The new issue of *British Medical Journal* includes an article: “Benzodiazepine use and risk of Alzheimer’s disease: case-control study.” In case you are not familiar with the terms Benzo’s are among the most common drugs used to treat anxiety and stress. They include: Xanax, Ativan, Klonopin, Valium, and Librium.
“Researchers followed a group of elderly adults who take Valium, Xanax or similar medications to treat insomnia and anxiety. Those who took these drugs for longer than three months were 51 percent more likely to develop Alzheimer’s disease.”
The study looked at the medical records of more than 1,700 Alzheimer’s patients over the age of 66 and 7,000 similar people without Alzheimer’s. Researchers found those who had taken the drugs over long periods of time were far more likely to be in the Alzheimer’s group.
To be clear, those involved in the study had been using benzodiazepine at least five years before they were diagnosed with Alzheimer’s.
Researchers seem confident benzodiazepine use is associated with an increased risk of Alzheimer’s, writing in the study, “The stronger association observed for long term exposures reinforces the suspicion of a possible direct association.”
Here’s how the article opens: Dementia is currently the main cause of dependency in older people and a major public health concern affecting about 36 million people worldwide.1 Because of population growth and demographic ageing, this number is expected to double every 20 years and to reach 115 million in 2050,1 resulting in tragic human consequences and social costs. As there are no effective treatments, the search for putative modifying factors remains a priority. Several studies have shown that benzodiazepine use could be one of these. This class of drugs is mainly used to treat anxiety or insomnia.10
Prevalence of use among elderly patients is consistently high in developed countries and ranges from 7% to 43%. International guidelines10 recommend short term use, mainly because of withdrawal symptoms that make discontinuation problematic. Although the long term effectiveness of benzodiazepines remains unproved for insomnia and questionable for anxiety, their use is predominantly chronic in older people.19
While the acute deleterious effects of benzodiazepines on memory and cognition are well documented, the possibility of an increased risk of dementia is still a matter of debate. The frequency of symptoms highly correlated with prescription of benzodiazepines (anxiety, insomnia, and depressive disorders) increases in the years before a diagnosis of dementia. Hence, benzodiazepines might not cause the disease but rather be prescribed to treat its prodromes. Adjustment for such a reverse causality bias is not easy in observational studies as prodromes are often not recorded as such. It might consist in the demonstration of a delayed risk or in the censoring of information on exposures started during the suspected prodromal phase. Moreover, few studies published on the topic have had sufficient power to investigate a cumulative dose relation, which is a compelling argument in the assessment of a potentially drug induced outcome.
We evaluated the association between past benzodiazepine use and the risk of Alzheimer’s disease using an administrative claims database with a long follow-up period and investigated the potential dose-effect relation.”
Another excerpt: “1796 people with a first diagnosis of Alzheimer’s disease and followed up for at least six years before were matched with 7184 controls on sex, age group, and duration of follow-up. Both groups were randomly sampled from older people (age >66) living in the community in 2000-09.”
Here’s how the Discussion section opens: “This case-control study based on 8980 individuals representative of elderly people living in the community in Quebec showed that the risk of Alzheimer’s disease was increased by 43-51% among those who had used benzodiazepines in the past. Risk increased with density of exposure and when long acting benzodiazepines were used. Further adjustment on symptoms thought to be potential prodromes for dementia–such as depression, anxiety, or sleep disorders–did not meaningfully alter the results.”
Another excerpt: “Our findings are congruent with those of five previous studies, two of which explored the modifying effect of the dose used.”
The study is provided online courtesy of Ken Pope at:
<http://bit.ly/KenPopeStudyOfBenzosAndAlz>
In all fairness, it’s not clear whether the drugs are a primary cause or AD or secondary. Since these drugs are used to treat ailments like prolonged stress, depression and insomnia, which other research has shown can contribute to Alzheimer’s. However, this study does suggest that rather than reducing the risk caused by these ailments, these drugs may be magnifying that risk – likely through the depletion of other brain essential nutrients such as the B-vitamins.
The study says “unwarranted” long term use should be a “public health concern.” That could be worrisome, as millions of people take these types of drugs daily.
See the other articles in this section on the underlying biological factors that contribute to stress and depression, and healthy ways of meeting the brain’s needs in this regard.
p.s. One new natural formulation with good potential for replacing these, or helping a person come off anti-anxiety meds, is Natural Stress from Life Extension. This actually addresses the same calming neurotransmitters but does so in a more natural less addicting way. Click here to learn more.
Dave Larsen, MFHD
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