6x Bananas a Day!? Meta-Analysis: Lower Glucose, Insulin and HbA1c Levels From 'Catalytic' Dose of 36g Fructose

Figure 1: At least according to the USDA data, the average US citizen did never in the last 40 years get even close to the "catalytic" dose of fructose - at least not if we go by his / her daily HFCS consumption.

I usually don't start these articles with a disclaimer, but in this case I want to make sure that this post is not misinterpreted as a corn-refiners advertisement (and contrary to one of the authors of the Sievenpiper study, Coca Cola has unfortunately as of yet never covered my travel expenses ;-)... anyways, whenever the word "fructose" is used in the following lines it to the simple monosaccharide found as part of a complex nutrient matrix in many plants and their fruits (who would have expected that?). It is not used to denote the controversial results of a three-step enzymatic isolation process (Cornstarch → alpha-amylase → oligosaccharides + glucoamylase →  glucose + xylose isomerase →  42% fructose + 50–52% glucose + other sugar; cf. Wikipedia. "High Fructose Corn Syrup") that's at the heart of a very emotional debate about who would be to blame for the current obesity epidemic, now that the bad fats are no longer bad enough to be the scapegoat and ultima ratio for why we get fat.

Junk food is more than HFCS and fruit is more than fructose!

Fortunately, you, as a "whole food eating" SuppVersity reader, don't really have to care about the whole HFCS business. With your minimal intake of processed foods, your exposure to high fructose corn syrup should ideally be identical to the one of the parents and grandparents of America's obese children in the flower power seventies (~0.1-1g, see figure 1); a time, when your parents would not tell you to "beware of high fructose corn syrup", but to stay away from "those hairy, drug-addicted, reprobate hippies next door". Against that background, today's SuppVersity article is to be understood as an incentive to rethink, whether or not it is really necessary, let alone beneficial to deprive yourself of a whole class of vitamin and micronutrient-laden foods, simply because they contain a small number of molecules of which you are told that they "must not to be eaten, if you want to stay lean & healthy".

To help your thought process along, I have compiled the data from a recently published meta-analysis (that's a study, the results of which are based on data from multiple previous trials, which was weighed and compiled to come up with "new" data with a larger empirical foundation and thus greater significance). And I am honestly curious whether or not the evidence Sievenpiper and his colleagues presented in favor of the existence of a"catalytic dose" of  ≤36g/day of fructose that's been shown to improve, not compromise, blood glucose, insulin and HBA1C, when it is consumed instead of 36g of carbs from other sources (the studies in the review used either starches or simple sugars with almost identical beneficial results, by the way) will have catalytic effects on your opinion making process ;-)

Figure 2:  Effect of isoenergetic exchange of "catalytic" fructose doses (≤36g/d) for other carbohydrates (starches or simple sugars) on glycaemic endpoints: HbA1c, fasting blood glucose and fasting blood insulin, data calculated based on analysis of the scarce literature that is currently available (adapted from Sievenpiper. 2012)

The improvements in HbA1C, which is still the gold standard for evaluating long-term blood sugar level, in fasting blood glucose and insulin levels were across the board statistically significant, regardless of whether or not you apply the quality criteria, Sievenpiper and his colleagues used to weigh the results of the individual studies (cf. figure 2). Accordingly, the authors are right, when they point out that

[...] this small meta-analysis of controlled feeding trials supports earlier13C NMR spectroscopy investigations and acute feeding studies showing that ‘catalytic’ doses (≤36g/d) of fructose may improve glycaemic control [and that this] benefit is seen without the adverse cardiometabolic effects reported when fructose is fed at high doses or as excessenergy. (Sievenpiper. 2012)

Based on the data in figure 1, which clearly shows that the "average American" does not and never did pass this "catalytic threshold level" it may - at first sight appear odd that 42% of your countrymen and -women are supposed to be obese by the year 2030 (Hellmich. 2012)... at least for so long until you realize that for every American who follows your lead and consumes virtually no HFCS, there must be another one who consumes this person's 43.3g of HFCS on top of his own 43.3g of HFCS on a daily basis and would thus easily surpass the "scientifically proven" catalytic threshold levels which was (and I leave it up to you to decide whether this is coincidence or not) in none of the studies achieved from HFCS intake, by the way (I guess I don't have to tell you that my calculation is of mere illustrative nature, despite the fact that the 43.3g /day HFCS intake are actually from the USDA dataset for 2010).

Bad news for the guy who eats / drinks your daily share of 43.3g of high fructose corn syrup, ...

...but what does that mean for you? As long as your only significant fructose source are whole fruits and the few vegetables that contain more than trace amounts of fructose, you can answer this question by taking a look at the data in figure 3. The small figures on top of the bars will tell you how many 100g servings of apples, dates, pears or tomatoes you can consume until you hit the catalytic limit*uhuhhh...*: 3.9x 100g servings, of apples, for examples, or 5x 100g servings of bananas, or a whopping 32.7x 100g servings of lemons... sounds plenty? Well, I don't know, but certainly plenty enough to finally stop worrying when Adelfo Cerame would not ruin his health, let alone his physique, when he eats a banana along with his postworkout shake, wouldn't you agree?

Figure 3: Number of 100g servings of various common fruits to get to the more or less arbitrary  ≤36g/day threshold.

Notwithstanding, this ≤36g/day limit does certainly appears more or less arbitrary. This is all the more true in face of previous results by Livesey & Taylor, who could not find evidence that such a thing as a "threshold dosage" for the Hb1AC improving effects of fructose even exists (Livesey. 2008) or the fact that a "low-GI fruit intake [and not the number of servings of fiber-laden cereals!] was the strongest independent predictor of [lowered] HbA1c" in a 2011 6-months low-GI diet experiment by Jenkins et al. who compared Kellog's... ah, pardon me, I meant the medical orthodoxy's gold standard, the high-cereal fiber diet in 152 participants with type 2 diabetes with a simple low-GI diet (Jenkins. 2011).

Can ≤35g of fructose per day really be the answer to everything?

Though the main reason for the arbitrariness of the 36g limit certainly is the scarcity of valid experimental data from well-controlled human trials, Sievenpieper et al. claim that their reference for the "catalytic range" was in accordance with "an emerging literature" that "has shown that low-dose fructose (≤10g/meal) may benefit glycaemic control".

Now, those of you who have read my "Carbohydrate Shortage in Paleo Land" post from back in June 2011, will probably remember that from a mere physiological point of view every healthy (=nondiabetic and with an intact liver) human being, including the tiniest woman, should be able to handle a minimum of ~100g of carbohydrates on a daily basis. If we now take the 2:1 glucose to fructose ratio, of which Walliset al. found that it is just as effective in repleting muscle gylcogen stores after a workout as the same amount (90g) of pure glucose, and apply it to the 36g fructose threshold this yields a "total carbohydrate threshold" of 108g - coincidence or physiological necessity?

And even when you didn't replace some of the starches or other simple sugars for your daily dose of 2kg of apples (another example of exclusively illustrative nature), you would maybe get fatter, but according to the results of Silbernagel et al. not a single gram fatter than from the same amounts of calories from glucose from fructose or glucose conducted with healthy young men; cf. Silbernagel. 2011).

