Researchers from Penn State College of Medicine evaluated existing information on five prescription CBD and delta-9-tetrahydrocannabinol (THC) cannabinoid medications: antinausea medications used during cancer treatment (Marinol, Syndros, Cesamet); a medication used primarily for muscle spasms in multiple sclerosis (Sativex, which is not currently available in the US, but available in other countries); and an antiseizure medication (Epidiolex). Overall, the researchers identified 139 medications that may be affected by cannabinoids. This list was further narrowed to 57 medications, for which altered concentration can be dangerous. The list contains a variety of drugs from heart medications to antibiotics, although not all the drugs on the list may be affected by CBD-only products (some are only affected by THC). Potentially serious drug interactions with CBD included
Absolutely. Inhaled CBD gets into the blood the fastest, reaching high concentration within 30 minutes and increasing the risk of acute side effects. Edibles require longer time to absorb and are less likely to produce a high concentration peak, although they may eventually reach high enough levels to cause an issue or interact with other medications. Topical formulations, such as creams and lotions, may not absorb and get into the blood in sufficient amount to interact with other medications, although there is very little information on how much of CBD gets into the blood eventually. All of this is further complicated by the fact that none of these products are regulated or checked for purity, concentration, or safety.
CBD can alter the effects of other drugs
CBD has the potential to interact with many other products, including over-the-counter medications, herbal products, and prescription medications. Some medications should never be taken with CBD; the use of other medications may need to be modified or reduced to prevent serious issues. The consequences of drug interactions also depend on many other factors, including the dose of CBD, the dose of another medication, and a person’s underlying health condition. Older adults are more susceptible to drug interactions because they often take multiple medications, and because of age-related physiological changes that affect how our bodies process medications.
Products containing cannabidiol (CBD) seem to be all the rage these days, promising relief from a wide range of maladies, from insomnia and hot flashes to chronic pain and seizures. Some of these claims have merit to them, while some of them are just hype. But it won’t hurt to try, right? Well, not so fast. CBD is a biologically active compound, and as such, it may also have unintended consequences. These include known side effects of CBD, but also unintended interactions with supplements, herbal products, and over-the-counter (OTC) and prescription medications.
Does the form of CBD matter?
While generally considered safe, CBD may cause drowsiness, lightheadedness, nausea, diarrhea, dry mouth, and, in rare instances, damage to the liver. Taking CBD with other medications that have similar side effects may increase the risk of unwanted symptoms or toxicity. In other words, taking CBD at the same time with OTC or prescription medications and substances that cause sleepiness, such as opioids, benzodiazepines (such as Xanax or Ativan), antipsychotics, antidepressants, antihistamines (such as Benadryl), or alcohol may lead to increased sleepiness, fatigue, and possibly accidental falls and accidents when driving. Increased sedation and tiredness may also happen when using certain herbal supplements, such as kava, melatonin, and St. John’s wort. Taking CBD with stimulants (such as Adderall) may lead to decreased appetite, while taking it with the diabetes drug metformin or certain heartburn drugs (such as Prilosec) may increase the risk of diarrhea.
You should, however, always consult your doctor if you’re on any medication before adding any other drug — even a natural one — to avoid possible interactions.
These mechanisms lead to increased neuronal transmission and hence stimulation.
Here’s a list of similar medications that share a similar level of risk when combined with CBD:
Is CBD a Viable Alternative to Amphetamine (Adderall)?
CBD and amphetamine (Adderall) are generally safe at a low therapeutic dose but can be hazardous when used in high doses for recreational use (not recommended). It could also become dangerous over time if both substances are taken together on a regular basis.
With that said, CBD could make amphetamines ineffective for treating ADHD, which would negate the entire point of using the medication in the first place.
What Are the Side Effects of Amphetamine (Adderall)?
Amphetamine enters the presynaptic axon terminal by diffusion or uptake by the monoamine transporters DAT, NET, and SERT . It displaces other stored neurotransmitters through vesicular monoamine transporter 2 (VMAT2) into the cytoplasm. From the cytoplasm, neurotransmitters are transported to the synaptic cleft by a retro-transport process resulting in the release of the stored neurotransmitters.
Amphetamine is prescribed for ADHD and increases attention span and focus, and helps control behavior problems. It may also help with organization and listening skills. It’s illegal to use amphetamine for recreational purposes.
Rats were acclimated to the startle chambers (Med Associates) for 5 min over 3 d. On the last day of acclimation, rats were tested in an input/output (I/O) function consisting of 12 increasing startle pulses (from 65 to 120 dB, 5 dB increments) to determine the appropriate gain setting for each individual rat. The testing procedure consisted of the following phases: the acclimation phase, a habituation phase (Block 1), and PPI measurement (Block 2). During acclimation, rats were exposed to the chambers and white background noise (68 dB) for 5 min. During Block 1, 10 pulse alone trials (110 dB white noise, 20 ms duration) were delivered at 15–20 s intertrial intervals. Block 2 consisted of 9 different trials presented 10 times in a pseudo-randomized order at 15–20 s intervals: 10 pulse-alone trials, and 10 of each of the three different prepulse-pulse trial types (72, 76, 80) with interstimulus intervals of 30 and 100 ms. Pulse-alone trials consisted of a startle stimulus-only presentation, whereas prepulse-pulse trials consisted of the presentation of a weaker nonstartling prepulse (white noise, 20 ms duration) before the startling stimulus. PPI was calculated for each animal and each trial condition as PPI (%) = (1 − average startle amplitude to pulse with prepulse/average startle amplitude to pulse only) × 100. The final number of rats in each group was as follows: VEH/Intra-NASh VEH group (VEH/VEH), n = 8; VEH/Intra-NASh CBD group (VEH/CBD), n = 9; AMPH/Intra-NASh VEH group (AMPH/VEH), n = 9; AMPH/Intra-NASh CBD group (AMPH/CBD), n = 9; AMPH/Intra-NASh Torin2+CBD, n = 10; and AMPH/Intra-NASh PF +CBD, n = 10.
