Eight HIIT Sessions on the Rowing Ergometer Cut Body Fat, Increase Adiponectin, VO2Max & Performance in National Level Rowers - Workmatched Classic "Cardio" Does Nothing

If you have hitherto ignored my previous advice (e.g. "Choosing Your Workout Style") to give the rowing machines a try, maybe the study at hand will rise your interest. Give it a try. It's an awesome whole body workout and highly effective, even if you just do 20min of steady state after lifting weights.

Yesterday you've learned that even the most idio... ah, I mean unconventional - not to say "experimental" in the literal sense - one-legged leg training routine is more likely to get you those six-pack abs, of which everyone appears to believe that it was a natural sign of outstanding health and a thing everybody must have (just like the new iPhone, you know ;-), than a bazillion of sit-ups. Today, you will see that a somewhat less "experimental" training regimen will not have you reach your goal faster and more efficiently, it will also have the welcome "side effect" of making you healthier and improving your conditioning. And you know what's the best about all that? It does not only work for sedentary baby-boomer, but also for highly trained athletes. 5 male and 2 female19(± 1.2)-year-old junior state and national level rowers from the Tasmanian Rowing Team (height: 1.77 ± 0.10 m, body mass: 74.0 ± 10.7 kg, body fat: 17.1%, VO2max 62.1 ± 7.0 mL·kg/min), to be precise (Shing. 2013).

Healthier, leaner, fitter - that's a HITTer ;-)

To evaluate the influence of two different training regimen, namely the traditional steady training (SST/LISS) on a rowing ergometer (a piece of equipment of which the regulars among you already know that I highly suggest you incorporate it into whatever cardio routine you may be doing), or a high intensity interval training (HIIT) variety of the latter the researchers from the School of Human Life Sciences at the University of Tasmania in Launceston, Australia put their participants, the aforementioned young national rowers, on two different workout protocols with matched cumulative energy expenditures (my emphases in Shing. 2013):

• SST: "The traditional training program involved rowers completing two ergometer sessions per week; one with a duration of 35 minutes and the other 40 minutes. [...] The intensity of each session
  was relatively low and more aerobic in nature when compared to the interval training protocol. The intensity of the traditional ergometer sessions was set to power outputs that corresponded to blood lactate concentrations of 2 and 3 mmol/l determined from the incremental exercise test."
• HIIT: "The interval training sessions consisted of eight 2.5 minute intervals at 90% of mean four-minute maximal power achieved during the incremental exercise test. Recovery between each interval was at an intensity of 40% of mean four-minute maximal power and the recovery duration was until heart rate returned to 70% of maximum heart rate, up to a maximum of five minutes."

The 2x four week experimental period (remember: we are dealing with a cross-over design, where all subjects participate in both protocols in random order) involved the incorporation of two ergometer sessions per week. Since all participants were part of the same squad the rest of their training regimen was identical, so that confounding factors - at least as far as the training is concerned - can be ruled out.

Body composition and adiponectin took a HIIT - a highly beneficial one that is ;-)

Performance tests were done and body fat mass (DXA), as well as a general blood profile and adiponectin values were taken at baseline and the end of both 4-week periods. Moreover, all participants had to keep a detailed training and diet log, so that the scientists could make absolutely sure that non of the effects they observed were due to unexpected changes in either activity levels or dietary habits.

Any potential influence of the randomized order, i.e. whether the rowers performed the classic training first and the HIIT sessions 2nd or vice versa was ruled out by statistical means before the scientists eventually analyzed their data sets and got the following results:

Figure 1: adiponectin levels before (pre) and after the respective workout at the beginning and end of the respective 4-week training period and body fat levels before and after 4 weeks of steady state (SST) or high intensity interval training (HIIT) in national level rowers (Shing. 2013)

I must admit, the changes are not earth-shattering, but there are changes - beneficial ones that is  - and they are statistically significant despite the small number of participants, and the fact that the subjects were already highly trained individuals and - I figure this may be the most convincing argument not to discard this effects - participated in no more than a total of only 8 HIIT sessions.

Bottom line: I guess, you could certainly argue that the novelty of the training stimulus was part of the reason, the HIIT regimen had so beneficial effects on the fitness, body composition and even the adiponectin levels of these already highly trained rowers (Adiponectin? That's the "new leptin", which promotes insulin sensitivity and exerts profound anti-inflammatory effects); but does this take away from the efficacy of this 4x2.5 min @90% max. + 5min active rest high intensity interval training regimen? I don't think so.

