To Drink or Not to Drink? That is the Question. Turns Out, if You Have Alzheimer’s, the Answer is NO
“We need to stop asking ourselves if we have a problem with alcohol and start to get curious about how much better our lives could be.” –
In a previous blog post, This Naked Mind, I discussed Catherine and I’s decision to stop drinking Alcohol. It all started in February, 2020 with the final decision being made to give it up all together, April 6th, three years ago. Instead of going down that road again here, I suggest all that are interested go back and read that blog post. I also reviewed that material in the last chapter of my book, Running All Over The World, Our Race Against Early Onset Alzheimers. You can preorder now, for the May 2nd release of the abridged version, by Morgan James Publishing.
Here are several articles that I wish I knew about when I first learned of Catherine’s diagnosis of Early Onset Alzheimer”s, back in 2014.
Summary: Even modest consumption of alcohol can accelerate brain atrophy and increase amyloid plaque formation. The findings reveal alcohol consumption can accelerate Alzheimer’s disease pathologies.
Source: Wake Forest University
Alzheimer’s disease is the most common form of dementia, accounting for 60% to 80% of dementia cases, according to the Alzheimer’s Association. While current research suggests alcohol use disorder is a risk factor in Alzheimer’s disease, the impact alcohol use disorder has on Alzheimer’s disease pathology is an area of continued research.
In a new preclinical study, scientists at Wake Forest University School of Medicine showed that even modest amounts of alcohol can accelerate brain atrophy, which is the loss of brain cells, and increase the number of amyloid plaques, which are the accumulation of toxic proteins in Alzheimer’s disease.
The study appears in Neurobiology of Disease.
“These findings suggest alcohol might accelerate the pathological cascade of Alzheimer’s disease in its early stages,” said Shannon Macauley, Ph.D., associate professor of physiology and pharmacology at Wake Forest University School of Medicine. The study was a collaboration led by Macauley and Jeffrey Weiner, Ph.D., professor of physiology and pharmacology at Wake Forest University School of Medicine, through the medical school’s Alzheimer’s Disease Research Center and Translational Alcohol Research Center.
Using mouse models of Alzheimer’s disease-related pathology, researchers used a 10-week chronic drinking approach where mice were given the choice to drink water or alcohol, mimicking human behavior regarding alcohol consumption. They then explored how voluntary, moderate consumption of alcohol altered healthy brain function and behavior and whether it altered the pathology associated with the early stages of Alzheimer’s disease.
The researchers found that alcohol increased brain atrophy and caused an increased number of amyloid plaques including a greater number of smaller plaques, potentially setting the stage for increased plaque proliferation in later life. Even modest amounts of alcohol can accelerate brain atrophy, which is the loss of brain cells, and increase the number of amyloid plaques, which are the accumulation of toxic proteins in Alzheimer’s disease. Interestingly, researchers also noted that acute withdrawal of alcohol increased the levels of amyloid-beta, which is a key component of amyloid plaques that accumulate in Alzheimer’s disease.
Further analysis showed that chronic alcohol exposure poorly regulated brain and peripheral metabolism—another way to accelerate Alzheimer’s disease pathology. Macauley previously showed that elevated blood sugar increases amyloid-beta and amyloid plaques. In the current study, researchers found that even moderate drinking caused elevations in blood sugar and markers of insulin resistance, which increases the risk not only for Alzheimer’s disease but also for other diseases such as type 2 diabetes and cardiovascular disease.
The study also found that moderate alcohol use altered anxiety and dementia-related behaviors.
“These preclinical findings suggest that even moderate consumption of alcohol can result in brain injury,” Macauley said. “Alcohol consumption may be a modifiable risk factor for Alzheimer’s disease and dementia.”
Alcohol consumption and Alzheimer’s disease research news
Ethanol exposure alters Alzheimer’s-related pathology, behavior, and metabolism in mice.
Epidemiological studies identified alcohol use disorder (AUD) as a risk factor for Alzheimer’s disease (AD), yet there is conflicting evidence on how alcohol use promotes AD pathology. In this study, a 10-week moderate two-bottle choice drinking paradigm was used to identify how chronic ethanol exposure alters amyloid-β (Aβ)-related pathology, metabolism, and behavior.
