Terminology
Cardiometabolic risk factors: a cluster of risk factors (e.g., high blood glucose levels) that predict a patient’s risk for developing diabetes and cardiovascular disease.
Cell energy charge: an index of a cell’s energy status, which controls various aspects of metabolism, and is represented, essentially, by the ratio of ATP to AMP in the cell.
Glycosylation: the enzymatic attachment of a sugar to a functional group of a protein, lipid, or other sugars. Glycosylated molecules have a myriad of functional roles in the body.
Maltose: a disaccharide made up of two glucose molecules, joined by an α-1,4 glycosidic bond.
Polysaccharide: very long carbohydrate molecules composed of repeating units of various sugars. Examples include cellulose, starch, and glycogen.
Triose/triose phosphate: intermediate sugars of glycolysis – namely glyceraldehyde-3-phosphate and dihydroxyacetone phosphate; phosphorylated trioses are much more reactive than unphosphorylated trioses.
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I hear and read often “sugar provides empty calories, and so displaces other more nutritious foods.” Especially coming from the paleo people and low carbohydrate dieters, who push for eating more and more dietary fat, I find this amusing.
Sugars (e.g., fructose, glucose, lactose, etc.) contain fewer calories than an equal measure of fats and oils. Saturated fats, though beneficial, aren’t any more nutritious than sugars are – especially considering the fact that, when eaten in excess, sugars can be converted to saturated fats (and monounsaturated fats) – namely palmitate (and palmitoleate) – and this is a highly energy-consuming process.
Furthermore, like fats, sugars are important structural elements of cells and form adducts with proteins, functioning as important signaling molecules. I think that this is important to know because, often, in these capacities, fats are highlighted and sugars are neglected. Sugar, for instance, via glycosylation, stabilizes the potassium channels found in the pancreatic β-cells, allowing for the proper regulation of insulin secretion.
On the matter of weight loss, fructose, as compared to sucrose, is 1.2-fold sweeter than sucrose (it’s glycemic index, however, is 4.5-fold less). So if the people who firmly hold that fructose should be eradicated eventually had their way, and if glucose displaced sucrose (and high fructose corn syrup [HFSC]), then food products would necessarily contain 20 percent more calories to achieve the same level of sweetness. Or even worse, artificial sweeteners – whose safety has yet to be decided on – would be increasingly used.
I also think that sugar is superior to starches – even whole food starches (a.k.a. “safe starches” as the “community” has taken a fancy to calling them).
Unbeknownst to most people, commercially available syrups (e.g., HFCS, corn syrup, and maltose syrup) contain tasteless starch molecules – for the purpose of increasing viscosity – that can go undetected in analyses – giving the impression that foods containing these syrups have fewer calories than they really do (see here).
Because they feed yeast, maltose syrups, which contain a mixture of glucose, maltose, and, predominantly, longer glucose chains, are employed to leaven baked goods.
In the intestines, many of these starch molecules can circumvent digestion, providing fodder for intestinal microbes – including yeast. Herein, I reiterate, is a problem with starches, and an advantage of fruit, as the overgrowth and excessive metabolic activities of intestinal microbes can lead to a myriad of adverse physical symptoms (e.g., bloating and gas) and metabolic derangements – discussed elsewhere on this blog (This is also why I prefer sucrose [table sugar] to HFSC and fruit juice to fruit.)
Incredibly successful diets have, at least to some extent, eradicated starches. To my knowledge, however, no one has made this insight, nor has anyone extensively drawn comparisons between fruit and starches in terms of their distinctive effects in the body.
Another polysaccharide that could afford some protection against starches is uncooked cellulose – an insoluble fiber. This is because cellulose, when uncooked, increases the rate at which food passes through the intestines, which should, in principle, decrease the absorption of the toxins produced by high rates of microbial metabolic activities in the intestines – such as lipopolysaccharide (LPS).
