Addictions and Recovery

1. A vignette about dementia and its effect on family members:

I would like to share a story involving a student of mine:

We were discussing the issue of having faith in a G-d or some Higher Power, and this student told me, with anger in her voice, that she had lost it some years earlier. She described how, at the age of 70, her grandfather taught her how to waterski, and yet 2 years later, he couldn’t recognize her and didn’t know her name. She was still shaking her fist at the heavens for taking away the grandfather that she had remembered and loved.

It’s not pretty, and it’s painful to watch.

2. What is dementia?

According to a 2024 article, https://granagardusa.com/blogs/news/what-is-dementia-causes-symptoms-and-support, dementia is an umbrella term covering various brain conditions that will affect thinking, memory, and behavior. Clinicians recognize several types of dementia, including Alzheimer’s Disease, vascular dementia, Lewy Body Dementia, and frontotemporal dementia.

We also know that chronic use of drugs, particularly illicit ones, will induce either reductions in brain volume and/or permanent changes in the functioning of neurons. Therefore, chronic use of drugs has the potential of causing dementia.

3. Alcohol

A. Is there evidence that shows that the likelihood of developing dementia is related to the amount of alcohol consumed?

We already know that ethanol and its metabolite acetaldehyde have direct neurotoxic effects (Rehm, et. al., 2019).

Conventional wisdom was that the consumption of moderate amounts of alcohol has a neuroprotective effect, such that individuals who are either abstainers or who are heavy drinkers (>60 grams of pure alcohol for men and >40 grams of pure alcohol for women) are at greater risk of developing dementia than those who are light- to moderate drinkers.

The evidence for this assertion is from a number of studies. For example, in a data meta-analysis of 15 prospective epidemiological cohort studies from countries situated in six countries, Mewton et. al. (2021) found that when compared with abstainers, the risk for dementia was lower in occasional, light-moderate, and moderate-heavy drinkers. Furthermore, in dose-response analyses, moderate drinking up to 40 grams/day was associated with a lower risk of dementia when compared with lifetime abstaining. They point out however, advising those who currently abstain to initiate drinking is not recommended. (Ed. note: “Whew!”)

Presumably, moderate drinking exerts its beneficial effects by increasing high-density lipoprotein and by affecting atherosclerosis and inflammation by decreasing fibrinogen levels and inflammation markers (Rehm, et. al., 2019).

However, a recent study suggests that even light alcohol consumption can increase dementia risk (Topiwala, et. al., 2025). In this study, 559,559 participants were recruited from the US Million Veteran Program (247,136) and the UK Biobank (312,423). Data collected from each participant included following;

• The number of standard drinks consumed on a typical drinking day;
• The frequency of binge drinking;
• Potential confounders;
  • Education qualifications
  • Smoking habits
  • Body mass index
  • History of head injury and post-traumatic stress disorder
  • Substance use disorders
  • Diabetes mellitus
  • Age
  • Mean systolic and diastolic blood pressures
• Genotyping using Minimac4

Of these participants, 10,564 developed incident all-cause dementia. Conventional observational analyses, i.e., omitting genetic data, found a U-shaped relationship between self-reported alcohol intake and incident dementia. This result is similar to previous research, which showed the lowest dementia risk to be among low-moderate drinkers, rather than non-drinkers.

However, when genetic data were incorporated into the analysis, the findings were quite different. Higher genetic risk for alcohol consumption, as well as problematic and dependent drinking was associated with an increased risk of all-cause dementia in European ancestry figures. For example, an increase from one to three drinks per week, or five to 16 drinks per week, was associated with a 15% increased risk of dementia risk. Furthermore, a twofold increase in genetic risk for AUD was found to be associated with a 16% increase in dementia risk.

Following his role as senior author of this study, Joel Gelernter, professor of psychiatry, genetics and neuroscience at Yale University School of Medicine and senior author of the study admitted that the “new evidence has caused him to avoid alcohol more than he used to”, according to an article appearing in the October 15, 2025 issue of The Washington Post (https://www.washingtonpost.com/wellness/2025/10/15/alcohol-dementia-risk/).

B. One possible consequence of prolonged consumption of alcohol is Wernicke-Korsakoff Syndrome

In a previous blog, https://addictionsandrecoverydotblog.com/2023/11/21/11-liver-cirrhosis-and-wernicke-korsakoff-syndrome-as-alcoholic-endpoints/, we looked at Wernicke-Korsakoff Syndrome as a consequence of prolonged drinking of alcohol, but it is worth repeating here.

