The four horsemen of the apocalypse.  The vision of death and destruction for humanity from the new testament is a chorus of the woes that can befall society.  It evokes hazard from all directions bringing misery and the pale horse called death.

When you come to grips with the health aspects of liver disease it is a surprise to learn that our understanding of our bodies as an integrated system is so poorly appreciated.  The mix of chemical processes that are done routinely by the liver cannot be duplicated by our chemists.  It is estimated that over 500 functions are performed by the cells of the liver and they affect every other kind of tissue in the body. Imagine that, all of that activity in a cell about one fifth the width of a human hair.

Want to know more about clinical trials? Here are some short videos from our partner Antidote.

FOR MORE INFORMATION AND LINKS TO TRIALS CLICK HERE

MK-3655 Trial

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.

About NASH

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.

https://www.sciencedaily.com/releases/2017/08/170818102308.htm

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.

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.

This is a page of links to the science that is important to you in terms of fatty liver disease, its consequences, and things you should be aware of. If you really want to dig in to fatty liver issues this is a good place to begin.

We claim that the current research shows that the best diet for anyone dealing with fatty liver disease or its more advanced cousins has calories of about 28% from omega 9 in extra virgin olive oil, less than 7% saturated fats, less than 5% refined sugar, about 7% omega 3 fatty acid, about 8% omega 6, about 25% complex carbs, and about 20% protein.

As a way to think about it we should start at the end and work backward. Consider the Mediterranean diet which is similar to the liver healthy diet that we discuss on this site. The Mediterranean diet is one of the most studied diets in science and medicine. In this section we'll summarize the research but the links will show you the original studies in a new page if you want the details.

Extra virgin olive oil is key to NAFLD management without restricted feeding -- living life not dieting

As a place to start, this very interesting study showed that a Mediterranean diet with extra virgin olive oil of at least 60ml per day reduced the incidence of NAFLD compared to a Med diet with supplemental nuts or a Med diet with reduced fat.  From a patient perspective an important point was that there were no feeding restrictions meaning it wasn't counting calories.  People ate until satisfied and still had the benefit.  The excess olive oil is a key feature of the study.  For a discussion of the typical Med diet recommendations here is a link to the Mayo information. The Mayo diet is a general diet discussion and does not focus on the value of increased olive oil consumption as a factor in liver disease as described in this study.

Practical Dietary Recommendations for the Prevention and Management of NAFLD in Adults

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. In the absence of effective pharmacological therapies, clinical guidelines focus primarily on weight loss to treat this condition. Established consensus, evidence-based, and clinical dietary recommendations for NAFLD are currently lacking. The aim of this paper is to provide evidence-based practical dietary recommendations for the prevention and management of NAFLD in adults. Five key dietary recommendations were developed:

1) follow traditional dietary patterns, such as the Mediterranean diet;

2) limit excess fructose consumption and avoid processed foods and beverages with added fructose;

3) PUFAs, especially long-chain omega-3 rich foods and MUFAs, should replace SFAs in the diet;

4) replace processed food, fast food, commercial bakery goods, and sweets with unprocessed foods high in fiber, including whole grains, vegetables, fruits, legumes, nuts, and seeds;

5) avoid excess alcohol consumption.

Improving diet quality may reduce the incidence and progression of NAFLD and associated risk factors. Many of the benefits are likely to result from the collective effect of dietary patterns.  AdvNutr2018;9:30–40.

Saturated Fat Is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars.

https://www.ncbi.nlm.nih.gov/pubmed/29844096

OBJECTIVE:

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.

RESULTS:

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.

CONCLUSIONS:

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.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5874578/

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

Lifestyle Interventions study in the EASL Journal of Hepatology

 Austrian Study of the Mediterranean Diet in BMC Gastroenterology Journal

The Med Diet in this study is characterized by a specific fatty acid profile: low in saturated fat (7–8 % of total energy) and high in monounsaturated fat (20 % of total energy) following a Spanish study which showed that treatment with a balanced diet rich in olive oil contributes to the recovery of the liver from hepatic steatosis or fatty liver. This was achieved by decreasing the activation of hepatic stellate cells resulting in a decrease in hepatic collagen or fibrosis by monounsaturated fatty acids. In addition monounsaturated fatty acid is less susceptible to lipid peroxidation as compared to polyunsaturated fatty acids so there are fewer free radicals produced. The patients in the Mediterranean Diet arm had significant improvements in insulin sensitivity and a significant reduction (39 %) in liver fat. In contrast there was no significant improvement in insulin sensitivity and only a 7 % reduction of liver fat with the low fat, high carbohydrate diet. The changes observed in the intervention group were without a significant reduction in weight. The diet has positive effects on insulin sensitivity, which has been attributed to the high content of bio-active phytochemicals with a range of antioxidant and anti-inflammatory activity. It has been shown that weight loss alone improves insulin sensitivity but this study was of shorter duration and not aimed at a weight loss goal.