You can have another apple today and will still (or rather hence?) live tomorrow ;-)

Image 3 (edited in response to anon & JP, thx!): Certainly impressive what lifelong caloric restriction did to the 27.6 year-old ape on the right, if you take a look at his wrinkled age-mate on the left, no? Suggested read: "Health and Longevity Effects of Intermittent Fasting"

Overall it does therefore seem more than unlikely that a healthy, non-sedentary or even athletic individual has to worry about eating another apple, when he or she already reached their purported catalytic limit of 36g with the pound of blackberries, two bananas and a huge grapefruit this person could have eaten earlier in the day.

Moreover, skipping on the apple would also mean that you would miss out on its recently confirmed life-extending effects (+130% in yeast; Palermo. 2012), of which Vanessa Palermo and her colleagues from the Dept. of  Biology and Biotechnology “Charles Darwin” have shown that they are the prerogative of the whole fruit and not a result of the high antioxidant or polyphenol content of apples, as they occurred only, when the yeast is treated with a handcrafted extract that had approximately 26.7 g/100ml of fresh apple in it... and guess what, that apple, Golden Delicicious, happens to be one of my personal favorites, taste-wise, or course ;-)

Bottom line: I know it is more than questionable to which extend (1:20, 1:100, not at all?) the lastly cited life-prolonging effects of whole apples can be extrapolated to human beings, but that does neither diminish the perplexing results of Sivenpiper's meta-analysis nor long-established cancer protective effects of fruits in general and apples in particular (eg.  Veeriah. 2006;  McCann. 2007; Yoon, 2007; Gerhauser. 2008; Zessner. 2008; Jedrychowsk. 2009; Liu. 2010; Reagan-Shaw. 2010) and should therefore suffice to put more than a non-legible font-size "1" questionmark behind any previously taken decision of yours that it would be better to deprive yourself of these delicious superfoods (=fruits) than trust on your livers ability to to what she has evolved to do and turn the slow influx of relatively low amounts of fructose and glucose into energy and deliver the rest of the vitamins, polyphenols, and other micronutrients via the bloodstream to other organs.

References:

• Gerhauser C. Cancer chemopreventive potential of apples, apple juice, and apple components. Planta Med. 2008 Oct;74(13):1608-24. Epub 2008 Oct 14. Review. 
• Hellmich J. Obesity could affect 42% of Americans by 2030. USA TODAY. Aug 05, 2012 < http://www.usatoday.com/news/health/story/2012-05-07/obesity-projections-adults/54791430/1 > accessed Aug 07, 2012
• Jandrain BJ, Pallikarakis N, Normand S, Pirnay F, Lacroix M, Mosora F, Pachiaudi C, Gautier JF, Scheen AJ, Riou JP, et al. Fructose utilization during exercise in men: rapid conversion of ingested fructose to circulating glucose. J Appl Physiol. 1993 May;74(5):2146-54.
• Jedrychowski W, Maugeri U. An apple a day may hold colorectal cancer at bay: recent evidence from a case-control study. Rev Environ Health. 2009
• Jenkins DJ, Srichaikul K, Kendall CW, Sievenpiper JL, Abdulnour S, Mirrahimi A, Meneses C, Nishi S, He X, Lee S, So YT, Esfahani A, Mitchell S, Parker TL, Vidgen E, Josse RG, Leiter LA. The relation of low glycaemic index fruit consumption to glycaemic control and risk factors for coronary heart disease in type 2 diabetes. Diabetologia. 2011 Feb;54(2):271-9. 
• Livesey G, Taylor R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008; 88, 1419–1437. 
• Liu L, Li YH, Niu YB, Sun Y, Guo ZJ, Li Q, Li C, Feng J, Cao SS, Mei QB. An  apple oligogalactan prevents against inflammation and carcinogenesis by targeting LPS/TLR4/NF-κB pathway in a mouse model of colitis-associated colon cancer. Carcinogenesis. 2010 Oct;31(10):1822-32. 
• McCann MJ, Gill CI, O' Brien G, Rao JR, McRoberts WC, Hughes P, McEntee R,  Rowland IR. Anti-cancer properties of phenolics from apple waste on colon carcinogenesis in vitro. Food Chem Toxicol. 2007 Jul;45(7):1224-30. 
• Reagan-Shaw S, Eggert D, Mukhtar H, Ahmad N. Antiproliferative effects of apple peel extract against cancer cells. Nutr Cancer. 2010;62(4):517-24. 
• Palermo V, Mattiv, F, Silvestri R, La  Regina G, Falcone CM. Oxidative Medicine and Cellular Longevity. 2012 [Article in press]
• Sievenpiper JL, Chiavaroli L, de Souza RJ, Mirrahimi A, Cozma AI, Ha V, Wang DD, Yu ME, Carleton AJ, Beyene J, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Kendall CW, Jenkins DJ. 'Catalytic' doses of fructose may benefit glycaemic control without harming cardiometabolic risk factors: a small meta-analysis of randomised controlled feeding trials. Br J Nutr. 2012 Aug;108(3):418-23.
• Silbernagel G, Machann J, Unmuth S, Schick F, Stefan N, Häring HU, Fritsche A.Effects of 4-week very-high-fructose/glucose diets on insulin sensitivity, visceral fat and intrahepatic lipids: an exploratory trial. Br J Nutr. 2011 Jul;106(1):79-86. 
• Veeriah S, Kautenburger T, Habermann N, Sauer J, Dietrich H, Will F, Pool-Zobel BL. Apple flavonoids inhibit growth of HT29 human colon cancer cells and modulate expression of genes involved in the biotransformation of xenobiotics. Mol Carcinog. 2006 Mar;45(3):164-74. 
• Wallis GA, Hulston CJ, Mann CH, Roper HP, Tipton KD, Jeukendrup AE. Postexercise muscle glycogen synthesis with combined glucose and fructose ingestion. Med Sci Sports Exerc. 2008 Oct;40(10):1789-94.
• Wikipedia contributors, "High-fructose corn syrup," Wikipedia, The Free Encyclopedia, < http://en.wikipedia.org/w/index.php?title=High-fructose_corn_syrup&oldid=505539604 > accessed August 7, 2012. 
• Yoon H, Liu RH. Effect of selected phytochemicals and apple extracts on  NF-kappaB activation in human breast cancer MCF-7 cells. J Agric Food Chem. 2007  Apr 18;55(8):3167-73. Epub 2007 Mar 21.
• Zessner H, Pan L, Will F, Klimo K, Knauft J, Niewöhner R, Hümmer W, Owen R,  Richling E, Frank N, Schreier P, Becker H, Gerhauser C. Fractionation of polyphenol-enriched apple juice extracts to identify constituents with cancer chemopreventive potential. Mol Nutr Food Res. 2008 Jun;52 Suppl 1:S28-44.

Glutamate: Can It Be Use To Your Advantage? Study Shows Insulin Sensitizing Effects of Dreaded Food Additive

"Now you've got me confused!"

In the context of MSG scare, glutamate has gotten such a bad rep that it seems highly counterintuitive to assume that there was anything good about the major excitatory amino acid in the human body and still, a recent study from the Department of Kinesiology at the University of Waterloo clearly suggests that "MSG and carbohydrate supplementation can be used to manipulate plasma glutamate" (Sebastiano. 2013)... and no, we are not talking about an in-vitro or rodent study here.

With 9 perfectly healthy, recreationally active men aged 23.9+/-1.9y and a BMI of 25kg/m² the results can however be taken as being representative for at least large parts of the ever-decreasing number of "normal-weight" individuals.

