Alcohol-Related Dementia: Rethink How Much You Drink

2021 ◽  
Vol 36 (7) ◽  
pp. 324-330
Author(s):  
Raquel Mateus ◽  
Jeannette Y. Wick

People have consumed alcohol for centuries. Most clinicians who work with people who have dementia acknowledge that alcohol may cause or exacerbate dementia's symptoms. Alcohol-related dementia (ARD) has been recognized since the 1960s, but clinicians rarely use this diagnosis. Regardless, it is common and develops pursuant to long-term excessive alcohol consumption. It may, in some cases, evolve into Wernicke-Korsakoff syndrome. Diagnosis can be obscured if patients are not truthful about their alcohol consumption. Often, friends or family provide a better picture of the patient's alcohol history than patients do themselves. Thiamine treatment may prevent or improve symptoms. Abstinence from alcohol is critical, but it is difficult for older people with long histories of heavy drinking. Consultant pharmacists can help the heath care team develop nuanced care plans for patients who have ARD.

2021 ◽  
Vol 36 (7) ◽  
pp. 324-330
Author(s):  
Raquel Mateus ◽  
Jeannette Y. Wick

People have consumed alcohol for centuries. Most clinicians who work with people who have dementia acknowledge that alcohol may cause or exacerbate dementia’s symptoms. Alcohol-related dementia (ARD) has been recognized since the 1960s, but clinicians rarely use this diagnosis. Regardless, it is common and develops pursuant to long-term excessive alcohol consumption. It may, in some cases, evolve into Wernicke-Korsakoff syndrome. Diagnosis can be obscured if patients are not truthful about their alcohol consumption. Often, friends or family provide a better picture of the patient’s alcohol history than patients do themselves. Thiamine treatment may prevent or improve symptoms. Abstinence from alcohol is critical, but it is difficult for older people with long histories of heavy drinking. Consultant pharmacists can help the heath care team develop nuanced care plans for patients who have ARD.


2012 ◽  
Vol 57 (2) ◽  
pp. 306-312 ◽  
Author(s):  
Stéphanie Faure ◽  
Astrid Herrero ◽  
Boris Jung ◽  
Yohan Duny ◽  
Jean-Pierre Daures ◽  
...  

Alcohol ◽  
2002 ◽  
Vol 27 (2) ◽  
pp. 99-105
Author(s):  
Matts Eriksson ◽  
Ulf Berggren ◽  
Claudia Fahlke ◽  
Ernest Hård ◽  
Jan Balldin

2020 ◽  
pp. 1-11
Author(s):  
Grace Gale ◽  
Katie Walsh ◽  
Vanessa E. Hennessy ◽  
L. E. Stemerding ◽  
Koa Sher Ni ◽  
...  

Abstract Background Alcohol use disorders can be conceptualised as a learned pattern of maladaptive alcohol-consumption behaviours. The memories encoding these behaviours centrally contribute to long-term excessive alcohol consumption and are therefore an important therapeutic target. The transient period of memory instability sparked during memory reconsolidation offers a therapeutic window to directly rewrite these memories using targeted behavioural interventions. However, clinically-relevant demonstrations of the efficacy of this approach are few. We examined key retrieval parameters for destabilising naturalistic drinking memories and the ability of subsequent counterconditioning to effect long-term reductions in drinking. Methods Hazardous/harmful beer-drinking volunteers (N = 120) were factorially randomised to retrieve (RET) or not retrieve (No RET) alcohol reward memories with (PE) or without (No PE) alcohol reward prediction error. All participants subsequently underwent disgust-based counterconditioning of drinking cues. Acute responses to alcohol were assessed pre- and post-manipulation and drinking levels were assessed up to 9 months. Results Greater long-term reductions in drinking were found when counterconditioning was conducted following retrieval (with and without PE), despite a lack of short-term group differences in motivational responding to acute alcohol. Large variability in acute levels of learning during counterconditioning was noted. ‘Responsiveness’ to counterconditioning predicted subsequent responses to acute alcohol in RET + PE only, consistent with reconsolidation-update mechanisms. Conclusions The longevity of behavioural interventions designed to reduce problematic drinking levels may be enhanced by leveraging reconsolidation-update mechanisms to rewrite maladaptive memory. However, inter-individual variability in levels of corrective learning is likely to determine the efficacy of reconsolidation-updating interventions and should be considered when designing and assessing interventions.


