Magnesium - Beyond Bioavailability: Bioaccumulation in the Brain 1.2-Fold Higher for Mg-Taurate | No Effect on Muscle

Brainiacs listen up: Magnesium + taurine can also be achieved from a (high seafood) diet.

You will remember that the year 2017 saw the publication of the first study to lend credible support to the use of transdermal magnesium. If you go back to my article discussing the results of the study, you will find the following items in the overview of CNS symptoms of magnesium deficiency (48% of the Americans don't get enough Mg | Moshfegh 1997): "Nervousness, increased sensitivity of NMDA receptors to excitatory neurotransmitters, migraine, depression, nystagmus, paraesthesia, poor memory, seizures, tremor, vertigo."

What you will also find is a figure depicting the effects of administering different forms of magnesium (orally) to rodents on plasma, bone, and red blood cell (#RBC) magnesium levels.

Mineral water contains Mg, a lot of other minerals and bicarbonate you don't want to miss:

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The figure is from another SuppVersity article from 2013, and it is still the most comprehensive comparisons of the oral bioavailability of magnesium compounds I know: What it does not provide, though is data that may explain the previously mentioned central-nervous-system effects of (low) Mg.

Figure 1: Where most of the magnesium in your body is found (based on Swaminathan 2003)

How's that? Well, as Uysal et al. point out, "[f]ollowing absorption from the digestive tract, magnesium enters the bloodstream [and] is then transported at different rate[s] of magnesium transport across cell membranes".

Fact 1: The rate of magnesium transport across cell membranes is higher in the heart, liver, and kidney and lower in the skeleton, red cells, and brain (Rude 1993).

Needless to say that this "penetration" is an important requirement for the previously hinted at (health) effects on the brain and the central nervous system... and guess what: a recent study by scientists from Turkey and the US suggests that previous measures of "bioavailability" may have underestimated the different absorption kinetics of organic and inorganic magnesium salts.

Hence, the aim of this study, which has just been published in "Biological Trace Element Research", was to investigate the bioavailability of different...

• organic (magnesium citrate, magnesium acetyl taurate, and magnesium malate), and ...
• inorganic (magnesium oxide and magnesium sulfate) magnesium compounds. 

As you may know, "[m]agnesium citrate and magnesium oxide are the most prescribed Mg compounds as dietary supplements", magnesium acetyl taurate (all about taurine), on the other hand, is something you will have to ask for, specifically -- however, after the publication of Uysal's paper, the number of people doing just that may keep increasing.

Fact 2: Dietary fermentable fiber improves, not impairs, magnesium absorption in the intestines (Coudray 2003) - probably by interacting with the microbiome.

Figure 2: The amount of magnesium in serum is only one parameter that determines its biological effect ... and probably not the most important one (data from Uysal 2018).

People who are less interested in further increasing the transport of Mg from the digestive tract into circulation, as it can be achieved by feeding your microbiome appropriately (fermentable fiber, guys), but rather in its (almost unique) ability to make it from their blood into their eyes and brains, where it stops the development/progress of cataracts (Choudhary 2016), and has been shown to have the very "preventive value in the treatment of migraine" (McCarty 1996b) other forms of magnesium don't seem to have.

As you can see in Figure 2, these effects are not a mere function of bioavailability, as the often derided magnesium sulfate (diarrhea-prone) will increase the level of plasma magnesium to the same extent as the 10-20x more expensive magnesium-taurate or magnesium malate salts (mg sulfate also displays all the beneficial anti-diabetes effects you may have heard about, by the way).

Figure 3: A new study shows that magnesium taurate (MgT) seems to have brain-specific effects (see larger figure) but may be less suitable to increase skeletal muscle magnesium levels (see smaller figure, both from Uysal 2018). What is noteworthy in this context is that Uysal et al. also observed the biological downstream effects on stress/anxiety you would expect to see from the restoration of optimal brain magnesium levels in their hairy rodent subjects.

The obvious question that arises if this is not your first visit to the SuppVersity is, whether you even have to take the taurine-bonded magnesium and/or cannot simply co-supplement with taurine and another form of magnesium like citrate, sulfate or carbonate to have enough taurine your #1 brain osmolyte (Oja 1996). Unfortunately, there's scant evidence to support the notion that a mere co-administration of both agents will have superior effects compared to other forms of magnesium.

DIY - MgTaurate? In theory, McCarty et al. provide you with all the information on how to produce your own magnesium taurate in their 1995 patent specifications, in which the simpler method to end up with MgTau is based on mixing magnesium hydroxide (433 mg, 7.46 mmol; Aldrich) and taurine (1.87 g, 14.9 mmol) in 20 ml water was heated under reflux for seven hours (learn more).

The idea that compounding the two has been first proposed by McCarty et al. more than a decade ago (McCarty 1996a). What the scientists who also own the previously referenced patent (see box) do yet fail to explain why the same 10:1 mix of unbound taurine:magnesium would not yield the same benefits as the compounded molecule.

In fact, studies in bone (Jeon 2007) or the epithelium (Katakawa 2016) seem to suggest that the mere presence of taurine may facilitate significant increases in cellular mg levels. If you take taurine, which is, by the way, one of the few supplements that consistently get a SuppVersity ThumbsUp!, buying MgTau be a waste of valuable dollars (Euros or Bitcoins) you would better spend on taurine- and magnesium-rich foods as they've been found by Yamori et al. (2017) to significantly reduce the risk of cardiometabolic disease in these benefits in Japanese seafood connoisseurs.

Fact 3: Food processing will reduce the magnesium content of your foods by up to 85% - and that's on top of the already declining Mg content of Western produce (Thomas 2007).

Speaking of real-food sources of magnesium, it is worth taking a parting look at the often-heard claim that "with the ongoing nutrient-depletion in our produce, it's simply impossible to get enough magnesium with your diet"... well, in short: that's naturopathic bullshit meant to have you spend money on overpriced supplements that are not better than those you could buy for 10% of the price at Walmart. The reason this myth is so diehard, though, is that it contains not one, but two sparks of truth: (1) Over the past decades, the magnesium concentration of US veggies, fruit, meat, dairy, and cheese has in fact declined. And (2) if you don't eat these foods right away, but after processing the magnesium loss can amount to 90%.

Figure 4: It's true, compared to the values from 1940, US veggies, fruits, meats, cheeses, and dairy contained an average 19% less magnesium in a study by Thomas using data from produce from 2002 (Thomas 2007).