There is a potential string attached

Usually, the "on the other hands", are something I am talking about at the end of the article, but in this case, of which I expect that it's going to become pretty controversial it appears prudent to address them right away: there was a hitherto unexplained dichotomy in the insulin response of the 9 subjects after the ingestion of the 150 mg/kg body weight MSG or placebo capsules, the subjects ingested after an overnight fast and 30 minutes before they consumed a 75 g carbohydrate or a non-energy placebo drink.

Figure 1: AUC for glucose and insulin across the trials (left); serum insulin and glucose concentrations in the post-prandial period during the glutamate and no-glutamate trials (Sebastiano. 2013)

What looks like a Taubs'ian nightmare is actually nothing but a perfectly normal insulin response to the ingestion of 75g of carbohydrates. In a healthy individual, the insulin response is proportional to the influx of glucose from the digestive tract and ensures that the latter is getting stored in muscle, liver and fat (with the former being topped of first, cf. figure 3 in previous article).

On average, we do the the same if not less insulin with a greater reduction in glucose

That being said, there is no debating that contrary to the scientists' working hypothesis, the average insulin secretion was not on augmented in the GLU+CHO, while the onslaught of glucose was significantly reduced (see figure 1, bottom right) compared with the CHO only trial.

Epidemiology paints a different picture of MSG (learn more)

"[I]t appears that glutamate, when combined with carbohydrate, elicits one of two insulin responses, depending on the individual.

Although the present study was not designed to explore this question, we did remark that the differences between these two groups of participants were not explained by factors associated with glucose handling, such as habitual activity levels (assessed using the Baecke questionnaire), fasting glucose, available glutamate or insulin sensitivity." (Sebastiano. 2013)

Now this is quite astonishing as it would suggest that the co-ingestion of glutamate does actually improve the insulin sensitivity only in some. In those the effect must yet have been so pronounced, though, that the "non-responders" didn't carry any weight...

---

Apropos weight, in order to confirm whether or not you can use glutamate to your advantage, we would need at least two follow up studies:

Will the additional butter on top of the potatoes reduce the insulin response? Learn the answer to this other questions in one of the famous installments of the "True or False?" Series on the SuppVersity (learn more)

• One study to elucidate the long-term consequence of the addition of glutamate to every (high) carbohydrate meal in healthy human subjects (the hypothesis would be that we should lower HOMA-IR and HbA1C levels as a sign of improved glucose metabolism).

• And another study to make sure that the obvious insulin-sensitizing effects glutamate appears to exert in at least some subjects are not adipose-tissue specific - or, in other words, that it is not an increase in fatty acid synthethase and subsequent storage of glucose as fat that's behind the significantly reduced glycemia the scientists observed.

What? You think all that is bullocks, because "we all know" that glutamate is going to make you fat? Well, in a non-calorically controlled scenario this may still be the case.

YamYol: Yeast extract = MSG

Did you know that almost all producers of convenience "food" are tricking their consumers by claiming their products were free of added flavor enhancer, MSG-free or at least free of artificial flavor enhancers only to add yeast extract as an ingredient. Now being an ingredient it's no longer an additive and in view of the fact that most consumers are not aware that it is basically MSG, nobody will complain... besides you, obviously ;-)

To understand that you will however have to get rid of your false prejudices against insulin, the release of which also acts as a satiety signal (in the insulin sensitive individual) and will have you stop eating (Verdich. 2001). With your glutamate laden super size fast food menu, your body may not even recognize that you have just been downing a Big Mac, XXL French fries and an XXL Coke, estimating that the stuff you ate was probably a Happy Meal with only 50% of the calories. In other words, in the real world, McGlutamate and ChinaMSG are probably still not the best places to dine regularly ;-)

References:

• Di Sebastiano KM, Bell KE, Barnes T, Weeraratne A, Premji T, Mourtzakis M. Glutamate supplementation is associated with improved glucose metabolism following carbohydrate ingestion in healthy males. Br J Nutr. 2013 Jun 11:1-8. [Epub ahead of print] 
• Verdich C, Toubro S, Buemann B, Lysgård Madsen J, Juul Holst J, Astrup A. The role of postprandial releases of insulin and incretin hormones in meal-induced satiety--effect of obesity and weight reduction. Int J Obes Relat Metab Disord. 2001 Aug;25(8):1206-14.

True or False: Xanthan Will Reduce The Glycemic Index of Your Meals, Increase Satiety and Have an Overall Beneficial Effects on Your Metabolic Health (Glucose, Lipids, Waist, ...)

Can xanthan reduce the glycemic response to "sweet treats" like this?

Have you ever heard of xanthan? Yep that's E-number E415. What? If it has an E-Number it can't be good? Well, what about vitamin C, then? That's E-Number E300. Does this make it "bad" for you? If so, I'd suggest you skip today's SuppVersity article and avoid xanthan out of principle. Otherwise, I would like to offer you to join me for another "True or False" Session (find more of these | RSS-compatible browser or plugin for Chrome like SlickRSS needed) at the end of which we will know whether the statement "Xanthan Will Reduce Your Meals Glycemic Index, Increase Satiety and Have Overall Beneficial Effect on Your Metabolic Health" is true, or false.

You can find more True or False articles at the SuppVersity

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High Volume Diet = Success

When it's added to juice (alongside with beta-glucans), xanthan will reduce the glucose response and thus help stabilize blood sugar levels (Paquin. 2012).

Figure 1: Mean (S.E.) changes of hunger, fullness, desire to eat, and prospective consumption after ingestion of 325 ml of a thin and thick shake. Ratings were provided on nine-point category scales. “*” indicates a significant difference in ratings for the two shakes (Mattes. 2001).

The stabilized blood sugar levels, in turn, will will eventually have beneficial effects on 24h satiety.

This goes, even though Julie Paquin and her colleagues did not detect an acute increase in their 2012 study on the effects of xanthan and β-glucan enriched juices on the glycemic response and satiety of healthy men. Previous studies suggest that the viscosity of a liquid meal, which is increased by the addition of xantham, may be an important determinant of the hunger response.

Mattes and Rothacker (2001), for example reported significantly greater and more prolonged reductions in hunger with thicker, but otherwise identical replacement shakes.

Marciani et al. (2001) even found that the viscosity of their high- vs. low-viscosity shakes with different macronutrient and energy content had a greater impact on the satiety than the fat, carbohydrate or energy content of the test meals.

Food Volume Matters!

SuppVersity Suggested Read: "True or False: High Volume + Nutrient + Low Energy Foods Keep You Lean. Bonus-Question: Will a High Volume Make Your Stomach Go Baggy & Mess Up Your Satiety Response?" | read more - Just in case you've already forgotten that I've covered the beneficial effects of a "high volume, high nutrient, low energy" diet and the corresponding increase in gastric volume in one of the last installments of the True or False Series | go trough previous installments.

The scientists from the University Hospital, Nottingham were also able to show a direct correspondence between the gastric volume of the viscous meal ad the satiety response. These observations support the dual hypothesis, i.e. that more viscous fibres exert their effect owing to distention in the gastric antrum and/or altered transport of nutrients to the small intestine, Caroline Hoad et al. put forward in their 2004 paper in the Journal of Nutrition (Hoad. 2004).

Table 1: Viscosity AUC values for solutions containing select dietary fibers during gastric digestion simulation

In view of the fact that a comparison of the total viscosity per gram of 12 different fiber types Dikeman et al. published in the Journal of Nutrition in April 2006 indicates that xanthan has by far the highest viscosity of all 12 tested types of dietary fiber (Dikeman. 2006), it appears to be certain that the polysaccharide, which is secreted by the bacterium Xanthomonas campestris, will exert significant beneficial effects on both the volume of a given liquid meal and the time it takes to pass through the digestive tract - and this will, as we have just learned, improve fullness and satiety, and decrease the energy intake of every dieter.

