Drug-related blackout is a phenomenon caused by the ingestion of any substance or medication and thus results in impairment of short-term or long-term memory, due to the complete inability to recall the past. Blackout is often described as having similar effects to anterograde amnesia in that the subject cannot recall any events after the event that caused the amnesia. EM Jellinek conducted research on alcohol-related blackout in the 1940s. Using data from a survey of Alcoholics Anonymous members, he came to believe that blackout would be a good marker of alcoholism. However, there are conflicting opinions as to whether this is true. The negative psychological effects of alcohol-related blackout are often increased by those with anxiety disorders. Liver dysfunction will also allow more alcohol to reach the brain and accelerate the individual's loss of consciousness. The term "blackout" can also refer to a complete loss of consciousness, blackout, or coma. Several studies have led to evidence of links between general alcohol consumption and its effects on memory capacity. These studies have shown in particular how a drunk or intoxicated person makes fewer connections between words and things than a normal person would. Studies of blackouts have later suggested that alcohol specifically impairs the brain’s ability to take short-term memories and experiences and transfer them to long-term memory. It is a common misconception that blackouts generally only occur in alcoholics; however, research suggests that individuals who engage in binge drinking, such as many college students, are also at risk. In a 2002 survey of college students by researchers at Duke University Medical Center, 40% of those surveyed who had recently consumed alcohol reported experiencing blackouts in the previous year. In one study, a sample of individuals was collected and divided into groups based on whether or not they had experienced partial blackouts within the past year. The groups were also divided based on those who had received alcohol and those who had not. In their drinking challenge, participants were given one drink for ten minutes until they achieved a target blood alcohol level of 0.08%. Drinks for the alcohol condition contained a 3:1 ratio of mixer to vodka. After 30 minutes, exhaled breath samples were recorded and recorded every 30 minutes thereafter. On a narrative recall test, those who received alcohol and FB+ recalled fewer narrative details after a 30-minute delay but there were no significant interaction effects. The following day, participants were recalled and tested on their narrative recall and cue recall. The results were that those who had consumed alcohol showed lower 30-minute delayed recall and next-day recall than those who had not consumed alcohol, but there were no significant effects on detail recall. Their study also revealed that those who had also consumed FB+ and alcohol performed worse on contextual recall than other participants. Alcohol impairs delayed recall and next-day narrative but not full cue recall the next day, suggesting that the information is available in memory but temporarily inaccessible. Those with a history of partial blackouts also performed worse on delayed recall than those who had not had previous blackouts. Neuroimaging shows that deleted recall and free recall are associated with differential neural activation in distinct neural networks: sensory and conceptual or imaginative. Together, these findings suggest that the differential effects of alcohol on free and emergent recall may be the result of a substance altering neural activity in conceptual networks rather than sensory networks. Previous experiences of unconsciousness also appear to be associated with impaired conceptual networks. Unconsciousness can be broadly divided into two categories, “global” unconsciousness and “partial” unconsciousness. Unconsciousness is generally characterized by the inability to recall any memories from the period of intoxication, even when prompted. These unconsciousness states are also characterized by the ability to easily recall things that happened within the last two minutes, with an inability to recall anything prior to this period. As such, a person experiencing global unconsciousness may not appear to do so, as they can carry on conversations or even perform difficult feats. The end of this type of unconsciousness is difficult to determine, as sleep usually occurs before the end of the sleep period, although it is possible for global unconsciousness to end if the sufferer stops drinking in the meantime. Fragmentary loss of consciousness is characterized by a person having the ability to recall specific events from a period of intoxication, yet not realizing that other memories are missing until reminded of the presence of these 'gaps' in the memory. Research suggests that such cases of partial loss of consciousness are more common than global loss of consciousness. Memory impairment during acute intoxication involves a disruption of episodic memory, a type of memory encoded by spatial and social context. Recent studies have shown that there are multiple memory systems supported by separate brain regions, and that the acute effects of alcohol, learning and memory, may result from alterations in the hippocampus and related structures at the cellular level. A rapid increase in blood alcohol concentration is consistently associated with the likelihood of loss of consciousness. However, not all subjects experience loss of consciousness, suggesting that genetic factors play a role in determining the susceptibility of the central nervous system to the effects of alcohol. The former may predispose an individual to alcoholism, as altered memory function during intoxication may affect an individual's anticipation of alcohol; one may perceive the positive aspects of intoxication while inadvertently ignoring the negative aspects.