Click here to learn more about the "Iranian HIIT Solution" a minimalist program with maximal results

There is nonetheless one thing I want to add before I close the SuppVersity doors for today. The 4x2.5 minute protocol is certainly appropriate for trained athletes; in fact, previous studies even suggest that it requires those long(er) intervals in order to elicit gains in VO2max in highly trained (endurance) athletes (e.g. Franch. 1998; Laursen. 2002). The initially mentioned sedentary baby-boomer - obese or not - may however be better off, if they follows a different regimen, such as the one I outlined in the "Iranian HIIT Solution" (see image on the right) and incorporate that in a three-day split (e.g. A, B, hypertrophy, C strength) or a two-day full body circuit training.

The main message here is that starting out "low" (in terms of both volume and intensity) is not just possible, it's even advisable, so that there is still enough room to do more, and/or preferably up the intensity. I know I have been telling you that before, but I feel it's worth stating again: Real cardio training, i.e. the type of training that strengthens the cardiovascular system is progressive. If you do the same thing day in and day out the best you can hope for is to keep the status quo. Remember that before you start out way too high (esp. on the volume side of things) and either bunk directly, or end up without any room to make progress.

References:

• Franch J, Madsen K, Djurhuus MS, et al. Improved running economy following intensified training correlates with re-duced ventilatory demands. Med Sci Sports Exerc 1998; 30: 1250-6.
• Laursen PB, Jenkins DG. The scientific basis for high-intensity interval training: optimising training programmes and maximising performance in highly trained endurance athletes. Sports Med. 2002;32(1):53-73.
• Shing CM, Webb JJ, Driller MW, Williams AD, Fell JW. Circulating Adiponectin Concentration AND BODY composition ARE Altered in Response to High-Intensity Interval Training. J Strength Cond Res. 2013 Dec 4.

The Female(?) Athlete Triad - Part II/III: LH, GH, IGF1, Insulin, Ghrelin, Leptin & Co Form a Self-Perpetuating Vicious Cycle

I usually rant against pizza and beer, but once the athlete triad has struck, they can be an occasional part of the "healing protocol".

In last Sunday's first installment of this series we have taken a look at the prevalence, etiology and fundamental cause of an entity that is, and I am repeating myself here, profoundly mislabeled as the "female athlete triad". In fact, it is, as we have learned in the last installment, neither an exclusively female thing, nor a triad. If anything, it is a quintet or sextet. To make that clear, and give you guys, who make the same mistakes, but usually with less detrimental consequences, I will once more refer to it as "athlete triad" = AT,  in this second part of the Female(?) Athlete Triad Series in which we will take a look at the endocrine underpinnings of the previously described consequences of the temporary and long-term energy deficiency we have identified as the single most important causative factor of the onset of the "triad" last Sunday.

Which endocrine factors are figuring, here?

Instead of overwhelming you with the details right from the start, I decided to compile a list based on a cross-section of the dozens of articles I have read in the course of my eventually futile quest for a single definitive answer to the question, "Which hormonal or metabolic consequence of restrictive eating and excessive training is to blame for the fatigue, the low sex hormones concentration,the  bone resorption, the anemia, the absence of menses / lack of libido, the performance decreases and the whole string of pathological features, we have explored in the last installment?"

"Refeeding is not an option, because you will only become fat!" FALSE! Yet another myth without substantial scientific foundation that probably arises from the disturbed self-perception of those affected by AT and AN. In fact, the fat stores are the last thing that will be restored (Golden. 2004). This is probably also one of the reasons why "refeeding" often does not appear to work, because the basal energy requirements will increase with every pound of lean tissue you add back to your frame, so that athletes suffering from the "triad" will have to continuously increase their energy consumption. Unfortunately, most athletes will fail to do the former (also because exercise & stress can blunt hunger) and instead react with an increase in workout intensity, now that they are finally able to work out, again. This, in turn, will restore or even exacerbate the energy deficit and thus worsen not improve their physiological problems, even if their scale shows that they have already gained 5-10kg. If you take a look at figure 1 you will also realize that, at least in women, a baseline level of total (not relative!) body fat appears to be necessary to maintain regular menses (in men to maintain normal total testosterone & SHBG, but not so much free testosterone levels or reproductive function).

• low luteinizing levels are unquestionably among the elemental features and causally responsible for the occurance of menstrual disorders / lack of libido and the correspondingly low estrogen and testosterone levels in women and men
• TSH levels are not a valid / reliable indicator for the presence of absence of AT, because they can be both slightly increased or normal in the presence of low T4 and low T3 levels, as  - and this is far more often the case - TSH can be low despite low free thyroid hormone levels (usually in the presence of a low T3/rt3 ratio; if anything this would be a good indicator of beginning or full-blown AT)
• the circadian cortisol rhythm is whacked in men and women, alike; characteristic are the absence of an appropriate cortisol spike in the morning as well as the normal decline in cortisol levels  in the course of the day; metaphorically speaking, as the athletes triad progresses, the "mountain range" turns into mesa and eventually into a plane lowland
• the quartet of (mostly) sub-clinical hypogylcemia, low insulin, extreme high / or totally blunted insulin sensitivity, low IGF-1 and high catecholamine levels cannot be seen in isolation, most detrimental are yet probably the first and last of these four glucose-related players in the AT concert, as the former entails the constant risk to run out of "brain fuel" (in the absence of alternative fuel sources) and can - in the absence of adequate corticosteroid expression - become potentially life-threatening and the latter, i.e. low IGF-1 levels and very low IGF-1 to IGF1 binding protein 4 being one of the, if not the central factor involved in the the long-term physical decline of muscle, bone, organ and even brain mass.