What mostly incited me to write this post tonight was a book, recently published, that offered a one-sided critique of sugar. So herein, some of the benefits of sugar (i.e., the other side) will be put forth – with a special focus on the predominant ketohexose in the body: fructose.
First, data from recent systematic reviews have, in effect, absolved fructose from the metabolic derangements, seemingly off-hand, attributed to it – such as raising blood pressure, uric acid levels, blood glucose levels, and the rate of weight gain in comparison to other carbohydrates. In turns out that much higher doses of fructose are needed to bring about these toxic effects. These systematic reviews were discussed previously on this blog (but unfortunately those posts were taken down due to overwhelming formatting issues). It’s important to note that in these systematic reviews, fructose was assessed based on studies that used moderate doses of fructose, and studies where fructose was exchanged, one for one, for other carbohydrates.
Nonetheless, I think studies like these are more informative than studies that use doses of fructose of, say, 30 percent of total calories. Americans consume fructose with glucose, and so in order to consume 30 percent of one’s calories as fructose, at least 60 percent of one’s calories would need to come from sucrose (or HFCS, which is, on average, in baked goods and processed foods, 53 percent glucose and 42 percent fructose, and in soft drinks, 42 percent glucose and 55 percent fructose). Of course this would be too unpalatable to do, and consumption data bear this out (Marriott, Cole, & Lee, 2009).
Also, studies in which subjects are fed sugar hyper-calorically always leave uncertainty as to whether an observed weight gain is due to an inherent fattening property of sugar, the excessive intake of calories, or a combination of both.
Second, with regard to diabetes, not only does fructose potentiate the use of glucose (discussed previously on this blog), but fructose also reinforces the counter-regulatory hormonal response to decreases in blood glucose levels, thereby providing a buffer against the potentially damaging consequences associated with a drastic decrease in glucose availability to cells (Gabriely, Hawkins, Vilcu, Rossetti, & Shamoon, 2002; Hawkins et al., 2002).
Fructose is also known to deplete intracellular phosphate, and this can – by decreasing the cell’s energy charge – increase the rate of oxidative metabolism (Díaz-Ruiz et al., 2008), and by increasing the ratio of triose sugars to triose phosphate sugars – the latter of which are highly reactive and decompose to glycators of proteins – provide protection against AGE formation and excessive flux through the respiratory chain and citric acid cycle apparatuses.
Fructose is also known to deplete intracellular phosphate, and this can – by decreasing the cell’s energy charge – increase the rate of oxidative metabolism (Díaz-Ruiz et al., 2008), and by increasing the ratio of triose sugars to triose phosphate sugars – the latter of which are highly reactive and decompose to glycators of proteins – provide protection against AGE formation and excessive flux through the respiratory chain and citric acid cycle apparatuses.
Third, fructose activates hepatic glucokinase - the enzyme that catalyzes the initial step of glucose oxidation in the liver (and is the focus of research in the interest of developing new diabetes drugs) (McGuinness & Cherrington, 2003; Watford, 2002). This partially explains why, according to a recent systematic review, fructose has a “catalytic” effect on glucose use: “Isocaloric exchange of fructose for carbohydrate [reduces] glycated blood proteins." This reduction in 'glycated blood proteins' was equivalent to a 0.53 percent reduction in glycated hemoglobin levels. The authors also concluded, as expected, that fructose consumption does not significantly affect fasting glucose or insulin levels (Cozma et al., 2012).
Fourth, fructose stimulates glycogen synthesis – which in diabetics is impaired – resulting in a decrease in hepatic (a.k.a. endogenous) glucose production. Fructose can exert this effect without the assistance of insulin – in stark contrast to glucose.
Fifth, fructose activates an enzyme, pyruvate dehydrogenase (PDH), which is inhibited in diabetics (and sometimes tumor cells) thereby permitting the oxidation of glucose. In doing so, fructose could provide additional protection against AGE formation by keeping levels of the phosphorylated reducing sugars in check (e.g., the triose phosphates).
