ONLINE DRIVERS MEDIA

Does her hair hold the secret to her fitness body? Actually thats unlikely, but it appears possible that a hair analysis could reveals whats keeping you back from a similarly amazing physique.

Hair mineral analyses have been discredited by certain snake oil vendors who use them to sell their "oils" in form of an endless list of "essential" supplements youd have to take if you dont want to end up as dead as the hair they used to produce the analysis. Still, they share one big strength with the more expensive RBC or other cell tests: They give you an idea of your actual calcium, magnesium, sodium and potassium balance.

Much in contrast to serum levels, by the way. If those are off, its either due to an acute event (like diarrhea, for example ;-) or you have a real reason to be concerned. There is after all a really good reason these minerals are also called "electrolytes": They are heavily involved in the ion and thus charge-exchange that keeps your heart beating!
Before we get to the actual hair mineral analysis data, lets briefly have a look at another set of striking and not so striking differences between the "normal" subjects and those with established metabolic syndrome:

Figure 1: Serum mineral concentrations, visceral (VAT) and subcutaneous body fat and smoking status in subjects w/ and w/out metabolic syndrome (Choi. 2014)

If you take a closer look at the data in Figure 1 you will see that - aside from marginal, but statistically non-significant differences in serum phosphor - the often-checked total Ca, Mg, K, Na & Ph concentrations did not differ between the two groups.
Moverover, visceral fat was a much more reliable parameter to distinguish the healthy and unhealthy subjects than subcutaneous fat and... a bit to my surprise: Smoking appears to be associated with a lower metabolic risk than non-smoking.

Lets take a look at the hair analysis, now

Much in contrast to the serum levels, the hair mineral analysis did reveal significant inter-group differences and corresponding correlations:
Of all potentially toxic molecules the researchers measured only the levels of arsenic and lead differed significantly between the two groups. The concentrations of cadmium, mercury, and aluminum were not different between the two groups, on the other hand, did not.
References:

• Choi, Whan-Seok, Se-Hong Kim, and Ju-Hye Chung. "Relationships of Hair Mineral Concentrations with Insulin Resistance in Metabolic Syndrome." Biological Trace Element Research (2014): 1-7.
• Rowe, John W., et al. "Effect of experimental potassium deficiency on glucose and insulin metabolism." Metabolism 29.6 (1980): 498-502.

Insulin sensitivity is a necessary pre- requisite for much more than a profane set of sixpack abs.

You will probably have realized that the number of short-news like articles on the SuppVersity has been increasing as of late. The reasons for that are twofold: For one, its the fact that it pisses me off (sorry, but thats how it is) that all the interesting stuff I post on the SuppVersity Facebook Page disappears into an oblivion of which I can only hope that it is not Mark Zuckerbergs *** Secondly, I am currently working my regular job, doing some additional University stuff and working on another nutrition and exercise science related project and dont have the time to do the extensive research thats necessary to produce articles like part II of the "perfect frying oil" article, you may (rightly) already be waiting for.

In other words: If you dont want me to switch to a twice or thrice (max) a week schedule, you will have to live with less in-depth articles like this - sorry! If you would prefer a new schedule, on the other hand, let me know.

Artemisia dracunculus and Lixisenatide, two names to remember?

Actually the first of these names, namely Artemesia dracunculus is a herb you should be vaguely familiar with, if you remember an old SuppVersity article with the title "SuppVersity Supplement Scrutiny: Athletic Edge Nutrition Creatine RT - More Than Yet Another Marketing Gag?" (refresh your memories). In said article I acknowledged the insulin-sensitizing prowess of Tarragon extract, but doubted that its purported effects on the uptake of creatine into the muscle had any real-world relevance.

I guess, some of you will probably say the same of the observation that the tarragon bioactives "improved insulin sensitivity in diabetic-obese myotubes to the level of normal-lean myotubes despite the presence of pro-inflammatory cytokines" in a recent in vitro study by scientists from the Louisiana State University. Before you do so, I would yet like to remind you of the existing evidence that supports the insulin-sensitizing (Wang. 2011), muscle-preserving (Kirk-Ballard. 2013), anti-diabetic (Watcho. 2010; Eisenman. 2011;  Scherp. 2012),  as well as anti-NAFLD (Wang. 2013) and eye (Watcho. 2011) and nervous system protecting (Singh. 2014) effects of this herb.

If you still dont trust a supplement that failed you once,...

there is obviously still BigPharmas answer to herbal supplements: Lixisenatide, a synthetic GLP-1 analogon that has just demonstrated that it could be the future of (type II) diabetes treatment.

Lixisenatide comes in a fool-proof pen - what else?