It stands out of the question that the latter (2) is the more likely reason why so many Americans are magnesium-deficient (often without correspondingly low serum levels). If you're concerned about these nutrient losses, though, you should be aware that magnesium is by no means the mineral with the highest reduction in US produce in the last 60 years: With average nutrient reductions of -62% and -37%, those are copper and iron, respectively, followed by a still astoundingly high -29% reduction of calcium in the aforementioned food groups.

Fact 4: You can get enough magnesium from the diet... if you consume a whole foods diet. If >50% of the foods you buy are heavily processed, you don't stand a chance.

So, if there's magnesium in your diet, how much do you need on top of it? Well, if you remember the recently published paper about vitamin D and magnesium (re-read it), you'll know that as little as 100mg can be plenty. In conjunction with the 300 mg you may be getting from your diet, you'll end up at the 400mg/d margin that's the RDA (for men, and won't hurt women).

Against that background, the crazy price of magnesium taurate does no longer sound so crazy - after all, it's not necessary to take more than the suggested serving size, which usually contains ~100-200mg elemental magnesium. However, if taken with food (to avoid diarrhea) and in reasonable amounts, magnesium sulfate would yet be a much cheaper alternative for those who don't want to give magnesium taurate a chance, because they suffer from migraines (McCarty 1996b) and those didn't improve from combining 'regular' magnesium supplements with some cheap taurine (buy in bulk for $20 per kg).

Figure 5: Magnesium in brain. Mg2 is an important regulator of glutamate signaling in the brain (de Baaij 2015).

So what should I remember? Different forms of magnesium differ in both, their bioavailability, i.e. the amount of magnesium that makes it into your bloodstream, and their bioaccumulation, i.e. the deposition of magnesium where you want it: in your cells.

In this context, magnesium taurate is of particular interest. In fact, a new study by Uysal et al. (2018) suggests that it delivers the important macromineral right to the brain, where it has been shown to enhance the brain mg levels and actually enhance learning and memory (Slutski 2010 | to elevate young & old rodents' brain levels, the researchers used Threonate, though).

Whether and to which extent the same brain-mg-boosting effects can be achieved by non-complexed (and non-patented) forms of taurine and magnesium (ratio 10:1) wouldn't yield similar effects is something future studies will have to investigate. And let's be honest: In view of the proven health benefits of high(er) dietary intakes of both from experimental and epidemiological studies (Yamori 2010), it seems likely that these studies could yield positive results | Comment!

References:

• Coudray, Charles, et al. "Two polyol, low digestible carbohydrates improve the apparent absorption of magnesium but not of calcium in healthy young men." The Journal of nutrition 133.1 (2003): 90-93.
• Choudhary, Rajesh, and Surendra H. Bodakhe. "Magnesium taurate prevents cataractogenesis via restoration of lenticular oxidative damage and ATPase function in cadmium chloride-induced hypertensive experimental animals." Biomedicine & Pharmacotherapy 84 (2016): 836-844.
• Jeon, Seol-Hee, et al. "Taurine increases cell proliferation and generates an increase in [Mg2+] i accompanied by ERK 1/2 activation in human osteoblast cells." FEBS letters 581.30 (2007): 5929-5934.
• Katakawa, Mayumi, et al. "Taurine and magnesium supplementation enhances the function of endothelial progenitor cells through antioxidation in healthy men and spontaneously hypertensive rats." Hypertension Research 39.12 (2016): 848.
• McCarty, M. F. "Complementary vascular-protective actions of magnesium and taurine: a rationale for magnesium taurate." Medical hypotheses 46.2 (1996a): 89-100.
• McCarty, M. F. "Magnesium taurate and fish oil for prevention of migraine." Medical hypotheses 47.6 (1996)b: 461-466.
• Moshfegh, A., et al. "Usual nutrient intakes from food and water compared to 1997 Dietary Reference Intakes for vitamin D, calcium, phosphorus, and magnesium." What we eat in America, NHANES 2005-2006 (2009).
• Oja, Simo S., and Pirjo Saransaari. "Taurine as osmoregulator and neuromodulator in the brain." Metabolic brain disease 11.2 (1996): 153-164.
• Rude, Robert K. "Magnesium metabolism and deficiency." Endocrinology and metabolism clinics of North America 22.2 (1993): 377-395.
• Slutsky, Inna, et al. "Enhancement of learning and memory by elevating brain magnesium." Neuron 65.2 (2010): 165-177.
• Thomas, David. "The mineral depletion of foods available to us as a nation (1940–2002)–a review of the 6th Edition of McCance and Widdowson." Nutrition and health 19.1-2 (2007): 21-55.
• Uysal, N., Kizildag, S., Yuce, Z. et al. "Timeline (Bioavailability) of Magnesium Compounds in Hours: Which Magnesium Compound Works Best?" Biol Trace Elem Res (2018). https://doi.org/10.1007/s12011-018-1351-9
• Vici, Giorgia, et al. "Gluten free diet and nutrient deficiencies: A review." Clinical nutrition 35.6 (2016): 1236-1241.
• Yamori, Yukio, et al. "Taurine in health and diseases: consistent evidence from experimental and epidemiological studies." Journal of biomedical science 17.1 (2010): S6.
• Yamori, Yukio, et al. "Taurine Intake with Magnesium Reduces Cardiometabolic Risks." Taurine 10. Springer, Dordrecht, 2017. 1011-1020.

Intermittent Fasting Beats Isocaloric Continuous Dieting (Fat Loss & Health) | New Study + Research Update 12/18

Is intermittent dieting the better form of dieting? Results are promising, but far from conclusive - even in 2018. Check out the latest study in Obesity and selected research from '18, now!

Let's get this straight, right away. The lion's share of the currently available literature on intermittent fasting vs. continuous dietary restriction suggests that "[i]ntermittent energy restriction [is] comparable to continuous energy restriction for short-term weight loss in overweight and obese adults" (Harris 2018).

And yes, there are numerous studies suggesting that intermittent (IER) is even superior to regular, continuous energy restriction (CER).

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However, with the plethora of different regimen and other essential differences in study design, such as subject characteristics, the in-/exclusion of exercise, or the nutritional composition of the diets the existing evidence is yet so heterogeneous that a general statement about the comparative efficacy of intermittent vs. continuous dietary restrictions seems unwarranted.

Just another promising study?

