Magnesium Round-Up: Know If You Are Deficient, Whether You Need More, Where to Find It, How Dietary Mg Contents Changed & How Magnesium Interacts W/ Vitamin D

24%, 23% and 22% of the DV for magnesium that's what you can find in one serving of sunflower seeds (0.25cup), halibut (4oz) and a large(r) banana - now you tell me it was impossible to get your magnesium from dietary sources.

After having handled half of the Science Round-Up from Thursday yesterday, yesterday, there is still something left to serve: seconds to the seconds, if you will and probably not so "new" as the average SuppVersity news. In order not to bore you, I will yet refrain from telling you how important magnesium is and how it is involved in thousands of enzymatic reactions ... you know the whole magnesium-guru-spiel all too well, anyway. I mean, anyone doing a cursory Google search will have to conclude that there is nothing magnesium cannot cure, right?. Whatever you may suffer from, someone has already found out that it must be related to magnesium deficiency or, even more profitable, taking the wrong form of magnesium supplements.

Apropos deficiency: How do you even know you are deficient?

What sounds like a question that could be answered in one, at best two sentences turns out to be one of the root causes of the whole confusion about magnesium. Based on a standard blood test you can only exclude that your levels are (a) so high or (b) so low that you better head straight to the emergency room. Magnesium is, just as the other electrolytes, simply too important for your body to have them drop below a certain margin in which your heart works optimally. So if there is not enough magnesium around, your body will tap into tissue stores the status of which is obviously not identical to the serum levels on a standard lab test.

Table 1:The lion's share of magnesium to replete your serum levels is not coming from your red blood cells and therefore RBC levels are only a proxy and not a 100% reliable marker of total body mg status (data based on Elin. 1987)

According to Maurice J. Arnaud who wrote a review with the telling title "Update on the assessment of magnesium status" in 2008, the most reliable method to assess the whole body magnesium status would be a metabolic ward study in the course of which a so-called "loading test" would be performed, But...

"[b]alance studies are time consuming, labour intensive and need well trained staff. They are often performed in a metabolic unit and require complete urine and faecal collections; therefore it is not a method that can be applied as a routine test for the evaluation of Mg status. Loading tests are simplified balance studies where absorption is supposed not to be disturbed when Mg is given orally so that body retention is calculated from urine elimination. Mg administration during a loading test can be either oral or intravenous and it is important that the subjects have normal kidney function. Urine is collected for 24 hours following administration of the Mg load as Mg excretion by the kidney has been shown to have a circadian rhythm . Under these conditions, the loading test is supposed to be a reliable indicator of Mg status." (Arnaud. 2008)

With the erythrocyte (red blood cell) test for magnesium, there is however an alternative available, which may not be just as reliable but appears to show a relatively high correlation with whole body magnesium levels in many, but not all studies (Malon. 2004).

How likely is it that you are deficient?

Honestly, I would hope that it is unlikely, because if that is the case for someone who is not taking supplemental magnesium you can almost be sure that her or she is following a healthy whole foods diet.

Table 2: Overview of age groups with more than 5 % of intakes below the lowest recommended intake levels in 7 European countries; T, toddlers (1–3 years (both sexes)); C, children (4–10 years); Y, youth (11–17 years); A, adults (18–60 years); S, seniors (.60 years); capitals, both sexes; lower case, women only; lower case italic, men only (Mensik. 2013)

If you take a look at table 2 you will see that even the average German gets enough magnesium in his diet, irrespective of his age, and much contrary to our neighbors in the East, West and Northwest (I could not resist to mark zinc another of those purported minerals of which conventional wisdom tells you that you simply cannot get enough from your diet).

Knowing that most of you are probably Americans, I can calm you down. You are not worse than your British friends. In fact, the NHANES data from 1999-2000 suggests that the average American Caucasian and Mexican man below 50 gets enough magnesium from his food only! Unfortunately, the same cannot be said for the women, and both male and female African Americans who have trouble meeting their requirements even if one accounts for the additional magnesium from supplements (NHANES).

Magnesium and the athlete

A note on magnesium and cramps: While there is evidence that altered serum osmolality and altered serum electrolyte concentrations, notably hypochloraemia, hyponatraemia, and hypocalcaemia (=not hypomagnesaemia) can cause generalized skeletal muscle cramping at rest in specific clinical settings, "data from well-conducted prospective cohort studies show that athletes with acute EAMC are not hyponatraemic, hypochloraemic, or hypocalcaemic and do not have an abnormal serum osmolality." (Schwellnus. 2008).

For the average athlete, a low magnesium intake is yet rather the exception and can even be problematic for athletes with a high anaerobic-to-aerobic ratio who suffer from increases in blood mg due to an overall reduction on blood volume after intense workouts, anyway (Cordova. 1992; Joborn. 1985; Monteiro. 2005; Monteiro. 2006). It is thus no wonder that not magnesium deficiencies, but high magensium levels are a problem that is commonly observed in athletes. I mean, what are you supposed to do, when even your mother "lies" to you about cramps being caused by magnesium deficiency?

"The most common alterations were higher serum phosphate (29/61, 47%) and magnesium concentrations (28/61, 46%). Abnormalities of serum phosphorus and magnesium concentrations were detected in almost half of the athletes. Hyperphosphataemia and hypermagnesaemia were the most common abnormalities." (Malliaropoulos. 2012)

The data Malliaropoulos et al. analyzed came from 130 elite track and field athletes (65 males and 65 females, age range 20-30 years) from the National Athletics Sports Medicine Center database in Thessaloniki, Greece. And maybe some of them were even on the proven non-ergogenic ZMA (zinc + magnesium + vitamin B6; cf. Wilborn. 2004).

So where do you get your supplemental magnesium from and how much?

I am not going to tell you to stop supplementing with magnesium if you feel that this has done you good in the past. It is after all an important mineral. What I want to remind you of is yet the fact that taking 100% of the RDA is imho the absolute maximum. Even if you don't end up with high levels due to supplementing more and don't care about wasting money, there is one thing that's commonly overlooked about human physiology and that is how the intake and excretion of nutrients are highly inter-related. In other words, if your body switches into a "get rid of magnesium" mode it is likely you are loosing other electrolytes you do not supplement in copious amounts (e.g. salt ;-), as well.

Figure 1: 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)

As far as the best forms are concerned the number of studies comparing multiple forms to each other is limited and the inter-comparison of different studies not really legit. Therefore I have simply copied + pasted the figure that went with a previous article on the matter - as you can see, you can generally use whatever form of magnesium you want - even the cheap oxides, which worked wonders for anxiety ridden ladies in a study by De Souza et al. that was published in the Journal of Women's Health & Gender-Based Medicine in March 2000. As long as you take your magnesium supplements in reasonably low doses - the dose in the De Souza study for example was 200mg + 50mg B6 - and over a long enough period, they are going to bring your levels back up - if not sooner, then later.

Magnesium depletion of our foods

A note on topical Epsom salt from the early 20th century: While I did tell you on the show that I could not find peer-reviewed adequately powered studies on the topical absorption of magnesium in the for of mg oil or Epsom salt, I found a comment in a 1915 paper on the potential harm caused by cosmetics quite enlightening, esp. the part on the economic value of respective products, where Martin I. Wilber writes that the ability of respective products to penetrate the "unbroken skin has as yet not been demonstrated" and cautions against the sue "of the now widely advertised lotions containing magnesium sulphate or Epsom salt", of which "the latter preparations serve very well to show the gullability of that portion of the public that is desirous of improving its facial appearance. As Epsom salt, magnesium sulphate can usually be purchased for 5 cents a pound, while in the form of any one of the popular skin or wrinkle lotions it is sold at the rate of from $2 to $4 a pound." (Wilbert. 1915) You see, there were snake,... ah I mean mg oil vendors all over the place even 100 years ago ;-)

Aside from the almost cult-like worship of epsom salt baths and topical ng oils, the notion of a general depletion of mg in the foods we eat is one of the favorites among the bazillion of websites run by people who hoax you to believe they were concerned with your physical health, when all they are concerned with is their own financial health.

Figure 2: Changes in mineral content of selected food types from 1940-2002 (Thomas. 2007)

It is, as the data in figure 2 goes to show you true that the amount of magnesium in many of the foods we consume is lower these days than it was amidst WW2. The mg loss in meats, for example, is  driven by the processing, while corned beef has lost almost 50% of its "original" mg content, the amount of mg in roast beef and steaks is still the same, the one in turkey is even up by ~30% and for chicken it remained 100% stable (Thomas. 2007). It is also a very intriguing coincidence that the same websites will usually also tell you how we are all not just magnesium deficient, but also copper toxic. Strange in view of the fact that the average reduction in copper is -62% and thus >2x higher than that of magnesium.

Magnesium supplementation for special conditions

Before closing this round-up with a bottom line, I am briefly listing a couple of things related to magnesium or rather a deficiency in this important mineral that could be solved by simply upping your dietary and/or supplemental magnesium intake.

