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

Exercise as a patient is a popular subject which reminded me of a recent experience.  If you have ever been a runner you likely know of what is called the "runners high".  It is a feeling of euphoria brought on by the release of endorphins.  Running is mostly hard work but occasionally it is magic.

There is a greenbelt along the river where I live that bikers and pedestrians enjoy.  It is really quite a nice amenity.  It is local custom for bikers to signal with a bell perhaps or more commonly to announce "on your left" when passing to avoid startling walkers. 

I was jogging along recently and it was a perfect day.  A gorgeous morning and I felt good.  As I went along everything came together.  I was the winged god Mercury floating effortlessly through space with the wind and gravity paying me hardly any mind as I flew past.  A glorious experience that I would gladly become addicted to. I could have run all day with no effort at all.

Several members have been asking about exercise lately.  The problem for anyone who is obese or ill is that it is so hard to do.  When you think about the fact that you have to walk a mile to burn off a single apple it is easy to be defeated by the task.  One apple is about 100 calories and to lose a pound you have to burn 3500 calories.  Crazy math, people who tell you to lose weight exercising probably don't face the challenges that you are dealing with.

We all agree that exercise is good for us and we all resolve to do more, but the simple truth is that most people fail to have an exercise program that affects their weight at all.  Since you wouldn't be here unless you or someone you care about was struggling perhaps there is a way to think about the exercise problem from a different perspective.

At the core, the lifestyle changes required to lose weight are about diet and the details of how to approach that are subjects we've commented on before.  If you would like to refresh your thinking about diet here is a link to our diet page

http://www.fattyliverfoundation.org/diet_compare

Let's look at exercise from the point of view of your liver.  The liver is a flexible mass of tissue and you might think of it as a very dense forest of veins with liver cells closely packed around all of them.  Every liver cell has blood moving past it and since a cell is only about 1/5 the width of a human hair the complexity is really quite extreme considering that each cell is involved in about 500 processes.

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.

A member was asking about why we didn't use lots of flaxseed oil instead of olive and why use coconut at all since it is so saturated.   This chart illustrates the fact that all of our oils are a mixtures unless they are specially processed.

There is a lot on advice on the internet about supplementing with omegas 3 as lots research supports its value.  Many are also advocating the use of coconut oil.  A few comments about the differences came out of that discussion so I thought I'd pass them along here.

I've written about the role of saturated and unsaturated fats and how they related specifically to liver disease and the development of inflammation and fibrosis development.  In that earlier post, which you can review here if you wish, I explained the research on fats and health which had a focus on diabetes for which liver function is critical. In that I commented only briefly on coconut oil since it is an intermediate, or medium chain, fatty acid.  It is a saturated fat so from the perspective of a liver patient the effect on liver bio-chemistry is important so I thought I would expand on the role of that intermediate length fat. 

A source I would like to refer you to for a broader discussion to the site of Jen Miller who discusses a lot of health issues. Her site is where you will find her article is here https://www.jenreviews.com/coconut-oil/.

Coconut oil has a specific value as it can be directly processed by the liver into ketones. When the body starts running low on blood sugar, the brain falls back on another source for its backup reserves. Its alternative energy is stored in what is known as a ketone body, or a ketone for short. Ketones are produced from fat that’s stored in the liver, and are made with a single purpose - to deliver energy to the brain in times of need. When blood sugar levels go down, the body amps up its production of ketones so the brain has a constant supply of energy.  As a brain supporting food coconut oil can be helpful to people who are struggling with energy after cutting out sugar.

One of the early consequences of a compromised liver is often a drift toward diabetes.  The pancreas and the liver work together to manage insulin and the use and processing of glucose so absent a specific pancreas disease liver function and fat processing are fundamental to health.  This discussion focuses on insulin and how it responds to different dietary fats but the conductor of the dance is the offstage liver.  If you read this carefully it shows the hazards of saturated fats and the benefit of extra virgin olive oil which is advocated by this foundation.  When you think about your diet understanding the bio-chemistry will help you as you consider how to change your lifestyle to be kind to your liver.   As a practical matter a diet that prevents diabetes will be just fine for your liver as well.  The smart plan is to not let your liver look like this one day.