Why does glycemia even matter? Aside from the fact that extreme glucose excursions after a meal are partly responsible for the development of diabetes, avoiding them will (1) stabilize your energy levels and curb your cravings, (2) decrease inflammation and oxidative stress, (3) help you maintain healthy blood lipid and body fat levels, (4) reduce your cancer and heart disease risk, and so on. You see, if xanthan can help you stability your blood sugar levels, this alone would have a long string of beneficial health consequences.

At this point, I could probably cite the dirty dozen of studies that support the appetite suppressing effects of PGX®, a combination of xanthan, sodium alginate and glucomannan (e.g. Jenkins. 2010; Tao. 2010; Kacinik. 2011; Reichert. 2013).

Figure 2: Postprandial glycemia in healthy subjects after the consumption of various breakfast meals (Jenkins. 2008) similar beneficial effects in response to the addition of a 70% glucomannan and 30% xanthan blend to the buiscuits were observed in diabetic subjects, as well.

In view of the fact that we are interested in the individual effects of xanthan, and not in the promotion of an expensive, albeit scientifically proven fiber supplement where xanthan is only one (but probably one of the most important) ingredients, I will leave the PGX-related evidence behind and turn to "xanthan only" studies to substantiate my assertion that xanthan gum is a beneficial, albeit not necessary, addition to the dietary regimen of both, lean and overweight physical culturists.

Warning! Xanthan is safe for adults (Eastwood. 1987), but probably not safe for infants. This is at least what a report from the US Food and Drug Administration in the Journal of Pediatrics would suggest (Beal. 2012). According to the USDA, the potential for thickened feeds to increase risk of necrotizing enterocolitis (NEC), a leading cause of morbidity and mortality in neonates, has not been thoroughly assessed. Nevertheless, the occurrence of 202 cases of NEC in formula-fed (obviously) infants over 12 years should yet be reason enough to keep your xanthan stash far away from your newborn, irrespective of the fact that the case series Beal et al. present cannot prove an association between the xanthan-containing thickening agent SimplyThick and NEC.

Odutola Osilesi and colleagues from various US Universities and the USDA were among the first to propose and demonstrate the potential usefulness of xanthan gum in dietary management of diabetes mellitus (Osilesi. 1985). In the corresponding experimental trial, they supplied 9 drug-free diabetics with moderately elevated serum glucose and four nondiabetic controls controls with - you guessed it - muffins that contained 12g of xanthan gum.

Figure 3: Muffins w/ 12g xanthan/day have significant beneficial effects on glucose management in diabetics and beneficial, but non-significant effects on fasting and post-prandial blood sugar in healthy subjects (Osilesi. 1985)

The subjects were randomly assigned to to a "xanthan first" or "control first" group for 2x six weeks. Before the study and at the end of the xanthan and xanthan-free periods, the scientists analyzed the blood before and 2 h after an oral glucose load.

Figure 4: Effect of the guar (G), xanthan (X), locust bean gum (LBG), and 1: 1 mixtures of X and LBG (X/LBG) and X and Meyprodyn (X/Mey) on the movement of radiolabeled glucose in the mixture (concentrations in % | Edwards. 1987)

You can see the results of this undertaking in Figure 4. Basically, what the researchers found were...

• significant reductions in fasting and postload serum glucose and reduced fasting levels of total plasma cholesterol in diabetic subjects, as well as
• lower fasting and postload levels of gastrin and gastric inhibitory polypeptide (GIP) and fasting levels of total and VLDL triglyceride and cholesterol in VLDL and LDL fractions

Moreover, all subjects reported a sense of fullness after consuming xanthan muffins but no severe digestive symptoms. The latter will usually become more prevalent, when xanthan is mixed with other fibres like galactomannan in a (successful) effort to promote its anti-cholesterol effect (Yamamoto. 2000).

In view of the fact that mixing with (obviously) lower viscosity fibers will not necessarily increase the hypoglycemic (glucose improving) effects, of which Edwards et al. (1987) demonstrated that they depend almost exclusively on the viscosity of the chyme, it appears unwarranted to spend the extra bucks on galactomannan or other fibers... Unless you are battling high cholesterol levels and would like to see a similar beneficial effects on your blood lipids as the rodents in the Yamamoto study, of course.

Yes, xanthan will increase satiety and have beneficial effects on glucose metabolism. Whether it is a "necessary" addition to everyone's diet, on the other hand, is questionable. It's a supplement and supplements are, as their name implies "supplemental".

A single teaspoon will already make a protein shake really thick! And remem- ber: more xanthan = high viscosity = slow gastric passage, high satiety, but slow nutrient release

There are, moreover, also situations, where you may not even want to reduce the transit of a liquid meal through your digestive tract. After a workout, for example, xanthan should be used only people who go hypogylcemic in response to the whey (+sugar) induced insulin spike in response to their post-workout shake.

As part of a high protein snack, on the other hand it does really make sense to combine xanthan, whey and maybe some resistant starch (RS4) into a energy-laden power-"shake"... just be careful: If you use more than a teaspoon your "shake" will easily turn into a pudding and you can spoon-feed yourself a fluffy protein pudding ;-)

Reference:

• Beal, Jennifer, et al. "Late onset necrotizing enterocolitis in infants following use of a xanthan gum-containing thickening agent." The Journal of pediatrics 161.2 (2012): 354-356.
• Dikeman, Cheryl L., Michael R. Murphy, and George C. Fahey. "Dietary fibers affect viscosity of solutions and simulated human gastric and small intestinal digesta." The Journal of nutrition 136.4 (2006): 913-919. 
• Edwards, C. A., et al. "Viscosity of food gums determined in vitro related to their hypoglycemic actions." The American journal of clinical nutrition 46.1 (1987): 72-77.
• Eastwood, M. A., W. G. Brydon, and D. M. W. Anderson. "The dietary effects of xanthan gum in man." Food Additives & Contaminants 4.1 (1987): 17-26.
• Hoad, Caroline L., et al. "In vivo imaging of intragastric gelation and its effect on satiety in humans." The Journal of nutrition 134.9 (2004): 2293-2300.
• Jenkins, Alexandra L., et al. "Comparable postprandial glucose reductions with viscous fiber blend enriched biscuits in healthy subjects and patients with diabetes mellitus: acute randomized controlled clinical trial." Croatian medical journal 49.6 (2008): 772.
• Jenkins, Alexandra L., et al. "Effect of adding the novel fiber, PGX®, to commonly consumed foods on glycemic response, glycemic index and GRIP: a simple and effective strategy for reducing post prandial blood glucose levels-a randomized, controlled trial." Nutrition journal 9.1 (2010): 58.
• Kacinik, V., et al. "Effect of PGX, a novel functional fibre supplement, on subjective ratings of appetite in overweight and obese women consuming a 3-day structured, low-calorie diet." Nutrition & diabetes 1.12 (2011): e22.
• Marciani, Luca, et al. "Effect of meal viscosity and nutrients on satiety, intragastric dilution, and emptying assessed by MRI." American Journal of Physiology-Gastrointestinal and Liver Physiology 280.6 (2001): G1227-G1233.
• Mattes, Richard D., and Dana Rothacker. "Beverage viscosity is inversely related to postprandial hunger in humans." Physiology & Behavior 74.4 (2001): 551-557.
• Osilesi, Odutola, et al. "Use of xanthan gum in dietary management of diabetes mellitus." The American journal of clinical nutrition 42.4 (1985): 597-603.
• Paquin, Julie, et al. "Effects of juices enriched with xanthan and β-glucan on the glycemic response and satiety of healthy men." Applied Physiology, Nutrition, and Metabolism 38.4 (2012): 410-414.
• Reichert, Ronald G., et al. "Meal replacements and fibre supplement as a strategy for weight loss. Proprietary PGX® meal replacement and PGX® fibre supplement in addition to a calorie-restricted diet to achieve weight loss in a clinical setting." Biotechnology and Genetic Engineering Reviews 29.2 (2013): 221-229. 
• Tao, Wendy. "A clinical observational study on PGX® conducted at the Canadian Centre for Functional Medicine." Alternative Medicine Review (2010) 15.1: 68-75.
• Yamamoto, Yukiko, et al. "Improved hypolipidemic effects of xanthan gum-galactomannan mixtures in rats." Bioscience, biotechnology, and biochemistry 64.10 (2000): 2165-2171.

