Paleo Diet + Kitchen-Sink Micronutrient Supp Sends Type II Diabetes into Remission | 14/17 Subjects Normalize HbA1c

I guess that would qualify as a "variation of the paleo diet", as well. 

No, this is not an advertisement for a diet book. In fact, the "variation" of the paleo diet the Canadian + US researchers used doesn't even require a cookbook, because it's as simple as "consisting of meat and vegetables, three times per day for three to five months" and "whole low glycemic fruit and nuts or seeds" as snacks between the meals  (Christensen 2017).

That I still expect some people to call the study "shady", though, is the use of Apex dietary supplements in those of the subjects with a predetermined micronutrient deficiency (I wouldn't mind that - what I do mind, though, is that the scientists do not explicitly declare if they received funding by Apex and 'forget' to report 36 of 38 lab values they claim to have tested).

As you would expect it from a "paleo diet", dairy was not on the menu

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Before you get overly mad at the researchers, let me say that I personally believe that the kitchen sink supplement combination (with vitamins and minerals no one really needs and minuscule amounts of everything that has a single rodent study to support its usefulness in T2DM | see Table 1) probably didn't contribute significantly to the success of the intervention.

Table 1: The Apex supplements used in the study at hand follow the highly popular (and at least as questionable) kitchen sink approach to micronutrient supplementation (ingredients according to Christensen 2017).

I mean, 40mg of taurine per serving? Studies show effects in T2DM with 6000mg per day. Or 20mg of NAC? Well, at least that's enough not to blunt your gains ;-)... Enough of the sarcasm, though, let's take a look at some tables/lists that actually matter:

Figure 1: Overview of the food groups (and respective foods) the subjects were allowed to eat.

The list of foods the subjects (11 females, 6 males | average age 69.7 ± 1.8 years) were allowed to eat (illustrated in Figure 1) looks pretty much like classic paleo: no dairy, for example,... on the other hand beans and peas are not exactly what paleo fanatics would eat voluntarily (esp. not unsoaked and sprouted ;-) -- be that as it may, what is important is, after all, that the diet had significant beneficial effects on the two most important of the 38 tested laboratory values (albumin, alkaline phosphatase, ALT, AST, bilirubin, bun and creatine, calcium, carbon dioxide, total CBC, chloride, c-reactive protein (CRP), creatine, ferritin, fibrinogen activity, glucose, GGT, hemoglobin (HbG) a1c, homocysteine, iron/TIBC, LDH, lipid panel, magnesium, phosphorus, citrated blood potassium, protein, sodium, TSH, T4 (free and total), T3 (free and total), T3 uptake, thyroglobulin antibody, thyroid peroxidase antibody, uric acid, serum urinalysis, vitamin D), i.e. the subjects' average glucose levels and the long-term blood glucose gauge HbA1c:

Figure 2: Changes in mean glucose and HbA1c in T2DM subjects and untreated (healthy) controls (Christensen 2017).

As you can see, significant reductions were achieved in both, the average glucose and the HbA1c levels. In fact, in 14 out of 17 subjects, the reduction of the A1C brought them out of the 6.5% - impressive for something as simple as cleaning up your diet.

In all fairness, though, it has to be said that the diet didn't to all that on its own... and no, I am not referring to the stupid supplement again, but rather to the fact that all diabetic participants received
diabetic medications while blood sugar A1C levels were above 6.5%. It would thus be haphazard to simply drop your medication, because "dat SuppVersity study shows that paleo cures T2DM, anyway". You understand?

Not a diabetic but trying to shed belly fat? Try this SV Classic: "10 Days of 'Paleo Life in the Wilderness' Will Strip up to 18 cm off Your Waist and Boost Your Insulin Sensitivity by 53%" | more

What are the implications? While we cannot be sure if and to which extent the multi-ingredient supplement contributed to the subjects' dieting success, the assumption that it had more than a minor additive effect to the diet (even the authors don't claim that) would be nothing but an unsustainable marketing claim.

Accordingly, the take-home message of the study at hand is not that an overpriced kitchen sink multi-micronutrient product, but a few months on a paleo diet, consisting of meat protein and vegetables, low glycemic fruit and nuts, can reduce the Hb1Ac of older male and female type II diabetics so significantly that, by definition, they would no longer be considered "diabetic" (<6.5%).

Next to the dubious supplementation regimen, the study does yet have another weakness: using healthy individuals who were not even changing their diet as control is like using no control at all. Furthermore, the authors fail to report the rest of the results (see the long list of blood markers they assessed) and do not disclose/negate a potential conflict or interest. A valuable control group would have been forced to adhere to another diet that has been associated with successful T2DM reversal like a high protein Mediterranean diet or (warning sarcasm inbound) the useless high carb + low-fat diet doctors will still prescribe to ensure that their patients are coming back for another prescription of their diabetes drugs | Comment!

References:

• Christensen, Kim D., and Karen Vieira. "A variation on the ‘Paleo’diet and its potential role in type 2 diabetes control."Sky Journal of Medicine and Medical Sciences Vol. 5(2), pp. 008 - 014, March, 2017

Each +30 Min/d of Physical Activity Reduce HbA1c by 11%, Protein + CHO Maintain Bone Mass, Overlooked Benefits of BFR, New Marker of Overtraining - Jan '17 Science Update

  This is what the Jan '17 Science Update has to offer? -11% HbA1c reduction per 30 minutes activity, new benefits of blood flow restricted tr., the bone protective effect of immediate post-workout whey plus carb ingestion, and a new overtraining gauge...

