Addiction

Question 1

is there a genetic basis to addiction?
1. alcoholic problems in adoptees
2. twin studies and probandwise concordance rate for alcoholism

Answer 1

1. children of alcoholics 4 times more likely to become alcoholics; adoptees with alcoholic bio parent were more likely to become alcholics than with sober bio parents based on fact that mother’s behaviours can influence her child’s environment in utero
2. probandwise concordance rate is probability of concordance of alcoholism in twins, C = concordant pairs have both alcoholic twins, X = discordant pairs only one is alcoholic using 2C/(2C+x) where x and c are number of pairs; higher PBWC of alcoholism b/w monozygotic twins than dizygotic twins indicate genetic basis to addiction

Question 2

predicting abuse based on response to drug
1. predicting alcoholism based on drinking response
2. genetics and alcohol addiction susceptibility

Answer 2

1. 20 y/o non-alcoholics consuming 0.75 mL/kg of alcohol self-reported feeling of drunkenness, 10 yrs later greater percentage of alcoholics with a family history of alcoholism and greater percentage of those reporting feeling less drunk became alcoholics
2. alcohol metabolized into acetaldehyde (30 times more toxic) by alcohol DH, acetaldehyde into acetic acid by acetaldehyde DH, ALDH2 gene on Chr 12 coding for ALDH enzyme determines response to alcohol, ALDH1 is function enzyme with guanine corresponds to low alcohol response (don’t feel it), ALDH2 is dysfunctional with adenine > high response; heterozygous is mod response; higher responders accumulate more AL since dysfunctional ALDH cannot break it down, feel more sick to protect against dev of alcoholism later in life

Question 3

dopamine and addiction
1. key characteristics of addiction
2. dopamine pathway and function
3. dopamine function and drug abuse

Answer 3

1. cravings, loss of control in frequency of use, compulsion, use despite consequences
2. drugs stim rewards sys ventral tegmental area nuclei to fire, axons in the medial forebrain bundle send AP to nucleus accumbens where dopamine is released into synase to act as neural incentive
3. dopamine regulates motivation for reward seeking behaviour such as food, sex, and exercise, brain is equipped to handle normal range from those behaviours but exposure to drugs releases so much dopamine that brain cannot handle it, decrease receptors as homeostatic response, normal reward seeking behaviours don’t give the brain the amount of dopamine it seeks thus less motivated to do them and compulsion to use drugs instead to provide brain with dopamine

Question 4

frontal lobe and addiction
1. activity in addicts
2. prefrontal cortex dev

Answer 4

1. frontal and prefrontal cortices responsible for rational thinking, empathy, and ability to delay gratification; frontal and prefrontal lobes of addicted brains are less active, lose control in amount or frequency of use and use despite consequences
2. pruning grey matter makes neural circuitry more efficient and functional; prefrontal cortex not fully dev until 25 thus adolescents are more susceptible to risk taking behaviour

Question 5

anticipation and reward
1. instrumental conditioning in addiction
2. cravings
3. drug environments and overdose

Answer 5

1. glutamate strengthens connections b/w drug and cues of drug administration to trigger drug-seeking behaviour after exposure to cues and context of drug
2. anterior cingulate cortex expectation of reward (drug) following drug cue, launch homeostatic counter response to drug activated to prepare body for drug’s effects; absence of drug after the cue leads to craving and withdrawal syndrome
3. cued drug administration leads to neutrality after drugs are taken, if no cues, no counter response, body not prepared, homeostasis imbalance after drug administration leads to higher chances of overdose and mortality

Question 6

1. THC and dopamine
2. how THC activates the reward system

Answer 6

1. low doses of THC in the nucleus accumbens close to natural rewarding levels of dopamine, high doses increases extracellular dopamine to near cocaine lvls, suggesting that THC has moderate addictive potential
2. GABA inhibits dopamine release, anandamide regulating dopamine binds to cannabinoid receptors to block GABA to allow dopamine release, THC mimics anandamide, allowing for unregulated indirect dopamine release

Question 7

effects of cannabis use
1. brain and dopamine
2. schizophrenia risk

Answer 7

1. 30% people using cannabis abuse it, especially those under 18, reward sys adapt to supernatural amount of dopamine leading to blunt release of dopamine to rewarding stimuli, desensitization, and dependency on THC to provide dopamine
2. with any cannabis use, increased risk of psychosis, females at higher risk, induce more psychosis by triggering schizophrenic phenotype expression in those with higher genetic risk; use worsens psychosis in schizophrenics

Question 8

psychedelics and mental healthcare
1. psilocybin mechanism
2. psilocybin application in depression
3. psilocin and dopamine

Answer 8

1. psilocybin is main psychoactive ingredient, metabolised into psilocin which mimics serotonin binding to serotonin receptors
2. more serotonin receptors occupied with higher dosage, boost amount of serotonin in body to enhance mood, instant effect, no delay unlike SSRI, effective for those req immediate help, effective for those resistant to SSRI
3. moderate dose does not effect dopamine beyond normal rewarding lvls, not addictive

Question 8

1. psilocybin and depression
2. psilocybin and alcohol abuse

Answer 8

1. single dose of 25 mg, 10mg, and 1 mg pure synthetic psilocybin reduced depressive symptoms in drug-resistance non-responders; adverse events occurred in 77% of participants, less in 1 mg
2. psilocybin as therapy for alcohol addiction reduced the number of heavy drinking days compared to the standard alcohol therapy control drug