This blog is part of a series on the interplay between substances and sex. In my previous posts, we discussed opioids and sex and alcohol and sex. In last week’s post and this week’s post, we look at stimulants and sex. Last week, we discussed the stimulant drug that is most commonly paired with sexual behavior: methamphetamine. This week we look at other stimulant drugs and how they affect us.
Cocaine, both in powder and crack (rock) form, has been consistently used since the early twentieth century and, since the 1970s, has had periodic surges of popularity. Cocaine, like methamphetamine, is an amphetamine that produces stimulating effects. Cocaine’s high is of much shorter duration, however, and does not release as much dopamine as meth. Another major difference between the two drugs is that cocaine is derived from a natural source, the coca plant, and cocaine molecules wash away from the receptor site.
As stated in my post last week, meth is a synthetic drug with a relatively large molecule that sits on the receptors for a long period of time, resulting in a longer period of intoxication and more toxic effects to nerve cells. Meth molecules do ultimately pass through the body and are expelled in the urine, a fact not lost on meth cookers who, when desperate for precursor materials, will sometimes recycle the molecules from their urine.
Another amphetamine sometimes paired with sex is MDMA (methylenedioxy-methamphetamine), a psychoactive drug that is chemically similar to both methamphetamine and mescaline. MDMA is also known as Ecstasy, sometimes abbreviated by users as X or XTC.
MDMA acts on the neurotransmitter serotonin, which affects tactile sensations as well as distortions in time and perception. It is primarily used for mood enhancement as well as to help people sustain dancing. However, the effects of X – an increased sense of empathy and connectedness – are qualitatively very different from meth. Meth, for example, can produce strong feelings of aggression, the polar opposite of empathy. The effects of MDMA are mellower than those of meth, although hostility can be associated with both drugs.[i] This may be the result of Mollies, which are increasingly popular pills reputed to be pure Ecstasy, but that often contain methamphetamine or a significantly adulterated form of MDMA.
As with meth, high doses of MDMA result in a spike in core body temperature that can result in death. MDMA also produces an increase in heart rate and blood pressure that is harmful and may result in long-lasting physical damage. Confusion, depression, and craving are among the psychological effects of MDMA. Adulterants in MDMA are common and represent a major risk to the user.
Adderall, Ritalin, and Other Prescription Amphetamines
These pharmaceutical formulations (clinically referred to as Desoxyn) have generally been considered safer than other amphetamines because they limit dopamine release to stored reserves, thus avoiding the neurotoxicity found with straight methamphetamine. Although they do elicit the release of both dopamine and norepinephrine, the potency of these drugs derives chiefly from the inhibition of the reuptake of these catecholamines (in biochemistry, a class of amines that includes many neurotransmitters). Examples include methylphenidate (Ritalin) and modafinil (Provigil).
These drugs are primarily utilized to treat conditions such as attention deficit hyperactivity disorder (ADHD) and mood disorders, and to improve wakefulness. Many college students believe these substances, particularly Adderall, not only reduce the need for sleep but improve information retention and test performance. These drugs are also misused by pairing them with sexual behavior to boost stimulation.
Anyone in recovery from methamphetamine or cocaine should be wary about using these drugs for ADHD or other conditions for which they may be prescribed. Alternatives that may not be as triggering include atomoxetine (Strattera), a selective norepinephrine reuptake inhibitor, and bupropion (Wellbutrin), which belongs to the aminoketone class of antidepressants.
Many addicts in recovery continue to use nicotine after giving up other drugs. This drug complicates recovery because, like meth, it has a powerful effect on the reward center of the brain. Researchers report[ii] that nicotine is the perfect drug for addiction because only a few exposures create a lasting memory of its rewards in the brain. Nicotine, like meth, triggers a release of dopamine, causing pleasurable feelings.
Even though nicotine triggers the release of dopamine for only a brief moment, the levels of dopamine in the brain remain high for much longer. Why this occurs was solved by research related to the interaction of nicotine with another neurotransmitter, GABA. Due to this interaction, the ‘reward’ of nicotine continues to be experienced by the user for up to sixty minutes, long after the nicotine levels in the blood have dropped, setting the stage for the use of a highly addictive drug and ongoing cravings.
Continuing to stimulate the reward center of the brain with nicotine at the same time that one is trying to eliminate cravings for methamphetamine and other drugs reduces the chance of quitting any of them. It has been said that nicotine primes the brain for addiction in that it quickly teaches the brain how to become addicted, and it maintains the addictive process of craving and satisfaction. This, at least indirectly, has implications for the overall comfort of anyone trying to extricate methamphetamine and other drugs from their life.
Caffeine is the most widely used drug in the world. While it does activate the sympathetic nervous system, it is not considered an adrenergic stimulant (stimulant compounds that mimic the effects of endogenous – or natural – agonists of the sympathetic nervous system). Its mechanism of action is mainly through antagonism (inhibition) of adenosine receptors, and then only at doses that far exceed normal daily consumption. Adenosine decreases numerous excitatory processes such as blood pressure, central nervous system activity, urine output, respiration, and others. Caffeine also increases the production of norepinephrine, epinephrine, dopamine, serotonin, and cortisol.
The arousal effect of caffeine is typically considered to follow an inverted-U principle, meaning that optimum performance is at intermediate levels of consumption. Low levels of caffeine can result in a state of under-arousal characterized by boredom and fatigue, and high levels of caffeine can produce hyperactivity and anxiety.
While caffeine’s effects are not as extreme as other amphetamines, it is not benign. Two to three cups of coffee can cause restlessness, insomnia, gastrointestinal disturbance, and cardiac arrhythmias. Five or more cups per day more than doubles the risk of heart problems and can aggravate disorders such as anxiety. Caffeine reduces cerebral blood flow through constriction of blood vessels in the brain. Any serious coffee drinker who has given it up will describe withdrawal symptoms that include headaches caused by a rebound effect of blood vessels
[i] Curran H.V., H. Rees, T. Hoare, R. Hoshi, and A. Bond. (2004). “Empathy and Aggression: Two Faces of Ecstasy? A Study of Interpretative Cognitive Bias and Mood Change in Ecstasy Users.” Psychopharmacology.
[ii] D’Souza, M., Markou, A. (2013). “The “Stop” and “Go” of Nicotine Dependence: Role of GABA and Glutamate.” Cold Spring Harbor Perspectives in Medicine. (2013), 10(6). doi: 10.1101/cshperspect.a012146.