Consumer books tend to not be factually reliable because the authors of them present data in a selective way to support their overarching message. Because I’m trusting and take what other people write very seriously, I stay clear of consumer books (and I think other should, too, especially those related to diet and weight loss). Nonetheless, as an exercise in learning only, herein, one of the claims made in a book (that I won’t reveal the title of) will be addressed. The claim in question:
"body fat is made almost exclusively from the carbohydrates in your diet….If you consume more than 200g, you will get fatter and fatter.”
To address this claim, first, we’ll look at several controlled over-feeding studies, where subjects are fed more than what's required to maintain their weights, because otherwise, conclusions would be less definitive.
In one such study, 6 subjects first ate 50 percent extra calories as carbohydrate for 5 days, and then – after a 2 week washout period – they ate 50 percent extra calories as fat for 5 days again . De novo synthesized fat from carbohydrate during the first phase of the study was calculated to amount to, on average, less than 10 grams per day (Schwarz, Neese, Turner, Dare, & Hellerstein, 1995).
The subjects in that study were eating just under 700 grams of carbohydrates and about 4,500 calories per day. So this means that most of the newly made fats, via de novo synthesis, were being oxidized or circulating in the blood in lipoproteins as triglycerides, which are essentially sinks for carbohydrates after meals. Unlike blood glucose concentrations, which fluctuate up and down throughout the day, blood triglyceride concentrations progressively increase (Parks, 2002). Anyway, of the 5.07 pounds gained by each subject on average, less than 1 percent came from carbohydrates.
Next, in another study of the same ilk, smokers were recruited and assigned to eat excessively – over 4,000 calories per day – of a mixed diet. In it, the subjects gained, on average, 2.5 grams and 1.1 grams of additional fat from de novo synthesis (calculated via fractional de novo synthesis data) per day during the two phases of the study: the smoking phase (CS phase) and non-smoking phase (non-CS phase), respectively (Neese et al., 1994).
In one such study, 6 subjects first ate 50 percent extra calories as carbohydrate for 5 days, and then – after a 2 week washout period – they ate 50 percent extra calories as fat for 5 days again . De novo synthesized fat from carbohydrate during the first phase of the study was calculated to amount to, on average, less than 10 grams per day (Schwarz, Neese, Turner, Dare, & Hellerstein, 1995).
The subjects in that study were eating just under 700 grams of carbohydrates and about 4,500 calories per day. So this means that most of the newly made fats, via de novo synthesis, were being oxidized or circulating in the blood in lipoproteins as triglycerides, which are essentially sinks for carbohydrates after meals. Unlike blood glucose concentrations, which fluctuate up and down throughout the day, blood triglyceride concentrations progressively increase (Parks, 2002). Anyway, of the 5.07 pounds gained by each subject on average, less than 1 percent came from carbohydrates.
Next, in another study of the same ilk, smokers were recruited and assigned to eat excessively – over 4,000 calories per day – of a mixed diet. In it, the subjects gained, on average, 2.5 grams and 1.1 grams of additional fat from de novo synthesis (calculated via fractional de novo synthesis data) per day during the two phases of the study: the smoking phase (CS phase) and non-smoking phase (non-CS phase), respectively (Neese et al., 1994).
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| (Neese et al., 1994) |
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| (Horton et al., 2005) |
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First, as mentioned in the study by Horton et al., the oxidation rate of carbohydrate is intensified, but also, the glycogen storage capacity expands greatly, so that additional carbohydrate can be accommodated (Acheson et al., 1988).
Second, when the above routes become saturated, so to speak, de novo synthesis kicks in, where carbohydrates are converted to fatty acids, namely palmitate, and then, palmitoleate, because de novo synthesis and desaturase enzymes are regulated in parallel (Chong et al., 2008). Thereafter, these newly made fats, via a futile cycle, are subsequently oxidized, so that body fat remains, more or less, unchanged.
Third, thermogenic mechanisms become activated when rates of glucose oxidation in the cell reaches a threshold level, and also in response to insulin itself. Fructose in this regard is more effective than glucose.
And fourth, the conversion of thyroid hormone to its active form, T3, becomes more efficient during these periods of excess carbohydrate intake, and as a result, cells throughout the body see a higher exposure to T3, whereby enzymes that regulate basal thermogenesis and oxidative energy production become expressed in higher amounts.
