The Daily Mail has reported that “a drug which appears to erase painful memories has been developed by scientists”. It said that bad memories were erased with beta-blocker drugs, which are usually prescribed to patients with heart disease. The newspaper said the treatment could help those with post-traumatic stress disorder (PTSD), which is caused by witnessing frightening or distressing events. It also warned that experts had said that the “breakthrough raises disturbing ethical questions about what makes us human”.
The relevance of this finding to the treatment of people with PTSD is limited. The study lasted three days, during which 60 healthy volunteers were ‘conditioned’ to feel fear by associating pictures of spiders with small electric shocks to the skin. The study found that subjects who were given a beta-blocker drug had less of a fear response when they were shown the picture again without the shock. Saying the drug ‘permanently erased painful memory’ is an overstatement, particularly as the study reports that the factual aspect of the memory (remembering that exposure had happened) remained intact.
More research is needed before the effects in vulnerable groups who have experienced extreme psychological trauma are known.
Dr Merel Kindt, Marieke Soeter and Bram Vervliet from the University of Amsterdam carried out this study. The research was funded by a Vici grant from the Netherlands Organization for Scientific Research. It was published in the peer-reviewed medical journal Nature Neuroscience .
Emotional memories are memories that are associated with emotionally charged situations, such as ones of stress or fear. The researchers say that once emotional memories are established, they appear to last forever. They maintain that even the most effective treatments only eliminate the fear response and do not get rid of the actual fearful memory. This leaves a person open to relapsing after apparently successful treatment. They say that if emotional memory “could be weakened”, then it might be possible to eliminate the root of disorders, such as PTSD, where recall of events is associated with extreme anxiety.
When a memory is converted from short-term to a long-term memory, the process is referred to as ‘consolidation’. The reactivation of a consolidated memory is called ‘reconsolidation’. The researchers say that reconsolidation of a fear memory can be affected by certain factors around the time of reactivation, and that the beta-blocker propranolol may have an effect. In this study, the researchers investigated these effects on recall of an emotional memory.
The researchers enrolled 60 students between 18 and 28 years of age from the University of Amsterdam. The participants were randomly allocated to receiving either the beta-blocker propranolol or placebo.
All the subjects took part in a series of complex experiments over a three-day period. In summary, the first day involved the subjects being shown pictures of spiders while being given electric shocks. This was designed to condition them to experience fear in response to these stimuli.
On the second day, the participants were given either the beta-blocker or placebo, and their blood pressure and anxiety levels were measured using a validated assessment scale. They were then exposed to one of the spider pictures from the previous day with the aim of reactivating the fear memory.
On the third day, ‘extinction’ experiments were carried out to decrease the conditioned fear response, that is to weaken the association between the pictures and the shocks. This was done by exposing the participants to spider images without the associated electric shocks. The researchers believed that the beta-blocker was likely to have cleared from the subjects’ systems by this point. They then tested the subjects’ response to pictures without the shocks, to three unexpected shocks and to more pictures and startles with noise and no shock.
The ‘startle response’ (eyeblink in response to a loud noise) was used to compare the fear response between treatment groups.
In terms of ‘fear learning’, there was no difference between the propranolol and placebo groups. During the fear reactivation experiments on day two, the groups had similar startle responses. The researchers also found that the fear memory was equally well consolidated in the two groups.
Following extinction of the fear association (on day three), the participants on propranolol appeared to have a reduced startle response when they were re-exposed to the spider pictures. Exposure to the trigger of the fear memory had less of an effect in those taking propranolol than placebo, i.e. the expression of the original fear memory was not reinstated.
The researchers conclude that beta-blockers weaken the fear response when given before reactivation of a fear memory.
They say that the finding that reinstating the fear memory did not produce a fear response suggests that either the memory was erased or it was not possible to retrieve it. They have a theory that beta-blockers may “selectively disrupt the protein synthesis of the amygdalar fear memory” while leaving the factual memory intact.
This is a small and complex study in healthy volunteers. Its findings have been over-simplified by the media. It is too early to suggest that the findings could be used to treat people with PTSD, a serious anxiety disorder resulting from exposure to extreme psychological trauma.
Although some newspapers have focused on the possible “ethical furore over drugs that threaten human identity”, these worries could be considered premature given the early stage of the research. Some professionals have expressed concern about the relevance of the study and the_ Daily Mail_ and the BBC quote Professor Neil Burgess from the Institute of Cognitive Neuroscience: “All they've shown so far is that the increased ability to startle someone if they are feeling a bit anxious is reduced.”
The newspapers also reported that a drug has been developed, but this is not the case. Beta-blockers, in particular propranolol, are long-established and widely used drugs that reduce the force and rate of heart contraction. They are not without risks and require careful monitoring. They are also not suitable drugs for everyone, particularly people with asthma and certain heart conditions. It is important that there is further testing of such treatments before they are used more widely.