True or False: Vinegar Reduces Postprandial Glycemia And Insulin Response. Vitamin D Must Be Taken With Fat or It Won't Work. Chewing Gum Will Help You Get & Stay Lean

This is quite an extraordinary Wednesday! To make sure that you don't have to go without your beloved Science Round Up, Carl and I are doing the show one day early, which means that you better make sure to make some room for listening to the show at 1PM EST (listen live!), if you want to be the first to learn the truth about the

Is it possible that your significant other outpaces you on all cardio activities, because she has the hormonal edge?

• effects of soy protein supplementation on the endocrine effects of exercise
• psychological effects of performance enhancing drugs & supplements
• interaction between dietary salt & your bodies ability to store magnesium
• vitamin D "dosage equivalent" of two tanning bed sessions per week
• estrogen's fat burning prowess
• better (?) alternatives to testosterone gel

... and all the other great topics, you will be able to listen to after you've witnessed Alex aka Primalkid's premier (what an alliteration) as SuppVersity guest author. I suppose that most of you will already have noticed that he helps me more than just "a lot" by answering questions in the comment section. Oftentimes these are pretty individual things, but sometimes they are downright "True or False"-compatible - just as the mini-article on Vinegar, Alex sent me a couple of days ago.

Vinegar Helps Reduce Postprandial Glycemia and Insulin Spike

True (minimally edited answer written by Alex aka Primalkid) Recently, apple cider vinegar has earned merit as a health tonic. No longer sold solely as a condiment in grocery stores, more and more people see apple cider vinegar as a remedy. Its wide availability and affordability make it appealing to those who have browsed the Internet, read various diet books, or even read the label on the bottle, all of which make fame of its weight loss ability. But is there any truth about those "rumors" or do they belong to the same class of "repeat it until everyone believes it must be true" gems of dietary wisdom like the notion that "fat will reduce the insulin spike from a carby meal" (learn more about this one in the previous of "True or False")

The discussion following last week's installment of "True or False", particularly about the way generations of dieters have been fooled to believe that it was a good idea to drown your carbs in fat in order to minimize the insulin spike was probably the incentive for Alex to author his first (and maybe not last) SuppVersity article... well, a part of an article ;-)

A 2006 review of all relevant epidemiologic studies and clinical trials found that "many recent scientific investigations have documented that vinegar ingestion reduces the glucose response to a carbohydrate load in healthy adults and in individuals with diabetes" (Alex' emphasis in Johnston. 2006). The review also concluded that "vinegar ingestion increases short-term satiety."

A fairly recent randomized controlled trial seeking to investigate if a combination of cinnamon and vinegar would have an additive blood glucose-lowering or satiety-enhancing effect compared to the substances in isolation, however, "did not see an effect of acetic acid on blood glucose" (Mettler. 2009). The study consisted of 27 non-smokers 20 to 30 years old with normal BMI and fasting blood glucose. In other words, they may be considered healthy adults. The control meal consisted of 194g vanilla milk rice and 33g glucose dissolved in water, providing a total of 75g carbohydrates, 5g fats, and 7g protein, and was consumed after an overnight fast of at least ten hours.

The researchers concluded that "the most apparent difference between the studies was the food matrix with which the acetic acid or vinegar was ingested," and admit ignorance as to why the vinegar might work more or less in different contexts.

Table 1: Tabular overview of the design of the four trials in the 2010 study by Johnston et al.

Fortunately, the answer comes three months later when a group of researchers at The College of Nursing and Health Innovation sought to investigate the dosage, timing and application of vinegar for reducing postprandial glycemia (PPG) (Johnston. 2010). This study recruited both healthy and type-2 diabetic individuals, and had them consume either a meal (white bagel, 20g butter, 200g juice) or a glucose drink after a ten to 12 hour fast in four different trials.

• Trial one examined whether small amounts (2 – 20g) of vinegar had any glycemic effects.
• Trial two sought whether this effect persisted for five hours after consumption of the vinegar.
• Trial three looked at whether the type of carbohydrate influenced vinegar’s antiglycemic effect.
• Trial four looked at whether the neutralized salt of acetic acid was effective in diabetics.  

One detail I want to bring to your attention pertains trial 3 and could in fact explain why other studies failed to observe an antiglycemic effect of vinegar: In Mettler’s study, the control meal consisted of milk rice and a dextrose solution, both of which can safely be classified as "simple" sugars.

So, Johnston’s research suggests that the antiglycemic effect of vinegar is best realized when ingested with foods composed of complex carbohydrates and that vinegar may not attenuate PPG following the consumption of foods sweetened with corn syrups or dextrose, as is the case for many processed beverages and foods.

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Bottom line: Aside from the fact that the last mentioned limitation implies that taking your vinegar with junk food is pointless, it appears that apple cider vinegar may in fact earn a place among the list of truly "functional" foods. And while the real-world benefits may be more pronounced for people who do already have slightly suboptimal (or worse ;-) insulin sensitivity, a small amounts of vinegar (2tsp - doesn't really matter which type) taken with a whole foods based meal may be considered one out of many proven dietary manipulations for reducing PPG. 

No Fat No Vitamin D - Fat's Necessary to Benefit from High Dose Vitamin D

Probably false. I know that you will now be citing an older post of mine discussing a study that showed quite conclusively that the usage of supplemental vitamin D is hampered, if it is not ingested with a significant amount of dietary fat (see "A Fat D-Ficiency").

Now, a soon-to-be-published paper by a group of scientists from the Human Nutrition Research Center on Aging at Tufts University and the Division of Endocrinology, Diabetes, and Metabolism at the Tufts Medical Center put a huge question mark after the results of the 2011 study by Raimundo et al. who had used an almost identical protocol in 20 likewise healthy subjects.

Figure 1: Changes in serum vitamin D3 and storage form of D3 (25OHD, small grey-scale graph) in response to 50,000 IU of vitamin D with / without a meal with high or low fat content (Dawson-Hughes. 2013)

As you can see in figure 1, the low fat meal did yield an even more rapid incline in plasma vitamin D3 levels, after the 90-day follow-up period the net "gain" in terms of serum 25OHD was yet identical in all three groups and brought the sixty-two 50-69 yrs subjects who were enrolled in this 3-month study well into the >70 nmol/L range for 25OHD - and that irrespective of whether they had ingested their D3 tablet** on empty or with an egg or egg white frittata with low or high amounts of olive oil and vegetables, turkey bacon, and Parmesan cheese topping, a slice of toast with either jelly (low-fat meal group) or butter, and a mango milk smoothie (mango, milk, ginger ale) with or without cream.

