scholarly journals Nutritional Status and Diet Style Affect Cognitive Function in Alcoholic Liver Disease

2020 ◽  
Author(s):  
Ye Rin Choi ◽  
Hyeong Seop Kim ◽  
Sang Jun Yoon ◽  
Na Young Lee ◽  
Haripriya Gupta ◽  
...  
Keyword(s):  
Liver Disease ◽  
Cognitive Function ◽  
Nutritional Status ◽  
Cognitive Dysfunction ◽  
Alcoholic Liver Disease ◽  
Digit Span ◽  
Alcoholic Cirrhosis ◽  
Synaptic Function ◽  
High Fat ◽  
High Carbohydrate

Malnutrition and cognitive dysfunction are typical features of alcoholic liver disease (ALD) and are correlated with the development of complications. The aim of this study is to explore the effect of nutritional state and diet on cognitive function in ALD. A total of 43 patients with compensated alcoholic cirrhosis were enrolled, and neuropsychological test was assessed according to body mass index (BMI, <22 and ≥22). In the ALD animal study, mice were divided into 5 groups (n=9/group; normal liquid, 5% EtOH+regular liquid, 5% EtOH+high-carbohydrate liquid, 5% EtOH+high-fat liquid, and 5% EtOH+high-protein liquid diet) and fed the same calories for 8-week. To assess cognitive function, we performed T-maze studies weekly before/after alcohol binging. In cognitive function (BMI <22 /≥22), language score of Korea mini-mental state (7.4±1.4/7.9±0.4), Rey-complex figure (72.0±25.9/58.4±33.6), Boston naming (11.7±2.7/13.0±1.8), forward digit span (6.7±1.8/7.5±1.6), Korean Color Word Stroop (24.2±26.5/43.6±32.4), and interference score (33.9±31.9/52.3±33.9) revealed significant differences. In the T-maze test, alcohol significantly delayed the time to reach food, and binge drinking provided a temporary recovery in cognition. The alcohol-induced delay was significantly reduced in the high-carbohydrate and high-fat diet groups. Synaptic function exhibited no changes in all groups. Cognitive dysfunction is affected by nutritional status and diet in ALD.

scholarly journals Nutritional Status and Diet Style Affect Cognitive Function in Alcoholic Liver Disease

Nutrients ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 185
Author(s):  
Ye Rin Choi ◽  
Hyeong Seop Kim ◽  
Sang Jun Yoon ◽  
Na Young Lee ◽  
Haripriya Gupta ◽  
...  
Keyword(s):  
Liver Disease ◽  
Cognitive Function ◽  
Nutritional Status ◽  
Cognitive Dysfunction ◽  
Alcoholic Liver Disease ◽  
Digit Span ◽  
Alcoholic Cirrhosis ◽  
Synaptic Function ◽  
High Fat ◽  
High Carbohydrate

Malnutrition and cognitive dysfunction are typical features of alcoholic liver disease (ALD) and are correlated with the development of complications. The aim of this study is to explore the effect of nutritional state and diet on cognitive function in ALD. A total of 43 patients with compensated alcoholic cirrhosis were enrolled, and a neuropsychological test was assessed according to body mass index (BMI, <22 and ≥22). In the ALD animal study, mice were divided into five groups (n = 9/group; normal liquid, 5% EtOH + regular liquid, 5% EtOH + high-carbohydrate liquid, 5% EtOH + high-fat liquid, and 5% EtOH + high-protein liquid diet) and fed the same calories for eight weeks. To assess cognitive function, we performed T-maze studies weekly before/after alcohol binging. In cognitive function (BMI < 22/≥22), language score of Korea mini-mental state (7.4 ± 1.4/7.9 ± 0.4), Boston naming (11.7 ± 2.7/13.0 ± 1.8), forward digit span (6.7 ± 1.8/7.5 ± 1.6), Korean color word stroop (24.2 ± 26.5/43.6 ± 32.4), and interference score (33.9 ± 31.9/52.3 ± 33.9) revealed significant differences. In the T-maze test, alcohol significantly delayed the time to reach food, and binge drinking provided a temporary recovery in cognition. The alcohol-induced delay was significantly reduced in the high-carbohydrate and high-fat diet groups. Synaptic function exhibited no changes in all groups. Cognitive dysfunction is affected by nutritional status and diet in ALD.

