I recently attended the meeting of the AASLD, the American Association for the Study of Liver Disease, which is a group of world leaders in research into liver disease. I was very encouraged by what I heard there and I've been wondering how to explain that to the community dealing with disease.
Fatty liver has mostly been dismissed as a medical problem because it was often benign and even if it wasn't there was no treatment anyway so dealing with it was a matter of waiting until some organ showed symptoms and try to deal with those until you die. Many doctors today leave their patients with that feeling of hopelessness with the phrase, I'm sorry but we have no treatment.
There are two very important points that I want to make. First, it isn't correct to say there is no treatment. Diet and lifestyle have been well proven to be treatments and there is a lot of information on our website about diets. If you want to review, here is a link
More importantly, we live in a very fortunate time because medical knowledge is advancing at a torrid pace. I've struggled to put that into perspective and decided to relate a discussion I had with Dr Peter Traber, the CEO of Galectin Therapeutics, one of the companies researching liver disease treatment.
Dr Traber is also the author of the blog, LiverLine, which I suggest you read. It is excellent. He was relating the changes in health care over his career. His example was Hepatitis C. When he began his career the virus was unknown. Over the course of several decades it was discovered and even though it was very difficult a cure was developed and now we can defeat that disease. His observation of the state of liver disease research is that we are now on the brink of developing real treatments for liver disease. Even a veteran researchers like him is impressed by the speed and quality of the work being done on liver disease today.
There are over 400 drugs being actively evaluated and only a few will turn out to be of value but the research community is confident that they now know enough to be sure that we will get useful therapies in the next several years. The message for current patients is that for now diet and exercise are your only friends but help is on the way so a hopeful attitude is also part of the therapy.
Want to know more about clinical trials? Here are some short videos from our partner Antidote.
If you have diabetes and are overweight, you can have silent liver disease too
Learn about fatty liver disease and NASH, and see if you may qualify for a clinical trial.
If you have diabetes or struggle with your weight, you may have fatty liver disease. A severe form of fatty liver disease, called nonalcoholic steatohepatitis (NASH), often has no symptoms but can cause significant damage to your liver if not diagnosed early.
About the Clinical Trial
The MK-3655 Clinical Trial is evaluating the safety and effectiveness of MK-3655, an investigational medication for people with NASH. This trial will test MK-3655 compared to placebo. A placebo looks like the study medication but contains no active ingredient.
You may be able to participate if you: *
- Are a male or postmenopausal female, 18 to 80 years of age [in Japan: 20 to 80 years of age]
- Have NASH confirmed by a liver biopsy
- Do not have type 2 diabetes OR have type 2 diabetes that is well controlled by diet or a stable dose of diabetes medication
- Have had a stable weight for at least 3 months
If you qualify and decide to participate:
- Your liver and your overall health will be monitored closely by an experienced study team
- You will receive the investigational medication and study-related doctor visits at no charge
- The information gathered may help advance medical knowledge about NASH and may improve patient care in the future
- Participation is voluntary and you are free to withdraw from the study at any time. Your privacy will be maintained throughout the clinical trial
To learn more, including the possible risks and benefits of participation, visit NASH3655Study.com.
For a copy of this information, you can download this flyer.
*There may be additional requirements to participate. The study doctor can provide you with more information. Additional potential risks and benefits will be fully described to you by your study team.
Historically fatty liver was viewed as being mostly benign. The theory was that while liver fat might make the organ vulnerable to other problems it was, after all just normal fat. This view naturally led to medicine focusing on other problems where symptoms existed. I thought that view made little sense if only because fat people died younger but the science wasn't there so that remained the story.
Research is now coming out which shows that a fatty liver is an active cause of disease in other organs. Did you ever wonder why people frequently get fat then get type 2 diabetes? Consider all the effort devoted to diabetes in the management of the symptoms and the long term medical needs. German research has now shown that a fatty liver begins to produce different secretions, such as one called fetuin-A, into the blood stream. Those substances enter other organs and trigger reactions there.
