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Liver Myths and Fatty Liver Disease

Every year, I see more and more people in my medical office with Fatty Liver Disease. I get at least two to three questions a week about it on social media sites. Fatty liver disease is now so common that many gastroenterologists are fearful that it will soon surpass viral hepatitis and alcohol use as the primary causes of cirrhosis.

Insulin resistance is the underlying driver for Fatty Liver Disease or Non-Alcoholic Fatty Liver Disease (NAFLD).  Fatty liver disease is also called hepatic steatosis (nonalcoholic steatohepatitis or NASH) when alcohol is not the primary cause of fat accumulation in the liver.  NAFLD can progress to cirrhosis and is an important cause of cryptogenic cirrhosis. 

In fact, we are now seeing more cirrhosis from NAFLD then we see caused from Hepatitis infections or even alcohol use.  NAFLD is the driver behind the majority of cases of cirrhosis. It is 3.9 times more prevalent among Hispanics and African Americans than European Americans, and it is caused by the same metabolic processes that cause obesity and diabetes (1).

30-35% of the population in 2004 who did not drink alcohol were demonstrated to have NAFLD (2).  And, 46% of US military personnel and their families had NAFLD by ultrasound in a 2011 study (3).

Insulin Resistance & NAFLD

It is interesting to me that NAFLD is directly associated with all of the diseases caused by insulin resistance including obesity, hypertension, abnormal cholesterol and overt diabetes.

Elevated insulin responses to starches, sugars and fructose in the diet cause increased fat deposition in the fat cells (adipocytes).  As we gain weight, and our fat cells fill to capacity, the fatty tissues (largest endocrine glands in the body) begins over-production of hormones like TNF-alpha, IL-1, and IL-6.  These hormones have an abnormal influence on the liver and the signaling of insulin from the pancreas.  Compensatory changes to handle these abnormal signals lead to increased glucose production from the liver and increased insulin from the pancreas.  This abnormal signaling causes increase triglcyeride (TG) deposition in the liver and increased deposition of non-esterified cholesterol in the liver (4).  Secondary oxidative injury from non-esterification of cholesterol, elevated hepatic iron, leptin resistance, antioxidant deficiencies and changes in intestinal bacteria all seem to play a part in the orchestration of fatty deposition in the liver.  This, concert of changes hormonaly and metabolically, leads to liver enlargement and can progress to non-alcoholic cirrhosis. 

Figure 1 – Interplay between glucose and lipid metabolism in the PRIM and SEC models of NAFLD. Liver-specific overexpression of SREBP-1c and increased hepatic DNL in the PRIM mouse model leads to accumulation of DAGs and triacylglycerols (TAG) and development of NAFLD. NAFLD in PRIM associates with decreased insulin signaling and higher hepatic glucose output. On the one hand, mitochondrial oxidative capacity (O2 flux) is increased under fasted conditions while emission of ROS remains unchanged. ChREBP-mediated lipogenesis in adipose tissue and fat mass are increased, which could protect from hyperglycemia and peripheral IR. On the other hand, SEC mice are characterized by loss of adipose tissue and ectopic lipid (DAG, TAG) accumulation in both liver and skeletal muscle. Moreover, accumulation of extrahepatic lipids in SEC but not intrahepatic lipids in PRIM associates with portal and lobular inflammation of the liver. In SEC, hepatic O2 flux is increased under fed conditions as well as systemic oxidative stress. Liver and skeletal muscle are both characterized by decreased insulin sensitivity. alb, albumin; AP2, adipocyte P2. (4).

How do you know if you have fatty liver disease? 

Elevated liver enzymes (AST and ALT) by 10-100 points are usually the first signal.  This is confirmed by ultrasound or CT scan of the abdomen.  Diagnostic imaging reveals a heterogenous texture (sandy or speckled appearance of a liver) that is often enlarged about 20% of the time – Liver width of > 18 cm). 

When liver enzymes are elevated for an unknown reason, the following lab testing is essential:

  • Anti-Hepatitis C virus antibody
  • Hepatitis A IgG
  • Hepatitis B surface antigen
  • Hep B surface antibody
  • Hep B core antibody
  • Plasma Iron
  • Ferritin
  • Total Iron Binding Capacity
  • Serum gammaglobulin levels
  • ANA titier
  • Anti-smooth muscle antibody
  • Anti-liver/kidney microsomal antibody-1

These tests should all be completed to rule out viral and auto-immune forms of hepatitis. 

Historically, most physicians had no idea why fatty liver disease starts happening. And, many physicians not well versed in how insulin resistance works metabolically, still don’t know why fatty liver disease occurs.

Because of what we now know about how insulin affects the fat cells, and the adverse effects of cholesterol oxidation, we have a much better understanding. This understanding now makes it possible to reverse fatty liver disease.

We aggressively treat insulin resistance in my office, and I have repeatedly seen fatty liver disease completely resolve in 12 months with the use of a ketogenic or carnivorous diet.   In fact, I’ve seen fatty liver disease reversed thousands of times over the last 20 plus years of my practice. 

Myth #1

“Liver cleanses or detoxes are important for daily health especially if you over indulge.”  

