Methamphetamine hydrochloride, also known as meth, is one type of amphetamine. There are many other names for this drug, and the names used are based on the form, effects, and how it’s used. General street names include meth, speed, go-fast, fire, crank, and tweak. Crystal meth or smokable forms include names like ice, shards, crystal, hot ice, batu, and quartz. Powder forms include names like methlies quick, and chalk. Tablet forms have names like Yaba, Scooby snacks, and Yellow Barn. Methamphetamine is a stimulant and is considered a Schedule II controlled substance. Schedule II controlled substances have a high potential for abuse and can cause extreme psychological or physical dependence; however, they also have very legitimate and accepted medical uses. Amphetamines, in general, are well known for their potential for abuse and have street names such as speed, and are commonly abused for their euphoric effects. There are also known medical uses for methamphetamine hydrochloride, in the form of “Desoxyn” for the treatment of ADHD or obesity.

There are other amphetamines prescribed for the treatment of ADHD. Vyvanse, also known as lisdexamfetamine dimesylate (LDX), is a medication that is used to treat attention deficit hyperactivity disorder (ADHD). Vyvanse is a central nervous system (CNS) stimulant and is classified as a Schedule II controlled substance by the federal Controlled Substances Act (DEA, 2023). However, Vyvanse does not have common street names and is typically referred to by the brand name or by terms such as “study drugs” or “uppers” by individuals who misuse the medication outside of prescribed medical indications.

The Vyvanse drug is prescribed for two different indications and uses. Vyvanse is approved to treat Attention Deficit/Hyperactivity Disorder (ADHD) in adult patients and children who are 6 years of age and older. Vyvanse is also used to treat adults with Moderate to Severe Binge Eating Disorder (BED). Lisdexamfetamine is the first and only FDA-approved stimulant for BED (Shire US Inc., 2007). In addition to its approved medical uses, many individuals take Vyvanse outside of the approved uses to enhance their cognitive functions as well as for weight control. This is typically seen in college students and young adults.

Methamphetamine comes in many forms, and because of this, it can be administered in many different ways, like ingestion, injection, and inhalation. The way it is administered influences the duration of each process from onset to peak, then coming down. When smoking, the onset takes 7 to 10 seconds, and the duration of effects is typically around 8 to 12 hours. When administered intravenously, the onset lasts around 15 to 30 seconds, and the duration of effects lasts 8 to 12 hours. When snorted, the onset lasts about 3 to 5 minutes, and the effects last about 6 to 8 hours. When ingested orally, the onset lasts around 20 to 30 minutes, and the duration of effects normally lasts around 12 to 24 hours (Cobb Outpatient Detox, n.d.). Route of administration influences intensity and risk when it comes to methamphetamine use because of the varying bioavailabilities based on route of administration. The way it is administered affects the amount absorbed into the body, how long it takes to be absorbed, and what kind of effects are felt.

Lisdexamfetamine is available in an oral capsule as well as in a chewable form. The drug must be swallowed as it is a prodrug in the GI tract. The lysine-amphetamine bond in LDX is cleaved by enzymes, peptidases, in the red blood cells to form d-amphetamine, the pharmacologically active drug.

Vyvanse begins to exert its effects in approximately 1 to 2 hours after administration, with maximum concentration (Cmax) approximately 3.8 hours post-dose. The prolonged duration of effect is a property of LDX and results from the activity of an RBC enzyme that releases d-amphetamine from the LDX prodrug. The amount of d-amphetamine released from LDX is determined by the amount of RBC peptidase present, and as a result, the rate of release is restricted. The resulting d-amphetamine is released slowly over a prolonged period of time, extending beyond the usual duration of action of typical immediate-release amphetamine products, lasting approximately 12 to 14 hours (Shire US Inc., 2007).

