Monday, April 30, 2012

Nonalcoholic Fatty Liver Disease


Nonalcoholic Fatty Liver Disease
Until recently I had not heard very much about Nonalcoholic Fatty Liver Disease.  In fact, I mainly attributed liver disease to those that used drugs and alcohol.  However, NAFLD is on the rise and many of us don't know anything about it.  NAFLD is the most prevalent liver disease in the Unites States, representing an estimated 24% of cases of liver disease!  You might be saying to yourself, "I don't drink alcohol and I feel fine. How could there be anything wrong with my liver?"  You might be very surprised.  In fact, most Americans are.

In its early stages (which can last for a decade or more), liver disease is symptom free. As a result, millions of people are living with nonalcoholic fatty liver disease (NAFLD) and don't even know it.

Take this Online Quiz --> Liver Disease Quiz

What Does the Liver Do?
The liver has two primary jobs. One is to detoxify the blood by converting substances like alcohol and medications to a usable form, then removing those chemicals from the body. The liver's second job is to turn food nutrients into compounds the body can use, storing excesses for future use.

Symptoms of Nonalcoholic Fatty Liver Disease
Generally, fatty liver disease has no symptoms, but as the condition progresses, individuals may experience one or more of the following:

-Fatigue
-Weight Gain
-Indigestion
-Loss of Appetite, Unintended Weight Loss
-Pain in the Upper-Right Abdomen
-Confusion or Disorientation
-Patches of Dark Skin on the Neck or Underarms
-Nausea
-Weakness

Fatty Liver Disease
Though mostly unknown until recently, fatty liver is reaching epidemic proportions in this country, affecting one in three Americans, even children


The Center for Disease Control reports that currently, approximately one half of the US adult population is overweight (BMI>25) and one quarter of the US adult population is obese (BMI>30). Projecting the prevalence of NAFLD and NASH in the obese subpopulation to the entire population would suggest that upwards of 29 million Americans have NAFLD and 6.4 million of these persons have nonalcoholic steatohepatitis (NASH).  The prevalence of simple fatty liver in obese persons can be estimated to be approximately 90% and that of NASH in obese persons to be 20%.


NASH is typically a disease of middle-aged overweight women with disproportionate abdominal fat distribution. However, there are also increasing reports of NASH related to obesity in men and even in pediatric populations. 

Symptoms can remain nonexistent for years but one very obvious sign of liver malfunction is weight-loss resistance or weight gain. However, as the disease progresses, it may also cause unexpected weight-loss or loss of appetite. Because of difficulty in diagnosing fatty liver disease it may be necessary to use an ultrasound or even a liver biopsy to make a diagnosis.


There is disagreement in the medical community as to whether fatty liver is a big deal.  Why is that?
Mainly it is because fatty liver itself is not considered to be life threatening.  It can escalate into far more serious conditions, though, including nonalcoholic steatohepatitis (NASH), cirrhosis of the liver, liver cancer, and ultimately liver failure.

While the liver does have the remarkable ability to regenerate and heal damage, that only works up to a point. A steady onslaught of poor diet, alcohol and/or drugs, exposure to everyday toxins, plus other health complications scar the liver, leading to permanent malfunctions. Eventually, the only remedy is a liver transplant, a costly, complicated procedure with no guarantee of success.

Why is this happening? 
The exact cause of NASH is still unknown but as the name suggests, fatty liver disease occurs when the liver is overrun by fat cells. These cells clog up the liver and interfere with its functions. 

Strong evidence, however, supports the concept that the process common to all stages of primary fatty liver disease (NAFLD) is insulin-resistance. While almost all patients with NASH are insulin resistant to some degree only a minority of patients who are insulin resistant develop NASH.  No evidence suggests that insulin resistance alone can lead to NASH.  A number of other factors may be involved as well in causing NAFLD and NASH and in progressing through the stages of NAFLD.

Fatty liver is often linked to other common health issues, particularly diabetes, prediabetes, high cholesterol and/or triglycerides, and obesity. Just having fatty liver makes an individual more likely to be diagnosed with type 2 diabetes and triples the risk of having a stroke.  Consumption of pills (prescription, nonprescription, or illegal) and too much alcohol play roles, too. 

Several theories, however, have been advanced.  First, it is possible that the accumulation of fat in the liver alone could lead to the development of NASH. According to this theory, the large quantity of fat in the liver is thought to be a source of peroxidation (removal of electrons from molecules). Peroxidation thereby generates so-called free radicals. These free radicals then damage proteins and organelles (small structures within a cell) in the liver cells. Finally, this damage leads to cell death and/or an inflammatory cell cascade that removes the afflicted cells. In other words, the fat could be thought of as potential fuel waiting to be ignited.

However, a growing body of work in animal models of fatty liver suggests a two-hit hypothesis. With this theory, the first hit is the fatty liver (steatosis). Then, a second event, or second hit, leads to the development of NASH. Multiple potential second hits have been suggested.