Though liver cleanses are packaged to claim that they’re a cure-all for daily liver health and overindulgence, I DO NOT recommend them.  These products and mixtures are not regulated by the FDA, and thus are not uniform and have not been adequately tested in any clinical trials. 

It has been my clinical experience over the last 20 years that liver cleanses actually do more harm than good.  While some common ingredients in liver cleanses have been shown to have positive results — milk thistle has been shown to mildly decrease liver inflammation, and turmeric extract has been shown to protect against liver injury by helping to stabilize glucose signaling — there have not been adequate clinical trial data in humans to recommend the routine use of these natural compounds for prevention.

As for overindulgence of alcohol or food, less is always best when it comes to liver health, and cleanses have not been proven to rid your body of damage from excess consumption.  The best way to cleans your liver is an 18-24 hour fast.

Myth #2

“Liver cleanses are a safe and health way to lose weight.” 

Many liver detoxification products are sold as weight loss cleanses. However, there is absolutely no clinical data to support the efficacy of these cleanses. In fact, some dietary supplements can actually cause harm to the liver by leading to drug-induced injury.  Any of these products should be used with great skepticism and caution.

Myth #3

“You cannot protect yourself against liver disease.” 

Contrary to this myth, there are many preventative methods to protect yourself from liver disease. 

  • Don’t drink alcohol in excess. In fact, abstinence is a fantastic way to avoid liver disease from alcohol.  However, if you must drink, limit your consumption to no more than two drinks per day.
  • Avoid simple sugars.  Carbohydrates and sugars contain fructose. Fructose is metabolized identically to alcohol in the liver.  Non-alcoholic fatty liver disease is driven by increased consumption of sugar, fruit juices and fruit.  Fatty liver disease can be reversed in 12 months with the use of a ketogenic diet. 
  • Avoid risky behaviors like illicit drug use, having unprotected sex with multiple partners or getting a tattoo in an unregulated setting. These behaviors increase the risk of acquiring viral hepatitis. 

Myth #4

“Liver cleanses can correct existing liver damage.” 

Liver cleanses have NEVER been proven to treat existing liver damage. However, if you already have liver disease, talk to your doctor about treatments know to be very effective in treatment of liver disease. 

  • Hepatitis A & B – vaccines exist that are very effective in prevention of these forms of hepatitis.
  • Oral medications are available to treat Hepatitis B infections. 
  • Hepatitis C – Very effective and well tolerated oral medications are available to treat those with hepatitis C.
  • Alcoholic Liver Disease – Discontinue all alcohol to provide the best chance of recovery. The liver has an amazing ability to heal, and recover once the damage has stopped. 
  • Non-alcoholic Liver Disease – The most effective method to reverse non-alcoholic liver disease is to cut out all simple sugars and starches from the diet. Use a ketogenic or carnivorous diet.

Myth #5

“Obesity does not increase your risk of liver disease.”   

This is the biggest myth of all.  The media has begun to push “healthy obesity” as a mindset.  Obesity increases your risk of fatty liver disease by 30-50%. If Non-alcoholic fatty liver disease (NAFLD) persists, this can cause fibrosis and cirrhosis later in life.  NAFLD is increasing rapidly and may surpass the prevalence of Hepatitis C in the next 20 years. 

Ultimately, the best thing you can do to keep your liver healthy is to treat it well. Avoid frequent overconsumption of sugary and starchy foods and alcohol, maintain a healthy low-carbohydrate or ketogenic diet and exercise regimen, and get screened if you have liver disease risk factors. If you do have liver damage, work with your physician to come up with the healthiest and safest plan for your personal needs.

References:

  1. Browning JD, Kumar KS, Saboorian MH, Thiele DL.  Ethnic differences in the prevalence of cryptogenic cirrhosis. Am J Gastroenterol. 2004 Feb;99(2):292-8. PubMed:15046220
  2. Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, Grundy SM, Hobbs HH. Prevalence of hepatic steatosis in an urban population in the United States: impact of ethnicity.  Hepatology. 2004;40(6):1387. PMID:15565570
  3. Williams CD, Stengel J, Asike MI, Torres DM, Shaw J, Contreras M, Landt CL, Harrison SA.  Prevalence of nonalcoholic fatty liver disease and nonalcoholic steatohepatitis among a largely middle-aged population utilizing ultrasound and liver biopsy: a prospective study. Gastroenterology. 2011;140(1):124. Epub 2010 Sep 19. PMID: 20858492
  4. Jelenik T, et al. Mechanisms of Insulin Resistance in Primary and Secondary Nonalcoholic Fatty Liver. Diabetes 2017 Aug; 66(8): 2241-2253.  Published online 2017 May 10. doi: 10.2337/db16-1147

Fatty Liver Disease – It Isn't Caused By Fat . . .

Two out of ten people that he sees in his office have signs of fatty liver disease.  What does that mean to society and how does it affect you?

Spend 11 minutes with Dr. Nally as he discusses the cause of Fatty Liver Disease and discusses the most effective method he has found to treat it.  What is the underlying cause?  Watch and find out.