Marijuana & Coffee

Marijuana and Coffee

Coffee and cannabis are the two most often utilized psychoactive drugs worldwide. Unlike cannabis, which is often consumed to relax the body, heighten perception, and promote creativity, coffee – along with tea and other caffeinated beverages – is typically consumed to energise and aid concentration, especially in the face of fatigue.

Does consuming cannabis and coffee together make sense? What is their interaction? Is it appropriate that decriminalized THC-rich cannabis was initially offered in Amsterdam coffee shops?

Several uncontrolled cannabis startups have recently began making and selling coffee flavored with CBD-derived from hemp. Are coffee and cannabidiol an effective combination, or is this merely a marketing ploy?

Marijuana and Coffee – The opposite effects

Caffeine is commonly considered a minor cognitive enhancer. It improves one’s capacity to concentrate and short-term memory. Caffeine stimulates fat metabolism and prevents tiredness on a physiological level. These effects are largely the opposite of those of THC, which can likewise improve concentration but temporarily impairs short-term memory and reduces fat metabolism.

Caffeine is a stimulant that activates the sympathetic nervous system, which is fundamental to the stress response in humans. However, THC mitigates numerous stress-related symptoms. Contrary to popular belief, THC can recover the memory of animals suffering from severe stress. Which effects prevail when coffee and marijuana are combined?

Since cannabinoids such as THC and CBD weakly impede caffeine’s metabolism via inhibiting the CYP1A2 enzyme, one could assume that caffeine would outweigh the cannabinoids.

Their interaction is not so straightforward as it turns out. Caffeine exacerbates the memory impairment brought on by THC. Furthermore, this effect may be limited to short-term memory. To comprehend how this occurs, one must examine the neurological features of these unique chemicals.

Low and high caffeine concentrations

There are two major metabolic consequences of caffeine. At low concentrations, it inhibits adenosine receptors (A1, A2A, and A3). Typically, these receptors are related with drowsiness. Adenosine affects both the sleep-wake cycle and blood vessel dilatation and constriction. Coffee and tea exert their energizing effects by inhibiting adenosine receptors. And the headaches experienced by some people during caffeine withdrawal are likely caused by constriction of the brain’s blood vessels.

At greater concentrations, caffeine inhibits phosphodiesterase enzymes (PDE). PDEs degrade crucial chemical messengers produced by both cannabis and adenosine receptors. These messengers are known as cyclic AMP (cAMP) and cGMP, which is closely related. They are among the most prevalent signaling molecules present in cells. PDE enzymes are the target of both asthma medicines and Viagra.

Adenosine: CB1 gatekeeper

Both CB1 cannabinoid receptors and A1 adenosine receptors are present in the hippocampus, which is important for many elements of memory. Particularly short-term memory is processed by transient neuronal alterations in the hippocampus. When hippocampus A1 is substantially active, cannabinoids at CB1 are less effective. THC, endogenous cannabinoids, or an experimental synthetic cannabinoid can still activate CB1, but even at high levels, the effect will be diminished.

In a 2011 study of marijuana and coffee conducted by Portuguese researchers at the University of Lisbon, THC’s impact was reduced by one-third when combined with an A1 adenosine receptor agonist. (An agonist activates a receptor, while an antagonist inhibits it.) In contrast, inhibiting the A1 receptor would amplify the action of cannabis, but only when A1 is already active. The precise method by which A1 decreases the effectiveness of CB1 remains unknown.

This study demonstrates that increasing adenosine levels may protect individuals from THC-induced memory impairment without affecting THC’s essential effects outside the hippocampus, which include neuroprotection, reduction of nausea, and painkilling, in addition to psychoactivity. Prior to sleep, adenosine levels are at their peak. Therefore, nocturnal cannabis usage may have a reduced impact on memory than daytime use, but this has not been scientifically determined.

In situations where cannabis is used to alleviate trauma, coffee consumers may benefit from combining the herb or its constituents with their morning brew. However, this may not be the case for a stressed-out individual who consumes coffee throughout the day. A few exploratory investigations have demonstrated that consuming coffee infrequently or frequently had the same effect: Both increased THC’s capacity to temporarily impair memory.