• 

  Higher vitamin D levels increase MG uptake from the gut and supplementation with VD has been shown to increase mg in obese, yet not in normal individuals (Farhanghi. 2009). On the other hand, mg has recently been found to be necessary for the production of calcitriol from 25OHD (Matsuzaki. 2013)

  anxiety - mg is the gate-keeper at the NMDA receptor and interacts with the GABA receptors; a deficiency can cause anxiety, the use of extra magnesium will yet not automatically solve the problem if you are not low to begin with
• depression - low cellular mg levels can precipitate if not cause depression(-like) symptoms, 150-300mg of magnesium glycinate or better taurinate can help (Eby. 2006)
• low vitamin D - while it is not yet sure if it helps with upping the storage form of vitamin D (25OHD), it has been recently established that magnesium is necessary for the production of calcitriol the active form of vitamin D; adequate levels of D also facilitate mg absorption very high levels of vitamin D, on the other hand, have been associated with low / imbalanced mg levels - probably due to their effects on calcium homestasis
• constant stress / burnout - initially low mg levels will lead to a hyper activity of the stress-axis within the HPTA; the constantly overtaxed CNS will then give in and you will end up totally burned out (Sartori. 2011); this state cannot be reversed by magnesium supplementation, alone, but it can aid the recovery process which is largely based on taking off of everything that stresses you

Whether or not simply eating more high magnesium foods will be enough or whether you actually have to buy supplements to work on these and other issues will also depend on whether

• you can digest / absorb it, which would be hampered due to vomiting, diarrhea, bowel resection, intestinal and biliary fistulas or hemorrhagic pancreatitis
• lose too much mg over the kidneys, due to chronic parental fluid therapy, osmotic diuiresis, hypercalcemia, diuretics, aminoglycosides, amphotericin B, pentamidine, cisplatin, cyclosporine, alcohol metabolic acidosis (ketosis, starvation, alcoholism), renal diseases, or
• suffer from endocrine disorders like primary or secondary aldosteronism, diabetes, hyperthyroidism or hyperparathyroidism

If anything of these sounds familiar, I would certainly consider testing my mg levels (erythrocyte test) before and while I was supplementing and that's not about wasting money on potentially unnecessary supplements, but much more about making sure that you actually get, absorb and retain enough magnesium.

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Bottom line: Magnesium is certainly an important mineral, but its effects must not be seen in isolation, it should not be supplemented in copious amounts in isolation without medical indication and it may not be misunderstood as a natural pharmacological agent - it works by (a) replacing a deficiency or (b) countering an imbalance. Plus: It is not generally impossible to get your 300-400mg of magnesium from your diet.

References:

• Arnaud MJ. Update on the assessment of magnesium status. Br J Nutr. 2008 Jun;99 Suppl 3:S24-36.  
• Bohl CH, Volpe SL. Magnesium and exercise. Crit Rev Food Sci Nutr. 2002;42(6):533-63. Review.
• Coudray C, Rambeau M, Feillet-Coudray C, Gueux E, Tressol JC, Mazur A, Rayssiguier Y. Study of magnesium bioavailability from ten organic and inorganic Mg salts in Mg-depleted rats using a stable isotope approach. Magnes Res. 2005 Dec;18(4):215-23.
• Cordova A. Changes on plasmatic and erythrocytic magnesium levels after high-intensity exercises in men. Physiol Behav1992; 52: 819-21.
• Eby GA, Eby KL. Rapid recovery from major depression using magnesium treatment. Med Hypotheses. 2006;67(2):362-70. 
• Elin RJ. Assessment of magnesium status. Clin Chem. 1987 Nov;33(11):1965-70. Review.
• Farhanghi MA, Mahboob S, Ostadrahimi A. Obesity induced magnesium deficiency can be treated by vitamin D supplementation. J Pak Med Assoc. 2009 Apr;59(4):258-61. 
• Joborn H, Akerstrom G, Ljunghall S. Effects of exogenous catecholamines and exercise on plasma magnesium concentrations. Clin Endocrinol (Oxf)1985; 23: 219-26; (Oxf).
• Malliaropoulos N, Tsitas K, Porfiriadou A, Papalada A, R Ames P, Del Buono A, Lippi G, Maffulli N. Blood phosphorus and magnesium levels in 130 elite track and field athletes. Asian J Sports Med. 2013 Mar;4(1):49-53.
• Malon A, Brockmann C, Fijalkowska-Morawska J, Rob P, Maj-Zurawska M. Ionized magnesium in erythrocytes--the best magnesium parameter to observe hypo- or hypermagnesemia. Clin Chim Acta. 2004 Nov;349(1-2):67-73.  
• Matsuzaki H, Katsumata S, Kajita Y, Miwa M. Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats. Magnes Res. 2013 May 1;26(2):83-6.
• Mensink GB, Fletcher R, Gurinovic M, Huybrechts I, Lafay L, Serra-Majem L, Szponar L, Tetens I, Verkaik-Kloosterman J, Baka A, Stephen AM. Mapping low intake of micronutrients across Europe. Br J Nutr. 2013 Aug;110(4):755-73.   
• Miriam C. De Souza, Ann F. Walker, Paul A. Robinson, and Kim Bolland. Journal of Women's Health & Gender-Based Medicine. March 2000, 9(2): 131-139.  
• Monteiro CP. Equilíbrio Oxirredutor: um estudo em nadadores e em não atletas, em repouso e em resposta ao exercício [PhD]. Lisboa: Faculdade de Motricidada Humana, Universidade Técnica de Lisboa, 2005.
• Monteiro CP, Santa Clara H, Raposo MF,et al. Effect of training and exercise intensity on magnesium status. In: Alpoim C, Vasconcelos Morais P, Santos MA, Cristóvão AJ,
  Centeno JA, Collery P, eds.Metal Ions in Biology and Medicine. Paris: John Libbey Eurotext, 2006: 546-52 
• Sartori SB, Whittle N, Hetzenauer A, Singewald N. Magnesium deficiency induces anxiety and HPA axis dysregulation: modulation by therapeutic drug treatment. Neuropharmacology. 2012 Jan;62(1):304-12. doi: 10.1016/j.neuropharm.2011.07.027. Epub 2011 Aug 4.
• Schwellnus MP. Cause of exercise associated muscle cramps (EAMC)--altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med. 2009 Jun;43(6):401-8. 
• Thomas D. The mineral depletion of foods available to us as a nation (1940-2002)--a review of the 6th Edition of McCance and Widdowson. Nutr Health. 2007;19(1-2):21-55. Review.
• Wilbert MI. Cosmetics as Drugs: A Review of Some of the Reported Harmful Effects of the Ordinary
  Constituents of Widely Used Cosmetics. Public Health Reports. 1896-1970; 30(42): Oct. 15, 1915. 3059-3066.
• Wilborn CD, Kerksick CM, Campbell BI, Taylor LW, Marcello BM, Rasmussen CJ, Greenwood MC, Almada A, Kreider RB. Effects of Zinc Magnesium Aspartate (ZMA) Supplementation on Training Adaptations and Markers of Anabolism and Catabolism. J Int Soc Sports Nutr. 2004 Dec 31;1(2):12-20.

The Neurotransmitter Depleting Effects of Branched Chain Amino Acids (BCAAs) and Their Potential Ergolytic, Anxiogenic & Depressive Downstream Effects

Oh yes, this will happen despite if not because you've taken large amounts of BCAA before the workout.

Usually you don't put the cart before the horse, but I guess you won't mind if I do so and postpone a summary of the information on magnesium from yesterday's installment of the Science Round-Up to tomorrow, when this means that we are going to take care of the "BCAA crisis" today.

Ok, maybe "crisis" is not the best word to describe the reverberations the recent publication of a study by SuJean Choi et al. should be having (=nobody buys BCAAs anymore), but I was looking for something better than the usual "the truth about..." Science, and I am not going to tire repeating that, is after all not about truth (that's what the confessional box is about), but about experimentally verifiable/verified and non-verifiable/non-verified hypothesis (Popper. 1994).

BCAAs can have ergolytic effects - A verifiable hypotheses?

Based on the observations Choi et al. made in by then decapitated lab animals (so much about the "why don't they prove this works in humans"-argument), the administration of a solution that contained either a BCAA + Arginine + Glutamine mix, or one out of two different EAA mixtures, it is safe to say that the hypothesis formulated in the subheading of this paragraph could belong to the former, i.e. the verifiable, hypothesis; and that despite the fact that the addition of glutamine and arginine to the human equivalent of 19:12:12 mg/kg body weight of leucine:isoleucine:valine (less than most BCAA products offer) would at least buffer the previously discussed performance decrements due to the accumulation of ammonia (learn more)

Table 1: Amino acid composition (mg/kg body weight) of the AA supplements tested (Choi. 2013)

In the end, the results Choi et al. present contradict both, the promises on the labels of the countless BCAA products and Newsholme's and Blomstrand's hypothesis that the inhibitory effect the BCAAs exert on the uptake of tryptophan from the blood into the brain and the way this forestalls the subsequent conversion of tryptophan to serotonin would lead to a reduction of central fatigue during exercise (Newsholme. 1996).

Figure 1: Effects of BCAA and BCAA + 100mg/kg l-tyrosine supplementation on serum and brain amino acid and neurotransmitter levels in sedentary rats; data expressed relative to vehicle (Choi. 2013)

Now, the data in figure 1 does confirm the first part of the Newsholme + Blomstrand hypothesis: The adminstration of BCAAs in an amount similar to many low dose BCAA supplements that are currently being marketed as ergogenic agents does blunt the increase in serotonin by competitively inhibiting the uptake of l-tryptophan from the bloodstream. The latter is a necessary consequence of the fact that both the BCAAs and the said 5-HTP (=serotonin) precursor are being transported by the same large amino acid transporter (think of it like a taxi that is allowed to pass the blood brain barrier) as l-tryptophan.