In a study that was conducted by no one else than the inventors over at Sanofi-Aventis in Frankfurt, Germany, injecting the drug subcutaneously 2 hours before an intravenous glucose challenge accelerated the disposal of glucose to "nearly physiological intensity" (Becker. 2014) - in other words: The mere injection of the GLP-1 analog reduced the insulin requirements of the diabetics to zero and helped push the glucose into the cells at a rate thats identical to the one of non-diabetics.

In view of the fact that it did not impair the counter-regulation to low glucose levels by glucagon, its probably just feasibility question (can you time it properly), if and when at least some diabetics will have Lixisenatide pens (see image to the right), instead of insulin syringes in the neat "I want that piece of cake now, so I have to inject tons of insulin"-bags they are carrying wherever they go.

And if you dont do drugs, ...

... a very simple and, as a recent study appears to confirm, effective way to improve your glucose management would be to increase your intake of calcium containing foods and/or "hard" (=high calcium) water around meals.
Why? Well, as a SuppVersity veteran you should actually remember that rumors had it for years that a high calcium intake would help with weight loss, but the observations in corresponding experiments were mixed and the contemporary scare about the connection between calcium supplements, on the one hand, and cardiovascular heart disease (CHD) and/or prostate cancer, on the other hand, put another question-mark, this time one that corresponds to safety issues, behind the "calcium for weight loss" paradigm.

Figure 1: Relative serum / blood levels of GIP, GLP-1, insulin, glucose, lactate and NEFA after meals with high calcium content compared to isocaloric meal w/ identical macronutrients w/ low calcium (Gonzalez. 2013).

Now, the results of a recent study from the Northumbria University in the UK wont make this question.mark disappear. What they definitely do, though, is clarify the underlying mechanism of action, which is - and this should be obvious, when you look at the data in Figure 1 - mediated by the calcium-induced 47 % and 22 % increases in GIP1–42 and GLP-1 respectively (Gonzalez. 2013).

Figure 2: Overview of the purported anti-obesity + anti-diabetic effects of calcium + vitamin D (Soares. 2014)

In conjunction with the 19 % increase in insulin areas under the curve for the 120 min following consumption of the macronutrient-matched meals these hormonal changes induced a 12 % reduction in appetite in the 10 healthy male subjects.

The combination of increased insulin levels and improved blood glucose clearance, on the one, and an increased production of the fat-burning satiety hormone GLP1, on the other hand, renders these observations interesting for both: The overweight, insulin resistant couch potato and the normal-weight individual on his / her way to a physique model body.
Reference:

• Becker, et al. "Lixisenatide Resensitizes The Insulin-Secretory Response To Intravenous Glucose Challenge In People With Type 2 Diabetes – A Study In Both People With Type 2 Diabetes And Healthy Subjects." Diabetes, Obesity and Metabolism (2014) - Accepted Article.
• Eisenman, Sasha W., et al. "Qualitative variation of anti-diabetic compounds in different tarragon (Artemisia dracunculus L.) cytotypes." Fitoterapia 82.7 (2011): 1062-1074. 
• Gonzalez, Javier T., and Emma J. Stevenson. "Calcium co-ingestion augments postprandial glucose-dependent insulinotropic peptide1–42, glucagon-like peptide-1 and insulin concentrations in humans." European journal of nutrition (2013): 1-11.
• Kirk-Ballard, Heather, et al. "An extract of Artemisia dracunculus L. inhibits ubiquitin-proteasome activity and preserves skeletal muscle mass in a murine model of diabetes." PloS one 8.2 (2013): e57112.
• Scherp, Peter, et al. "Proteomic analysis reveals cellular pathways regulating carbohydrate metabolism that are modulated in primary human skeletal muscle culture due to treatment with bioactives from< i> Artemisia dracunculus</i> L." Journal of proteomics 75.11 (2012): 3199-3210.
• Sakhaee, Khashayar, et al. "Meta-analysis of calcium bioavailability: a comparison of calcium citrate with calcium carbonate." American journal of therapeutics 6.6 (1999): 313-322.
• Singh, Randhir, Lalit Kishore, and Navpreet Kaur. "Diabetic peripheral neuropathy: Current perspective and future directions." Pharmacological Research 80 (2014): 21-35. 
• Soares, Mario J., Kaveri Pathak, and Emily K. Calton. "Calcium and Vitamin D in the Regulation of Energy Balance: Where Do We Stand?." International Journal of Molecular Sciences 15.3 (2014): 4938-4945.
• Vandanmagsa, B. et al. "Artemisia dracunculus L. extract ameliorates insulin sensitivity by attenuating inflammatory signalling in human skeletal muscle culture." Diabetes, Obesity and Metabolism (2014) - Accepted Article.
• Wang, Zhong Q., et al. "An extract of Artemisia dracunculus L. enhances insulin receptor signaling and modulates gene expression in skeletal muscle in KK-A y mice." The Journal of nutritional biochemistry 22.1 (2011): 71-78.
• Watcho, Pierre, et al. "High-fat diet-induced neuropathy of prediabetes and obesity: effect of PMI-5011, an ethanolic extract of Artemisia dracunculus L." Mediators of inflammation 2010 (2010).
• Wang, Zhong Q., et al. "< i> Artemisia scoparia</i> extract attenuates non-alcoholic fatty liver disease in diet-induced obesity mice by enhancing hepatic insulin and AMPK signaling independently of FGF21 pathway." Metabolism 62.9 (2013): 1239-1249.
• Watcho, Pierre, et al. "Evaluation of PMI-5011, an ethanolic extract of Artemisia dracunculus L., on peripheral neuropathy in streptozotocin-diabetic mice." International journal of molecular medicine 27.3 (2011): 299-307.