Adding fats to carbohydrate containing meals is a common recommendation to diabetics to make meals “healthier” by reducing the glycemic response to the meal. The primary mechanism through which fat does this is by slowing the rate of gastric emptying, which leads to a slower appearance of glucose into the blood. Given that postprandial glycemia is an important risk factor for many diabetic complications, it makes complete sense to want to minimize post-meal blood glucose excursions.

However, to focus solely on the blood glucose response of a meal misses the forest for the trees. There is a considerable amount of evidence to suggest that consuming starchy carbohydrates in combination with excessive dietary fat, especially saturated fat, causes an acute state of insulin resistance that may last for hours after the meal. This has been known since at least 1983, when Collier and O’Dea published research showing that adding butter to a potato meal significantly blunted the rise in blood glucose without significantly affecting insulin in young and healthy men and women. Thus, the amount of insulin required to handle a similar amount of glucose in the blood was 3-fold greater when butter was added to the potato compared to eating the potato alone.

So while postprandial glycemia was reduced, more insulin was required to dispose of the glucose in the blood and insulin levels remained elevated for a longer period of time. Collier and O’Dea conclude,

These changes found after the co-ingestion of fat may indicate an acute insulin insensitivity or at least a potentiation of insulin secretion which could form the basis of the insulin resistance associated with the chronic consumption of high fat diets.

Suppose a member of your close family has NASH/Cirrhosis.  Should you be concerned for your own health?

Would you think about your lifestyle choices if you knew your odds of having liver disease were high?

An interesting study was just released which show that you are 12 times as likely to have fatty liver disease than does a person without a family member suffering from end stage liver disease.  Unbelievable?  Here is a link to the study.

https://www.healio.com/hepatology/family_risk_of _liver_disease

These data may impact and potentially change clinical practice in increasing awareness of advanced fibrosis in NAFLD in high-risk populations such as those with a first-degree relative with NAFLD-cirrhosis,” the researchers concluded. “Further studies are needed to determine the interval for surveillance after initial screening. The clinical implications of this study are potentially significant, as earlier detection of cirrhosis would perhaps lead to earlier initiation of hepatocellular carcinoma screening and surveillance.” – by Talitha Bennett

Did you ever wonder what dying from cirrhosis might be like?  Pain and how we tolerate disease is a very individual thing but some statistics are instructive.  Study this image for a minute.

NOTE: Hepatitis C is a cirrhosis disease, it is just categorized separately because we know the cause.  When you combine the other cirrhosis stat of 2.3 you see that cirrhosis sufferers are 11.4 times as likely to abuse pain killers as the average person.  If that doesn't suggest to you that avoiding this particular sadistic angel of death is wise, you aren't paying attention.

You can learn about liver disease at this link

http://www.fattyliverfoundation.org/liver-disease

Liver cancer mortality rates resulting from cirrhosis are increasing and in the coming decades will become a leading cause of death.  Liver cancer has increaesed 300% since 1980 in step with the obesity and fatty liver disease epidemics. It is currently the 5th most common cancer in men and the 8th in women but increasing rapidly in both sexes.

If you know someone at risk consider passing this information along.

“Liver cancer death rates are increasing at a faster pace than any other cancer. A major factor contributing to this increase is the comparatively high prevalence of hepatitis C virus (HCV) infection among those born during 1945 through 1965, also called ‘baby boomers.’ The sustained rise in obesity and type 2 diabetes over the past several decades has also likely contributed to the increasing liver cancer trend,” Farhad Islami, MD, PhD, from the American Cancer Society, Georgia, and colleagues wrote. “The incidence of liver cancer varies by race/ethnicity and state, mainly because of differences in the prevalence of major risk factors and, to some degree, because of disparities in access to high-quality care.”

These are among the reasons that we are developing our mobile liver van. Many at risk people never have an opportunity to be evaluated for fatty liver disease and the problem is worse for women and ethnicities.  By taking our service directly to the people we can do our small part to reduce these problems

Average yearly rate of the attacks doubled in people with the liver disease

From Cornell -- Cirrhosis -- a stiffening of liver tissue that's often tied to excessive drinking of alcohol -- may also raise an older person's odds for a stroke, a new study suggests.

"In a nationally representative sample of elderly patients with vascular risk factors, cirrhosis was associated with an increased risk of stroke, particularly hemorrhagic stroke," wrote a team led by Dr. Neal Parikh, of Weill Cornell Medicine and New York-Presbyterian Hospital in New York City.