This image from IDM shows pancreatic islet cells surrounded by fat cells. The study was reported in Science Daily at this link but I'll summarize it below.Read more
The foundation was spawned out of my personal journey through undiagnosis, misdiagnosis, and finally a stage 4 NASH so I've chronicled my journey through our website. I just completed a checkup at the transplant center and now that we are two years into my treatment plan I am starting to get enough data that might be helpful.
I do have some very encouraging results to report. In 2015 I had an MRI elastography which reported my liver stiffness as 4.8 kPa. Their scale shows that to be a stage 3 moving into full cirrhosis which they start at 5.0 kPA. My biopsy called it cirrhosis and I also had a fibroscan that year which read as 21.5. Anything above 12 is considered to be cirrhosis. A long way around to say I really do have a liver in trouble even though I have never had a symptom of any kind. Go figure.
There are many ways to support the efforts of the Fatty Liver Foundation. General purpose donations are welcome from anyone concerned about public health in general or liver disease specifically. At the program level, we invite sponsorship in the following ways:
The Platinum level sponsor has provided a contribution to the Foundation of at least $200,000. Platinum sponsors may fund a mobile screening system or other project of interest and may be featured prominently with logos and other information in all of our media efforts promoting their support for public health.
The Gold level sponsor has provided a contribution to the Foundation of at least $100,000. Gold sponsors have the opportunity to direct their contributions to particular projects in partnership with the Foundation. While the screening project is our most visible patient outreach program but there are many needs within the obesity, fatty liver, and cirrhosis challenged patients that benefit from efforts surrounding the screening events.
The Silver level sponsor is anyone who has provided a contribution to the Foundation of at least $50,000. Silver level sponsors are honored on our sponsorship webpage with their logo and a link to their webpage for more information.
The Bronze level sponsor is anyone who has provided a contribution to the Foundation of at least $10,000. They are honored on our sponsorship webpage with their logo in recognition of their contributions.
Blue ribbon level contributions are all those less than $10,000. They are honored on our sponsorship webpage with their logo in recognition of their contributions.
Whatever level of support you can give is greatly appreciated and will be used to maximize benefit for current and future patients of liver disease and the complications of obesity which is at the heart of most fatty liver disease.
This is an overview of our site. Liver disease is complex and we invite you to study it but if all you want is a quick summary the site probably isn't for you
I was shocked to learn I am a cirrhosis patient and because of that I became a patient advocate. I decided the best way to have a voice was to create a non-profit foundation. If you are here, you or someone you care about, is obese, is ill, has or is at risk for liver disease or a co-morbidity associated with it. Obesity is a major cause of the problems. You won’t care about this topic except as a health or diet issue.
This is what you will find here:
- Non-technical explanation of how your body actually works
- How the liver develops disease over time
- Why fats are a critical source of fuel for your cells
- How the liver manages triglycerides
- How the course of fatty liver disease depends on triglycerides and carbohydrates
- How the kind of dietary fat you use matters
- Information by a liver patient for liver patients
- Information about diet based upon bio-chemistry not fads
This site is not trying to sell you anything.
We are a nonprofit foundation and we do not represent anyone but the patient. If you are looking for advice on supplements or quick fixes this is not the place for you. We offer extensive information about the body in general, the liver specifically, and we recommend lifestyle strategies that have worked for me specifically and which I believe are valuable for anyone concerned about liver health to be familiar with. The strategies are also the best we know of for weight control and management. If you struggle with weight you need to understand how the body works rather than just buy expensive stuff from the guru of the month. Our goal is to help you understand the problem so that you can deal with it effectively.
This site offers you extensive opportunity to add your own comments and experiences to the pages. We invite you to add your own thoughts if you would like to. Patient and caregivers stories are especially helpful to other sufferers.
Saturated Fat Is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars.
Nonalcoholic fatty liver disease (i.e., increased intrahepatic triglyceride [IHTG] content), predisposes to type 2 diabetes and cardiovascular disease. Adipose tissue lipolysis and hepatic de novo lipogenesis (DNL) are the main pathways contributing to IHTG. We hypothesized that dietary macronutrient composition influences the pathways, mediators, and magnitude of weight gain-induced changes in IHTG.