Journal article from Diabetologia studying the effect on liver enzymes in obese type 2 diabetes patients.

In numerous studies, the Mediterranean diet has been reported to have a beneficial effect on cardiovascular risk factors. Analysis of a subgroup of 772 participants in the PREDIMED study, a large trial including individuals at high risk of cardiovascular disease, demonstrated a beneficial effect of a Mediterranean diet on lipid profiles, insulin resistance, blood pressure and inflammatory markers compared with a low fat diet. In a smaller trial with longer follow up (2 years), the Mediterranean diet was found to be more effective for reducing weight, BMI, waist circumference, inflammatory markers, glucose, total cholesterol, triacylglycerol, and insulin resistance, increasing HDL, improving endothelial function, and reducing the prevalence of the metabolic syndrome compared with the low fat control diet. Taken together, these results suggest that relatively high dietary fat intake, in itself, is probably not associated with accumulation of fat in the liver or other cardiovascular risk factors, and that the type of dietary fat (saturated fat, monounsaturated fat and polyunsaturated fat) may be more important than the amount.

World Journal of Gastroenterology - Mediterranean diet and non-alcoholic fatty liver disease

The Mediterranean diet is characterized by a high consumption of fruit, vegetables, legumes, and complex carbohydrates, with a moderate consumption of fish, and the use of olive oil as the main source of fats. This eating pattern has been promoted worldwide as a model for healthy eating and has been reported to contribute to a favorable health status and to a better quality of life, as well as allowing an optimal intake of antioxidant vitamins, polyunsaturated fats and other beneficial nutrients for the prevention of chronic degenerative diseases. In terms of NAFLD prevention, the beneficial effects of such dietary habits can be explained through several mechanisms that can vary from an effective dietary approach for weight loss, to a model diet that is plentiful in some beneficial nutrients such as MUFA and vitamins, to the presence of olive oil as the main contributor of fats. Indeed, olive oil has been demonstrated to have several different beneficial effects on metabolic syndrome and NAFLD, by improving glucose and lipid metabolism and preventing atherogenesis. All these factors likely contribute, as a whole, in determining the preventive and therapeutic role of a Mediterranean diet on fatty liver disease.

Olive oil prevents CCL4 induced hepatic fibrosis in mice from the Journal Gastroenterol

The study of the bio-chemistry of oleic acid can't be done on humans so a mouse model is used where carbon tetrachloride causes massive liver damage so this is the research method used to compare treatment strategies. This material is technical but shows why olive oil protects liver cells and is central to understanding why the diet plan we recommend is effective. In the study, serum alanine aminotransferase levels and the mRNA expression of TGF-b and colla2 were significantly reduced by treatment of olive oil. Dietary olive oil blunted the expression of a-SMA in the liver and liver injury and hepatic fibrosis were prevented by treatment of olive oil. The number of a-SMA positive cells was significantly lower in HSCs co-cultured with oleic acid than in those co-cultured with linoleic acid. Concentration of hydroxyproline in culture medium was significantly lower in cells co-cultured with oleic acid than in the control. Previous studies have reported that fatty acids prevented liver injury induced by chronic administration of CCl4 or intragastric alcohol feeding in rats. The protective effects of olive oil against liver injury due to oral intake of CCl4 have also been reported. In the present study, serum transaminase levels were blunted by dietary olive oil. Furthermore, the expression of a-SMA in the liver was markedly inhibited by dietary olive oil and liver fibrosis induced by intraperitoneal injection of CCl4 was prevented by olive oil. Thus, olive oil had anti-inflammatory and anti-fibrogenic effects.

Oleic acid stimulates complete oxidation of fatty acids through protein kinase A - dependent activation of SIRT1-PGC1α complex

Oleic acid potently accelerated rates of complete fatty acid oxidation in skeletal muscle cells. These results illustrate how a single long chain fatty acid specifically controls lipid oxidation through a signaling/transcriptional pathway. Fatty acids are essential components of the dynamic lipid metabolism in cells. Fatty acids can also signal to intracellular pathways to trigger a broad range of cellular responses. Oleic acid is an abundant monounsaturated omega-9 fatty acid that impinges on different biological processes to modulate rates of fatty acid oxidation. In skeletal muscle cells, oleic acid treatment increased intracellular levels of cyclic adenosine monophosphate (cAMP) that turned on protein kinase A activity. This resulted in SIRT1 phosphorylation at Ser-434 and elevation of its catalytic deacetylase activity. A direct SIRT1 substrate is the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1α), which became deacetylated and hyperactive after oleic acid treatment. Importantly, oleic acid, but not other long chain fatty acids such as palmitate, increased the expression of genes linked to fatty acid oxidation pathway in a SIRT1-PGC1α-dependent mechanism. Complicated but what it means is that there is less oxidation stress in cells using oleic acid as the primary fat source.