Hemorrhagic or "bleeding" stroke comprises about 13 percent of strokes and occurs when a blood vessel ruptures, according to the American Stroke Association. The majority of strokes (87 percent) are ischemic -- meaning they are caused by clots.

In the new study, Parikh's team tracked 2008-2014 data for more than 1.6 million Medicare patients older than 66.

The research showed that while just over 1 percent of people who did not have cirrhosis suffered a stroke during the average year, that number jumped to just over 2 percent for people with the liver disease.

The study couldn't prove that the cirrhosis actually caused any of the strokes. According to the authors, possible explanations for the association between cirrhosis and increased stroke risk include impaired clotting ability. Or, patients' heart risk factors may be exacerbated by cirrhosis and the underlying causes of cirrhosis, such as alcohol abuse, hepatitis C infection and metabolic disease, they said.

Unhappiness with modern medicine is becoming pretty common, at least our ability to tell the stories has expanded.  The internet has become the campfire we sit around and share the tales of our lives and as our expectations of medicine have grown our impatience with its problems has flowered.  In the liver community the stories of delayed or missed diagnosis, lack of communication, hurried explanations, and fear of the future are common.  Some of that kind of stress led to the creation of this foundation as I went through years of being told I was OK when that just couldn't be really true. At times the anger I felt post diagnosis about my loss of time and life energy was heavy on my soul.  I'm perhaps a bit wiser now as I've been able to understand the bigger picture and the challenges doctors face with the limitations of our tools and the mindless bureaucracy that has bound us all in soul searing edicts.  I recently found a wonderful blog by a doctor who speaks of his profession with a clear eye but unbounded humanity.  I'd like to share one of his posts with you and encourage you to get acquainted with his work.  He is Dr Jeremy Topin and this is a link to his blog

https://jtopin.wordpress.com/

I want to share a little from one of this entries called "Walk with me".

Walk with me, why don’t you? It’s about time, don’t you think? We have been avoiding this for quite a while. But it is best to bring this out from the shadows and into the light. Let’s take a walk… Thru a part of my day. But be careful. You won’t like what you see. Push open that door. Let’s take a peek. Could have been a lot of things behind “door number one” but probably best we start here. Walk inside. She won’t mind.  Yes. I assure you she is alive. I am very good at what I do and what I am doing for her is keeping her alive.  This can be hard. One might say it’s just semantics, but I do believe in the power of words. “Keeping someone alive” sounds good. Feels good. Invokes heroism and strength and knowledge and courage and bravery. But I promised to be honest. And honestly, she is alive. Because I am preventing her from dying. Because if you get rid of the fuzzy and you really take a look here… you would be hard pressed to say she is living. Alive yes. Living no. You looked, you know that although she is alive, she is not living.

What we have here is “a failure to communicate”. But to be fair, there is more to the story than just poor bedside communication skills between the doctors and her family. I mean I am a doctor. I am her doctor. And being biased, I view myself as a decent human being. Empathic, compassionate even. So there must be more to the story.

Family. Each bring to this room layers. Years of complicated relationships filled of love, hate, resentment, guilt. Overtones of religion and cultural bias.  Pre-conceived notions of health, life, disease, prognosis with variable degrees of inaccuracy. And in this powder-keg, we will add the specter of death as an accelerant. We don’t know any of them. The chances of having any relationship or trust prior to crossing that threshold are slim to none. But I am supposed to guide this family, with these layers, to a better understanding of what lies ahead for mom or dad or sister or brother. Five minutes maybe? How about ten? Not really a lot of extra time in my day to work thru this mess. Virtual piles of notes and documentation still to be done.  Beware of the son who knows it all. Beware of the daughter who doesn’t trust doctors. Beware of the child from the coast who hasn’t seen mom in years and decides to play an active role now. Beware of giving any information that contradicts any given prior that will fuel the seeds of mistrust. Beware of the primary MD or the consultants who give updates. Now you think you can do this in 5 minutes?  10 minutes? A day? A week? Would you sacrifice going to your son’s baseball game to work through this? How about your daughter’s musical recital? Do you skip your lunch when you haven’t had breakfast? Best to kick that can down the road a little bit.