Against that background it will also hardly surprise you that the latest investigation to compare intermittent fasting (IF) versus continuous energy intakes at 100% or  70%  of  calculated  energy  requirements  on  insulin  sensitivity,  cardiometabolic  risk,  body  weight,  and  composition ends on the following conclusion:

"When prescribed at matched energy restriction,  IF reduced weight and  fat mass and improved total and low-density lipoprotein cholesterol more than DR. IF prescribed in energy balance did not improve health compared with other groups, despite modest weight loss" (Hutchinson 2018). 

And guess what, with their results, the researchers from the Adelaide  Medical  School are in good company. Only recently, Antoni et al. identified potentially life-saving differences in the effects of intermittent vs. continuous dietary restrictions. In their study, the scientists from the University of Surrey, observed significantly more pronounced improvements in blood pressure, as well as the postprandial C-peptide (part of the glucose metabolism) and triacylglycerol response in the IF group who dieted for only 2/7 days of the week (Antoni 2018a).

What? Oh yes, there's this impressive 2014 study I discussed in detail - it's worth checking out if you haven't done so already | read it!

Is refeeding "intermittent fasting"? With no clear-cut definition of what constitutes an intermittent fasting regimen, it makes sense to include the results of a recent review in "Obesity Reviews" in this research update. In the eponymous paper, the authors outline a "[r]ationale for novel intermittent dieting strategies to attenuate adaptive responses to energy restriction" (Sainsbury 2018) and report that of the five randomized controlled trials in adults with overweight or obesity that have tested the effects of "refeeding" (=energy balance or absence of energy restriction), two reported greater weight loss than CER, whereas three reported similar weight loss between interventions.

Figure 1: Markers of postprandial lipid (left) and glucose metabolism before and after 5 % weight loss via intermittent energy restriction (IER, black circles) and continuous energy restriction (CER, black squares) in Antoni 2018.

Researchers from the same group have also been able to show that time-restricted feeding aka "intermittent fasting" (feeding window ≥3 h reduced vs. baseline) triggers significant reductions in energy intake in overweight subjects on an ad-libitum (=eat as much as you want) diet (Antoni 2018b).

On the other hand, studies like Schübel et al. (2018) failed to demonstrate significant inter-group differences between continuous and intermittent dietary restriction in their recent 50-week-study (Schübel 2018). Others even report that "in normal-weight subjects have shown detrimental effects of intermittent diets on fat distribution and metabolic homeostasis, raising safety concerns and the need for further investigation" (Brinia 2018). Moreover, another 1-year study found that subjects in the IF group reported greater hunger - that's in contrast to the general consensus among practitioners, but it's what Sundfør et al. report in their recent paper in NMCD (2018).

Table 1: As a review of Ganesan et al. (2018) illustrates, "intermittent fasting" can be effective in form of various regimens. 

There are multiple ways to shed that body fat w/ intermittent fasting: As the tabular overview on the left goes to show you, the studies in Ganesan et al's (2018) review of studies showing statistically highly significant reductions in body fat (p < 0.01) used very different iterations of an "intermittent fasting"-diet, ranging from alternative day fasting to refeeding.

Noteworthy: The alternative day fasting studies were conducted in normal-weight individuals who likewise saw improvements in their body composition.

And the study at hand seems to support the hunger-increasing effects of intermittent fasting (see Figure 2) - interestingly enough, in both IF groups and thus irrespective of the total energy intake:

Thus having returned from a short overview of the latest and greatest in IER vs. CER (or IF vs. CD) returned, it's about time to take a closer look at the initially introduced study by Hutchinson et al. (2018). In said study, the subjects, women with overweight (n = 88;  50 ± 1  years,  BMI  32.3 ± 0.5  kg/m2) were randomized to one of four diets (IF70, IF100, dietary restriction [DR70], or control) in a 2:2:2:1 ratio for 8 weeks:

"IF groups fasted for  24 hours after breakfast on three nonconsecutive days per week.  All foods were  provided and diets matched for macronutrient composition  (35%  fat,  15%  protein,  50%  carbohydrate).  Insulin sensitivity by a hyperinsulinemic-euglycemic  clamp,  weight, body composition, and plasma markers were assessed following a “fed” day (12-hour fast) and a 24-hour fast (IF only)" (Hutchinson 2018).

But how exactly did that work? Well, on fed days, IF70 participants were provided with ~100% and IF100 with ~145% of energy requirements.

"IF groups consumed breakfast before 8 am on fasting days (~32% of energy requirements at breakfast on fasting days in IF70 and ~37% in IF100), and then commenced a ~24-hour 'fast' until 8 am the following day on three nonconsecutive weekdays per week. During the fast, participants were allowed water, small amounts of energy-free foods (e.g., 'diet' drinks, chewing  gum/mints),  black  coffee,  and/or  tea  and  were  provided  with  250 mL of very-low-energy broth (20 kcal/250 mL, 2.0 g protein, 0.1 g fat, 3.0 g carbohydrate) for lunch or dinner" (Hutchinson 2018). 

As previously pointed out, the diets were matched for macronutrient composition (35% fat, 15% protein, 50% carbohydrate). How adherent the subjects actually were, though, is difficult to tell, even though the scientists delivered free foods every 2 weeks to their home - I mean, the "few" cookies at the office and the White Hot Chocolate (worth 590kcal) from Starbucks can easily ruin any dieting effort without appearing on ashamed subjects' 7-day food logs.

Figure 3: Changes in anthropometric outcomes following 8 weeks of intermittent or continuous intake at 70% and 100% of daily energy requirements.  (A)  Weekly weights;  (B)  change in body weight, (C)  fat mass and (D) fat-free mass (all as mean ±  SEM). Pairwise comparisons: *P  <  0.05 vs. control; ^P < 0.05  vs.  IF100; ‡P  <  0.05 vs. DR (Hutchinson 2018)

In view of the fact that this is not an IF-specific problem, though, it raises no general doubts about the most relevant results in Figure 3: the subjects on the F70 protocol displayed greater reductions in weight and fat mass.

The lean mass issue: an intermittent fasting specific problem?

In that, we cannot ignore, though, that the IF70 subjects also recorded the greatest reduction in fat-free mass (=muscle + organs). With ~1.4kg FFM per 4kg FM, the fat-to-organ (including muscle) weight loss ratio was yet worse than the one in the DR70 group, i.e. those subjects who cut their calories by 30% every day (35% in F70 vs. 20% in DR70) - a lean mass sparing effect as it was reported by Varady et al. in both 2009 and 2013.