The oral prodrug form of Vyvanse has a significant impact on the potential for abuse by different routes of administration. As an oral drug, Vyvanse must first be processed in the gut to produce its active form. This limits the production of d-amphetamine by routes other than oral ingestion. Therefore, intravenous, insufflation, and inhalation of Vyvanse will not efficiently produce d-amphetamine to create typical amphetamine-like effects of euphoria and increased alertness. This abuse-deterrent property was an explicit design goal of lisdexamfetamine, distinguishing it from conventional amphetamine formulations (Pennick, 2010). However, high doses of oral Vyvanse could potentially produce d-amphetamine levels high enough to be of abuse.

The primary brain regions impacted by methamphetamine are the prefrontal cortex, amygdala, and the nucleus accumbens. All of these regions affect motivation, emotional regulation, and decision making. The specific neural pathway involved is the mesolimbic dopamine system, which is the brain’s primary reward pathway. It works by transporting dopamine from the ventral tegmental area to the nucleus accumbens, amygdala, and hippocampus. It plays a major role in motivated behaviors, pleasure, and incentives. Acute brain effects caused by meth are an abrupt release of dopamine, norepinephrine, and serotonin, which causes an intense euphoric feeling. Physiological effects caused by acute methamphetamine use are things like increased blood pressure, increased heart rate, and higher body temperature. Complications caused by acute use can be paranoid psychosis, agitation, seizures, and a chance of stroke. Chronic brain effects caused by methamphetamine are persistent cognitive or psychiatric dysfunction, structural damage to the brain, and neurotoxicity. The primary neurotransmitters affected by methamphetamine use are three of the main monoamine neurotransmitters. These include dopamine, norepinephrine, and serotonin (Patel & Saadabadi, 2025). Methamphetamine raises the level of these neurotransmitters by promoting their release, then blocking their reuptake. It acts as a reuptake inhibitor of dopamine, norepinephrine, and serotonin. It also does not really fit the traditional description of an agonist or antagonist because it forces the neurotransmitters out of storage vesicles and reverses the transporter molecules, sending them into the synaptic space. Methamphetamine exerts a massive downstream effect on neural communication. It induces a huge, sustained surge of neurotransmitters; this disruption of neurotransmitters leads to neurotoxicity.

The effects of Vyvanse are felt in the central nervous system, specifically as a result of the drug’s active ingredient, d-amphetamine. Within the CNS, amphetamines primarily act on regions heavily innervated with dopamine and/or norepinephrine-containing axons. Among these, the prefrontal cortex (PFC) is the primary region affected. The PFC contains a high number of neurons involved in a number of cognitive functions and in behavior such as working memory, sustained attention, and others. Children and adults with attention-deficit/hyperactivity disorder (ADHD) are characterized by an impaired ability to regulate such functions within the PFC. Several studies have reported a decrease in the signal-to-noise ratio, for example, in the amount of information-related activity relative to background activity within prefrontal circuits of ADHD patients. D-amphetamine increases the amount of catecholamines, dopamine and norepinephrine, released in the synapse between neurons, and as a result it is possible to allow the PFC to function (Arnsten, 2006).

The nucleus accumbens (NAc), or ventral striatum, is the key brain area where the reward effect of drug abuse is believed to occur. Dopamine release in the NAc causes the user to feel a sense of pleasure or euphoria. This is due to the activation of the mesolimbic dopamine system. The mesolimbic dopamine system refers to a pathway that originates in the ventral tegmental area (VTA) of the brain and projects to the NAc, amygdala, and hippocampus. This system assigns salience to a stimulus. It determines the degree to which a stimulus will grab the user’s attention. In the case of drug abuse, the salience of the drug is determined by its ability to release high levels of dopamine in the NAc. Thus, drugs of abuse have the potential to be “addictive” because of their ability to reinforce their use. Repeated use of a drug of abuse causes long-lasting changes in the sensitivity of the mesolimbic dopamine system, which can result in tolerance, a requirement for increased doses of the drug to produce the same effect, and physical dependence (Koob & Volkow, 2016).

