Your liver could be an alcoholic even though you are not!

One doesn’t have to be an alcoholic to acquire liver disease. As a matter of fact, more people in the United States are diagnosed with Non-Alcoholic Fatty Liver Disease (NAFLD) than Alcoholic Liver Disease (ALD). Thirty percent of the population is affected, it is often asymptomatic and may not be detected! The clinical picture ranges from no symptoms at all to discomfort in the area of the liver, fatigue, poor quality sleep, obesity with abdominal (brown) fat and abnormal blood tests.

So how does this happen? The liver is the master filter of the blood stream, pulling out toxic chemicals, extra hormones, metals and excess sugars. It’s a complex set of processes that essentially require the liver have a store of materials to pull from, creating the protective network that is essential to life and health.

Risk factors abound for NAFLD. The usual suspects include diabetes type 2 (what we associate as adult onset), obesity, high lipids in the blood (elevated cholesterol and triglycerides) and insulin resistance/metabolic syndrome. Other risk factors that may not be as evident can lead to the deposition of fats in the liver as well, these include: celiac disease*, drug use (steroids, aspirin, AZT, calcium channel blockers, synthetic estrogens and others), surgical gastric procedures for weight reduction, a few genetic diseases (Wilson’s, Weber-Christian), and environmental/work toxin exposure (benzenes, toluene, styrene, hexane, vinyl chloride, and others). Stress is often not identified as part of this inflammatory cascade, however, adrenal-stress leading to hypercortisolemia is a potent stimulator of chemical injury and should not be overlooked. Cortisol levels are implicated in many neuro-endocrine disorders such as  insulin resistance, inflammation and obesity, at a minimum.

Current belief is the progression of this pathology begins with a sensitivity to too much sugar in the blood stream that is not accessing the cells for proper energy usage. Excess sugars are stored in the liver in the form of fat as a reserve for periods of starvation. Insulin levels are high in insulin resistance, the cells are not receptive to the insulin knocking on the door of the cell wall to deliver the glucose-energy needed for normal cell-life. Resulting fatty storage, oxidation of fatty acids and decreased release of liver storage of triglycerides occurs. There is increased stress in the cells causing fats to transform into harmful bad fats, resulting in release of cytokine chemicals of inflammation. Fat storage, inflammation, liver cell damage, scar tissue and liver cell death ensue. Liver cell death is a normal, pre-programmed event. A healthy liver cell lives out its life and at an appropriate time is replaced by a copy of itself (hepatocyte). The amount of chemical-oxidative stress from injurious substances interrupt the normal copying of a mature hepatocyte, resulting in malformed cells that mimic healthy liver cells but actually form scar tissue which can progress to liver/hepatocellular carcinoma.* Besides all of this, complications with other organs can be contributors to NAFLD. Increased gut permeability (AKA leaky gut) in infection, autoimmune inflammation, food sensitivities/allergies, alcohol consumption and the standard American diet (SAD) can be part of the bigger picture. Small intestine bacterial overgrowth (SIBO) is identified as a condition debated by scientists where a specific microbiome toxins are linked as a key player in NAFLD*. SIBO results in increased bacteria that stimulate the immune response causing inflammation throughout the body but more specifically local liver inflammation and damage.

Diagnosing NAFLD includes measuring alcohol consumption. Less than 20 grams of alcohol per day is a key factor. One standard drink contains 10 grams of alcohol, one average beer, a small glass of wine (3 ½ ounces) or a nip of spirits (1 ounce). There are conflicting reports regarding alcohol consumption in NAFLD, although generally avoidance is recommended, “moderate use of alcohol is thought to reduce the risk of cardiovascular disease, but not for those with NAFLD.”* ALD, by comparison, results in hepatocyte swelling and Mallory bodies inside the cell (alcoholic hepatitis), fibrosis of the activated (stellate) cells and fibroblasts. This evolves slowly into alcoholic cirrhosis of the liver. RSNA.org reports MRI imaging and CT scans show promise for evaluating the amount of liver fat accumulation.*

Blood and serum testing include the liver transaminases (AST, ALT, GGT), triglycerides, HDL-c, fasting insulin, C peptide, HOMA-IR, IL-6, and serum zonulin. All of these markers are higher in the NAFLD group than in controls according to a study done by Hendy in 2017. Salivary hormone tests for cortisol and DHEA are useful in identifying a disruption as well as tracking progress over time.

At home, a simple waist circumference test could indicate storage of the visceral (bad) fat accumulation on the frame. Measuring at the waist level where the naval would naturally be (not when it has dropped in an obese form) will inform as to whether the healthy woman is less than 35 inches and man is less than 40 inches.

The good news is that the liver has an uncanny ability to repair and regenerate, given optimal circumstances! Of course, there is always the chance one has waited too long, is un/mis-diagnosed, is unable to implement adequate lifestyle changes. The opportunities for restoring health requires an intimate conversation covering all the facts in the case and the resources available for change. The two primary approaches include avoiding alcohol and/or other liver-offending substances and implementing the Mediterranean Diet plan. In 2015 Malhotra discovered that a diet low in high fructose corn syrup decreased fibrous tissue changes of the liver, and subsequently others (Jensen, DiNicolantionio and Chen) found NAFLD is driven by HFCS and sugar. Monosodium glutamate induces liver fatty changes and the viscera*.

