Non alcoholic fatty liver disease (NAFLD) is today the most common cause of chronic liver disease, causing steatohepatitis, cirrhosis, hepatic failure and hepatocellular carcinoma. Newer insights into the issue have revealed a  simple truth that it’s the sugars, fruits and grains that are the source of every alcoholic beverage and the actions and metabolism of these sugars, particularly of fructose, have several similarities with those of alcohol. Therefore, prevention and management of NAFLD have got lot to do with restriction of these dietary factors.

Toxic Truth of Sugar: Source

Fructose and nonalcoholic fatty liver disease (NAFLD): the multifaceted aspects of fructose metabolism. [See]

The Toxic Truth: Too much fructose can damage your liver, just like too much alcohol [See]

Sugar is Toxic: The growing scientific evidence, both epidemiological and mechanistic, very clearly shows that excess sugar induces all of the diseases associated with the metabolic syndrome, Robert H. Lustig et al write in Nature. See Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature. 02 February 2012;482:27–29. doi:10.1038/482027a[Link][Report | Report | Report | Report]

Lim J, Mietus-Snyder M, Valente A et al. The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome. Nat Rev Gastroenterol Hepatol 2010;7:251–264.

Jegatheesan P, Bandt J-PD. Fructose and NAFLD: The Multifaceted Aspects of Fructose Metabolism. Nutrients 2017;9(3):230. Available at

Zhang D-M, Jiao R-Q, Kong LD. High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions. Nutrients 2017;9(4):335. Available at

Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. Hepatology. June 2013;57(6):2525-2531. Available at

Duarte S, Stefano JT,  Vanni D, Carrilho F, Oliveira C. Impact of current diet at the risk of non-alcoholic fatty liver disease (NAFLD). Arquivos de Gastroenterologia. 2019;56.  DO – 10.1590/s0004-2803.201900000-67. Available at

Prussick RB,  Miele L. Nonalcoholic fatty liver disease in patients with psoriasis: a consequence of systemic inflammatory burden? Br J Dermat. July 2018;179(1):16-29. Available at

Gastaldelli A, Cusi K. From NASH to diabetes and from diabetes to NASH: Mechanisms and treatment options. JHEP Reports. October 2019;1(4):312-328. Available at

Aron-Wisnewsky J, Gaborit B, Dutour A, Clement K. Gut microbiota and non-alcoholic fatty liver disease: new insights. Clinical Microbiology and Infection. 2013;19(4):338-348. Available at

Mann JP et al. Nonalcoholic Fatty Liver Disease in Children. Semin Liver Dis 2018;38:1–13. Available at

Duwaerts CC, Maher JJ. Macronutrients and the Adipose-Liver Axis in Obesity and Fatty Liver. Cellular and Molecular Gastroenterology and Hepatology2019;7(4):749-761. Available at

Taskinen M-R, Packard CJ, Borén J. Dietary Fructose and the Metabolic Syndrome. Nutrients 2019;11(9):1987. Available at

Akhtar DH, Iqbal U, Vazquez-Montesino LM, Dennis BB, Ahmed A. Pathogenesis of Insulin Resistance and Atherogenic Dyslipidemia in Nonalcoholic Fatty Liver Disease. J Clin Transl Hepatol. 2019;7(4):362. doi: 10.14218/JCTH.2019.00028. Available at

Chen Q, Wang T, Li J et al. Effects of Natural Products on Fructose-Induced Nonalcoholic Fatty Liver Disease (NAFLD). Nutrients 2017;9:96.Available at

Godoy-Matos AF, Silva Júnior WS, Valerio CM. NAFLD as a continuum: from obesity to metabolic syndrome and diabetes. Diabetol Metab Syndr 2020;12:60. Available at

El-Agroudy NN et al. Are Lifestyle Therapies Effective for NAFLD Treatment? Trends in Endocrinology & Metabolism 2019;30(10):701-709. Available at

Lambertz J, Weiskirchen S, Landert S,  Weiskirchen R. Fructose: A Dietary Sugar in Crosstalk with Microbiota Contributing to the Development and Progression of Non-Alcoholic Liver Disease. Front. Immunol., 19 September 2017. Available at


Obesity is now not only more common, but also affecting kids more often. It’s linked to all other problems of metabolic syndrome. In recent years, evidence has been mounting to link the consumption of sugar and sweetened foods with increasing prevalence of obesity, across the ages. Although several therapeutic approaches are being tried, including surgical interventions, the root cause of the obesity epidemic being the modern diet, the most important, most effective, most healthy and least invasive intervention is dietary intervention itself.

