Fighting Fatty Liver, Part 1 of 2
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How the gut, microbes, inflammation, and diet affect the liver, and what to do about it
The fatty liver epidemic
Sedentary lifestyles, nutrient-poor diets, chemical exposures, and an excess of sugar and refined foods are wreaking havoc on and in our bodies more than ever before. And the effects aren’t just cosmetic – beyond bulging waistlines, the incidence of high blood pressure, high blood sugar, and high cholesterol associated with metabolic syndrome are all on the rise, along with the rate of nonalcoholic fatty liver disease (NAFLD).
As the name implies, NAFLD (casually pronounced “naffled”) is a condition in which the liver stores excess fat occurring in those who drink little to no alcohol. Over time NAFLD can not only increase the risk of cardiovascular disease, but can also lead to further ailments of the liver like cirrhosis and liver cancer – conditions also seen in heavy alcohol consumers, but now more commonly seen in non-drinkers. In fact, NAFLD is the leading cause of liver disease in the West, often concurrent with other metabolic conditions: approximately 40 to 80% of people with the disease also have type 2 diabetes, and 30 to 90% are obese.[i] As with metabolic syndrome, the incidence of NAFLD is also on the rise among children, affecting an estimated 3 to 12% of children with normal body mass and an alarming 40 to 80% of obese children.[ii]
NAFLD is the leading cause of liver disease in the West, often concurrent with other metabolic conditions: approximately 40 to 80% of people with the disease also have type 2 diabetes, and 30 to 90% are obese.
The umbrella term NAFLD encompasses two sub-categories: nonalcoholic fatty liver (NAFL), which is characterized by fatty liver with little to no inflammation; and nonalcoholic steatohepatitis (NASH), which is the more harmful of the two and is defined as fatty liver with inflammation. It’s estimated that 30 to 40% of American adults have NAFL and about 3 to 12% have NASH.[iii]
How did all this fat get in my liver?
The causes of NAFLD are not fully known, but a large piece of the puzzle has to do with the liver holding onto excess triglycerides. Triglycerides (TGs) are a form of fat that the body produces from excess calories, such as those that come from carbohydrates and sugar. Insulin resistance and blood sugar levels clearly play a role in the progression of NAFLD, which may very well explain why so many individuals with the disease are also diabetic. It has also been demonstrated that oxidative injury further exacerbates the situation, contributing to the progression of NASH.
But what causes that oxidative injury? It’s still being researched, but some explanations include iron overload conditions (like hemochromatosis), low antioxidant defenses, and an over-abundance of opportunistic or pathogenic bacteria in the gut (also known as dysbiosis), which contributes to inflammation and “leaky gut.”[iv]
What’s the gut got to do with it?
Living in close quarters, the liver and gut work together to aid digestion and elimination. One role of the gut wall is to ensure that nutrients are allowed to enter the body and that harmful agents – like toxic bacteria and viruses – are not. In the presence of agents that irritate the gut – like environmental toxins, non-steroidal anti-inflammatory drugs (NSAIDs),[v],[vi] alcohol,[vii],[viii] stress, a high fat diet,[ix] nutritional deficiencies,[x],[xi] food allergies, infections, and/or certain diseases such as celiac disease[xii] and irritable bowel disease (IBD) – the walls of the intestine undergo injury and thus lose integrity.
This state of increased intestinal permeability is called “leaky gut,” and quickly leads to a domino effect of disaster in the body. As the spaces between the cells of the intestinal wall grow wider, bacteria and other toxins begin traveling between these cells and into the bloodstream, where they create inflammation. And the liver bears the brunt of that inflammation. In fact, leaky gut and bacterial overgrowth are both correlated with the severity of fatty liver, and it has been shown that 50% of those with NASH also have small intestinal bacterial overgrowth (SIBO).[xiii]
In fact, leaky gut and bacterial overgrowth are both correlated with the severity of fatty liver, and it has been shown that 50% of those with NASH also have small intestinal bacterial overgrowth (SIBO).
