Thinking You Are Bullet Proof might just Kill You.

Alcohol seemed to fortify me, make me stronger limbed, heroic, thrusting and invincible. With alcohol in me I communed with the Gods.

The blood seemed to flow around my body better, muscles seemed to get enhanced. I was less inhibited, funnier, nicer, more humane, better company. I looked on the world and it’s troubles with a kinder, gladder heart. People sought me out for advice. I was often sage-like. Especially compared to the insecure, disconnected from people, sober me.

People would comment on how transformed I became with the drink, nicer, more trusting, more human, more warmed up and less distant.

Alcohol was my first profound spiritual awakening –  alcohol brought about a profound alteration in how I felt and thought about the world and it’s people. How I acted towards them.  It made me connect with humanity, become a part of, not separate.  It made me exhale and go “phew”.  My wife said the main reason I gave for drinking when I was in the midst of chronic alcoholism was to escape from myself – not to get drunk but to escape the unbearable lightness of being ME.

The second, and most vital and absolutely necessary profound spiritual awakening I had was when I came into recovery via the 12 steps. Then I found a program that also enabled let me go “phew” and also connected me to my fellow human beings. With much less damage and tragedy wrought!

Don’t get me wrong I wasn’t some shy kid, fidgeting in the corner.  I was not. I was not all there, a character, wired to the moon some would say. I was extrovert, but I was also insecure, uncertain, distrusting of people. Sure I was someone who appeared to get  on with people but in a manipulative way. People worried me so I have a whole bundle of strategies to keep them happy, at arms reach. This included my family.

I was also less than whole when sober. Not properly filled in, felt like I was missing something or was protecting some indescribable weakness or deficit in me, although I was never sure want this was, this undefined sense of lacking. Always attending to, protecting some invisible psychic wound.

When drinking I underwent some transformation of spirit. I connected better with my fellow human beings. I became someone I liked more than the sober me. Other people seemed to like the sober me less also and much preferred the company of the wisecracking, fun seeking drinking me.

The drinking me was a shinier, more colourful me, expansive, inclusive, connecting, less manipulative. The sober me was greyer, more insular, cut off and suspicious of people.

When I drank I could drink a lot and rarely had the negative impairments to speech, gait and behaviour that I saw frequently in friends and others.

Alcohol did not make me drowsy or make me want to hug my friends and family. It made me slap people on the back, high five. It was not a sedative it was a major stimulant and much more. A wonderful cocktail of effects. For me it is the most brilliantly designed concoction of effect, and I have tried quite a few other drugs in my time.

In fact it wasn’t a drug to me so much as a homecoming to myself.

If you could mix cocaine with opium in liquid form then that was what  alcohol was me. Not only did it give me a warm glow of absolute well being, in a way no other drug has – although opium was pretty good at that! – it also made me feel that I could conquer the world, that everything was possible. It made me dream big dreams, plan my next imaginary offensive.




Alcohol made me more me! Seemed to make me work better. I became more the  me I wanted to be, that is before  the magic began to dissipate in later years until the point in the end of drinking the alcohol had not affect but to calm the delirium tremens or stave off that imminent alcoholic fit, or momentarily quietened the auditory and visual hallucinations, before reigniting and refuelling them again. Alcoholism gives you many heavenly feelings as it drags you to hell!

The thrill was long gone by this stage. So why did alcohol have this effect. Is it only alcoholics that get this euphoric alive and kicking reaction to alcohol? And for years I got away with the physiological withdrawals and hangovers too. Alcohol made me feel bullet proof, it made me stronger. Invincible, like my internal organs were steam powered and made of metal. That I was beyond human.

In this response to alcohol, in this lack of impairing effects of alcohol, in this thinking I was invincible, that the drink was my greatest ally may well have lain the seeds of my eventually destruction. In this combination of impulsive seeking and stimulative effects of alcohol was an alcohol fuelled propulsion into eventual chronic alcoholism and compulsive addictive behaviours. Alcoholism would never be something I ever had to consider because I was good, very good, at drinking!!


We cite and quote directly from a very interesting article on how a family history of alcoholism contributes to impulsivity, the one psychological domain that turns up repeatedly and is supported in studies of alcoholics, addicts and those at risk genetically from these addictive disorders. Impulsivity from an early age is one variable that appears central to later addictive disorders.

“A family history of alcoholism (FHA) doubles the risk of alcohol dependence (Nurnberger et al., 2004). Beyond the risk for alcohol use disorders, familial alcoholism is also significantly associated with impulsive and externalizing behaviors (Marmorstein et al., 2009)–behaviors thought to be relevant to drinking initiation, escalation, and treatment relapse (Perry & Carroll, 2008).



