TRIAL: A test to determine whether the species will create new organ designs to accommodate chronic over feeding or fail and result in mortality and long term decline.  The alternate endpoint, increased intelligence in feeding strategies.

OVERVIEW;

The test subjects all like sugar but dietary advice mostly says give it up.  The question, what really happens when they eat excess sugar over time?

OK, but sugar is glucose and it is known that glucose is a fundamental fuel so what is wrong with that? Let's take a walk down bio-chemistry lane.  Just a peak so easy peasy. This is really important if one has concerns about livers so don't run away yet.

Improving together the medical learning about NASH to better address its causes and consequences, and serve patients.

As a recognized leader in the NASH field, the endowment fund has a responsibility for being proactive in NASH disease awareness.

The NASH Education Program^TM defines and drives initiatives in collaboration with an independent scientific committee² composed of four international key opinion leaders, well-known and respected in the field, with a footprint in both hepatic and metabolic diseases, and a strong presence in the United States as well as in Europe.

The objective of this public health initiative is to place the practitioner and the patient at the heart of tomorrow's awareness and education actions. It aims at producing essential and relevant scientific and medical knowledge, and at disseminating it towards targeted audiences:

• All physician specialties, going beyond hepato-gastroenterology, i.e. including diabetologists, endocrinologists, obesity specialists, cardiologists, OB-GYN and general practitioners who will all have a key role to play in the clinical management of NASH patients;

• Patients and their families, but also individuals at risk, who all need to understand causes, mechanisms and consequences of the disease, to fully appreciate the importance of an early diagnosis and a treatment well-suited to their condition.

Through this approach, The NASH Education Program^TM creates opportunities to increase awareness through relevant and impactful education actions. It is obviously open to all key stakeholders in the NASH space who are committed to improving NASH patient care.

Videos from The NASH Education Program^TM

 * NASH: A Major Public Health Issue & Growing Concern

Learn about the vital role of the liver in the body, as well as about NASH, or non-alcoholic steatohepatitis.  You will see the progression of the disease from a healthy liver to a liver with steatosis and necro-inflammation, the driving force of the disease, leading to fibrosis and ultimately to life-threatening outcomes such as cirrhosis or liver cancer – both requiring a liver transplant – or cardiovascular disease.

* Why Early Diagnosis is Important

Learn why NASH is becoming a significant economic and societal issue globally. With its high prevalence and the recent FDA approval of Rezdiffra, there is now a treatment option for adults with noncirrhotic NASH/MASH with moderate to advanced liver fibrosis, alongside diet and exercise. Healthcare system expenses related to NASH are expected to grow, making early diagnosis a critical challenge. This emphasizes the need for simple, cost-effective, and non-invasive solutions in NASH management.

* Biopsy:  The Gold Standard for Diagnosis

Learn about biopsy, the current gold standard to diagnose NASH in individuals at risk, and the most complete diagnostic solution allowing clinicians to study key characteristics of the disease. Also learn why it is not considered an ideal solution and needs complementary diagnostic tools: mainly due to its low availability, invasiveness and cost.

* What is NASH?

Stephen A. Harrison, MD, Medical Director of Pinnacle Clinical Research, San Antonio, introduces us to NAFLD (Non Alcoholic Fatty Liver Disease), and more specifically NASH (Non-alcoholic Steatohepatitis). He explains the definition of the disease, as well as its characteristics & the risks induced by its progression. He also highlights how the disease is related to the double epidemic of obesity and diabetes.

* Who is at Risk?

Mary E. Rinella, MD (Associate Professor of Medicine, Northwestern University Feinberg School of Medicine, Chicago) describes who are the patients at risk of developing NAFLD and NASH, as well as the link between NASH and cardiovascular events, the ultimate consequences of the disease, and the importance of a multidisciplinary approach to be successful in the fight against NASH.

* Improving Access to NASH Diagnosis

Arun J. Sanyal , MD (Virginia Commonwealth University Medical Center, Richmond) explains that NASH is under diagnosed because a biopsy is usually necessary to confirm diagnosis. Because NASH is a silent disease and most patients are asymptomatic until late stages of the disease, it is crucial that a new, easy-to-use, accessible non-invasive diagnostic tool becomes available soon.

* How to Resolve NASH

Kenneth Cusi, MD (Chief of the Division of Endocrinology, Diabetes and Metabolism at the University of Florida, Gainesville) explains how beneficial weight loss is for NASH patients. But most people struggle to lose weight, and more importantly keep it off. Therefore, because of the prevalence of NASH and its rapid progression, increasing awareness around NASH could help to better manage patients, but that new treatments remain a priority.

* NASH:  The Future

Vlad Ratziu, MD (Professor of Hepatology at the Pitié-Salpêtrière Hospital, Paris) explains that resolving NASH (inflammation and ballooning), the underlying cause of cirrhosis, is a recommended endpoint for clinical trials. He tells us more about the key requirements for an anti-NASH drug, especially the importance of safety and tolerability on top of efficacy.

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.

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

http://www.fattyliverfoundation.org/diet_compare

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.

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

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.

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