Blood Alcohol Concentrations (BAC) and blackouts
        Drinking large quantities of alcohol often precedes blackouts, but several other factors also appear to play important roles in causing such episodes of memory loss. As Goodwin and colleagues (1969a) stated with regard to subjects in one of their studies, "Although blackouts almost always were associated with heavy drinking, this alone seemed insufficient to produce one. On many other occasions, subjects said they had drunk as much or more without memory loss" (p. 195). Among the factors that preceded blackouts were gulping drinks and drinking on an empty stomach, both of which lead to rapid rises in BAC.  In other words, drinking in this way results in a lot of alcohol getting into the body very fast. As we will discuss in the section on brain function and blackouts, flooding the system with alcohol quickly might catch critical brain regions unprepared, thus essentially knocking them offline for a while.
       Subsequent research provided additional evidence suggesting a link between blackouts and rapidly rising BACs. Goodwin and colleagues (1970) examined the impact of acute alcohol exposure on memory formation in a laboratory setting. The author recruited 10 male subjects for the project, all but one through the unemployment office in St. Louis, Missouri. Most subjects met diagnostic criteria for alcoholism and half had a history of frequent blackouts. The men were asked to consume roughly 16 to18 ounces of 86-proof bourbon in approximately 4 hours. Beginning 1 hour after subjects began drinking, memory was tested by presenting subjects with several different stimuli, including a series of children's toys and scenes from erotic films. Subjects were asked to recall details regarding these stimuli 2 minutes, 30 minutes, and 24 hours after the stimuli were shown. Half of the subjects reported no recall for the stimuli or their presentation 30 minutes and 24 hours after the events, though most seemed to recall the stimuli 2 minutes after presentation. Lack of recall for the events 24 hours later, while sober, represents clear experimental evidence for the occurrence of blackouts. The fact that subjects could remember aspects of the events 2 minutes after they occurred but not 30 minutes or 24 hours afterward provides compelling evidence that the blackouts stemmed from an inability to transfer information from short-term to long-term storage.  For all but one subject in the blackout group, memory impairments began during the first few hours of drinking, when BAC levels were still rising. The average peak BAC in this group occurred approximately 2.5 hours after the onset of drinking and was roughly 0.28%.
       In a similar study, Ryback (1970) examined the impact of alcohol on memory in seven hospitalized alcoholics given access to alcohol over the course of several days. All subjects were white males between the ages of 31 and 44. Blackouts occurred in five of the seven subjects, as evidenced by an inability to recall salient events that occurred while drinking the day before (e.g., one subject could not recall preparing to hit another over the head with a chair). Estimates of BAC levels during blackout periods suggested that they often began at levels around 0.20% and as low as 0.14%. The duration of blackouts ranged from 9 hours to 3 days. Based on his observations, Ryback concluded that a key predictor of blackouts was the rate at which subjects consumed their drinks. He states, "It is important to note that all the blackout periods occurred after a rapid rise in blood alcohol level" (p. 622). The two subjects who did not black out, despite becoming extremely intoxicated, experienced slow increases in blood alcohol levels.