Obesity: new bad news on eating patterns, liver disease, and shortened life – Clinical Tips
Ann M. Coulston
The dire consequences of obesity are not limited to diabetes, high blood pressure, and osteoarthritis, because body fat cell mass increases the risk for fatty liver disease and a reduced total lifespan rises sharply.
Medical journals, newspapers, and popular magazines brim with reports about the adverse effects of obesity. Yet the incidence and prevalence of obesity keeps increasing. (1,2). Health warnings about obesity aren’t getting through to the public, aren’t understood, or are viewed as irrelevant.
The best known health consequences of obesity include hypertension, which can lead to stroke; hyperlipidemia or risk for coronary heart disease; hyperinsulinemia (the forerunner of type 2 diabetes); osteoarthritis; and risk for some types of cancer. (3) However, there are other less well known risks of obesity, including reduced lifespan and nonalcoholic fatty liver disease (NAFLD) and its consequences. Americans are still reluctant to conform their food choices to the Food Guide Pyramid, resulting in their frequent overconsumption of calorie-dense foods and underconsumption of nutrient-rich lower calorie fruits and vegetables. Americans need a “wake-up” call. Perhaps the new bad news that follows will help you to communicate a wake-up call to patients, colleagues, family, and friends.
Food Choices: “Hourglass” Instead of “Pyramid” Eating Patterns Don’t Help
A recent report from US Department of Agriculture’s (USDA’s) Economic Research Service revealed that Americans’ food choices resemble an hourglass more than a pyramid? Consumers eat mostly from the tip and the foundation of the Food Guide Pyramid, enjoying lots of food high in fat and added sugars, along with refined grain products, such as pasta, crackers, and white bread. Many Americans eat too much. Approximately 12% more calories crept into the American diet between 1985 and 2000. That’s approximately 300 calories per person per day–enough to gain approximately 30 pounds if eaten routinely. Despite the reported benefits of fruits and vegetables, Americans still don’t eat the recommended minimum of 3 to 5 servings of vegetables and 2 to 4 servings of fruit. Oranges, apples, and bananas comprise half the fruit consumed. Iceberg lettuce, frozen potatoes (mostly French fries!), and potato chips accounted for one third of all vegetables. Most people exceed the 9 servings a day of the grains base of the Pyramid recommendation for a 2,200-calorie diet, eating approximately 50 more pounds of refined flour and cereal in 2000 than in 1985. Americans’ diets are missing whole grains, which have more vitamins, minerals, phytonutrients, and fiber that may help protect against heart disease and diabetes. Also, milk consumption dropped 24% between 1970 and 2000, whereas more yogurt and cheese were consumed. Yogurt consumption jumped 209% during that same time. Cheese consumption rose 61%. Mozzarella cheese alone increased 365%. Consumption of added sugars found in foods, such as soft drinks, fruit drinks, cakes, cookies, candy, and ice cream, rose 22% between 1980 and 2000–reaching 31 teaspoons of added sugars per person per day.
Medical reports indicate that Americans are paying for their indiscretions in new and different ways. There is an alarming increase in fatty liver disease among adults and children who are obese and insulin-resistant. Plus, some adults may not live long enough to enjoy their well-earned retirements or grandchildren.
Nonalcoholic Fatty Liver Disease
The incidence of obesity-related liver disease in children and adults is alarming doctors. (5,6) Excess body fat is deposited in the liver, as well as in subcutaneous adipose tissues, but obesity-associated hepatomegaly has often been overlooked, perhaps because it was so rare. Now, with the obesity rates rising among children and adolescents, medical experts are focusing on abnormalities of liver function that result when fat deposits build up in the liver (Figure 1).
[FIGURE 1 OMITTED]
Several terms have been used to describe this condition, including nonalcoholic steatohepatitis (NASH) (Figure 2). The term NAFLD is preferred, because it refers to liver damage ranging from simple steatosis to steatohepatitis, advanced fibrosis, and cirrhosis (Figure 3). (7) NAFLD represents a clinical and histologic spectrum of liver diseases associated with fatty infiltration of the liver (steatosis) in the absence of an obvious cause or alcohol abuse. Any condition that leads to fatty liver can progress to NAFLD. Without treatment, these fatty deposits in the liver can lead to more serious inflammation and fibrosis of the liver and, ultimately, cirrhosis, liver failure, and death. NAFLD occurs more commonly in people with type 2 diabetes, truncal obesity, hyperlipidemia, and insulin resistance. (7)
[FIGURE 2 OMITTED]
[FIGURE 3 OMITTED]
Up to 75% of adults who are obese have fatty liver on ultrasonography. More than 50% of these individuals with steatosis on biopsy have more serious histologic findings of inflammation and fibrosis. These are accompanied by a 25% incidence of developing cirrhosis, with a 10% to 15% risk for liver-related death. (7,8) What is so alarming is that up to 53% of children who are obese have NAFLD and face similar disease consequences as adults.
