Another hormone Lipoprotein lipase (LPL) is moderated by insulin levels. Increases in insulin (due to carbohydrate consumption) increase LPL and elevated levels of this hormone are seen in line with elevated blood triglycerides. This is because LPL’s role is to break down triglycerides in the chylomicrons releasing free fatty acids which are then available for energy metabolism or indeed to be restored by the body as fat. If it was all about high insulin equals no fat burning and low insulin levels equalling fat burning it would be a simplification.
This highlights that even during carbohydrate consumption and elevated insulin we will still metabolize fat- a good reason not to exclude carbohydrate from consumption as standard in the long term as a lot of “dietrary extremists” suggest.
There has been tentative research in to the importance of Acylation Stimulating Protein (ASP) which plays a role in the breakdown of triglycerides as well as the transport of glucose. This enzyme which is stimulated by insulin is also stimulated by high numbers of chylomicrons in the blood stream indicating again that high insulin is not the sole mechanism for fat storage.
So what does the science behind fat burning tell us? Well there are a range of factors that influence the rate of fat breakdown and storage.
It is clear to see that focussing upon one part of this process would be ineffective as a mechanism for fat loss. This also highlights why if you over eat on carbohydrate or indeed fat you will convert excess fuel to be stored as fat regardless of food combinations, timings or amounts.
Taking one supplement may help one part of this process but it may also limit another process in the body over a period of time.
Current obesity research highlights this point in that eating excessive calories from one food source or indeed all the major macronutrients may not be the sole cause of obesity and fat gain:
“…Obesity can arise in the absence of calorie over consumption. In addition, opposite models can show how obesity can be prevented by increasing expenditure to waste energy and stabilize body weight when challenged by hyperphagia (over consumption).”
(Rampone, AJ, Reynolds, PJ. Life Sci. 1988; 43(2):93-110).
“The regulatory systems (of the body) control both energy input and output so that for a given steady state, compensatory changes on the input side are made if expenditure is challenged, or on the output side (expenditure or efficiency) if intake is challenged…Realizing human obesity is caused by the interaction of an obesigenic environment with a large number of susceptibility genes, successful treatment will require uncoupling of these compensatory mechanisms”
(Jequier et al 2002).
“The critical issue in addressing the problem of alterations in body weight
regulation is not intake or expenditure taken separately, but the adjustment of one to the other under ad libitum food intake conditions”
(Buchholz et al 2004).
In the end, as these papers suggest, understanding the relationship between “energy in” and “energy out” requires a more complex energy balance model than currently espoused by the media and health authorities, again this is an example of where there has been an oversimplification (and where a calorie may not necessarily be a calorie) of the science behind not weight loss but fat loss.