Smoking and Dementia: Exploring the Studies

Studies surrounding nicotine and reduced dementia risk and improved learning and memory have sparked interest in many people. However, smoking cigarettes significantly increases the risk of cardiovascular disease—a well-known risk factor for dementia development. In fact, the World Health Organization estimates that as many as 14% of Alzheimer’s disease cases worldwide are potentially attributed to smoking. 

Many questions remain regarding the relationship between smoking and dementia risk. In this article, we will evaluate research surrounding smoking and dementia, highlighting the limitations of current research and the path toward a greater understanding of this relationship.

Smoking and Dementia Risk

While several studies have linked nicotine with improved cognitive function and reduced dementia risk, it seems the harmful effects of cigarette smoking may outweigh the potential beneficial effects of nicotine. According to the 2020 Lancet Commission on dementia prevention, intervention, and care, smoking is the third largest modifiable risk factor for dementia. In later life, smoking was found to be the top modifiable risk factor for dementia.

A growing number of studies have linked smoking to an increased risk of the two most common causes of dementia: Alzheimer’s disease and vascular dementia. 

Smoking, Alzheimer’s Disease, and Vascular Dementia

Although the prevalence of cigarette smoking appears to be declining, there are still approximately 1.1 billion smokers around the globe. Understanding the relationship between smoking, cognitive decline, and dementia risk and raising awareness will be important for reducing the prevalence of smoking and, consequently, the incidence of dementia.

A meta-analysis of prospective studies (with at least 12 months of follow-up) found that current smokers at baseline, relative to never-smokers, had a risk ratio of 1.79 for Alzheimer’s disease, 1.78 for vascular dementia, and 1.27 for all-cause dementia.

A more recent meta-analysis of prospective studies found that current smokers, compared to never-smokers, had a risk ratio of 1.4 for Alzheimer’s disease, 1.38 for vascular dementia, and 1.3 for all-cause dementia. For all-cause dementia, the risk increased by 34% for every 20 cigarettes smoked per day. They also found that former smokers did not show an increased risk for all-cause dementia, indicating that smoking cessation may reduce the risk of dementia to that of never-smokers.

The association between smoking and dementia risk is believed to be due in part to the link between smoking and the cardiovascular system. Because smoking increases the risk of stroke, cerebrovascular and cardiovascular disease, silent infarction, and atherosclerosis as well as increased oxidative stress and inflammation, smoking may impact the development of dementias such as vascular dementia and Alzheimer’s disease. 

Secondhand Smoke and Dementia Risk

Worldwide, an estimated 35% of non-smoking adults and 40% of children are exposed to secondhand smoke. Additionally, vulnerable people are disproportionately affected by secondhand smoke exposure due to having less control over their living and working conditions. Thus, understanding the impact of secondhand smoke exposure on dementia risk will be important for informing global and national strategies to reduce dementia incidence.

Although there are minimal studies analyzing the effects of exposure to secondhand smoke on dementia risk, preliminary studies are giving us some clues. One study found that moderate and high secondhand smoke exposure levels were not independently associated with dementia risk, where moderate exposure was defined as 16-25 years and high exposure was defined as greater than 25 years. However, they did find that those with high exposure and greater than 25% carotid artery stenosis had a 3-fold increase in dementia risk compared to those with no or low exposure (0-15 years).

A cross-sectional analysis of a national population-based study found that exposure to secondhand smoke may be associated with increased odds of cognitive impairment, with those with higher cotinine concentrations being at a higher risk of cognitive impairment compared to those with lower cotinine concentrations. Together, these studies suggest a possible dose-response risk, though further research is needed to confirm this relationship.

Limitations of Research Surrounding Smoking and Dementia

While a large body of research indicates that smoking increases dementia risk, these studies don’t come without limitations. Limitations of current research include the following:

• Many risk factors for dementia that are related to lifestyle behaviors are difficult to isolate. There are several potential overlapping risk and protective factors that may influence study results. Smoking is associated with other lifestyle, dietary, and social factors. For example, people who smoke are more likely to use other substances, such as alcohol. Alcohol consumption (>21 units/week) is a known risk factor for dementia. 
  
  Additionally, smoking is more prevalent among those with lower levels of education and less education is a known risk factor for dementia. While adjustment factors for such situations can be utilized, many studies surrounding smoking and dementia do not adjust for these overlapping factors, whether due to limitations in available participant data or study design.

• For many of these studies, smoking status is determined via a questionnaire, meaning it may not perfectly reflect the status of each participant. Additionally, exposure to secondhand smoke was not included in the majority of these studies which may slightly skew study results.

• There are more than 7,000 chemicals in tobacco smoke, with at least 250 known to be harmful. This makes it difficult to understand the specific chemical(s) influencing dementia risk.

• Many studies assessing the relationship between smoking and dementia rely on outdated pencil and paper or computerized neuropsychological assessments, such as the Mini-Mental State Examination (MMSE), for outcome measures. These assessments only test a small subset of neurocognitive domains and often produce noisy, highly variable data that lacks the specificity and granularity needed to determine dementia outcomes.

Although many of these limitations are difficult to eliminate, there are ways to improve clinical research in this space by utilizing newer neuropsychological assessment tools that assess a greater breadth of neurocognitive domains, offer high accuracy and reliability, and produce more granular data. Oftentimes, this can be accomplished by utilizing digital endpoints. Digital endpoints have the potential to offer previously inaccessible precision and accuracy and provide new, previously unattainable insights about the relationship between smoking and dementia.