It's almost, February... almost and that's why today's SuppVersity article still qualifies as a January '17 research update. One that is based on the latest (ahead of print) papers from the peer-reviewed journal "Medicine & Science in Sports & Exercise" - papers about the large impact of short bouts of moderate-to-vigorous physical activity (MVPA) on the messed up glucose management of people with an increased T2DM risk, the bone-preserving effects of a mix of whey and dextrose and how this effect depends on timing, the belated and thus overlooked beneficial effects of blood flow restriction on muscular rapid force development and, last but not least, a potential new marker of overreaching and -training that could also explain the dichotomous role of IL-6 in the adaptive and maladaptive response to exercise.

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• Scientists find new marker of overreaching and potentially -training: You know that exercise will increase the levels of the allegedly "bad" cytokine IL-6. Now, as a SuppVersity reader, you will yet also know that this "cytokine" is, in fact, a "myokine" if it is released in response to muscle contractions and that it appears to figure in the hormetic response to exercise stress... or, in other words, without it, you're not going to get the adaptational response in form of strength and size gains you're training for. With that being said, studies also show that significantly elevated levels of IL-6 can also occur with overtraining and are - in this situation - a sign of dysfunctional adaptation.
  
  Recent research does now suggest that the "dichotomous nature of IL-6 signalling appears to be determined by the respective concentration of its receptors (both membrane-bound (IL-6R) and soluble (sIL-6R) forms)" (Cullen. 2017) - measuring these concentrations could thus provide important information about whether the circulating IL-6 is going to trigger a hormetic response or not. Accordingly, Cullen et al. conducted a study that investigated the response of sIL-6R to long-term training, and the relationship between sIL-6R, self-reported measures of wellbeing, and upper respiratory illness symptoms (URS) in highly-trained endurance athletes.
  

  

  Figure 1: Unlike cortisol, which has a long history as a suspected, but rarely useful overtraining gauge, sIL-6R doesn't have a circadian rhythm (see explanation in green box). This doesn't mean it's an accurate marker of overtraining, but it does mean that it is less complicated and more convenient to use, because with overtraining the circadian rhythm can be so messed up that simply measuring at the same time won't suffice to get comparable and thus useful results to gauge your training status.

  Their results are quite conclusive: Firstly, they confirmed that sIL-6R is responsive to prolonged periods of exercise training. And second- and more importantly, the subjects' sIL-6R levels varied according to the individual training volume and could be linked to common symptoms of overreaching such as high levels of stress, and/or depressed mood.
  
  This is obviously not enough to use sIL-6R as an overtraining gauge. With future studies that determine the level of sIL-6R in overreaching and overtraining athletes, it may thus be possible to distinguish between these states (and regular training) and to use this information to optimize athletes and gymrats workout routines. 
• Rapid Force Capacity (RFC) increases sign. with blood flow restriction, but study shows: Adaptation takes time: This observation Nielsen, et al. (2017) made in their recent study is an important one, because it implies that previous studies on the effects of blood flow restriction + low-intensity training may simply have missed the beneficial effects when they measured (just as Nielsen, et al. did it, too), the adaptational response only 5 days after having subjects participate in a series of standardized workouts.
  
  In the study at hand, this series constituted of twenty-three training sessions which were performed within 19 days. In all 10 male subjects (22.8+/-2.3 years) who performed four sets of knee extensor exercise (20%1RM) to concentric failure during concurrent BFR of the thigh (100mmHg), and the eight work-matched controls (21.9+/-3.0 years) who trained without BFR (CON), the scientists tested the maximal slow and fast knee joint velocity muscle strength and rapid force capacity (e.g. RTD) as well as evoked twitch contractile parameters before and after the study.
  

  

  Figure 2: Changes in rate of force development (left) and mean muscle fibre area (right | Nielsen. 2017).

  Now, that's nothing new. What was new, however, is that they tested before (Pre) and 5 and 12 days after training (Post5, Post12). In conjunction with the data from the biopsies, Nielsen et al. were thus able to detect the improved rate of torque development for the first time. The sign. difference in muscle fiber area (Figure 2, right), on the other hand, is - interesting as it may be - no news: after all, we're comparing light load with BFR to light load w/out BFR and not, as many other studies did, light load BFR to regular high load training, where time and again the regular training group saw the greater muscle increases.
• Each extra 30 minutes of daily moderate to vigorous physical activity improve HbA1c of subjects at increased T2DM risk by 11%: MVPA aka "moderate to vigorous physical activity" is the buzzword of the fitness tracker generation. Now, a three-year study confirms what the medals your fitness tracker software will award to you already suggested: each minute spend moving at moderate to vigorous intensity is an investment into your health and well-being.
  
  

  

  How Accurate Are Activity Trackers? EE Data From Omron, Fitbit, Jawbone & Other Devices Reveals 10% Error & More | read the full SV article

  The above is the result of a recent study that correlated longitudinal (three-year follow-up) activity tracker data with changes of the long-term glucose marker HbA1c in a sample of 489 men and women at high risk of developing type II diabetes, participants (mean age 64.2 +/- 7.3 years, BMI 31.7 +/- 5.1, 63.4% male). And it's a result based on which the authors, Mathew McCarthy, and colleagues, rightly conclude that "[i]ncreases in MVPA and body weight were associated with a reduction and increase in HbA1c respectively, particularly in those with dysglycemia" (McCarthy. 2017).
• Immediate Protein + CHO post-workout nutrition protect your bone from the bone resorption in the hours after exhaustive running: Next to its important result, there are two things which make a recent study by Rebecca Townsend et al. particularly interesting. Firstly: The subjects were young, healthy men, not post-menopausal women as in so many other bone health studies; and second- and not less importantly, the study tested both the efficacy of a mix of 1.5g/kg dextrose + 0.5g/kg whey as a means to reduce bone resorption (=calcium leeching) markers and the effects of timing.
  