A note on the pro-obesity effects mentioned during the show: While some scientists invoke the increased BCAA levels in obese individuals and the subsequent blockade of serotonin (and dopamine) production in the brain to the constant insatiable cravings, anxiety and depression in these individuals (Breum. 2003; She. 2007; Coppola. 2013) a more fundemental contribution to the obesity pandemic has been proposed by Newgard et al. (2009). Their hypothesis is that a continuous presence of BCAAs in the blood will lead to a continuous overexpression of mTOR that increases the susceptibility to diet induced obesity and insulin resistance.

Now, it is also true that this will blunt the increase in 5-HTP synthesis in the brain (-48%; in the absence of exercise; see figure 1), but with the concomitant -25% decline in hypothalamic DOPA (=dopamine, the "get going neurotransmitter") in the brain after ~30min, the net ergogenic effect will, just as it was the case in the majority of pertinent rodent and human studies, be negligible, at best!

Modulatory Effects of Different Macronutrient & Stress Compositions on Serotonin (read more)

"Following oral intubation with the ‘‘BCAA’’ mixture to sedentary rats (see Table1; n=3/group), serum TRP and TYR concentrations showed non-significant reductions; the serum TRP and TYR ratios, and cortical TRP and TYR concentrations dropped markedly at 30 min. Cortical TRP and TYR concentrations remained low for the duration of the study (120 min), while the ratios began to recover at 90–120 min. DOPA and 5HTP synthesis dropped to nadir values at 60 min; DOPA synthesis remained low, while 5HTP synthesis had rebounded by 120 min (bottom panels, Fig.2).

Inasmuch as the maximal effects on DOPA and 5HTP synthesis occurred 60 min following intubation, all subsequent studies used 60 min as the experimental endpoint." (Choi. 2013)

In fact, the overall and as you've just read persistent drop in neurotransmitter levels can not only make you tired, previous research even suggests that it may be invoked in the etiology of depression / central fatigue (see previous SuppVersity post "Study Investigates Modulatory Effects of Different Macronutrient Compositions on Serotonin in the Presence and Absence of Stress" | read more).

Balancing leucine with tyrosine at a ~1:1 ratio helps

The data in figure 1 does however also tell you that you can mitigate the problem by the addition of 100mg/kg body weight of l-tyrosine to the supplement. With that being roughly equivalent to the amount of leucine in the BCAA formula (cf. table 1), this is yet far more of the dopamine precursor than your average BCAA product is going to have... after all it's a maximal leucine concentration that sells and is propagated as being "modern" and "maximal anabolic".

Figure 2: Hypthalamic DOPA and 5HTP levels after BCAA or BCAA + 100mg/kg tyrosine ingestion with / without exercise, left (Choi. 2013); effects of BCAA or l-tyrosine supplementation on time to exhaustion (Strüder. 1998)

With the addition of 100mg/kg l-tyrosine, you may yet in fact expect to see some benefits. Unfortunately, the currently available literature will put you right in a study that was conducted by Strüder et al. for example neither 21g of BCAAs nor the whopping dose of 20g of pure l-tyrosine resulted in the expected increase in the time-to-exhaustion during time trials in trained cyclists (see figure 2, right; Strüder. 1998) and Blomstrand concludes in his review for the British Journal of Sports Medicine's A-Z Supplement Review Series:

"Under certain conditions, BCAA supplementation can also improve physical performance, although the majority of studies have found no effect of BCAA on performance when supplied together with carbohydrates." (Blomstrand in Burke. 2009)

This, on the other hand, tells you that the performance enhancing effects are a mere result of the oxidation of BCAAs of which both Blomstrand, who is by the way defending his own hypothesis here, and the recently discussed by Falavigna et al. (see SuppVersity News) indicate that the ensuing increased release in ammonia production "may be detrimental to performance" (Blomstrand in Burke. 2009). If you also take into consideration that a study by van Hall et al. from 1995, i.e. before Newsholme & Blomstrand came up with the hypothesis the whole BCAA myth was built on, basically falsified the tryptophan hypothesis of fatigue, In the pertinent study the scientists were after all able to show that the provision of BCAAs as workout fuel is not superior to that of tryptophan and that despite a 8-12% reduction in brain tryptophan uptake at exhaustion with BCAAs and a 7- to 20-fold increase in response to the ingestion of a tryptophan supplement (van Hall. 1995).

Milk protein EAAs: An option, but a logical one?

If you finally take a look at the data in figure 3  you will notice that the head-to-head comparison would place an amino acid pattern as the one you can find in milk proteins, would probably be the best amino acid supplement source to resort to (don't ask me what exactly it is that makes the difference, I can't tell, but suspect it could be related to lysine which is also going to block the same small AA channel into the brain + the inclusion of non-essential amino acids in milk protein vs. pure EAAs).

Figure 3: Comparison of the the effects of BCAA, regular EAAs and an EAA amino acid mix from milk protein; composition of the mixtures see table 1 (Choi. 2013)

But let's be honest, does it really make sense to buy an additional supplement, when you already have a pouch of cheap and tasty whey and/or another fast digesting high BCAA protein such as pea protein lying around at home?

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So what's the verdict then? As you've heard on the Science Round-Up, yesterday, I personally think that this does not make sense, because ...

1. .

   

   Suggested Read: "Spiking Whey W/ EAA Will Provide Inferior Results" (read more)

   .. neither the total amount of amino acids that are obsorbed within 1h from free form EAAs, nor the the utilization speak in favor of EEAs - both have been shown to be +7% and +92% higher with slightly hydrolized whey vs. EAAs (Monchi. 1993),
2. ... nor is there any anabolic benefit to the addition of EAAs or leucine to whey, in fact "25 g of whey is better suited to increase resistance exercise-induced muscle anabolism" compared to lower amount of whey that has been pimped with additional EAAs and leucine to offer the same amount of the purpoted "anabolics" as the 25g dose of plain whey protein (click on the picture to the right to learn more; Churchward-Venne. 2012)

Contrary to Carl's jovial suggestion to simply throw away your BCAA supplements, I would suggest you keep them (unless you already have problems with anxiety, etc.), cut back on the dosage and monitor your response closely. The latter is especially true, when you take them on an empty stomach. After you've run out, train a month with nothing but cheap protein and decide afterwards whether or not your past "great training experience", "superior intensity" and whatever else the ads tell you the respective products will do was more than just another instance of the brocebo effect (learn more about brocebos).

References:

• Breum L, Rasmussen MH, Hilsted J, Fernstrom JD. Twenty-four-hour plasma tryptophan concentrations and ratios are below normal in obese subjects and are not normalized by substantial weight reduction. Am J Clin Nutr. 2003 May;77(5):1112-8. 
• Burke LM, Castell LM, Stear SJ, Rogers PJ, Blomstrand E, Gurr S, Mitchell N, Stephens FB, Greenhaff PL. BJSM reviews: A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance Part 4. Br J Sports Med. 2009 Dec;43(14):1088-90.
• Choi S, Disilvio B, Fernstrom MH, Fernstrom JD. Oral branched-chain amino acid supplements that reduce brain serotonin during exercise in rats also lower brain catecholamines. Amino Acids. 2013 Aug 1. [Epub ahead of print] 
• Coppola A, Wenner BR, Ilkayeva O, Stevens RD, Maggioni M, Slotkin TA, Levin ED, Newgard CB. Branched-chain amino acids alter neurobehavioral function in rats. Am J Physiol Endocrinol Metab. 2013 Feb 15;304(4):E405-13.
  
• Churchward-Venne TA, Burd NA, Mitchell CJ, West DW, Philp A, Marcotte GR, Baker SK, Baar K, Phillips SM. Supplementation of a suboptimal protein dose with leucine or essential amino acids: effects on myofibrillar protein synthesis at rest and following resistance exercise in men. J Physiol. 2012 Jun 1;590(Pt 11):2751-65.
• Monchi M, Rérat AA. Comparison of net protein utilization of milk protein mild enzymatic hydrolysates and free amino acid mixtures with a close pattern in the rat. JPEN J Parenter Enteral Nutr. 1993 Jul-Aug;17(4):355-63. 
• Newgard CB, An J, Bain JR, Muehlbauer MJ, Stevens RD, Lien LF, Haqq AM, Shah SH, Arlotto M, Slentz CA, Rochon J, Gallup D, Ilkayeva O, Wenner BR, Yancy WS Jr, Eisenson H, Musante G, Surwit RS, Millington DS, Butler MD, Svetkey LP. A branched-chain amino acid-related metabolic signature that differentiates obese and lean humans and contributes to insulin resistance. Cell Metab. 2009 Apr;9(4):311-26.
• Newsholme EA, Blomstrand E. The plasma level of some amino acids and physical and mental fatigue. Experientia. 1996 May 15;52(5):413-5. Review.
• Popper, KR. Zwei Bedeutungen von Falsifizierbarkeit [Two meanings of falsifiability]. In Seiffert, H.; Radnitzky, G. Handlexikon der Wissenschaftstheorie. München: Deutscher Taschenbuch Verlag. 1994.  
• She P, Van Horn C, Reid T, Hutson SM, Cooney RN, Lynch CJ. Obesity-related elevations in plasma leucine are associated with alterations in enzymes involved in branched-chain amino acid metabolism. Am J Physiol Endocrinol Metab. 2007 Dec;293(6):E1552-63. Epub 2007 Oct 9.
• Strüder HK, Hollmann W, Platen P, Donike M, Gotzmann A, Weber K. Influence of paroxetine, branched-chain amino acids and tyrosine on neuroendocrine system responses and fatigue in humans. Horm Metab Res. 1998 Apr;30(4):188-94.  
• van Hall G, Raaymakers JS, Saris WH, Wagenmakers AJ. Ingestion of branched-chain amino acids and tryptophan during sustained exercise in man: failure to affect performance. J Physiol. 1995 Aug 1;486 ( Pt 3):789-94.

