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.

Shouldnt it be obvious that the "happy medium" must be the solution, when high protein leads to brittle bones, and low protein to frail muscle? Sure! But where is this "happy medium"?

Some of you may remember my recent Facebook post "High Protein Diet in the Firing Line. Rodent Study Says: Kidneys Are at Risk". It was based on a press release you could read on all the major science-news outlets on the Internet; a press release that will give the average reader the impression that the corresponding study by Aparicio et al. would "prove" that high protein diets will ruin your kidneys and eventually jeopardize your health (read more).

Another paper (Cao. 2014), Jose Antonio, the CEO of the ISSN and the editor of the ISSNs journal posted on Facebook yesterday, didnt get as much media attention, though.

No wonder, the message of this study is after all not in line with one of the fundamental arguments you will hear, whenever you question the allegedly necessary restriction of total protein intake to 0.8g/kg, maximally 1.2g/kg protein per kilogram body weight day in the current nutritional guidelines:

"[...S]hort-term consumption of high-protein diets does not disrupt calcium homeostasis and is not detrimental to skeletal integrity."

Thats not what you will learn at med-school and it is certainly not in line with the hysteria about protein intakes that are 2x or even 3x higher than the 0.8g protein per kilogram body weight we are supposed to consume. Apropos RDA, the subjects in the control group of the said study by Jay J Cao et al. consumed a diet that contained exactly those 0.8g/kg body weight thats supposed to be good for us. The 21 human guinea pigs in the treatment groups, on the other hand, consumed 2x and 3x more than the average dietitian would recommend and they did so for 31 days (Cao. 2014).

Figure 1: Protein intake (in g/day; left), mineral intake (in mg/day; middle)  and calculated renal acid load (in mEq; right) of 49 normal weight, healthy men (n=32) and women (n=7) who consumed normal (0.8g/day), high (1.6g/kg per day) and very high protein (2.4g/kg per day) energy restricted (40%) diets for 4 weeks (Cao 2014)

If you take a look at the PRAL values in Figure 1, you can see that math (not bio- or physiology!) tells us that this reckless practice could compromises the acid-base balance of the healthy, normal-weight subjects, whose energy restricted diets were modeled on the increasingly popular high protein weight loss diets.

Equations vs. experiments | PRAL vs. urinary calclium loss | theory vs. practive

The urinary analysis the scientists conducted does yet speak a very different language. There is, as the scientists emphasize in the discussion of the results no evidence that

Suppversity Suggested Read: "High protein diet = high protein loss" | more

"habitual consumption of dietary protein at levels above the RDA [would] significantly alter urinary calcium excretion, dietary calcium retention, or markers of bone turnover or BMD, despite increased urinary acidity. These results indicate that diets that are 2 or 3 times the RDA for protein are not detrimental to calcium homeostasis when calcium and vitamin D are consumed at recommended intake"

In that I would like to emphasis the importance of adequate calcium (min. 800mg/day) and vitamin D intakes (800-1000IU/day) and the fallacy of the word "habitual". The study at hand did not test the effects of "habitual" high protein consumption. It tested the effects of short-term (28 days) high protein consumption in a low calorie scenario, which is by definition less prone to produce adverse inflammatory and thus potentially pro-osteoporotic side effects (Mundy. 2007).

Not eating enough protein could increase bone loss, when youre dieting

In view of the fact that the evidence I am about to cite, stems from rodent model of postmenopausal bone metabolism, I deliberately used the word could in the headline of this paragraph. And still, the way in which the low protein diet  "negatively impacted bone mass and magnified the detrimental effects of vitD and/or estrogen deficiencies" (Marotte. 2013) in the pertinent study from the Buenos Aires University is particularly disturbing.
The (postmenopausal) women the scientists try to model with their ovariectomized rats (=rats whose ovaries have been removes) are after all one of the many patient groups who are advised to carefully control their protein intake to make sure that the additional acid load will not compromise their bone health even further and that in spite of the fact that there is ample evidence that the current RDA for protein is inadequate to maintain optimal health, particularly when the total energy intake is restricted and especially in populations who are susceptible to bone loss (Kerstetter. 2005; Chernoff. 2004).

Figure 2: We know for quite some time not that low protein diets decrease the absorp- tion of protein (Kerstteter. 2005). Its not certain if this is "just" a homeastatic me- chanism to stabilize the net/acid balance.

In their 2005 study, Kerstetter et al. were in fact able to show that protein intakes that are 2.6x higher than the RDA increase the effective absorption of calcium from the diet (see Figure 2).

This increase stands in contrast to the significant decrease in calcium absorption the researchers observed in the healthy young (age: 26y) women in the low protein arm (0.7g protein per kg body weight) of the study and should remind us that a reduction in protein intake is not going to stop the insidious loss of bone thats caused by the triage of low estrogen, no exercise and a diet that may be low in protein, but high in acid producing grains (Remer. 1995) and devoid of alkaline fruit and vegetables.

I could now go more into details, but I will just leave you with the notion that the "paleo diet" is, despite its high meat content, among the most kidney-, and above all bone-friendly diets we know. In fact, its fruit and vegetables content yield a net alkaline renal load, and will lead to significant improvements in urinary calcium excretion rates (Appelet. 1997; Frassetto. 2013).   

? Note: If you want more about the "Paleo connection" - let me know this (best on Facebook) and what you would be most interested in and I will address that in a future SuppVersity article.

References

• Aparicio, V. A., et al. "High-protein diets and renal status in rats." Nutrición hospitalaria: Organo oficial de la Sociedad española de nutrición parenteral y enteral 28.1 (2013): 232-237.
• Appel, Lawrence J., et al. "A clinical trial of the effects of dietary patterns on blood pressure." New England Journal of Medicine 336.16 (1997): 1117-1124. 
• Cao, Jay J., et al. "Calcium homeostasis and bone metabolic responses to high-protein diets during energy deficit in healthy young adults: a randomized controlled trial." The American journal of clinical nutrition 99.2 (2014): 400-407.
• Chernoff, Ronni. "Protein and older adults." Journal of the American College of Nutrition 23.sup6 (2004): 627S-630S. 
• Frassetto, L. A., et al. "Established dietary estimates of net acid production do not predict measured net acid excretion in patients with Type 2 diabetes on Paleolithic–Hunter–Gatherer-type diets." European journal of clinical nutrition 67.9 (2013): 899-903.
• Kerstetter, Jane E., et al. "The impact of dietary protein on calcium absorption and kinetic measures of bone turnover in women." Journal of Clinical Endocrinology & Metabolism 90.1 (2005): 26-31.
• Mundy, Gregory R. "Osteoporosis and inflammation." Nutrition reviews 65.s3 (2007): S147-S151.
• Remer, Thomas, and Friedrich Manz. "Potential renal acid load of foods and its influence on urine pH." Journal of the American Dietetic Association 95.7 (1995): 791-797.