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.
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
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