A high ratio of dietary n-3/n-6 polyunsaturated fatty acids improves obesity-linked inflammation and insulin resistance

Compared to saturated fat fed rats, PUFA¹:¹ fed rats exhibited decreased body and visceral fat weight, lowered blood lipids, and improved glucose tolerance and insulin sensitivity. Interestingly, these changes were accompanied with decreased expression levels of circulating pro-inflammatory cytokines, including tumor necrosis factor α, interleukin-6, and C-reactive protein. Moreover, the TLR4 protein and mRNA levels were markedly down-regulated by PUFA¹:¹ compared with saturated fatty acids.

omega 6 omega 3 fatty acid ratio, can it kill you

The essential fatty acids are called that because they can't be synthesized by the body and must come from the diet. Therefore the proper question is how much of each is good for me and is there an amount that is harmful? The answer to that comes from nutritional research. Looking at human diets over time, we estimate that as hunter gatherers humans probably had a diet that ranged between one to one up to four to one omega 6 to omega 3. In simple terms, more 6 than 3 but not an overwhelming difference.

In our modern society things have changed. Some research suggests that our industrial diet may have an omega ratio as high as 50 to 1. The fat balance in our diets has changed dramatically in the past two generations and mirrors the obesity epidemic raging in our society. An important class of chemicals are the eicosanoids. These chemicals participate in the inflammatory process by encouraging or promoting inflammation.The thing to understand is that both omega 6 and 3 fatty acids can be converted to eicosinoids. That is important to the unsaturated fat debate because both corn and soybean oil are rich in omega 6 while olive oil is primarily omega 9. As our industrial food system uses more and more corn and soybean oil it is easy to see why our omega ratio has become one sided.

IF YOU WOULD LIKE TO DELVE INTO MORE OMEGA 3 INFORMATION CLICK HERE FOR A PAGE DEDICATED TO OMEGA 3

Eating your carbs as resistant starch is good for your health refined sugar is not

Glucose is the primary fuel of the body but eating glucose in quantity, in a form that enters the blood stream quickly, is part of the process that leads to metabolic resistance and diabetes.  Your source of glucose should be in resistant starches which are not absorbed in the small intestine but are digested slowly in the colon.

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.

Resistant starch (RS) is any starch or starch digestion products that are not digested and absorbed in the stomach or small intestine and pass on to the large intestine. RS has been categorized into four types:

• RS1 – Physically inaccessible or undigestible resistant starch, such as that found in seeds or legumes and unprocessed whole grains.
• RS2 – Resistant starch is inaccessible to enzymes due to starch conformation, as in high amylose corn starch
• RS3 – Resistant starch that is formed when starch-containing foods are cooked and cooled, such as pasta. Occurs due to retrogradation, which refers to the collective processes of dissolved starch becoming less soluble after being heated and dissolved in water and then cooled.
• RS4 – Starches that have been chemically modified to resist digestion

It is important not to eliminate all carbs from your diet but pay attention to the kind of carbs you eat. Resistant starch is digested by bacteria in the colon producing a variety of short chain fatty acids. The short-chain fatty acid butyrate is particularly important for colon health because it is the primary energy source for colonic cells and has anti-carcinogenic as well as anti-inflammatory properties that are important for keeping colon cells healthy.Butyrate inhibits the growth and proliferation of tumor cell lines in vitro, induces differentiation of tumor cells, producing a phenotype similar to that of the normal mature 

Fructose, Fatty Liver and Insulin Resistance

Fructose is even more strongly linked to obesity and diabetes than glucose. From a nutritional standpoint, neither fructose nor glucose contains essential nutrients. As a sweetener, both are similar. Yet fructose is particularly malevolent to human health compared to glucose due to its unique metabolism within the body. Large quantities of ingested fructose goes straight to the liver, since no other cells can help utilize or metabolize it, putting significant pressure on the liver. Levels of carbohydrates and insulin may be 10 times higher here than in other parts of the circulation. Thus the liver is exposed to far higher levels of carbohydrates – both fructose and glucose than any other organ.