Marijuana and Coffee – Neurobiology of memory

So how exactly does THC impact short-term memory?

Memory is not encoded in the firing of a single neuron; rather, it evolves through changes in the network of neurons in the brain. If some neuronal connections are heavily exploited, it makes logical for the brain to reinforce those pathways. Conversely, if two neurons communicate infrequently, it would be advantageous to waste little energy sustaining the connection. A major element of brain plasticity is the constant strengthening and weakening of neuronal connections.

By controlling what scientists refer to as “long-term potentiation” (LTP) and “long-term depression,” endocannabinoids play an important role in synaptic plasticity (and total neuroplasticity) (LTD). Both of these processes have a direct impact on memory and a variety of other cognitive processes.

LTP includes potentiating or strengthening neuronal connections between cells; this can take place by raising the amount of neurotransmitters released by the presynaptic (signal-sending) neuron or by boosting the sensitivity of the postsynaptic (signal-receiving) neuron. LTD involves the opposite process, which ultimately diminishes neural activity’s effect. LTD in the hippocampus aids in the elimination of old memories.

By activating the CB1 receptor, endogenous cannabinoids and plant cannabinoids suppress neurotransmitter release. Depending on which neurotransmitters are blocked, this could have bidirectional physiological effects. CB1 is present on both glutamatergic (excitatory) and GABAergic (inhibitory) neurons. When CB1 reduces the release of the inhibitory neurotransmitter GABA, brain activity is increased (“disinhibited”). In addition, by slowing glutamatergic neurons, cannabinoids (through CB1) promote LTD and the erasure of old memories in the hippocampus.

Fine-tuning the brain

When it come to marijuana and coffee mall amounts of adenosine are continuously released onto the same region of the hippocampus that contains cannabinoid, adenosine, and glutamate receptors. By activating the A1 receptor, adenosine diminishes the effectiveness of THC and other cannabinoids at CB1. In addition, this partially inhibits cannabinoid-mediated LTD, hence improving short-term memory.

However, caffeine inhibits A1 receptors. This enhances the effect of cannabis activation, leading to increased LTD and transient working memory deficits.

There are CB1 and A1 receptors on GABAergic neurons in the hippocampus. A1 performs a similar gatekeeping function for CB1 in these neurons (it prevents CB1 from inhibiting the inhibitory neurotransmitter GABA). In the hippocampus, GABAergic neurons serve as the primary brake decreasing glutamate release.

Under certain conditions, cannabinoids can promote either LTD or LTP by activating the CB1 receptor. LTD seems to be more prevalent. By decreasing LTD, adenosine acting on A1 receptors will improve memory. These intricate interactions and feedback loops offer neurons subtle means for fine-tuning the brain.

CBD & Adenosine

Cannabidiol does not activate CB1 directly, but exerts its effects through a variety of different mechanisms. For instance, high dosages of CBD increase adenosine levels in the brain by inhibiting adenosine reuptake. This may explain CBD’s potential to mitigate the short-term memory deficits associated with THC, according to certain research. It may be one among several ways that contribute to the “ensemble effect,” in which the various chemicals in cannabis lessen each other’s adverse effects and enhance each other’s potency.

In addition to being a neurotransmitter, adenosine is also recognized to have anti-inflammatory properties. Reuptake is the primary mechanism by which the body stops adenosine signaling. Cannabidiol is protective in certain models of heart attack, multiple sclerosis, lung injury, and retinal issues due to CBD’s indirect activation of A2A and A1 receptors (through adenosine reuptake inhibition).

The sleepy effect of high dosages of CBD may potentially be caused by an increase in adenosine. In clinical trials of the sublingual CBD isolate Epidiolex, one of the most common side effects was sedation. Although the exact molecular mechanism is unknown, a large dose of CBD may enhance adenosine signaling and lead to fatigue.

CBD’s effects on adenosine would likely be overshadowed by caffeine’s antagonistic activities at adenosine receptors when combined. Unknown is the extent to which this may impair CBD’s therapeutic qualities. Given the several mechanisms of action of cannabidiol, it is doubtful that this would pose a significant concern. However, there are now no obvious advantages to mixing or promoting CBD and caffeine.

We hope you enjoyed our article about marijuana and coffee!

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