The locus coeruleus is a brain region that contains the cell bodies of the neurons that make up the brain’s norepinephrine system. These neurons release NE to the cerebral cortex, where it increases arousal, and NE is also released to other parts of the brain from neurons in the brain stem. Within the PFC, the axons of the locus coeruleus neurons release NE to enhance signal transmission between the neurons in the PFC. An increase in the release of dopamine in the PFC is associated with an increase in the activity of NE in the PFC as well. The increase in dopamine and NE activity in the PFC, produced by d-amphetamine, results in an increase in the ability of the PFC to regulate behavior that is dependent on the PFC. Acutely, the increased activity of dopamine and NE in the PFC results in an improvement in attention and a decrease in distractibility. With chronic use of d-amphetamine, however, the increased activity of dopamine in the PFC can result in a decrease in the activity of dopamine in other regions of the brain (Arnsten, 2006).

Lisdexamfetamine has effects on the same primary neurotransmitters as other amphetamines (i.e., dopamine and norepinephrine). However, because of its unique mechanism of action, it produces somewhat different pharmacological effects. As a substrate for the dopamine transporter (DAT) and norepinephrine transporter (NET), lisdexamfetamine is first taken into the neuron where it is a substrate for reverse transport by these two transporters. In reverse transport, lisdexamfetamine is first taken into the neuron by the DAT and NET in its intact form. Then, within the neuron, it is moved across the neuronal membrane in its intact form by reverse transport by the two transporters. The drug is released from the neuron in the form of d-amphetamine. Because lisdexamfetamine is a prodrug for d-amphetamine, all of the pharmacological actions of the amphetamine are exerted by this portion of the molecule. Therefore, lisdexamfetamine acts as a monoamine releaser and is classified as an amphetamine (Fleckenstein et al., 2007). Other drugs that act as monoamine releasers include methamphetamine, methylphenidate, and fenfluramine.

D-amphetamine can also enter into the synaptic vesicles. Once inside the vesicles, D-amphetamine can be released by the drug into the cytoplasm of the neuron. From here, D-amphetamine can be reabsorbed back across the plasma membrane of the neuron by the DAT to be released into the synapse. This reverse transport of D-amphetamine can result in a large amount of D-amphetamine being released into the synapse for a long period of time. This is in contrast to the normal phasic release of dopamine into the synapse that is dependent on action potential activity in the neuron. Instead, there is a large, tonic amount of D-amphetamine in the synapse available to bind to the postsynaptic neuron’s dopamine receptors (Fleckenstein et al., 2007).

With doses of d-amphetamine above those used therapeutically for ADHD in both children and adults, the effect of the drug on the SERT will also become apparent at supratherapeutic doses. D-amphetamine activation of D1 and D2 receptors in the PFC and NAc enhances executive functions such as working memory, cognitive flexibility, and monitoring, while simultaneously increasing the rewarding salience of all stimuli. As with all drugs, with chronic use of high doses of d-amphetamine, there will be a down-regulation of these receptors, the number of receptors for the drug will decrease, and the drug will have less of an effect at the same dose. This is defined as tolerance to a drug (Koob & Volkow, 2016).

Common psychological effects reported by methamphetamine users are a rapid feeling of euphoria/immediate rush, increased energy, increased alertness, and heightened confidence. Methamphetamine changes mood by making the user feel high energy, intense pleasure, hyperalertness, and a sense of euphoria. Chronic use can result in chronic depression and issues with finding pleasure in things naturally. Chronic users also report mood swings, anxiety, violent behavior, and increased irritability (Rusyniak, 2013). It affects perception because high doses and chronic use can cause psychosis, paranoia, hallucinations, and delusions (Rusyniak, 2013). Methamphetamine affects motivation by making users seek the drug more often to try to keep feeling the euphoria that the drug brings. It can also cause users not to feel motivated outside of drug-seeking behavior, making them do nothing or strive for nothing when it comes to everyday life. Methamphetamine creates changes in cognition because of the damage it does to the brain. It causes damage to the prefrontal cortex, which controls decision-making, critical thinking, etc. It also affects a user’s ability to focus and can cause issues with memory, more specifically, working memory. When it comes to high versus low doses of methamphetamine, high doses are more likely to cause a rush, an intense feeling of euphoria, and an increased chance of toxicity. Low doses are more likely to stimulate behavioral activation and cause acute brain injury. Variability across individuals who use meth is high. It often leads back to the individual user’s habits. Things like negative emotions, cravings, and daily usage depend on the person (Takano et al., 2026).

