Just as the public has started to recognise that it’s an excess of carbs, not an excess of fats, in the diet that are central to our current obesity epidemic, a new US study at the National Institutes of Health (NIH) has sparked more confusion than ever. Unsurprisingly, the media have picked up the news and brandished headlines around the world claiming that low-fat might, after all, be better than low-carb. Not so, we say, and we give you 10 reasons why we think the study is flawed.

Ensuring that the take home message wouldn’t be lost, the authors from NIH as well as two US, one Canadian and a UK university entitled their paper “Calorie for Calorie, Dietary Fat Restriction Results in More Body Fat Loss than Carbohydrate Restriction in People with Obesity”. It’s a big claim in the face of the current interest in low carb, higher fat, keto-adapted lifestyles that are helping tens of thousands to manage their weight and develop levels of fitness they thought were beyond their reach.

But is it right and should you ditch your new metabolically savvy nutritional regimen like it was yesterday’s news?

Here are 10 reasons we don’t think the NIH Clinical Center study is worth the paper it’s written on:

1. Study population is not representative. All 19 subjects were obese, some of these subjects may have single nucleotide polymorphisms (SNPs) which affect metabolism, including ones affecting fat metabolism. In this study the average BMI of the subjects was c.36 and they were confined to a metabolic ward at the NIH Clinical Center for duration of study.
2. Design not reflective of real-world scenarios. Key aspects of study design involved 5 days baseline diet, followed by 6 days on carb or fat restricted diet. After that they had a 2-4 week wash-out period (anything goes!), then a further 5 days baseline phase before the final 6 days on the alternate restricted diet to the one they had the first time round. All the diets were isocaloric, meaning they had the same caloric value. The prime outcome measure was termed “metabolic balance”, which included selective isocaloric reduction of dietary carbohydrate versus fat on body weight, energy expenditure, and fat balance in obese volunteers. An hour treadmill activity per day was included, but the intensity is unspecified by the study authors and it appears not to have been HIIT.
3. Carb or fat restriction periods (6 days) far too short. The carb and fat restriction periods were far too short to allow fundamental changes in metabolic fuelling. Transitioning one’s metabolism, from carb-burning to fat-burning, can take most individuals at least 3 months.
4. Quality of carbs, fats and proteins unknown. No detail is provided on the nature of the carbohydrates (e.g. complex vs simple), fats (e.g. n-6:n-3 ratio, monounsaturated:polyunsaturated:saturated), protein quality, anti-inflammatory phytonutrients, etc.
5. No intermittent fasting or HIIT. There was no attempt to accompany the caloric restriction (including carbohydrate restriction) with intermittent fasting and an activity regimen (e.g. HIIT) that helps trigger the mTOR pathway. Added to this is the fact that eating causes a certain amount of inflammation. The gut mucosal immune system faces more challenges in one day than our entire immune system does in a lifetime, as it must separate friend from foe and deal with the latter if necessary. Eating 6 meals a day, as subjects did in the study, left no time for activation of the mTOR pathway or an inflammation-lowering pause.
6. Too little physical activity. The one hour of treadmill activity per day would generally only be sufficient to burn stored glucose in the form of glycogen and is just not long enough to strongly trigger the beta-oxidation of fats. The latter is usually most pronounced when activity, at moderate levels of intensity, is extended beyond one and a half to two hours, the time it takes most people to deplete their liver and muscle glycogen.
7. Inadequate measures of body composition. There appears to be no plausible explanation for why the authors didn’t measure body composition thoroughly, using a state-of-the-art DEXA measurements or even a commercial, professional body composition analyser such as one of the Tanita scales. This would have helped ascertain just how much of the weight loss was caused by a reduction of water, fat or muscle, or combinations thereof. It’s nutrition 101 and it’s been omitted.
8. Long-term effects of restricted diets ignored. The fat restricted diet included an extremely low level of fat (only 8% of total daily energy intake), which could even be harmful and pro-inflammatory in the long-term. Administering a food composition with a level of fat over a 6-day period when it’s known to be harmful and concluding this might be best in the long-term is scientifically irrational at the very least. The study was far too short to observe the real effects of such fat deprivation, which would include deleterious effects on brain chemistry and body repair, so it’s absurd that such definite conclusions have been drawn as well as having found their way into the title, ready to be picked up by the media.
9. Predictive model unrealistic. While the model simulation predicted that restricted fat diet would lead to 3 kg more fat loss than restricted carbohydrate diet, this is very speculative given that an individual body’s responses are so variable. In the real world, people’s diets are not isocaloric and they contain very significant variations in daily energy expenditure.
10. Wacky theories in the face of known mechanisms. The study’s leader, Kevin D. Hall, makes a peculiar comment about looking for a new hormone, when the energy- and nutrient-sensing protein kinase systems like mTOR and AMPK are very well established as prime regulators of fuel use and storage. The paper doesn’t even pay lip service to these evolutionary pathways, let alone allow the participants to benefit from true “metabolic balance”.

Conclusion: fat is still your friend and most benefit from lowering carb intake

As always, the devil is in the detail. Headlines are often crafted by well meaning journalists, but they often lack the scientific skills to interrogate a paper and determine how relevant it is to people’s lives – or their life-long eating habits.

Scientifically, there are some interesting aspects that emerge from the NIH study. There are also a lot of questions. One of them is why were the diet restriction periods so short? The most interesting finding, we think, is that changes to carb intake or fat intake can change body composition. That reminds us how important food composition is, as opposed to individual food groups or macronutrients. The effects of micronutrients are also key. Many argue this is a detailed study – but there is so much that wasn’t measured.

In our view, looking at the overall weight of evidence, there is nothing to suggest that overall, it’s an excess of carbs, especially sugars and starchy simple carbs, not an excess of fat, that is among the biggest dietary culprits in our present obesity crisis.

But we also need to look closely at the quality as well as the relative amounts of our macronutrients. We can’t ignore micronutrients, whether from our foods or our supplements, as they offer vital signals to the communication networks that control our metabolism. We would be equally foolish to ignore the effects of food frequency – and eating ‘little and often’ is increasingly losing its shine, being replaced with intermittent fasting. How you exercise is as important, but of course, that’s another story.