What then is the fate of the carbohydrates eaten in excess?
First, as mentioned in the study by Horton et al., the oxidation rate of carbohydrate is intensified, but also, the glycogen storage capacity expands greatly, so that additional carbohydrate can be accommodated (Acheson et al., 1988).
Second, when the above routes become saturated, so to speak, de novo synthesis kicks in, where carbohydrates are converted to fatty acids, namely palmitate, and then, palmitoleate, because de novo synthesis and desaturase enzymes are regulated in parallel (Chong et al., 2008). Thereafter, these newly made fats, via a futile cycle, are subsequently oxidized, so that body fat remains, more or less, unchanged.
Third, thermogenic mechanisms become activated when rates of glucose oxidation in the cell reaches a threshold level, and also in response to insulin itself. Fructose in this regard is more effective than glucose.
And fourth, the conversion of thyroid hormone to its active form, T3, becomes more efficient during these periods of excess carbohydrate intake, and as a result, cells throughout the body see a higher exposure to T3, whereby enzymes that regulate basal thermogenesis and oxidative energy production become expressed in higher amounts.
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After eating a 1,600 kcal high-fat diet, subjects were placed on a hypercaloric high-carbohydrate diet (86 percent carbohydrate), thyroid output increased and the conversion to T3 did, too (Acheson et al., 1988).
Although body fat from carbohydrate overfeeding does not, at first, come from de novo synthesis per se, over time – on the order of weeks – de novo synthesized fats contribute more and more to stored body fat. And in parallel, the fat oxidation rate progressively decreases and insulin secretion rate progressively increases (in order to clear NEFA and intensify carbohydrate oxidation). But at some point, the storage of de novo synthesized fats surpasses the oxidation of them. In the obese, these processes are more efficient.
Nonetheless, diets that include upwards of 200 grams of carbohydrate per day, contrary to what the author of the quotation declared, do not necessarily lead to weight gain, as long as they are not eaten hypercalorically.
Finally, several mechanisms begin to progressively kick in as more and more carbohydrate is eaten, and culminates in changes in the expression of genes that make the aforementioned processes more efficient. These mechanisms, in effect, dispose of excessive carbohydrate so that blood glucose concentrations don’t fall out of range too much.
References
Acheson, K. J., Schutz, Y., Bessard, T., Anantharaman, K., Flatt, J. P., & Jéquier, E. (1988). Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man. The American journal of clinical nutrition, 48(2), 240–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3165600
Barrows, B. R., & Parks, E. J. (2006). Contributions of different fatty acid sources to very low-density lipoprotein-triacylglycerol in the fasted and fed states. The Journal of clinical endocrinology and metabolism, 91(4), 1446–52. doi:10.1210/jc.2005-1709
Chong, M. F.-F., Hodson, L., Bickerton, A. S., Roberts, R., Neville, M., Karpe, F., Frayn, K. N., et al. (2008). Parallel activation of de novo lipogenesis and stearoyl-CoA desaturase activity after 3 d of high-carbohydrate feeding. The American journal of clinical nutrition, 87(4), 817–23. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/18400702
Horton, T. J., Drougas, H., Brachey, A., Reed, G. W., Peters, J. C., & Hill, J. O. (1995). Fat and carbohydrate overfeeding in humans: different effects on energy storage. The American journal of clinical nutrition, 62(1), 19–29. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/7598063
Neese, R. A., Benowitz, N. L., Hoh, R., Faix, D., LaBua, A., Pun, K., & Hellerstein, M. K. (1994). Metabolic interactions between surplus dietary energy intake and cigarette smoking or its cessation. The American journal of physiology, 267(6 Pt 1), E1023–34. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/7810617
Parks, E. J. (2002). Macronutrient Metabolism Group Symposium on “ Dietary fat : how low should we go ?” Changes in fat synthesis influenced by dietary macronutrient content, (July 2001), 281–286.
Schwarz, J. M., Neese, R. A., Turner, S., Dare, D., & Hellerstein, M. K. (1995). Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection. The Journal of clinical investigation, 96(6), 2735–43. doi:10.1172/JCI118342