Impulsive behavior is associated with both alcohol use disorders and a family history of alcoholism (FHA). One operational definition of impulsive behavior is the stop signal task (SST), which measures the time needed to stop a ballistic hand movement.

Stop signal reaction time (SSRT) is distinct from delay discounting, which measures impulsive devaluing of reward as a function of time, the motor impulsiveness assessed by SSRT represents the speed  (or slowness) with which an individual can accommodate an environmental demand to halt a behavior. Using the stop signal task (SST) to quantify SSRT, Nigg et al. (2004) found that alcohol-naïve adolescent offspring of alcoholic fathers had slower SSRTs than children from control families, and that SSRT predicted aggregate future alcohol and drug problems (Nigg et al., 2006).

Twenty two family history positive (FHP; age = 22.7 years, SD= 1.9) and 18 family history negative (FHN; age = 23.7, SD= 1.8) subjects performed the SST in fMRI in two randomized visits: once during intravenous infusion of alcohol. The results showed FHP being less sensitive to alcohol’s effects.

Beyond its potential as a reflection of baseline behavioral impulsiveness, SSRT and inhibition success (but not choice reaction time) are worsened by alcohol intoxication (e.g., De Wit et al., 2000; Fillmore & Vogel-Sprott, 1999).

Thus, as inhibitory control worsens during intoxication, so does ad lib alcohol consumption (Weafer & Fillmore, 2008), speaking to a potential mechanism in the loss of control of drinking.

The principal finding from this experiment (1) was a significant interaction between alcohol exposure and those with family history of alcoholism (FHA) in right prefrontal BOLD activation during motor inhibition. During clamped alcohol infusion, however, this right frontal activation in FHN was significantly reduced, while in FHP activation remained essentially unchanged. Those subjects with a smaller right prefrontal BOLD response during behavioral inhibition (FHN) also tended to need more time (had a longer SSRT) to successfully inhibit their behavioral responses so SSRT may have been lengthened by alcohol infusion.

While we found only an insignificantly smaller difference in frontal responses to correct stop signal responses in FHP subjects, which is consistent with data on another task measuring impulsivity, the Go/No-Go, of Schweinsburg, et al. (2004), which showed only FHN subjects’ activation frontal activation was significantly reduced by alcohol.

Schuckit et al. (1980) first proposed that individuals with FHA are less sensitive to alcohol’s effects. A recent meta-analysis (Quinn & Fromme, 2011) found that, when compared to lower drinkers, heavier drinkers are more sensitive to alcohol’s stimulant effects, and less sensitive to alcohol’s sedative effects.

The data form this study (1)  the data are generally consistent with the concept that FHP subjects are less susceptible to (in this case, the adverse cognitive) effects of alcohol exposure in a brain region that plays an important role in behavioral inhibition.

…a resistance to the cognitively impairing effects of intoxication may carry its own risks, as subjects may perceive a reduced vulnerability to alcohol’s punishing consequences— or in this case the adverse effects in brain systems regulating behavioral control. Thus, the combination of an increased sensitivity to reward and a tolerance to alcohol’s cognitively impairing effects could represent a mechanism of increased risk of progression to heavier drinking, in particular by creating expectancies in drinkers that they can increase their consumption without adverse consequences to their behavior (Vogel-Sprott & Sdao-Jarvie, 1989).”

So to summarise, solely from our own perspective, it may not be the effect of alcohol that prompts  impulsive, loss of control drinking observed in alcohol dependent individuals but impulsivity that prompts drinking behaviour initially and with an apparent lack of cognitive impairment as the result of drinking then leading some individuals to thinking they can “handle the drink” and it negative psychological effects and consequences when, over time and chronic use, it may be progressively contributing to an increased impulsive behaviour to the point where this impulsivity becomes  compulsivity.

It may be that in thinking they are “in control” of drinking and it’s consequences that this paradoxically gives rise to loss of control in drinking via an increased compulsivity but much more on this another time!


1. Kareken, D. A., Dzemidzic, M., Wetherill, L., Eiler II, W., Oberlin, B. G., Harezlak, J., … & O’Connor, S. J. (2013). Family history of alcoholism interacts with alcohol to affect brain regions involved in behavioral inhibition.Psychopharmacology, 228(2), 335-345.


How does the First Drink really get you Drunk?

In treatment circles, I have constantly heard the refrain “one is not enough and two is too many!” and “the first drink gets you drunk” which points to a difficulty certain people have with stopping once they start drinking; a “loss of control” over drinking.