The liver metabolizes fructose into glucose, lactose and glycogen. There are no limitations on this system of metabolism for fructose. The more you eat, the more you metabolize. When the limited glycogen stores are full, the excess fructose is changed directly into liver fat through de novo lipogenesis. Fructose overfeeding can increase DNL five fold, and replacing glucose with a calorically equal amount of fructose increases liver fat by a massive 38% within only eight days. It is precisely this fatty liver is crucial to the development of insulin resistance. Fructose’s propensity to cause fatty liver is unique among carbohydrates. The fatty liver directly causes insulin resistance setting in motion the vicious cycle of hyperinsulinemia – insulin resistance. Furthermore, this harmful effect of fructose does not require high blood glucose or blood insulin levels to wreak havoc. Further, this fattening effect, because it acts through fatty liver and insulin resistance, cannot be seen in the short term – only in the long term.

If you want to explore liver disease in more depth watch these short videos

Part of dealing with liver disease is to understand it.  There is a lot of information here.  It is important to understand liver disease if you are going to deal with it.  In order to provide you with a solid understanding, we are working with Armando Hasudungan. Armando produces superb short videos to explain complex medical subjects.  We use them throughout the site to help you understand your body and specifically your liver.

What is a recommended diet for a compromised liver

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 

legal Disclaimer - This information is not FDA approved

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?

Here is a link to more discussion of our recommended eating strategy.

After all that, if you really want to dig into the subject, click here

So what really is a diet if I have a fatty liver? In order to avoid the supplementation debate, lets assume that we can get all the vitamins and nutrients we need from our food. We start with the fact that the fundamental process is the bio-chemical flow mediated by the liver.  The liver performs over 500 individual chemical reactions which are all important to your health so to simplify the problem, if we treat the liver well most other organs will do fine. In simple terms the goal is to avoid or minimize what stresses the liver and load up on foods that are nutritional or protective. Easy peasy right. Well let's take a look.

• limit alcohol consumption, remember it is a liver poison
• limit saturated fat to less than 7% of calories and go easy on red meat
• when possible use low fat or skim dairy products
• eliminate trans-fat and all hydrogenated oils
• eliminate all high fructose corn syrup
• cut way down on salt -- the goal is 1500 mg/day
• minimize added dietary sugar
• limit the use of processed grains
• be aware that there are unknown health consequences for many chemicals

Well, that doesn't sound very easy. Not possible to enjoy life that way. OK, take a breath. The goal is to provide proper nutrition in a lifestyle that doesn't feel painful every day but allows your body to thrive. So what do you do?

• Use extra virgin olive oil for cooking and take three tablespoon per day like cough medicine
• Don't buy prepared foods without reading the label, there isn't actually much that you can buy
• Eat lots of fruits and vegetables but watch the salt
• Learn to like kale, lima beans, brussel sprouts, etc.
• Look for fiber like whole wheat bread no white breads and use brown rice
• Eat fatty fish like salmon at least a few times a week
• East skinless chicken or turkey and lean pork
• Minimize processed meats like ham
• Explore new foods like quinoa as a grain
• Eat plenty of vegetable protein like beans.
• Drink 3 to 4 cups of paper filtered coffee daily.
• Keep in mind that eating out is mostly unhealthy so be thoughtful

You get the idea. you might call this a type of Mediterranean diet but the olive oil is specifically a medicine. The rest is mostly nutrition. The salt limitation is good for you and lowers your blood pressure. So why should you think this might work for you? Without getting too technical your energy systems are built around triglycerides. Many oils can be used by the body to make them but if made with unsaturated oil they are better for the body. More importantly olive oil is mostly an omega 9 fatty acid. Good olive oil is a complex mixture of around 30 oils and phyto chemicals which support liver function and soothe inflammation. Just something to understand, good olive oil causes a burning feeling at the back of your throat when you take it straight. Those are the phyto chemicals and more is better if you ever go to an oil tasting bar you can try different grades.

DISCLAIMER: Be aware that I am not a doctor.  I cannot give medical advice.  I am a cirrhosis patient and I have apparently halted the progression of my disease following a more strict version of this strategy.

There is a lot of information below.

If you would like a short summary click this link.

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. 

Palmitic acid is a major body component of the body and is made primarily in the liver.

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.

https://www.fattyliverfoundation.org/tags/fructose

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.

What is a good diet for a healthy person

What is a diet for fatty liver or NAFLD

What is a diet for a damaged liver NASH or cirrhosis

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.

USDA Dietary Guidelines

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,

US News has an excellent summary of popular diets which you can look at here for an overview.

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.

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).^[10] 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.^[10][12]

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.^[13][14] The fermentation of resistant starch produces more butyrate than other types of dietary fibers.^[15]

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,^[16] an amount exceeding the total recommended intake for dietary fiber of 25–38 grams per day.^[17] When isolated resistant starch is used to substitute for flour in foods, the glycemic response of that food is reduced.^[18][19]

Here is a link to a discussion of Resistant Starch

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 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.  

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