Graphic by Dr. Carrie Decker
A healthier diet for a happier liver
When it comes to preventing and managing NAFLD, it’s important to remember that the origins of the condition are multifactorial and include high blood sugar levels, leaky gut, dysbiosis, and excess cholesterol production. Making dietary choices that avoid these insults to the body are therefore the cornerstones of NAFLD prevention and care. Specifically, avoiding refined carbohydrates and foods high in sugar can not only keep blood glucose levels in a healthy range, but can also serve to deprive the harmful intestinal bacteria of the fuel they need to overpopulate, cause leaky gut, and wreak further havoc in the body.[xiv],[xv]
Consuming fiber may also help reduce fat accumulation in the liver.[xvi] In fact, those with NAFLD were on average found to consume 50% less fiber than those without NAFLD in one study,[xvii] and consuming more fiber improved liver markers in NAFLD patients in another.[xviii],[xix] The Mediterranean diet – rich in vegetables, fruits, seeds, nuts, whole grains, and legumes, with moderate consumption of animal-sourced protein – has been shown to lower the degree of fatty liver and insulin resistance in patients with NAFLD/NASH.[xx],[xxi] Dietary changes such as these have been observed to have a positive effect on NAFLD even without caloric restriction and/or weight loss.
Those with NAFLD were on average found to consume 50% less fiber than those without NAFLD in one study, and consuming more fiber improved liver markers in NAFLD patients in another.
Check out Part 2 of this article, which explores the botanicals and nutrients that can help prevent and battle NAFLD.Click here to see References
[i] Spengler EK, Loomba R. Recommendations for diagnosis, referral for liver biopsy, and treatment of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Mayo Clinic Proceedings. 2015;90(9):1233-46.
[ii] Berardis S, Sokal E. Pediatric non-alcoholic fatty liver disease: an increasing public health issue. Eur J Pediatr. 2014 Feb;173(2):131-9.
[iii] Brunt EM, et al. Nonalcoholic fatty liver disease. Nature Reviews Disease Primers. 2015;1:15080.
[iv] Sheth SG, Chopra S. Epidemiology, clinical features, and diagnosis of nonalcoholic fatty liver disease in adults. Waltham (MA): UpToDate. 2017.
[v] Bjarnason I, Takeuchi K. Intestinal permeability in the pathogenesis of NSAID-induced enteropathy. J Gastroenterol. 2009;44 Suppl 19:23-9.
[vi] Bjarnason I, et al. Side effects of nonsteroidal anti-inflammatory drugs on the small and large intestine in humans. Gastroenterology. 1993 Jun;104(6):1832-47.
[vii] Vishnudutt Purohit, et al. Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences (Symposium Summary). Alcohol. 2008 Aug; 42(5): 349-361.
[viii] Bjarnason I, et al. The leaky gut of alcoholism: possible route of entry for toxic compounds. Lancet. 1984 Jan 28;1(8370):179-82.
[ix] Pendyala S, et al. A high-fat diet is associated with endotoxemia that originates from the gut. Gastroenterology. 2012 May; 142(5):1100-1101.e2.
[x] Assa A, et al. Vitamin D deficiency promotes epithelial barrier dysfunction and intestinal inflammation. J Infect Dis. 2014 Oct 15;210(8):1296-305.
[xi] Kong J, et al. Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G208-16.
[xii] Drago S, et al. Gliadin, zonulin and gut permeability: effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scandinavian Journal of Gastroenterology 2006;41:408-419.
[xiii] Schnabl B, Brenner DA. Interactions between the intestinal microbiome and liver diseases. Gastroenterology. 2014 May;146(6):1513-24.
[xiv] Guerville M, et al. Western-diet consumption induces alteration of barrier function mechanisms in the ileum that correlates with metabolic endotoxemia in rats. Am J Physiol Endocrinol Metab. 2017 Aug 1;313(2):E107-20.
[xv] Frazier TH, et al. Gut microbiota, intestinal permeability, obesity-induced inflammation, and liver injury. JPEN J Parenter Enteral Nutr. 2011 Sep;35(5 Suppl):14S-20S.
[xvi] Cantero I, et al. Fruit fiber consumption specifically improves liver health status in obese subjects under energy restriction. Nutrients. 2017 Jun 28;9(7):667.
[xvii] Cheng Y, et al. Associations between dietary nutrient intakes and hepatic lipid contents in NAFLD patients quantified by H-MRS and dual-echo MRI. Nutrients. 2016 Aug 27;8(9):527.
[xviii] Eslamparast T, et al. Dietary composition independent of weight loss in the management of non-alcoholic fatty liver disease. Nutrients. 2017 Jul 26;9(8):800.
[xix] Musso G, et al. Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis. Hepatology. 2003 Apr;37(4):909-16.
[xx] Eslamparast T, et al. Dietary composition independent of weight loss in the ,management of non-alcoholic fatty liver disease. Nutrients. 2017 Jul 26;9(8).
[xxi] Zelber-Sagi S, et al. The Mediterranean dietary pattern as the diet of choice for non-alcoholic fatty liver disease: evidence and plausible mechanisms. Liver Int. 2017 Jul;37(7):936-49.
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