The new normal at most chiropractic practices is watching patients suffer from chronic illnesses.
These are often worsened by diets that are high in sugar and saturated fat, and low in plant-based nutrients and fiber.
These characteristics are typical of today’s fast-food-centered Western diet. An excellent film to recommend to these patients is Morgan Spurlock’s Super Size Me.
During the film, Spurlock decides to spend a month consuming only McDonald’s menu items—the gold standard for processed food that is unfortunately part of the standard American diet. Throughout his “experiment,” he gets periodic medical exams to assess his blood work and overall health. The food Spurlock ate for each meal was the only variable of his daily routine.
Not surprisingly, with each medical visit, his health was seen to decline. In addition, he began to gain considerable fat around his belly. Unbeknownst to him, he was also gaining omental fat (particularly around his liver).
The job of the liver
The liver has many bodily functions, most significantly regulating the amounts of sugar, protein, and fat that enter the bloodstream. The liver is also a detoxification site where the conversion of toxic substances to nontoxic metabolites occurs.1
When a person regularly eats too much food containing saturated fatty acids, omega-6 fatty acids, and fructose, the risk of non-alcoholic fatty liver disease (NAFLD) is increased.2
NAFLD is typically comorbid with obesity, type 2 diabetes, metabolic syndrome, and steatohepatitis.3
Although the pathogenesis of NAFLD is intricate, lipid accumulation appears to be the primary impetus. This phenomenon of turning carbohydrates into fat has been referred to as de novo lipogenesis (DNL), and the latest research has concluded that it is a major contributor to the pathogenesis of NAFLD.3
Before Spurlock started his experiment, his team of doctors evaluated his health by taking his blood work. When he had his routine liver enzymes checked, they were unremarkable: SGPT 20 IU/L and SGOT 21 IU/L.
Toward the end of his experiment, his liver enzymes were unbelievable: SGPT 290 IU/L and SGOT 130 IU/L.4
Elevated levels of SGPT and SGOT originating from the liver are caused by damage to the hepatocytes or liver cells. The optimal ranges are between 10 and 30 U/L. Readings greater than 100 U/L are warning signs of liver pathology that may include NAFLD.12
These results are eye opening: As a result of Spurlock’s consuming a 30- day steady diet of McDonald’s foods, his liver started to leak enzymes into his bloodstream because there was an overabundance of fat accumulating in his liver cells. This is a tell-tale sign of liver damage. Interestingly, this can occur without the use of alcohol or drugs, which are the usual culprits.
It became obvious throughout the film that the energy imbalance resulting from consuming excess calories without increasing his activity level was what facilitated Spurlock’s weight gain. What stymied his providers was how quickly the ectopic fat accumulated around his liver.
The challenge with patients who have NAFLD is that often the disease is asymptomatic. The presentation (as seen when Spurlock visits his doctor for an exam) is usually coincidental from routine blood tests.5
It’s customary for your overweight patients to have elevated liver enzymes without showing any overt symptoms of morbidity.
Co-occurring with NAFLD are insulin resistance and cardiac inflammation, so elevated fasting glucose and lipids, in addition to elevated homocysteine and C-reactive protein, may also appear. Although NAFLD patients may be referred to a hepatologist to avoid progression toward end-stage liver disease, the overall prognosis is usually good following dietary modification and weight loss.
Patients with even minor elevated blood values (lipids, glucose, and liver enzymes) must be educated on being at increased health risk. Intervention should begin by targeting gradual weight loss of one to two pounds per week. A vital step in this process is educating the patient about reading food labels to steer clear of processed carbohydrates and saturated fats.
Depending on the prescription medications they’re taking, if any, certain nutraceuticals and micronutrients that aid in the liver’s detoxification process are recommended. There is strong clinical research supporting the use of supplements that have hepato- protective properties, such as vitamin D7, vitamin E8, astaxanthin, omega-3 fatty acids, and coffee.9
Addressing this preventable disease begins with weight loss and diet modi-ication because NAFLD is co-occurring with excess fructose consumption and consequent insulin resistance. Educating the patient on the dangers of added high-fructose corn syrup (HFCS) is paramount because HFCS represents over 40 percent of caloric sweeteners in foods and soft drinks. Healthcare providers should understand the impact this has on the incidence of NAFLD.6
Sucrose and HFCS intake have increased 1,000 percent over the last 40 years, and now account for up to 10 percent of caloric intake.11
The big culprits are the sugary beverages often sold and marketed to children. In addition, many fruit smoothies, fruit juices, and recovery drinks contain as much or more sugar than soda.