Wernicke-Korsakoff Syndrome, also called “wet brain” is a consequence of the depletion of vitamin B₁ (thiamine).

Thiamine itself is a water-soluble vitamin found in wholegrain cereals, yeast and some legumes. Populations at risk for the development of thiamine deficiency include pregnant and lactating women and their offspring, patients with HIV-AIDS, and chronic alcoholics.

The two most common disorders associated with thiamine deficiency are beriberi and Wernicke’s encephalitis (Butterworth, 2003).

Briefly, beriberi is described as either dry or wet:

In the case of chronic alcoholics, the thiamine deficiency leading to Wernicke’s encephalitis results from a combination of factors:

• Inadequate dietary intake of the vitamin due to poor nutrition;
• Poor gastrointestinal absorption of thiamine as a consequence of gastric disease;
• Loss of liver thiamine stores associated with alcoholic liver disease.
• Ethanol itself directly inhibits the transport of thiamine in the gastrointestinal tract;
• Ethanol also inhibits the conversion (phosphorylation) of thiamine to its active diphosphate ester form, which is necessary for cellular energy metabolism and synthetic functions (Butterworth, 2003).

The results of this thiamine depletion are not pretty. First, we can see that parts of the brain have literally shrunk, while the ventricles (cavities in the brain which are filled with cerebrospinal fluid) have become enlarged:

^{Magnetic resonance imaging (MRI) scans of a healthy male (top) compared to a male of the same age with WK syndrome (bottom). The WK brain has less brain volume and larger cavities within the brain (called ventricles). Credit: Adapted from a figure by A. Pfefferbaum, SRI International. Image extracted from https://www.niaaa.nih.gov/publications/brochures-and-fact-sheets/wernicke-korsakoff-syndrome .}

The following is a quote from Alcohol’s Effects on Health, https://www.niaaa.nih.gov/publications/brochures-and-fact-sheets/wernicke-korsakoff-syndrome , which describes the symptoms of Wernicke’s encephalitis:

Symptoms of Wernicke’s disease include: 

• Confusion 
• Lack of energy, hypothermia, low blood pressure, or coma
• Lack of muscle coordination that can affect posture and balance and can lead to tremors (i.e., involuntary movements in one or more parts of the body)  
• Vision problems such as abnormal eye movements (e.g., back and forth movements called nystagmus), double vision, misaligned or crossed eyes, and eyelid drooping

Some of the symptoms can be reversed with prompt administration of thiamine. However, if the alcoholic continues to drink, the condition worsens to a point that the disease progresses to Korsakoff’s Psychosis, which is not reversible. Again, the following is a quote from the website mentioned above:

Although some symptoms of Wernicke’s disease such as muscle and vision problems are reversible with prompt thiamine treatment, other symptoms may respond more slowly or may not be completely reversible. Without prompt treatment, Wernicke’s disease can progress to Korsakoff’s psychosis, which is not reversible.²

Symptoms of Korsakoff’s psychosis include those listed above (i.e., for Wernicke’s encephalitis), as well as: 

• Potentially severe, irreversible memory impairments, including problems forming new memories (called anterograde amnesia) and recalling memories²
• Making up inaccurate stories about events (i.e., confabulation) or remembering events incorrectly
• Experiencing hallucinations (i.e., seeing or hearing things that are not really there)
• Repetitious speech and actions^1,2
• Problems with decision making as well as planning, organizing, and completing tasks²
• Lack of motivation and emotional apathy²

4. Cannabis (Weed)

In 2022, the American Journal of Psychiatry published a fascinating article by Meier, et. al., involving a study spanning 45 years to determine whether long-term cannabis use is associated with cognitive deficits and smaller hippocampal volume in midlife. These two issues are important because they are risk factors for dementia.

The participants in this study were members of a representative cohort of 1,037 individuals born in Dunedin, New Zealand in 1972-1973, and followed to age 45. Cannabis use and dependence were assessed at ages 18, 21, 26,32, 28 and 45. Long-term cannabis users (N=86; 64%) were compared with individuals separated into 5 groups in terms of cognitive tests, trusted informant-reported memory and attention problems, and hippocampal volume:

• Lifelong cannabis nonusers (N=202; 41% male)
• Long-term tobacco users (N=75; 40% male)
• Long-term alcohol users (N=57; 56% male)
• Midlife recreational cannabis users (N-65; 59% male)
• Cannabis quitters (N-60; 62% male)

Hippocampal volume was measured because of its importance in memory. According to the text in https://my.clevelandclinic.org/health/body/hippocampus, it converts short-term memories into long-term memories by organizing, storing and retrieving memories within your brain. Furthermore, it also helps you learn more about your environment (spatial memory), so you’re aware of what’s around you, as well as remembering what words to say (verbal memory).