Many patients with early signs of NAFLD are only moderately obese, with a body mass index (BMI) of approximately 30. However, NAFLD’s prevalence increases with increasing obesity severity. NAFLD is most common in people with central obesity and insulin resistance, but it also occurs in some individuals who are not obese.
An NAFLD diagnosis is suspected in asymptomatic persons with chronic mild elevation of aminotransferase enzymes, hepatomegaly, and radiologic findings of fatty liver. Laboratory findings are summarized in Table 1. (7) Excessive alcohol use (>20-40 g/day) must also be excluded, as should viral hepatitis and other liver diseases. For reference, 12 oz of beer, 4 oz of wine, and 1.5 oz of hard liquor each contain 10 g of alcohol. Liver biopsy histology is used to confirm the diagnosis, stage of disease, and level of severity.
NAFLD is a “two-hit” disease. Once hepatic steatosis is established, the liver becomes more susceptible to the “second hit,” perhaps resulting from oxidative stress and steatohepatitis. The oxidative stress hypothesis of its development is that reactive oxygen species, unchecked by antioxidants, may trigger steatohepatitis by lipid peroxidation and cytokine induction. These events lead to cell death, necrosis, and collagen synthesis with fibrosis. (7) Based on the oxidative stress hypothesis, medical scientists are conducting trials of vitamin E supplements for NAFLD prevention and treatment, but findings are not yet in, although they show some promise. Vitamin E is a potent lipid-soluble antioxidant and is effective against lipid peroxidation. In a pilot study, 11 children (aged 8-14 years) with BMI of 28-42 were treated with vitamin E after a 3-month elevation of aspartate aminotransferase/ alanine aminotransferase (AST/ALT). By 5 months follow-up, all children had normalization of AST/ALT. (9)
Treatment involves reversing the risk factors for obesity, diabetes, and hyperlipidemia. Good metabolic control of blood glucose and lipids helps but is not always effective in reversing NAFLD. Marked biochemical improvement has been noted in response to a 10% decrease in body weight. For every 1% reduction in body weight, an 8% reduction of ALT was noted. Unfortunately, drastic weight loss schemes, such as gastric bypass techniques or very low-calorie diets, do not work and may worsen portal inflammation and fibrosis. (7,8) A nutrition treatment plan that promotes gradual weight loss of no more than 0.5-1 lb/week for children and 1-2 lb/week for adults and normalization of glucose and lipid concentrations is presently the first line of treatment. This is the only treatment recommended for pure steatosis with no evidence of fibrosis.
No medications directly reduce or reverse liver damage. Vitamin E, metformin, and gemfibrozil improve liver tests, and betaine, vitamin E, and clofibrate may also improve liver histology, but further clinical testing is needed before specific recommendations for drug treatment can be made. (7)
NAFLD may represent a hepatic component of the metabolic syndrome that, in the presence of obesity, includes the “deadly quartet” of insulin resistance, diabetes, hypertriglyceridemia, and hypertension. Soon we may have to add NAFLD as a fifth player and make a “deadly quintet.”
Years of Life Lost From Obesity
Obesity in young adults decreases their length of life or increases their years of life lost (YLL). The association between height, weight, exercise, and risk of dying before age 90 was examined in the Leisure World Cohort Study, a population-based prospective investigation of people with an average age of 75 years in a California retirement community The odds of dying before age 90 were associated with height, weight, weight at age 21, BMI, and outdoor exercise, even after adjusting for sex, smoking, cardiovascular-related conditions, diabetes, fractures, and cancer. After 11 years of follow-up, age, height, and weight at baseline were not associated with mortality. However, a low body weight during early adulthood and physical activity in the 70s increased chances of survival to age 90. (11)
A follow-up of Framingham Heart Study participants also looked at the probability of death before age 70 and its relationship to overweight (BMI of 25-29) and obesity (BMI = 30) at age 40. (12) Because the relationship between weight and mortality is affected by underlying disease, those who had cardiovascular disease and those who were very underweight (BMI < 18) were excluded. The probability of death before age 70 increased with each higher category of BMI group. Obesity at age 40 was associated with a 7-year decrease in life expectancy for women and a 6-year decrease in men, even after adjustment for physical activity and education.
