I’ve been discussing SIBO, small intestinal bacterial overgrowth, quite a bit lately, as I believe it represents a huge epidemic, an epidemic as large as that of the epidemics of overweight and obesity, bigger than the epidemics of pre-diabetes and type 2 diabetes. It’s not an infectious epidemic, of course, but a man-made one. Flawed dietary guidelines, predatory practices of the food industry, pharmaceuticals, herbicides, and many other factors have all contributed to this massive distortion of the human microbiome. The long-term health implications of unaddressed SIBO are significant, ranging from coronary disease, to type 2 diabetes, to neurodegenerative diseases, to colon cancer. Yet it continues to be ignored, denied, and simply not addressed in most conventional medical settings.
As bad as SIBO can be for many aspects of health, it is especially bad for liver health because of some fundamental facts.
Blood from the entire gastrointestinal (GI) system drains into the portal system that connects to the liver. The portal vein drains venous blood from the intestinal tract, spleen, gallbladder, pancreas and other abdominal organs and delivers it to the liver, where various components are processed. The liver is therefore the organ that first receives whatever flows out of abdominal organs, a protective process that limits the entry of toxic components into the main, “systemic,” bloodstream.
Recall that, in SIBO, unhealthy shifts in bowel flora species have occurred, favoring species like Klebsiella and E. coli at the expensive of favorable species such as Lactobacillus, Bifidobacteria, and selected Clostridia species. There can be overgrowth of fungal species, as well, such as Candida and Malassezia species. For not entirely clear reasons (intermittent dissolution of the mucus barrier, non-steroidal anti-inflammatory drugs, stomach acid-blocking drugs, maltodextrin, chlorinated drinking water, and others are among the likely reasons), unhealthy species have ascended up the ileum, jejunum, duodenum, and stomach, constituting 30 feet of unhealthy microbes. The lifespan of bacteria and fungi is measured in hours to days, not years. It therefore means that there is rapid turnover of trillions of microbes within the 30 feet of your GI tract. Upon dying, the debris that is generated gets metabolized by intestinal cells and microbes, while some of it penetrates into the bloodstream, a process labeled “endotoxemia,” since one of the dominant and most destructive bacterial components to enter the body is bacterial endotoxin, also called “lipopolysaccharide,” or LPS, a component of the cell walls of the species most dominant in SIBO.
Because the portal circulation is the first to receive venous blood draining the GI tract, the level of LPS in the portal system is high, as much as 10-fold higher than that in the main circulation. A substantial quantity of LPS does indeed bypass the liver, raising systemic levels 200-400% higher. But it is the liver that receives the greatest amount of LPS.
LPS from SIBO therefore means that your poor liver receives a beating, an enormously powerful inflammatory stimulus. (Nanogram quantities of LPS injected into a human induces an acute illness, for instance.) In someone who consumes plenty of carbohydrates and sugars, such as someone following U.S. Dietary Guidelines, or someone consuming a typical American diet rich in processed foods and sugars, the liver is busy converting carbs and sugars to triglycerides, the process called “de novo lipogenesis.” Some triglycerides exit the liver, thereby raising blood levels of triglycerides, while some are retained within the liver, yielding fatty liver. The process is further amplified by insulin resistance that typically develops in someone consuming carbs and sugars, increasing the rate at which carbs are converted to triglycerides.
The delivery of LPS via the portal circulation to a liver busy with de novo lipogenesis and insulin resistance is therefore exposed to a huge inflammatory stimulus, a major factor in causing progression of fatty liver to non-alcoholic steatohepatitis, then cirrhosis, then liver failure. Outwardly, this is not a pretty process, as it leads to portal hypertension, accumulation of fluid in the abdomen (ascites), impaired liver metabolic capacity (e.g., reduction in serum proteins), esophageal varices (essentially varicose veins in the esophagus) that leads to upper GI hemorrhage (vomiting blood), and jaundice. At this point, you are quite ill, incapable of conducting the normal affairs of your life, and dependent on the medical system. And your doctor advises you all along that there is little they can do until they put you on the liver transplant list, if you qualify.
I hope that you now recognize that, if you understand the process, you have the answer to NOT engaging in this process. As I have outlined previously, all you need to do to avoid this process and regain normal liver status is to:
- Not consume foods that fuel liver de novo lipogenesis–i.e., avoid wheat and grains that contain amylopectin A, minimize exposure to sugars, such as those in soft drinks and snacks
- Address common nutrient deficiencies that allow insulin resistance–vitamin D, omega-3 fatty acids, iodine, magnesium
- Recognize, then address, SIBO
In my view, if you are diagnosed with fatty liver and are not advised of the above, then doctor ignorance and malpractice are the issues. Reversing fatty liver and regaining health are really fairly straightforward, but it will not involve any prescription drugs nor medical procedures and are thereby of little interest to most conventional healthcare practitioners. So it is up to YOU to take the reins.