Perhaps the greatest misconception I’ve encountered over my times spent in the gym – and believe me, there are many – is that you can’t eat carbs past a certain time because they’ll get stored as body fat due to insulin being released. The funny part is that most of these guys, despite believing this dogma, try to induce the biggest insulin spike possible post-workout to drive carbs into the muscle (as glycogen). Along a similar vein, I want to look at this question of carbohydrate and fat storage and try to answer the question of carbs being stored as fat in adipose tissue. I think the low-carb craze (Atkins for example, there are many others), along with perceptions of low-carb diets being popularized by dieting bodybuilders who are known for ridiculous low levels of body fat, have contributed significantly to this mindset, and it needs to be unraveled. And don’t get me wrong, low-carb diets have their time and place. However, the misconception that carbs get stored as body fat and are the reason you should do low-carb is a completely misguided assumption.
First off, can dietary carbohydrate even be stored as body fat? The quick and easy answer is yes, they absolutely can. However, the more pertinent question is, do they get stored as body fat, and to what extent? The fact of the matter is that although we have the ability to store dietary carbohydrate as body fat, our body’s capacity for doing so is very limited . This process is called de novo lipogenesis (DNL), and luckily for us it doesn’t contribute greatly to our fat stores.
So what’s the alternative? Well, our body has a wonderful storage form of carbohydrate called glycogen. Once we ingest a meal containing carbohydrate our levels of blood glucose increase causing the beta-cells of the pancreas to sense this increase and release insulin (a storage hormone) to clear the bloodstream of glucose (gym-rats you were right about one thing). In doing so a majority of the glucose is shuttled off to muscle tissue where it is converted to glycogen and stored for future use while some goes directly into glycolysis for immediate use. Any active tissue that can use glucose most likely will (save the heart which runs on a mixture of fatty acids, glucose and ketone bodies to some extent) while shutting down the body’s ability to make its own glucose (gluconeogenesis). The remaining glucose (if any depending on the meal size) is stored as glycogen in the liver. I should note that some of the glucose is also delivered to the brain where it is oxidized completely to CO2 (~120g/day for a normal, well fed person).
It is right about at this point where it gets a little tricky. If glycogen stores are full and the body is oxidizing carbohydrate as best it can (which actually increases as consumption increases), then yes, some carbohydrate will go to glycerol-3-phospate (G3P) and synthesized into triglyceride (our body’s storage form of fat) . But, like I pointed out, this is limited and in most cases doesn’t exceed fatty acid oxidation.
As promised, what I’ve said thus far is supported by a number of studies which show that storing triglyceride made from carbohydrate is not the major pathway for carbohydrates in the human body [1, 3], even under conditions of excess calories from carbohydrate given in conjunction with a mixed diet [4-6]. It should be recognized that these studies used indirect calorimetry (a measure of heat production via CO2) which does not measure DNL directly, but rather Net DNL (synthesis – oxidation). Either way, NDNL exceeded lipolysis only after 5 days of overeating (175% daily kcal needs). This is probably not very realistic (or comfortable) for most people to do, unless you’re consciously eating almost twice as much as you need.
Furthermore, short-term studies looking at a single meal excessively high in carbohydrate (500g or about 2,000kcals from carbs alone!) were not shown to significantly contribute to fat gain after 24 hours [7, 8]. In fact, glycogen storage was seen as the primary fate of the excess carbohydrate, with stores increasing up to 1kg (or 2.2lbs for the metrically challenged)! Again, these studies used indirect calorimetry, but the theme remains the same: DNL < oxidation.
Studies using more accurate measure, such as stable isotopes have found limited DNL in subjects consuming very low-fats diets (high carbohydrate), but lipogenesis again did not exceed oxidation and contributed insignificantly to body fat stores [9, 10]. Even using more accurate measures yielded similar results. And because normal “Western Diets” are not typically very low in fat, DNL is probably not very active in most people under normal dietary consumption patterns anyway.
So although DNL in fact does exist as a pathway in the human body, it doesn’t exist to any significant extent that you should label carbohydrates as “bad,” or fat promoting, or worse yet, exclude them past some arbitrary time. The fact of the matter is that any fat gain from DNL is likely to be trivial at best and shouldn’t worry you in the least.
1. Hellerstein, MK., Schwarz, JM., Neese, RA. Regulation of hepatic de novo lipogenesis in humans. Annu Rev Nutr 1996;16:523-557.
2. Labayen I, Forga L, Martinez JA. Nutrient oxidation and metabolic rate as affects by meals containing different proportions of carbohydrate and fat in healthy young women. Eur J Nutr. 1999;38(3):158-66.
3. Hellerstein, MK. De novo lipogenesis in humans: metabolic and regulatory aspects. Eur J Clin Nutr 1999;53(1):S53-65.
4. Minehira K, Vega N, Vidal H, Acheson K, Tappy L. Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tisue of lean and overweight humans. Int J Obes Relat Metab Disord. 2004;28(10):1291-8.
5. Hellerstein, MK. Synthesis of fat in response to alterations in diet: insights from new stable isotope methodologies. Lipids 1996;31:S117-25.
6. Schwarz, JM, Neese, RA., Hellerstein, MK., et al. Short-term alterations in carbohydrate energy intake in humans: striking effects on hepatic glucose production, de novo lipogenesis, lipolysis and whole-body fuel selection. J Clin Invest 1995;96:2735–43.
7. Acheson, KJ., Schutz, Y., Bessard, T., et al. Nutritional influences on lipogenesis and thermogenesis after a carbohydrate meal. Am J Physiol 1982;246:E62–70.
8. Acheson, KJ., Flatt, JP., Jequier E. Glycogen synthesis versus lipogenesis after a 500-g carbohydrate meal. Metabolism 1982;31:1234–40
9. Hudgins LC, Hellerstein M, Neese R, et al. Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet. J Clin Invest 1996;97:2081–91.
10. Hudgins LC, Seidman CE, Diakun J, Hirsch J. Human fatty acid synthesis is reduced after the substitution of dietary starch for sugar. Am J Clin Nutr 1998;67:631–9.