There’s an interesting study published in the British Medical Journal this week which concerns the relationship between use of drugs known as benzodiazepines and risk of dementia in elderly individuals [1]. Benzodiazepines are drugs which are usually used to treat anxiety and/or insomnia (diazepam – trade name Valium – is an example). In this study, benzodiazepine use was associated with about a 50 per cent increase in risk of dementia.
The authors of the study concluded that: “Considering the extent to which benzodiazepines are prescribed and the number of potential adverse effects of this drug class in the general population, indiscriminate widespread use should be cautioned against.”
It may indeed by the case that benzodiazepine drugs have the capacity to damage the workings of the brain and bring on dementia. This study does not prove this, however, because it is ‘epidemiological’ in nature. This means that the study has found an association between benzodiazepine use and dementia, but that does not mean that the drugs are causing the dementia. It might be that the real cause of the problem is other factors that are themselves associated with benzodiazepine use. In this study, some potential so-called ‘confounding factors’ were taken into consideration. However, this adjustment is an imprecise science and the end result is still something that only tells us that benzodiazepine use and dementia are linked.
Coincidentally, this week I came across a study in which dementia-prone mice (due to genetic glitches in their make-up) were subjected to exercise (running on a wheel), melatonin therapy (melatonin the chief brain chemical which regulates sleep) or both [2] Compared to no intervention at all, the mice subjected to one or both of the interventions over time ended up doing better in terms of learning, behaviour and memory.
Some researchers have previously put forward the theory that melatonin may help to counter the pathological processes thought to be involved in the development of Alzheimer’s disease [3]. Noting in nailed down in this area just yet, but the possibility exists that low melatonin levels may predispose to dementia. Of course, low melatonin levels will also predispose to insomnia too. So, might the association between benzodiazepine use and dementia be, at least in part, because those with melatonin ‘deficiency’ are more likely to suffer from insomnia and more likely to be treated with benzodiazepines as a result?
We’re unlikely ever to be able to unravel this, but I do think it’s good that the role of melatonin in health appears to have attracted more interest in recent years. Melatonin secretion is responsive to light. Getting decent light exposure in the day (particularly the morning) is one way to ensure enough melatonin is made when the evening comes. However, as I discussed recently here, light exposure in the evening (from room lighting or electronic devices) has the capacity to suppress melatonin secretion. Keeping light exposure low in the hours before bed may therefore promote good sleep and might possibly help us maintain our mental faculties as we age too.
References:
1. Billioti de Gage S, et al. Benzodiazepine use and risk of dementia: prospective population based study BMJ 2012; 345 doi: 10.1136/bmj.e6231 (Published 27 September 2012)
2. García-Mesa Y, et al. Melatonin plus physical exercise are highly neuroprotective in the 3xTg-AD mouse. Neurobiology of Aging, 2012; 33 (6): 1124
3. Rosales-Corral SA, et al. Alzheimer’s disease: pathological mechanisms and the beneficial role of melatonin. J Pineal Res. 2012 Mar;52(2):167-202
