Author: James Anderson

Alcohol Interaction with Cocaine, Methamphetamine, Opioids, Nicotine, Cannabis, and γ-Hydroxybutyric Acid PMC

People abusing alcohol or suffering from alcoholism tend to use multiple illegal and addictive drugs either sequentially or simultaneously [4,5]. Powerful stimulants like meth cause physical jitteriness, intense wakefulness, and anxiety. However, these effects do not last very long, especially when combined with illicit drugs.

Hungund et al. [198] showed that alcohol did not cause the release of DA in CB1−/− mice or SR141716A, a selective cannabinoid receptor antagonist, administered wild-type mice. Cohen et al. [199] showed that SR141716A reduced alcohol consumption, possibly via reducing DA release in the NAc in mice. These results strongly suggest that administration of cannabis and alcohol may additively enhance DA release the NAc. Therefore, it is important to tailor multi-substance treatments to specific needs when a single-substance intervention may not be effective.

This stronger response may be caused by the pharmacologically active metabolite cocaethylene [59]. For this reason, many people who have a meth addiction often binge drink or become alcoholics. Scientists have shown that alcohol actually slows down the metabolism of meth so that the drug stays in the body longer. Scientific studies have also demonstrated that alcohol bolsters the rate at which the brain absorbs meth.

Recommended Drug and Alcohol Rehab-Related Articles

Alcohol has been shown to enhance the sedative effect of GHB in humans and animals [212,213]. Co-administration of GHB and alcohol induces sedation stronger than the sum of the sedation induced by the individual substances [214], possibly due to a pharmacokinetic interaction resulting in an increased concentration at the site of action (Figure 19). Alcohol administration has been shown to increase the plasma concentration of cocaine [97], leading to an increase in cocaethylene concentration in plasma and decrease in benzoylecgonine renal excretion [98]. Although alcohol ingestion did not alter cocaine half-life, it significantly increased cocaethylene’s half-life [99], thus increasing the exposure to cocaethylene’s deteriorating toxic effects. Cocaine and alcohol co-exposure also has deleterious effects on cardiovascular and endocrine systems as evidenced by an increase in heart rate, systolic blood pressure, cortisol, and prolactin concentrations, and cerebral blood perfusion [100].

1. Just as alcohol amplifies a meth “rush,” it also worsens a meth “crash,” the aftermath of meth abuse.
2. Brains were rapidly removed and prefrontal cortex and striatal tissue were dissected and frozen immediately on dry ice.
3. Co-administration of GHB and alcohol induces sedation stronger than the sum of the sedation induced by the individual substances [214], possibly due to a pharmacokinetic interaction resulting in an increased concentration at the site of action (Figure 19).
4. This stronger response may be caused by the pharmacologically active metabolite cocaethylene [59].
5. However, these effects do not last very long, especially when combined with illicit drugs.
6. Body temperatures were monitored remotely throughout Meth injections via transponders (IPTT-300 transponder, BMDS) implanted subcutaneously and body temperatures were remotely measured every 30 min.

Alcohol exposure augments the opioid’s analgesic response by co-activating both OPR and GIRK2 channel activations [161,162]. Unlike the opioid-induced analgesia, the NMDAR-mediated analgesia may occur independently of GIRK2 channels are not modulated by alcohol exposure [162]. In 2015, the estimated global prevalence among the adult population was 18.4% for daily heavy alcohol use, 15.2% for daily tobacco smoking, 3.8% for cannabis, 0.77% for amphetamine/methamphetamine (METH) use, 0.37% for opioid use, and 0.35% for cocaine use [1]. Europe had the highest prevalence of heavy episodic alcohol use and daily tobacco use.

What is Crystal Meth (Meth)?

Parker and Laizurs [32] studied effects of alcohol on pharmacokinetics of cocaine administered via oral and intravenous (i.v.) administration (Table 1). They showed cocaine area under the curve (AUC0–∞) and benzoylecgonine (BE) AUC0–∞ values were approximately 5.5-fold and 2-fold, respectively, higher after i.v. Alcohol exposure significantly increased (3 to 4 folds) oral cocaine systemic bioavailability and peak concentration (Cmax) values, respectively, but alcohol did not affect oral cocaine elimination half-life. The BE AUC0–∞ values were approximately 2.5-fold higher with alcohol cocaine co-administration than with oral cocaine given alone.

Effects of alcohol on cocaine and benzoylecgonine pharmacokinetic parameters [33]. All procedures performed in studies involving animals were in accordance with the ethical standards of the institution or practice at which the studies were conducted. Body temperatures were monitored remotely throughout Meth injections via transponders (IPTT-300 transponder, BMDS) implanted subcutaneously and body temperatures were remotely measured every 30 min. This website is using a security service to protect itself from online attacks.

Possible CNS mechanisms underlying the addictive effects of opioids alone or in combination with alcohol are hypothesized in Figure 13. Acute alcohol exposure causes reinforcing (euphoria, red font) and weak analgesia, while acute opioid exposure (blue font) causes strong analgesia (Figure 13A red font). Acute alcohol activates DAergic neurons, thus releasing endogenous opioids (eOPs) that inhibits GABAergic activity either by directly binding to the OPRs or via inhibiting Glu release from the Gluergic neurons [170].

It exhibits a steep dosage-response curve, thus, exceeding the intoxicating dose can result in severe adverse effects occurring within 15 minutes of ingestion of GHB [218,219]. Figure 12 shows signaling pathways for analgesic effects of opioids and effects of alcohol drinking on it. In addition to the OPRs, type-2 G-protein coupled inwardly rectifying potassium (GIRK2) channels are also implicated in analgesic action of opioid drugs (Figure 16) [158]. This hypothesis is supported by the observations that the analgesic effects of opioids were absent in GIRK2 null-mutant mice [159,160] or by OPR antagonist [161].

What Is Meth? Why Is It Mixed with Alcohol?

Since some participants did not feel the effects of alcohol as strongly as one would expect. This could cause risky behaviors because of people underestimating their intoxication. Additionally, individuals could seek more alcohol to increase feelings of intoxication; they might engage in cycles of binging or heavy drinking. Lastly, conditions like alcohol toxicity can occur if those combining both drugs abuse large quantities of alcohol to offset Meth’s side effects. The increase in inflammatory mediators is not limited to the periphery but can also readily cross the blood-brain barrier (BBB) to promote neuroinflammation (see Banks 2005 for review). The brain lymphatic system could also readily transport immune cells such as T-cells across the BBB (Louveau et al. 2015).

An increase of eOP peptides increase alcohol consumption that is blocked by nonselective opioid antagonists such as naloxone and naltrexone [177,178]. Blomqvist et al. [134,135] have proposed that alcohol modulates the reinforcing effects of nicotine by directly interacting with the nAChRs, β2 and β4 [136,137]. Lüscher and Malenka [138] have shown that chronic nicotine exposure triggers a conformational change in β4 nAChRs that initiates various forms of synaptic plasticity and modify the VTA-DA neuron’s responses to alcohol and alcohol drinking behaviors.