A calorie is a calorie, right? If you eat more than you burn, you gain weight; if you burn more than you eat, you lose weight. It doesn’t matter where your calories are coming from; it’s a simple equation of calories in and calories out. Or is it? Not according to Dr. Lustig, it isn’t.
Dr. Robert Lustig, MD, is one of the leading experts on childhood obesity; he is Director of the Weight Assessment for Teen and Child Health (WATCH) Program at the University of California, San Francisco and has written 85 peer-reviewed articles and 30 reviews. His research has been highly significant in understanding how sugar is metabolised in the body.
His book, Fat Chance: The Hidden Truth About Sugar, Obesity and Disease, brings together the science in this area and unpacks the way in which different calories are processed. You can also view a number of his lectures on youtube, such as this one. Here’s what he has to say.
The obesity crisis
We’re getting bigger. According to the World Health Organisation (WHO), worldwide obesity has more than doubled since 1980. Body mass index (or BMI, an indicator of body fatness that is calculated from a person’s weight to height ratio), recordings show that 39% of adults (1.9 billion people) are overweight and 13% are obese (600 million people)1 and it’s on the rise.
So what has happened in the last 30 years?
We are eating more calories, on average 530 calories per person each day 2. We’re eating more, but we’re not eating more of everything. We’re eating more of some things and less of others.
The changes in the breakdown of where our calories are coming from, Lustig explains, point us to one of the crucial points in understanding obesity. According to the U.S. Department of agriculture: there has been decrease in dietary fat (from 40 to 30%) and protein intake has remained the same (15%). However, our intake of carbohydrates has increased from 40-55%3 with fructose, as apposed to starches, showing the biggest rise. In actual fact, our consumption of fructose has doubled in the past 30 years and has increased six fold in the last century4.
What is fructose exactly? Fructose is the carbohydrate that is found in table sugar and High-Fructose Corn Syrup (used widely in the United States and increasingly in Europe) both of which are approximately 50% glucose and 50% fructose.
Don’t we already know this?
So, it’s in the sugar. Everyone already knows that we should be eating less of it. In fact we should be eating less in general and exercising more, we know that. But if we already know this, why aren’t we?
Why can’t we do it?
This is where we need to understand a bit about what the body does to maintain energy balance. This is a highly complex process controlled by the hypothalamus, a small area at the base of the brain. It works in conjunction with the pituitary gland to control energy storage versus energy expenditure. The hypothalamus receives meal-to-meal information from the GI (gastrointestinal) tract on both hunger and satiety. It also receives long-term information on fat stores and nutrient metabolism. This information is conveyed by the hormones leptin and insulin to the hypothalamus where it either stimulates or suppresses appetite, and adjusts energy expenditure accordingly.
Insulin primarily acts as an energy storage hormone. When we eat, after food has been broken down by the stomach and then small intestine, amino acids and simple sugars (glucose) travel to the liver. The liver is the first to process each of these classes of nutrient. The glucose that isn’t taken up by the liver, appears in the general circulation, causing a release of insulin.
Insulin rises in accordance with the volume of glucose consumed, ultimately allowing muscle cells to store glucose in the form of the polysaccharide glycogen. Consuming excess levels of glucose can lead to the glucose being stored in adipocytes or fat cells, which is at the root of our current obesity crisis.
The hormone leptin was discovered in 1994 and was initially believed to be the answer to the obesity crisis. Leptin is a protein made and released by fat cells, which circulate in your blood stream and signal to the hypothalamus that you’ve got enough energy stored in your fat5. It was originally thought, that those who were overweight were simply not producing enough leptin. Clinical trials involving administration of leptin were however, unsuccessful in reducing weight6 and we have come to the realisation that what we are actually suffering from is not Leptin deficiency but leptin resistance.
Leptin resistance, is the key to the obesity epidemic and with a few rare exceptions, the 1.9 billion overweight or obese people on the planet are suffering from this. These people have plenty of leptin, the problem is that their hypothalami can’t see their leptin, so their brains think they’re starving and will therefore try to increase energy storage and conserve energy usage.
Recent experiments suggest insulin acts as a leptin antagonist7. Many scientists have shown that insulin actions in the hypothalamus block leptin signalling8,9. When insulin levels at the hypothalamus are chronically high (hyperinsulinemia), leptin cannot signal the hypothalamus.
The root cause
So what causes insulin levels to be so high? You guessed it, it’s the fructose. Lustig argues that the changes in our dietary habits over the last few decades, in particular our increased consumption of processed food, which (amongst other pitfalls) is characteristically high in sugar, has a cascading effect. Sugar is far more than empty calories, it is throwing off the whole body’s appetite-control system; for this reason, a calorie is not a calorie. Processed food, with fructose in particular, is driving the obesity epidemic10.
If you want to know just how different the metabolism of fructose is, as apposed to glucose, check out the next post which looks further into Lustig’s key message that a calorie is not in fact a calorie.
- World Health Organisation, Fact Sheet: Obesity and Overweight (2016)
- Profiling Food Consumption in America: United States Department of Agriculture Factbook
- P. Chanmugam et al., “Did Fat Intake in the United States Really Decline Between 1989-1991 and 1994-1996? J. Am. Diet Assoc. 103 (2003): 867-72
- R. H. Lustig, Fat Chance: The Hidden Truth About Sugar, Obesity and Disease p.21
- J.S. Flier, “What’s in a Name? In Search of Leptin’s Physiologic Role,” J. Clin. Endocr. Metab. 83 (1998): 1407-13
- S.B. Heymsfield et al., “Recombinant Leptin for Weight Loss in Obese and Lean Adults: A Randomized, Controlled, Dose-Escalation Trial,” JAMA 282 (1999): 1568-75
- R. H. Lustig et al., “Childhood Obesity: Behavioral Aberration or Biochemical Drive? Reinterpreting the First Law of Thermodynamics,” Nature Clin. Pract. Endo. Metab. 2 (2006): 447-58
- M. Kellerer et al., “Insulin Inhibits Leptin Receptor Signalling in HEK293 Cells at the Level of Janus KInase-2: a Potential Mechanism for Hyperinsulinaemia Associated Leptin Resistance, in Mice,” J. Clin. Invest.118 (2008) 1796-805
- T. Klockener et al, “High-fat Feeding Promotes Obesity via Insulin Receptor/PI3K-Dependent Inhibition of SF-1 VMH Neurons,” Nat. Neurosci. 14 (2001): 911-18
- R. H. Lustig, E. Isganaitis, “Fast Food, Central Nervous System Insulin Resistance, and Obesity” Arteriosclerosis, Thrombosis, and Vascular Biology: 25: 2451-2462