Interesting article over at Medscape on the role of bariatric surgery in the treatment of non-alcoholic fatty liver disease (NAFLD) and (NASH).
For the uninitiated, non-alcoholic fatty liver disease is a serious condition where functional tissue of the liver (used to metabolize and detoxify everything we ingest including medications) is replaced with fat tissue, and eventually fibrosis. As more and more healthy tissue becomes fatty & fibrotic, the liver function deteriorates until it progresses to cirrhosis and eventual liver failure.
Currently, the only treatment for cirrhosis and liver failure is liver transplantation (which is still only a temporary measure, even in the best case scenarios*.)
But why is the happening? and who does it affect? Obesity and obese patients.
To better understand what’s going on – we need to review some basic pathophysiology:
First, lets look at food. Not in cultural or psychosocial way, or even in food preferences, but food as the body sees it: Fuel for all of our cellular functions. Just as we run our houses, appliances and cars on different types of fuel – gasoline, natural gas, electricity etc. our body runs on different types of fuels (proteins, fats, sugars) that all get broken down to serve as energy. Like fossil fuels – the metabolism of each of these fuels requires different mechanisms (ie. gas-powered versus electric cars) and creates different by-products.
Now I want you to think of a scale.
No, not this kind of scale
No – I want you to think of a scale, as in a delicate balance between differing metabolisms for different fuels.
Think of a multi-tiered scale, where a delicate balance between the types of metabolism and waste products is required for continued good health – anything that upsets the balance such as diabetes – throws everything out of whack.
Normally, as fuel (food) in consumed – the body uses insulin to transport the fuel into the cell for processing (metabolism), so think of insulin as a wheelbarrow carrying in complex carbohydrates (sugars) into the cell.
Now, in a person with obesity & diabetes – two things are occurring – too much fuel and not enough wheelbarrows**. These means that:
1. Excess fuel is converted into fat (adipose tissue – which we are all familiar with).
2. Without the wheelbarrows, the body has to find another way to break down the fuel. This other pathway – for fat metabolism has a lot of by-products – namely free fatty acids (cholesterol and triglycerides.) This leads to numerous problems (hypercholesterolemia and cardiovascular disease for one), and fatty liver disease.
(This is a gross oversimplification of a series of very complex mechanisms, but for today’s discussion – it is sufficient.)
Just as the rates of obesity, and diabesity (diabetes caused by obesity) have skyrocketed, so has cardiovascular disease (which we’ve talked about before) and the prevalence of non-alcoholic liver disease. In fact, the authors of the study below found that 70% of the people with a BMI greater than 35 have some degree of non-alcoholic liver disease, and over 30% have the more severe form – NASH.
The article by Rabl & Campos (2012) looks at the literature on the outcomes (progression or regression of disease) after bariatric surgery in patients previously diagnosed with NAFLD. (I’ve linked a pdf version of the entire article under the full reference.)
They looked at the current bariatric procedures including the ever popular lap-band procedure and it’s effectiveness in treating NAFLD. What they found was that in the majority of cases – with certain procedures (formal gastric bypass surgery aka Roux en Y, and biliopancreatic diversion procedures) the disease process was not only halted, but regressed as a result of both weight loss, and a reversal of altered metabolism. They also found that as a result of a reduced stomach surface area (in comparison to lap-band procedures where the stomach remains intact) – reduced ghrelin leads to increased weight loss.
(If you don’t know about ghrelin – think of it as an evil gremlin (the one that makes you want cookies when you know you are about to eat dinner) – since it is a potent appetite stimulant produced by the stomach. The larger the stomach – the more ghrelin released – so the surgical procedures such as gastric bypass where a portion of the stomach is actually surgical removed are significantly more effective overall that lap-banding procedures.)
This is a significant advancement for medicine and the treatment of obesity related disease – since as we suggested above, multiple authors including Burianesi et. al (2008) suggest that the true prevalence of non-alcoholic fatty liver disease is much higher than we realize, (thus affecting a lot more people.)
* There is a tendency in American society to ‘gloss over’ many of life’s harsh realities, and no where is this more evidence than in the public perceptions of organ transplantation as a ‘cure’ or permanent solution for organ failure. Transplanted organs do not have the same life expectancy as native organs (even in the best case scenarios) – and for most people who need non-kidney transplants – they get one opportunity, not multiple. Transplanted organs last ten years – maybe fifteen at the outside – so this is not a cure (particularly in young patients). Transplantation also carries a whole host of other problems with it – such as the development of opportunistic infections and cancer from the drugs used to prevent rejection, or rejection itself. The very drugs used to prevent rejection of some organs may cause failure of others – so relying on transplantation as a ‘cure’ for a disease that is becoming more and more prevalent is a pretty poor strategy.
** This balance between mechanisms can be upset in other ways – by starvation, for example, when the body starts catabolizing proteins.. Catabolizing – think cannibalism – as the body consumes it’s own muscle tissue because there is nothing left for it to eat, after it has exhausted all other sources of fuel.
References and Resources
Rabl, C. & Campos, G. M. (2012) The Impact of Bariatric Surgery on Nonalcoholic Steatohepatitis. Semin Liver Dis. 2012;32(1):80-91 [Article under discussion above].
Body Mass Index calculator – West Virginia Dietetic Association.
Bugianesi et. al. (2008). Clinical update on non-alcoholic fatty liver disease and steatohepatitis. Annals of hepatology, 2008; 7 (2): April – June 157-160. The authors ask, “What is the real prevalence of disease?”
Goldstein, B. J. (2001) Insulin Resistance: Implications for Metabolic and Cardiovascular Diseases. This is a good presentation that explains how alterations in glucose metabolism (from diabetes) affects fat metabolism.
Overview of NASH/ NAFLD with classifications, diagnostics, prognostics : University of California, San Diego – Dan Lawson, 2010 [notes]. Good reference for medical students, health care professionals wanting a brief review.
Salt, W. B. (2004). Nonalcoholic fatty liver disease (NAFLD): A comprehensive review. J Insur Med, 2004; 36: 27 -41.
For more about Bariatric surgery – including the Pros & Cons