Citrulline = The Dieter's Amino Acid? Citrulline Maintains Muscle Protein Synthesis & Strength Endurance During Caloric Deficits Better Than Leucine!?

Can citrulline supplementation prevent you from hitting a catabolic wall, when you are dieting? And is it more potent than leucine?

You have been told "leucine is the most anabolic amino acid known to man", by the guy at your local GNC, the bros in the gym and the "experts" on the board.

And yeah, in a way, they all are "right", but the surprising negative effects of HMB supplementation on the muscle catabolism during overtraining (read more) should have reminded you that this does not imply that it will also protect your muscles against muscle breakdown and/or have similar "anabolic" effects on a diet.

Dieting is a major change in the metabolic stage and another stage means a different cast, among whom citrulline could turn out to be the new star... at least if we trust the results of a recent rodent study.

Different metabolic stage - new stars on the scene

In their most recent paper Ventura et al. describe the results of a rodents experiment in the course of which they  evaluated the effect of sequential administration of leucine (LEU) and citrulline (CIT) to preserve lean body mass during food restriction. In a 2009 study, Moinard et al. had already observed that the provision of 1.0 g/kg/day of CIT (HED ~10-15g) to exert beneficial effects on body composition in aged rats (Moinard.2009) and if you go by the abstract of the study at hand, it would sound as if citrulline was not simply "lean mass protective", but also much more potent than leucine:

Only CIT administration (1 g/kg) was able to restore MPS [muscular protein synthesis] (CIT1: 3.4±0.3 vs.R: 2.5 ±0.2 %/day,p=0.05) and increase muscle maximum tetanic force (CIT1: 441 ±15 vs.R: 392 ±22 g,p=0.05) and muscle strength (CIT1: 4,259±478 vs. R: 3,045 ±663 A.U., p=0.05). LEU had no effect and CIT+LEU supplementation had few effects, limited to adipose mass and fatigue force. The results of this study highlight the ability of CIT alone to preserve muscle function during dietary restriction. Surprisingly, LEU antagonized some effects of CIT." (Ventura. 2013)

This observations have been made after the rats dietary provisions had been cut by 60% for 2 weeks while the amino acid composition of their diet had been increased by the provision of additional amino acids: 

• R-CIT 0.2 - low dose citrulline: 0.2g/kg
• R-CIT 1- high does citrulline: 1.0g/kg
• R-LEU - leucine: 1.0g/kg
• R-LEU-CIT - leucine + citrulline: 1.0g/kg + 1.0g/kg

By addding valine (130 mg/kg/day) and isoleucine (220 mg/kg/day) to the diet, the researchers had also ensured that the natural BCAA balance would be maintained and ....

Figure 1: Changes in body composition during the 2 weeks on 60% of the regular energy intake with different amino acid supplements in the diet (Ventura. 2013)

... well if you look at the "net result" in terms of weight loss, it would in fact seem that citrulline is the way to go... if you do yet take a look at the lean mass measurements, it becomes plain obvious that there was no difference to the starved control group in any of the AA supplemented rodents.

Figure 2: Muscle contractile properties (fatigue AUC), myofibrillar and sarcoplasmic protein synthesis (PS) after 2 weeks on the different 40% dietary restricted diets (Ventura. 2013)

This is interesting, as it stands in contrast with the directly measured influx of protein into the myofibrillar part of the skeletal muscle of the rodents, and does not mirror the pronounced benefits on muscular fatigue the researchers observed and is not appropriately discussed in the study, the authors of which were so fascinated by the miniscule increase in protein synthesis that they did not even notice that they effectively produced a null-result.

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The hormonal response (esp. testosterone & GH) to workouts is another of those things that don't predict real world results (learn more)

Real results count: So does it really matter that the protein synthesis increased? No, just as it does not matter in the countless post-exercise protein synthesis studies. If you want to inflate a tire, you are not interested in how much air you can pump into it, but rather how much of the air will stay inside and the results of the study at hand only confirm that the former cannot predict the latter.

And let's face it: None of the treatments actually had to prevent lean mass loss, because much contrary to the bro-scientific believe that you would lose tons of muscle mass within a day, if you don't get all your shakes and pills in just in time. The rodents lost no lean mass at all.

So if you want take home messages, don't rely on protein synthesis rates alone and don't freak out about muscle loss too much.

Sequential or Alternating Resistance Training for Maximal Size, Strength and Endurance Gains!? Plus: Basic Blueprint for a 2x2 Day Alternating Muscle Split Workout

If you want to try something new, but feel that this is a bit over the top, why don't you try an alternate workout regimen to escape the daily grind?

It's funny and sad that studies like the one at hand, which investigate basic training principles and their effect on your real world results in the gym are so scarce. I mean, let's be honest. With a few exceptions, all of us will probably get much more out of training optimization than of any available supplement and maybe even drug. As far as supplements goes, you are bombarded with unwarranted claims and the occasional non-significant (per design) study on newly available products. On the training side of things, on the other hand, there is little to no innovation - probably for a good reason, but still: Would you be able to tell me for sure if and why training sequentially, i.e. finishing all sets of one exercise, is "better" than alternating training, where you would, for example do a set of leg curls followed immediately by leg extensions (not necessarily without rest)?

What's better sequential or alternating?

I see, you are scratching your head... well, maybe you'll feel enlightened, after having read what Hamid Arazi, Siavash Rahmati and Samira Zaheri from the Department of Exercise Physiology, Faculty of Sport Sciences at the University of Guilan in Rasht, Iran have found in their most recent study on the effectiveness of 10 weeks of alternating vs. sequential push and pull training of the large and small muscle groups in 24 healthy male athletes (age 22y, BF% 14, weight 72kg) with a history of at least 3-6 months of weight training (Arazi. 2013).

The actual training protocol, the two groups followed was virtually identical except for the exercise order, of course:

• frequency: 3x /week
• rest: 48h between workouts; 2 min between upper, 3 min between lower body ex.
• duration: 70-80min per workout (20 minutes warm-up + cool down) 
• progression: linear, every two weeks - 60%1RM\12reps < 65%1RM\12reps < 70%1RM\10reps < 75%1RM\10reps < 80%1RM\8reps

• exercise selection: 3 sets of leg extensions, leg curls, rows and bench presses for the major and 3 sets of bicep curls and triceps extensions for the smaller muscle groups
• push vs. pull: leg extension, chest press, and triceps extension are push exercises; leg curl, biceps curl and rowing are pull exercises

• sequential training: "Sequence means each exercise is performed for 3 sets (with intervals of rest) and then next exercise starts moving again." (Arazi. 2013)
• alternating training: "Each session was conducted by leg extension (1 set) and leg curl (1 set). The alternative means the opposing muscles (requires push and pull) that were trained alternatively ." (Arazi. 2013)

The main outcome measures were muscle circumference (hypertrophy), muscle strength and muscular endurance, and the results look like this:

Figure 1: Relative changes in arm and thigh circumference (Arazi. 2013)

As you can see in figure 1 the increases in arm and thigh circumference were more yet not statistically significantly more pronounced in the sequential training group. An observation that would suggest that hypertrophy requires a certain amount of body part specific training density, which is obviously reduced it you do one set of one exercise, rest for 2-3 min, do one exercise for the other muscle group and rest for another 2-3 minutes - that's 4-6 minutes of passive and ~1 min of active rest (while you perform the other exercise) between sets and that's imho simply too much to gain.

Figure 2: Changes in muscular strength and endurance (Arazi. 2013)

Both, strength and strength endurance don't show a clear response - overall maybe a marginal benefit for the longer rest times, but certainly not impressive. At least wrt to the increase in strength endurance once could maybe argue that is may be a simple result of an increased total training volume and - maybe even more importantly - more reps per set, when you train alternately instead of sequentially.

Suggested read: "Intra-Set Rest Periods Boost Power (+38%) & Strength Gains (+65%) Without Hampering Skeletal Muscle Hypertrophy" (read more)

Unfortunately, the "discussion" of the results, the authors provide is not exactly helpful in this regards (it is not exactly legible, either, by the way, and I am usually the last to criticize other non-native speakers for their command of the English language).

Still the overall message the researchers formulate in the conclusion to their paper, where it says that it would be "suggested to use the opposing exercises for strengthening agonist –antagonist exercises" (Arazi. 2013) is not totally beside the point. Nevertheless,I'd expect better hypertrophy effects if you reduce the inter-set rest times  from 2 minutes to 60s and from 3 minutes to 90s for the large and small muscle groups, respectively.

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Blueprint for a 2-day alternating muscle split to be trained twice a week: Day 1: 4x6-8 bench presses / pull-ups, 3x8-10 military press / your favorite version of rows, 3x12 biceps curls / nose breakers; Day 2:  4x6-8 squats / stiff legged deadlifts, 3x8-10 bent over lateral / front raises, 3x15 leg extensions / hamstring curls; optional 5 min ab training on day 1 and 5 min calve training on day 2; inter-set rest 90s for complex, 60s for isolation exercises.