Potential mechanisms for fructose-induced insulin resistance. [See]
Main pathways of fructose metabolism that lead to insulin resistance, metabolic syndrome and obesity [See]

Sugar is Toxic: The growing scientific evidence, both epidemiological and mechanistic, very clearly shows that excess sugar induces all of the diseases associated with the metabolic syndrome, Robert H. Lustig et al write in Nature. See Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature. 02 February 2012;482:27–29. doi:10.1038/482027a[Link][Report | Report | Report | Report]

Isganaitis E, Lustig RH. Fast Food, Central Nervous System Insulin Resistance, and Obesity. Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:2451–2462. Available at

Modern day food causes all the ills: The highly processed, calorie-dense, nutrient-depleted diet frequently leads to exaggerated supraphysiological post-prandial spikes in blood glucose and lipids. This post-prandial dysmetabolism induces immediate oxidant stress, which increases in direct proportion to the increases in glucose and triglycerides after a meal. The transient increase in free radicals acutely triggers atherogenic changes including inflammation, endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity. To attenuate the increase in glucose, triglycerides, and inflammation after a meal,  a diet rich in minimally processed, high-fiber, plant-based foods, including vegetables and fruits, whole grains, legumes, and nuts is recommended. Other dietary interventions that can significantly ameliorate postprandial dysmetabolism include intake of lean protein, vinegar, fish oil, tea, and cinnamon. Additional benefits may result from calorie restriction, weight loss and exercise.See O’Keefe JH, Gheewala NM, O’Keefe JO. Dietary Strategies for Improving Post-Prandial Glucose, Lipids, Inflammation, and Cardiovascular Health. J Am Coll Cardiol 2008; 51:249-255 Abstract at | Anti-Inflammatory” Diet May Improve Postprandial Glucose, Cardiovascular Health

Dietary fructose linked to metabolic syndrome and diabetes mellitus: In a new study from Vanderbilt University in Nashville, Tennessee, a diet with 30 percent of total energy from fructose was given to 29 adult male rhesus monkeys aged 12 to 20 years for a period of 12 months. Starting at six months and by the end of the 12-month feeding study, ALL (100%) the monkeys developed certain metabolic syndrome components including body adiposity, insulin resistance, and dyslipidemia and four monkeys (15%) developed type 2 diabetes mellitus. [Bremer AA et al. Fructose-Fed Rhesus Monkeys: A Nonhuman Primate Model of Insulin Resistance, Metabolic Syndrome, and Type 2 Diabetes. Clinical and Translational Science. August 2011;4(4):243–252. Full Text | Report]

Increased fructose consumption from fruits increases metabolic syndrome risk: A cross-sectional population based study on 2537 subjects (45% men) aged 19-70 y has shown that higher consumption of dietary fructose may have adverse metabolic effects and increase the risks for metabolic syndrome. [Firoozeh Hosseini-Esfahani et al. Dietary fructose and risk of metabolic syndrome in adults: Tehran Lipid and Glucose study. Nutrition & Metabolism 2011, 8:50 doi:10.1186/1743-7075-8-50 Full text]

Mortera RR, Bains Y, Gugliucci A. Fructose at the crossroads of the metabolic syndrome and obesity epidemics. Frontiers In Bioscience, Landmark. Jan 1, 2019;24:186-211. Available at

Malik VS, Hu FB. Fructose and Cardiometabolic Health. Journal of the American College of Cardiology. 2015;66(14):1615-1624. doi: 10.1016/j.jacc.2015.08.025 Available at

Zhang D-M, Jiao R-Q, Kong LD. High Dietary Fructose: Direct or Indirect Dangerous Factors Disturbing Tissue and Organ Functions. Nutrients 2017;9(4):335. Available at

Tappy L, Lê K-A. Metabolic Effects Of Sweetened Beverages: Pathophysiology And Mechanistic Insights. CMR e Journal. December 2010;3(3):13-18. Available at

Tappy L, Lê K-A. Metabolic Effects of Fructose and the Worldwide Increase in Obesity. Physiological Reviews January 2010;90(1):23-46. Available at

Tappy L. Fructose-containing caloric sweeteners as a cause of obesity and metabolic disorders.