Ethanol-exposed mice showed increased brain atrophy and an increased number of amyloid plaques. Further analysis revealed that ethanol exposure led to a shift in the distribution of plaque size in the cortex and hippocampus.
Ethanol-exposed mice developed a greater number of smaller plaques, potentially setting the stage for increased plaque proliferation in later life. Ethanol drinking mice also exhibited deficits in nest building, a metric of self-care, as well as increased locomotor activity and central zone exploration in an open field test. Ethanol exposure also led to a diurnal shift in feeding behavior which was associated with changes in glucose homeostasis and glucose intolerance.
Complementary in vivo microdialysis experiments were used to measure how acute ethanol directly modulates Aβ in the hippocampal interstitial fluid (ISF). Acute ethanol transiently increased hippocampal ISF glucose levels, suggesting that ethanol directly affects cerebral metabolism. Acute ethanol also selectively increased ISF Aβ40, but not ISF Aβ42, levels during withdrawal.
Lastly, chronic ethanol drinking increased N-methyl-d-aspartate receptor (NMDAR) and decreased γ-aminobutyric acid type-A receptor (GABAAR) mRNA levels, indicating a potential hyperexcitable shift in the brain’s excitatory/inhibitory (E/I) balance. Collectively, these experiments suggest that ethanol may increase Aβ deposition by disrupting metabolism and the brain’s E/I balance.
Furthermore, this study provides evidence that a moderate drinking paradigm culminates in an interaction between alcohol use and AD-related phenotypes with a potentiation of AD-related pathology, behavioral dysfunction, and metabolic impairment.
Do symptoms of Alzheimer’s get worse when you drink alcohol?
Alzheimer’s disease is a progressive neurodegenerative disorder that affects memory, thinking, and behavior. While there is no cure for Alzheimer’s, individuals with the condition can take steps to manage symptoms and improve quality of life. One factor that can have a significant impact on symptoms is alcohol consumption.
Does drinking alcohol increase your risk of developing Alzheimer’s?
When it comes to drinking and Alzheimer’s risk, the jury is still out. Alcohol use comes with plenty of other lifestyle factors that can be variables in risk of negative effects on the brain, including the long-term risk of neurodegeneration, and studying the long-term effects of alcohol use in a controlled environment is virtually impossible. So, while study after study shows that chronic drinking is linked to higher dementia risk, other studies have found some alcohol consumption can actually be good for the brain — if not just neutral. Long story short, more research is needed to determine the link between alcohol and brain health definitively.
For people living with Alzheimer’s, does alcohol make symptoms worse?
In the meantime, for people already living with Alzheimer’s, scientists do have more solid data to go on. While Alzheimer’s disease typically progresses through seven stages, every individual with Alzheimer’s experiences a different journey, and care plans for people living with Alzheimer’s and other forms of dementia should be individualized. That said, research shows that excessive alcohol consumption can worsen symptoms of Alzheimer’s disease. Alcohol is toxic to the brain and can lead to brain damage, which can result in a decline in cognitive function, memory, and motor skills.
Further, alcohol can interfere with medications used to treat Alzheimer’s, making it harder to manage symptoms. Alcohol consumption can also lead to dehydration, which can exacerbate symptoms of Alzheimer’s. Dehydration can cause confusion, fatigue, and difficulty with coordination, which can be especially challenging for individuals with Alzheimer’s. I wrote a previous blog post article on dehydration, seizures and Alzheimer’s.
Given the potential negative effects, experts recommend that people living with Alzheimer’s avoid alcohol consumption. This can help with the management of Alzheimer’s symptoms — and it can improve one’s quality of life.
With this information now in hand I am glad we stopped drinking when we did. At the same time, I wish, for Catherine’s sake, that many years ago when Catherine said she was willing to stop drinking, but I had to join her, that I had taken her up on the offer to stop drinking much sooner.
I am not saying this lifestyle just like putting everything in storage and running all over the world is for everyone but if you read or listen to the book, This Naked Mind, it just might be for you. As I often say, to each their own. In closing, one thing to consider, just because you decide to be AF does not mean you have or had a problem. Just maybe you will realize, like I did, Alcohol no longer does anything, “FOR”, you. Also if you are caring for someone with Alzheimer’s, sooner is probably for the better.