Bottom line: While the study at hand certainly doesn't provide a conclusive answer to the question whether alternate or sequential training is the way to go for strength trainings, my personal experience is that alternating between exercises for antagonistic muscle groups as in a chest / lat,  biceps / triceps, front delts / upper back, and quads / hams + glutes 4- or 2-day split with relatively short inter-set rest periods (90s for larger, and 60s for smaller muscle groups) can be more than just a diversion from the daily grind at the gym.

You can be in and out of the gym in <40 min and still lift a pretty decent amount of weight; and that, at a lower risk of CNS burnout than with a classic super-set training, where you would not rest between the push and pull movements, at all. The latter allows for a relatively high training frequency, but I would still take a day off between workouts, unless you are trying to cut weight at all costs. In that case, a fast paced training split build around the concept of alternating back and forth between exercises for agonist and antagonist can actually be worth way more than hours of classic "cardio" training or HIIT training. Just don't overdo it! While the individual muscles may still get enough rest, any increase in workout density will also increase the load on the central nervous system.

References:

• Arazi H, Rahmati S, Zaheri S. The Effect Of Two Sequence Patterns In Resistance Training On Strength, Muscular Endurance And Circumference In Novice Male Athletes. Hrvat. Športskomed. Vjesn. 2013; 28: 7-13.

How To Get Rid Of Pregnancy Weight? Exercise, Diet Or A Combination Of Both? What Works And Is Safe? Plus: Full Breastfeeding Alone Sheds 12kg of Pregnancy Weight

Mother's love is a natural instinct, the worries about pregnancy weight not, simply because it would hardly ever occur in nature. If anything you'd be worried not to "make" enough weight to nurture your baby after the pregnancy.

If the name “Cochrane review” does not ring a bell, let me briefly fill you in on what the Cochrane Database and the Cochrane reviews are, before we are delving deeper into the topic at hand, which is, or rather which are the results of the latest Cochrane Review on “Diet or exercise, or both, for weight reduction in women after childbirth” by Amorim Adegboye & Linne YM (2013).

I guess, the elevator pitch on what distinguishes Cochrane Reviews from the rest of the pack, would read as follows: They are comprehensive, they are systematic, they review only primary research in human health care and health policy, and they are internationally recognized as the highest standard in evidence-based health care.  When you’ve read one, you should know what the effects of interventions for prevention, treatment and rehabilitation and how reliable the actual results presented are.

Ok, that’s my assessment, now let’s see what the Cochrane Foundation says about their own work:

“Each systematic review addresses a clearly formulated question; for example: Can antibiotics help in alleviating the symptoms of a sore throat? All the existing primary research on a topic that meets certain criteria is searched for and collated, and then assessed using stringent guidelines, to establish whether or not there is conclusive evidence about a specific treatment. The reviews are updated regularly, ensuring that treatment decisions can be based on the most up-to-date and reliable evidence.”

Sounds similar, right? Now, although they certainly have a high standard and are internationally acclaimed for that, this does not protect these review from being subject to scientific bias, themselves and it’s quite normal to get at least 10 rebuttals to rebuttals after one of these reviews is published. Still, I guess the 77 page report from which I will pick just the most important facts for you is at least the most comprehensive review of the post-pregnancy weight-loss I’ve come across up to now.

Enough of the foreplay let’s get right to the time after the pregnancy now ;-)

So guys - I am deliberately addressing YOU, because you usually don’t care how, just that your significant other gets back in shape - what are you supposed to do if you just became a daddy? If you did everything right during the pregnancy and did not support your wife’s tendency to finally overeat after years of chronic starvation, you are already in a pretty good starting position. Otherwise, you and your wife or girlfriend are probably going to have a rough time to get her back in shape. So…

A. To diet or not to diet?

Assuming that you did not support the nutritional super-size escapades of your significant other during the pregnancy you are best advised to keep her from restricting her food intake.

The latter would probably increase the weight loss (-1.7kg), but most of this weight loss would come from lean mass and would set your wife or girlfriend up for the notorious yoyo effect, or life-long dieting; and that for a meager -0.4% less body fat and at the expense of a reduction in breast milk volume of -18g/day.

B. To work out or to sit still?

You don't have to lie around and eat 24/7, just because you are pregnant: 85 sessions (general fitness class, three times/week, 55-60 min/session from weeks 8-10 to weeks 38-39 of pregnancy are nothing but healthy for mother + child (learn more)

While it is not necessary for weight loss in breast feeding women, it is certainly necessary for your significant other’s overall health, fitness (+6.73mL/kg VO2Max) and lean mass (+0.88kg). Just keep her away from arduous hours of cardio exercise if you don’t want your baby to starve or your wife / girlfriend being forced to fed him/her formula and thus set your offspring up for metabolic and immune problems in the future.

While not being significant the Cochrane review still reports a trend for greater reductions in body fat percentage (-2.51%) for women who worked out in the post-partum period. And while it was beyond the scope of this review, SuppVersity readers will be aware that working out offers protection against post-partum depression, as well (Dennis. 2013).

As mentioned above doing too much entails the risk of reduced milk production and thus depressed infant weight gain. Both were yet not found to be statistically significant and occurred only in some of the pertinent studies.

C. What about working out & dieting

Contrary to dieting alone this is a very favorable approach to get rid of the pregnancy weight. In fact, the likelihood of returning to pre-pregnancy weight was doubled in the three trials that investigated the effects of combined exercise and diet programs. The chances to get back to a health weight after crazy pregnancy binges was even four times higher!

Against that background it is not surprising that we see an overall -1.93kg increase in body weight loss and -2.19% higher losses of body fat in women who diet and work out (sanely) after their pregnancy. The fat free mass loss observed with diet alone was not an issue and most importantly the volume of breast milk, infant length growth and infant weigh gain increased (probably alongside the mother’s health).

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Figure 1: Pregnancy-weight left (in kg) in Danish mothers breastfeeding for different time periods 6 months after the baby was born; the x-axis indicates the pregnancy weight gain in kg (Baker. 2008)

So what are the implications for mother's and fathers to be? For the guys, I would say you better make sure to keep the fridge well-stocked with fresh healthy foods to nourish your family and be prepared to watch for the kid (or kids if this is not your first-born), while your wife is at the gym.

For the ladies, on the other hand, it’s actually quite simply. Just eat a clean diet, work out regularly, not arduously and endlessly and by all means, breastfeed your baby. That alone has been shown to suffice to eliminate up to 12kg of pregnancy weight during the recommended 6-months period of exclusive breast feeding in a 2008 study from Denmark (Baker. 2008)

And lastly don't put yourself under too much pressure. Better slow and steady, than fast and failure-prone. 


References:

• Baker JL, Gamborg M, Heitmann BL, Lissner L, Sørensen TI, Rasmussen KM. Breastfeeding reduces postpartum weight retention. Am J Clin Nutr. 2008 Dec;88(6):1543-51.
• Dennis CL, Dowswell T. Psychosocial and psychological interventions for preventing postpartum depression. Cochrane Database Syst Rev. 2013 Feb 28;2:CD001134.

High Fish, Soy, Lard & Low Fat Diets: How Do They Affect Body Composition, Lipid and Glucose Metabolism? Results From Study on Rats That Don't Get Obese on High Fat Chow

(Un!)Surprising results: The "healthy" soy oil is the only fat in the study at hand that causes NAFLD.

I know, it is not certain whether or not the results of rodent studies will transfer to human beings and believe me, I would rather have seen this study conducted on humans or at least pigs. And while the latter are simply to expensive, the former are unreliable and don't like to be caged in metabolic wards... well, unless they receive a monetary compensation that costs about as much as a whole pigsty ;-)

That being said, let's stick with what we have and take a look at the results, Yoko Hashimoto and her colleagues published in a recent issue of the medical journal Lipids (Hashimoto. 2013).

The "obesity resistant" wistar rat and it's reaction to different dietary fats

I promise, the results are interesting and probably highly relevant, because the strain of Wistar rats (Slc:Wistar/ST) used in this study does not become obese simply because there is some fat in their chow. In fact, this is exactly the reason why the Japanese researchers picked the Wistar/STs. They wanted to examine the effects of various high-fat diets on plasma and hepatic lipid parameters and lipid metabolism in an obesity "resistant" rodent strain (everyone and every rat can become obese, but these don't get obese just by feeding them fatty chow) who were kept on either standard low fat chow or 3 different high-fat diets for 4 weeks (45% of the energy from fat) .

Figure 1: Fatty acid composition of the different diets (Hashimoto. 2013)

The primary outcomes of the study were the body and tissue weights, total food consumption, fatty acid composition, and energy metabolism, as well as the plasma and liver lipid profiles of the rodents.

Figure 2: Food intake, organ/body weight (Hashimoto. 2013)

If you take a look at the first set of results, namely the energy intake and body/organ weights, and focus on the distribution of white and brown fat you will realize that all rats on the high fat chow were significantly fatter than their low fat fed peers. For the fish oil group, however, the fat gain was almost exclusively from metabolically active brown fat.

Figure 3: Serum an liver lipid profiles (Hashimoto. 2013)

Against that background it is actually not surprising that the "fish oil rats" were the ones with the most favorable blood lipid profile. The rats in the soy group, on the other hand carried the highest amount of white fat and that also shows up in their messed up liver lipids.