At therapeutic doses of Vyvanse, individuals with ADHD report subjective effects that enable them to concentrate and complete daily tasks. These positive effects on concentration are vastly different from the high caused by individuals misusing Vyvanse. The majority of patients report a “normalized” mental state or a return to their typical functioning when they are taking the medication for their ADHD. Individuals taking Vyvanse for ADHD report a sense of being “clear” or having a “mental reset” (Ginsberg et al., 2011). The amount of catecholamines optimal for functioning in the PFC is thought to follow an inverted-U shape. The individual may display difficulty with attention, executive function, etc. at low levels of activity in the PFC, but increased focused attention and other positive effects, along with increased reward from typically non-rewarding tasks, at higher levels (Arnsten, 2006). Studies into Vyvanse report similar subjective effects, such as mild anxiety, improved attention, and irritability (Pietrangelo, 2025).

Some observable behavioral changes when it comes to methamphetamine are hyperactivity, mood swings, “tweaking” behavior, social withdrawal, and neglect of hygiene/appearance (Rusyniak, 2013). Some effects on attention when it comes to methamphetamine use are a reduced ability to concentrate. It can also cause issues with suppressing irrelevant information, which can increase errors within attention-based tasks. When it comes to how methamphetamine affects impulse control, it creates an increased amount of impulsivity. It can also cause issues with understanding how to stop a task once it is in the process of being done, and it promotes “tweaking” behavior, which is repeated involuntary movements and behavioral actions. Methamphetamine affects decision-making by increasing emotional decision-making, and because of damage to the prefrontal cortex, it causes poor judgment. When it comes to methamphetamine’s effects on social behavior, methamphetamine causes users to socially isolate, causes users to be hostile and violent towards others, and can cause psychosis in users, which can result in irrational reactions to friends and family. Physiological effects of methamphetamine include rapid heart rate, irregular heartbeat, insomnia, appetite suppression, rapid weight loss, and increased body temperature, among others (Patel & Saadabadi, 2025).

The amphetamine effects of lisdexamfetamine reported by users at doses typically considered supratherapeutic or inductive of recreational effects are euphoria, increased energy, increased drive/motivation/sexual performance, decreased need for sleep, decreased appetite, and increased sociability. Amphetamine effects of lisdexamfetamine are reported to onset slowly and to be of lower peak intensity than similar doses of amphetamine, although the effects are reported to last longer. For example, the positive effects typically are reported by users to peak approximately 10 hours after ingestion of a dose, in stark contrast to immediate-release amphetamine, where peak positive effects are reported by users to occur 1 to 3 hours after ingestion. Of importance to the user, the effects of lisdexamfetamine are reported to last long after the typical amphetamine positive effects have waned and can leave the user feeling “dosed” or “foggy” for 24 hours or more after ingestion of the dose. Individual response to lisdexamfetamine varies based on baseline dopaminergic tone, rate of enzymatic conversion, and genetic factors including transporter polymorphisms. Vyvanse can also cause nausea and loss of appetite, leading to weight loss in users (Pietrangelo, 2025).