  

  Figure 3: Overview of the study design, note that active treatment or PLA were administered at three different time points with two servings of placebo ensuring that the subjects could not differentiate between the immediate supplementation, the 2h-post and 4h-post supplementation trial (Townsend. 2017).

  And guess what. The study, in the course of which the dextrose + whey drinks were administered either before or after a placebo drink immediately or 2h after the run (see Figure 3) did not just confirm that the nutrient mix can ameliorate and shorten the exercise-induced (75% VO2Max run to exhaustion) increase in the bone resorption markers β-CTX and P1NP, it also found that this effect is time-dependent with the administration of the dextrose + whey mix right after the workout having more beneficial effects than taking it 2h post. With the immediate consumption reducing the levels below pre-exercise levels (-22% to -61%) within 1h, while it remained elevated with the placebo drink and/or in the DF group in which the supplement was consumed 2h after the workout. Now all that could well be a mere time-shift in the bone anabolic response. The scientists' observation that "[t]he overall β-CTX response was significantly lower in the IF trial than the DF trial (P=0.019, d=0.37) and the PLA trial (P≤0.001, d=0.84)" (Townsend. 2017) does however clearly suggest a definite benefit of immediate (IF) vs. postponed (DF and PLA) nutrient consumption after exhaustive workouts.
  
  In this context, however, it is important to realize that that, eventually, i.e. 3-4h after the run, the level of β-CTX decreased to similar below pre-test levels in all groups. Practically speaking this means that the net effect of a single session of exhaustive exercise on the young men's bone was almost certainly positive, irrespective of whether and when they ingested the supplement.

What's the take away of the studies in this Science Update: For me personally, the most important lesson comes from the MVPA study by McCarthy et al. (2017). A mere 30 minutes of "exercise" (even fast walking would qualify) is after all an easily manageable workload of that will contribute to statistically and, more importantly, clinically significant improvements in blood glucose management.

Drop the weights, grab the shake! Timing matters for advanced trainees.

Sort of surprising was the time-dependence of the beneficial effects of a dextrose + whey mix on bone resorption after exhaustive running in young male subjects. As I hinted at in the discussion of the study, however, we got to be careful not to mistake a timeshift in the response for an actual improvement.

Imho, future (best longitudinal studies) should investigate the net effect on bone mass to avoid a similar confusion as we've had them for protein supplements of which the majority of studies refutes that their ingestion in the immediate vicinity of the workout would improve your gains.

Last but not least, there's Nielsen's BFR study, which doesn't just prove another hitherto overlooked benefit of blood flow restricted low-intensity training, but also constitutes a lesson in study design, which reminds us that the timing of a retest will often determine if you find an effect or not. Apropos timing, while the latter may matter less for sIL-6R data than it does for cortisol, there's still a lot of research necessary to confirm the validity of this new marker of overreaching and -training and develop reliable tests for athletes and gymrats | Comment on Facebook!

References:

• Cullen, Tom; Thomas, Andrew W.; Webb, Richard; Phillips, Thom; Hughes, Michael G. "sIL-6R Is Related to Weekly Training Mileage and Psychological Well-being in Athletes." Medicine & Science in Sports & Exercise: Post Acceptance: January 24, 2017.
• McCarthy, Matthew; Edwardson, Charlotte L; Davies, Melanie J; Henson, Joseph; Gray, Laura; Khunti, Kamlesh; Yates, Thomas. "Change in Sedentary Time, Physical Activity, Bodyweight, and Hba1c in High-Risk Adults." Medicine & Science in Sports & Exercise: Post Acceptance: January 24, 2017.
• Nielsen, Jakob Lindberg; Frandsen, Ulrik; Prokhorova, Tatyana; Bech, Rune Dueholm; Nygaard, Tobias; Suetta, Charlotte; Aagaard, Per. "Delayed Effect of Blood-Flow-Restricted Resistance Training on Rapid Force Capacity." Medicine & Science in Sports & Exercise: Post Acceptance: January 23, 2017. 
• Townsend, Rebecca; Elliott-Sale, Kirsty J.; Currell, Kevin; Tang, Jonathan; Fraser, William D.; Sale, Craig. "The Effect of Postexercise Carbohydrate and Protein Ingestion on Bone Metabolism." Medicine & Science in Sports & Exercise: Post Acceptance: January 24, 2017.

Cinnamon as Nutrient Partitioner and 1st-Line Treatment for Pre-Diabetes? 5% Decrease in Fasting Glucose per Month in Human Studies, Up to 24% in 40 Days W/ High(er) Doses

Yes, that's how real cinnamon look like. It does not grow as powder in plastic boxes on trees as I suspect the members of the generation McBurgerSubway believe ;-)

No, this is not absolutely new. In fact this is just "another" SuppVersity articles on the anti-diabetic effects of cinnamon, but I promise it's going to be the most comprehensive one. One that discusses the currently available evidence from human trials, as well as the things we know and believe to know about how cinnamon acts its anti-diabetic magic qualitatively and quantitatively.

Before I even go into further details, though, I would like to address one of the "cinnamon myths" that says that only the highly expensive Ceylon or Sri Lankan Cinnamon would do the trick, while the commonly sold Cinamon cassia would be useless or even dangerous due to its high (and in fact toxic) coumarin content.