The changes in the blood lipid levels the researchers observed went hand in hand with a few, but statistically significant differences in the local expression of important epigenetic regulators of fatty acid oxidation Acat1 / Acox1, in particular in the "fish oil rats":

Suggested read on the effects of fish oil on liver fat: "TTA + Fish Oil - Fat Burning Superfats or Hepatoxic Pro-Oxidants?" (read more)

"Nineteen genes involved in inflammation response genes as well as lipid metabolism-related genes were selected and their mRNA expression levels were measured by qRT-PCR. No significant differences were detected between the groups in the expression levels of genes encoding microsomal triglyceride transfer protein (MTP), ACAT2, 3-hydroxy-3-methylglutaryl-Coenzyme A reductase (HMG- CoA R, EC 1.1.1.34), and prostaglandin-endoperoxide synthase 1 (PTGS1, COX-1). In contrast, the expression levels of Acat1 and Acox1 mRNAs were the most abundant (p < 0.01) in the livers of the [fish] group." (Hashimoto. 2013)

Interestingly enough, the fish oil group was yet not the only group with metabolically relevant changes in the genetic landscape of the liver:

"Lipogenesis was not significantly increased in the [soy] group [...] Moreover, the level of VLDL secretion in the [soy] group was lower than that in the [lard] group group, because the mRNA expression levels of Apob and Mttp were not up-regulated in the [soy] group. The normal levels of VLDL secretion contributed to hepatic lipid accumulation in the [soy] group"(Hashimoto. 2013)

Overall, the results of the study at hand do not simply highlight the differential effects of various forms of fatty acids on the development of metabolic derangements, they are also testimony to the fact that their effects on the metabolism of obesity-resistant Slc:Wistar/ST rats are much different from those of the obesity-susceptible animals that are usually used in studies like that. The latter become hyperphagic (ravenously hungry => overeating) and acquire hepatic lipid accumulation, almost irrespective of the source of dietary fat. The results of Hashimoto et. al. on the other hand demonstrate that "obesity-resistant Slc:Wistar/ST rats are isocaloric and do not exhibit hepatic lipid accumulation even when consuming high-fat diets, except one that includes soybean oil." (Hashimoto. 2013)

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These results remind me of another SuppVersity article with the telling title "If You Go 'High Carb', You Better Go Really High! Seven Meals/Day, More than 800g of Carbs, Less Than 50g of Fat & 1000kcal Over Maintenance and Still Lean Gains!" (read more)

Bottom line: For me there are three messages to take away from this study. (1) The Slc:Wistar/ST rat could be a much better model to study the effects of high fat diets on human metabolism, than the regular rodents that are in fact actually selected for their high susceptibility to become obese on diets with 45% vs. just 11% of the energy in form of fat. (2) In a high fat diet scenario fish oil is the most effective way to keep the liver clean; the increase in body fat on the other hand is identical and the higher brown (=metabolically active) vs. white fat accumulation is probably irrelevant for humans. And what's more, if you take into consideration that all animals weighed the same at the end of the study, you just have to do the math to know that the "low fat rodents" were not just leaner, but also more muscular than their peers. (3) Lastly, there is the issue of omega-3 vs. omega-6 fatty acids where the comparison between the effects of lard and soybean oil do not contradict the importance of ratios, but still underline that the ratio interacts with the total PUFA (and omega-6) intake and that nothing compares to high soybean oil, when it comes to ruining your health deliberately.


References:

• Hashimoto Y, Yamada K, Tsushima H, Miyazawa D, Mori M, Nishio K, Ohkubo T, Hibino H, Ohara N, Okuyama H. Three Dissimilar High Fat Diets Differentially Regulate Lipid and Glucose Metabolism in Obesity-Resistant Slc:Wistar/ST Rats. Lipids. 2013 Aug;48(8):803-15

Chocolicious Statin: One Week "on" 100g/day of 70% Dark Chocolate Improves Cholesterol Profile and Reduces Waist Circumference in "Skinny Fat" Women

With the average German eating 9-10kg of chocolate per year we should be pretty heart healthy... well, if more than 10g of those were dark chocolate, I suppose.

You know what? I am pretty enervated by the reverberations of the notorious "chocolate makes Nobel Laureates" study. Even now, month after the publication, the media hype and the head-shaking on part of anyone who does have the slightest idea of the difference between association and causation, it's still all over the place.

On my part this has lead to a "desensitization" with respect to the word "chocoloate" in medical journals, so that I had almost missed this ground-braking study from the Department of Neuroscience at the University of Tor Vergata in Rome, the National Institute for Mediterranean Diet and Nutrigenomic in Cosenza and the UOS of Pharmacology, Department of Pharmacology at the University Magna Graecia,Roccelletta di Borgia in Catanzaro, Italy (di Renzo. 2013)

Chocolate for the skinny fat

As if it was not already enough that this is a "non-Nobel-Laureate-infected" study on chocolate consumption, it's also study on skinny fats: 15 women in the age of 20-40 years with a normal BMI, but high total body fat mass (FM) percentage (FM% > 30%) and significantly higher values of proinflammatory cytokines, such as IL-1, IL-6, IL-8 and TNF-α. SuppVersity reader what else can you ask for?

Well, ok.... probably you could ask what the study was all about. So, the intervention was pretty simple:After a dark-chocolate-free (DC) washout period, the subjects received 100g of dark chocolate per day for 7-days (50g in the morning another 50g as an afternoon snack or at dinner).The dark chocolate contained (only) 70% cocoa and was provided as an unrestricted gift from Valrhona, Tain l’Hermitage, France. Of the 70% cacao in it, 42.5% were cacao butter with a fatty acid composition of 64.6% saturated fats, 34% monounsaturated fats and only 4.4% PUFA. The sugar in the chocolate was almost exclusively saccharose.

Chronic diet = skinny fat!? (learn more)

Did you know? In previous studies, di Renzo et al. found that 10% of the Italian women fall into the "skinny fat", or as they put it "normal-weight obese" category. These women had similar increased cardiovascular disease (CVD) risk indexes values, as their pre-obese peers, but did not manifest the metabolic syndrome, despite a cluster of metabolic and genetic features associated with increased CV mortality (di Renzo. 2006, 2009, 2010; Marques-Vidal. 2010).

Moreover, the chocolate contained 2% polyphenols, and 0.7% theobromine, as well as 444mg/kg naturally occurring catechins, 908mg/kg epicatechin and 20, 20 and 40mg/kg epigallocatechin gallate epicatechin gallate, Epigallocatechin, respectively.

Improved blood lipids, improved body composition, improved....

The main outcomes of the study were the changes in body composition (DXA), blood pressure, anthropometric measurements, biochemical parameters and plasma levels of some cytokines within the 7-day intervention period.

Figure 1: Changes in lipid and glucose metabolism during the 7-day chocolate intervention (di Renzo. 2013)

And as you can see in figure 1, the results were ambiguous. We have the great and statistical signifcant improvement on the cholesterol side of things, as well as a reduction in specific markers of infallamtion, i.e. IL-6 (-33%), TNF-α (-19%) and IL-1Ra (-33%) and a 1cm reduction in waist circumferene. On the other hand, we do also see increases in fasting insulin and insulin resistance, which did not reach statistical significance, but remind me of the inverse effects on lipid and glucose metabolism we see with so many other agents with cholesterol lowering effects.

Still if we rely on statistics, the overall effects is a beneficial one, but...

There is another string attached, though, due to which I still cannot wholeheartedly recommend to add those 100g of chocolate to your diet, because the scientists did not have the funds for a control group... that's a major bummer. After all, we don't really know if the changes were not brought about by the standardization of the diet, which took place at the beginning of the DC abstinence period and of which the authors write:

Did you know? In another study 40g of dark chocolate consumed on a daily basis for 2 weeks were able to reduced the urinary excretion of the stress hormone cortisol and catecholamines and partially normalized stress-related differences in energy metabolism in 30 human subjects, who were classified in low and high anxiety traits using validated psychological questionnaires. (Martin. 2009)

"Total daily energy content of the diet was determined on an individual basis, calculated using De Lorenzo et al. prediction equation for the Italian population. Initial caloric levels were adjusted, when necessary, to maintain the body weight. All subjects received about 1700 kilocalories/day. The recommended composition of the dietary regimen was as follows: carbohydrates, 55% to 60%; proteins, 15% to 20% (of which about 50% was comprised of vegetable proteins); total fat, 25% (saturated fat acids (SFA), less than 10%, and cholesterol consumption, less than 300 mg per day), and 30 g of fibre.

[...] The composition of the diet in terms of foods and food combinations was planned to obtain an animal to vegetable protein ratio as close to 1:1 as possible. The Italian Recommended Dietary Allowances were incorporated to ensure proper vitamin and mineral intake."

Otherwise, the subjects were were advised "not to consume any other chocolate for the duration of the study" and to make "no further changes to their diet and lifestyle habits" (di Renzo. 2013).

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Bottom line: I do not question the value of adding a chunk of dark chocolate to your diet from now to then and I believe the beneficial effects on your blood lipids is well-established enough to even suggest the supplementation with "pure" chocolate (90%+) just for this porpose.