For individuals with ADHD, clinical and behavioral measures that assess attention, working memory, or inhibition are significantly lower than those of individuals without ADHD. For those with ADHD who are taking Vyvanse to treat their ADHD, behavioral measures from a variety of studies indicate significant improvement in their attention, working memory, ability to inhibit interference, and hyperactivity (Biederman et al., 2007). When individuals with BED were given Vyvanse in randomized, placebo-controlled clinical trials, they reported, on average, a significant decrease in the number of binge eating days per week compared to those taking placebo (McElroy et al., 2016). As mentioned, the mechanism that underlies the actions of d-amphetamine in the mesolimbic system is likely to be a key factor. Therefore, it is hypothesized that the effect lisdexamfetamine has on BED is an indirect one: enhanced impulse control or decreased salience of rewarding food.

Similar to other agents classified as sympathomimetics, Vyvanse can produce a host of physiologic effects. Some of these can have serious consequences, particularly in relation to the use of this agent via its peripheral adrenergic receptors. For children with ADHD, lisdexamfetamine has been shown to decrease appetite for food, with significant consequences for children of growing age (Faraone et al., 2010). This agent can also cause a host of sleep-related problems, primarily in the form of increased sleep onset latency and decreased amounts of time spent in slow-wave sleep and REM sleep. Additional side effects reported by a number of patients taking Vyvanse include dry mouth, likely as a result of decreased salivation caused by the drug’s adrenergic effects on salivary glands. In addition to these commonly reported side effects, high doses of this agent can cause patients to experience hyperthermia or an action tremor, and in extreme cases can cause serious cardiovascular problems.

Evidence for tolerance development in methamphetamine users is well documented in both clinical and preclinical studies, specifically in sleep disturbance studies and cardiovascular effects. In sleep studies conducted on both humans and monkeys, it was found that the initial sleep disruption/wakefulness caused by methamphetamine decreased with repeated administration. In studies of cardiovascular effects, monkeys showed that after long-term self-administered intravenous injection, the initial increase in blood pressure and heart rate no longer occurred. Both studies show that in order to get the same effects from the initial dose, users would have to increase the amount administered (Berro et al., 2017). Physical dependence on methamphetamine is characterized by the heart and other parts of the body “getting used to” the dose administered and progressively needing more to get the same effects. Psychological dependence on methamphetamine is characterized by needing the drug in order to feel happy or “normal.” It is also followed by withdrawal. Withdrawal symptoms typically begin within 24 hours after last use. Symptoms like agitation, dysphoria, and anxiety typically peak a little after someone’s last use (American Addiction Centers, 2026). Neurobiological explanations for the withdrawal effects of methamphetamine are severe neurotransmitter depletion, activated stress systems, and diminished neuroplasticity (McKetin et al., 2025).

The majority of patients on long-term therapy with Vyvanse will note the development of tolerance to the therapeutic effects of the drug at some point during their course of treatment. This is typically evidenced by a need for an increase in dose on a regular basis in order to continue receiving the same therapeutic effects that had been achieved prior to the time when the need for an increase in dose began. The neurobiological basis for the development of tolerance to the therapeutic effects of Vyvanse is thought to be a homeostatic response by the brain to the drug’s effects on the levels of dopamine in the synaptic cleft. The chronic increases in levels of synaptic dopamine that are produced by the drug’s effects on the release and uptake of dopamine lead to down-regulation of D2 receptors in the PFC and a decrease in the expression of the DAT. These changes result in a decrease in the amount of dopaminergic activation produced by a given dose of the drug, thereby requiring an increase in dose in order to achieve the same amount of activation (Koob & Volkow, 2016).

There is a likelihood that Vyvanse carries significant potential for psychological dependence. The rewarding effects of dopamine release in the mesolimbic system can drive compulsive use, and some individuals report being unable to function without the medication. Physical dependence also develops with long-term use, resulting from neuroadaptation of the brain’s catecholamine systems (Koob & Volkow, 2016).