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Interestingly, all human studies have been done with the "cheap toxic stuff from the supermarket". In view of what you are about to learn about its effects on blood glucose later in this article, the first take-home-message from today's article is thus: "Cheap cinnamon cassia will work just fine as a blood glucose management supplement!" Unfortunately, long-term studies the safety of "common cinnamon" with its highly variable coumarin content (0.31 g = harmless to 6.97 g = potentially dangerous per kg raw powder | Wang. 2013 | see Table 1) are non-existent.

Table 1: Content of Coumarin 1, Cinnamyl Alcohol 2, Cinnamaldehyde 3, Cinnamic Acid 4, Eugenol 5, Cinnamyl Acetate 6 in Cinnamomum Species and Commercial Samples (g/kg) | DUL = Detected under limits of quantitation; ND = not detected (Wang. 2013).

The only advise I can give you is thus to rely on supplements with standardized (low to non-detectable) amounts of this potentially carcinogenic substance (Wang. 2014) if you plan to take it regularly for years. Using the next best cinnamon powder from the supermarket next door on the other hand is probably not advisable even though some of the scientists who conducted the studies Arjuna B. Medagama reviewed for his (or her?) latest paper in Nutrition Journal (Medagama. 2015) probably did just that: Buy cinnamon powder from the supermarket next door to test its effects on blood glucose management in 40-days- to 4-months-studies in cinnamon-naive patients with (pre-)diabetes.

If you take a closer look at the data, though, it becomes obvious that some studies used plain cinnamon powder, while others used regular or commercial water-extracts (CinSulin. Anderson).

Effect of 6g of cinnamon on post-prandial blood glucose in healthy subjects (Hlebowicz. 2007). This hefty dose also slowed down gastric emptying and triggered non-significant increases in satiety in 14 healthy subjects after high CHO meals.

What's the optimal dosage? Even though the overview in Figure 1 suggests that "more helps more", Anand, et al. (2010) observed negative effects on the liver of rodents at dosages that would tantamount to ~40g of cinnamon per day. Ok, I assume you already apprehended that this is madness, but in the world of fitness maniacs and mad bodybuilders I thought it would be worth mentioning that even the coumarin free Ceylon cinnamon appears to have ill side effects when it is consumed in extremely high dosages. It would thus appear to be more reasonable to target an intake of 3-6 g of cinnamon with every major meal (it slows down gastric emptying and reduces postprandial blood glucose, therefore it makes sense to take it with a meal | Hlebowicz. 2007, see Figure to the left).

If you scrutinize the results I've plotted for you in Figure 1, you will notice that (a) the improvements in fasting blood glucose were significantly more pronounced than those of the long-term blood sugar maker HbA1c, that (b) the former appear to increase with the dosage that was used (Klan and Mang observed the highest reductions and used the highest amounts of cinnamon powder), and that (c) the reductions in HbA1c take time, i.e. several months and are not guaranteed, even if there are significant reductions in fasting blood glucose (cf. Belvins).

Figure 1: Relative changes in fasting blood glucose and HbA1c levels of pre-diabetic subjects (Medagama. 2015)

On average, the fasting blood glucose levels of the study participants in all studies decreased by 4.7% in four weeks; the HbA1c, on the other hand, by only 1%. Since part of the effects on blood glucose are merely a results of the reduced gastric emptying and will thus affect the peak values, yet not the overall glycemia, it appears logical that the HbA1c reacts slowly to the intervention. As Medagama points out, the effects of cinnamon are yet more far-reaching, so that more pronounced effects on the slow-reacting HbA1c levels can be expected to be seen in the hitherto non-existent long-term (= 1-2 year) studies, because cinnamon will also have ...

• 

  Figure 2: Molecular mechanisms of Cinnamon by which it exerts hypoglycaemic activity. (Medagama. 2015).

  direct effects on the insulin receptor have been observed for Cinnamtannin B1, a proanthocyanidin isolated from the stem bark of Ceylon cinnamon that activates the phosphorylation of the insulin receptor β-subunit on adipocytes as well as other insulin receptors,
• indirect effects on glucose management that are mediated by increased GLP-1 levels, a satiety hormone that decreases the amount of insulin that is necessary to clear glucose from your blood - as Medagama points out, probably by improving glucose transport,
• direct effects on the GLUT-4 glucose uptake receptor, the expression of which is increased by 42.8 % to 73.1 % in brown adipose tissue and muscle by cinnamon in a dose dependent manner,
• indirect effects on insulin sensitivity that are mediated by the effects of cinnamon on the expression of PPAR (α) and PPAR (γ), the increase of which is linked to increased glucose uptake - unfortunately, also in fat cells,
• direct effects on carbohydrate availability that are mediated by the inhibition of the amylase enzyme that is responsible for breaking down complex carbs into simple sugars,
• indirect effects on the endogenous production of glucose in the liver that is inhibited by cinnamon (glucogenesis, i.e. the storage of sugar in the liver, on the other hand, is promoted), and
• indirect effects that are brought about by the reduced rate of gastric emptying that will naturally slow down the absorption of glucose after a meal.

If that was too much for you to remember, I guess the graphical overview Medagama created may serve as a memory aid, when you come back to this article to refresh your knowledge about cinnamon and pre-diabetes. Speaking of which...

Glucose Control Beyond Carb Reduction ➲ Amino Acids, Proteins, Peptides | learn more!

