Affective instability is a psychophysiological symptom observed in some psychopathologies. It is a complex construct that encompasses (1) primary emotions, or affects, and secondary emotions, with each category having its own characteristics, amplitude, and duration, (2) rapid shifting from neutral or valenced affect to intense affect, and (3) dysfunctional modulation of emotions. Affective instability is often confused with mood lability, as in bipolar disorders, as well as with other terms. To clarify the concept, we searched databases for the term affective instability and read related articles on the topic. In this article we situate the term within the current affective nomenclature and human emotional experience, explore its psychophysiological features, and place it within the context of psychopathology. We explain why the term can potentially be confused with mood pathology and then define affective instability as an inherited temperamental trait modulated by developmental experience.

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78 subjects who had participated in experiments involving deception and the use of aversive contingencies were interviewed and completed a questionnaire concerning their reactions to the study. Of the subjects, 20% were “bothered” by some aspect of the experiment. Subjects' dissatisfaction was greatest and lasted longest for issues other than deception and the use of aversives.

Two studies were conducted to examine the interaction between sucrose and ethanol in normal young fasting adult males. The first experiment employed a 3 (100 g sugar, 35 g sugar, 0 g sugar) x 3 (alcohol, placebo and sober) factorial design, which was carried out double-blind using aspartame to ensure that all the drinks were equally sweet. Subjects were tested for mood, memory, subjective intoxication and psychomotor performance at baseline and at times up to 3.5 h after ingestion of the drinks. An alcohol by sugar interaction was seen at 0.5 after drinking. Sugar attenuated alcohol intoxication at this time without influencing blood alcohol levels. Contrary to previous reports, the combination of alcohol and sugar failed to produce significant hypoglycemia, or any of the adverse behavioral effects associated with hypoglycemia, at later times after drink ingestion. The second experiment involved a simpler design, carried out single-blind in which the subjects receiving no sugar did not get aspartame. This was to rule out the possibility that aspartame was exacerbating alcohol intoxication instead of sugar attenuating it. The second experiment also showed that sugar can attenuate alcohol intoxication in fasting humans without altering blood alcohol levels significantly.

Forty-eight male subjects participated in an aggression task after having received either alcoholic or placebo beverages and after being told that they had received either a high dose or low dose of alcohol. All subjects in the alcohol group actually received the same dose. Measures of aggression were the intensity and duration of shock given to a bogus partner in a reaction time-pain perception task and a score on a posttask attitude questionnaire. Blood alcohol readings were taken three times during the session, and a locus of control scale was administered before and after drinking. For subjects in the alcohol conditions, blood alcohol levels averaged .079% before the task and .085% upon completion of the task. Alcohol resulted in higher aggression scores only on the questionnaire measure, and an interaction between drug and attribution was found for the measure of shock duration. Attribution alone resulted in greater aggression on the measure of shock intensity. Subjects in groups where the attribution was discrepant with the drug condition were the most aggressive on the measures of both shock intensity and duration. These subjects became more external, reflecting a high correlation between their aggression and a stimulus tone. The results of this study suggest that a person's increased aggressiveness when intoxicated results from an interaction situation between alcohol and an alteration in responsivity to provoking stimuli.