Drugs and food Flashcards

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1
Q

What are 5 positive impacts of alcohol?

A

– Tax revenues from Alcohol in Australia have averaged around 6 Billion Dollars per year over the last decade
– Alcohol consumption reduces cardiovascular deaths by approximately 800 cases per year, and prevents around 20,000 hospitalisations
– It also acts to reduce kidney/gall-bladder stones and increases bone density
– Hotels can act as focal point for communities
– Alcohol consumption can be a pleasurable experience

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2
Q

What are 7 negative impacts of alcohol?

A

– 15% percent of men and women aged 20-29 drink at a rate likely to cause them harm (> 2 standard drinks/day).
– Among this age group 50% of men and 20% of women have engaged in binge drinking (> 7/5 standard drinks drunk consecutively) at least once a week in the past year.
– Harms from excessive intake include:
• Cirrhosis (liver damage)
• Heart disease
• Brain damage
• Road trauma
• Violent behaviour
• Relationship breakdown
• Lost productivity
– The rate of excessive consumption in Indigenous Australians is 2-3 times higher even though fewer drink

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3
Q

What are the metabolic effects of alcohol? (6)

A

• Metabolism and male vs female differences
– Alcohol enters the bloodstream and is rapidly absorbed by the brain, but much more slowly by muscle (women have less muscle)
– Alcohol is primarily (90%) metabolised by the liver (and 10% by stomach - but women are less efficient at this)
• Alcohol is broken down into Acetaldehyde (women less efficient at this as well)
• Acetaldehyde is broken down into Acetate
• Acetate is then fed into the ACoa pathway yielding 7Kcal for every gram of alcohol consumed
• The body can metabolise a maximum of 6-8g per hour

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4
Q

What are the psychological effects of alcohol? (6)

A

• General - euphoria, disinhibition, reduced anxiety, impaired motor control
• Specific - effects of alcohol need to be distinguished from peoples expectations of what happens on ingestion
– Expectation free research designs tell us that
• Alcohol lengthens reaction time
• Alcohol narrows attention
• Alcohol promotes risk taking
• Alcohol enhances aggression
– This makes for a very unfortunate cocktail when combined with a car and an inexperienced driver

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5
Q

What are the effects of alcohol on the brain? (7)

A

• Alcohol acts upon multiple brain systems, which is why it is called a promiscuous drug
• Its effects also vary by dose
• The key changes appear to be:
– It acts akin to anaesthetics by increasing the permeability of nerve cell membranes (consumption of the anaesthetic agent ether is also intoxicating)
• Alcohol can be used as an anaesthetic but its therapeutic dose is so close to its lethal dose it was never of much practical use
– It acts upon the same GABA receptors as anti-anxiety drugs such as diazepam (which is 4000X more potent)
– It alters brain dopamine levels, especially in the Nucleus Accumbens (driving wanting)
– It increases levels of endogenous opioids (producing liking)

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6
Q

What are the 2 types of tolerance we can have to alcohol?

A

• The behavioural and pharmacological effects of alcohol change with exposure - that is, tolerance
• Acute tolerance
– Within a drinking session rising blood alcohol (BA) correlates well with behaviour change. After drinking ends BA can still be elevated but there can be a disconnect between behaviour and BA:
• One can feel sober even with both an elevated BA and significant impairment in things like reaction time, attention etc
• The classic example is driving the morning after heavy drinking the night before – feeling sober, but impaired and with an elevated BA
• Chronic tolerance - metabolic and tissue
– Regular drinking affects the way the body metabolises alcohol and the way in which cells respond to the same level of alcohol. Chronic tolerance is lost after 3 weeks of abstinence in all drinkers

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7
Q

What is addiction to alcohol?

A

• Addiction is a problem in around 10% of regular drinkers
• It is defined by the American Medical Association as:
– Alcoholism is an illness characterised by a preoccupation with alcohol and a loss of control over its consumption, such as to lead to intoxication if drinking is begun; the condition is chronic, progressive, and has tendency to relapse. It is typically associated with physical disability and impaired emotional, occupational and/or social adjustment as a direct consequence of persistent and excessive use of alcohol
• Around 1 person in a 100 becomes an alcoholic

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8
Q

How does alcoholism affect neurology? (7)

A

• Wernicke-Korsakoff syndrome
• Two components that may occur alone or together
– Wernicke’s encephalopathy – dementia, ataxia, visual disturbances
– Korsakoff’s syndrome – anterograde amnesia (i.e., an inability to learn new things), confabulation, language difficulties
• Cause
– Chronic alcohol abusers tend to have poor diets, and hence have low intakes of thiamine (vitamin B1)
– Alcohol may interfere both with thiamine uptake and adversely affect metabolic pathways that are dependent on thiamine
– There may also be a genetic susceptibility
• Disease course is irreversible following amnesia/dementia onset

• Other neuro-degenerative disorders
– Marchiafava-Bignami disease – degeneration of corpus callosum and dementia
– Haemotomas – small blood clots resulting from frequent bumps to the head (occurring during intoxication)
– Hepatic encephalopathy, Central pontine myelinolysis, Alcoholic cerebellar degeneration, Alcohol related dementia

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9
Q

What are the withdrawal symptoms from alcohol?