scholarly journals Dissociation of hepatic insulin resistance from susceptibility of nonalcoholic fatty liver disease induced by a high-fat and high-carbohydrate diet in mice

2014 ◽  
Vol 306 (6) ◽  
pp. G496-G504 ◽  
Author(s):  
Akihiro Asai ◽  
Pauline M. Chou ◽  
Heng-Fu Bu ◽  
Xiao Wang ◽  
M. Sambasiva Rao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Diet Group ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Akt Phosphorylation ◽  
High Carbohydrate

Liver steatosis in nonalcoholic fatty liver disease is affected by genetics and diet. It is associated with insulin resistance (IR) in hepatic and peripheral tissues. Here, we aimed to characterize the severity of diet-induced steatosis, obesity, and IR in two phylogenetically distant mouse strains, C57BL/6J and DBA/2J. To this end, mice (male, 8 wk old) were fed a high-fat and high-carbohydrate (HFHC) or control diet for 16 wk followed by the application of a combination of classic physiological, biochemical, and pathological studies to determine obesity and hepatic steatosis. Peripheral IR was characterized by measuring blood glucose level, serum insulin level, homeostasis model assessment of IR, glucose intolerance, insulin intolerance, and AKT phosphorylation in adipose tissues, whereas the level of hepatic IR was determined by measuring insulin-triggered hepatic AKT phosphorylation. We discovered that both C57BL/6J and DBA/2J mice developed obesity to a similar degree without the feature of liver inflammation after being fed an HFHC diet for 16 wk. C57BL/6J mice in the HFHC diet group exhibited severe pan-lobular steatosis, a marked increase in hepatic triglyceride levels, and profound peripheral IR. In contrast, DBA/2J mice in the HFHC diet group developed only a mild degree of pericentrilobular hepatic steatosis that was associated with moderate changes in peripheral IR. Interestingly, both C57BL/6J and DBA/2J developed severe hepatic IR after HFHC diet treatment. Collectively, these data suggest that the severity of diet-induced hepatic steatosis is correlated to the level of peripheral IR, not with the severity of obesity and hepatic IR. Peripheral rather than hepatic IR is a dominant factor of pathophysiology in nonalcoholic fatty liver disease.

Assessment of nutritional status and in vivo immune responses in alcoholic liver disease

1983 ◽  
Vol 38 (6) ◽  
pp. 849-859 ◽  
Author(s):  
P R Mills ◽  
A Shenkin ◽  
R S Anthony ◽  
A S McLelland ◽  
A N Main ◽  
...  
Keyword(s):  
Liver Disease ◽  
Nutritional Status ◽  
Immune Responses ◽  
Alcoholic Liver Disease

scholarly journals Alkoholos májbetegség: a genetikai-epigenetikai tényezők szerepe és az absztinencia hatása

2019 ◽  
Vol 160 (14) ◽  
pp. 524-532 ◽  
Author(s):  
Alajos Pár ◽  
Gabriella Pár
Keyword(s):  
Risk Factors ◽  
Liver Disease ◽  
Environmental Factors ◽  
Alcoholic Liver Disease ◽  
Liver Toxicity ◽  
Hepatitis Virus ◽  
Alcoholic Cirrhosis ◽  
Protective Role ◽  
Micro Rna ◽  
Alcoholic Fatty Liver