There are actually two hippocampus structures, one on the left and the other on the right side of the brain.

Finally, it has a high density of receptors which respond to cannabinoids, is important for learning and memory, and has been shown to be the most consistently impaired cognitive domains in cannabis users.

(Figure from https://my.clevelandclinic.org/health/body/hippocampus)

With this cohort, Meier, et. al. were able to show that long-term cannabis users showed the following:

• An IQ decline averaging -5.5 points from childhood to midlife;
• Poor learning and processing speed relative to their childhood;
• Memory and attention problems as verified by trust informants;
• Smaller hippocampal volume. However, smaller hippocampal volume did not statistically mediate cannabis-related cognitive deficits.

In 2025, Myran et. al. (2025) published an article showing that those individuals who have an acute care encounter, such as an emergency department visit or hospitalization, are at considerably higher risk of being diagnosed with dementia within 5 years.

Their study was a population-based, retrospective, matched cohort study of 6,086,794 individuals, using health administrative data from Ontario, Canada, between 2008 and 2021, with follow-up until 2022. These individuals were aged 45 to 105 years and living in Ontario and did not have a diagnosis of dementia at cohort entry.

Annual rates of incident acute care due to cannabis use increased 5.0-fold in individuals aged 45 to 64, from 10.10 to 50.65 per 100,000, and 26.7-fold in individuals aged 65 years or older, from 0.65 to 16.99 per 100,000 between 2008 and 2021. Individuals with incident acute care due to cannabis use were at a 1.5-fold and 3.9 increased risk of a new dementia diagnosis within 5 years compared with individuals with an all-cause acute care encounter and the general population, respectively.

The concern that cannabis can lead to dementia is significant because of three reasons:

• An increasing number of elderly people are resorting to using cannabis for recreational or medical uses, such as treating pain or insomnia;
• The proportion of elderly people in the general population is increasing;
• The potency of cannabis has increased over the past 30 years.

Butterworth, R.F. (2003). Thiamin deficiency and brain disorders. Nutrition Research Reviews 16:277-283, https://doi.org/10.1079NRR200367.

Meier, M.H.; Caspi, A.; Knodt, A.R.; Hall, W.; Ambler, A.; Harrington, H.; Hogan, S.; Houts, R.M.; Poulton, R.; Ramrakha, S.; Hariri, A.R.; Moffitt, T.E. (2002). Long-Term Cannabis Use and Cognitive Reserves and Hippocampal Volume in Midlife. American Journal of Psychiatry. 179:5 (362-374).
 doi: 10.1176/appi.ajp.2021.21060664.

Mewton, L.; Visontay, R.; Hoy, N.; Lipnicki, D.M.; Sunderland, M.; Lipton, R.B.; Guerchet, Maelenn; Ritchie, K.; Najar, J.; Scarmeas, N.; Kim, K-W; Heller, S>R.; van Boxtel, M.; Jacobsen, E.; Brodaty, H.; Anstey, K.J.; Haan, M.; Scazufca, M.; Lobo, E.; Sachdev, P.S.; Collaborators from the Cohort Studies of Memory in an International Consortium (COSMIC). (2021). The relationship between alcohol use and dementia in adults aged more than 60 years: a combined analysis of prospective, individual-participant data from 15 international studies. Addiction 118:412-424. DOI: 10.1111/add.16035.

Myran, D.T.; Pugliese, M.; Harrison, L.D.; et. al. (2025). Risk of Dementia in Individuals With Emergency Department Visits or Hospitalizations Due to Cannabis. JAMA Neurology 82(6):570-579. doi:10.1001/majaneurol.2025.0530.

Rehm, J.; Hasan, O.S.M.; Black, S.E.; Shield, K.D.; Schwarzinger, M. (2019). Alcohol use and dementia: a systematic scoping review. Alzheimer’s Research & Therapy 11:1. https://doi.org/10.1186/s13195-018-0453-0.

Topiwala, A.; Levey, D.F.; Zhou, H.; Deak, J.D.; Adhikari, K.; Ebmeier, K.P.; Bell, S.; Burgess, S.; Nichols, T.E.; Gaziano, M.; Stein, M.; Gelernter, J. (2025). Alcohol use and risk of dementia in diverse populations: evidence from cohort, case-control and Mendelian randomisation approaches. BMI Evidence-Based Medicine, Published Online First: 23 September 2025. doi: 10.1136/bmjebm-2025-113913