Figure 4: Pooled effect sizes (Weighted Mean Difference) of secondary outcomes, calculated as difference between the reductions in IER vs. CER, i.e. intermittent vs. continuous energy restriction (Harris 2018)

Whether the greater lean mass losses were a result of the ~30g/d lower protein intake in the IF70 vs. DR70  group (~70 vs. 100g/d that's 0.78g/kg body weight and ~1.3g/g in the intermittent and continuous dieting group, respectively | see Figure 6 in the bottom line, too) is not clear - to me, however, it doesn't sound unrealistic to assume that a mere lack of total daily protein may have been driving these changes in body composition which were not observed with a more intense protocol (alternating every 24-h between consuming 25% or 125% of energy needs), which found that...

"[t]he FFM:total mass ratio increased in both ADF (0.03 ± 0.00) and CR (0.03 ± 0.01) compared to the control group (P < 0.01), with no differences between the intervention groups" (Trepanowski 2018).

In fact, a recent effort to pool and compare the data on IER and CER for a meta-analysis by Harris et al. (2018) found no difference in muscle and a significantly higher reduction in waist circumference (-2.14 cm | p = 0.002) and fat mass (-1.38kg | p = 0.014) - with only six studies and the previously described methodological heterogeneity in study design it would yet be premature to subscribe to any claims about the fat loss specificity of either form of dieting (see Figure 4).

Would more protein help? A study by Harvie was conducted to vary the protein intake and see its effects on body composition and metabolism, but failed to induce relevant intake differences in 2013; overall resistance training and increased protein intakes are yet going to slow down muscle loss when dieting (Hector 2018) - on every diet. If you scrutinize the results of Harris' meta-analysis in Figure 3 you will see that the changes in the subjects' insulin levels were likewise among the handful of statistically significant differences between IER and CER - again with an advantage for the intermittent dieting groups. With 70g

This leads us back to the latest contribution and actual subject of today's article, Hutchinson's recent study in Obesity and its non-aesthetic (ok, body fat is also health-relevant) outcomes, where significant improvements in markers of glucose metabolism (see Figure 5)...

Figure 5: Changes in markers of insulin sensitivity and biochemical markers following 8 weeks of intermittent or continuous intake at 70% and 100% of daily energy requirements. (A) Change in insulin sensitivity as assessed by hyperinsulinemic-euglycemic clamp; completers analysis (DR70 n = 22;  IF70 n = 18;  IF100 n = 19;  C n = 10);  (B) change in fasting blood glucose; (C) change in fasting insulin; (D) change in HOMA-IR; (E) change in nonesterified fatty acids (NEFA); (F) change in aspartate transaminase; (G) change in fibroblast growth factor-21; (H) change in beta-hydroxybutyrate. Data are shown as mean ±   SEM. Filled bars: change from baseline to fed visit; open bars: change from baseline to fasted visit. Pairwise comparisons: *P < 0.05 vs. C; ^P < 0.05  vs.  IF100; ‡P   <   0.05 vs. DR70 (Hutchison 2018).

as well as reductions in total and LDL cholesterol and triglycerides were observed only in the IF70 group, i.e. those subjects who reduced their energy intake by 30% by intermittent fasting (lipids not shown in Figure 5) and hence, ultimately, to the claim from the headline of this article: "Intermittent Fasting Beats Isocaloric Continous Dieting" - an article that turned out to be more of a research update than the analysis of Hutchinson's latest results.

Figure 6: You can hardly argue that the real-world nutrient intakes (in g/d) in the IF70 group come close to what we know would be optimal for lean mass retention (Hutchinson 2018).

So what's the verdict, then? Even though Hutchinson et al. are not the first to diagnose clinically relevant advantages of intermittent vs. isocaloric continuous dieting interventions, we'll need a  lot more research to be able to understand important confounding variables such as protein intake, concurrent exercise, the mere type of IF protocol that is used, subject-specificity...

I could continue this list forever, but instead of doing so, I will tell you this: If skipping breakfast "lean gains"-style allows you to effortlessly reduce your energy intake by 500kcal/day - do it!

Don't fret, though, if intermittent fasting just doesn't seem to work for you even after you've given it enough time (2 weeks+) for your circadian rhythm to adjust.

If there's one thing we seem to be able to tell for sure it's that the main driver of (intermittent fasting-induced) weight loss is the calorie deficit you're generating - add heavy resistance training and sufficient protein 2g/kg to the mix and watch your progress in the mirror. Much better progress than the subjects in the Hutchinson study who didn't skip breakfast, but reduced their energy intakes by 500kcal/d without either working out or eating close to sufficient amounts of protein (see data in Figure 5) | Leave a comment on Facebook!

References:

• Antoni, Rona, et al. "Intermittent v. continuous energy restriction: differential effects on postprandial glucose and lipid metabolism following matched weight loss in overweight/obese participants." British Journal of Nutrition 119.5 (2018a): 507-516.
• Antoni, Rona, et al. "A pilot feasibility study exploring the effects of a moderate time-restricted feeding intervention on energy intake, adiposity and metabolic physiology in free-living human subjects." Journal of Nutritional Science 7 (2018b).
• Brinia, M. E., et al. "The effects of intermittent energy restriction on metabolic and cardiovascular function and overall health." Arch. Hell. Med 35 (2018): 1-17.
• Ganesan, Kavitha, Yacob Habboush, and Senan Sultan. "Intermittent Fasting: The Choice for a Healthier Lifestyle." Cureus 10.7 (2018).
• Harris, Leanne, et al. "Intermittent fasting interventions for treatment of overweight and obesity in adults: a systematic review and meta-analysis." JBI database of systematic reviews and implementation reports 16.2 (2018): 507-547.
• Harvie, Michelle, et al. "The effect of intermittent energy and carbohydrate restriction v. daily energy restriction on weight loss and metabolic disease risk markers in overweight women." British Journal of Nutrition 110.8 (2013): 1534-1547.
• Hector, Amy J., and Stuart M. Phillips. "Protein recommendations for weight loss in elite athletes: A focus on body composition and performance." International journal of sport nutrition and exercise metabolism 28.2 (2018): 170-177.
• Hutchinson, et al. "" Obesity  27 (2019): 50-58. Ahead of print.
• Sainsbury, A., et al. "Rationale for novel intermittent dieting strategies to attenuate adaptive responses to energy restriction." Obesity Reviews 19 (2018): 47-60.
• Schübel, Ruth, et al. "Effects of intermittent and continuous calorie restriction on body weight and metabolism over 50 wk: a randomized controlled trial." The American journal of clinical nutrition 108.5 (2018): 933-945.
• Smith, Gordon I., et al. "Effect of Protein Supplementation During Diet‐Induced Weight Loss on Muscle Mass and Strength: A Randomized Controlled Study." Obesity 26.5 (2018): 854-861.
• Sundfør, T. M., M. Svendsen, and S. Tonstad. "Effect of intermittent versus continuous energy restriction on weight loss, maintenance and cardiometabolic risk: A randomized 1-year trial." Nutrition, Metabolism and Cardiovascular Diseases (2018).
• Trepanowski, John F., et al. "Effects of alternate-day fasting or daily calorie restriction on body composition, fat distribution, and circulating adipokines: secondary analysis of a randomized controlled trial." Clinical Nutrition 37.6 (2018): 1871-1878.
• Varady, Krista A., et al. "Short-term modified alternate-day fasting: a novel dietary strategy for weight loss and cardioprotection in obese adults–." The American journal of clinical nutrition 90.5 (2009): 1138-1143.
• Varady, Krista A., et al. "Alternate day fasting for weight loss in normal weight and overweight subjects: a randomized controlled trial." Nutrition journal 12.1 (2013): 146.