Finally, recent research suggests that leptin resistance may contribute to the development of NASH.  Leptin is a very small hormone that is secreted by the brain, fat, and stomach cells in response to eating. Its main effect is to curb the appetite. Patients with NASH have abnormally elevated levels of leptin but experience no loss of appetite. That is, they are resistant to the appetite-curbing effect of leptin. The leptin also helps control the processes of inflammation and scarring within the liver cells. Furthermore, leptin also increases insulin sensitivity. But the fact that patients with NASH are insulin resistant supports the idea that the leptin receptors are malfunctioning. 

Raw Foods Get Results
Doctors have found that people with fatty liver disease who follow a predominantly organic raw-foods diet have the best results. Eating more raw organic fruits and vegetables accomplishes several things. First, it's good for losing weight, one of the most important remedies for fatty liver. Second, by taking in fewer toxins with organic produce, your liver has fewer poisonous substances to process. Third, raw organic food supplies vital nutrients and fiber, something you aren't going to get with processed, prepared meals.

With proper care and by avoiding the wrong foods, fatty liver disease can be prevented from turning into something more serious. Here's an example: Researchers have found that diets high in saturated fats and fructose not only contribute to weight gain but also to NASH, the fatty liver-related condition mentioned earlier. Saturated fats and fructose are commonly found in fast foods, as well as prepared, packaged meals. Please avoid these!

LIVER-SUPPORTIVE FOODS

Beets Broccoli Cantaloupes
Garlic Onions Plums
Peppers Artichokes Blueberries
Tomatoes Oranges Raspberries
Carrots Pink Grapefruit Blackberries
Cabbage Apples Radishes

Supplements for Liver Health
There is evidence that some nutritional supplements that can help support a healthy liver.

Milk thistle: In clinical trials involving silymarin, the active ingredient in milk thistle, researchers found the herb rejuvenates and repairs damage to the liver. It is recommended to take 200 mg of milk thistle three times each day.
Vitamin E: A powerhouse antioxidant, vitamin E prevents damage to cell membranes, among other things. Look for a product containing natural vitamin E, which you can identify by its chemical name, d-alpha-tocopherol. The form dl-alpha-tocopherol is synthetic and not nearly as effective.  400 IU daily.
Curcumin: The active ingredient in the spice turmeric, curcumin has a long list of benefits, including heart health and fewer signs of aging. A recent study has found that curcumin protects liver cells from the type of damage commonly found in fatty liver and related conditions. Take 500 mg daily. If you are taking blood-thinning medications (including Coumadin or warfarin), please consult your physician before adding curcumin to your daily regimen.

These next supplements have recently been receiving mixed results from research but are still highly recommended:
Phosphatidylcholine (PC): This extract of lecithin helps liver cells regenerate. Try 900 mg twice daily.
Probiotics: Our intestinal tract is home to billions of good bacteria that are absolute necessities for a healthy immune system, proper digestion, and much more. Now research is showing that probiotics can prevent fat from accumulating in the liver. Look for a product containing at least 10 billion live organisms, and take one dose daily with a meal.
Fish oil: Try 2,000 to 3,000 mg taken in two or three 1,000 mg doses during the day.
Digestive enzymesFor some people, when switching to a raw-food diet they may experience problems with digestion.  If this happens, taking digestive enzymes can help. These enzymes target specific types of foods.    
Sources
Ying I, Saposnik G, Vermeulen MJ, et al. "Nonalcoholic fatty liver disease and acute ischemic stroke." Epidemiology. 2011 Jan;22(1):129-30.
Sung KC, Kim SH. "Interrelationship between fatty liver and insulin resistance in the development of type 2 diabetes." Journal of Clinical Endocrinology & Metabolism. 2011 Apr;96(4):1093-7.
Tang Y, Zheng S, Chen A. "Curcumin eliminates leptin's effects on hepatic stellate cell activation via interrupting leptin signaling." Endocrinology. 2009 Jul;150(7):3011-20.
Kang Q, Chen A. "Curcumin eliminates oxidized LDL roles in activating hepatic stellate cells by suppressing gene expression of lectin-like oxidized LDL receptor-1." Lab Invest. 2009 Nov;89(11):1275-90.
Kohli R, Kirby M, Xanthakos SA, et al. "High-fructose, medium chain trans fat diet induces liver fibrosis and elevates plasma coenzyme Q9 in a novel murine model of obesity and nonalcoholic steatohepatitis." Hepatology. 2010 Sep;52(3):934-44.
Xu RY, Wan YP, Fang QY, et al. "Supplementation with probiotics modifies gut flora and attenuates liver fat accumulation in rat nonalcoholic fatty liver disease model." Journal of Clinical Biochemistry and Nutrition. 2012 Jan;50(1):72-7.


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