Updated: Sep 17
An important study from 1984 is often cited as evidence that the fat components of meals is the most important cause of obesity. This was the politically correct theory at the time" but reinterpretation of the data can lead to the exact opposite conclusion and certainly questions the wisdom of "all things in moderation"
The study produced wonderful data that show how "moderate amounts" of high glycemic carbohydrate in a mixed meal dominated metabolism through massive insulin secretion.
Effects of Dietary Fat on Postprandial Substrate Oxidation and on Carbohydrate and Fat Balances. J. P. Flatt, Eric Ravussin, Kevin J. Acheson, and Eric Jequier. J. Clin. Invest. t© The American Society for Clinical Investigation, Inc. , 1985, Vols. Volume 76, September 1985, 1019-1024
The study involved giving 7 healthy young men 3 test meals and subsequently following glucose, insulin, free fatty acids, and substrate oxidation for 9 hours after the meals. All meals had 75gm carbohydrate but two had an additional 40gm of fat. They were one of three different breakfasts of white bread, jam and margarine but meals 2 and 3 had an extra 360 kcal of 2 different types of fat:
1. 482 kcal: 27% protein, 62% carbohydrate, and 11% fat
2. 858 kcal: 15% protein, 35% carbohydrate, and 50% fat as long-chain triglycerides
3. 858 kcal: 15% protein, 35% carbohydrate, and 50% fat as medium chain triglycerides
In these healthy young men plasma glucose and insulin concentrations rapidly increased to peak at 95% & 1000% above baseline values respectively 45 min after the start of the meals.
When compared with the low fat meal, the addition of fat in the other 2 meals had no effect on circulating glucose and insulin concentrations or respiratory quotient. Nine hours after the breakfasts, the amounts of substrates oxidized were similar resulting in positive fat balance when the additional 376 kcal fat was consumed. The results demonstrated that the rates of fat and carbohydrate oxidation are not influenced by the fat content but totally dominated by the carbohydrate content of a meal. If the authors had run another test meal with just fat and no carbohydrate they would have seen no increase in glucose or insulin and continued unchanged oxidation of fat (as seen in the fat tolerance tests in the last two figures below)
The authors conclusions below in italics reflects the political correctness of the times: which was demonization of fat and justification of the official advice to reduce fat intake.
The results of the present experiments are relevant to the problem of weight maintenance. It seems reasonable that conscious efforts to avoid excessive food intake should be expected to be most needed, and most worthwhile, when directed at that sector of metabolism where metabolic regulation is least effective in assuring the maintenance of substrate balance. Our investigations show that this is the case for fat, which suggests that deliberate efforts to facilitate weight control may be most likely to be effective in the long run when they serve to limit fat intake. This provides a metabolic rationale in support of current recommendations to counter the trend toward obesity by reducing the diet's fat content, and, thereby, the caloric density of the foods consumed.
However, we have subsequently learned increasing insulin levels 1000% by consuming a modest 75g of high glycemic carb three times every day (as recommended in official government guidelines and accepted as perfectly normal for decades) has dire consequences for weight gain, diabetes, inflammation, and the risk of age related diseases.
The study data highlights the often neglected influence of insulin on blood (FFA) free fatty acid levels which dropped to 1/3 of fasting levels by 2 hours and took up to 9 hours to recover to fasting levels. The brain hunger centers sense available energy levels in the circulation and respond to either low blood glucose or low fatty acid levels. In this study glucose levels returned to normal in 2 hours but fatty acid levels remained low for a further 2-3 hours after the high glycemic meal and hunger sensors in the brain perceive an energy deficit to trigger hunger despite being in positive fat balance.
Respiratory quotient is the ratio of CO2 to O2 in expired breath and indicates either use of fat (RQ 0.7) or carbohydrate (RQ 1.0) for energy. As indicated in the graph suppression of FFA levels by insulin is reflected in decreased fat oxidation as inverse RQ closely follows FFA.
The authors point out the free glucose pool present in extracellular fluids (ECF) of the body is just 10 grams so it is not surprising that 75 gm of rapidly absorbed carbohydrate swamps the free glucose pool and prompts the emergency switch to glucose storage in the form of glycogen and fat in muscle and adipose tissue to avoid what would otherwise be toxic levels of blood glucose.
Put this further in perspective the average American consumes 500 grams a day of high glycemic carbohydrates; maybe 170 g three times a day and a permanent positive fat balance in the face of low circulating energy levels to virtually guarantee progressive weight gain.
We also have vast amounts of data on glucose and insulin levels from glycemic index testing of foods and glucose tolerance tests for suspected diabetes where 100gm of available carbohydrate is used in test meals in the figures below . Note the difference in glucose and insulin levels between glucose tolerance (squares) and fat tolerance tests (circles).
In the light of government recommendations that we must consume more than 50% of our calories as carbohydrate and virtually the only carbohydrates available in supermarkets and convenience stores are sugar and starches from flour, potatoes, corn and rice: little wonder that 2/3 of the population are overweight and the rest may be struggling with hunger inducing diets just to keep their weight within normal levels.