Since the 1970s the availability and consumption of high fructose corn syrup (HFCS) increased considerably, while sucrose – from sugar cane and beets – decreased by about the same amount. Overall, however, the caloric intake of sugars from all added sources decreased subtly, as did the consumption of fruits and vegetables, which are additional natural sources of sugars.
It should be noted that HFCS is distinct from corn syrup in that the latter contains only glucose. However, corn syrup can be enzymatically turned into HFCS, in a process that transforms some of the glucose molecules found in corn syrup to fructose.
HFCS contains 55 percent fructose and 42 percent glucose in soft drinks and 43 percent fructose and 55 percent glucose in baked goods and processed foods; sucrose, on the other hand, contains an equal amount of each. Also, due to the way that it's processed, fructose and glucose are found in "free" form in HFSC, whereas in sucrose, each molecule of glucose is joined to a molecule of fructose by α-1,4 glycoside bonds.
However, an intestinal enzyme readily degrades the glycosidic bonds between glucose and fructose, such that the absorption kinetics between sucrose and HFCS are effectively the same. What's more, soft drinks usually sit on shelves, exposed to heat and acids, and over time, under these conditions, many of the α-1,4 glycoside bonds are broken down. So most of the sugars in sucrose-sweetened soft drinks are "free" glucose and fructose molecules – just like in HFCS-sweetened products.
However, an intestinal enzyme readily degrades the glycosidic bonds between glucose and fructose, such that the absorption kinetics between sucrose and HFCS are effectively the same. What's more, soft drinks usually sit on shelves, exposed to heat and acids, and over time, under these conditions, many of the α-1,4 glycoside bonds are broken down. So most of the sugars in sucrose-sweetened soft drinks are "free" glucose and fructose molecules – just like in HFCS-sweetened products.
Bray was mentioned briefly in the previous post for putting blame on HFCS for the obesity epidemic. Bray’s hypothesis was grounded on observational data, like Yudkin’s decades before (Bray, Nielsen, & Popkin, 2004). Between 1960 and 2000, the use of HFCS correlated positively with rising obesity rates, but circa 2002, HFCS consumption has been on the decline. And generally, HFCS consumption doesn't correspond to obesity rates in other countries, like
In a previous post, a study in which subjects were given sucrose, as 25 percent of total calories, without any adverse effects, was referenced. These results can be carried over to HFCS as well because the metabolic effects of sucrose and HFCS are, in effect, identical–even at very high doses (e.g., Melanson et al., 2007, 2008). Pure fructose given at very high doses will, in fact, produce metabolic derangements, but as I keep laboring the point of, fructose is not a good model for HFCS, so this line of experimentation, for the most part, should be ignored.
Fructose has a lower glycemic index (GI) than glucose, and this has led people to suggest that fructose is more "satiating" than glucose (Brand-Miller, Holt, Pawlak, & McMillan, 2002). The premise here is faulty, as there is little evidence to assume that the GI of carbohydrates contributes significantly to satiety or weight regulation (e.g., Sloth et al., 2004).
One study compared the satiety producing effects of 12 ounces of a sucrose-sweetened soft drink, an artificially-sweetened soft drink, or mineral water in healthy subjects. After drinking each of these liquids, all three groups ended up eating the same amount of food. What was confusing, however, was that the researchers attributed this outcome to the volume of liquid ingested (Holt, Sandona, & Brand-Miller, 2000). This is probably mistaken, as is the reflex to assign blame to the ability of liquid calories to somehow circumvent the body's satiety mechanisms. I doubt these interpretations and instead, tend to think that the status of energy stores provides the predominance of the stimuli for satiety and eating behavior (For instance, when glycogen stores are replete, satiety centers in the hypothalamus become active, and the desire for food falls away [Kendall, Levitsky, Strupp, & Lissner, 1991; Lissner, Levitsky, Strupp, Kalkwarf, & Roe, 1987].)
Sugar is an intense metabolic stimulant as well – due to its fructose moiety – so hunger after drinking a can of soda is unsurprising. For what it’s worth, the water and diet soda didn’t curb eating in this study, laying waste to the theory that water and diet soda somehow “trick” the brain into eliciting a state of "fullness."
Finally, herein, the mechanistic reasons as to why sugar can’t be the cause of obesity will be put forth herein (Please bear with me.)