So, what's the verdict about cinnamon and pre-diabetes? As Medagama points out in the conclusion to the previously referenced recently published review, "[b]oth true cinnamon and cassia cinnamon has the potential to lower blood glucose in animal models and humans" (Medagama. 2015). The problem is yet that we do not have reliable long-term safety studies for both, the problematic, potentially coumarin-laden regular cinnamon, as well as the expensive 99% coumarin-free Ceylon cinnamon, which has actually never been tested in human studies (rodent studies suggest that it works at least as well, though).

Addendum: As previously hinted at, there is no evidence from human studies that the "healthier", "true cinnamon" aka Ceylon cinnamon even works. Well, I just noticed that there's a single, rarely cited study in healthy individuals from the Lund University in Sweden that says that Ceylon cinammon has no effect whatsoever on glycemia and thus concludes "The Federal Institute for Risk Assessment in Europe has suggested the replacement of C. cassia by C. zeylanicum or the use of aqueous extracts of C. cassia to lower coumarin exposure. However, the positive effects seen with C. cassia in subjects w/ poor glycaemic control would then be lost." (Wickenberg. 2012)

To recommend regular cinnamon as a standard-supplement, you'd take everyday for years, on the other hand cannot really be recommended - not for pre-diabetics and by no means for healthy, active individuals who have no reason to take supplements with non-muscle specific glucose partitioning effects, anyways. If you want to improve your glucose management folks, work out - a glycogen-depleting strength or HIIT workout, that's the only scientifically proven muscle specific glucose repartitioner | Comment on Facebook!

References:

• Akilen, R., et al. "Glycated haemoglobin and blood pressure‐lowering effect of cinnamon in multi‐ethnic Type 2 diabetic patients in the UK: a randomized, placebo‐controlled, double‐blind clinical trial." Diabetic Medicine 27.10 (2010): 1159-1167.
• Anand, Prachi, et al. "Insulinotropic effect of cinnamaldehyde on transcriptional regulation of pyruvate kinase, phosphoenolpyruvate carboxykinase, and GLUT4 translocation in experimental diabetic rats." Chemico-biological interactions 186.1 (2010): 72-81.
• Anderson, Richard A., et al. "Cinnamon extract lowers glucose, insulin and cholesterol in people with elevated serum glucose." Journal of Traditional and Complementary Medicine (2015).
• Blevins, Steve M., et al. "Effect of cinnamon on glucose and lipid levels in Non–insulin-dependent type 2 diabetes." Diabetes care 30.9 (2007): 2236-2237.
• Crawford, Paul. "Effectiveness of cinnamon for lowering hemoglobin A1C in patients with type 2 diabetes: a randomized, controlled trial." The Journal of the American Board of Family Medicine 22.5 (2009): 507-512.
• Hlebowicz, Joanna, et al. "Effect of cinnamon on postprandial blood glucose, gastric emptying, and satiety in healthy subjects." The American journal of clinical nutrition 85.6 (2007): 1552-1556.
• Khan, Alam, et al. "Cinnamon improves glucose and lipids of people with type 2 diabetes." Diabetes care 26.12 (2003): 3215-3218.
• Mang, B., et al. "Effects of a cinnamon extract on plasma glucose, HbA1c, and serum lipids in diabetes mellitus type 2." European journal of clinical investigation 36.5 (2006): 340-344.
• Suppapitiporn, Suchat, and Nuttapol Kanpaksi. "The effect of cinnamon cassia powder in type 2 diabetes mellitus." Journal of the Medical Association of Thailand= Chotmaihet thangphaet 89 (2006): S200-5.
• Vanschoonbeek, Kristof, et al. "Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients." The Journal of nutrition 136.4 (2006): 977-980.
• Wang, Yan-Hong, et al. "Cassia cinnamon as a source of coumarin in cinnamon-flavored food and food supplements in the United States." Journal of agricultural and food chemistry 61.18 (2013): 4470-4476.
• Wickenberg, Jennie, et al. "Ceylon cinnamon does not affect postprandial plasma glucose or insulin in subjects with impaired glucose tolerance." British journal of nutrition 107.12 (2012): 1845-1849.

Magnesium & Type II Diabetes - Link not as Straightforward as Some Experts & Supp. Recommendations Suggest

If Mg is the solution, then in form of high Mg foods, not supplements.

If you've ever googled "magnesium and diabetes", you will probably have read a sentence like this "magnesium (Mg) is actively involved in a number of metabolic reactions as an important co-factor with special emphasis on carbohydrate metabolism (Mooren. 2015). Unlike the latest paper by the German scientists Frank C. Mooren from the Justus-Liebig-University in Giessen from which I've grabbed the previously cited statement, your Google results will yet probably have treated this observation as if it was conclusive evidence that the provision of extra-magnesium would solve the T2DM-crisis of the Western wordl.

In his review, Mooren doesn't make the same mistake, instead he provides a brief, but in-depth overview of the regulation of intra- and extracellular Mg and the regulatory role of Mg in important metabolic pathways involved in energy metabolism and glycaemic control.

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An overview Mooren concludes by stating that a "critical consideration of the pros and cons of a Mg replacement therapy" that accounts for various "parameters such as Mg status, stage of disease and glycaemic control" is still lacking.

The fact that we do not yet understand all the confounding factors, though, does not mean that we are still completely in the dark. Rather than that we do know that,,,

• ...diabetes predisposes to magnesium deficiency - It may seem to be a chicken or egg question, but an impartial review of the evidence suggests that diabetes or rather pre-diabetes comes first and hypomagnesaemia = low magnesium levels are a consequence of the development of diabetes.
  