Magnesium Could be in Charge of Your Vitamin D Levels: Supplements Lower High and Increases Low 25OHD Levels

D3 and Mg Supplements not mandatory w/ sun + balanced diet

If you subscribed to the @SuppVersity Facebook Page, you will have read the news, already: "Magnesium status and supplementation influence vitamin D status and metabolism" (Dai 2018) - that is both the title and the main results of a recent study from the Vanderbilt University that is important enough to make it from the short format on Facebook to a detailed SuppVersity article of its own - the article at hand ;-)

The 25OHD-balancing effects Dai et al. observed in their 180 participants (aged 40–85 y) could after all do much more than point towards a reason why everyone and his mama seems to be D-ficient - it could force us to redefine what "optimal" 25OHD levels are - significantly below those many Internet "health experts" recommend.

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The study is a National Cancer Institute independently funded ancillary study, nested within the "Personalized Prevention of Colorectal Cancer Trial" (PPCCT), which enrolled 250 participants at risk of developing colorectal cancer. The PPCCT is a double-blind 2 × 2 factorial randomized controlled trial conducted in the Vanderbilt University Medical Center.

Customized supplementation with magnesium glycinate brought the subjects' total magnesium into the range of the RDA (men 400-420 mg/d, women 310-320 mg/d)

What makes the study stick out is that doses for both magnesium and placebo were customized based on baseline dietary intakes - in other words: The less magnesium in the diet, the more was supplemented. Furthermore, the scientists tested not just 25OHD (which is what your doctor will test if you ask for a "vitamin D test") but also changes in plasma 25-hydroxyvitamin D3 [25(OH)D3], 25-hydroxyvitamin D2 [25(OH)D2], 1,25-dihydroxyvitamin D3, 1,25-dihydroxyvitamin D2, and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] - all by liquid chromatography–mass spectrometry.

Based on the somewhat disappointing observation that vitamin D was not related to cardiovascular disease in the recent VITAL trial (Kubiak 2018) - even in subjects with baseline vitamin D insufficiency(!) - the researchers whose current main objective is to elucidate the role that magnesium may play with cancer as part of the previously mentioned "Personalized Prevention of Colorectal Cancer Trial" speculated that "magnesium supplementation differentially affects vitamin D metabolism dependent on baseline 25-hydroxyvitamin D [25(OH)D] concentration" (Dai 2018).

In previous experiments, the scientists had already observed that people's ability to synthesize "vitamin D" depended on their magnesium status.

About both, the US's vitamin D and magnesium status, co-author Martha Shrubsole, Ph.D., research professor of Medicine, points out in the corresponding press release:

Magnesium is at the center of vitamin D metabolism - as part of CYP, cytochrome P450 enzymes (dark gray indicates deactivating enzymes, and light gray indicates activating enzymes | Dai 2018)

"Vitamin D insufficiency is something that has been recognized as a potential health problem on a fairly large scale in the U.S. A lot of people have received recommendations from their health care providers to take vitamin D supplements to increase their levels based upon their blood tests. 

In addition to vitamin D, however, magnesium deficiency is an under-recognized issue. Up to 80 percent of people do not consume enough magnesium in a day to meet the recommended dietary allowance (RDA) based on those national estimates" (from Vanderbilt press release). 

[Worth mentioning:] "Shrubsole stressed that the magnesium levels in the trial were in line with RDA guidelines, and she recommended dietary changes as the best method for increasing intake. Foods with high levels of magnesium include dark leafy greens, beans, whole grains, dark chocolate, fatty fish such as salmon, nuts and avocados." (ibid.). 

Incidentally, the hypothesis that these two deficiency nutrients may interact is not even new. You can go back as far as 50 years and will find (rodent) studies showing how vitamin D affects not just calcium but also magnesium levels (Harrison 1964). Hitherto, though, this interaction has often been ascribed to the ability of vitamin D to increase Mg absorption irrespective of one's vitamin D status.

Having high(er) 25OHD levels was found to be associated with 11-13% reduced all-cause mortality hazards in a 2013 study using data from NHANES 2001-06 - for those of the subjects that consumed high(er) amounts of magnesium the hazard reduction compared to D-ficient levels of <20ng/ml was 23%-30% and the overall HRs up to 20% lower (Deng 2013).

The opposite, i.e. putative effect of magnesium on vitamin D, on the other hand, has been largely ignored - despite the fact that more recent studies, such as Deng et al. 2013, in which the authors analyzed NHANES data from 2001 to 2006 seem to suggest that there's a two-way interaction of magnesium and vitamin D in relation to risk of both vitamin D deficiency and insufficiency - with literally life-threatening/saving implications (Deng 2013).

Which Mg is best? Plasma an bone (primary axis) as well as red blood cell (RBC; 2ndary axis(!)) content after 14 days of supplementation with identical amounts of magnesium in different organic and inorganic forms (Coudray. 2005 | learn more) - unfortunately, the study was conducted in rodents and used only gluconate, not glycinate as it was used in the PPCT trial.

Now, we shouldn't forget that, in Deng's study, we're talking about correlations/associations of which Zittermann in a 2013 writes that it "provides important findings concerning potential metabolic interactions between magnesium and vitamin D and its clinical relevance.

