The Preventable, Silent Disease Afflicting 30 Percent of Adults

It afflicts an estimated 20 to 30% of people in Western countries, yet most people have never heard about nonalcoholic fatty liver disease (NAFLD), nor have they heard about nonalcoholic steatohepatitis (NASH), an advanced form of NAFLD, which afflicts around 17% of the population.1,2,3

Pharmaceutical companies, however, are rushing to develop drugs for these lifestyle-related diseases. Within the next 5 years, the market for such drugs is expected to swell to $8 billion.4

What are these diseases and why are they so unknown? In this article, we’ll answer those questions, while also examining why the Paleo diet can play a big role in treatment.

What Causes Liver Fat Accumulation?

NAFLD is characterized by the accumulation of liver fat (triglycerides) by people consuming less than 20 grams of alcohol per day.5 This accumulation, which develops slowly and subtly over the course of many years, can progress into NASH and even cirrhosis. NASH is the advanced form of NAFLD, which features inflammation and fibrosis (scar tissue) within the liver, plus increased fat accumulation.

The precise etiology (the manner of causation) of NAFLD is unknown, but the disease is strongly associated with obesity, insulin resistance, diabetes, and hyperlipidemia (excessive levels of fat within the blood). For example, about 80 to 90% of obese adults have NAFLD, as do 30 to 50% of diabetes patients, and upwards of 90% of hyperlipidemia patients.6 Furthermore, as reported by Tolman et al., “what is common to virtually all patients with NAFLD is insulin resistance.”7

Preventing NAFLD and NASH therefore starts by preventing insulin resistance, which in turn starts by adopting a healthy diet and lifestyle practices. By eliminating cereals, sugar, and other rapidly digestible carbohydrates, for example, the Paleo diet helps normalize insulin levels. Those types of carbohydrates are what Dr. David Ludwig refers to as “the ultimate fat cell fertilizer.” They produce the most insulin, thereby triggering fat accumulation.8

Put another way, it’s not dietary fat that makes you fat; excessive carbohydrate consumption, particularly sugar, is the far more likely culprit. The same holds true for liver fat accumulation. Perhaps to an even greater extent. For example, Sevastianova et al. administered high-carb diets to overweight adults for 3 weeks, resulting in “a >10-fold greater relative change in liver fat (27%) than in body weight (2%).”9

Compared to glucose, excessive fructose consumption is particularly detrimental for liver health because the liver bears most of the burden of fructose metabolism.10 In a recent review published in Hepatobiliary Surgery and Nutrition, Basaranoglu et al. characterized fructose as a “weapon of mass destruction” with respect to NAFLD. The authors wrote, “ingested carbohydrates are a major stimulus for hepatic de novo lipogenesis (DNL) and are more likely to directly contribute to NAFLD than dietary fat.”11 They went on to demonstrate that high fructose corn syrup (HFCS) consumption, particularly HFCS-containing beverages, is associated with NAFLD based on the lipogenic and proinflammatory effects of fructose.

Risks and Solutions

According to Dr. Manal Abdelmalek, a liver disease specialist at Duke University, NAFLD doesn’t necessarily pose a problem for most people. “You may live and die with your fatty liver and never know it,” he explains.12 The main problem is the potential for NAFLD to progress into NASH or cirrhosis.

With NASH, the liver becomes damaged by fibrosis, so much so that by 2020, NASH is expected to overtake hepatitis C as the leading reason for liver transplants within the US.13 As the fibrosis develops, the next stage is cirrhosis, which severely impairs liver function. Cirrhosis is the 12th leading cause of death in the US14. Once cirrhosis sets in, 30 to 40% of patients die of liver failure over a 10-year period.15

The easiest and most logical way to avoid NAFLD and its downstream diseases is through diet and lifestyle choices that prevent insulin resistance. Unfortunately, portions of the medical community are giving up on this solution. Scientific American, for example, recently informed its readers that despite the liver’s extraordinary ability to regenerate healthy cells following dietary adjustments, “unfortunately, studies have shown again and again that people are unable to stick to a healthier regime, and liver specialists would like to be able to offer treatments. The need for drugs is made more urgent by the fact that obese, diabetic people are often low on the liver transplant list.”16

There are currently no FDA-approved drugs for the treatment of NASH, but a series of recent trials has catalyzed a huge increase in the number of companies vying for approval. According to Rohit Loomba, director of the University of California, San Diego’s NAFLD Translational Research Unit, “suddenly we went from five to 15 companies overnight, and now we are at 50 companies.”17 Will NASH drugs become the next statins – another huge pharmaceutical cash cow foisted upon large portions of the population? As usual, the profit motive tends to obfuscate the most practical and most effective solution, which in this case is the Paleo diet.