Overfeeding saturated fats increased liver triglycerides more (+55%) than unsaturated fats (+15%, P < 0.05). Carbohydrate feeding increased liver triglycerides (+33%) by stimulating DNL (+98%). Saturated fat significantly increased while unsaturated fat decreased lipolysis. Saturated fat induced insulin resistance and endotoxemia and significantly increased multiple plasma ceramides. The diets had distinct effects on adipose tissue gene expression.
Macronutrient composition of excess energy influences pathways of liver triglycerides: Carbohydrates increases DNL, while saturated fat increases and unsaturated fat decreases lipolysis. Saturated fat induced the greatest increase in triglycerides, insulin resistance, and harmful ceramides. Decreased intakes of saturated fat could be beneficial in reducing liver triglycerides and the associated risk of diabetes.
Overfeeding polyunsaturated and saturated fat causes distinct effects on liver and visceral fat accumulation in humans
The importance of dietary fat composition for fat storage in humans is unknown. We investigated liver fat accumulation and body composition during overfeeding saturated fatty acids or polyunsaturated fatty acids Thirty-nine young and normal-weight individuals were overfed muffins high in palm oil or sunflower oil for 7 weeks. Liver fat, visceral adipose tissue, abdominal subcutaneous adipose tissue, total adipose tissue, pancreatic fat, and lean tissue were assessed by magnetic resonance imaging. Both groups gained similar weight. Saturated fats, however, markedly increased liver fat compared with unsaturated fats and caused a twofold larger increase in visceral fat than poly unsaturated fats. Conversely, poly unsaturated fats caused a nearly threefold larger increase in lean tissue than saturated fats. Genes involved in regulating energy dissipation, insulin resistance, body composition, and fat-cell differentiation saturated fats were differentially regulated between diets. In conclusion, overeating saturated fats promotes hepatic and visceral fat storage, whereas excess energy from poly unsaturated fats may instead promote lean tissue in healthy humans
We start with the fact that the fundamental problem is the bio-chemical flow between the liver and fat cells. When diet is poorly balanced, over time fat accumulates in the liver and by itself is rather benign but when other chemistries like insulin management begin to degrade you get inflammation which leads to fibrosis and if not stopped progresses to cirrhosis. Since there is no treatment your tool is diet and the question is to avoid anything that stresses the liver and load up on anything that is protective. Easy peasy right. Well let's take a look
- eliminate all alcohol
- eliminate saturated fat and no red meat
- eliminate all non skim dairy products
- eliminate trans-fat and all hydrogenated oils
- eliminate all high fructose corn syrup
- eliminate most sodium -- the goal 1,500 mg per day
- eliminate all added dietary sugar
- eliminate processed grains, no white flour or white rice
- Avoid most products hustled by the supplement industry
- Make sure that any medications you take are not harming your liver
The goal of this website is to share my experiences and information as I seek to use nutrition and a health supportive lifestyle to manage my liver disease. I have to tell you the legal things because our society is riddled with lawyers. Please go to the link above to see the full statement. By using this site, you signify your assent to these Terms and Conditions. If you do not agree to all of the Terms and Conditions of use, do not use this site.
OK, I get it, but what kind of diet can meet all those goals?
DO YOU KNOW HOW TO KILL YOUR LIVER?
Your liver is like a very complex factory
There are many diets being advocated but most of them do not talk to you about specific liver health issues like how their program impacts your liver. The assumption is that weight loss alone is good for you. While generally true, if we consider the liver the kind of calories you consume is important. You can feed it almost anything and it will try to make something out of it. It is filled with about 500 robots that each know how to do one thing. As long as a robot knows what to do with what you send it and the supply isn't overwhelming all is well. However, if you supply more than it can process bad things happen. With too much raw material things in the factory can pile up. When a robot is broken or over supplied, the wrong product might be made or the robot might fail. Break too many of your liver robots and the entire factory fails. These are the reasons why what you eat really does matter to your long term health.