Treatment considerations point to reducing inflammation which causes cellular injury, correcting the insulin resistance and repairing the gut. Naturopathic medicine and Functional medicine approaches healing the cells by changing the diet and lifestyle. Addressing the vis, the core energy creating healthy and well cellular activity, incorporates mindfulness, dietary habits, appropriate levels of physical activity, nutritional supplementation and reducing environmental exposure. Weight loss, normalizing blood fats and sugar via the diet, stress management and supplementation have the greatest impact of all and offer solutions to nearly everybody without investing in expensive interventions.
  • A slow, steady weight loss not exceeding 3 ½ pounds a week for adults to reach a total of 10% reduction of body weight is the first goal.
  • Avoidance of alcohol, added sugar, fructose, soda/pop, artificial additives and preservatives.
  • Food choices within the Mediterranean Diet fit the program, generally, although some may need to modify this diet, such a Celiac eliminating wheat/gluten. It is felt that the NAFLD individual is better off eliminating all gluten and grains as well as starchy vegetables. A high protein and vegetable diet with a low glycemic load and frequent small meals seems to work best.
  • Nutrients to correct glucose, insulin and fat in NAFLD: alpha lipoic acid, B complex, Chromium, Zinc, Magnesium, Manganese, Vanadium, Betaine HCl, N-acetyl Cysteine, Vitamin E and probiotics (order ProBio SAP on https://us.fullscript.com/welcome/drnancydoreo). Robust antioxidant levels are beneficial. Vitamin D levels, when low, can cause poor response to treatment or increased risk of fibrosis.
  • Herbs to support liver function:  Green Tea, Black Tea, coffee.  Herbal choleretics and addressing the cortisol/DHEA levels are also crucial factors. Mahonia, Cynara, Silybum, Taraxacum, Cichorium and Curcuma longa. Mixed carotenoids (lycopene, beta carotene, alpha carotene and phytoene/phytofuene).
Addressing chronic disease is a big project and requires support and direction. Please research, learn and make informed decisions in your health care. After all, no one knows you better than you!

Are you looking for some help with NAFLD? Contact Dr. Doreo for a consultation to see if you are a fit for the scientifically natural approach she uses in restoring health through Science-based Nutrition.

Yours in Health and Wellness,
Dr. Doreo

  




References
Kennedy AS. Radiation Therapy for Hepatocellular Carcinoma. Hepatocellular Carcinoma. 2009:615-640. doi:10.1007/978-1-60327-376-3_23.

Pooler BD, Wiens CN, Mcmillan A, et al. Monitoring Fatty Liver Disease with MRI Following Bariatric Surgery: A Prospective, Dual-Center Study. Radiology. 2019;290(3):682-690. doi:10.1148/radiol.2018181134.

Korpimäki S et al, Gluten-sensitive hypertransaminasemia in celiac disease: an infrequent and often subclinical finding. Am J Gastroenterol. 2011 Sep;106(9):1689-96.

Chen HL, Tsai TC, Tsai YC, Liao JW, Yen CC, Chen CM. Kefir peptides prevent high-fructose corn syrup-induced non-alcoholic fatty liver disease in a murine model by modulation of inflammation and the JAK2 signaling pathway. Nutr Diabetes. 2016;6(12):e237. Published 2016 Dec 12. doi:10.1038/nutd.2016.49

Saltzman ET, Palacios T, Thomsen M, Vitetta L. Intestinal Microbiome Shifts, Dysbiosis, Inflammation, and Non-alcoholic Fatty Liver Disease. Front Microbiol. 2018;9:61. Published 2018 Jan 30. doi:10.3389/fmicb.2018.00061moderate use of alcohol is thought to reduce the risk of cardiovascular disease, but not for those with NAFLD Ajmera VH. 2017

Hendy OM, Elsabaawy MM, Aref MM, Khalaf FM, Oda AMA, Shazly HME. Evaluation of circulating zonulin as a potential marker in the pathogenesis of nonalcoholic fatty liver disease. Apmis. 2017;125(7):607-613. doi:10.1111/apm.12696.

Jensen T, Abdelmalek MF, Sullivan S, et al. Fructose and sugar: A major mediator of non-alcoholic fatty liver disease. Journal of Hepatology. 2018;68(5):1063-1075. doi:10.1016/j.jhep.2018.01.019.DiNicolantonio JJ, 2017

Dinicolantonio JJ, Subramonian AM, O’Keefe JH. Added fructose as a principal driver of non-alcoholic fatty liver disease: a public health crisis. Open Heart. 2017;4(2). doi:10.1136/openhrt-2017-000631.

Malhotra N, Beaton MD. Management of non-alcoholic fatty liver disease in 2015. World J Hepatol. 2015;7(30):2962–2967. doi:10.4254/wjh.v7.i30.2962

Collison KS, Maqbool ZM, Inglis AL, et al. Effect of Dietary Monosodium Glutamate on HFCS-Induced Hepatic Steatosis: Expression Profiles in the Liver and Visceral Fat. Obesity. 2010;18(6):1122-1134. doi:10.1038/oby.2009.502.

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