2020 ◽  
Author(s):  
Grace. Gale ◽  
Vanessa E. Hennessy ◽  
Katie. Walsh ◽  
Sunjeev K. Kamboj ◽  
Ravi. K. Das

ABSTRACTBackgroundAlcohol use disorders can be conceptualised as a learned pattern of maladaptive alcohol-consumption behaviours. The memories encoding these behaviours centrally contribute to long-term excessive alcohol consumption and are a key therapeutic target. The transient period of memory instability sparked during memory reconsolidation offers a therapeutic window to directly rewrite these memories using targeted behavioural interventions. However, clinically-relevant demonstrations of the efficacy of this approach are few. We examined key retrieval parameters for destabilising naturalistic drinking memories and the ability of subsequent counterconditioning to effect long-term reductions in drinking.MethodsHazardous/harmful beer-drinking volunteers (N=120) were factorially randomised to retrieve (RET) or not retrieve (No RET) alcohol reward memories with (PE) or without (No PE) alcohol reward prediction error. All participants subsequently underwent disgust-based counterconditioning of drinking cues. Acute responses to alcohol were assessed pre- and post-manipulation and drinking levels assessed up to 9 months.ResultsGreater long-term reductions in drinking were found when counterconditioning was conducted following retrieval (with and without PE), despite a lack of short-term group differences in motivational responding to acute alcohol. Large variability in acute levels of learning during counterconditioning were noted. ‘Responsiveness’ to counterconditioning predicted subsequent responses to acute alcohol in RET+PE only, consistent with reconsolidation-update mechanisms.ConclusionsThe longevity of behavioural interventions designed to reduce problematic drinking levels may be enhanced by leveraging reconsolidation-update mechanisms to rewrite maladaptive memory. However, inter-individual variability in levels of corrective learning is likely to determine the efficacy of reconsolidation-updating interventions and should be considered when designing and assessing interventions.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Young Soo Han ◽  
Yong Woo Kim ◽  
Yu Jeong Kim ◽  
Ki Ho Park ◽  
Jin Wook Jeoung

Abstract The present study investigated the effect of aldehyde dehydrogenase2 (ALDH2) rs671 polymorphism and alcohol consumption on the severity of primary open-angle glaucoma (POAG). The questionnaire for alcohol consumption pattern and targeted genotyping for ALDH2 rs671 polymorphism was performed from 445 Korean POAG patients. Retinal nerve fiber layer (RNFL) and ganglion cell-inner plexiform layer (GCIPL) thicknesses were measured and compared according to alcohol consumption and ALDH2 rs671 genotype. Heavy drinking group eyes had thinner RNFL thickness than did abstinence group eyes (65.0 ± 10.9 vs. 70.9 ± 11.5 µm, P = 0.023). Both mild (65.8 ± 9.6 µm) and heavy (63.8 ± 8.4 µm) drinking group eyes had significantly thinner macular GCIPL thickness than did abstinence group eyes (68.1 ± 8.2 µm, P = 0.003). However, ALDH2 rs671 polymorphism did not show any significant association with RNFL or GCIPL thickness. Alcohol consumption was significantly associated with GCIPL thinning (β = –0.446, P = 0.035) after adjustment for multiple confounding factors. As excessive alcohol consumption was significantly associated with thinner GCIPL thickness while ALDH2 polymorphism had no significant effect on RNFL or GCIPL thickness, glaucoma patients should avoid excessive alcohol consumption regardless of ALDH2 polymorphism.


2018 ◽  
Vol 4 (1) ◽  
pp. 44-50
Author(s):  
Dwi Purbayanti

Long-term and excessive alcohol consumption is a risk factor for chronic diseases such as impaired kidney function. Acute and chronic alcohol consumption can increase blood pressure which is a risk factor for kidney damage. Oxidative stress play a role in the kidney damage that induced by ethanol. In this study aims to the description of creatinine levels in moderate and heavy alcohol drinkers in Jalan Mendawai Kota Palangka Raya. This study used the descriptive method to describe the effect of consuming alcohol on kidney function using creatinine level parameters. Total sample used is 20 people with snowballs Sampling technique. The inclusion criteria such as male, age over 20 years old, consumed alcohol more than 5 years, consumed alcohol every day. Creatinine examination was done by Jaffe Reaction method using Photometer 5010 V5 +. The results showed that 15 people (75%) had high creatinine levels and 5 people (25%) had normal creatinine levels.


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