Ingested carbohydrates have 3 main metabolic fates through which they are "disposed":
(1) Oxidation for energy
(2) Storage as glycogen
(3) Conversion to fats via de novo lipogenesis (DNL), and subsequent storage as triglycerides
(1) Oxidation for energy
(2) Storage as glycogen
(3) Conversion to fats via de novo lipogenesis (DNL), and subsequent storage as triglycerides
In everyday life, numbers 1 and 2 predominate, whereas 3 occurs mainly under experimental settings, where subjects are fed massive amounts of carbohydrate . . . because otherwise, satiety would set in. For example, measurements of palmitate – a major product of DNL in VLDL particles – showed that, in humans, DNL accounts for only about 0.5 percent and 2 percent of the palmitate in VLDL particles in the fasting and fed states, respectively (Hellerstein et al., 1991).
Furthermore, glycogen stores can be greatly expanded to accommodate extra carbohydrate. Day to day whole body glycogen stores are usually maintained at a constant level – around 250-500 grams – even after eating a big meal. But on consecutive days of massive carbohydrate overfeeding – pushing through satiety – the storage capacity of glycogen increases substantially. When carbohydrate oxidation and storage (as glycogen) become insufficient to "dispose" of additional ingested carbohydrate, DNL kicks in, and eventually becomes significant, to where storage of de novo synthesized fats outpace their oxidation (Acheson et al., 1988).
Normal blood glucose levels are maintained, as a result, at the expense of some body fat storage. Of course most people aren’t gluttonous enough to make and store much body fat through this pathway – from carbohydrates to fat – as eating this much would be, really, in a word, epic.
As compared to glucose, fructose is unique in that it induces thermogenesis after eating and stimulates total carbohydrate oxidation and energy expenditure without insulin's help (Tappy et al., 1986). More CO2 is produced as a result – in fact, more than any other carbohydrate, denoted by its very high respiratory quotient. Insulin resistant (or obese) people present with an unusually low thermogenic response to carbohydrates, and thus produce less CO2. But fructose can normalize thermogenesis, through various mechanisms (Simonson, Tappy, Jequier, Felber, & DeFronzo, 1988), and improve glucose oxidation in the obese or in diabetics to near normal.
Normally on the ingestion of a mixed meal, insulin is secreted in response to rising blood glucose levels, and insulin in turn suppresses fatty acid mobilization and increases the expression of LPL by fat cells. LPL breaks down – like maggots on a carcass – in a chemical reaction that involves water, food triglycerides, which are carried in lipoproteins called chylomicrons, into their component fatty acids. These liberated fatty acids are thereafter, by mechanisms that are less clear, taken up (near completely) by fat cells, where they are subsequently reesterified into triglycerides. So in effect, insulin "clears" lipids out of the blood, creating the optimal conditions for efficient carbohydrate "disposal." Insulin, at the same time, also stimulates the uptake and oxidation of glucose at high rates through various mechanisms. Taken together, these insulin-mediated effects work to maintain normality (within a certain range) of nutrients in the blood so that they don't fall out of range too much.
The Randle cycle, or the inhibition of glucose use by fatty acids, is an immediate, normal, physiological, and readily reversible phenomenon. High fat diets tend to raise blood NEFA levels moderately, but the resultant insulin resistance is not readily reversible due to the accumulation of lipid metabolites inside cells, which, in one way or another, degrade the insulin receptor, producing glucose intolerance and apparent diabetes. A distinction should therefore be drawn between these two phenomena (Experimentally produced insulin resistance falls along the lines of the Randle effect.)
Hypocaloric high fat diets can raise blood NEFA levels, too, but insulin resistance is not necessarily produced because fatty acid oxidation keeps up with fatty acid mobilization and delivery to tissues in this scenario (Kim et al., 2000). It seems therefore that a high fat, low carbohydrate dieter lives on the edge of subsistence.
The Randle cycle, or the inhibition of glucose use by fatty acids, is an immediate, normal, physiological, and readily reversible phenomenon. High fat diets tend to raise blood NEFA levels moderately, but the resultant insulin resistance is not readily reversible due to the accumulation of lipid metabolites inside cells, which, in one way or another, degrade the insulin receptor, producing glucose intolerance and apparent diabetes. A distinction should therefore be drawn between these two phenomena (Experimentally produced insulin resistance falls along the lines of the Randle effect.)
Hypocaloric high fat diets can raise blood NEFA levels, too, but insulin resistance is not necessarily produced because fatty acid oxidation keeps up with fatty acid mobilization and delivery to tissues in this scenario (Kim et al., 2000). It seems therefore that a high fat, low carbohydrate dieter lives on the edge of subsistence.
In summary, the metabolic effects of HFCS and sucrose are effectively a wash, and there is inadequate evidence to conclude whether either one causes obesity or diabetes. The bad rap on sucrose and fructose derive mainly from rat studies, in which large doses of pure fructose are used, and from observational data (that cannot provide causal information). Sucrose can be beneficial, and fructose provides benefits that glucose can’t, in health, disease, youth, or old age.