Fontaine and colleagues reported on YLL resulting from obesity. (13) YLL is the difference between the number of years that you would be expected to live if you were not obese and life expectancy if you were obese. Using a nationally representative database, Fontaine et al found that even a moderate amount of excess weight confers a noticeable increase of years of life lost and that as degree of overweight increases there are striking, steady YLL increases. For example, the maximum YLL was 13 years in severely obese (BMI > 45) white men aged 20-30 and 8 years for women of the same age. There were also racial differences. Among Blacks with severe levels of obesity (BMI > 45), the maximum YLL was observed: some 20 years for men and 5 years for women. For every degree of increased body weight over BMI of 25, younger adults had greater YLL than older persons.
Can our concern about the increasing trend toward obesity be translated into changes in food consumption patterns? Will we acknowledge the health risks of obesity when faced with some less common conditions, such as NAFLD? Can the expectation of a decreased life expectancy reverse the epidemic of obesity in this country? Only time will tell.
Table 1. Liver Enzyme Laboratory Data Primer
Aspartate aminotransferase (AST) <50 U/L
Alanine aminotransferase (ALT) <45 U/L
Alkaline phosphatase <200 U/L
Gamma glutamyltransferase (GGT) <40 U/L
Prothrombin time 10.4-12.6 sec
Findings in Nonalcoholic Fatty
Aspartate aminotransferase (AST) Mild to moderate elevation
Alanine aminotransferase (ALT) Mild to moderate elevation
AST/ALT Mild to moderate elevation
Alkaline phosphatase Mildly elevated
Prothrombin time Normal
(1.) National Center for Health Statistics. Available at: www.cdc.gov/nchs/products/pubs/pubd/hestats/obese/obse 99.htm. Accessed April 26, 2003.
(2.) Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA. 2003;289:76-79.
(3.) Pi-Sunyer FX. Medical hazards of obesity. Ann Intern Med. 1993;119:655.
(4.) Squires S. Pecking at the Pyramid. Washington Post, April 8, 2003, HE03.
(5.) Mehta K, Van Thiel DH, Shah N, Mobarhan S. Nonalcoholic fatty liver disease: pathogenesis and the role of antioxidants. Nutr. Rev. 2002;60:289-293.
(6.) Sinatra F. Non-alcoholic steatohepatitis (NASH): fat kids and fatty livers. Presented at Advances in Perinatal and Pediatric Nutrition; Stanford, Calif; July 23, 2001.
(7.) Angulo P. Nonalcoholic fatty liver disease. New Engl J Med. 2002;346:1221-1231.
(8.) Angulo P, Lindor K. Treatment of nonalcoholic fatty liver: present and emerging therapies. Semin Liver Dis. 2001;21:81-88.
(9.) Lavine J. Vitamin E treatment of nonalcoholic steatohepatitis in children: a pilot study. J Pediatr. 2000;136:734-738.
(10.) Palmer M, Schaffner F. Effect of weight reduction on hepatic abnormalities in overweight patients. Gastroenterology. 1990;99:1408-1413.
(11.) Kawas CH, Corrada MM, Paganini-Hill A. Low weight in early adulthood and later life exercise increase chances of surviving to age 90 [abstract]. Presented at American Academy of Neurology meeting 2003. Available at: http:// am.aan.com/scientific/index/htm. Accessed April 7, 2003.
(12.) Peeters A, Barendregt JJ, Willenkens F, Mackenbach JP, Mamun AA, Bonneux L. Obesity in adulthood and its consequences for life expectancy: a life-table analysis. Ann Intern Med. 2003;138:24-32.
(13.) Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB. Years of life lost due to obesity. JAMA. 2003;289:187-193.
Ann M. Coulston, MS, RD, FADA, is an established expert in clinical nutrition and research. She currently serves as a nutrition consultant to the food and healthcare industry, public relations firms, and Internet companies. She has more than 20 years of clinical research at Stanford University Medical Center, where her research centered on the nutritional management of diabetes and insulin resistance. She is Past-President of the American Dietetic Association and a member of the American Diabetes Association, the American Society for Nutritional Sciences, and the American Society for Clinical Nutrition. Ms Coulston received her master’s degree in nutritional science from Cornell University.
Corresponding author: Ann M. Coulston, MS, RD, FADA, Nutrition Consultant, 1386 Cuernavaca Circulo, Mountain View, CA 94040 (e-mail: email@example.com).
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