In 10 lab-workers, the mean serum 25(OH)D varied widely [from 17.1 (4.6) to 35.6 (5.2) ng/ml; P < 0.005] between laboratories (error bars represent SEM). B, Similarly, marked within-individual variation was observed in 25(OH)D measurement in different laboratories. This means: Whether an individual has hypovitaminosis D (threshold = dashed line) depends on which laboratory was used. 

I've heard the vitamin D test is inaccurate - Is that accurate or #fakeNews? Accurate. As Holick points out in a 2009 paper, "the first assays for 25(OH)D used the competitive protein binding format with the vitamin D binding protein (DBP) as the binder" - advantage: recognizes 25(OH)D2 equally as well as 25(OH)D3; disadvantage: the assay will also measure all sorts of D-metabolites including 24,25-dihydroxyvitamin D [24,25(OH)2D], 25,26-dihydroxyvitamin D and the 25,26-dihydroxyvitamin D -26, 23-lactone, which reduces the accuracy by ~10-15%.

The same issue(s) exist(s) for the radioimmunoassay (RIA | Diasorin@) which "typically overestimated 25(OH)D levels by approximately 10-20%" (ibid). Moreover, IDS has recently developed an RIA "which has a 100% specificity for 25(OH)D3 and only 75% specificity for 25(OH)D2 (ibid) and could thus be a more accurate alternative (still, if you're D-ficient or not often depends on which lab you're using (see Figure on the right | from Binkley 2004)

So how do you get the absolute accurate levels? You don't... well, actually you don't have to. Scientists, on the other hand, should use liquid chromatography tandem mass spectroscopy (LC-MS) to measure 25(OH)D in human serum, directly. This assay quantitatively measures both 25(OH)D2 and 25(OH)D3.

However, results should be considered preliminary since biochemical data on individual magnesium status were lacking, [and] confounding cannot be excluded" (Zittermann 2013). That's in contrast to the more recent observations by Dai et al. whose data come from a tightly controlled clinical trial - a trial that clearly suggests this link could be mechanistic.

The relationship between 25OHD and magnesium is complex and probably U-shaped

Mechanistic, but not simplistic, to be more precise: In the latest study by Dai et al. the relations between magnesium treatment and plasma concentrations of 25(OH)D3, 25(OH)D2, and 24,25(OH)2D3 were significantly different depending on the baseline concentrations of 25(OH)D, and significant interactions persisted after Bonferroni corrections (meaning including statistical correction of multiple comparisons which increase the likelihood of false positives). More specifically, the subjects from the "Personalized Prevention of Colorectal Cancer Trial" whose data the Vanderbilt scientists analyzed revealed that ...

• 

  The main result of the study: The provision of adequate (RDA) amounts of magnesium seems to help balance the 25OHD levels of the subjects in the PPCCT trial at ~30ng/ml.

  magnesium supplementation increased the 25(OH)D3 concentration when baseline 25(OH)D concentrations were close to 30 ng/mL, ...
• but decreased the levels of 25(OH)D3 when the baseline 25(OH)D was higher (from ∼30 to 50 ng/mL | insufficient data to reliable statements about even higher concentrations);
• moreover, at higher baseline 25OHD concentrations, other 25OHD metabolites, i.e. 25-hydroxyvitamin D2 [25(OH)D2], and 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] were likewise affected by magnesium supplements, how and at which levels this affects the hitherto often ignored ratio of these D-metabolites and hence our health will have to be elucidated in future studies, though (see figure below).

Overall, the provision of (sufficient =RDA) magnesium seems, as the authors from Vanderbilt University rightly point out, to allow our bodies to keep our 25OHD levels within the middle range of a previously established and repeatedly confirmed U-shaped curve that illustrates the general or specific cardiovascular disease risk as a function of serum 25OHD levels (Ross 2011; Abraham 2011).

Somewhat surprising for the "more is more" proponents, high 25OHD3 and 24,25(OH)2D3 decreased with magnesium supplementation; the often derided 25(OH)D2, on the other hand, increased (Dai 2018).

In the discussion of the results, Dai et al. (2018) write that "magnesium supplementation may not only accelerate the metabolism and degradation of 25(OH)D3 but also shift CYP3A4 to selectively degrade vitamin D3 over vitamin D2 when plasma 25(OH)D is high" - it doesn't take a scientists to realize that the findings of the study at hand thus "provide the first evidence that adequate magnesium status could potentially prevent vitamin D–related adverse events" (Dai 2018).

The existence of such a "comfort zone" is also in line with some recently published paper in the Journal of Steroid Biochemistry and Molecular Biology in which Mohammed S. Razzaque highlights that "Vitamin D status is more likely to be a consequence rather than a cause of a disease" (Razzaque 2018). That magnesium may help keeping your levels within this "comfort zone" may hence be either the results of direct interactions or simply the consequence of the well-proven cardiovascular and metabolic benefits of getting enough of the precious mineral in your diet.

More Than a Diet Myth? Dark Chocolate/Cacao Won't Get You Jacked, but it May Help Maintain a Slim Waist Over Time | read the whole SuppVersity Classic

Another reason to eat more chocolate... just kiddin', although Dai et al. rightly point out that, in spite full-blown deficiency intakes in  79% of US adults (NHANES), sufficient amounts of magnesium can be easily consumed with our diet if the latter contains copious amounts of foods with high levels of magnesium include dark leafy greens, beans, whole grains, fatty fish such as salmon, nuts, avocados and dark chocolate!

In this context, it seems appropriate to remind you that the overall result of the study at hand underlines the futility of the Western concept "more helps more", which doesn't seem to hold for vitamin D. In fact, it may well fail you when it comes to magnesium supplementation, too... and I am not just talking about magnesium (and other nutrient) losses due to the laxative effects of the Internet's favorite macromineral, here (noteworthy in this context: 1st study on transdermal magnesium + Mg-bioavailability).