Asian foods are low in SFAs. So the researchers had to add it to the pan.

From a physiological perspective, the observation researchers from the Nakamura Gakuen University, the  Akita University, the Chiba University and the University of Copenhagen appear counter-intuitive, why should fat increase the insulin response to a meal. The presence of fat in a meal should slow down the absorption of glucose, right?

Obviously you havent read my previous article on the fallacies of adding fat to glucose in the false believe that the reduced digestive speed would reduce the post-prandial insulin spike ("True or False? Adding Fat to A Carby Meal Lowers Insulin Response." | read more) - a highly suggested read you may want to read either, before or after you devour todays SuppVersity article.
Dont worry, todays article still has something new to offer. While the previously reported data dealt with acute responses to high(er) fat meals, Itoh et al. (2014) whose study is available as an "ahead of print paper" on the website of Nutrition Research, looked at the effects of sub-chronic, not acute high saturated fat intakes.

Figure 1: Graphical overview of the procedure  (Itoh. 2014)

In that, they conducted an intervention study to investigate the insulin and plasma GIP responses in 11 healthy women, including a dietary control. Subjects were provided daily control meals (F-20; saturated fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P] ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental meals for 7 days each. All meals were standard Japanese meals, the recipes for both experimental meals were identical, only a different cooking oil was used.
Talking about "test meals" (I dont like to call them thus, as they were consumed for a couple of days and not just for a "test), these meals comprised 60 E% carbohydrate, 15 E% protein, and 30 E% fat with the fat being distributed as follows:

• in the high saturated fatty acid meal (FB-30): S/M/P, 5:4:1; 
• in reduced saturated fatty acid meal (F-30): S/M/P, 3:4:3

Tests were conducted after two days on the FB-20 meal (pre) and at the end of the FB-30 and F-30 phases (see Figure 1), before and 30, 60, and 120 minutes after a meal tolerance test.

Figure 2: Comparison of glucose, insulin, and C-peptide levels after the control, F-30, and FB-30 meals (Itoh. 2014)

Interestingly, the plasma glucose responses did not differ between F-20 and FB-30 or F-30. The insulin levels, on the other hand, were higher after the FB-30 than after the F-20 (P<.01).

The GIP response, i.e. the response of the non-satiating non-fat burning insulin release triggering brother of GLP-1 (learn more) that does neither reduce hunger, not appetite nor improve glucose control (increased amount of insulin used to store away the same amount of glucose; cf. Edholm. 2010), after the FB-30 was higher than that after the F-30 (P< .05).

"In addition, the difference in the incremental GIP between FB-30 and F-30 correlated significantly and positively with that of the insulin." (Itoh. 2014)

The scientists believe that their results clearly prove, what scientists have believed for quite some time, now: "a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion." (Itoh. 2014)
References:

• Boden, Guenther, et al. "Mechanisms of fatty acid-induced inhibition of glucose uptake." Journal of Clinical Investigation 93.6 (1994): 2438.
• Edholm, T., et al. "Differential incretin effects of GIP and GLP?1 on gastric emptying, appetite, and insulin?glucose homeostasis." Neurogastroenterology & Motility 22.11 (2010): 1191-e315.
• Itoh, Kazue, et al. "High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals." Nutrition Research (2014).
• Nuutila, P., et al. "Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo." Journal of Clinical Investigation 89.6 (1992): 1767.
• Roden, Michael, et al. "Mechanism of free fatty acid-induced insulin resistance in humans." Journal of Clinical Investigation 97.12 (1996): 2859.