Why the addiction-brain connection has to be part of the addiction treatment picture

Dr. Dodes recent article, apparently trying to blow up the myth of addiction as a neurophysiological disorder, sounded persuasive, although its underpinning was oversimplified and it’s understanding of the brain-science involved in addiction, and other associated mental health disorders, was lacking. Hopefully, by presenting a more complete picture of the evidence for a brain-aspect to addiction, I can un-bias the discussion somewhat. I, for one, don’t believe that neuroscience will ever be the only factor important in addiction – an individual’s environment, social influences, and other factors will always end up playing important parts as well – still, I think that to dismiss all of the evidence for biological factors at play in the development of addiction is foolhardy. Especially when there’s so much of it that was glossed over in Dr. Dodes’ introduction.

Pleasure center activation is only part of the picture in addiction

Firstly, supporters of the notion that addiction is, at least partly, an outcome of specific brain function point not only to pleasure center activation, but also to a whole host of findings showing genetic variability that is either protective from, or a risk factor for, dependence on drugs and likely also behavioral addiction like eating disorders, compulsive gambling, and maybe sex addiction as well (you can start out looking up ALDH2-2 variability and alcoholism and cocaine addiction, DRD4 and stimulant addiction, and many more).

While it is true that all those who consume addictive substance activate the brain similarly, there are considerable differences in the specific of that activation in reaction to drugs. Some release more dopamine while others have more “active” versions of specific important receptors; neurotransmitter recycling is quick in some, but not all, and drug metabolism is different in different individuals in ways that have been shown to be important not just for addiction risk, but also for the probability of treatment success. Just look at the nicotine and CPY26 literature for an example. It’s right there.

Additionally an entire body of literature exists that shows differential activation, as well as structural differences, between addicts and non-addicts in regions as varied as the OFC, PFC, Insula, and more. This is not to mention a slew of evidence that shows different behavioral test performance on risk-taking, impulsivity, and delay-discounting, all personality variables highly associated with addiction. If one simply ignore all of this evidence, it may be easy to believe that there is no biological explanation for these phenomena, but that’s just wrong.

To say that mesolimbic activation (what the good doctor called “pleasure centers”) is the only evidence for physiological factors in addiction is dismissive at best.

Drug addiction develops in only some drug users

The notion that not everyone who takes drugs becomes addicted is nothing close to evidence against a brain explanation for addiction. Everyone’s motor–cortex, striatum, and substantia nigra (the areas of the brain responsible for movement) activate in the same way during movement, but only a small group ends up suffering from Parkinson’s or Huntington’s disorders. One fact does not preclude the other but instead may specifically point to the fact the group which develops the disorder has somewhat different neurological functioning. Researchers aren’t concerned with explaining why all individuals can become addicted to drugs, but rather why that small subgroup develops compulsive behavior. A short reading of the literature makes that fact pretty clear. Additionally, while Dr. Dodes’ claims otherwise, imaging technology HAS produced evidence explaining this “mystery”, including differences in the ways addicted smokers respond to smoking-related triggers, and an increased dopamine response in cocaine addicts to cues, and well as to cocaine.

As mentioned in the motor disorder section above, ingestion of chemicals is not at all necessary for brain disorders to occur or indeed develop later in life. Dr. Dodes example of shifting addiction could be used as evidence for an underlying neurological difference just as well as it would serve to make his point… Or even better. If there’s a faulty basic mechanism attached to rewarding behaviors, it doesn’t really matter what the behavior is, does it? Sex addiction, gambling, and more can all be explained using a similar mechanism, though drugs of abuse may just have a more direct impact. I know, I’ve written about them all.

The Vietnam vet heroin story used by Dr. Dodes as evidence that emotional, rather than physiological, factors are responsible for addiction actually fits right in line with the notion of predisposition and underlying differences, and I’m surprised to hear a physician point to group differences as an indicator of no neurobiological basis. Indeed, when it comes to the emotional reactivity associated with drug associated cues, normal learning literature, as well as drug-specific learning research, has revealed over and over that drug-related stimuli activate brain regions associated with drug reward in the same way that natural-reward predictors do for things like food and sex. Once again, these facts are part of the basic understanding of the neuroscience of learning, with or without drug abuse involvement.

My own dissertation work shows that it is very likely that only a subsection of those exposed to nicotine will develop abnormal learning patterns associated with that drug. However, among those, learning about drug-related stimuli (as in “triggers”) continues in an exaggerated manner long after the other “normal” animals have stopped learning. That sort of difference can lead to a seriously problematic behavioral-selection problem whereby drug-related stimuli are attended to, and pursued, more so than other,  non-drug-related ones. If that sounds familiar, it should, since drug users continuously pursue drug-associated activities and exposures in a way that seems irrational to the rest of the world. It just might be due to such a mechanism and others like it.