From a mechanistic perspective, the interaction could be a result of the previously illustrated role of magnesium in vitamin D metabolizing enzymes: 1α-hydroxylase (i.e., CYP27B1) and 24-hydroxylase (i.e., CYP24A1), which synthesize and metabolize 25(OH)D and 1,25(OH)2D, respectively. In that, the study at hand is the first large(r)-scale study to (a) be done in people w/out severe Mg-deficiency and to (2) show that normalizing magnesium will not simply increase 25OHD, but seems to modulate it towards ~30-40ng/ml. This warrants mentioning that similar interactions do/could exist with calcium & phosphorus (Harrison 1958; Gray 1977), as well as potassium (Bikle 1978; Rafferty 2008) and salt (Breslau 1982). And guess what: One of them, i.e. calcium or rather a Ca:Mg ratio of ≥2.6, which has previously been found in >76% of the US general adult population, is also characteristic of the subjects in the study at hand - whether high Ca:Mg diets actually 'cause the vitamin D deficiency epidemic will yet have to be elucidated in future studies | Comment!

References:

• Abraham, Paul S., et al. "The vitamin "D-bate": what vascular risk in geriatric inpatients?" Journal of the American Geriatrics Society 59.8 (2011): 1556-1558.
• Bikle, Daniel D., and H. Rasmussen. "A biochemical model for the ionic control of 25-hydroxyvitamin D3 1alpha-hydroxylase." Journal of Biological Chemistry 253.9 (1978): 3042-3048.
• Binkley, N., et al. "Assay variation confounds the diagnosis of hypovitaminosis D: a call for standardization." The Journal of Clinical Endocrinology & Metabolism 89.7 (2004): 3152-3157.
• Breslau, Neil A., et al. "The role of dietary sodium on renal excretion and intestinal absorption of calcium and on vitamin D metabolism." The Journal of Clinical Endocrinology & Metabolism 55.2 (1982): 369-373.
• Dai, et al. "Magnesium status and supplementation influence vitamin D status and metabolism: results from a randomized trial." The American Journal of Clinical Nutrition, 108.6(1) (2018).
• Deng, Xinqing, et al. "Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III." BMC medicine 11.1 (2013): 187.
• Gray, Richard W., et al. "The importance of phosphate in regulating plasma 1, 25-(OH) 2-vitamin D levels in humans: studies in healthy subjects, in calcium-stone formers and in patients with primary hyperparathyroidism." The Journal of Clinical Endocrinology & Metabolism 45.2 (1977): 299-306.
• Harrison, Helen C., Harold E. Harrison, and Edwards A. Park. "Vitamin D and citrate metabolism: effect of vitamin D in rats fed diets adequate in both calcium and phosphorus." American Journal of Physiology-Legacy Content 192.2 (1958): 432-436.
• Harrison, Harold E., and Helen C. Harrison. "The interaction of vitamin D and parathyroid hormone on calcium phosphorus and magnesium homeostasis in the rat." Metabolism-Clinical and Experimental 13.10 (1964): 952-958.
• Holick, Michael F. "Vitamin D status: measurement, interpretation, and clinical application." Annals of epidemiology 19.2 (2009): 73-78.
• Kubiak, Julia, et al. "Vitamin D supplementation does not improve CVD risk factors in vitamin D-insufficient subjects." Endocrine connections 7.6 (2018): 840-849.
• Rafferty, Karen, and Robert P. Heaney. "Nutrient effects on the calcium economy: emphasizing the potassium controversy." The Journal of nutrition 138.1 (2008): 166S-171S.
• Ross, A. Catharine, et al. "The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know." The Journal of Clinical Endocrinology & Metabolism 96.1 (2011): 53-58.
• Tuohimaa, Pentti, et al. "Both high and low levels of blood vitamin D are associated with a higher prostate cancer risk: a longitudinal, nested case‐control study in the Nordic countries." International Journal of Cancer 108.1 (2004): 104-108.
• Zittermann, Armin. "Magnesium deficit-overlooked cause of low vitamin D status?." BMC medicine 11.1 (2013): 229.

AM Cardio for Fat Loss W/ 25g Casein vs. 25g Whey Isolate, 25 g Maltodextrin Preload, or Truly Fasted - What's "Best"?

Don't believe a word when someone tells you that a new study would show that you can burn extra body fat if you consume a casein shake before your (by then no longer fasted) AM cardio workouts.

While the scientific evidence doesn't seem to confirm the superiority of fasted AM cardio (learn more), there's no doubt that it can help you shed body fat if the energy you expend on treadmill ergometer, or rowing machine helps you sustain a >10% energy deficit over the next 24h.

What is highly debated, though, is whether you got to take precautions in form of protein powders (or BCCAs) to protect your muscle from falling apart.

A final answer to this question has yet to be found, but with the results of a recent study by Bradley T. Gieske and colleagues from the Lindenwood University (Gieske 2018), this ostensibly super-important question *rofl* may become redundant, anyway...

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... How's that? Well, in their study, the US scientists write that "[p]rotein consumption before fasted moderate-intensity treadmill exercise significantly increased post-exercise energy expenditure compared to maltodextrin ingestion and tended to be greater than control" (Gieske 2018). 

For the naive supplement nerd this sounds like "you can have your protein and eat it, too"

SuppVersity readers, on the hand, have learned too much about the futility of post-exercise excess oxygen consumption (aka EPOC) and its (ir-)relevance in terms of fat loss to buy into premature supplement advice a la "Ingest 30.3g of casein 32.4 minutes before your AM cardio workout".Ah... and that's not just Gieske's randomized, double-blind, placebo-controlled, crossover study tested not 30.3g/session, but rather...

• 25g protein in form of 25 g of similarly colored and flavored whey protein isolate, of casein protein (real micellar casein, no cheap caseinates), and compared the effects of this protein preload to 25 g of maltodextrin, or a non-caloric control. 

After the ingestion of the supplement, the participants sat quietly for 30 min before completing a standardized warm-up protocol consisting of whole-body dynamic movements that lasted approximately ten minutes. Hence, the actual testing session, a medium-to-low intensity 30-minute 'cardio' session on the treadmill (55% heart rate reserve) took place 40 minutes after the bolus ingestion of casein, whey, maltodextrin or the zero-calorie control drink. 

Figure 1: Acute exercise-induced (kcal total on the primary axis) and extrapolated post-exercise 24h energy expenditure (kcal/kg/day on the secondary axis) in the study by Gieske et al (2018).

In conjunction with the 15 minutes, it took for the subjects to get their resting metabolic rate post workout (re-)assessment started, the data in Figure 1 was thus generated at roughly T=60 minutes in the early postprandial phase (note: don't forget that the exercise itself will have slowed down the digestion significantly).

"The postprandial phase is not exactly where you'd expect fat oxidation to peak, no?"