When you hear the term fatty liver you instinctively assume that eating fat is what caused it and the siren song of low fat diets that get so much attention have appeal. The problem is that the important thing is not what you eat but what does your liver do with what you eat. As you think about the rest of this material remember this one fact as you learn about fatty liver disease and lifestyle. The first step in carbohydrate metabolism is to turn the carbs to fat in the form of palmitic acid. Excess carbohydrates in the body are converted to palmitic acid which is the first fatty acid produced during fatty acid synthesis and is the precursor to longer chain fatty acids. The critical idea here is the presence of excess carbohydrates.
Sugar is also half fructose. Unlike glucose, which is a direct fuel for all organs, fructose can only be processed by the liver and it is turned into fat inside the liver cells. That process is unlimited so unlike glucose it just keeps building fatty acids in the liver and if you exceed what the liver can manage bad things happen. You can learn about that here.
When you eat too much sugar some of it is converted to fat in your liver cells and if the amount exceeds what the liver can dispose of you get accumulation. There are many other chemical pathways in the liver but you can probably see how this might apply to you.
Much of this advice will be familiar to you, however, there is one critical food item which under official US food advice is different. That is the extensive use of extra virgin olive oil. It is important to be aware that the Official American Dietary Guidelines advise calorie reduction and exercise with limited dietary fat. It limits saturated fats but ignores the differences between various oils. If you want to study the official recommendation you can do it here. You might wonder whether the official federal policy has anything to do with the vast amount of disease afflicting our society.
The nutritional approach to fatty liver disease has a broad base of support among providers, including MDs. The optimal approach is still a matter of investigation and debate. However, the Mediterranean diet is one of the most studied diets in science and medicine. As the most common cause of mortality among patients with NAFLD is cardiovascular events, the impact on mortality alone make it worthwhile to adopt. The anti inflammatory and anti-fibrotic literature for the diet are also compelling and since we are focused on liver disease that is the focus of this information.
Much of our advice is built around extra virgin olive oil. If you would like
more information see this link on olive oil
but if your interest is about
fatty liver disease and its complication click here.
If you have a liver problem, you should be aware that liver disease is ignored by almost all diet plans. The reason is that it is mostly symptom free and there are no treatments so most of the research has been on heart and diabetes issues. If you are concerned about your liver you are part of an ignored patient group. If you would like to test that theory,
Just be aware that they ignore the questions that brought you here. Diet plans mostly ignore the liver even though its health is the foundation upon which most of the bio-chemistry that is you depends. So look around but come back here when you find out that the diet plan advocates ignore you.
A COMMENT ABOUT POPULAR LOW CARB DIETS
Please note that extreme low carb plans are probably bad for you. Your body must have fuel and when we eliminate sugar that comes significantly in the form of fats and carbs. The kind of carbs is what you need to pay attention to. Ideally you want to eat a good supply of resistant starch, that is starch that is digested in the colon and not the small intestine. This is very important for the health of the colon as much of its energy is in the form of short chain molecules called butyrate which are produced by the healthy bacteria. Take those away and the cells lining the colon suffer.
Resistant starch is considered both a dietary fiber and a functional fiber, depending on whether it is naturally in foods or added. Although the U.S. Institute of Medicine has defined total fiber as equal to functional fiber plus dietary fiber, U.S. food labeling does not distinguish between them.
|Examples of naturally occurring resistant starch|
|Food||Serving size||Resistant starch
|Banana flour, from green bananas||1/4 cup, uncooked||10.5-13.2|
|Banana, raw, slightly green||1 medium, peeled||4.7|
|High amylose RS2 corn resistant starch||1 tablespoon (9.5 g)||4.5|
|Oats, rolled||1/4 cup, uncooked||4.4|
|Green peas, frozen||1 cup, cooked||4.0|
|White beans||1/2 cup, cooked||3.7|
|Lentils||1/2 cup cooked||2.5|
|Cold pasta||1 cup||1.9|
|Pearl barley||1/2 cup cooked||1.6|
|Cold potato||1/2" diameter||0.6 - 0.8|
|Oatmeal||1 cup cooked||0.5|
IMPORTANT LITTLE KNOWN OR UNDERSTOOD FACTS ABOUT STARCH
Processing may affect the natural resistant starch content of foods. In general, processes that break down structural barriers to digestion reduce resistant starch content, with greater reductions resulting from processing. Whole grain wheat may contain as high as 14% resistant starch, while milled wheat flour may contain only 2%.