One week after surgery, rats received Intra-NASh bilateral infusions of CBD (Tocris Bioscience, 100 ng in 20% DMSO and 80% NaCl (0.9%); 0.50 μl per side), vehicle (VEH, 20% DMSO and 80% NaCl (0.9%); 0.50 μl per side), coadministration of Torin2 (Tocris Bioscience, 40 ng in 20% DMSO and 80% NaCl (0.9%); 0.50 μl per side) and CBD (Torin2+CBD) and coadministration of PF 4708671 (PF, Tocris Bioscience, 100 ng in 50% DMSO and 50% NaCl (0.9%); 0.50 μl per side) and CBD (PF+CBD) over 5 consecutive days using an injection cannulae connected to a Hamilton syringe with Teflon tubing and a microinfusion pump. A total volume of 0.5 μl per side was delivered over a period of 1 min. Microinjectors were left in place for an additional 1 min following drug infusion to ensure adequate diffusion from the tip. Immediately following the microinfusions, the rats received an intraperitoneal injection of d -AMPH sulfate (AMPH; Sigma-Aldrich; 5 mg/kg in 0.9% NaCl) or VEH (0.9% NaCl). Following the final AMPH or VEH treatment injection (on day 5), rats were left undisturbed in home cages until test day (locomotor activity or prepulse inhibition [PPI]) on sensitization day 16, when rats received the VEH or AMPH challenge (1 mg/kg; i.p.).
AMPH-induced hyperlocomotor activity
In conclusion, the present findings demonstrate, at the behavioral, molecular, and neuronal levels of analysis, direct mechanistic effects of CBD linked to antipsychotic-like phenomena within the mesolimbic pathway. CBD attenuates DAergic sensitization phenomena within the mesolimbic pathway, the primary brain target for antipsychotic efficacy. Furthermore, we demonstrate a novel mechanistic pathway though which CBD may exert its antipsychotic-like properties. These findings have critical implications not only for understanding how specific phytochemical components of MJ may differentially impact neuropsychiatric phenomena, but demonstrate a potential mechanism for the therapeutic effects of MJ derivatives in the treatment of DA-related, psychiatric disorders.
Effects of Intra-NASh VEH versus CBD (100 ng/0.5 μl) pretreatment on AMPH-induced hyperlocomotion. A, Schematic representations of microinfusion locations in the NASh of AMPH-sensitized rats. Black circles represent CBD (100 ng). Gray circle represents VEH. B, Microphotograph of a representative Intra-NASh injector placement. C, Exposure to AMPH (5 d, 5 mg/kg) followed by an 11 day sensitization period caused a typical pattern of AMPH-induced psychomotor sensitization in Intra-NASh VEH-pretreated rats. D, Ambulatory activity assessed in 5 min epochs over the 60 min recording session and total ambulatory activity. Intra-NASh CBD pretreatment significantly decreases the AMPH-induced locomotor activity observed in Intra-NASh VEH-pretreated rats. E, Intra-NASh CBD pretreatment significantly decreases AMPH-induced rearing observed in Intra-NASh VEH-pretreated rats. F, Intra-NASh CBD pretreatment significantly decreases AMPH-induced stereotypy observed in Intra-NASh VEH-pretreated rats. VEH/ Intra-NASh VEH, n = 9; VEH/Intra-NASh CBD, n = 10; AMPH/Intra-NASh CBD, n = 10; AMPH/Intra-Nash VEH, n = 8. **p < 0.01 (one-way ANOVA). *p < 0.05 (one-way ANOVA). ns, Not significant. Error bars indicate SEM. ac, Anterior commissure; NACore, core subdivision of the nucleus accumbens; VP, ventral pallidum.
Drug preparation and administration
Effects of Intra-NASh VEH versus CBD on VTA DA neuronal activity following AMPH challenge. A, Histological localization of microinfusion sites in the NASh and recording sites in the VTA for each treatment condition performed during electrophysiological recordings. Black circles represent CBD (100 ng). Gray circle represents VEH. A total of n = 19 VTA DA neurons were sampled: Intra-NASh VEH group, n = 10 cells in 8 rats; Intra-NASh CBD (100 ng/0.5 μl) group, n = 9 cells in 6 rats. B, Microphotograph of a representative VTA neuronal recording placement. C, Time-dependent consequences of Intra-NASh VEH and CBD (100 ng/0.5 μl) treatments on VTA DA neuronal firing frequency following the challenge dose of systemic AMPH (1 mg/kg). D, Time-dependent consequences of Intra-NASh VEH and CBD (100 ng/0.5 μl) treatments on VTA DA spikes firing in burst mode following AMPH challenge. E, Representative histogram showing the increase response activity of one DA neuron following the microinfusion of Intra-NASh VEH and systemic AMPH (top) or Intra-NASh CBD and systemic AMPH (bottom). Inset, Action potential waveform of the selected neuron. F, Activity patterns observed 20 min after the microinfusions of either Intra-NASh VEH (top) or CBD (bottom) and systemic AMPH. **p < 0.01 (two-way repeated-measures ANOVA). *p < 0.05 (two-way repeated-measures ANOVA). Error bars indicate SEM.