Foods & the Sun are the natural vitamin D sources, listen to today's Science Round Up to learn more about the latter.

** Note: I mentioned this before on the Science Round-Up: You better don't put too much faith into what the label of your D3 supplement says. Even with the supplement used in the study (50,000 IU vitamin D3 tablets that were purchased from BioTech Pharmacal) there was a >10% difference between what the label said the tabs would contain (obviously 50,000IU) and the measured amount of 57,000 IU of vitamin D3 the tabs actually contained. In the aforementioned study by Garg et al,. one of the tested vitamin D3 tabs contained more than twice of the labeled amount (Garg. 2013).

Just like Dawson-Hughes and colleagues, I can only speculate about the underlying reasons for the differences between the study at hand and the Raymundo study. The scientists' hypothesis that the unexpectedly high and early increase in the high fat (25.6g) group of the study by Raimundo et al. could be attributable to "inadvertent sun exposure or supplemental vitamin D ingestion in the second half of that study", would yet be a plausible explanation. Another one could be the use of cabs instead of tabs, as they were used in the study at hand. After all, the content of the 50,000IU vitamin D cap Raimundo et al. have used is like to be released much more rapidly so that the fat may have been necessary to slow the gastric emptying and thus facilitate absorption.

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Bottom line: For you it does not really matter if you can ingest your vitamin D without fat. It's not the "better" alternative, so why would you bother anyway? So have it with a fatty meal, but don't forget that testing is not optional, but obligatory - I mean you do not even know how much vitamin D your Vitamin D product actually provides.

Chewing gum Helps to Get & Stay Lean (Note: This is just about regular chewing gum!)

True.  I know it may sound hilarious, but in view of the fact that research has shown "gum chewing is sufficiently exothermic that if a person chewed gum during waking hours and changed no other components of energy balance, a yearly loss of more than 5 kg of body fat might be anticipated." You can certainly argue that chewing of calorie-free gum, of which James Levin points out that it "can be readily carried out throughout the day", the "potential effect on energy balance should not be discounted" (Levin. 1999).

Mint chewing gums are incompatible to the "6x Bananas a Day!?" approach to lowering your glucose, insulin and HbA1c levels (learn more)

Chewing mint gums will reduce fruit consumption (Swobody. 2013) -- Why? Give it a try, I bet you will not recognize the delicious pineapple when you try to eat it right after you've been through a packet of Orbit Mint ;-) This may sound like it was not important, but it could in fact diminish or even blunt the effects of chewing gum... I mean think of Mr. Average Obese American at a barbecue. If he had not been chewing mint-flavored gum all the time, he may well have had his share of filling, refreshing & libido enhancing water melon before the barbecue was even ready to be served. Now that he missed on that, he will stick to the meat (+) and tons of salty junk (-). Not a good bargain, right?

Now, all of you know that I am no fan of the "calories in vs. calories out"-hypothesis Levin is referring to, here, but in view of the fact that chewing (sugar free!) gum has also been shown to

• 8% reduced food intake on a "snack break" and generally reduced cravings and perceived likelihood of snacking on sweet foods in 40 women and 20 men (21.7+/-4 years; BMI=22.7+/-3.4) who participated in a 2007 study at the Glasgow Caledonian University) who came to the laboratory four times for lunch and then returned 3 h later for a snack after either chewing gum or not chewing gum for 15 minutes before the snack break (Hetherington. 2007). 
• chewing gum will reduce the size of snacks even in moderately restraint eaters, although the effect is not as pronounced as it is in people who are not thinking about what and how much they are eating all day (Hetherington. 2011)

So, in general, it is probably advantageous to chew gum. The probability that it will result in significant weight loss is however small. A 2012 one of those pathetic randomized controlled trials, in the course of which the researchers provide their subjects with dietary advice and expect something to happen, the 102 of the 201 overweight and obese adults who were furthermore required to chew gum for at least 90min/day did not lose significantly more body weight or inches off their waist. Contrary to their non chewing gum chewing peers in the control group there was a greater heterogeneity so that only the difference to baseline reached statistical significance only in the chewing gum group.

If there is anything bad to say about chewing gums it would probably pertain to the (imho) not fully elucidated side effects xylitolm a proven "antimicrobial" (Mäkeläinen. 2007), could theoretically have on the gut microbiome, but since we do not know if that would be a detrimental and not even a beneficial effect (initial evidence exists, cf. Salminen. 1985), I just want to mention it as an "would be interesting to see more research in this direction". Possible artificial sweetener related distortions of the hedonic response to sweet foods, on the other hand, are not very likely... well, as long as you stick to the spearmint and peppermint varieties and refrain from those disgustingly sweet fruit gums.

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There may be more advantages of chewing gum. People with GERD / reflux disease, for example have been shown to benefit from chewing gum for 1 h after the meal. The effect lasted for up to 3 h and occured in both patients with and without chronic reflux disease (Avidan. 2001). Chewing gum has also been shown to reduce the symptoms of depression (Erbay. 2013), alleviate acute psychological stress (Scholey. 2009), and increase alertness on "intellectual" performance during regular intelligence tests (Smith. 2009; similar effects in previous studies with sugar- and artificially sweetened gums, cf. Stephens. 2004)

Bottom line: The Shikany study is actually a perfect example of what chewing gum can do for the average dieter. Although it overall effects on caloric expenditure are non-significant the act of chewing and what my friend Carl Lanore once aptly called "cleaning one's pallet" with a sugar-free peppermint gum can help you (a) not to return to the buffet, once you've decided that you've had enough and started chewing gum and (b) not grab another snack between your main meals.

Against that background, the statement "chewing gum can help you lose weight" is actually correct. What is yet a hilariously unrealistic expectation is that you would - just like Levin mentioned it in the initially cited letter to the editor - be able to lose X pounds of pure body fat per year, because chewing gum increased the caloric expenditure of the subjects in the Levine study by 12kcal per hour.

That's what people in Germany call a "Milchmädchenrechnung" or as you would call it, my dear American friends, "naive fallacy" - a type of naive fallacy which is unfortunately still pretty common especially among people who make not one, but two major mistakes and don't read the SuppVersity and listen to Super Human Radio ;-)

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That's it for the written part (don't miss the Science Round Up at 1PM EST, though!), I hope you enjoyed this installment of True or False and though I will be hard pressed to answer all the questions, just keep the suggestions coming. I will take the weekend to compile a detailed list to make sure I don't overlook any of them, when I tackle at least one of your suggestions in the future installments of this series.