Educating your patients
Twenty-four-hour food recalls are helpful to assess how frequently a patient consumes refined and processed carbohydrates that contribute to chronically elevated blood sugar and ectopic fat production. The interplay between diet and NAFLD is crucial.
The patient must realize NAFLD does not exist solely by itself but as a result of a series of aberrant physiological functions that start with high plasma levels of both glucose and insulin, which contribute to NAFLD.
The diet that appears to work the best with weight loss and decreased inflammation is the Mediterranean Diet (see sidebar). The Mediterranean diet consists of an abundance of olive oil, fruits, vegetables, nuts, legumes, deep cold-water fish, and monounsaturated fatty acids.
The foods your patients should avoid are fatty meat products, omega-6 fatty acids, processed grains, fruit juices, and soft drinks.
Louis Miller, DC, MS, is the owner and operator of advanced Chiropractic of South Florida and Healthy Weight Solutions. He graduated from New York Chiropractic College in 2000 and has been practicing chiropractic ever since. In 2015 he completed his Master of Science Degree in applied clinical nutrition. He is currently writing his first book regarding the many nutritional cases he’s been presented during practice. He can be contacted at 561-432-1399 or through healthyweightsolutions.org.
1 Bland JS, et al. (2004). Clinical Nutrition: A Functional Approach (2nd ed. pp. 247-252). Federal Way, WA: The Institute of Functional Medicine.
2 Yu J, Marsh S, et al. The Pathogenesis of Nonalcoholic Fatty Liver Disease: Interplay between Diet, Gut Microbiota, and Genetic Background. Gastroenterol Res Pract. 2016;2016:2862173. doi: 10.1155/2016/2862173.
3 Chen G, Ni Y, et al. Micronutrient Antioxidants and Nonalcoholic Fatty Liver Disease. Int J Mol Sci. 2016;17(9):1379.
4 Morley JR (Producer), Spurlock M (Director). (2004). Super Size Me. [Motion picture]. United States: The Con.
5 Vuppalanchi R, Chalasani N.. Non-alcoholic fatty liver disease and non- alcoholic steatohepatitis: Selected practical issues in their evaluation and management. Hepatology. 2009;49(1):306-317. http://doi.org/10.1002/hep.22603.
6 Ludwig DS. Examining the health effects of fructose. [ITAL]JAMA.[/ITAL] 2013;310(1):33-4.
7 Wang X, Li W, Zhang Y, Yang Y, Qin G. Association between vitamin D and non-alcoholic fatty liver disease/non-alcoholic steatohepatitis: results from a meta-analysis. [ITAL]Int J Clin Exp Med.[/ITAL] 2015;8(10):17221-34. eCollection 2015.
8 Fukui A, Kawabe N, Hashimoto S, et al. Vitamin E reduces liver stiffness in nonalcoholic fatty liver disease. [ITAL]World J Hepatol.[/ITAL] 2015;7(27):2749-56. doi:10.4254/wjh.v7.i27.2749.
9 McCarty MF. Full-spectrum antioxidant therapy featuring astaxanthin coupled with lipoprivic strategies and salsalate for management of non-alcoholic fatty liver disease. [ITAL]Med Hypotheses.[/ITAL] 2011;77(4):550-6. doi:10.1016/j.mehy.2011.06.029.
10 Sofi F, Casini A. Mediterranean diet and non-alcoholic fatty liver disease: new therapeutic option around the corner? [ITAL]World J Gastroenterol.[/ITAL] 2014;20(23):7339-46. doi: 10.3748/wjg.v20.i23.7339.
11 Abdelmalek MF, Suzuki A, Guy C, et al. Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease. [ITAL]Hepatology.[/ITAL] 2010;51:1961-1971.
12 Weatherby D, Ferguson S. (2002). [ITAL]Blood chemistry and CBC analysis: Clinical laboratory testing from a functional perspective.[/ITAL] Jacksonville, OR: Bear Mountain Pub.