As I have repeatedly emphasized in the last installment, the underlying cause, the trigger, maintaining factor and thus most important setscrew of the athlete triad (female or male) is an over-exaggerated and / or  long-lasting (weeks to months, in the worst case years; see Sundgot-Borgen. 2000) discrepancy between energy intake and expenditure, your body will initially try, but eventually fail to compensate by

• tapping into its energy stores in form of body fat, muscle and organ mass, the insulating fat around nerves and organs, etc.,
• continuously decreasing its metabolic activity (esp. thyroid metabolism),
• shutting down non-vital, but energy-intensive (e.g. immune and reproductive system) bodily functions, to prioritize short term survival of the individual over long-term survival and the conservation of the species

Therefore it is an indispensable and in many cases even sufficient prerequisite to restore an adequate supply of nutrients, and abolish temporarily better reverse the discrepancy between "energy in" and  "energy out" (please read the information in the red box next to the list of the previous paragraph, as well).

And what about leptin, ghrelin, adiponectin ... ?

Figure 1: In female athletes, only total fat mass, not body fat % or BMI are associated w/ AT (here identified by amenorrhea; top, left); the correspondingly low pulsatile (not baseline, see lower left) of LH correlate negatively with ghrelin and positively with leptin (top, right); while LH and leptin show a lack of pulsality, the ghrelin levels are not simply elevated, they also have a higher pulse size, amplitude and total polsatile secretion compared to control and eumenorrhetic athletes (bottom; LH, ghrelin, leptin expressed relative to non-athletic control; based on Ackerman. 2013)

Similar to the facilitative effects of the "hunger high", the "evolutionary advantage" that's turning its ugly face on everyone, who's willing to dig a deep enough whole (see Part I), the endocrine imbalances, as well as the reduced leptin) or over-pronounced (adiponectin) release of adipokines and the disturbances of the glucose, fatty acid and cholesterol metabolism start to take on a life of their own.

And as if that alone would not already make it difficult enough to separate cause and effect, it does actually appear likely that the order may even be reversed over time - not unlike the chicken that will hatch and eventually lay an egg. 

As discussed in the last installment, the combination of over-exercising and fasting, which may at time-point T0 actually have been the root cause of the problem will often turn into a strategy to stave off the impeding total breakdown. It becomes sort of a conditioned response to the constant starvation, which  will then no longer manifest itself in the form of hunger, but as anxiety and an almost compulsive urge to exercise (this is particularly well-established for anorexics; Teufel. 2008). And while the latter can be motivated by the desire to increase athletic performance and/or lose even more body fat, it does have a very real, often under-appreciated, physiological underpinning.

If you like, you could argue that the urge of the starved athlete to exercise is yet another "evolutionary conserved" automatism that mirrors the well-known food-seeking behavior rodents display  in periods of food deprivation and in response to the stimulatory effects of ghrelin on the orexin neurons in the brain (Yamanaka. 2003).

From ghrelin to growth hormone to IGF-1 and back

At the same time, the combination of exercise, low triglyceride, low free fatty acid and exuberant levels of the "hunger hormone" ghrelin leads to an overexpression of growth hormone (Scacci. 2003), subsequent increases in adiponectin (Wölfing. 2008), which will in turn decrease progesterone and androstenedione production and LH receptor expression in ovarian cells (Lagaly. 2008) and GnRH and LH release in the pituitary (Rodriguez-Pacheco. 2007; Lu. 2008). The surprisingly high adiponectin levels (surprisingly in view of the often dangerously low levels of adipokine producing body fat) will further increase the borderline pathological insulin sensitivity and thus lower the already rock bottom blood glucose and basal, as well as (post-)prandial insulin levels even further.

Figure 2: Illustration of the self-perpetuating vicious cycle of the athlete's triad (AT)

With their suppressive effect on leptin (Böni-Schnetzler. 1999), the high growth hormone levels and low body fat reserves are probably the most important contributers to the pathologically low, in fact quasi non-existent basal leptin secretion (see figure 1). And the low insulin levels don't just compromise the normal food-induced prandial suppression of ghrelin (Murdolo. 2003), they also hamper the production of IGF-1 (especially in the liver), so that athletes who suffer from the "triad" cannot derive any anabolic benefits from their high growth hormone levels, since the latter are largely mediated by the stimulatory effect of growth hormone on the production of IGF-1... what you are seeing here is thus a self-perpetuating vicious circle, you can extricate yourself from only by a multi-faceted approach the pillars of which are an..