Fructose (Fruit Sugar) is a more important cause for metabolic disorders like diabetes, hypertension, fatty liver disease, obesity

Fructose in fruits can increase obesity: A new study reports that when fructose was consumed, absolute lipogenesis was 2-fold greater and that an early stimulation of lipogenesis after fructose, consumed in a mixture of sugars, augments subsequent postprandial lipemia. Acute intake of fructose stimulates lipogenesis and may create a metabolic milieu that enhances subsequent esterification of fatty acids flowing to the liver to elevate TG synthesis postprandially. See Parks EJ, Skokan LE, Timlin MT, Dingfelder CS. Dietary Sugars Stimulate Fatty Acid Synthesis in Adults. J. Nutr. June 2008;138:1039-1046 Abstract

Energy Drinks Pose Serious Health Risks for Young People: According to a review of scientific literature and Internet sources, published in Pediatrics, energy drinks that contain caffeine, taurine, sugars and sweeteners, herbal supplements etc., are regularly consumed by 30% to 50% of children, adolescents, and young adults and and are associated with risks for serious adverse health effects such as liver damage, kidney failure, respiratory disorders, agitation, confusion, seizures, psychotic conditions, nausea, vomiting, abdominal pain, rhabdomyolysis, tachycardia, cardiac dysrhythmias, hypertension, myocardial infarction, heart failure, and death. [See Seifert SM, Schaechter JL, Hershorin ER, Lipshultz SE. Health Effects of Energy Drinks on Children, Adolescents, and Young Adults. Pediatrics. 2011;127:511-528. DOI: 10.1542/peds.2009-3592. Free Full Text | Report]

Sugar sweetened beverages increase the risk of weight gain, development of metabolic syndrome and type 2 diabetes, meta analysis shows [See Malik VS et al. Sugar-Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes A meta-analysis. Diabetes Care November 2010;33(11):2477-2483 Free Full Text]

Sugar Sweetened Beverages Increase the Risk of Metabolic Syndrome, Diabetes and Obesity Vasanti S. Malik et al. Sugar Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes: A Meta-analysis Diabetes Care. August 2010;33(8) Full Text | Report]

Duwaerts CC, Maher JJ. Macronutrients and the Adipose-Liver Axis in Obesity and Fatty Liver. Cellular and Molecular Gastroenterology and Hepatology2019;7(4):749-761. Available at

Lakhan SE, Kirchgessner A. The emerging role of dietary fructose in obesity and cognitive decline. Nutr J 2013;12:114. Available at

Metabolic disorders striking the young: Should the stress be on ‘Stress’ or on Food? Many reports emerging from India reveal increasing incidence of metabolic syndrome disorders in young children and many things such as stress at school, sedentary life style, computers, TV, genes and junk food have been blamed. Some have even advised the kids to stop schooling and do yoga for relaxation! Is it not ironical that the so called experts who sought changes in our school education, so as to make it less stressful, now blame the changed methodology for increasing stress? In blaming many things, the strongest reason is bound to be missed: and that reason is the FOOD! See The Young Are Ageing. Outlook Sep 13, 2010 Full Text | Delhi kids suffer from adult ailments! Wonder Woman Sep 8, 2010 Full Text]

Apple Or Pear-Shaped Body Type Equally Dangerous: A study of 220,000 people suggests that being obese – having a body mass index (BMI) of 30 or more – is a major risk factor for heart disease, but found the distribution of fat on the body has no impact on that risk. [The Emerging Risk Factors Collaboration Separate and combined associations of body-mass index and abdominal adiposity with cardiovascular disease: collaborative analysis of 58 prospective studies. The Lancet. 11 March 2011. doi:10.1016/S0140-6736(11)60105-0 Full Text | Report]