References:

• Avidan B, Sonnenberg A, Schnell TG, Sontag SJ. Walking and chewing reduce postprandial acid reflux. Aliment Pharmacol Ther. 2001 Feb;15(2):151-5.
• Dawson-Hughes B, Harris SS, Palermo NJ, Ceglia L, Rasmussen H. Meal conditions affect the absorption of supplemental vitamin D(3) but not the plasma 25-hydroxyvitamin D response to supplementation. J Bone Miner Res. 2013 Feb 20.
• Erbay FM, Aydın N, Satı-Kırkan T. Chewing gum may be an effective complementary therapy in patients with mild to moderate depression. Appetite. 2013 Jun;65:31-4.
• Garg S, Sabri D, Kanji J, Rakkar PS, Lee Y, Naidoo N, Svirskis D. Evaluation of vitamin D medicines and dietary supplements and the physicochemical analysis of selected formulations. J Nutr Health Aging. 2013 Feb;17(2):158-61.
• Hetherington MM, Boyland E. Short-term effects of chewing gum on snack intake and appetite. Appetite. 2007 May;48(3):397-401.
• Hetherington MM, Regan MF. Effects of chewing gum on short-term appetite regulation in moderately restrained eaters. Appetite. 2011 Oct;57(2):475-82.
• Johnston CS, Steplewska I, Long CA, Harris LN, Ryals RH. Examination of the antiglycemic properties of vinegar in healthy adults. Ann Nutr Metab. 2010;56(1):74-9. 
• Johnston CS, Gaas CA. Vinegar: medicinal uses and antiglycemic effect. MedGenMed. 2006 May 30;8(2):61.
• Levine J, Baukol P, Pavlidis I. The energy expended in chewing gum. N Engl J Med. 1999 Dec 30;341(27):2100.
• Mäkeläinen HS, Mäkivuokko HA, Salminen SJ, Rautonen NE, Ouwehand AC. The effects of polydextrose and xylitol on microbial community and activity in a 4-stage colon simulator. J Food Sci. 2007 Jun;72(5):M153-9. 
• Mettler S, Schwarz I, Colombani PC. Additive postprandial blood glucose-attenuating and satiety-enhancing effect of cinnamon and acetic acid. Nutr Res. 2009 Oct;29(10):723-7. 
• Salminen S, Salminen E, Koivistoinen P, Bridges J, Marks V. Gut microflora interactions with xylitol in the mouse, rat and man. Food Chem Toxicol. 1985 Nov;23(11):985-90.
• Scholey A, Haskell C, Robertson B, Kennedy D, Milne A, Wetherell M. Chewing gum alleviates negative mood and reduces cortisol during acute laboratory psychological stress. Physiol Behav. 2009 Jun 22;97(3-4):304-12. 
• Smith A. Effects of chewing gum on mood, learning, memory and performance of an intelligence test. Nutr Neurosci. 2009 Apr;12(2):81-8.
• Shikany JM, Thomas AS, McCubrey RO, Beasley TM, Allison DB. Randomized controlled trial of chewing gum for weight loss. Obesity (Silver Spring). 2012 Mar;20(3):547-52.
• Stephens R, Tunney RJ. How does chewing gum affect cognitive function? Reply to Scholey (2004). Appetite. 2004 Oct;43(2):217-8; discussion 221-3.
• Swoboda C, Temple JL. Acute and chronic effects of gum chewing on food reinforcement and energy intake. Eat Behav. 2013 Apr;14(2):149-56.

Instant Coffee, Glycemia & Caffeine Powered Post-Workout Glycogen Repletion. Fish Oil, Arachidonic Acid Release & Prostaglandin Modulation. Adipocyte Sizes & Yoyo Dieting

Judged by the way they are looking at each other they don't care about their differential glucose / insulin response too coffee, but if you do, I suggest you scroll down and read the pertaining news item.

7.3% and 21.4%, those are the SuppVersity figures of the week. Figures that stand for the 2011 youth- and 2010 adult obesity rates in Colorado and they represent the nationwide "optimum" - at least according to CDC data from the respective years. Now, it was already hard to find US states with obesity rates below the nationwide average of 13% (youths) and 27.6% (adults). What is yet even harder or rather impossible is to dig up studies which try to elucidate why Colorado is the "leanest" of the 50 US states. Non-exhausting physical activity, for example, would be a candidate, but according to Wyatt et al. the "[e]ven in Colorado, one of the leanest states, very low levels of physical activity are seen in much of the population." (Wyatt. 2005).

Wouldn't it be worth taking some time to try to elucidate what the citizens in Colorado may be doing, their fellow Americans in Mississippi (highest adult obesity rate of 34.5%) or Alabama (highest youth obesity rates of 17%) ain't doing? Are they maybe having more or less fish oil or drinking only half the amount of caffeine? I don't know, but based on today's installment of "On Short Notice", you should be able to answer whether or not it is likely that factors like these could make a difference ;-)

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Coffee, Sex and Your Physique (Gavrieli. 2013) -- The latter two, i.e. sex and your physique are what determines your postprandial glucose and insulin concentrations after escalating dosages of caffeinated coffee. That's at least what Anna Gavrieli from the Harokopio University in Athens and her colleagues from overseas write in a soon-to-be-published paper.

To examine the effects of different amounts of coffee on blood glucose and insulin concentrations in the postprandial phase (after a meal) the scientist recruited thirty-three volunteers [16♀/17♂, 16 normal-weight and 17 overweight/obese, 27.3 ± 7.2 (19–44) y] who came to the lab fasted and obviously without having  had a "wake up coffee" early in the morning. When they arrived, the subjects received a standardized meal, i.e. a slice white bread, 5 g of butter and 10 g of white sugar, providing 142 kcal (6.5% of energy from proteins, 62.5% from carbohydrates and 31.0% from lipids) along with 200 mL of water or instant coffee containing either 3 or 6 mg of caffeine/kg body weight on three different occasions.

Figure 1: Usual and experimental caffeine intake in the subjects (left); effects on glucose metabolism after standardized "breakfast" (=sugar binge) + water or different dosages of instant coffee (Gavrieli. 2013)

As you can see in figure 1, the blood samples the scientists obtained before, immediately after and in regular intervals over the remaining 3 hours after the ingestion of the "breakfast" do support the hypothesis that men and women, light and heavy weights react very differently to the ingestion of 200-500mg.

So what's the verdict then? Is coffee the way to go?

Post workout caffeine supplementation?! Just like dieting, working out is one of the confounding factors which render results like the one at hand valid only in certain scenarios. Against that background it is not surprising that a 2008 study by Pedersen et al., the results of which I have plotted for you in the figure above (Pedderson. 2013), found statistically significant improvements in glycogen resynthesis w/ 8mg/kg caffeine being coingested with 4mg/kg glucose after a workout. Whether this will yield real world benefits is obviously another story ;-)

While coffee delayed the rise of insulin in response to the standardized meal and the fall of glucose concentrations from its maximum levels in the entire study sample, the glucose incremental area under the curve (IAUC) was not just different between the interventions (with both coffee amounts inducing a greater area compared to water, p = 0.009), but also varied according to the sex and body weight of the subjects:

"Secondary, subgroup analysis at the nominal level showed that this might be more evident among females (PIAUC = .05) and overweight/obese participants (PIAUC = .03). Furthermore, coffee, mainly the 6 mg dose, could be lowering insulin concentrations the first 30 min after its consumption compared to water in men and overweight/obese participants." (Gavrieli. 2013)

So what do we make of these results, now? Well, first of all, even if your breakfast does not deserve the name food, having a single regular sized cup of coffee is unlikely to to any harm. Reversing the ratio of breakfast to coffee on the other hand and having a "Sex & The City" breakfast with a croissant and a large cup of breakfast will have you run the risk of having high blood sugar afterwards (esp. if you drink that 400mg+ pot of coffee with tons of sugar).