And sixth, studies generally show that when fructose is exchanged isocalorically with other carbohydrates, weight loss is modestly increased (Sievenpiper et al., 2012). I think this will be obvious to people who have embarked on diets with the intent to lose weight: Diets centered on fruit is highly conducive to weight loss, and weight loss in turn is associated with a host of favorable changes in cardiometabolic risk factors (e.g., lower blood glucose levels).
I say it’s time stop the unfair crusade against sucrose, because only then can we begin to appreciate the wide range of benefits offered by this sugar – of course, in the context of a nutrient replete diet. Fructose and glucose, together, provides a punch that each alone can’t deliver, and, in effect, can curtail the damages of eating either alone.
I say it’s time stop the unfair crusade against sucrose, because only then can we begin to appreciate the wide range of benefits offered by this sugar – of course, in the context of a nutrient replete diet. Fructose and glucose, together, provides a punch that each alone can’t deliver, and, in effect, can curtail the damages of eating either alone.
But then again, did we have, realistically – based on how it is consumed in the US – reason to believe that sugar could be the cause of the metabolic derangements or a major contributor to the burden of diseases commonly attributed to it (Dolan, Potter, & Burdock, 2010)?
Leave your comments and questions below.
A few other posts on the topic:
- Carbon dioxide, glycation, and the protective effects of fructose
- Fruit, starches, and the perils of low carbohydrate diets
- Are starches safe? Part 1 (UPDATED)
- Are starches safe? Part 2
- Fructose is > glucose Part IV
A response to (half-baked) attacks on sugar
References
Cozma, A. I., Sievenpiper, J. L., De Souza, R. J., Chiavaroli, L., Ha, V., Wang, D. D., Mirrahimi, A., et al. (2012). Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials. Diabetes care, 35(7), 1611–20. doi:10.2337/dc12-0073
Dolan, L. C., Potter, S. M., & Burdock, G. A. (2010). Evidence-based review on the effect of normal dietary consumption of fructose on blood lipids and body weight of overweight and obese individuals. Critical reviews in food science and nutrition, 50(10), 889–918. doi:10.1080/10408398.2010.512990
Díaz-Ruiz, R., Avéret, N., Araiza, D., Pinson, B., Uribe-Carvajal, S., Devin, A., & Rigoulet, M. (2008). Mitochondrial oxidative phosphorylation is regulated by fructose 1,6-bisphosphate. A possible role in Crabtree effect induction? The Journal of biological chemistry, 283(40), 26948–55. doi:10.1074/jbc.M800408200
Gabriely, I., Hawkins, M., Vilcu, C., Rossetti, L., & Shamoon, H. (2002). Fructose amplifies counterregulatory responses to hypoglycemia in humans. Diabetes, 51(4), 893–900. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11916904
Hawkins, M., Gabriely, I., Wozniak, R., Vilcu, C., Shamoon, H., & Rossetti, L. (2002). Fructose improves the ability of hyperglycemia per se to regulate glucose production in type 2 diabetes. Diabetes, 51(3), 606–14. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11872657
Marriott, B. P., Cole, N., & Lee, E. (2009). National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. The Journal of nutrition, 139(6), 1228S–1235S. doi:10.3945/jn.108.098277
McGuinness, O. P., & Cherrington, A. D. (2003). Effects of fructose on hepatic glucose metabolism. Current opinion in clinical nutrition and metabolic care, 6(4), 441–8. doi:10.1097/01.mco.0000078990.96795.cd
Sievenpiper, J. L., De Souza, R. J., Mirrahimi, A., Yu, M. E., Carleton, A. J., Beyene, J., Chiavaroli, L., et al. (2012). Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis. Annals of internal medicine, 156(4), 291–304. doi:10.1059/0003-4819-156-4-201202210-00007
Watford, M. (2002). Small amounts of dietary fructose dramatically increase hepatic glucose uptake through a novel mechanism of glucokinase activation. Nutrition reviews, 60(8), 253–7. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/12199300