References

[1] Bellentani S, et al. (2010). Epidemiology of non-alcoholic fatty liver disease. Digestive Diseases, 28(10). Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/20460905

[2] Clark JM, et al. (May, 2002). Nonalcoholic fatty liver disease.

[3] Tolman KG, et al. (Dec, 2007). Treatment of non-alcoholic fatty liver disease. Ther Clin Risk Manag, 3(6). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2387293/

[4] Jarvis LM. (Oct 4, 2016). Facing a Silent Liver Disease Epidemic. Scientific American. Retrieved from https://www.scientificamerican.com/article/facing-a-silent-liver-disease-epidemic

[5] Szczepaniak LS, et al. (Feb 2005). Magnetic resonance spectroscopy to measure hepatic triglyceride content: prevalence of hepatic steatosis in the general population. Am J Physiol Endocrinol Metab, 288(2). Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/15339742/

[6] Bellentani S, et al. (2010). Epidemiology of non-alcoholic fatty liver disease. Digestive Diseases, 28(10). Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/20460905

[7] Tolman KG, et al. (Dec, 2007). Treatment of non-alcoholic fatty liver disease. Ther Clin Risk Manag, 3(6). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2387293/

[8] Levin, L. (May-Jun 2016). Are All Calories Equal? Harvard Magazine. Retrieved from http://harvardmagazine.com/2016/05/are-all-calories-equal

[9] Sevastianova K, et al. (Oct 2012). Effect of short-term carbohydrate overfeeding and long-term weight loss on liver fat in overweight humans. American Journal of Clinical Nutrition, 96(4). Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/22952180

[10] Chong MF, et al. (Feb 2007). Metabolic interaction of dietary sugars and plasma lipids with a focus on mechanisms and de novo lipogenesis. Proc Nutr Soc, 66(1). Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17343772/

[11] Basaranoglu M, et al. (Apr 2015). Carbohydrate intake and nonalcoholic fatty liver disease: fructose as a weapon of mass destruction. Hepatobiliary Surgery and Nutrition, 4(2). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405421/

[12] Jarvis LM. (Oct 4, 2016). Facing a Silent Liver Disease Epidemic. Scientific American. Retrieved from https://www.scientificamerican.com/article/facing-a-silent-liver-disease-epidemic

[13] Jarvis LM. (Oct 4, 2016). Facing a Silent Liver Disease Epidemic. Scientific American. Retrieved from https://www.scientificamerican.com/article/facing-a-silent-liver-disease-epidemic

[14] National Institute of Diabetes and Digestive and Kidney Diseases. (Apr 2014). Cirrhosis. Retrieved from https://www.niddk.nih.gov/health-information/health-topics/liver-disease/cirrhosis/Pages/facts.aspx

[15] McCullough AJ. The epidemiology and risk factors of NASH. In: Farrell GC, George J, Hall P, et al., editors. Fatty liver disease: NASH and related disorders. Oxford: Blackwell; 2005. pp. 23–37. Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/9780470987438.ch3/summary

[16] Jarvis LM. (Oct 4, 2016). Facing a Silent Liver Disease Epidemic. Scientific American. Retrieved from https://www.scientificamerican.com/article/facing-a-silent-liver-disease-epidemic

[17] Jarvis LM. (Oct 4, 2016). Facing a Silent Liver Disease Epidemic. Scientific American. Retrieved from https://www.scientificamerican.com/article/facing-a-silent-liver-disease-epidemic

About Christopher James Clark, B.B.A.

Christopher James Clark, B.B.A.Christopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.

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“2” Comments

  1. The think that always leave me astonished every time is the claim:”you can live anyway with X or Y…”. The fact that we can survive despite X issues is the real double edge sword. Thriving is a far cry from surviving.
    Do we have to wait to get really sick before taking the deserved health into our hands?
    This trick is being well exploited by drug companies, because it’s about all what they do: disguising the symptoms and overlooking the cause, making people life dependant on their products.
    Insulin resistance is indeed the main trigger of most problems, including the aforementioned.
    Anyway, insulin resistance is not all about carbs, but about grains, HFCS and all the refined stuff.
    The main focus should always be about real species appropriate food.
    It’s easy to focus on macronutrients, especially carbs, but the problem is more about their concentrations.
    Aside from dietary toxins, that I believe have a lot to do with inflammation, it’s about concentration that is an evolutionary mismatch, that drives proinflammatory pathways mostly mediated by the microbiota.
    Thus, for me, the problem is also about protein powders and even concentrated fats may be hazardous in this sense, though at a lower extent than carbs.

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