Given the Taubes/Lustig view on sugar, why not use dextrose everywhere?
April 7, 2016 7:30 AM   Subscribe

If we assume the (increasingly accepted) view that sugar, in any decent quantity, is a highly unhealthy thing to eat, and that the main culprit is actually fructose, is there any good reason to not aggressively replace sugar or HFCS with dextrose?

I've been keeping an interested on eye on what I think of as the emerging Gary Taubes/Robert Lustig consensus, which blames our increasing consumption of sugar for the obesity and various metabolic diseases that have plagued the west in recent decades.

More specifically, this consensus says that when fructose is metabolised, much more of it is converted to fat than is the case with glucose, and that fructose metabolism in general is very hard on the liver and the endocrine system as a whole.

As someone with both a personal and geeky interest in nutrition, and also a serious sweet tooth, it sounds to me like we could ameliorate a lot of the harm by replacing sucrose (table sugar) or HFCS with dextrose (glucose). Dextrose works just fine to sweeten tea, coffee, or lemonade. It's not as intense or purely sweet as sugar, but I'm sure many recipes for baked goods could be rejiggered to use dextrose as well. I'm under no illusion that dextrose is a health food, but from my layperson's understanding, it seems much more benign than fructose. So, if you accept the sugar-is-the-new-tobacco view, but still want to have, and eat, your cake, what are the arguments against putting Dextrose in All The Things?
posted by tempythethird to Health & Fitness (10 answers total) 5 users marked this as a favorite
Sugar is sugar. There's no Dark Molecular Magic at work with HFCS that makes it, gram for gram, more evil. The problem is that it's economically cheap and it still tastes good, so it's put into everything.
posted by Cool Papa Bell at 7:43 AM on April 7, 2016 [7 favorites]

Totally hear where you're coming from. In my recollection there are two main problems with table sugar:

1) The fructose is metabolized in your liver in a way similar to alcohol, causing metabolic problems such as fatty liver disease and just general adipose tissue and taxing your liver.

2) Excess glucose in your bloodstream causes insulin to be released, which if done too much for too long can cause various problems, one of which is diabetes, and another is increased appetite.

Your dextrose fix solves #1 as far as I can see, but not #2. Using dextrose in everything would basically be similar to eating more starchy foods (e.g. potatoes and rice) because their starch molecules would get broken down into glucose in your body after digestion, although it would be a slower process than just eating a bolus of dextrose. Taubes doesn't really recommend eating a diet of potatoes and rice for reason #2, just having so much carbohydrate in your diet and glucose in your bloodstream causes problems over time.

As for why people don't do it, I'd imagine cost is one and HFCS probably tastes sweeter/better is another.
posted by permiechickie at 7:51 AM on April 7, 2016 [2 favorites]

I wonder what the relative resource/environmental costs of producing each are.

Also, are there any foods with naturally-occurring pure dextrose?
posted by amtho at 7:59 AM on April 7, 2016

There is a lot of evidence that a diet high in carbohydrates, particularly refined carbohydrates, can cause health problems. There is very little reliable evidence (some would say none) that these problems are caused exclusively by the fructose component of sucrose, or that glucose is harmless.

Therefore, encouraging consumption of a refined carbohydrate, dextrose/glucose, would be irresponsible without first showing conclusively (with rigorous trials) that it is any better than sugar, which we already know to be harmful. Better to recommend against refined carbohydrates as a whole.
posted by randomnity at 8:13 AM on April 7, 2016 [6 favorites]

Table sugar is a glucose and fructose stuck together. I think one reason sugar is better than HFCS because the glucose and fructose bond has to be broken apart before it can be digested.

Any time digestion of food occurs outside the body (ie the breaking of the glucose and fructose bond) your body has to spend fewer calories digesting. Just as an example a rare steak gives you fewer calories than a very well cooked steak, because the well cooked steak has been digested more by heat.