Metabolic Syndrome May be Due to Disease Causing Fat Cells: UC Davis Health System researchers have reported a novel observation that subcutaneous fat of MetS has increased macrophage recruitment with cardinal crown-like structure features and contributes to the increased cellular inflammation that produces increased levels of biomarkers that are correlated with both insulin resistance and low-grade inflammation. [Bremer AA et al. Adipose Tissue Dysregulation in Patients with Metabolic Syndrome. The Journal of Clinical Endocrinology & Metabolism August 24, 2011 jc.2011-1577. Abstract | Report]

Diet and Obesity May be Linked to Alzheimer’s: A Swedish study that included 8,534 twins over the age of 65, has found that the risk of dementia was almost double in those who were overweight versus those of normal weight and those who were obese had almost a fourfold increase in risk. [Johansson K at al. Longer term effects of very low energy diet on obstructive sleep apnoea in cohort derived from randomised controlled trial: prospective observational follow-up study BMJ 2011; 342:d3017  Abstract | Report | Older Paper]

Premature Death Awaits Obese Kids
Paul W. Franks et al., New Eng Journal Med., 11 February 2010 | Business Week Report

Childhood Obesity Alone May Increase Risk of Later Cardiovascular Disease Being obese by as early as 7 years of age may raise a child’s risk of future heart disease and stroke, even in the absence of other cardiovascular risk factors such as high blood pressure, according to a new study accepted for publication in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM). Abstract | Report in Science Daily | Report in Modern Medicine

Overweight Kids Risk Weak Bones, Diabetes: Abdominal Fat May Play a Role in Bone Strength Norman K Pollock et al. Lower bone mass in prepubertal overweight children with pre-diabetes Journal of Bone and Mineral Research Jul 2010 Abstract | Report]

Higher-Protein/Low-GI Diet Best for Maintaining Weight Loss [See Larsen TM et al. Diets with High or Low Protein Content and Glycemic Index for Weight-Loss Maintenance. N Engl J Med November 25, 2010; 363:2102-2113 Abstract | Report]

A Randomized Trial of a Low-Carbohydrate Diet vs Orlistat Plus a Low-Fat Diet for Weight Loss A new randomized trial comparing a low-carbohydrate diet with a low-fat diet in combination with the weight-loss drug orlistat has found that both strategies produced meaningful weight loss and the low-carb diet in addition produced significant improvements in blood pressure. William S. Yancy Jr, et al., Published in Arch Intern Med. on Jan 25, 2010 [Abstract] | Report]

Low-Carb and Mediterranean Diets Better than Low-Fat for Weight Loss, Lipid Changes at 2 Years: Mediterranean and low-carbohydrate diets may be effective alternatives to low-fat diets, offering more favorable effects on lipids (with the low-carbohydrate diet) and on glycemic control (with the Mediterranean diet). See Shai I, Schwarzfuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008;359:229-241 Full text Article

Low carbohydrate and high monounsaturated fat diets help weight loss and offer metabolic benefits Brehm BJ,  D’Alessio DA. Weight Loss and Metabolic Benefits With Diets of Varying Fat and Carbohydrate Content: Separating the Wheat From the Chaff Nature Clinical Practice Endocrinology & Metabolism Available at

Rely on internal cues of meal cessation to keep off obesity Wansink B, Payne CR, Chandon P. Internal and External Cues of Meal Cessation: The French Paradox Redux? Obesity 2007;15:2920-2924. Available at

Higher Fat at Breakfast May Be Healthier: University of Alabama research reveals that mice fed a meal higher in fat had normal metabolic profiles and in contrast, mice that ate a more carbohydrate-rich diet in the morning and consumed a high-fat meal at the end of the day saw increased weight gain, adiposity, glucose intolerance and other markers of the metabolic syndrome. [MS Bray, J-Y Tsai et al. Time-of-day-dependent dietary fat consumption influences multiple cardiometabolic syndrome parameters in mice. International Journal of Obesity. 30 March 2010.] doi:10.1038/ijo.2010.63 [Abstract] | UAB Report]