Some important points about science in Dr. Dodes’ article

One very true fact about mental health pointed out by Dr. Dodes is that diseases like schizophrenia, which used to be explained simply as demon possession and evidence of witchcraft can now be, to a large extent, explained by the study of behavioral neuroscience and cognition. The same is true for bipolar disorder, depression, ADHD, and a host of other such conditions. In fact, the study of psychology has only been able to rely on technological advances that allow us to “see” brain function for a few short decades, leading to incredible advances in the field that I think will continue. The thinking that no such advances have, or will continue to be, made in the study of addiction is, in my opinion short sighted.

As I mentioned above, I don’t for a second think that the entire explanation for drug abuse and addiction will come from neurophysiological evidence. The doctor points out that “If we could take a more accurate image of addiction in the brain, it would encompass much of the history and many of the events that make us who we are.” I agree that we need to advance our technology as well as expand our understanding, but I think that to discount neuroscientific explanations completely is a big mistake.

Understanding Blood Alcohol Content (BAC levels)

Contributing co-author: Andrew Chen

Blood Alcohol Content (BAC) is a measure of alcohol concentration in a person’s bloodstream. The more a person drinks, the higher their BAC and the more they experience alcohol-related impairments. The following table shows the behavioral, physical, and mental changes brought on by alcohol at various BAC levels:

Progressive Effects of Alcohol with rising BAC levels

Blood Alcohol
Concentration
Changes in Feelings
and Personality
Physical and Mental
Impairments
0.01 — 0.06 Relaxation
Sense of Well-being
Loss of Inhibition
Lowered Alertness
Joyous
Thought
Judgment
Coordination
Concentration
0.06 — 0.10 Blunted Feelings
Disinhibition
Extroversion
Impaired Sexual Pleasure
Reflexes Impaired
Reasoning
Depth Perception
Distance Acuity
Peripheral Vision
Glare Recovery
0.11 — 0.20 Over-Expression
Emotional Swings
Angry or Sad
Boisterous
Reaction Time
Gross Motor Control
Staggering
Slurred Speech
0.21 — 0.29 Stupor
Lose Understanding
Impaired Sensations
Severe Motor Impairment
Loss of Consciousness
Memory Blackout
0.30 — 0.39 Severe Depression
Unconsciousness
Death Possible
Bladder Function
Breathing
Heart Rate
=> 0.40 Unconsciousness
Death
Breathing
Heart Rate

BAC levels can be accurately measured through blood, breath, or urine tests. Currently, the legal limit to drive in the U.S. is .08 for individuals over the age of 21. That limit is similar to those used in other states, but there is some variation.

How many drinks for a BAC of .08?

The answer to this question is a little more complicated than it seems. Alcohol affects everyone differently. In general, smaller individuals reach higher BAC levels more quickly than larger individuals, fatter individuals reach higher levels more quickly than muscular individuals, and women reach higher levels more quickly than men. These factors are all related to the amount of water present in the body. The more water a person has in their body, the more diluted the alcohol will be in their blood. (smaller individuals have less water than bigger people, fatty tissue has less water than muscle, and women typically have a higher % of body fat than men).

Chronic drinkers can develop a tolerance to alcohol, allowing them to metabolize alcohol more quickly and giving them added resistance to the functional impairments of alcohol.

Furthermore, alcohol can affect the same person differently under different circumstances. Eating before drinking can delay alcohol absorption and reduce a person’s peak BAC levels by as much as 40%. Exhaustion, illness, and dehydration impair a person’s ability to metabolize alcohol, promoting higher BAC. Depressed mood and stress can also magnify the effects of alcohol. Finally, medications can react with alcohol, potentially causing serious health complications.

You’ve had too many – can you lower BAC?

Contrary to popular belief, there is no magic food or drink that can lower your BAC levels. Exercising and taking a cold shower will also do nothing to lower BAC. BAC levels will only decrease with time. On average, a person metabolizes alcohol at a rate of one drink (0.5 oz alcohol) per hour. Spacing out drinks is a good way to manage BAC levels as it gives your body time to metabolize alcohol while delaying further increases in BAC.

Understanding your body is the first step towards preventing dangerous BAC levels. Plan ahead make sure you don’t ruin your night or someone else’s by drinking more than you can handle.

Additional Resources:

BAC table for men

BAC table for women

Check out the Virtual Bar at www.b4udrink.org for a really fun way to learn about your own limits!