Lowering sodium intake has been a constant in dietary guidelines for decades and is widely recommended as part of healthy eating advice. The conventional view is that eating too much sodium increases blood pressure and thereby increases the risk for cardiovascular disease. Yet the benefits of sodium reduction are being hotly debated with experts around the globe trading arguments in journals, on-line debates and the mainstream media. What’s driving this debate?
In November 2011, O’Donnell and colleagues published a study on the relationship between urinary sodium and the risk for cardiovascular disease. Urinary sodium is a good way to estimate how much sodium people are eating as, generally speaking, ‘sodium in equals sodium out’. As higher sodium intake is known to be linked with higher blood pressure, the expectation might have been that the higher the sodium excretion, the higher the risk for cardiovascular disease. However, the relationship turned out to be J-shaped. In other words, high intakes of sodium were indeed associated with higher risk for cardiovascular disease, but so were low intakes of sodium. How can that be? Does eating too little sodium cause harm?
High fat, calorie-rich foods have long been thought to be fattening and policymakers continue to recommend their restriction in order to prevent obesity. However, scientific support for this advice has fallen away. The latest research suggests that identifying foods that promote future weight gain is much more challenging than previously thought, with carbohydrate quality playing a central role.
Traditional dietary advice for preventing obesity has revolved around eating less calorie-rich food. In the 1980s and 1990s the best way of achieving this was thought to be by limiting total fat intake and this became the core strategy for the prevention of obesity. It made good sense as gram-for-gram fat contains more calories that protein or carbohydrate – lower fat foods are lower calorie foods. By the turn of the century, dietary advice for obesity prevention evolved to limiting intake of ‘energy dense’ (calorie dense) foods. This was a small change in emphasis as the key drivers of energy density are fat and water content.
Lowering the fat content or energy density of the diet as a means of preventing obesity makes so much sense to nutritionists and dietitians that it is seldom challenged but the unfortunate reality is that these recommendations can no longer be supported scientifically.
The current ‘debate’ about sugar and health descended into farce last Sunday night with the broadcast of a 60 Minutes program in which it was suggested that sugar ‘is as addictive as the hardest drugs’.
The argument behind this claim rests on the supposedly similar responses in the brain to sugar and cocaine. The brain contains a reward centre that is designed encourage survival behaviours, such as eating and sex. If these things were not pleasurable humans would not eat or reproduce and the species would disappear. Foods, sugar, fat and especially the combination of sugar and fat trigger this reward centre, and so does cocaine. So, with a huge leap of faith and imagination, sugar equals cocaine.
An American neuropsychologist on the program claimed that … sugar kills way more people than any psychoactive drug – an absurd claim that simply cannot be supported scientifically. I have never seen any credible scientific study that attempted to associate sugar intake with increased risk of death. Scientists have gone to great lengths to investigate the role of dietary factors in preventable disease but sugar intake simply does not feature in their calculations. In susceptible people, the risk for tooth decay may increase with the consumption of carbohydrates i.e. added sugars, natural sugars in fruits and even breast milk, and starch. But that’s it – that’s the health risk posed by sugar. Eating sugar does not kill people.