The EDC Program - Exercise + Diet + Chocolate (learn more)

The question is yet, do you need that? If you are skinny fat, probably. If you work out regularly and have your diet in check, unlikely. So, why would you want to run the risk of being among those of the ladies in the study at hand who must have experienced pretty extreme elevations in fasting insulin. If we were talking about something that happened across the board to all of them, the data would be statistical significant. The way it is, my best bet is that the increase in circulating free fattty acids in response to the combination of catechins + theobromine may be to blame. And this response can very well be very different from one individual to the other. But who knows, maybe it was just the dietary switch (?) to an up to 60% carbohydrate diet that was to blame for these results!?

References:

• Di Renzo L, Bigioni M, Bottini FG, Del Gobbo V, Premrov MG, Cianci R, De Lorenzo A. Normal Weight Obese syndrome: role of single nucleotide polymorphism of IL-1 5Ralpha and MTHFR 677C-->T genes in the relationship between body composition and resting metabolic rate. Eur Rev Med Pharmacol Sci. 2006 Sep-Oct;10(5):235-45. 
• Di Renzo L, Gloria-Bottini F, Saccucci P, Bigioni M, Abenavoli L, Gasbarrini G, De Lorenzo A. Role of interleukin-15 receptor alpha polymorphisms in normal weight obese syndrome. Int J Immunopathol Pharmacol. 2009 Jan-Mar;22(1):105-13.
• Di Renzo L, Galvano F, Orlandi C, Bianchi A, Di Giacomo C, La Fauci L, Acquaviva R, De Lorenzo A. Oxidative stress in normal-weight obese syndrome. Obesity (Silver Spring). 2010 Nov;18(11):2125-30.
• Marques-Vidal P, Pécoud A, Hayoz D, Paccaud F, Mooser V, Waeber G, Vollenweider P. Normal weight obesity: relationship with lipids, glycaemic status, liver enzymes and inflammation. Nutr Metab Cardiovasc Dis. 2010 Nov;20(9):669-75.

Colostrum Maintains Testosterone, Cortisol and Heart Rate Recovery, Where Whey Fails - During a Five Day Cycling Event With 10 Highly Trained Male Road Cyclists

Legal gear fresh from the udder? If it works for cyclist, it must be real ;-)

Some of you will probably remember the corresponding installment of "Ask Dr. Andro" from 2011 that dealt with the question whether colostrum and milk products in general are healthy muscle builders, a waste of money or toxic waste (read more). If you do, you will also remember that my review of the literature did support the general benefits of milk proteins, but it did not provide significant evidence that benefits that have been observed in the few existing studies on the ergogenic value of colostrum could not be achieved by whey and/or casein proteins as well. Now, the latest study from the University of Queensland appears to suggest that just this could yet in fact be the case (Shing. 2013) - at least if the outcome measures are the salivary testosterone concentration and modulated autonomic activity over consecutive days of competitive cycling.

10g of whey vs. 10g of cholostrum "isolate"

The scientists from the School of Human Movement Studies recruited 10 highly trained cyclists with an average age of 22.5y and a body weight of ~70kg and put them on two different supplemental protocols

• the control group received consumed 10g whey protein concentrate (“Alacen® 80” Fonterra Co-op Group Limited, Auck- land, New Zealand) per day 
• the colostrum group consumed 10 g Intact® bovine CPC (Numico Research Australia Pty Ltd, South Australia) per day

Neeldess to say, both supplements were isocaloric, packed in identical sachets to and had to be used for the same timespan, which were the 8 weeks prior to and the whole five days of the cycle race that was used as the litmus test for the efficacy of the supplementation regimen.

Colostrum muscle builder or murky allergen (learn more)?

In that it, may be worth adding that the cyclists consumed the in the morning mixed with 50 mL of water and 100 mL of skim milk and that the scientists picked Intact® CPC 3-6, 14 as their colostrum supplement of choice, because the various available products vary largely in their amino acid and protein content. Therefore it appeared sensible to use the same brands that have been used in previous studies, as well. According to Shing et al. Intact® is a standardized, low heat  treated, low fat, low lactose colostrum powder containing 20%  IgG that retains both casein and whey proteins (just as a side note: there was no sponsorship involved in the study, although the brand names may suggests otherwise).

Aside from the objectively measurable saliva responses, the scientists had the participants fill diet and training, as well as illness logs. The latter reflects the hypothesis that the IgG content in the colostrum would strengthen the immune system of the cyclists and should thus result in lowered infection rates. With two vs. four illnesses in the whole study period the differences between the colostrum (2 illnesses) and the whey group were yet statistically not significant.

Figure 1: Change in heart rate recovery (left), salivary testosterone and cortisol levels (right) during the 5-day cycling event (Shing. 2013)

Much contrary to whey group, where the naturally cyclic testosterone rhythm is completely lost and the cortisol rhythm attenuated, both remained intact in the colostrum group. This goes hand in hand with the loss of heart rate variability in the whey control and the increases of the parameter in the colostrum group. Both results in conjunction with the smaller reduction in vigor and the ameliorated change in fatigue in the colostrum group clearly suggest that the cyclists in the whey group were already parasympathetically overtrained, while the stress reducing effects colostrum kept the cyclists in the active arm from falling into the same trap.

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For short time-trials sodium bicarbonate may be the supp of choice (learn more).

Bottom line: The scientists state it in their conclusion "the number of participants in this pilot study was small", too small for my liking, so that it is - as a standalone - simply not enough to prove anything.

The scientists are yet right that "the present data support the potential for bovine CPC supplementation to maintain testosterone concentrations and influence heart rate variability response" in a training regimen that is notorious for its negative impact on the central nervous system and the HPTA. "Support" and "potential" - not more, but not less either.

References:

• Shing CM, Peake JM, Suzuki K, Jenkins DG, Coombes JS. A pilot study: bovine colostrum supplementation and hormonal and autonomic responses to competitive cycling. J Sports Med Phys Fitness. 2013 Oct;53(5):490-501.

Abdominal Fat Annihilation With Clay-Wraps, Microcurrents & Aerobic Exercise? There is Something in This List That Works, But It's Probably Not the Clay ;-)

This, probably won't cut it (the fat), because the electrodes and the wraps are missing.

I suppose that the headline of today's SuppVersity article will probably split the SuppVersity Readership into two camps. Those who say: "Pah, I am not a pussy: Clay-Wraps are not an option. I'd rather do a couple of additional HIIT sessions than getting one of those!" And the other camp saying: "Wtf, finally I have a reason to go to the spa regularly!"

In the end, it does not matter on which side of this divide you are, the results a group of scientists from the Oporto Polytechnic Institut in Vila Nova de Gaia in Portugal present in their most recent paper in Clay Sciences (no, this is not a joke, there really is a peer-reviewed journal on "clay science"), will probably surprise all of you.

"Clay wraps? Really?"

Assuming you would read the full-text of the study, you would, just like me, initially be enlightened that clay has been used for centuries not just as a cosmetic to make your skin look younger and healthier, but also as a means to reduce abdominal fat (Melo. 2013). Usually, these clays are composed of "green clay" (which has natural calcium and aluminum as components), green tea and magnesium sulfate. The clay is impregnated in a bandage that compresses the tissue and enhances fluid drainage from the abdominal region through the superficial lymphatic system (Standring. 2008).

• 

  Green tea reduces thyroid hormoness. Reason for concern? (learn more)

  Green tea: I am quite certain that all of you are familiar with the fat liberating effects green tea has on adipose tissue, as well as its ability to induce apoptosis in mature fat cells, to inhibit adipogenesis (storage of fat) and differentiation of preadipocytes (formation of new fat cells). Accoding to Belo (2009) and Heinrich (2004) these effects are retained within the adipose tissue, when its applied topically and only very little of the agent will actually make it into circulation.

• Magnesium sulfate: Being an essential mineral to the activity of hormone-sensitive lipase, magnesium can facilitate triglyceride breakdown. It's topical application may be particularly useful, in people with circulatory problems (as in cellulite; learn more). The way the author's present it as an "active fat burner" (in between the lines, only) is yet unwarranted.

• Calcium: Contrary to magnesium, calcium actually plays a more active role in the promotion of body fat loss. An increase in extracellular calcium concentration leads to an augmented enzymatic activity and promotes a reduction of calcitriol (active vitamin D) that will in turn trigger lipolysis (Somaet. 2003; Zemel. 2005). Whether this works via topical application has AFAIK not been well-established.

Another not fully understood factor that could make clay and the minerals in it a valuable tool for minimalist local body reshaping is their ionic nature. The latter can have direct effects on the microcurrents (electrolipophoresis; the movement of molecules due to electric currents) and may thus promote triglyceride degradation by increasing bloodflow and metabolism and by provoking changes in cell membrane polarity.

Ultrasound, caliper and body impedance

The subjects the scientists selected for this research were 20 young women (faculty students), with a body mass index that would rank them as either normal (18.5–24) or pre-obese (25–29). To make sure they would not be fooled by mere changes in the fluid levels of the tissues, the scientists used a combination of ultrasound, body fat caliper and body impedance measures, to access the effects of the "clay-wrap intervention" on the body composition of the ladies.

For the women in the active arm of the study, the protocol, which they went trough two times a week over a course of five weeks (10 interventions altogether) looked like this:

1. 

   In case it's not the amount of fat, but the orange peel look you want to get rid off, check out the SuppVersity Cellulite Special and listen to the show.