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The tissue incorporation of regular triglyceride based fish oils is inferior to their phospholipid bound brethren. Want to learn more? Check out my article on that matter from June 2012 (learn more)

3g of fish oil modulate the eicasonoid production from omega-6 fatty acids in young men (Zulyniak. 2013) -- 2g of EPA and 1g of DHA that was the dosage the 10 young healthy males (23.4 ± 1.7 years) had to consume on every day of the 3-months supplementation period in Zulyniak et al.'s experiment which was designed to "better understand the potential health benefits of fish oil supplementation in young healthy males" (Zulyniak. 2013).

What the researchers observed were the expected decreases in serum triglycerides (-38%), a significant increase in the proportion of HDL-c relative to total cholesterol, as well as - and this is the actual news - an increase in eicosanoids production, namely prostaglandin-F2α (P < 0.0001) and thromboxane-B2 (P = 0.0296), after fish oil supplementation.

The latter two are products of omega-6 metabolism and confirm the replacement of arachidonic acid (AA, the long-chain omega-6 fatty acid and the quasi-analogon to DHA) in the cell membranes of the erythrocytes by EPA and DHA. This process must have triggered the increase in PGF2α and TXB2 production of which the scientists state that

On a side note: The results of this study don't change my opinion as far as the usefulness, let alone necessity of fish oil supplementation in healthy, athletic, fish eating SuppVersity readers is concerned. I don't see any.

"[...]previous work by both Boughton-Smith et al. and Scott et al. suggest that PGE2, PGF2α, TXB2, and 6-keto-PGF1α are the primary products of the COX2 pathway when AA is in abundance. Furthermore, Scott and colleagues suggested that with chronic elevation of AA, PGF2α and TXB2 production is more likely to be up-regulated due to their vasoconstrictive qualities, which would prevent the efflux of AA and other more-damaging eicosanoids from cells into circulation." (Zulyniak. 2013)

Whether this is actually a good thing does yet appear at least somewhat questionable to me and even Zulyniak et al. have to admit that future research was necessary to confirm "the production of eicosanoids capable of regulating vasoconstriction" and thus "substantiate this hypothesis" (Zulyniak. 2013). As you can see, we are still learning new stuff about things of which every disciple of Dr Oz believes he already knew everything.

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Study supports hypothesis that regression in adipocyte size during weight loss could be reason for fat loss plateaus and "walls" (Verhoef. 2013) -- As a seasoned SuppVersity veteran, you are probably aware of the possible influence the size of your fat cells could have on weight loss success, failure or stagnation (learn more).

In a previous post on the Yoyo effect, I already discussed some aspects of adipocyte morphology - including the way lower body fat tends to be more stubborn than upper body fat (read more)

A recent study from the Maastricht University does now offer further support for my previously expressed hypothesis that the reduction of adipocyte size that comes with profound weight loss in then formerly obese individuals could be at the heart of the weight loss plateaus and over-pronounced metabolic downregulation formerly obese individuals experience at way higher body fat levels than someone who has never been obese in his / her whole life. Verhoef et al. put a group of twenty-eight overweight (BMI 28-35kg/m²) healthy subjects on a very low energy diet for 2 months. The 500kcal/day period (50g carbs, 52g protein, 7g fat + multi-mineral supplement delivering the RDA of all nutrients) was followed by a 10-month period of weight maintenance.

Over the course of the low energy diet intervention period, the adipocyte size decreased by -16.7%, the body fat level, on the other hand dropped by only 4.7%. Still, the leptin levels plummeted from 20.3 to 13.1 µg/L and did not return to baseline in the course of the "weight maintenance" phase.

Figure 2: Relative changes (compared to baseline) in body composition, adipocyte volume and leptin after the dieting intervention and the miserable weight maintenance phase (Verhoef. 2013)

In how far the suppressed leptin levels were actually responsible for the fact that the "weight maintenance" phase turned out to be a very dirty, fat only bulking phase cannot be said, but we know from previous studies, that the process of shrinking in itself

"has been reported to generate cellular stress and the more [the adipocytes] shrink, the higher will be the resistance against increasing mitochondrial beta-oxidation via HADHsc [hydroxyacyl-Coenzyme A dehydrogenase] during follow-up." (Verhoef. 2013)

And as if that was not enough the slight increase in ATGL (lipolytic protein) and HADHsc in the "weight maintenance" phase are, as the scientists point out, indicative of the appearance of newly differentiated adipocytes that are are metabolically active contribute to an "improved physiological status", but could potentially make future weight loss (esp. the aesthetic one) even more difficult.

"Empty" adipocytes <> lower leptin <> more glucose-to-fat conversion <> rapid fat gain

If CLA worked in humans as it does in rodents, it could solve the "small adipocyte" problem (learn why)

Moreover, the glycolyctic and thus potentially glucose-to-fat conversion promoting enzyme Aldolase-C did not just distinguish the successful weight maintainers (low Aldolase-C) from the yoyo dieters (high Aldolase-C), it also correlated with the leptin production of the fat cells, of which we know from previous studies that it is in turn negatively correlated to their size (Skurk. 2007)... too complicated?

Ok, let's express it the other way around. The "emptier" your adipocytes are (=smaller size), the less leptin they will produce and the more likely they are to convert glucose to fat and stash that away in their empty "tummies".

Suggested read for those who want to dig further into the purported underlying effects of weight regain: Maclean PS, Bergouignan A, Cornier MA, Jackman MR. Biology's response to dieting: the impetus for weight regain. Am J Physiol Regul Integr Comp Physiol. 2011 Sep;301(3):R581-600.

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That's it for an allegedly too lengthy installment of "On Short Notice"... about as much a misnomer as the "weight maintenance" phase in the Verhoef study, I guess. Maybe some of today's Facebook news can make up for that? In the end news like

Want to make HIIT a hit for you? Not a problem, the SuppVersity holds all the information you need. Start out with the respective two post article series and descend into the archives, where you are going to find more about HIIT, how it compares to LISS and which different regimen have shown some promise in peer-reviewed research (learn more)

• High fat dieting reduces the beneficial effects of resistant starch - Reduction in abdominal obesity with 42% fat diet = zero (read more)
• HIIT hits home in 8 young, untrained men - 12 HIIT sessions lead to increased V02 kinetics (read more)
• Ice slurries are the new energy gels - Scientists observe significant increases in cycling performance (read more)
• Physical therapy as effective as surgery for a meniscal tear and osteoarthritis - Unfortunately patients are too lazy and the revenue for the doctors too small to be used more often (read more)
• Evolution is to blame for inflammatory disease - At least that's what the latest "paleo" research would suggest (read more)

are eventually the reason that the saturdaily short news are always so lengthy. The really short stuff is already on Facebook ;-)

References:

• Gavrieli A, et al. Gender and body mass index modify the effect of increasing amounts of caffeinated coffee on postprandial glucose and insulin concentrations; a randomized, controlled, clinical trial. Metabolism.2013 [ahead of print]
• Pedersen DJ, Lessard SJ, Coffey VG, Churchley EG, Wootton AM, Ng T, Watt MJ, Hawley JA. High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine. J Appl Physiol. 2008 Jul;105(1):7-13.
• Verhoef SP, Camps SG, Bouwman FG, Mariman EC, Westerterp KR. Physiological response of adipocytes to weight loss and maintenance. PLoS One. 2013;8(3):e58011.
• Wyatt HR, Peters JC, Reed GW, Barry M, Hill JO. A Colorado statewide survey of walking and its relation to excessive weight. Med Sci Sports Exerc. 2005 May;37(5):724-30.
• Zulyniak MA, et al. Fish oil supplementation alters circulating eicosanoid concentrations in young healthy men. Metabolism. 2013 [ahead of print]