Abstract: The pathogenesis of alcoholic liver disease depends not only on the toxic effects of alcohol, but also on the complex interaction of host’s and environmental factors. Thus, the genetic pre-disposition, co-morbidities and behavioral factors all play a role in the individual variations in the disease outcomes. On the other hand, the essential part of the therapeutic strategy is the complete withdrawal of the harmful etiological agent. The present paper is devoted to overview the genetics, the environmental factors and the effects of abstinence in alcoholic liver disease. Genetic variants in two enzymes involved in the metabolism of ethanol, alcohol-dehydrogenase ADH1B *2 and aldehyde-dehydrogenase ALDH2 *2 through increasing the blood level of acetaldehyde, may play a “protective” role against alcoholism. The P450 CYP2E1 *5 c2, an inducible microsomal oxidase, upregulated by ethanol and by formation of acetaldehyde and reactive oxygen species, increases liver toxicity. Three novel gene polymorphisms – such as the patatin-like phospholipase domain-containing 3 (PNPLA3 I148M C>G), the transmembrane 6 superfamily member 2 (TM6SF2 E167K), and the membrane-bound O-acyltransferase domain-containing 7 (MB0AT7 rs641738 C>T) – have been proven as risk factors of steatosis, fibrosis and even hepatocellular carcinoma in both alcoholic and non-alcoholic fatty liver disease patients. Alcohol-induced epigenetic effects, reversible but inheritable gene expression alterations – as histon modulations, DNA methylation and micro-RNA-s – are of importance in the pathogenesis as well, and in the future, they may serve as diagnostic markers and therapeutic targets. Women are at greater risk of developing alcoholic cirrhosis, furthermore, malnutrition, obesity, diabetes, smoking, and hepatitis virus infections are also risk factors. Alcoholic liver disease should be regarded as a preventable disease. Several clinical studies revealed that abstinence may result in the regression of steatohepatitis and fibrosis, compensation of cirrhosis, improving disease outcome and increasing survival even in patients with advanced stages. Early diagnosis and multidisciplinary interventions are highly required to achieve long-term abstinence and to prevent alcoholic cirrhosis. Orv Hetil. 2019; 160(14): 524–532.

scholarly journals Three consecutive weeks of nutritional ketosis has no effect on cognitive function, sleep, and mood compared with a high-carbohydrate, low-fat diet in healthy individuals: a randomized, crossover, controlled trial

2019 ◽  
Vol 110 (2) ◽  
pp. 349-357 ◽  
Author(s):  
Stella Iacovides ◽  
David Goble ◽  
Bronwyn Paterson ◽  
Rebecca M Meiring
Keyword(s):  
Cognitive Function ◽  
Sleep Quality ◽  
Visual Learning ◽  
Normal Weight ◽  
Healthy Individuals ◽  
High Fat ◽  
Low Fat ◽  
High Carbohydrate ◽  
Cohen’S D ◽  
Cohen's D

ABSTRACTBackgroundThe high-fat ketogenic diet (KD) has become an increasingly popular diet not only in overweight/obese populations, or those with clinical conditions, but also in healthy non-overweight populations.ObjectiveBecause there are concerns about the association between high-fat diets and cognitive decline, this study aimed to determine the effects of a KD compared with an isocaloric high-carbohydrate, low-fat (HCLF) diet on cognitive function, sleep, and mood in healthy, normal-weight individuals.MethodsEleven healthy, normal-weight participants (mean age: 30 ± 9 y) completed this randomized, controlled, crossover study. Participants followed 2 isocaloric diets—an HCLF diet (55% carbohydrate, 20% fat, and 25% protein) and a KD (15% carbohydrate, 60% fat, and 25% protein)—in a randomized order for a minimum of 3 wk, with a 1-wk washout period between diets. Measures of β-hydroxybutyrate confirmed that all participants were in a state of nutritional ketosis during post-KD assessments (baseline: 0.2 ± 0.2 mmol/L; KD: 1.0 ± 0.5 mmol/L; washout: 0.2 ± 0.1 mmol/L; and HCLF: 0.3 ± 0.2 mmol/L). Cognitive function was assessed using a validated, psychological computer-based test battery before and after each diet. Subjective measures of mood and sleep were also monitored throughout the study using validated scales.ResultsThree weeks of sustained nutritional ketosis, compared with the HCLF diet, had no effect on speed and accuracy responses in tasks designed to measure vigilance (speed: P = 0.39, Cohen's d = 0.26; accuracy: P = 0.99, Cohen's d = 0.04), visual learning and memory (speed: P = 0.99, Cohen's d = 0.04; accuracy: P = 0.99, Cohen's d = 0.03), working memory (speed: P = 0.62, Cohen's d = 0.26; accuracy: P = 0.98, Cohen's d = 0.07), and executive function (speed: P = 0.60, Cohen's d = 0.31; accuracy: P = 0.90, Cohen's d = 0.19). Likewise, mood, sleep quality, and morning vigilance did not differ (P > 0.05) between the dietary interventions.ConclusionThe results of our randomized, crossover, controlled study suggest that 3 wk of sustained nutritional ketosis had no effect on cognitive performance, mood, or subjective sleep quality in a sample of healthy individuals. This trial was registered in the Pan African Clinical Trial Registry as PACTR201707002406306.

