Introduction: Dementia Prevention, Intervention, and Care
The Lancet Commission on Dementia Prevention, Intervention, and Care, in partnership with too many organizations to list in this article, met to compile the research showing progress in knowledge of what can be done to prevent and manage dementia. The conclusions of the Commission are presented in a 2017 guidance document that represents the state of the field on this topic. Briefly, the key messages and recommendations for medical, social, and support care are very focused on providing interventions and care once a diagnosis has been reached, with only minimal attention given to preventing it. Prevention interventions address known modifiable risk factors for dementia which vary by life stage and include:
- Early life (age <18 years): Less Education
- Midlife (age 45-65 years):
- Hearing loss
- Later life (age > 65 years):
- Physical inactivity
- Social isolation
Reducing these risk factors could potentially delay or prevent a third of dementia cases. Most of the recommendations contained in the document are about management and treatment of dementias. The emphasis on managing rather than preventing the condition may have to do with the fact that until recently dementia was viewed as neither preventable nor treatable. Emerging research is beginning to clarify that dementia is both manageable and preventable. Research is also showing dementia of all types is extremely complex to address from the prevention standpoint and yet modifiable risk factors do exist. The result is a focus on brain resilience, or cognitive reserve and on strategies to reduce risk factors in those areas or for other known and modifiable risk factors.
New Research on the Effects of Alcohol on the Brain
This is where alcohol and other drugs have begun to enter the picture. In the Lancet document it states that there are many different types of dementia, including Alzheimer’s disease, the most common; vascular dementia; dementia with Lewy bodies; mixed dementia; frontotemporal degeneration; and dementias associated with brain injury, infections, and alcohol abuse, which are less common (Livingston, et al, 2017). This is interesting because the less common forms of disease often have a less broad knowledge base due to the existence of less research. A key point is that alcohol use can lead to alcohol-related dementia, which implies alcohol in some amount has an impact on the development of dementia. In the discussion of interventions to prevent dementia by addressing known and modifiable risk factors, the lack of data on the connection between alcohol and dementia is hinted at: “We do not have data to include dietary factors and alcohol in our calculations, but we believe that they could be important.” And in describing risk factors not included: “We have not incorporated other potential risk factors, such as diet, alcohol, living near major roads, or sleep, which could be relevant. Therefore, the potentially preventable fraction of dementia might be underestimated in our figures.” How little research into the connection between dementia and alcohol is evident in the fact that the word alcohol is used just four times in the 63-page document (Livingston, et al, 2017). The studies described below are an example of the type of research that may lead to alcohol (and other drugs) being recognized as another “known and modifiable” risk factor for dementia.
Patterns of Regional Cerebral Blood Flow as a Function of Age Throughout the Lifespan
In this recent study, researchers analyzed 62,454 brain SPECT (single photon emission computed tomography) scans of more than 30,000 people aged nine months to 105 years old to identify factors that contribute to brain aging. Their analyses of blood flow in 128 brain regions was used to predict chronological age (CA) and brain estimated age (BEA). Accelerated brain aging was considered to be present when the age predicted by the scan (BEA) was older than the actual chronological age (CA). Findings showed that certain disorders such as depression, dementia, substance use, and anxiety increased brain aging, with the greatest impacts being on:
- those with schizophrenia, whose brains measured as 4 years older than chronological age;
- those who misused cannabis, whose brains measured 2.8 years older than chronological age;
- those with bipolar disorder with brains measuring 1.65 years older than chronological age;
- those with attention deficit hyperactivity disorder (ADHD), with brains measuring 1.4 years older than chronological age;
- those who misused alcohol, whose brains age measured 0.6 years older than chronological age;
- those with anxiety disorder, with brains measuring 0.5 years older than chronological age (Amen, et al., 2018).
Interestingly, the authors of the study did not find accelerated aging in dementia, though they did note that different dementias affect different regions of the brain and that dementia was not believed to be a disease of accelerated aging. But according to the Lancet guidance document, dementia risk increases with age, making the possibility of further studies very intriguing. If actual aging of the brain is not the cause of dementias, could one component be the cumulative or long-term effect of some of the substances and conditions that put people at risk? Although this is just one study, the authors plan further investigation into the connection between psychiatric conditions, alcohol and other drugs, and brain aging.
Alcohol consumption and risk of dementia: 23-year follow-up of Whitehall II cohort study
This 2018 study found that people who drank more than 14 units—10 milliliters or 8 grams—of alcohol per week on a regular basis had an increased risk of dementia (Sabia, et al., 2018). In a commentary about this research one of the study authors, Séverine Sabia, PhD, related that the study originated as a search for ways the might delay the onset of or prevent dementia. She further stated that because the prolonged preclinical phase of dementia involves changes in biomarkers over the course of several years, longitudinal studies are needed to show the impact of health behaviors on the risk of cognitive decline and dementia. The new analysis of the consumption of alcohol relative to aging populations was largely conducted because alcohol was not among the risk factors in the most recent guidelines for dementia prevention, the Lancet Commission’s Dementia Prevention, Intervention, and Care. In her commentary about the study, Dr. Sabia said further that “Most previous studies on alcohol and dementia have been in the elderly population. As people tend to drink less as they get older, alcohol consumption in these studies might not reflect previous behaviour. Furthermore, one-off measures to identify abstainers and heavy drinkers are prone to misclassification. This prompted us to use data from several time points, starting in midlife, to identify regular heavy drinkers and to differentiate long term abstainers from former and occasional drinkers. We found similar excess risks among long term abstainers, former drinkers, and occasional drinkers.”
Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline: longitudinal cohort study
A 30-year follow-up study showed that higher alcohol consumption was associated with dose-dependent hippocampal atrophy. The consumption of alcohol resulted in increased risk of atrophy, even at moderate doses (Topiwala, 2017).
Association of relative brain age with tobacco smoking, alcohol consumption, and genetic variants
A more recent study revealed similar aging effects on the brain. According to the research, every gram of alcohol consumed per day ages the brain. Researchers at the University of Southern California looked at brain scans of 17,308 people between the ages of 45 to 81, then trained a computer to assess the ages of the brains in the scans. The researchers compared the results with the participants’ chronological ages and their self-reports on how much they drink and smoke. As a result, they concluded that just one gram of alcohol consumed per day ages the brain 0.2 years, or about a week. The study also showed that the brains of people who reported drinking on a daily basis looked about five months older on average than those who consumed more moderate amounts of alcohol. The effects of smoking were even more pronounced. Smoking a pack of cigarettes a day for a prolonged period of time revealed brains that looked six to seven months older on average than those of people who only smoked occasionally or not at all (Ning,et al., 2020).
The Oscar-Berman Lab
Additional research on alcohol and its effects on the brain has been funded by the National Institutes of Health and the US Department of Veterans Affairs since the 1970s at The Oscar-Berman Lab. Publications specific to alcohol effects regarding gender differences, chronic pain, psychiatric disorders, memory decline and dementia, and other relevant topics can be found on the Publications page.
“We know that, in general, drinking to excess—more than 21 drinks in a week for four or five years—is bad for brain health in most individuals,” Marlene Oscar Berman, PhD, a leading researcher on the brain effects of alcohol, told Mass General Hospital in 2017. “For many people it boils down to this: If you want to drink, stay healthy. And consider cutting down or stopping when you reach middle age to reduce the growing risk of harmful effects on your brain. … The bottom line is: Be sensible. Alcohol consumption is an aspect of brain health that should be carefully considered.”
Takeaways for Behavioral Health Providers
With new research pointing the way to changes in what we know about alcohol and its effects, particularly on the brain, behavioral health providers may want to know how their clients can benefit from this evolving knowledge and the fact that not all of the evidence is in yet. Here are a few takeaways from the latest research for clients who need just one more reason to enter treatment or stay in recovery:
- Alcohol (and tobacco and other drugs) directly impact the brain, causing it to age more rapidly, atrophy, and lose functioning ability. At this point in time the research has not revealed the full extent of the damage that is done or its full implications.
- Alcohol (and tobacco and other drugs) have no established “safe” level of consumption with the possible exception of “none.”
- Alcohol (and tobacco and other drugs) interact with other substances and with other mental health and physical health conditions in the body. Although some effects have been identified, the full extent of these interactions are not fully identified and those that have been are not associated with positive outcomes.
- Groups of studies of alcohol (and tobacco and other drugs) that show inconclusive, mixed, or inconsistent results do not mean that use of alcohol is safe; they mean that no safe level of consumption has been established.
What are your takeaways from the research described here? Can you add to the list in the comments below?
Amen, D., Egan, S., Meysami, S., Raji, C., & George, N. (2018). Patterns of regional cerebral blood flow as a function of age throughout the lifespan. Journal of Alzheimers Disease, 65(4), 1087-1092. doi:10.3233/JAD-180598
Livingston, G., Sommerlad, A., Orgeta, V., Costafreda, S. G., Huntley, J., Ames, D., . . . Mukadam, N. (2017). Dementia prevention, intervention, and care. The Lancet, 390(10113), 2673-2734. doi:10.1016/S0140-6736(17)31363-6
Ning, K., Zhao, L., Matloff, W., Sun, F., & Toga, A. W. (2020). Association of relative brain age with tobacco smoking, alcohol consumption, and genetic variants. Scientific Reports, 10(1), 10-10. doi:10.1038/s41598-019-56089-4
Sabia, S., Fayosse, A., Dumurgier, J., Dugravot, A., Akbaraly, T., Britton, A., . . . Singh-Manoux, A. (2018). Alcohol consumption and risk of dementia: 23 year follow-up of whitehall II cohort study. Bmj-British Medical Journal, 362, k2927. doi:10.1136/bmj.k2927
Topiwala Anya, Allan Charlotte L, Valkanova Vyara, Zsoldos Enikő, Filippini Nicola, Sexton Claire et al. Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline: longitudinal cohort study BMJ 2017; 357 :j2353. doi: https://doi-org.unr.idm.oclc.org/10.1136/bmj.j2353
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