As I’ve written here previously, the condition of non-alcoholic fatty liver disease (NAFLD) has seemed to come out of nowhere, is still creating confusion within the medical profession, and is continuing to grow in prevalence. It’s a follow-up to a previous post here, see: Just Read: Global epidemiology of nonalcoholic fatty liver disease-Meta-analytic assessment of prevalence, incidence, and outcomes.
This paper, published in 2011, is a trek back in time, to see when this phenomena started,
There was a starting point – 1988 -1994
Researchers used NHANES data from 1988 to 2008 to compare the presence of markers of metabolic disease. I’ve charted the relevant ones in the image above.
What can be seen is that in the 1988-1994 time period
- About the same percentage of Americans had diabetes type II and NAFLD
- NAFLD was a much smaller percentage (but not trivial) – 46 % of chronic liver disease
Contrast that to 2005-2008
- Diabetes increasing to 9.1 %
- NAFLD to 11 %
- Percentage of liver disease from NAFLD – 75 %
These eclipse the formerly dominant causes of liver disease – the causes those of us who trained in the 20th Century were used to: hepatitis, and alcohol, which didn’t increase very much at all during this time period ( 0.34 % – 2.0 % )
Together, these studies indicate that NAFLD is poised to become the most important cause of CLD with a substantial clinical and economic impact.
These estimates are an under-estimation by as much as 50 %
This paper precedes the newer one I previously referenced, that uses more accurate methods for determining NAFLD. This paper uses blood testing, which can take a lot longer to show the effects of NAFLD. As a comparison, the newer paper showed a prevalence of 24 % in North America by imaging, 12 % by blood testing.
For one thing:
Is obesity the cause or is it a symptom of the same cause, looking at carbohydrates:
There is no known drug treatment for non-acoholic fatty liver disease, and good evidence that’s made worse by the same things that make obesity and diabetes worse, so it may not be “because” of obesity but rather an effect of the same thing that causes obesity.
Note in the chart above that insulin resistance (as roughly calculated) was also increasing, from 23 % to 35 % in 2005-2008.
During chronic positive calorie balance, any excess carbohydrate must undergo de novo lipogenesis. There is no other available pathway, and it can only occur in the liver. This particularly promotes fat accumulation in the liver. As insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will increase liver fat more readily than others due to the higher plasma insulin levels. The increased liver fat will cause relative resistance to suppression of hepatic glucose production by insulin. Over many years, this will bring about a small increase in fasting plasma glucose level, and hence increased basal insulin secretion rates. The consequent hyperinsulinemia will further enhance the conversion of excess calories into liver fat. A vicious cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established.
It’s been thought that losing weight was the treatment. However, this recently published study disputes that, in that changing the diet without weight loss resulted in immediate changes (for the better) in fat deposition in the liver.
Citation:Younossi ZM, Stepanova M, Afendy M, Fang Y, Younossi Y, Mir H, et al. Changes in the Prevalence of the Most Common Causes of Chronic Liver Diseases in the United States From 1988 to 2008. Clin Gastroenterol Hepatol [Internet]. Elsevier; 2011 Jun 1 [cited 2018 Mar 14];9(6):524–530.e1. Available from: http://linkinghub.elsevier.com/retrieve/pii/S154235651100317X