scholarly journals Effects of almond consumption on the post-lunch dip and long-term cognitive function in energy-restricted overweight and obese adults

2017 ◽  
Vol 117 (3) ◽  
pp. 395-402 ◽  
Author(s):  
Jaapna Dhillon ◽  
Sze-Yen Tan ◽  
Richard D. Mattes
Keyword(s):  
Weight Loss ◽  
Cognitive Function ◽  
Weight Loss Intervention ◽  
Performance Indices ◽  
High Fat ◽  
Obese Adults ◽  
Memory And Attention ◽  
High Carbohydrate ◽  
Attention Performance

AbstractThe post-lunch dip in cognition is a well-established phenomenon of decreased alertness, memory and vigilance after lunch consumption. Lunch composition reportedly influences the post-lunch dip. Moreover, dieting is associated with cognitive function impairments. The negative effects of dieting have been reversed with nut-supplemented diets. The aims of this study were to (1) evaluate the acute effect of an almond-enriched high-fat lunch or high-carbohydrate lunch on the post-lunch decline in cognitive function, and (2) evaluate the effects of chronic almond consumption as part of an energy-restricted diet on the memory and attention domains of cognitive function. In total, eighty-six overweight and obese adults were randomised to consume either an almond-enriched diet (AED) or a nut-free control diet (NFD) over a 12-week weight loss intervention. Participants were also randomised to receive either an almond-enriched high-fat lunch (A-HFL) (>55 % energy from fat, almonds contributing 70–75 % energy) or a high-carbohydrate lunch (HCL) (>85 % energy from carbohydrates) at the beginning and end of the weight loss intervention. Memory and attention performance indices decreased after lunch consumption (P<0·001). The A-HFL group ameliorated the decline in memory scores by 57·7 % compared with the HCL group (P=0·004). Both lunch groups had similar declines in attention. Moreover, memory and attention performance indices increased after the 12-week intervention period (P<0·05) with no difference between the AED and NFD groups. In conclusion, almond consumption at a midday meal can reduce the post-lunch dip in memory. However, long-term almond consumption may not further improve cognitive function outcomes in a weight loss intervention.

Alcoholic liver disease

2020 ◽  
pp. 3142-3147
Author(s):  
Ewan Forrest
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Alcoholic Liver Disease ◽  
Alcoholic Hepatitis ◽  
Early Recognition ◽  
Clinical Manifestations ◽  
Alcoholic Cirrhosis ◽  
Diagnostic Uncertainty ◽  
Short Term Mortality ◽  
High Index Of Suspicion

The incidence of alcoholic liver disease (ALD) follows the trend of per capita alcohol consumption, with hepatic injury which extends from fatty liver to alcoholic hepatitis and cirrhosis. It is unclear how alcohol causes liver disease, but postulated mechanisms include (1) oxidative stress and acetaldehyde generated by the metabolism of ethanol, and (2) innate and adaptive immune responses. Factors determining the susceptibility to liver disease in heavy drinkers are believed to include a variety of host and environmental factors, with genetic factors increasingly recognized. Clinical manifestations are extremely variable, and some patients remain relatively well while others suffer the effects of severe hepatic failure. Although patients can come to light with a life-threatening complication, most often they develop symptoms which are not immediately related to the liver, such as nonspecific digestive symptoms or psychiatric complaints. The key to the early recognition of alcohol-related disease is having a high index of suspicion, with confirmation by (1) direct questioning for alcohol history and alcohol-related symptoms; (2) clinical examination for signs of chronic liver disease; (3) supportive investigations, including aspartate aminotransferase, which is less than 500 IU/litre and greater than the alanine aminotransferase level; and (4) liver biopsy, which may be required in some cases of diagnostic uncertainty and to confirm the stage of the disease, revealing alcoholic fatty liver, alcoholic hepatitis, or cirrhosis. Management is governed by the stage and severity of the liver disease, but always includes abstinence and adequate nutritional support. In selected patients with severe acute alcoholic hepatitis, corticosteroids can reduce short-term mortality. Transplantation remains the only effective treatment for advanced alcoholic cirrhosis, although this remains controversial, mainly because of concerns about post-transplant recidivism.

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