Alcohol and the Risk of Developing Alzheimer’s Disease

Alcohol and the Risk of Developing Alzheimer’s Disease

Alcohol and the Risk of Developing Alzheimer’s Disease

Researchers from the University of Illinois at Chicago revealed alcohol may increase the risk of developing Alzheimer’s disease by disrupting the way amyloid beta is cleared

  • Amyloid beta is a protein implicated in Alzheimer’s disease that can clump together in the brain, building up into groups of clumps or a sticky plaque that may disrupt cell-to-cell signaling
  • The study focused on rat microglial cells, which are immune system cells in the brain and spinal cord that actively work to clear amyloid beta in a process known as phagocytosis
  • Microglial phagocytosis was affected by alcohol, decreasing by about 15% after 1 hour of exposure
  • The study reveals that binge drinking or heavy alcohol consumption may make it more likely that the brain will accumulate these damaging proteins, contributing to the development of Alzheimer’s disease

Drinking alcohol has been found to have both a protective and damaging effect on the brain, depending on which study you read and how much alcohol is consumed.

It is not yet known whether light or moderate consumption may be good for your brain, but it is becoming increasingly clear that heavy drinking is not.

Researchers from the University of Illinois at Chicago even revealed how alcohol may increase your risk of developing Alzheimer’s disease, by disrupting the way amyloid beta is cleared.

Amyloid beta is a protein implicated in Alzheimer’s disease that can clump together in the brain, building up into groups of clumps or a sticky plaque that may disrupt cell-to-cell signaling.

The study, published in the Journal of Neuroinflammation, reveals that binge drinking or heavy alcohol consumption may make it more likely that the brain will accumulate these damaging proteins, contributing to the development of Alzheimer’s disease.

The study focused on rat microglial cells, which are immune system cells in the brain and spinal cord that actively work to clear amyloid beta in a process known as phagocytosis.

Researchers exposed the microglial cells to alcohol in a level comparable to that found in people who drink heavily or binge drink, inflammatory cytokines or a combination of alcohol and cytokines for 24 hours.

The expression of over 300 genes was altered following exposure to alcohol, while exposure to cytokines resulted in changes in more than 3,000 genes and the combined alcohol and cytokines exposure caused changes in over 3,500 genes.

Many of the altered genes were involved in phagocytosis and inflammation.3 Notably, microglial phagocytosis was also affected by alcohol, decreasing by about 15 percent after one hour of exposure.

Although the tests were performed in isolated rat cells, which means real-life alcohol consumption in humans may lead to a different result, they suggest that alcohol may hinder the microglia’s ability to clear amyloid beta, thereby increasing the risk of Alzheimer’s.

The study’s lead author, Douglas Feinstein, Professor of Anesthesiology in the University of Illinois at Chicago College of Medicine, suggested people at risk of developing Alzheimer’s may want to be especially careful with alcohol consumption:

“There is a large literature supporting the idea that low amounts of alcohol can be beneficial; not only peripherally but in the brain. However, it might be prudent that if someone is at risk to develop AD [Alzheimer’s disease], they should consider to reduce their alcohol intake; and certainly avoid binge or heavy drinking.”

If you believe you have an alcohol use disorder (alcoholism), seek professional help. If you drink excessively on occasion and would like to cut back, you can try keeping track of how much you drink and setting limits on how much or little to consume.

You should also avoid places, activities and even people who may tempt you to drink and seek out new positive hobbies and friendships to replace them.

Exercise is also essential.

When people drink, it chemically alters the brain to release dopamine, a chemical your brain associates with rewarding behaviors.

When we exercise, this same reward chemical is released, which means we can get a similar “buzz” from working out that you can get from alcohol.

In one study, hamsters that ran the most consumed less alcohol, while less active hamsters had greater cravings for and consumption of alcohol.

In addition, exercise may help to mitigate some of the risks of alcohol consumption.

Longtime drinkers who exercise regularly have less damaged white matter in their brains compared to those who rarely or never exercise. As a bonus, exercise may also reduce declines in cognitive performance attributed to aging as well as protect against changes related to neurodegenerative diseases like Alzheimer’s.

  • NAD is also known to be depleted in Alzheimer’s disease.
  • Small doses of NAD (not time released) can be very helpful when provided while weaning off alcohol

If you are a social drinker who perhaps could benefit from cutting back on your drinking, also consider N-acetyl cysteine (NAC).

NAC is a form of the amino acid cysteine and is known to help increase glutathione and reduce the acetaldehyde toxicity that causes many hangover symptoms. In addition, NAC is known to reduce alcohol consumption and withdrawal symptoms in rodents and cut down cravings in humans.

In a study of people who averaged 1 drink a week, NAC increased the likelihood of alcohol abstinence and reduced drinks per week and drinking days per week.

Meanwhile, if you are planning to have a drink, try taking NAC (at least 200 milligrams) 30 mins before to help lessen the alcohol’s toxic effects.

NAC is a powerful antioxidant known to directly target free radicals, especially oxygen radicals, which is important since oxidative damage is believed to be involved in Alzheimer’s disease. NAC, in turn, may decrease levels of oxidative damage by protecting mitochondrial function, and in so doing reduce Alzheimer’s risk, especially when combined with lipoic acid (LA).

As noted in a review published in Cell Journal:

“Combination of both LA and NAC maximizes this protective effect suggesting that this may prevent mitochondrial decay associated with aging and age-related disorders such as AD. Antioxidant therapies based on LA and NAC seem promising since they can act on mitochondria, one key source of oxidative stress in aging and neurodegeneration.”

As for whether or not alcohol can be good for your brain, there is some research showing that light-to-moderate drinking may have neuroprotective effects.

For instance: consumption of up to 3 servings of wine daily is associated with a lower risk of Alzheimer’s disease in elderly people without the apolipoprotein E4 (APoE4) gene, the gene thought to be most strongly associated with Alzheimer’s disease.14

However, as James A. Hendrix, Alzheimer’s Association director of global science initiatives, cautions, “no one should start drinking alcohol as a means of lowering dementia risk.”

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Paul Ebeling

Paul A. Ebeling, polymath, excels in diverse fields of knowledge. Pattern Recognition Analyst in Equities, Commodities and Foreign Exchange and author of “The Red Roadmaster’s Technical Report” on the US Major Market Indices™, a highly regarded, weekly financial market letter, he is also a philosopher, issuing insights on a wide range of subjects to a following of over 250,000 cohorts. An international audience of opinion makers, business leaders, and global organizations recognizes Ebeling as an expert.

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