You might read In Defense of Food: An Eater's Manifesto by Michael Pollan; it has a pretty solid discussion of why food can't be broken down to just sugar, fat, and protein.
posted by gregr at 8:30 AM on April 7, 2016

1) The fructose is metabolized in your liver in a way similar to alcohol, causing metabolic problems such as fatty liver disease and just general adipose tissue and taxing your liver.
The last paragraph of this comment explains how untrue that statement is. That entire thread is interesting reading on sugar.
posted by soelo at 8:39 AM on April 7, 2016 [2 favorites]

what I think of as the emerging Gary Taubes/Robert Lustig consensus

Just because those guys get a lot of play in the media doesn't mean their views represent an emerging consensus.

Re your suggestion, as you point out, dextrose is less sweet than sucrose -- 74% as sweet, according to this chart -- so it would take more to achieve the same sweetness.

And with fructose, as with anything, the dose makes the poison -- deleterious effects are only observed when it's consumed in large amounts.
posted by ludwig_van at 8:41 AM on April 7, 2016 [6 favorites]

From a food manufacturer's view, switching is expensive, difficult and unwanted by buyers compared to changes like blending in zero-calorie sweetener, achieving a "natural" ingredients labdl , etc. I agree with those writers but we are nowhere close to consensus. Low fat products are popular.
posted by michaelh at 8:53 AM on April 7, 2016

If the biochemistry doesn't scare you off, this is Lustig's more technical article on the pathways that fructose uses in the liver. Obviously, ethanol and fructose are different molecules, but his assertion is that they both stimulate de novo lipogenesis (DNL) in a way that glucose doesn't in the liver. Nobody is suggesting they are the same molecule, but the body has a finite set of metabolic pathways and some of them intersect.

From the article (FFA = Free Fatty Acid; VLDL = very low density lipoprotein):
Hepatic ethanol metabolism
The hepatic pathway of ethanol metabolism is different from that of glucose in its regulation and the disposition of intermediary metabolites (Fig. 2). Ethanol enters the hepatocyte through osmosis, it does not require insulin for its metabolism, and it does not stimulate insulin secretion. Ethanol does not undergo glycolysis. Instead, it is converted by alcohol dehydrogenase 1B to form acetaldehyde, which, due to its free aldehyde, can generate reactive oxygen species (ROS) formation and toxic damage (19) if not quenched by hepatic antioxidants such as glutathione and ascorbic acid (see ROS formation and aging section) (20). Acetaldehyde is then quickly metabolized by the enzyme aldehyde dehydrogenase 2 to the intermediary acetic acid. From there, acetic acid is metabolized by the enzyme acyl-CoA synthetase short-chain family member 2 to form acetyl-CoA, which can then enter the mitochondrial tricarboxylic acid cycle (as per glucose). However, in the event of consumption of a large dose of ethanol producing a large amount of acetyl-CoA or due to the presence of other caloric substrate (i.e., as in beer in which ethanol and glucose are consumed together), the ethanol will more likely be converted to FFAs through DNL (21). Furthermore, acetaldehyde stimulates SREBP-1c, activating the enzymes of DNL (22) to increase rate of formation of FFAs. Although the absolute rate of DNL of ethanol (i.e., that which is metabolized to VLDL) is relatively small, fractional DNL increases from 1% at baseline to 31% after an ethanol bolus (21); thus, the liver is primed to convert ethanol to FFAs. Normally, intrahepatic lipid is exported as VLDL. Ethanol suppression of MTP alters VLDL production and lipid export machinery (23) to increase VLDL production and contribute to hypertriglyceridemia (24–26). By increasing intrahepatic lipid formation, ethanol drives hepatic insulin resistance (27, 28). Although the mechanism is still unclear, dyslipidemia and hepatic insulin resistance may be due to hepatic diacylglycerol and triglyceride accumulation seen in hepatic steatosis, with resultant activation of the enzyme c-jun N-terminal kinase 1 (JNK-1) (see the following) (29).