A

– Mild (tremor, anxiety, insomnia)
– Moderate (severe tremor, convulsions, hallucinations [typically in peripheral vision])
– Severe – AKA Delirium tremens (confusion, persecutory hallucinations, systemic circulatory problems, status epilepticus; 15% mortality if untreated)
– Gets worse with repeated cycles

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10
Q

What other health problems can alcoholism cause? (8)

A

– Cardiomyopathy, myopathy, hepatitis, cirrhosis, impotence, sterility etc
– Cancer of mouth, tongue, oesphagus
• 5x base rate in heavy drinkers, 8x base rate in smokers, 44x base rate in heavy drinkers & smokers

• Fetal alcohol syndrome
• Characterised by facial abnormalities (absent philtrum, flattened bridge) and significant developmental delays of varying severity
• 6% of alcoholic mothers (heavy consumption during 1st trimester)
• 1200 cases (?) per year in US
• Lifelong social and intellectual disability

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11
Q

What are the risk factors for alcoholism? (3)

A

• Several lines of evidence suggest genetic susceptibility
• Increased risk in offspring of alcoholics
• Risk higher if both parents alcoholic
Risk the same if offspring raised by non-alcoholics
• No risk (relatively) for the offspring of non-alcoholics adopted by alcoholic parents
• Higher concordance in MZ than DZ twins
– Individuals with alcoholic relatives show:
• Less sensitivity to low levels of alcohol
• Abnormalities in DA receptors (wanting)
• Abnormalities in 5HT metabolism (relating to heightened risk for anxiety, depression and impulsivity)

• Genes combined with…
– Drinking culture
• Socially sanctioned
• Widespread availability (the outlet effect)
– Comorbid conditions
• Alcoholism tends to be comorbid with anxiety disorders such as panic attacks, OCD and phobias - self medication
• Alcoholism results from an unfortunate synergy of genetic predisposition (alcohol or non-alcohol related) combined with our alcohol tolerant culture

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12
Q

How do we treat alcoholism?

A

• Pharmacological
• Acute withdrawal (Benzodiazepines)
• Chronic
– Disulfiram (antabuse) which prevents reduction of acetaldehyde
– Naltrexone which appears to be useful in preventing relapse by reducing craving (as with tobacco)
• Psychological
• AA, Therapy (varied), Relapse prevention training
• The long-term (4 year) spontaneous abstinence rate is around 30%. Virtually no treatment appears to exceed this benchmark, although drug/psychological therapies may assist continued abstinence

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13
Q

What are the psychological effects of caffeine? (6)

A

• Cognitive
– Decreases reaction time
– Attentional effects
• Increases vigilance (especially on monotonous tasks)
• Benefits both endogenous (voluntary capacity to direct attention) and exogenous (ability to attend to external events) attention
• Mood
– Increases feelings of alertness
– Increases feelings of subjective wellbeing
• It exerts these effects equally in both sleep deprived and non-sleep deprived individuals
• Important caveat!
– There is much uncertainty as to whether the cognitive and mood effects of caffeine JUST reflect the alleviation of withdrawal symptoms. This is because almost everybody consumes caffeine.

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14
Q

What are the physiological effects of caffeine? (7)

A

• Mild diuretic
• Increases blood pressure, heart rate
• At high doses, tremors, anxiety, racing heart
• Some evidence for adverse effects on pregnancy
• Adenosine (involved in energy metabolism) increases during the day and is elevated whilst asleep. Caffeine prevents adenosine binding to its receptor
• Caffeine also interacts with GABA receptors, slowing the binding of benzodiazepines and other hypnotic agents
• It indirectly modulates striatal dopamine and MAY potentiate the effects of certain addictive drugs

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15
Q

Is caffeine addictive?

A

• Is it abused?
• In very rare instances (caffeine intoxication >1000mg/day)
• It does not appear to produce a high and animals do not self administer this drug, but it is a positive reinforcer in animals and people (i.e., both like it)
• Tolerance?
• There is some evidence of acute tolerance but little or no evidence of chronic tolerance
• Withdrawal?
• Many suggest there is a withdrawal syndrome
– Headache, fatigue, cognitive dulling, low mood, which are readily alleviated by consuming caffeine
• This is disputed by others
– Some say these symptoms are expectancy effects
– A prior headache history may predict this particular symptom
– Guatemala study - heavy coffee intake in kids (6x adult US consumption) followed by abrupt cessation found no withdrawal symptoms

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16
Q

Are certain foods addictive?

A

• It has been claimed that certain foods are‘addictive’
• Fast food (high fat/high salt or high fat/high sugar)
• Hyper-processed foods (chocolate, crisps, ice cream…)
• This is a very live and controversial issue – why?
• It is because of blame
– If the sort of foods that make people fat are addictive then if I overeat it is not my fault
– If such foods are not addictive, then I am choosing to eat them, in which case if I overeat it is my fault
• This is the same argument taken by tobacco and gun lobby of the sort “…guns don’t kill – it’s who pulls the trigger”.
• This has major legal and social ramifications because if certain foods are addictive, then food manufacturers are to blame for the obesity epidemic and can be sued