Question: Is long-term treatment with benzodiazepines (BDP) associated with an increased risk of dementia in the elderly?
Background: Elderly people are often treated with benzodiazepines. It is known that these drugs can impair attention and memory. Some studies have even suggested that long-term treatment with benzodiazepines increases the risk of dementia. However, because the onset of dementia can be associated with sleep disturbances, anxiety, and depression – symptoms that are often treated with benzodiazepines – these studies may have been based on apparent causality.
PATIENTS AND METHODS: There were 3434 participants (from Seattle, USA) enrolled in this prospective, population-based cohort study and followed up for a mean of 7.3 years. All were at least 65 years old at baseline and without dementia symptoms. All had to have computerized pharmacy data on drug prescriptions for the preceding ten years. Assessments (at baseline and every two years) were conducted with a standardized clinical interview.
Results: During the observation period (7.3 years), 23.2% of participants developed dementia, the majority of which was Alzheimer-type dementia. In relation to the cumulative amount of benzodiazepines consumed, the following was found: Overall dementia risk was slightly but significantly increased at low levels of BDP (hazard ratio 1.25; 95% CI 1.03-1.51). The same was true for the risk of developing Alzheimer’s dementia specifically (HR 1.27; 95% CI 1.03-1.57). In contrast, no increased risk of dementia was found with moderate and high BDP use.
Authors’ conclusions: In the elderly, low levels of BDP are associated with a slightly increased risk of dementia. This relationship is probably based on an apparent causality, namely that sleep disturbances – a prodromal symptom of dementia – are preferentially treated with BDP. Intermediate and higher levels of BDP are not associated with altered dementia risk. Thus, a causal relationship between BDP use and dementia cannot be substantiated.
Comment: Benzodiazepines not only have an antianxiety and sleep-promoting effect, they sometimes also have an amnesic effect. But does that already make them “dementia-inducing”?
A Canadian study from 2014 affirmed this (see issue 4/2016). There, the association between a high cumulative dose of BDP with an increased risk of Alzheimer’s disease had been confirmed. So why not here too? Methodological deficiencies do not jump to mind as an explanation. It was studied prospectively, the case number was large and population-based, the BDP quantities were from documented prescriptions, and participants were followed for a sufficiently long period and assessed for dementia symptoms every two years. A connection was found where it was not expected – in the small BDP quantities. Should we therefore prefer the large quantities in terms of dementia risk? Of course not! There are enough other reasons to be cautious about BDP.
The present study finds no association between moderate or high levels of BDP and the risk of developing dementia. This is reassurance, but not an all-clear, because “lack of evidence” is far from being “evidence of lack.”
InFo NEUROLOGY & PSYCHIATRY 2016; 14(5): 33.