I frequently talk about how to test for or stop liver fibrosis but it is also important to understand how to manage it.  An important consideration is that the disease is usually symptom free until it is severe and there are a lot of medical tests that are needed to manage secondary problems.  It is valuable to know when a particular test would be useful in order to avoid the cost, discomfort, and risk associated with many of them.

The American Gastroenterolgy Association recently released guidelines for how to use Fibroscan to decide whether the liver disease is advanced enough to consider testing for complications of portal hypertension or esophageal varices.

It isn't common to be able to report really important clinical research results where liver disease is concerned, but today is one of those days.  Intermountain Hospital's lead researcher and associate director of the medical center's transplant program, Dr Charlton, announced their results at a Czech medical conference.  The study found that seriously ill patients who exhibited a positive reaction to the drug sofosbuvir were also 50 times less likely to die from severe cirrhosis, a liver illness usually brought on by hepatitis C or alcoholism, than similar patients never given the drug.

Why do I get so tired? Even when I don't feel sick I am sooo tired.

Is there anything I can do? It just seems so hopeless.

OK, lets take a look at this.  Fatigue is common to a lot of problems, but with liver disease it makes everything much harder.  These comments will apply to a lot of fatigue issues but I'll refer to liver in this discussion.

When you think about energy you have to forget that you like to imagine yourself as a "person".  You have to understand that at the core of your problem you are a bunch of mitochondria.  These are small, self contained structures that float inside of your cells.  They are the focus of this discussion because they are the power source of the cell.  There is a vast and very complex chemistry that does its magic to allow you to live but at the root of everything is energy.  You eat to get fuel for your body but ask yourself just when does that fuel turn to the energy?  What the heck is energy anyway?  Ah, there you have it. That is the nut isn't it? when you feel fatigue, even when you eat good food, why doesn't it work for you?

Since the function of the liver is so very complex, it should not come as a surprise that it can play a role in a vast array of diseases.  Like so many problems, psoriasis has been treated symptomatically as a skin problem but research is now coming along which links it to more profound causes and suggests that addressing liver damage may be the best way to treat psoriasis.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209456/pdf/PG-11-25606.pdf

 Psoriasis is a chronic inflammatory disease that affects the skin. Studies have shown that psoriasis is not merely a skin problem; psoriasis is linked with various comorbid conditions, especially obesity and metabolic syndrome [1–5], which are known risk factors for non-alcoholic fatty liver disease (NAFLD).

The amount of alcohol required to produce hepatitis or cirrhosis varies among individuals, but as little as 40 g/day (Table 1) for 10 years is associated with an increased incidence of cirrhosis. There is considerable evidence to suggest that females require less total alcohol consumption (20 g ethanol/day) to produce clinically significant liver disease.

Patients with cirrhosis who were treated with human albumin experienced improvement in a number of outcomes, including overall survival, compared to standard therapy, according to data presented at the International Liver Congress.

“Long-term albumin administration to patients with decompensated cirrhosis could be seen as a disease-modifying treatment,” Mauro Bernardi, MD, of the University of Bologna, in Italy, said in a press conference. “At the moment, the only curative approach is transplant. Treatment to influence the survival of these patients is most needed.”

A new study of how the different saturated fats produce different illnesses

Saturated fatty acids induce development of both metabolic syndrome and osteoarthritis in rats

The predominant saturated fatty acids (SFA) in human diets are lauric acid (LA, C12:0) from coconut and palm oil, myristic acid (MA, C14:0) mainly from palm kernel oil, coconut oil, and butter fat, palmitic acid (PA, C16:0) naturally present in butter, cheese, milk, and meat , as well as cocoa butter, soybean oil, and sunflower oil and stearic acid (SA, C18:0) abundant in animal fat (up to 30%) , cocoa butter and shea butter.

The aim of this study was to investigate whether diets containing individual SFA together with excess simple carbohydrates induce osteoarthritis (OA)-like changes in knee joints and signs of metabolic syndrome in rats. Rats were given either a corn starch diet or a diet composed of simple carbohydrates together with 20% LA, MA, PA, SA or beef tallow for 16 weeks. Rats fed beef tallow, SA, MA or PA diets developed signs of metabolic syndrome, and also exhibited cartilage degradation and subchondral bone changes similar to OA.