  Next to the low magnesium content of the pro-diabetic junkfood Western diet (Pham. 2014), recent data indicate that hyperglycaemia and resulting osmotic diuresis overwhelm the kidneys’ reabsorption capacity for Mg leading to hypermagnesuria. In conjuction with various disturbances of metabolic and electrolyte variables, such as hypokalaemia and metabolic acidosis, which are common among diabetics, the elevated glucose levels trigger a redistribution of Mg within its compartments that will eventually lead to the depletion of intracellular Mg and an enhanced urinary Mg excretion (Pham. 2014).
• ...hypomagnesaemia accelerates the transition from pre- to full-blown diabetes - The hyperglycemia-induced depletion of magnesium levels triggers a viscous cycle, because a balanced Mg status seems to be an important prerequisite for an adequate carbohydrate metabolism.

Overall, there is no doubt that there is a strong independent relationship between low serum magnesium levels and metabolic syndrome (Odds ratio (OR)=6.8, CI95% 4.2-10.9).

Are we talking serum of intracellular Mg levels? Both serum and intracellular Mg levels were reduced in patients with metabolic syndrome and were inversely correlated with BMI. Hypomagnesaemia (=low serum levels) as well as intracellular Mg depletion have been shown to be more prevalent (23.2 % and 36.1 %, respectively) in T2DM patients than in control group (3.3 % and 9.8 %, respectively | de Lourdes Lima. 2009). The reason that intra-cellular levels may still be a better predictors of future disturbances in glucose metabolism is the time-course of magnesium depletion which will begin in the cells and surface in form of low serum magnesium levels only when the intracellular stores are already critically low.

Six cross sectional studies have also reported associations between magnesium intake and risk of metabolic syndrome were reviewed in a recent meta-analysis by Diaba et al. (2014). More than 24,000 individuals of both sexes have been included.

Figure 1: Multivariable adjusted odds ratios (95% CI) of having prevalent metabolic syndrome in participants with the highest level of dietary magnesium intake compared with those with the lowest (Diba. 2014).

Despite the fact that the data shows a 31% reduced risk of metabolic syndrome (see Figure 1) and a 17% reduced risk per 100mg/day of magnesium in the diet in subjects in the highest vs. lowest Mg intake groups, and were compared (OR=0.69, CI95% 0.59-0.81), the evidence from studies investigating the effects of oral Mg supplementation as an adjunct therapy for type 2 diabetes is quite heterogeneous.

Table 1: Absolute changes in fasting plasma glucose after Mg supplementation in people with impaired glucose regulation | FPG – Fasting plasma glucose; * indicates the inclusion of hypomagnesaemic subjects only (Mooren. 2015).

Fourteen randomized controlled studies have been identified which investigated the effect of Mg supplementation on type 2 diabetes (Table 3). In total, 825 people with diabetes were enrolled, who had suffered from the disease for a mean duration of about 10.8+4.1 years. 10 studies reported values for glycosylated haemoglobin (HbA1c) at study onset. Their long term glucose control failed the recommended values for diabetic patients (target range HbA1c from 6.5-7.5 %) as indicated by a mean HbA1c of 9.3+2.1 %. 3 studies included patients with initial HbA1c levels lower than 7.5 %. Serum Mg concentrations at study onset have been reported in 12 studies. 5 out of 12 studies included diabetic people with hypomagnesaemia (Mg < 0.74mmol/l), while patients of another 5 studies showed serum Mg levels in the lower segment of the normal range (between 0.74 and 0.85 mmol/l).

Different Mg salts (Mg-pidolate; Mg-lactate-citrate; Mg-oxide; Mg-chloride; Mg-aspartate; Mg sulfate) were applied during a wide range of treatment periods which lasted from 4-16 weeks (mean treatment duration 9.6 weeks). After Mg supplementation, only 50 % of the studies reported significant improvements in serum Mg (7 out of 14 studies). Such a limited supplementation efficacy might partially result from different bioavailabilities of the various Mg salts (organic vs. inorganic) applied" (Mooren. 2015).

In a similar vein, most of the studies did not observe significant improvements in glucose control and the long-term glucose measure HbA1c in response to magnesium supplementation (only 23% and 18%, respectivels). The closely related triglyceride levels were not affected in any of the studies.

Magnesium vs. Diabetes - Which Form is Best? Find out in this SV Classic!

So is Mg supplementation useless? As Mooren rightly points out, the "results are somewhat surprising in the light of the previously shown epidemiological data about the relationship between altered Mg status and diabetic disease" (Mooren. 2015). This does not mean, though, that it was pointless to give mg supplements a try. In fact, the short duration of the majority of the studies (6 weeks in 6 out of 14 of the studies) may simply not have been enough to fully replete the intra-cellular magnesium stores of the subjects.

What should not be forgotten, though, is the fact that the two studies on subjects with the lowest serum Mg and highest HbA1c levels yielded the most beneficial results. Specifically for those with exuberantly high and badly controlled blood glucose levels the provision of Mg supplements in form of magnesium citrate or magnesium gluconate of which my previous review of the literature showed that they are the most bioavailable forms is clearly indicated | Comment on Facebook!

References:

• de Lourdes Lima, Maria, et al. "Serum and intracellular magnesium deficiency in patients with metabolic syndrome—evidences for its relation to insulin resistance." Diabetes research and clinical practice 83.2 (2009): 257-262.
• Dibaba, D. T., et al. "Dietary magnesium intake and risk of metabolic syndrome: a meta‐analysis." Diabetic Medicine 31.11 (2014): 1301-1309.
• Mooren, Frank C. "Magnesium and disturbances in carbohydrate metabolism." Diabetes, Obesity and Metabolism (2015): Accepted Article.
• Pham, Phuong-Chi T., et al. "Hypomagnesemia: a clinical perspective." International journal of nephrology and renovascular disease 7 (2014): 219.