Other types of processing increase resistant starch content. If cooking includes excess water, the starch is gelatinized and becomes more digestible. However, if these starch gels are then cooled, they can form starch crystals resistant to digestive enzymes such as those occurring in cooked and cooled cereals or potatoes (e.g., potato salad). Cooling a boiled potato overnight increases the amount of resistant starch for example.
Resistant starch does not release glucose within the small intestine, but rather reaches the large intestine where it is consumed or fermented by colonic bacteria (gut microbiota). On a daily basis, human intestinal microbiota encounter more carbohydrates than any other dietary component. This includes resistant starch, non-starch polysaccharide fibers, oligosaccharides, and simple sugars which have significance to colon health.
The fermentation of resistant starch produces short-chain fatty acids, including acetate, propionate, and butyrate and increased bacterial cell mass. The short-chain fatty acids are produced in the large intestine where they are rapidly absorbed from the colon, then are metabolized in colonic epithelial cells, liver or other tissues. The fermentation of resistant starch produces more butyrate than other types of dietary fibers.
Modest amounts of gases such as carbon dioxide, methane, and hydrogen are also produced in intestinal fermentation. One review estimated that the acceptable daily intake of resistant starch may be as high as 45 grams in adults, an amount exceeding the total recommended intake for dietary fiber of 25–38 grams per day. When isolated resistant starch is used to substitute for flour in foods, the glycemic response of that food is reduced.
There is a concept of "healthy" saturated fat. Since being saturated refers to a bio-chemistry definition in which all available carbon bonds are used by a hydrogen atom I've wondered what that meant. I had never considered how the research on fibrosis is actually done with animal trials but I was fortunate to be able to recently attend a conference of about 200 of the top liver researchers in the world. The official focus was to update everyone on the progress on the most interesting 20+ drugs inching closer to human trials and possibly a treatment for fibrosis but I was struck by the specifics of how the research is done.
When you want to study how a drug might work against liver disease in a mouse or rat you first have to give it liver disease. How might that be done quickly and cheaply and mimic human disease you might be moved to ask. Well, suppose there are two really good diets you can feed them. It is that simple. There are two main ones that are named the "Western Diet" and the "Fast Food Diet".
I wonder what might be in that food. Would it surprise you to learn they have two main components? Would you bet on lots of saturated fat and sugar? It is that simple. You can give a mouse cirrhosis in weeks by just feeding them what you eat and feed your kids every day.
The information on the bio-chemistry was absolutely fascinating but I was dumbfounded by the little detail of how to create illness that ran through the conference. I'm pondering how to make that more clear to people in general but I offer it here for whatever it may be worth.
My mother, Geneva Eskridge, was one of the inspirations for this foundation. She passed away, a few days short of her 94th birthday of complications arising from her lung cancer. Her family was there and had been with her during her final days. She was well and truly loved by those who knew her and she rarely met anyone whom she did not befriend. She will be sorely missed by many.
For anyone not familiar with her and for those who knew her well I’d like to offer a brief visit with her indomitable spirit. Geneva exemplified the best of us and we can but hope to approach our lives in the same spirit. When diagnosed with lung cancer at the age of 91 she decided to go skydiving rather than retreat from life. The link below is to her first jump and the second is when she jumped again at 92
I only hope that I can live up to her example with my life and our family offers her memory to you as an example of a life well led. I regret that the role of caregiver, which I worried that I might be unable to perform adequately, was cut tragically short by unforeseen events.