New York City has taken the initiative, passing the first legislation of its kind, banning the sale of soft drinks larger than 16 ounces in restaurants and certain venues. Although there's been strong opposition, there are plans to create more barriers to obtaining sugar, as if measures like these will stop or eradicate the obesity and diabetes epidemics.
Last year Danny Roddy made special reference to a study wherein researchers analyzed HFSC sweetened beverages for their glucose and fructose contents, by first, the addition of enzymes that hydrolyzed the glycosidic bonds between the sugar molecules. Measurements made after hydrolysis revealed about 400 to 500 percent more calories than what was listed on the soft drink labels, pointing to the presence of undigested cornstarch molecules – from which corn syrup and HFCS are predominantly derived. Inasmuch as this is true, the talk about implementing laws to curb the consumption of soft drinks has some validity, as people who drink HFCS sweetened beverages are getting significantly more calories than they fancy (about 600 to 750 calories more per 12 ounce can).
Still I don’t know . . . not only is this ban misguided, but other issues are raised by it as well. To place limitations on a food, however unhealthy, seems extreme, and not in accordance with what this country is about – freedom of choice. Though, we will have ample time to judge.
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
Brand-Miller, J. C., Holt, S. H. A., Pawlak, D. B., & McMillan, J. (2002). Glycemic index and obesity. The American journal of clinical nutrition, 76(1), 281S–5S. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12081852
Bray, G. A., Nielsen, S. J., & Popkin, B. M. (2004). Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. The American journal of clinical nutrition, 79(4), 537–43. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15051594
Hellerstein, M. K., Christiansen, M., Kaempfer, S., Kletke, C., Wu, K., Reid, J. S., Mulligan, K., et al. (1991). Measurement of de novo hepatic lipogenesis in humans using stable isotopes. The Journal of clinical investigation, 87(5), 1841–52. doi:10.1172/JCI115206
Holt, S. H., Sandona, N., & Brand-Miller, J. C. (2000). The effects of sugar-free vs sugar-rich beverages on feelings of fullness and subsequent food intake. International journal of food sciences and nutrition, 51(1), 59–71. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10746106
Kendall, A., Levitsky, D. A., Strupp, B. J., & Lissner, L. (1991). Weight loss on a low-fat diet: consequence of the imprecision of the control of food intake in humans. The American journal of clinical nutrition, 53(5), 1124–9. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2021123
Kim, J. Y., Nolte, L. A., Hansen, P. A., Han, D. H., Ferguson, K., Thompson, P. A., & Holloszy, J. O. (2000). High-fat diet-induced muscle insulin resistance: relationship to visceral fat mass. American journal of physiology. Regulatory, integrative and comparative physiology, 279(6), R2057–65. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11080069
Lissner, L., Levitsky, D. A., Strupp, B. J., Kalkwarf, H. J., & Roe, D. A. (1987). Dietary fat and the regulation of energy intake in human subjects. The American journal of clinical nutrition, 46(6), 886–92. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3687822
Melanson, K. J., Angelopoulos, T. J., Nguyen, V., Zukley, L., Lowndes, J., & Rippe, J. M. (2008). High-fructose corn syrup, energy intake, and appetite regulation. The American journal of clinical nutrition, 88(6), 1738S–1744S. doi:10.3945/ajcn.2008.25825E
Melanson, K. J., Zukley, L., Lowndes, J., Nguyen, V., Angelopoulos, T. J., & Rippe, J. M. (2007). Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women. Nutrition (Burbank, Los Angeles County, Calif.), 23(2), 103–12. doi:10.1016/j.nut.2006.11.001
Simonson, D. C., Tappy, L., Jequier, E., Felber, J. P., & DeFronzo, R. A. (1988). Normalization of carbohydrate-induced thermogenesis by fructose in insulin-resistant states. The American journal of physiology, 254(2 Pt 1), E201–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3279802
Sloth, B., Krog-Mikkelsen, I., Flint, A., Tetens, I., Björck, I., Vinoy, S., Elmståhl, H., et al. (2004). No difference in body weight decrease between a low-glycemic-index and a high-glycemic-index diet but reduced LDL cholesterol after 10-wk ad libitum intake of the low-glycemic-index diet. The American journal of clinical nutrition, 80(2), 337–47. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/15277154
Tappy, L., Randin, J. P., Felber, J. P., Chiolero, R., Simonson, D. C., Jequier, E., & DeFronzo, R. A. (1986). Comparison of thermogenic effect of fructose and glucose in normal humans. The American journal of physiology, 250(6 Pt 1), E718–24. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/3521319