   Vigorous 5 min massage with an alcoholic extract of green tea (96% ethanol) macerated for 5 days, about which the scientists say: "[A] combination of ethyl alcohol with green tea provides a good extraction of the tea components . In addition, ethanol promotes the mechanical removal of contaminants and dissolves lipids in the lipid membrane, increasing the permeability of the skin" (Melo. 2003)
2. Application of a solution of 33.79 g of green clay combined with 18.56 g of magnesium sulfate (proportion in volume of 6 measures of green clay for 4 measures of sulfate) dissolved in 16.67 ml of distilled water to the abdomen. 
3. Application of a low elasticity bandage soaked in an infusion of 3.12 g of green tea, 6.94 g of magnesium sulfate (1 measure, in volume) and 0.5 l of water was applied with increased pressure from the center to the periphery. 
4. Application of microcurrents to the abdominal region with electrodes in a parallel position, and at an intensity below the sensitivity threshold (max. of 1 mA, frequencies of 25 Hz and 10 Hz) for 15 minutes. The polarity changed every second.

The protocol also included 30 min of aerobic moderate-intensity exercise (50%) on a cycloergometer
which had to be performed with the clay body wrap on the abs.

Figure 1: Before vs. after local (ultrasound) and total (body fat caliper in %) in the active arm of the study (Melo. 2003)

If we look at the main study outcomes, it's hard to argue that the intervention was kind of successful. "Kind of", in this case, implies that the effects were not earth-shattering and nothing you couldn't achieve by diet + exercise alone. More importantly, though, the results of the control group were within statistical margins the same. So what does that tell you about the usefulness of clay wraps?

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If you are in his position, clay is certainly the last thing you want to rely on, to reduce your weight to a healthy level. Stick to what works dieting and the glucose repartitioning effects of exercise about which you've read in an article from Friday, July 5 (read it)

Bottom line: So what can we learn from a study like this? Well, personally, I would say: "Just because it's science, this does not mean it does make sense!" And I guess you will concede that going through the ardeous procedure is not exactly worth the statistically non-significant additional 1 cm reduction in waist circumference in the intervention group.

Not convinced,yet, well if you put any faith in the data from body-fat calipers and body impedance devices which tell us that the total trunk fat loss was (non significantly) larger in the control group (-2.1% vs. -1.6) and the total body fat loss measured using triceps, suprailiac, thigh and abdominal skinfolds, were -1.9% and -1.8% for the women in the control and intervention group, respectively, I guess that should suffice to shelve the idea of going to the spa to actively burn fat. That does not mean, however that the relaxing effect it can have may eventually promote body fat loss, but this would be the topic for another study ;-)

References:

• Belo SE, Gaspar LR, Maia Campos PM, Marty JP. Skin penetration of epigallocatechin-3-gallate and quercetin from green tea and Ginkgo biloba extracts vehiculated in cosmetic formulations. Skin Pharmacol Physiol. 2009;22(6):299-304.
• Heinrich M, Barnes J, Gibbons S, Williamson EM.Fundamentals of Pharmacognosy and Phytotherapy. Churchill Livingstone—Elsevier Limited. 2004.
• Melo et al. Clay body wrap with microcurrent: Effects in central adiposity. Applied Clay Science. 2013; 80-81:140–146.
• Soma MR, Gotto AM Jr, Ghiselli G. Rapid modulation of rat adipocyte lipoprotein lipase: effect of calcium, A23187 ionophore, and thrombin. Biochim Biophys Acta. 1989 Jun 28;1003(3):307-14.
• Standring S. Anterior abdominal wall (chapter 61). Standring, S, Gray's Anatomy—The Anatomical Basis of Clinical Practice. Elsevier, 40th Churchill Livingstone. 2008; p1059.
• Zemel MB, Richards J, Milstead A, Campbell P. Effects of calcium and dairy on body composition and weight loss in African-American adults. Obes Res. 2005 Jul;13(7):1218-25.

Fat Burning Silk Peptides From Korean Labs: You Don't Even Have to Eat Worms to Gear Your Personal Energy-In-VS-Energy-Out Equation Towards Weight & Fat Loss

It does resemble a birds nest but what you see here are silk proteins not swallow eggs and birds poop.

Let's first get two things out of the way: Yes this is yet again a rodent study and no, it has not been sponsored by BPI, who are trying to tell you that you should buy their silk protein based supplement instead of any other amino acid product if you want to get bigger, leaner, faster and... well, they don't say that, but obviously also poorer.

Now that we have got the sarcastic introduction out of the way, let's get back to the facts the study at hand is not the first to describe beneficial effects that may be brought about by the consumption of silk peptides.

Silk the traditional protein base fat burner from the far East?

What may sound gross to some of you, does in fact have a longstanding tradition in the Asian countries and has already been shown to suppress adipogenesis in preadipocytes of rodents on high fat diets by Lee et al. in 2012.

The mashes that are used to cover up hernias could soon be made of silk, as well.

Silk as tissue substitute: To be honest, the effects silk proteins could have on your belly, are actually not the really exciting stuff about silk. While it is not the silk of the common silkworm, but the stronger silk variety of spiders, the latter may in fact soon replace conventional materials that are currently used to manufacture "implants" like the meshes that are used to fix hernias (Schäfer-Nolte. 2013). They are more stable than most of the conventional materials and, more importantly, are not identified as a "foreign" object and thus not attacked by our own immune system.

Scientists from the Tufts University and other renowned research facilities are also developing new silk-based delivery devices for drugs (Pritchard. 2010).

The results of the most recent study from Korea (Kim. 2013), on the other hand, render a supplement that has hitherto been investigated mainly as an anti-diabesity interesting for physique athletes and gymrats, as well. The researchers from the Konkuk University used an open-circuit calorimetry system to measure the energy expenditure of mice that received either 800mg/kg of silk peptides of placebo or 2 weeks and had to exercise on a treadmill for 50 minutes five times a week (20m/min in week 1, 25m/ming in week 2).

Figure 1: Fat oxidation in control and silk peptide group at the end of the study period (Kim. 2013)

As you can see in figure 1, the mice in the active arm of the study had a higher total oxygen consumptions, a higher fat oxidation and correspondingly lower respirator exchange ratios (indicating a higher contribution of fat to the energy expenditure).

Figure 2: The 66% reduction in food efficiency does basically mean the rodents hat to eat 3x more to gain the same amount of body weight, the high isoleucine content in the silk peptides should remind you of a previous SuppVersity article on the beneficial effects of isoleucine containing peptides in whey hydrolysates (read more)

The combination of exercise and silk protein also led to a statistically significantly lower body weight gain and a 66% reduction in feed efficacy. In other words: Despite eating much more, the mice with the silk protein in their diets gained significantly less body weight.

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Read my past elaborations on silk proteins, when BPI first announced their new "BLOX" silk protein supplement (read the whole article)

Bottom line: As a standalone study the latest results from Korea are interesting, but not impressive. In conjunction with the results from previous studies, where Shin et al. (2010) observed direct ergogenic effects in an exhaustive exercise scenario, the anti-diabetic effects of respective hydrolysates (Do. 2012) , its ability to increase GLUT-4 activity and thus facilitate glucose uptake (Lee. 2011), it would be impressive, if we had (a) human data to prove that you me and every of our non-hairy cousins would see similar results; and (b) if silk protein would stand the test against another source of small peptides... which one? Well what about plain hydro-whey (WPH)? You've read about WPH's ability to improve blood glucose management, as well as its antioxidant effects before. So until this data is available, it may be worth to keep silk on the radar, but would be an N=1 experiment with an undetermined chance of success if you bought it.

Speaking of whey hydrolysates: If your goal is to build mass and lose body fat the similarity of silk proteins to whey hydrolysates may, in fact be another reason not to literally buy into the hype (which has by the way already abated ;-) Why?  Well you must have missed Tuesday's post "Is hydrolized Whey, the New Way to Go? 12 Week Human Study Suggests: Yes, If Your Goal is to Ward Off Oxidative Damage. No, If You Want to Build Muscle & Lose Fat" (read more) otherwise you wouldn't be asking.

References:

• Do SG, Park JH, Nam H, Kim JB, Lee JY, Oh YS, Suh JG. Silk fibroin hydrolysate exerts an anti-diabetic effect by increasing pancreatic β cell mass in C57BL/KsJ-db/db mice. J Vet Sci. 2012 Dec;13(4):339-44.
• Kim J, Hwang H, Yun HY, Kim B, Lee CH, Suh H, Lim K. Silk Peptide intake increases fat oxidation at rest in exercised mice. J Nutr Sci Vitaminol (Tokyo). 2013;59(3):250-5.
• Lee HS, Lee HJ, Suh HJ. Silk protein hydrolysate increases glucose uptake through up-regulation of GLUT 4 and reduces the expression of leptin in 3T3-L1 fibroblast. Nutr Res. 2011 Dec;31(12):937-43. 
• Lee SH, Park D, Yang G, Bae DK, Yang YH, Kim TK, Kim D, Kyung J, Yeon S, Koo KC, Lee JY, Hwang SY, Joo SS, Kim YB. Silk and silkworm pupa peptides suppress adipogenesis in preadipocytes and fat accumulation in rats fed a high-fat diet. Eur J Nutr. 2012 Dec;51(8):1011-9.
• Pritchard EM, Valentin T, Boison D, Kaplan DL. Incorporation of proteinase inhibitors into silk-based delivery devices for enhanced control of degradation and drug release. Biomaterials. 2011 Jan;32(3):909-18.