The COVID-19 pandemic has put everything on hold and suddenly we find ourselves in the midst of a major health crisis. While keeping track of the developments in COVID-19 treatment and pathogenesis, the other pandemic that has been around for over the last decade is that of metabolic syndrome. This involves the commonly found clinical features of obesity, Type II diabetes, dyslipidemia, fatty liver disease, arterial hypertension, and cardiovascular disease. All these conditions are defined under a broad term called metabolic syndrome or simply metabolic disease.
Besides these conditions, individuals with metabolic syndrome are susceptible to other conditions such as polycystic ovary syndrome, cholesterol gallstones, asthma, sleep disturbances, some forms of cancers, and elevated uric acid levels. Excessive nutrition and sedentary lifestyle are the fundamental causes of metabolic syndrome, which has become a major health problem with more than 90% of obese, about 70% of overweight, and about 25% of normal weight patients being affected. In the US, over two-thirds of adults are overweight or obese with 1/20 considered as extremely obese. Very alarmingly, nearly a third of American children are obese or overweight.
Obesity including Type II diabetes and non-alcoholic fatty liver disease are among strong risk factors associated with metabolic syndrome. According to recent reports, the prevalence of diabetes is increasing in every country of the world and in the US alone there are now more than 100 million individuals who are overweight or obese. In one study, jointly conducted by the International Diabetes Federation and the Madras Diabetes Research Foundation, reported that in 2011, India had 62.4 million people with Type II diabetes. In 2010, the number was 50.8 million. Further the study reports that nationwide prevalence in India is above 9%. In southern cities, the incidence is as high as 20%. A report released in 2014 said that India had 65 million diabetic patients. The latest report released by Indian Diabetes Federation (IDF) suggests that India had 73 million patients in 2017 and the number is expected to be 100 million by 2030.
These diabetics are at risk of developing advanced fatty liver disease called non-alcoholic steatohepatitis (NASH) and different forms of cancer. Population-based cohort studies like EPIC (European Prospective Investigation into Cancer and Nutrition) suggest that obesity may play a role in 16% of hepatocellular carcinoma (liver cancer) cases. Many epidemiological studies have shown that obesity is a strong risk factor for liver cancer. Other epidemiological studies suggest a strong association between body mass index (BMI) and liver cancer. With each 5 kg/m2 increase in BMI, the risk of liver cancer increases by 24%. Compared to high prevalence of metabolic disease in western countries (20%-30%), the prevalence in Asia was considered to be lower (5%-20%). However, a growing body of literature has highlighted metabolic disease as a global epidemic.
In India the prevalence of non-alcoholic fatty liver disease is estimated to be 16%-32%. This is believed to be due to increased industrialisation along with changes in lifestyle and diet. Furthermore, recent evidence has suggested that fatty liver disease can affect non-obese patients in Asia. This effect has come to be known as the Asian paradox.
Sugar consumption is often considered as a key contributor to the obesity epidemic and associated cardiovascular disease. A global change in dietary habits has occurred over the last few decades and data have shown temporal associations between increased total sugar consumption, increased use of high fructose corn syrup (HFCS), and the obesity epidemic. The addition of sweeteners such as fructose and sucrose by food industries has increased to a large extent in the last few decades. For example, regular soft drinks (SD) and fruit drinks, major sources of fructose or sugar, have increased from 3.9% of the total energy intake in 1977 to 9.2% of the total energy intake in 2001. The terminology varies across different countries. Most commonly used names are: carbonated beverages, fizzy drink, fizzy juice, cool drink, cold drink, lolly water, pop, seltzer, soda, soda pop, tonic and mineral water. In most of the populations worldwide, two types of soft drinks are used: regular SD which is sweetened with sugar (fructose) and another type, Diet SD, which is sweetened with non caloric sweeteners (aspartame).
Up to 1980s, SD contained most of their food energy in the form of refined cane sugar or corn syrup. Nowadays, high fructose corn syrup (HFCS) is used almost exclusively as a sweetener throughout the world because of its lower cost. These added sweeteners constitute about 16% of all calorie intakes. HFCS made by the enzymatic isomerisation of glucose to fructose was introduced as HFCS-42 (42% fructose) and HFCS-55 (55% fructose) was introduced in 1967 and 1977 respectively, and opened a new frontier for the sweetener and SD industries.
The fructose component of sugar sweeteners is considered as a harmful macronutrient. Evidence suggests that increased consumption of fructose, a more lipogenic sugar, has been suggested to lead to obesity, hyperlipidemia, NAFLD, visceral adiposity, Insulin resistance and cardiovascular disease. Individuals consuming >1SD per day had a higher prevalence of metabolic syndrome than those consuming <1SD per day.
The first line of treatment for NAFLD and other associated problems is behavioural change that involves weight loss through a combination of healthy diet and physical activity (exercise). It is noteworthy that at present there is no FDA-approved for NAFLD in the market. The option that is available to medical practitioners in addition to lifestyle change is:
Vitamin E: This is a drug of choice for most clinicians and might be helpful for people with liver damaged by NAFLD. However, there is a strong caution. Vitamin E has been linked to increased incidence of prostate cancer in men. A clinical trial is underway regarding Vitamin E and its dosage for NAFLD patients at National Institute of Health, USA. The data may provide us with something that clinicians can make best use of.
Sugar has built empires and industries, but it now threatens global health. Fructose consumption increases the risk of developing metabolic syndrome. So, reducing fructose intake is crucial. Of course, behavioural changes could also help. For example, the American Academy of Paediatrics provides clear guidelines to limit juice and sweetened beverage intake in children and advocates limiting sales of sugar-sweetened beverages (SSB) in schools. Recently Mexico enacted a 1 peso/liter excise tax of Sugar Sweetened Beverages (SSB) in 2013, and recent data have shown that this move has decreased purchases of SSB. Further research into the role of dietary fructose in the development of metabolic diseases will be necessary to better inform clinical investigators and policy-makers.
Need for population based (epidemiological) study and making policy for reducing the consumption of sweetened beverages might help. In this connection, gastroenterologists need to play a leading role. This will help us understand the disease in a better way in our society. An informed, coordinated, and comprehensive approach will provide the much-needed path out of this epidemic and back to a healthy society. Once we understand the problem, together we will find a solution.
Take home message
Non-alcoholic fatty liver disease and other associated problems is emerging at greater rate than expected. To avoid metabolic disease such as diabetes and fatty liver, take precautionary measures. Avoid sedentary lifestyle and increase physical activity. Reduce your Fructose (Sugar intake). Look for the symptoms and consult a clinician.
The writer is Assistant Professor & Graduate Programme Councillor at Department of Biochemistry, HED, J&K. He has worked on understanding the basic mechanism of lipotoxicity in NAFLD and NASH at CSIR-IIIM Jammu, Group on Molecular and Cell Biology of Lipids at University of Alberta, Canada, and is currently engaged in understanding the molecular basis of disease pathogenesis.