Hepatic fructose metabolism
Only the liver possesses the Glut5 transporter (30), and the liver has a very high fructose extraction rate (31); thus, virtually an entire ingested fructose load finds its way to the liver. In contrast to the majority of hepatic glucose being converted to glycogen in the liver under the influence of insulin, fructose does not get converted to glycogen directly [although in case of glycogen depletion due to starvation or exercise, it can be converted to fructose-6-phosphate, which is isomerized to glucose-6-phosphate, which can rebuild glycogen (32)]. Rather, fructose is phosphorylated independently of insulin to fructose-1-phosphate by the enzyme fructokinase (Fig. 3), which undergoes glycolysis, and is metabolized to pyruvate, with the resultant large volume of acetyl-CoA entering the mitochondrial tricarboxylic acid cycle. Any extra intermediary will be available for DNL, similar to ethanol. Alternatively, a proportion of early glycolytic intermediaries will recombine to form fructose-1,6-bisphosphate, which then also combines with glyceraldehyde to form xylulose-5-phosphate (33). Xylulose-5-phosphate is a potent stimulator of protein phosphatase 2A (34), which activates carbohydrate response element binding protein (35), stimulating the activity of DNL. Furthermore, fructose also stimulates PPAR-γ coactivator 1β, a transcriptional coactivator for SREBP-1c, which further accentuates DNL enzymatic activity (36). In other words, fructose drives “double DNL” because carbohydrate response element binding protein and PPAR-γ coactivator 1β drive these enzymes additively. Human studies demonstrate a rate of fractional DNL of 2% with glucose, yet up to 10% after 6 d of high fructose feeding (37, 38) A recent human study demonstrated that fructose feeding increased fractional DNL to 17% (39). More importantly, when the liver receives glucose and fructose simultaneously, the glucose occupies the glycogenic pathway, forcing the fructose down the lipogenic pathway, thus tripling the rate of DNL compared with fructose alone (40). The attachment of hepatic triglyceride to apolipoprotein B by MTP completes its conversion to VLDL, which is exported out of the liver to contribute to fructose-induced hypertriglyceridemia (39, 41–43), along with the production of “small dense” LDL (44), which is particularly atherogenic because it can be oxidized rapidly and is small enough to get under the surface of vascular endothelial cells to start the foam cell process (39, 45–47). Some of the fatty acyl-CoA products from DNL escape packaging into VLDL for export and instead accumulate as lipid droplets in the hepatocyte (48), driving hepatic steatosis, similar to ethanol. In doing so, the enzyme JNK-1 (49) is activated, which induces serine phosphorylation of IRS-1 in the liver (50), thereby preventing normal insulin-mediated tyrosine phosphorylation of IRS-1 and promoting hepatic insulin resistance. This drives hyperinsulinemia (51), with resultant obesity causing worsening insulin resistance. Furthermore, fructose increases the expression of FoxO1 (52). In the face of hepatic insulin resistance, FoxO1 is not phosphorylated to maintain its exclusion from the nucleus, with resultant transcription of gluconeogenic enzymes and hyperglycemia, requiring an even greater β-cell insulin response. Eventually, in response to the hepatic insulin resistance, gluconeogenesis, and the phenomena of glucotoxicity, lipotoxicity, endoplasmic reticulum stress (53–56), and the unfolded protein response (57) at the β-cell, this leads to inadequate insulin secretion in relation to the degree of peripheral insulin resistance and type 2 diabetes (58).
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posted by permiechickie at 9:19 AM on April 7, 2016 [2 favorites]

I think one reason sugar is better than HFCS because the glucose and fructose bond has to be broken apart before it can be digested.

The enzyme that does that is in the surface of the gut, and operates before the sugar even hits the bloodstream. The amount of energy involved is tiny compared to that obtained by metabolizing the resulting glucose and fructose.

If there is any discernible metabolic difference at all between HFCS and sucrose (a dubious proposition at best) it will be because the HFCS 55 typical for soft drinks is 55% fructose rather than sucrose's 50%. In solid foods, HFCS 42 tips the balance slightly the other way.

Dextrose works just fine to sweeten tea, coffee, or lemonade. It's not as intense or purely sweet as sugar, but I'm sure many recipes for baked goods could be rejiggered to use dextrose as well.

To get the same subjective sweetness, you'd need more dextrose. To get the same sweetness as any given amount of sucrose or HFCS 55 from glucose alone, you'd end up ingesting none of the fructose but roughly triple the glucose. It's not instantly obvious that this would confer an overall benefit.
posted by flabdablet at 9:28 AM on April 7, 2016 [2 favorites]

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