Energy Drinks Before Workout Make You Thirsty. Single HIIT Session Every 14 Days Maintains Fitness in the Off-Season. Postprandial Walk Decreases HbA1c by 5%. Cardio Before Weights Increases pAKT +87% Over Weights Alone

You simply cannot start "working out" too early - even if it's just child's play.

"Three for one!" No, I am not trying to sell you three bottles of "uberpotent" test-boosters for the rat of one. Three for one that's the SuppVersity Figure of the Week and it is the ratio of the decrease in breast cancer risk in women and the hours of physical activity per week during their adolescence.

According to a 2004 review by Lagerros, Hsieh and Hsieh, each additional* hour of weekly physical activity is associated with a -3% risk of developing breast cancer later in life (Lagerros. 2004)

Needless to say that the "additional" hours are in addition to the low physical activity in the laziest of the study participants, who had a 20% higher risk of developing breast cancer than their most active peers.

So what else do we have today? With this primer on the importance of physical activity esp. in the critical periods of your / your children's and grand-children's lives, let's delve right into a "special edition" of the Saturdaily "Short News" with a focus on a selection of very recent results from exercise-related studies.

• Energy drink before a workout make you thirsty. don't enhance performance (Tanskanen. 2013) While the mantra of the "intra-workout" beverage producer that you need at least a small amount of carbohydrates to optimally absorb the added salts, a recent study from the University of Jyväskylä in Finland showed that the ingestion of both high- and low-carb (33g vs. 10g) caffeine-containing energy drinks before the workout resulted in a temporary increase in thirst compared to to both caffeinated (106mg, just as the two energy drinks) an non-caffeinated water.
  
  

  

  With +1kg Fat in 4 Weeks from less than 2 energy drinks/day, thirst may be the least problem you will have if you guzzle "energy drinks" (learn more).

  The fact that the increase in thirst was only transient, and decreased in the course of the 60min cycling exercise (60% VO2max) the healthy young adults had to perform, as well as the non-existent differences in hydration status between the groups do yet show that these effects were practically irrelevant. Incidentally, the latter has to be said for the promised / expected performance enhancing effects of energy drinks - with the relatively low amount of caffeine in the drinks, there were no significant differences between the the time the 10 participants cycled on an incremental test to exhaustion that followed the "steady-state-cardio" during each and every of the four testing days of this randomized, crossover study.

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  Putting things into perspective: The fact that previous trials yielded different results, esp. wrt to the performance enhancing effects of caffeine, is probably attributable to a the low dosage of caffeine. Another very recent study by Ranchordas & Kenzie, for example has just confirmed that a compbination of 32g of carbs and 300mg of caffeine can "enhance some aspects of soccer-related fitness including acceleration, maximal velocity, 20-m sprint speed, speed-endurance, and lower RPE during repetitive sprints compared with CHO-only and PLA beverages." (Ranchordas. 2013)

 

• 

  Remember the "Iranian HIIT Solution" - 9% body fat in 12 weeks? Perfect evidence: HIIT is not for athletes, only.

  It does not take much to stay fit, a single every other week HIIT session is enough (Rønnestad. 2013) Right from the former Olympia "Metropolis" *rofl* Lillehammer comes a study which shows that trained athletes like semiprofessional soccer players can maintain their baseline fitness levels in the off-season by no more than a single HIIT session, which consisted of five bouts of 4 min running at 87–97% of age-predicted maximum heart rate, every other week.
  
  The overall loss in the distance the subjects covered during the 20-m shuttle run did obviously decline (-8% ± 6%), but the difference to the control group that performed the same HIIT sessions on a weekly basis was non-significantly different from the every-other-week group.Moreover, both groups maintain their VOmax over the whole six week study period.

  ---

  Bottom line: A little of HIIT can go a long way ... wait, this is almost the title of a previous SuppVersity post, i.e. "Some HIIT For Life & Less LISS For More! How to Burn 27,300 Kcal Extra W/out Losing a Single Extra Pound of Fat!", of which I would really suggest you read it now, in case you are still not convinced that a reasonably dosed amount of HIIT makes a valuable addition to almost every trainees regimen.

 

• Hit the weights! If you want to do more than just increase your daily activity levels to lower your HbA1c, don't waste your time on the treadmill. Increase your daily activity level and lift weights! Three supervised resistance training sessions per week for 10 weeks have been shown in a 2009 study by Bweir to be significantly more effective in lowering the Hb1Ac levels than in adults with type II diabetes than an isoenergetic (=spending the same energy during the workout) treadmill exercise (Bweir. 2009).
  The postprandial stroll in the bark is an effective means to lower your HbA1c (Nygaard. 2013) While the former post on the conservation of the conditioning of a trained athletes by HIIT does confirm the notion that "aerobic exercise" in the original sense of the meaning, which would imply that you increase your body's exercise capacity (as evidenced by VO2max), another recently published study shows that metabolic benefits of exercise can be achieved with much lower intensities.
  
  At least in the in the South Asian immigrants with high risk of type 2 diabetes who participated in a recently conducted 12-week intervention, it took nothing but the figurative "walk in the park" (30min+ of physical activity of any sort) after a meal, to reduce their HbA1c levels - a marker of long(er) term glucose levels - by allegely relatively unimpressive, but statistically highly significant ~3% (p = 0.012). That the intervention in the course of which the average subject increased his / her daily activity by 40min compared to the control group did not yield any significant changes in body composition should yet be as evident as the fact that it was 100% side-effect free.

