Drugs & the Brain
Nicotine is a specific ingredient within cigarettes which promotes a continued desire to smoke. Nicotine stimulates nicotinic receptors in the brain which causes dopamine to be released in the nucleus accumbens (a central component of the reward system of the brain), mimicking the neural effects common to many other drugs of addiction. Nicotine can reach the brain within just ten seconds of inhalation of a cigarette.
Nicotine can alleviate anxiety and stress, reduce anger and aggression and induce pleasant states of relaxation and bliss. These behavioural effects are less troubling and less obvious than the behavioural effects of other drugs. However, these pleasant effects tend to reinforce the desire to continue smoking. Nicotine tolerance is common and means that for users to keep nicotine in the blood at an optimal level for experiencing its rewarding effects, they are likely to need to increase the rate and frequency with which they smoke. Between one third and a half of all smokers become dependent.
When nicotine levels in the blood drop, withdrawal syndrome occurs, making it difficult for some people to quit or reduce their nicotine intake. Symptoms of withdrawal include craving, depression, restlessness, irritability and increased hunger.
Nicotine is considered both a stimulant and a sedative. Users will experience a ‘kick’ after immediate exposure to nicotine caused by stimulation of the adrenal glands and the resultant release of epinephrine (adrenaline). Nicotine can also produce a sedative effect, depending on the level of arousal of the smoker’s nervous system and the amount of nicotine absorbed by the brain.
A 2011 study investigated the effects of smoking on 78 participants’ prospective memory (prospective memory is responsible for enabling us to remember to carry out future activities such as remembering to buy milk on the way home from work). Participants ranged in age from 18 to 35 years and were considered not to be affected by age-related memory impairments, given their youth. Participants smoked an average of nine years and an average of 65 cigarettes per week. Significant impairments in prospective memory were observed in the participants who were persistent smokers.
The endocannabinoid system plays an important role in the development of the central nervous system (CNS), synaptic plasticity and responding to environmental and endogenous insults. Marijuana/cannabis contains chemicals that resemble naturally occurring neurotransmitters produced by the brain’s endocannabinoid system. The main chemicals found in marijuana/cannabis include CBD (cannabidiol) and THC (tetrahydrocannabinol).
In normal brain function, cannabinoid neurons (like CB1 and CB2) will fire off but will then become temporarily unresponsive so as to not overwhelm the brain. However, marijuana/cannabis use causes THC and CBD (agonists) to bind to CB1 and CB2 neurons in the brain causing them to fire off continuously. When these neurons are prevented from temporarily ‘switching off’, thoughts, perception and imagination become amplified. Users may experience an inability to see the ‘big picture’ and will instead tend to become fixated on a particular idea. Neurons continue to fire until a new idea forms and the user then veers off on a new tangent.
Cannabinoids also alter the brain’s dopamine levels. Short-term use has been shown to increase dopamine levels, with users reporting sensations of euphoria, relaxation and even pain modulation. However, abuse of marijuana tends to alter the brain’s reward system by depleting dopamine levels, causing increased negative emotions and decreased motivation (Bloomfield et al., 2017). Whilst there may be no physiologically addictive components to marijuana, it may cause psychological dependence as the brain craves higher levels of dopamine.
Recent research has discovered cannabinoid receptors in the amygdala (a region of the brain which regulates anxiety and our ‘fight or flight’ response). Some cannabis users report that cannabis relieves their symptoms of anxiety. However, little research has been conducted to substantiate these claims. In fact, one study showed that dependent cannabis users were more likely to have a lifetime diagnosis of generalised anxiety disorder (GAD). Another Australian study reported higher prevalence rates of anxiety disorders among cannabis dependent users compared to those who did not use cannabis.
Regular cannabis use has been linked to the later development of psychotic disorders, and some studies have identified cannabis use in adolescence as increasing the risk of psychosis (Moore et al. 2007) and earlier onset of psychosis (Large et al., 2007). THC is known to produce temporary but generally mild psychotic effects in intoxicated users, and it can also worsen symptoms for people with schizophrenia (Di Forti, Morrison, Butt, and Murray 2007). Yet there have also been studies of cannabis use that have shown improved cognition in people with schizophrenia (Yucel et al. 2012).
As the above information indicates, further research is needed to truly understand the risks associated with long-term use of marijuana and, in order to reduce these risks, the safest option is to avoid the drug altogether.
