Learning as the causeWatson and Rayner’s (1920) study, helps us understand the development of phobias by classical conditioning. This demonstrates, if we learn phobias, our learning experiences and environment dictate the development of phobias. Learning is supposedly the mechanism for developing irrational fear; a phobia. If fear is learned through stimulus-stimulus pairing by classical conditioning it can also be unlearned; this idea inspired reconditioning studies. It is important to evaluate the findings as information on little Albert is lacking after the study.Conditioning little AlbertWatson and Rayner (1920) claimed to condition a fear of white rats and associated objects in an eleven-month-old boy, little Albert.
Through classical conditioning, inducing fear of a previously neutral stimulus. They struck a metal bar making a loud noise which frightened him, while simultaneously presenting a white rat. The noise acted as an unconditioned stimulus as he already showed fear to this. Before conditioning they checked for pre-existing fears of white rats and other furry objects associated; he showed no fear. After seven conditioning trials over a period of weeks, he showed fear to the rat alone. The rat served as a conditioned stimulus causing a conditioned response; fear.
Watson (1920) chose him as he was a “stolid and unemotional” baby who rarely cried (p.1). An anxious child would have confounded the results as the acquisition of fear would have been easier and quicker with fewer trials. They intended to investigate what effect time would have on the fear response, and if fear generalised to similar objects; he feared objects associated with the rat e.g. Santa Claus mask. They intended to remove the fear but never did.
Fear or phobia? It is not known if little Albert maintained the fear. Fridlund, Beck, Goldie and Irons (2012) found he was Douglas Meritte, who died at age six of hydrocephalus. If so, we do not know of any long-term impact; he lived a short life. As he was so unemotional he may not have retained the fear thus devaluing the study. They had to continuously restore the fear, it would have reduced significantly if they did not keep conditioning him. His fear became weaker, thus showing learning may not be the only reason for phobias but a genetic predisposition. Not every person with a phobia experienced a traumatic event.
Seligman (1970) stated we are biologically prepared to associate stimuli with fear for survival. Little Albert lacks the strong responses we would perceive with a phobia, it takes him a lot to cry. Watson relied on his subjective interpretation of fear. An objective scale of fear should have been used as it seems he overestimated his fear; he shows weak fear.
Inducing fear in a “normal” child?There are visible social and communicative deficits in little Albert, which causes doubts in Watson’s (1920) judgements of healthy and normal. From his lack of responsiveness to stimuli that would normally cause a reaction in other infants e.g. fire, to lack of facial expression. He barely smiles and does not seek support from observers when distressed.
Physically, he is overweight and does not move much; far from normal. Even if Watson was not aware of any problems, it is clear from observation he is not normal. If Watson was oblivious to his deficits, he was also neglectful in not checking his medical history. If little Albert died of hydrocephalus, did the experiment exacerbate an underlying brain condition, or did it cause the brain condition? “We never saw him cry until after our experiments were made.” (Watson, 1930 p.
159). This suggests they induced impairment or exacerbated underlying problems; not protecting him from harm. If they knew of his condition they should not have continued as they did not know what damage they could cause. The most unethical action was not reconditioning him; due to removal by his mother. However, if she was well-informed about the study she would have wanted her son to be reconditioned.
They knew how much time they had with little Albert, this should have been prevented. To conclude, this study was unethical to not just condition fear and not remove it, but the possibility of inducing fear causing damage or exacerbating a pre-existing brain condition. Although beneficial for understanding the development of phobias, it does not offer a method for its removal. We do not have any information on long-term effects and whether he retained the phobia which provides weak evidence for learning in phobias.
However, through his suffering, this inspired reconditioning studies to develop treatments for thousands of phobia sufferers.