Short-term physiological side effects of methamphetamine include a sense of euphoria, increased energy, rapid breathing, decreased appetite, increased blood pressure, increased heartbeat, and increased body temperature. Short-term psychological effects are feelings of anxiety/panic, paranoia, irritability, aggressive behavior, and insomnia. Long-term health risks associated with methamphetamine use include cognitive impairment, chronic insomnia, heart conditions, depression, meth-induced psychosis, and the possibility of developing schizophrenia. Methamphetamine’s interactions with other drugs, like alcohol and various medications, are not good and can result in death. It can cause things like stroke, heart attack, or liver issues.

Amphetamine crash or withdrawal from Vyvanse typically begins within 24 hours after the last dose and can last up to two weeks. While the physical effects of Vyvanse withdrawal are considered less severe than withdrawal from alcohol or other narcotics, the crash can be psychologically very distressing. Users report extreme fatigue, feelings of depression or intense dysphoria or sadness, sleepiness or hypersomnia, increased appetite, and feelings of being slow or irritable (Shire US Inc., 2007).

Short-term side effects of Vyvanse include decreased appetite, decreased sleep, dry mouth, headache, increased heart rate and blood pressure, irritability, and stomach upset or pain. All of these short-term side effects of Vyvanse are typically dose-related and can be expected in most children and adolescents taking the medication for ADHD. Vyvanse is contraindicated in children and adolescents with a variety of serious heart conditions, including structural heart defects, heart failure, and serious heart rhythm or other serious heart problems (Shire US Inc., 2007).

As with all amphetamines, there are some long-term health effects to be concerned about. While there is limited information regarding the long-term cardiovascular effects of increased heart rate and blood pressure due to Vyvanse, there is potential for serious health problems. In addition, children and adolescents on Vyvanse may experience growth suppression, which is believed to be due to reduced caloric intake (Faraone et al., 2010). In general, as with all medications, there is potential for the emergence of psychiatric problems in individuals who have a history of psychiatric problems, or whose families do. These potential problems could include increased anxiety, rare instances of psychosis, mania, or even increased aggression/hostility. Also, as with all stimulants, there is potential for long-term neuroadaptation of both a structural and functional nature. These potential long-term changes could result in decreased sensitivity of amphetamine-sensitive dopamine receptors and also changes in reward processing within the brain.

On rare occasions, individuals taking high doses of Vyvanse have experienced serious and potentially life-threatening reactions, including increases in heart rate and blood pressure and very high body temperature. Agitation, increased aggression, hallucinations, and, in rare instances, seizures have also been reported in individuals taking high doses of Vyvanse. In rare cases, Vyvanse can cause a fatal stroke. No specific treatment for a Vyvanse overdose is available, and treatment is generally supportive in nature (Shire US Inc., 2007). There are also several potential drug interactions that individuals taking Vyvanse must be aware of. For example, there is the potential for a serious and potentially life-threatening hypertensive crisis when taken with MAOIs (e.g., phenelzine [Nardil], tranylcypromine [Parnate]), and an increased risk of developing serotonin syndrome when taken with other medications that increase serotonin levels. Amphetamines are alkalinized in the urine, and thus alkalinizing agents used to treat kidney stones may increase the risk of side effects of amphetamines. On the other hand, urinary acidifiers may decrease the absorption of amphetamines and thus may also decrease the risk of side effects.

Methamphetamine is known for being an illicit drug, but there are some medical uses for it. The medicine Desoxyn is the only FDA-approved medication that contains meth, and it is used to treat ADHD and obesity. Desoxyn is a Schedule II drug that is only prescribed for ADHD or obesity if other options were unsuccessful. Some harm reduction strategies when it comes to methamphetamine use are being mindful of the possibility of contaminated drugs and using harm-reduction strategies such as drug testing and clean needles.

