syndrome from amyloid plaques, which has been linked to the cognitive deficits which also occur in those suffering from Alzheimer’s disease.
How cannabis works on Down Syndrome
CBD can also help with the seizures that occur in about 8% of people with Down syndrome . In fact, CBD has been shown to be an effective seizure treatment and CBD-based drug Epidiolex received FDA approval for treating specific seizure conditions including Dravet Syndrome and Lennox-Gastaut in 2018. The research in this area is quite promising, suggesting that CBD may treat a variety of seizures:
Regular, THC-rich cannabis (commonly known as marijuana) can cause dry mouth, red eyes, sleepiness, dizziness, impaired memory and reaction time, and increased heart rate. Some individuals might also experience feelings of paranoia and anxiety.
A very concerning consensus is now emerging relating to cannabis-induced teratogenesis, embryotoxicity and fetotoxicity. A 2007 Hawaiian study found that 21 birth defects including many cardiovascular defects, Downs syndrome, orofacial clefts, gastroschisis and arm and hand defects were elevated in offspring of women exposed only to cannabis gestationally with odds ratios up to 40-fold and upper confidence intervals to 123-fold. 11 A report on Canada found that total congenital defects were three times more common in the northern territories where cannabis is smoked about three times as much. 12 , 13 In October 2018 Colorado Health reported an excess of 20,152 total birth defects beyond their baseline expected 67,620 defects 2000–2013 across the period of cannabis legalization when the use of other drugs was falling, representing an elevation of 29.8% above background rates. 14 In a high cannabis use area of Australia 13 defects were found to be elevated compared to Queensland, which for methodological reasons is a conservative estimate. 15 Concerningly elevated rates of Downs syndrome in Colorado, Hawaii, Australia and Canada clearly indicate that heritable cannabis genotoxicity can occur at the hundred megabase chromosomal scale. 11 , 12 , 14 , 15 A close association of atrial septal defect (secundum type) with rising patterns of cannabis use across space and time in the US was recently reported, suggesting that the list of known teratological associations of prenatal cannabis exposure is as yet incomplete. 16 This epidemiological literature is closely concordant with studies in experimental animals. 17 – 19 Again an abrupt rise in genotoxicity with increasing cannabinoid exposure has been demonstrated for many cannabinoids and is of particular concern. 20 – 23
Links between cannabis and several paediatric cancers including acute lymphoid leukaemia (ALL), acute myeloid leukaemia, rhabdomyosarcoma and neuroblastoma suggest further implications of cannabinoid genotoxicity. 24 – 28 Since these tumours together encompass the common tumours of childhood, it is at least possible that cannabis is responsible for the 43% elevation in total childhood cancer across US 1975–2017. 29 Indeed Downs syndrome is well known to be associated with a 2,000-fold elevated risk of childhood ALL from 2/100,000 to around 5/100. 30 , 31
In the September/October 2020 Missouri Medicine, Polocaro and Vettraino raise the important issue of the transgenerational effects of prenatal cannabinoid exposure (PCE) on subsequent generations. 1 The implications of multigenerational toxicity of cannabinoids is very far-reaching with major policy implications.
The picture presented by Polcaro and Vettraino relating to the mental health implications of PCE is correct if too conservative. As they observe the subject is deeply confounded with multiple other factors impacting post-natal neurological development. For these reasons the significant concordance between reports from five longitudinal studies of childhood development relating to impaired indices of concentration, startle, excitability, poor visuospatial processing and executive functioning including ADHD-like and autism-like features are of particular concern. 2 – 6 Under a legalization paradigm the state effectively condones unlimited all day every day exposure to extremely high concentrations of THC, other cannabinoids and cannabis tars. What is especially concerning about this is that many of the neurotoxic and neurodevelopmental toxicities of cannabis exhibit threshold dose effects above which severe damage becomes commonplace. 7 In the context of an increasingly solid consensus relating to the harmful impacts of adult and adolescent cannabis exposure 8 the implications of PCE-neurotoxicity have not been carefully considered. It has been shown that nationwide autism rates are undergoing an exponential rise and indeed New Jersey has been shown to have 4.5% of 8-year-old boys who carry an autism spectrum disorder diagnosis. 9 , 10 Our space-time and causal inference studies demonstrate that indeed cannabinoid exposure to THC and cannabigerol amongst other fractions of cannabis, is a principal driver of this nationwide epidemic (manuscript submitted). 9 , 10
This diverse assemblage of highly congruent evidence of severe cannabis-related neurotoxicity and genotoxicity from varied locations can only be described as extremely concerning indeed. In view of its well described epigenetic and chromoanagenetic effects 32 – 34 and its clearly transgenerational-multigenerational impacts one can only conclude that if the evidence base is not admitted to the cannabis debate and access to fetotoxic and embryotoxic cannabinoids is not immediately restricted the community will inevitably pay a heinous price in terms of avoidable paediatric neurotoxicity, congenital birth defects, heritable cancerogenesis and multigenerational epigenotoxicity.