Well, in terms of bro-science the above question seems to be very reasonable. As the pros (here Gieske et al.) point out, though, anyone who knows a thing or two about the metabolic effects of protein and the potential issues w/ training fasted will be hardly surprised to see that 

the researchers' hypothesis "that pre-exercise protein ingestion would increase post-exercise energy expenditure and fat oxidation compared to both carbohydrate and fasting conditions" (Gieske 2018)...

... was confirmed when the data from the eleven healthy, college-aged males (23.5 ± 2.1 years, 86.0 ± 15.6 kg, 184 ± 10.3 cm, 19.7 ± 4.4% fat | recreationally active, doing both cardio and weights, being active most of the days - but no athletes) was analyzed. In that it's important to note the following:

• Dietary standardization in form of a replication of the average four-day diet composition reported by participants prior to Visit 1 was as follows: 2446 ± 800 kcal (28.44 ± 9.30 kcal/kg), 132 ± 56 g (1.53 ± 0.65 g/kg) protein, 235 ± 101 g (2.73 ± 1.17 g/kg) carbohydrate, 99 ± 37 g (1.15 ± 0.43 g/kg) fat on the remaining test visits was successful.
• Exercise standardization as measured using one-way ANOVA revealed no significant differences (p = 0.743) in intra-exercise heart rate, rating of perceived exertion (p = 0.985), or oxygen consumption (p = 0.993) between conditions, suggesting that intensity was sufficiently standardized across all testing sessions.
• And the pre-treatment and pre-exercise rates of energy expenditure (Absolute: 1873 ± 189 kcal/day, Relative: 22 ± 2 kcal/kg/day) were not significantly different across conditions (p > 0.99). 

All three factors can thus not explain why the scientists found visible (Figure 1) and statistically significant inter-trial differences between the pre-treatment/exercise energy expenditure and post-exercise energy expenditure. More specifically, the researchers were able to show that, ... 

• 

  #Evidence: Meta-analysis says: "Fasted AM Cardio - No Measurable Physiological Benefits in Terms of Fat Loss & Body Composition" | more

  the energy expenditure after consuming the whey protein isolate (WPI | 3.41 ± 1.63 kcal/kg) was significantly greater (p < 0.05) than the within-group change in REE following consumption of maltodextrin (MAL | 1.57 ± 0.99 kcal/kg, p = 0.010) and tended to be greater than the non-feeding control group (2.00 ± 1.91 kcal/kg, p = 0.055); 
• similarly, the energy expenditure after consuming the casein protein (CAS | 3.38 ± 0.82 kcal/kg) was greater than those following consumption of MAL (p = 0.012) and tended to be greater than the non-feeding control group (p = 0.061) 

About the trend towards statistically significant effects of whey vs control the scientists write that it "is notable, as 73% of the participants during the WPI condition exhibited a change in REE toward the direction of significance" (Gieske 2018 | note: the success rate in terms of being able to observe beneficial effects on energy expenditure was yet highest in the casein group, where 9 out of 11 subjects vs 6 out of 11 participants in the WPI group saw significant increases). 

The researchers calculated within-condition effect sizes for each nutrient (WPI, CAS, and MAL) - with effect sizes for WPI and CAS being moderate to large compared to MAL and CON.

So far, so good, now for the bad news: With a total intra-exercise EE of 345 ± 31 kcal, 362 ± 32 kcal, and 349.17 ± 70 kcal, the increase in energy expenditure compared to the control trial (293 ± 37 kcal) is below the amount of energy, circa 100kcal, in the protein/carbohydrate supplements. 

Figure 2: Individual effects on energy intake and expenditure (left) and corresponding net effect (right).

You can see that very well if you check out the subjects' energy balance right after the workout (Figure 2, left); and things don't look much better if we assume that the post-workout increase in energy expenditure persists, i.e. that the scientists' calculated "increase in energy expenditure" remains stable (or whatever they assumed it did, when they used the data from 20-25 minutes after the workout and extrapolated it to 24h), and calculate the effect of consuming whey, casein, or maltodextrin on the net energy balance.

Do not get me wrong, though... AM cardio aids fat loss!

#Popular: "Ever Wondered Why the Fat Keeps Falling Off When You Embark on Intermittent Fasting Regimens? Calories, Bro!" | read more

I've experienced that repeatedly, myself. For me, personally, doing AM cardio means doing cardio at all. If I postpone it to "later", it is not unlikely that I don't do it at all and fail to burn those extra 300-500kcal which are then not missing from my net energy balance - a balance I deliberately keep in the red while dieting, 'cause there's no metabolic magic in AM cardio that would make the fat fall off, it is pretty much like "fasting": It's all about calories ... well, calories, coffee ('cause you always need it ;-) and weight training + enough protein to optimize your lean mass retention aka "keep your gainz" ;-)

No, no, and no: It does not make a difference! It makes no difference if you consume whey or casein or any other form of protein before your low-to-moderate intensity AM cardio. While the insulin spike from whey may blunt the fat oxidation during the initial 5 minutes of your training that's not relevant for your real-world fat loss.

The same goes for the 14.42kcal difference in the NET energy balance between whey and casein and the overall difference to control, of which we (a) do not even know if those 75-90kcal wouldn't simply be compensated for at lunch or dinner, and/or (b) nullified by potential compensations in REE later in the day (which were not measured).

So what's the verdict, then? In the absence of practically relevant changes in energy expenditure, let alone net energy balance, it would be stupid to expect to lose more body fat if you consume 25g of either whey or casein before your by then no longer "fasted" AM cardio sessions.

What's more, the measurable, but overall small and medium effects (Cohen's d) of casein and whey protein isolate on the subjects' intra- and post-workout total fat oxidation and respiratory exchange rate (ratio of carbohydrates to fats that are used to fuel your metabolic requirements), respectively, are likewise irrelevant when it comes to the alleged "fat burning effects" of AM cardio.

In the end, it's just a zero-sum-game! One of which I can guarantee, however, that it is going to be completely misinterpreted on the average bodybuilding and physique boards, though... especially with the scientists' imho somewhat unfortunate emphasis on the "significantly increased rates of post-exercise fat oxidation and energy expenditure with casein" and "the reduction in [...] total fat oxidized during the exercise bout [with WPI preingestion] compared to casein" in the first paragraph of the discussions | Leave a comment on Facebook!

References:

• Gieske, et al. (2018). "Metabolic impact of protein feeding prior to moderate-intensity treadmill exercise in a fasted state: a pilot study." Journal of the International Society of Sports Nutrition 15:56.