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Progression of liver disease in NAFLD
NAFLD DIABETES AND ALCOHOL: IS THERE A SAFE
THRESHOLD?
Stefano Bellentani*, Andrea Barchetti, Fabio Nascimbeni and Amedeo Lonardo
*Shrewsbury and Telford NHS Trust,
Department of Gastroenterology,
Shrewsbury, The United Kingdom
E-mail: stefano.bellentani@nhs.net
Take home message
• Is alcohol a good guy or a bad guy? It depends on the dose!
Introduction
The effect of alcohol on health depends on daily intake, the means of drinking and the type of alcoholic
beverage consumed. The dose-response relationship between alcohol consumption and all-cause
mortality follows a J- or U-shaped curve, which suggests that all-cause mortality is reduced among
those with light to moderate alcohol intake compared to those with high consumption. This effect is
mainly due to a reduction in CVD, attributed to a beneficial effect on plasma lipid levels, decreased risk
of thrombosis and prevention of MetS. Moreover, moderate alcohol consumption is a protective factor
toward the risk of NAFLD development and it seems to enhance IS, leading to a decreased risk of MetS.
Alcohol and NAFLD
Our group was first in identifying a safe threshold level of alcohol consumption for chronic liver disease
in the general population [1]. This threshold level of 30 g of alcohol/day (i.e. 3 drinks/day) is very
close to that conventionally adopted (<20 g/day) to distinguish NAFLD from AFLD. Individuals who
consume more than 30-50 g/d of alcohol for more than 5-10 years have a significantly higher risk of
developing ALD. Not all these drinkers, however, develop liver disease. Indeed, host- and environment-
related factors promote the development of ALD [2]. For example, genetic polymorphisms of alcohol
dehydrogenase and their interaction with genes involved in the generation and scavenging of free radicals
influence susceptibility to ALD [2]. Obesity, diabetes, IR, MetS, NAFLD, as well as chronic HCV
infection increase the deleterious effects of alcohol on the liver.
NAFLD may evolve in 4-5% of the cases in NASH (although these two conditions may be unrelated
according to recent views), and patients with NASH are at a high risk of cirrhosis and HCC related
mortality. Patients with NAFLD are at increased risk of CVD or CHD. Indeed, they are twice more likely
to die from CVD than from liver diseases. Evaluation of cardiovascular risk and management of CHD
risk factors is, therefore, mandatory in these patients. As well as being associated with reduced CVD
morbidity and mortality, moderate alcohol consumption also improves metabolic risk factors related to
both CVD and NAFLD and is partially protective against NASH and NAFLD. Interestingly, a recent
study suggests that even somewhat excessive alcohol consumption (>280 g/week, i.e. >4 drinks/day),
especially in men, is likely to reduce the development of NAFLD over time [3]. Moreover, preliminary
evidence suggests that the benefits of alcohol on CVD observed in the general population may extend
to individuals with established NAFLD. Indeed, modest alcohol consumption has been shown to have
an inverse association with carotid artery plaques and stenosis, independently from age, smoking and
MetS, in men with NAFLD [4]. According to these studies, patients with NAFLD who drink no more
than two to three drinks per day could perhaps be allowed to continue their drinking habits.
The International Liver Congress™ 2015 • Vienna, Austria • April 22–23, 2015 99
NAFLD DIABETES AND ALCOHOL: IS THERE A SAFE
THRESHOLD?
Stefano Bellentani*, Andrea Barchetti, Fabio Nascimbeni and Amedeo Lonardo
*Shrewsbury and Telford NHS Trust,
Department of Gastroenterology,
Shrewsbury, The United Kingdom
E-mail: stefano.bellentani@nhs.net
Take home message
• Is alcohol a good guy or a bad guy? It depends on the dose!
Introduction
The effect of alcohol on health depends on daily intake, the means of drinking and the type of alcoholic
beverage consumed. The dose-response relationship between alcohol consumption and all-cause
mortality follows a J- or U-shaped curve, which suggests that all-cause mortality is reduced among
those with light to moderate alcohol intake compared to those with high consumption. This effect is
mainly due to a reduction in CVD, attributed to a beneficial effect on plasma lipid levels, decreased risk
of thrombosis and prevention of MetS. Moreover, moderate alcohol consumption is a protective factor
toward the risk of NAFLD development and it seems to enhance IS, leading to a decreased risk of MetS.
Alcohol and NAFLD
Our group was first in identifying a safe threshold level of alcohol consumption for chronic liver disease
in the general population [1]. This threshold level of 30 g of alcohol/day (i.e. 3 drinks/day) is very
close to that conventionally adopted (<20 g/day) to distinguish NAFLD from AFLD. Individuals who
consume more than 30-50 g/d of alcohol for more than 5-10 years have a significantly higher risk of
developing ALD. Not all these drinkers, however, develop liver disease. Indeed, host- and environment-
related factors promote the development of ALD [2]. For example, genetic polymorphisms of alcohol
dehydrogenase and their interaction with genes involved in the generation and scavenging of free radicals
influence susceptibility to ALD [2]. Obesity, diabetes, IR, MetS, NAFLD, as well as chronic HCV
infection increase the deleterious effects of alcohol on the liver.
NAFLD may evolve in 4-5% of the cases in NASH (although these two conditions may be unrelated
according to recent views), and patients with NASH are at a high risk of cirrhosis and HCC related
mortality. Patients with NAFLD are at increased risk of CVD or CHD. Indeed, they are twice more likely
to die from CVD than from liver diseases. Evaluation of cardiovascular risk and management of CHD
risk factors is, therefore, mandatory in these patients. As well as being associated with reduced CVD
morbidity and mortality, moderate alcohol consumption also improves metabolic risk factors related to
both CVD and NAFLD and is partially protective against NASH and NAFLD. Interestingly, a recent
study suggests that even somewhat excessive alcohol consumption (>280 g/week, i.e. >4 drinks/day),
especially in men, is likely to reduce the development of NAFLD over time [3]. Moreover, preliminary
evidence suggests that the benefits of alcohol on CVD observed in the general population may extend
to individuals with established NAFLD. Indeed, modest alcohol consumption has been shown to have
an inverse association with carotid artery plaques and stenosis, independently from age, smoking and
MetS, in men with NAFLD [4]. According to these studies, patients with NAFLD who drink no more
than two to three drinks per day could perhaps be allowed to continue their drinking habits.
The International Liver Congress™ 2015 • Vienna, Austria • April 22–23, 2015 99