It is as if drinking gives you a thirst rather than taking it away. Many thousands of recovering alcoholics will tell you about this phenomenon – how they had only intended to have a couple but then lost a weekend to drinking instead.

It is an essential question to get to the bottom of, why do certain people not have the ability  or have a reduced ability to stop once they start.

I came across an article from a few years back which addressed this issue (1) .

In those with a family history of alcoholism,  drinking alcohol affects how the brain responds to an alcohol cue – in other words these individuals appear to want more compared to controls when they see alcohol cues. So drinking alcohol heightens a wanting for alcohol  rather than causing a  feeling of having had enough (not wanting). 

Although a family history of alcoholism is the strongest risk factor for developing alcohol dependence, there are few studies of the association between familial alcoholism and the human brain’s reward system activity. This study used a functional magnetic resonance imaging (fMRI) to determine how family history affects the brain’s response to subjects’ preferred alcoholic drink odors (AO).

A family history of alcoholism doubles the odds of developing alcoholism (Hasin et al., 1997; Nurnberger et al., 2004). While environmental influences exert considerable influence in early adolescence, twin studies show an increasingly larger genetic influence by age 18 (Dick, Rose, & Kaprio, 2006), with a family history of alcoholism being a significant factor in the transition from abusive to dependent drinking (Hasin, Paykin, & Endicott, 2001).

While a number of studies have examined the human cerebral response to alcohol-related cues, particularly in alcoholics (e.g., Bragulat et al., 2008; Filbey et al., 2008b;Kareken et al., 2004; Myrick et al., 2008; Tapert et al., 2004;Wrase et al., 2007), very little research shows how familial alcoholism affects the brain response to alcohol-related cues— particularly in at-risk individuals who have yet to become dependent.



Animal research suggests that selective breeding for alcohol preference might affect the heavily dopaminergic mesocorticolimbic reward system. For example, rodents selectively bred to prefer alcohol have reduced dopamine in the striatum (see Murphy et al., 2002; Strother et al., 2005) and medial prefrontal cortex (Engleman et al., 2006), but greater striatal dopaminergic responses to alcohol itself (Bustamante et al., 2008; also see Smith & Weiss, 1999;Weiss et al., 1993). In at least one case, alcohol-preferring rats (compared to Wistar rats) showed a greater dopaminergic response in the ventral striatum during alcohol anticipation (Katner, Kerr, & Weiss, 1996). In non-abusive drinkers without a family history of alcoholism there is greater striatal dopamine receptor availability (Volkow et al., 2006), suggesting a potential protective factor.

Family history affects the brain’s response to alcohol’s olfactory (smell) cues in non-dependent, at-risk heavy drinkers and this study  sought to determine how acute alcohol exposure affects the reward system’s response to alcohol’s conditioned cues by using intravenous (IV) alcohol infusion— a method that prescribes a constant level of brain alcohol throughout functional imaging and avoids the highly variable time courses of breath alcohol concentrations that accompany oral consumption (O’Connor et al., 1998; Plawecki et al., 2007;Ramachandi et al., 2004; Ramchandani et al., 1999).

So in effect alcohol was infused rather than simply drunk.

The researchers hypothesized that a family history of alcoholism would be associated with stronger responses to alcoholic drink aromas in the mesocorticolimbic reward system, and that a low-level of steady-state brain exposure to alcohol would potentiate these stimulus-induced responses (Bragulat et al., 2008). Such a potentiation could reflect a possible substrate for priming, when alcohol exposure increases desire to drink (De WitDe Wit, 2000).

In this study (1) fourteen non-dependent heavy drinkers (HD) who were family history positive (FHP) participated, as did 12 HD who were family history negative (FHN). Subjects were imaged under both alcohol intoxication and placebo.

In this study alcohol intoxication dampened this “cued” response in the HD-FHP but potentiated (heightened)  it in the HD-FHN.

This suggests that a family history of alcoholism and brain exposure to alcohol interact in heavy drinkers to differentially affect how the brain responds to alcohol cues.

In conclusion, frontal regions thought to process reward value may respond differently to alcohol’s classically conditioned cues in subjects with a family history of alcoholism. While alcohol appears to dampen medial frontal responses to alcohol cues in HD-FHP, it may enhance it in HD-FHN. Genetic background may therefore determine when, and under what circumstances, cues activate the reward network


Kareken, D. A., Bragulat, V., Dzemidzic, M., Cox, C., Talavage, T., Davidson, D., & O’Connor, S. J. (2010). Family history of alcoholism mediates the frontal response to alcoholic drink odors and alcohol in at-risk drinkers. Neuroimage,50(1), 267-276.