For children with ADHD, lisdexamfetamine has the positive feature of a long duration of action, extending to 13 hours or more, potentially allowing for once-daily dosing with the option of delaying a second dose in the middle of the day to address afternoon “rebound” or “wear-off” of medication effects. Furthermore, as a prodrug, this agent has been designed with an abuse-deterrent feature that should serve well in the school setting in order to minimize the potential for diversion and misuse by other students with ADHD. For adults with BED, lisdexamfetamine offers a positive pharmacological advance in treating this condition, given that no previously effective pharmacological agents were available for this disorder. The findings from two multicenter, double-blind, placebo-controlled studies conducted with adults with BED demonstrated a significant reduction in the number of binge eating days per week for individuals with BED who were treated with lisdexamfetamine, as compared to those who received placebo, with both studies having large and clinically meaningful effect sizes (McElroy et al., 2016).

The primary concern with off-label use of Vyvanse for weight loss or cognitive enhancement is the significant cardiovascular risk the drug carries, which is compounded by the lack of long-term safety data for these purposes. For individuals who are prescribed Vyvanse for ADHD, the benefits of a long-acting formulation like Vyvanse can be significantly negated by the need for periodic medication breaks in order to determine whether the medication is still needed and to allow for growth in pediatric patients on long-term therapy for ADHD. For individuals with ADHD who need Vyvanse, the fact that it is a Schedule II controlled substance, is only available in a 30-count bottle, and cannot be refilled by phone can pose significant problems for individuals in rural and other underserved areas of the country who are already at a disadvantage due to a number of factors and currently experiencing a shortage of Vyvanse for which there is currently no alternative. Vyvanse can also be used off-label for treatment-resistant depression and narcolepsy (Ross-Hazel, 2024).

Many studies have shown that other stimulants could be effective in treating methamphetamine addiction. Though methamphetamine use can cause psychosis, it might not be permanent. Some studies have shown that brain damage after meth use could be at least partially reversed with other medications that affect serotonin and dopamine absorption, among others.

A misconception about d-amphetamine is that it has different effects on individuals with ADHD and those without the disorder. The former report dramatic effects that are normalized by the medication, whereas individuals without the disorder report minimal effects. There are several reasons why this misconception exists. Many people believe that amphetamines must work in different ways on individuals with and without ADHD. Actually, d-amphetamine affects the catecholamine systems of the brain in all individuals. The only difference is that the net effect of d-amphetamine can be a normalized, therapeutic effect or a very powerful, euphoric stimulant effect, depending on an individual’s baseline level of dopamine and the dose of amphetamine they take. On average, individuals with ADHD report different subjective effects and clinically relevant behavioral effects at equivalent doses of amphetamine than individuals without the disorder. These average differences are due to average differences in the baseline catecholamine levels of the two groups (Hart & Ksir, 2024).

The issue of overdiagnosis of ADHD also seems to be a source of controversy. Some argue that the increase in the prevalence of the diagnosis is due to a better understanding of ADHD, allowing more people to receive a valid diagnosis. Others attribute the increase in prevalence to overdiagnosis, arguing that the line between normal variation in children and symptoms considered indicative of ADHD is often drawn in a way that is culturally and contextually relative, leading to inconsistencies in diagnosis rates (Hart & Ksir, 2024).

Vyvanse is one of many stimulant medications on the market today, and as with any of these medications, many people mistakenly refer to Vyvanse as the “safer” alternative to other amphetamines. This has led some to believe that because the drug is a prodrug and is supposed to be “abuse-deterrent,” it must be safe to take. There are, however, many dangers of this drug for those who take it for reasons other than what it is intended for, namely treatment of Attention-Deficit/Hyperactivity Disorder and Binge Eating Disorder. And, as with any controlled substance, this drug is a Schedule II controlled substance with considerable residual abuse potential, a fact the FDA and DEA recognize (DEA, 2023). Stimulants in general are viewed with a great deal of fear or distrust. On the one hand, there is a fear that these medications are too powerful for individuals with Attention-Deficit/Hyperactivity Disorder and that their condition could worsen over time. On the other hand, there are individuals who do not have this disorder who take these same medications in order to perform better in school or at work. This stigma has caused some individuals with a legitimate ADHD diagnosis to conceal their use of prescribed medication.

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