  ---

  Bottom line: It really depends on where you are and if you are a sedentary slob, even 40min of extra (light) activity a day can make a difference. After all, previous studies have shown that each 1% increase in HbA1c is associated with a 1% increase in cancer risk (data fro 25,476 patients with type 2 diabetes registered in the Swedish National Diabetes Register; cf. Miao Jonasson. 2012). 

• Rodent study says: Cardio does not hamper anabolic signalling (Souza. 2013) While the comprehensive review by Wilson et al. you've read about here at the SuppVersity several times (e.g. April 2012, January 2013, etc.) found that there is a
  

  "significant negative relationships between frequency (-0.26 to -0.35) and duration (-0.29 to -0.75) of endurance training for hypertrophy, strength, and power." (Wilson. 2012)

  a very recent study from the Universidade de Sao Paulo would suggest that the negative influence of endurance training on the anabolic stimulus of restistance training is either
  
  1. species specific and occurs only in humans, but not in rodents,
  2. occurs only with chronic high volume trainging, or
  3. is at least not related to changes in the AMPK, TSC2, mTOR, or p70S6K1 ratios
  Now while each of the former is certainly possible, my best bet would be that the training volume, i.e. 5 sets of 10 reps on a "rodent leg trainer" and a 60min endurance workout on the treadmill, and the fact that the protocol was performed only once are the main reasons that the AMPK, TSC2, mTOR, or p70S6K1 ratios were identical.

  ---

  

  Doing cardio before strength workouts results in a higher testosterone:cortisol ratio after the workout (learn more)

  One thing is remarkable, however: The scientists observed a pretty remarkable +87% increase in Akt phosphorylated/total ratio that occurred 2h post only in those rodents who performed a 60min bouts of treadmill running before their leg workout. What? Yeah, that's actually what Carl and I have been talking about in the past - "pre-workout glycogen depleting cardio as intensity technique" (learn more)

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So what's left to do now? Ah, yes of course. The best wishes for the weekend and a brief link-list for those of you who can't be without SuppVersity news for another 24h.

• 

  "Going Nuts On Berries: Ellagic Acid in Rasp- and Blueberries, Pecans, Walnut & Co Protects Against Visceral Obesity" - I hope you are not one of the guys who spits the tiny seeds of the raspberries out. That is not just disgusting, you would also spit away ~90% of their ellagic acid content (learn more).

  Do you stand right? Scientists investigate the influence of dynamic vs. static posture on leg stiffness and future risk of fall (read more)
• Anabolic steroid use has distinct effects on tendons. Scientists speculate that the increased stiffness and higher modulus contribute to the frequent ruptures in chemical athletes (read more)
• Oldie but goldie: Do you cook the creatine out of your steaks? A mid 20th century paper shows that cooking degrades creatine to creatinine (read more)
• More walnut lovin' Despite the fact that you have to be careful with what you say about the health effects of walnuts, these days a group of reseachers does not fear the repressions from the FDA and says: "We found two novel mechanism that explain why walnuts are good for your heart!" (read more)

These and other news are already waiting for you on Facebook and you can bet that there will be at least half a dozen additional ones posted before the next official SuppVersity article will see the light of the day, tomorrow.

References:

• Bweir S, Al-Jarrah M, Almalty AM, Maayah M, Smirnova IV, Novikova L, Stehno-Bittel L. Resistance exercise training lowers HbA1c more than aerobic training in adults with type 2 diabetes. Diabetol Metab Syndr. 2009 Dec 10;1:27. doi: 10.1186/1758-5996-1-27.
• Miao Jonasson J, Cederholm J, Eliasson B, Zethelius B, Eeg-Olofsson K, Gudbjörnsdottir S. HbA1C and cancer risk in patients with type 2 diabetes--a nationwide population-based prospective cohort study in Sweden. PLoS One. 2012;7(6):e38784.
• Nygaard H, Grindaker E, Rønnestad B, Holmboe-Ottesen G, Høstmark AT. Long-term effects of daily postmeal physical activity - Preliminary results.International Journal of Sport Nutrition and Exercise Metabolism,2013, 23, S1 -S15.
• Ranchordas M, Kenzie J.Effect of carbohydrate only and carbohydrate plus caffeine co-ingestion on a battery of reliable soccer-specific tests. International Journal of Sport Nutrition and Exercise Metabolism,2013, 23, S1 -S15.
• Rønnestad BR, Slettaløkken G. High-intensity interval training every second week maintains VO2max in soccer players. International Journal of Sport Nutrition and Exercise Metabolism,2013, 23, S1-S15.
• Souza EO, Tricoli V, Bueno Junior C, Pereira MG, Brum PC, Oliveira EM, Roschel H, Aoki MS, Urginowitsch C. The acute effects of strength, endurance and concurrent exercises on the Akt/mTOR/p70S6K1 and AMPK signaling pathway responses in rat skeletal muscle. Braz J Med Biol Res. 2013 Apr 19:0.
• Tanskanen M, Heikkinen T, Linnamo V. Effects of caffeine drinks on endurance performance, fluid balance, and subjective feelings. International Journal of Sport Nutrition and Exercise Metabolism,2013, 23, S1 -S15.
• Wilson JM, Marin PJ, Rhea MR, Wilson SM, Loenneke JP, Anderson JC. Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises. J Strength Cond Res. 2012 Aug;26(8):2293-307.