Relatives of people with NAFLD have been warned to get tested for a dangerous disease

Relatives of people with NAFLD have been warned to get tested for a dangerous disease

Non-alcoholic fatty liver disease (NAFLD) affects a quarter of the general population worldwide and encompasses a number of liver conditions affecting people who drink little or no alcohol.

However, a new study by researchers at the University of California, San Diego School of Medicine has found that first-degree relatives of people with NAFLD who have advanced fibrosis are 15% more likely to get the disease. themselves.

Over the past 40 years, changes to our urban environment and diet have had a major impact on our lifestyles as we are more sedentary and the quality of our diet and sleep are at their lowest in decades.

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These changes, coupled with an increase in life expectancy, are associated with an increase in the number of people with “cardiometabolic” diseases such as type 2 diabetes, heart disease, certain cancers or certain neurodegenerative diseases.

Another cardiometabolic disease that often goes unnoticed is non-alcoholic fatty liver disease. The liver is an important organ for food digestion, energy metabolism and nutrient management, and communicates with the intestine and adipose tissue (the main component of our body fat).

But non-alcoholic fatty liver disease is a fairly silent disease, as there are few or no symptoms associated with it.

Fatty liver disease and its consequences

Non-alcoholic fatty liver disease is a disease that affects an average of one in four adults and nearly one in 10 children worldwide. The disease progresses from reversible to irreversible stages.

The first stage is defined by the presence of steatosis (excessive lipid accumulation in the liver to at least five percent of the total liver mass).

The next stage, also reversible, is characterized by inflammation of liver cells (called hepatocytes). This inflammation may be accompanied by scar tissue (called fibrosis).

Progression of the disease to irreversible stages, in the most severe cases, can lead to cirrhosis and/or liver cancer. By 2025, non-alcoholic fatty liver disease will be the leading cause of liver failure and transplantation.

Its complications, however, are not limited to liver disease. It is strongly associated with several other cardiometabolic diseases such as type 2 diabetes and cardiovascular disease (the leading cause of death for people with non-alcoholic fatty liver disease).

What are the risk factors?

Non-alcoholic fatty liver disease develops gradually and can progress differently from one individual to another, depending on genetic factors and certain risk factors, including diet.

The consumption of added sugars, such as fructose in sugary drinks, can contribute to its development, by activating a metabolic process called “de novo lipogenesis”, the production of fatty acids from sugar.

Ultra-processed products, common in the North American diet, have a high energy density and provide a high intake of sugar, fat and salt.

Moreover, alcohol consumption, even in the absence of alcoholism, could have a synergistic effect on hepatic metabolism and accelerate the progression of non-alcoholic fatty liver disease.

Being overweight is also a risk factor for non-alcoholic fatty liver disease: about half of obese people (people with a body mass index (BMI) greater than or equal to 30) could develop the disease.

However, non-alcoholic fatty liver disease is commonly seen in people who are of “healthy weight”. Although BMI may have some utility in measuring the consequences of high body weight, its clinical usefulness is increasingly being questioned.

BMI provides little or no information on the location of fatty tissue: fat has much more harmful consequences when it is located in the abdomen than in the arms, hips or thighs.

Genetic factors

Our research team believes that identifying the genetic factors that contribute to chronic diseases such as non-alcoholic fatty liver disease will allow us to better understand, prevent and treat them.

To this end, we conducted the largest genetic study of this disease to date.

We compared the genome variations of 8,434 people with non-alcoholic fatty liver disease in four countries (Estonia, USA, Finland and UK) with those of 770,180 people without the disease, and identified several susceptibility genes, including an association between a gene called LPL and non-alcoholic fatty liver disease.

This gene, which codes for an enzyme called lipoprotein lipase, plays an important role in the storage of blood lipids in our fatty tissue. A disruption in the activity of the LPL gene could increase the chances of lipid deposition elsewhere in the body, such as in the liver.

This genetic study also allowed us to clarify the role of the distribution or localization of adipose tissue and obesity in the development of non-alcoholic fatty liver disease. In a recent study, which is currently undergoing peer review, we investigated the contribution of BMI and waist circumference to the presence of non-alcoholic fatty liver disease.

A larger waist circumference was strongly associated with an increased risk of developing non-alcoholic fatty liver disease, independent of BMI. Conversely, BMI alone had no effect on risk after controlling for waist circumference.

So, is it necessary to lose weight to prevent fatty liver disease?

Prevention or cure?

Although some of the medications used to treat type 2 diabetes can reduce liver inflammation in patients with non-alcoholic fatty liver disease, there are currently no specific treatments or recommended supplements for the condition.

We believe that identifying the genes involved in non-alcoholic fatty liver disease will expedite its treatment. Until then, targeting the risk factors associated with non-alcoholic fatty liver disease seems to be the most promising avenue.

Interestingly, several studies have shown that improving nutrition and increasing physical activity levels can reduce fat accumulation in the liver, although these factors have been associated with relatively modest weight loss.

Like other chronic societal diseases such as cardiovascular disease and type 2 diabetes, fatty liver disease can be prevented to some degree.

Daily activity, cooking a good variety of foods, improving sleep and limiting time spent in front of screens, consumption of ultra-processed products and exposure to stress, can prevent or delay the development of such diseases.

We believe that by democratizing access to healthy food and transforming urban planning to promote active travel, it will be possible to slow the progression of these diseases in the population as a whole.

Benoit Arsenault is an associate professor in the Department of Medicine at Laval University and a researcher in the cardiology axis at the Research Center of the University Institute of Cardiology and Pneumology of Quebec (IUCPQ)

Émilie Gobeil is a master’s student in clinical and biomedical sciences, Université Laval

This article first appeared in The Conversation

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