Cocaine is an illicit stimulant drug in Australia, and typically comes in the form of a white powder that is snorted by the user. It may also be injected. Crack cocaine is derived from the same coca bush that cocaine is extracted from, except that crack cocaine takes the form of white crystals and is usually smoked. Historically, the leaves of the coca bush were chewed by labourers and farmers who had to work long hours under harsh conditions with little food.
In the brain, dopamine is typically released into a synapse (small space in between two neurons), where it then binds to dopamine receptors and allows the reward signal to be passed on to the next neuron. This is known as the mesolimbic dopamine system and is responsible for stimulating feelings of ‘reward’ and motivation. When the message has been passed on, the dopamine transporter then removes the attachment that the dopamine has on its receptor. When cocaine is consumed, however, the user experiences feelings of euphoria and excitation as the molecules in the cocaine bind themselves to dopamine transporters, preventing the dopamine from being removed. Dopamine builds up in this process and produces the ‘high’ that users experience. In other words, the brain is being flooded with these reward neurotransmitters, which lead to feelings of pleasure, elation and excitement.
As with many other drugs, continued use of cocaine leads to dependency and tolerance, where the original dose does not produce the same ‘high’ as before, and users who seek the rush of hyperstimulation increase their dosage. This is because when the brain is tuned to the ‘high’ mode for an extended period of time, it starts to accept it as the default resting mode. From that point on, even more cocaine is required to stimulate the brain to reach the same ‘high’ as before. Withdrawal symptoms are experienced when a user suddenly ceases use. Emotionally, the user experiences a ‘crash’, characterised by anxiety, discomfort, and cravings. They may even experience feelings of depression and have thoughts about suicide as a result.
In the long term, cocaine use can be very damaging for the brain, and cause cognitive impairments. It causes deficits in attention, processing speech, and verbal and visual memory. Of these domains, the areas showing the greatest deficit are attention, verbal memory and working memory. Addicted individuals also displayed more impulsivity, indicative of the impairments that cocaine has caused for their reward pathway – they are more likely to perform actions without first considering the consequences because they are unable to suppress their desire to seek the reward. When users abstained from the drug for at least 12 weeks, it was found that this deficit decreased in magnitude but remained present. Current literature has demonstrated that addiction to cocaine has profound impacts for the individual emotionally and cognitively in the long term.
Ecstasy, or MDMA, is an illicit recreational drug that is usually ingested orally in the form of a pill. It is a drug with both stimulating and hallucinogenic effects that affect the brain by exciting neurotransmitters and preventing their uptake. Ecstasy primarily affects serotonin, a neurotransmitter that is responsible for emotion regulation. Unlike marijuana and cocaine which are derived from plants, ecstasy is a ‘designer drug’, meaning that it was created in a laboratory environment by altering the chemical makeup of existing drugs.
When consumed, ecstasy brings with it feelings of euphoria, elation and hallucinations. Users describe that everything around them feels more ‘pronounced’ and clear. For this reason, ecstasy is frequently used by party-goers. Using ecstasy brings with it the risk of dehydration and exhaustion. Users often do not feel the need to eat or drink when ‘high’ on ecstasy. Combined with long hours of physical exertion without hydration, this can result in severe dehydration in the user. Other side effects of consuming ecstasy include hallucinations, tremors and nausea.
Using ecstasy in the long term results in similar impairments seen in cocaine-addicted individuals. They are more prone to anxiety, depression and hallucinations. Whenever ecstasy is used, the brain produces floods of serotonin, which help the user experience their ‘high’. Over a period of time, however, the brain increasingly loses its natural ability to produce serotonin on its own, causing a lack of serotonin. This manifests in the form of a ‘crash’, characterised by low mood, lack of motivation and problems with sleep.
Cognitively, ecstasy can be very damaging and cause lasting impairments. It has been found that even ecstasy users who have not used the drug recently had problems with both their verbal and visual memory – that is, remembering what was said or seen, indicating that the damage caused by ecstasy is long-lasting and not easily reversible. They also had problems with their attention and were easily distracted when instructed to complete tasks. When given particularly cognitively challenging tasks, ecstasy users had difficulty completing them even when given multiple chances, whereas marijuana users were able to complete the tasks at almost the same competency as controls.