Study highlights the urgent need to evaluate deficiencies in the energy balance model for the prevention and treatment of obesity

In a recent study published in the European Journal of Clinical Nutrition, researchers highlighted the urgent need to substitute highly processed carbohydrates with minimally processed carbohydrates or healthy fats to cease the obesity pandemic that relentlessly continues.

Background

There are two possible explanations for the failure of public health campaigns focused on decreasing energy intake (eating less) and increasing energy expenditure (moving more) or the energy balance model (EBM). The first explanation is that the public has not adequately adopted the EBM approach. Another possibility is that the EBM is erroneous itself.

The EBM primarily attributes rising obesity to the availability of inexpensive, ultra-processed foods with high fat and sugar content. The alternative carbohydrate-insulin model (CIM) proposes that processed carbohydrates shift energy partitioning toward deposition in adipose tissue or adiposity, which causes higher calorie intake to compensate for the impounded calories. Nevertheless, both models target highly processed carbohydrates as drivers of obesity, albeit for different reasons.

The study

In the present study, researchers described how the EBM and CIM view the pathophysiology governing obesity and highlighted EBM deficiencies that impede the design of new models to guide the prevention and treatment of obesity. They compared features of both models, competing for almost a century, assessed evidence supporting each, and specified improvements in the EBM formulation.

In particular, the researchers highlighted main disagreements with the new EBM proposed by Hall et al., which explicitly states that diet ultimately drives fat deposition by increasing total energy intake, disregarding the role of calorie-independent effects on substrate partitioning.

EBM vs. CIM

Though rodents and humans do not eat similar diets, Hall et al. showed that a diet comprising 70% carbohydrate and 10% fat protected rodents from obesity, and 20% carbohydrate and 60% fat resulted in the highest weight gain. Another study also concluded that increased dietary fat was associated with higher variations in body weight. However, Tordoff and Ellis observed that rodent diets consuming equal amounts of fat and carbohydrates were the most obesogenic. Kennedy et al. established that an ultra-low-carbohydrate diet (with low protein) induced a unique metabolic state concordant with weight loss in mice.

Hall et al. also dismissed studies of insulin action as non-discriminating, although downplaying its significance risks creating an EBM so general as to be untestable. While in the CIM, more insulin secretion stimulates fat storage via direct peripheral mechanisms, the EBM seems to predict the opposite, given the insulin-induced anorectic actions in the brain.

Furthermore, Hall et al. stated that nervous systems have evolved to control energy intake. However, as per Claude Bernard, the brain controls practically all aspects of metabolism, including glucose metabolism.

In some models, disproportionate adiposity instinctively develops without augmented food intake or body weight. It is odd as genetic studies have attributed the prevalence of more obesity-related polymorphisms in the brain than adipocytes in support of the EBM.

As per Hall et al., evidence suggesting that carbohydrate intake explicates differences in body weight are non-existent between the two countries. On the contrary, countries with high carbohydrate intake tend to be poor, with a substantial undernourished population. Also, in the United States (US), BMI increased swiftly from 1970 to 2000, parallelly with increased consumption of refined grains and sugar.

Further, Hall et al. concluded that, in agreement with the EBM, the epidemiological data suggested several potential dietary drivers of excess calorie intake. However, Mozaffarian raised new questions about this conceptualization. He provided quantitative evidence that despite adhering to EBM recommendations for many decades, Americans have eaten less on a population basis. Subsequently, energy intake plateaued or declined since 2000 in the US, but obesity rates continue to increase. BMI deduced trends might be underestimating the extent to which the obesity epidemic has progressed since 2000. Therefore, these trends need careful consideration of alternative underlying explanations, including those involving metabolic dysfunction.

Per the 1992 Consensus Development Conference on Methods for Voluntary Weight Loss and Control organized by the National Institutes of Health (NIH), participants who remained in weight loss programs usually lost ~10% of their weight. They regained all the weight within five years. Therefore, obesity treatment should reduce the insulin-to-glucagon ratio, not just calorie restriction.

The physician’s job, it seemed, was simply to explain that semistarvation reduces fat stores, to prescribe a diet for this purpose, and to sit by. If the patient lost weight as predicted, this merely confirmed the comfortable feeling that treatment of obesity was really a pretty simple matter. However, if, as so often happened, the patient failed to lose weight, he was dismissed as uncooperative or chastized as gluttonous. It was the rare physician who entertained the possibility that failure to follow a regimen might in itself be a medical problem.”

– Albert Stunkard and Mavis McLaren-Hume

Conclusion

The current review demonstrated that the EBM failed to meet the specifications of a good scientific model that could effectively guide the design of informative research, elucidate causal mechanisms of obesity, or suggest apt approaches for its prevention or treatment. Yet, it dominated for nearly a century and never let other views come to notice until highlighted by expanded formulations of the CIM by Ludwig et al. and EBM by Hall et al. in The American Journal of Clinical Nutrition.

The future scientific model should specify testable causal pathways of obesity, elucidate how metabolic responses defend the increased population-level BMI and demonstrate ways to integrate calorie-independent effects of diet.

New models should be studied, not suppressed, to curtail the rising toll of obesity-related diseases.

To conclude, unbiased studies should rigorously test all the acceptable versions of competing models and ensure that the clash between competing paradigms remains constructive and conducive to recognizing evidence that obesity pathogenesis in humans may involve elements of all competing models.

Written by

Neha Mathur

Neha is a digital marketing professional based in Gurugram, India. She has a Master’s degree from the University of Rajasthan with a specialization in Biotechnology in 2008. She has experience in pre-clinical research as part of her research project in The Department of Toxicology at the prestigious Central Drug Research Institute (CDRI), Lucknow, India. She also holds a certification in C++ programming.