“Heart pills taken by millions of people in Britain could dramatically reduce the risk of dementia,” the Daily Express reports.
A study from Taiwan has found an association between the use of statins (cholesterol-lowering drugs) and reduced dementia risk.
In this large study of older adults, researchers recorded people’s first prescription of statins and looked at their later development of dementia – comparing statin users with non-statin users.
Over an average five-year period, statin use was associated with a 22% reduced risk of dementia. Risk reduction was greater among females than males, and greatest with high-dose statins and with statin use for more than three years.
However, this type of study cannot definitely prove cause and effect – only an association. The researchers also attempted to adjust for factors that could influence any association, such as history of heart disease. But this still may not fully account for these, or other, factors that may be involved in the relationship.
And because it studied Taiwanese people, its results cannot be directly generalised to other populations, such as those of the UK.
Overall it is not clear whether statins definitely reduce the risk of dementia, and if they do, how it is they act to reduce risk. Also it is not known whether they may reduce risk of all dementias, or only specific types.
Where did the story come from?
The study was carried out by researchers from National Yang Ming University, Taipei and other institutions in Taiwan. The study was supported by the National Science Council Taiwan and published in the peer-reviewed medical journal International Journal of Cardiology.
The Daily Express’s reporting on the study is broadly accurate, but does not consider the limitations of this research.
What kind of research was this?
This was a population-based cohort study.
The study included over 33,000 people aged over 60 years from Taiwan and looked back at whether dementia developed in people who were and were not prescribed statins.
The researchers say that there has been some controversy in past research over whether there is any link between statin use and risk of dementia, and Alzheimer’s disease in particular.
The main limitation of this study, as with all cohort studies, is that it can demonstrate an association, but it cannot definitely prove cause and effect.
The study has adjusted for a number of potentially contributing factors (confounders) that could be influencing the association including:
- sociodemographic variables
- various long-term medical conditions coded in medical records (for example high blood pressure, heart disease, stroke, diabetes, and liver and kidney disease)
Still, this may not fully account for these or other health or lifestyle factors that may be involved in the relationship; especially for such a complex condition as dementia.
What did the research involve?
The research used the Longitudinal Health Insurance Database 2000, which includes a randomly sampled group of 1 million individuals included in Taiwan’s National Health Insurance Research Databases (NHIRD) between 1996 and 2010. The NHIRD contains registration information, claims data, and information on clinical visits, diagnostic codes for diseases (according to the International Classification of Diseases) and prescription details.
For the purposes of this trial they included only people above the age of 60 years, who had not had a statin prescription or dementia diagnosis in the three years prior to the start of the cohort. They excluded people who had been diagnosed with dementia prior to prescription of statins.
Statin use was defined as receipt of at least one prescription of statins in the cover period of cohort.
Statin users were each matched by age and gender to a person who was not taking statins. The researchers recorded statin use:
- by individual drug
- by mechanism of drug action
- according to duration of use
New cases of dementia were defined as the first time a diagnostic code was given for any type of dementia, from the date of the statin prescription onwards to the end of the study in 2010. However, they excluded from their analyses anyone diagnosed with dementia within one year of statin prescription, or who had less than one year of follow-up.
The researchers considered many potential confounders, including age and various sociodemographic factors recorded at the time the statin was first prescribed. They also took into account various diseases recorded at the time that the statin was prescribed (such as high blood pressure, heart disease, stroke, diabetes, and liver and kidney disease).
What were the basic results?
Just over half of the 16,699 statin users and their 16,699 non-statin-using comparison group were female. The average follow-up time was five years.
Comparing sociodemographic and health characteristics, there were few significant differences between the statin users and non-users. An exception to this was age and history of chronic diseases such as high blood pressure.
Overall, the incidence of dementia was lower among the statin users than non-users, which calculated to statin use being associated with a 22% reduced risk of dementia (hazard ratio [HR] 0.78, 95% confidence interval [CI] 0.72 to 0.85).
The risk reduction with statin use was greater for women (24%) than men (14%).
When looking at the type of statin, risk reduction was greatest with high-dose statins, and with use for more than three years.
However, on sub-analyses by type of dementia, the only significant association was found between statin use and any type of dementia with the exclusion of vascular dementia. There was no significant association between statin use and Alzheimer’s disease specifically, or statin use and vascular dementia specifically.
How did the researchers interpret the results?
The researchers conclude that: “Statin use was associated with a significantly lower risk of dementia in the elderly patients in Taiwan. The potency and the cumulative duration of statin utilised played critical roles.”
This study using a large, older age, Asian population finds an association between statin use and reduced risk of developing dementia over an average five years of follow-up.
The main limitation of this study is that it can demonstrate an association, but it cannot definitely prove cause and effect. The study has adjusted for a number of measured confounders, but this may not fully account for these or other factors (such as lifestyle habits) that may be involved in the relationship.
Also, while the research has used what can be expected to be a fairly reliable research database, there is also the possibility for some of these health variables to have been inaccurately coded. In particular, there may be inaccurate assumptions around the use of statins. However, statin use was based on first recorded prescription and duration of prescription, we do not know for definite whether the person actually took them as described.
And as the study population was Taiwanese, the results cannot be generalised to other populations who may have socioeconomic, health and lifestyle differences and different dementia risk.
Overall, these results suggest a possible beneficial effect of statins in reducing risk of dementia, but the possible biological mechanism is not clarified.
It may be expected that statin use could be associated with risk of vascular dementia, through both statin prescription and vascular dementia having a common cardiovascular risk association.
However, surprisingly, no specific association was found between statin use and vascular dementia. Statins were only found to reduce risk of dementia when vascular dementia was excluded. Also, no association was found specifically with Alzheimer’s disease, which is the most common type of dementia and which has no firmly established cause (age and genetics being the most associated risk factors).
So, overall, the possible association between statin use and dementia risk needs to be further studied and clarified.
Until then, statins are not licensed as a possible preventative treatment for dementia. Statins should only be used within their licensed indication for reduction of cholesterol in people considered to be at risk of cardiovascular disease.