* in view of the insulinogenic effects of whey and the pro-IGF-1 effects of casein (Hoppe. 2009), and the anti-catabolic effects of CLA & omega-3 you should - if by any means possible - incorporate dairy products from preferably grass fed dairy (butter, milk, cheese, yoghurt, quark / curd cheese, fermented dairy and if you want protein powders) in your diet regularly, better daily.

1. adequate and continuous energy supply to control ghrelin levels and help stabilize blood sugar (and thus glucocorticoid) levels and restore normal leptin and adiponectin expression,
2. increased low GI (to avoid reactive hypoglycemia) carbohydrate and protein intakes to normalize glucose levels, suppress ghrelin, increase insulin and IGF-1 levels* (Foster-Schubert. 2008; suggested read: "Carbohydrate Shortage in Paleo Land"),
3. balanced intakes of all types of natural fats, with an emphasis on long-chain PUFAs from food including a reasonable amount of "bad" omega-6 fatty acids and w/out fish oil or other omega-3 supplements, which would further blunt the already compromised glucocorticoid response and the leptin secretion (Kratz. 2002; suggested read "Omega-3 and Low Cortisol"), and
4. profound reductions in training volume to lower GH, cortisol, catecholamin and energy requirements and a (temporary) reorientation towards low volume strength training that will help increase bone density and IGF-1 expression (Davee. 1990)

Now, this may sound hilarious, but for the time being, laziness, pizza and beer - in moderation - are actually your friends. In that, I am not suggesting that you have to copy the patient, Chris Kresser mentioned several times on the old "Healthy Skeptic" podcasts (now RHR) about a client, who "cured" his longstanding physiological, and as I suspect psychological problems with pizza and beer, but the third pillar of this guy's regimen is actually a must: Go out with friends and start to enjoy your life again! Without thinking about food and exercise and sticking to whatever form of restrictive "diet" all the time.

Figure 3: Development of BMI (blue), leptin (red), adiponectin (green) levels in 8 female adolescent malnourished AN patients (based on Modan-Moses. 2007)

Apropos, third pillar. I have already had my short intense workout for the day, I have eaten well, but I have not hung out with friends. In other words, I will postpone the in-depth discussion of the energy and nutrient requirements, useful and detrimental supplements and medications, as well as necessary and facilitative tweaks to your workout routine to the next week, add another Roman "I" to the second "II" in "Part II/II" in the preliminary headline of this post and leave you (hopefully not too frustrated) with the graphical illustration of the effects re-feeding, alone, and a normalization of the body weight from a BMI of 16kg/m² to ~19kg/m² can have on the skewed basal leptin and adiponectin in figure 3.

In view of the fact that other studies have shown that this increase in weight, which must not be confused with a mere increase in adiposity, i.e. body fat percentage (go back to figure 1 if you already forgot that the absolute not the relative fat mass counts and please remember that the latter includes the fat in the myelin sheaths of your nerves, the protective fat around the organs, the fat in your brain etc.), does help with the normalization of both insulin and ghrelin (Otto. 2001), growth hormone and IGF-1 (Argente. 1997) and is in some cases even sufficient to restore most of the endocrine abnormalities (Scheid. 2010), many of the lessons we will learn in the next (and according to my current plans last ;-) installment can also be applied to a lean bulk - and that goes irrespective of your gender and your whether or not you have already fallen victim to the athlete triad!

References

• Ackerman KE, Slusarz K, Guereca G, Pierce L, Slattery M, Mendes N, Herzog DB, Misra M. Higher ghrelin and lower leptin secretion are associated with lower LH secretion in young amenorrheic athletes compared with eumenorrheic athletes and controls. Am J Physiol Endocrinol Metab. 2013 Apr 1;302(7):E800-6.
• Argente J, Caballo N, Barrios V, Muñoz MT, Pozo J, Chowen JA, Morandé G, Hernández M. Multiple endocrine abnormalities of the growth hormone and insulin-like growth factor axis in patients with anorexia nervosa: effect of short- and long-term weight recuperation. J Clin Endocrinol Metab. 1997 Jul;82(7):2084-92.
• Beals KA, Manore MM. Disorders of the female athlete triad among collegiate athletes. Int J Sport Nutr Exerc Metab. 2002 Sep;12(3):281-93. 
• Boag F, Weerakoon J, Ginsburg J, Havard CW, Dandona P. Diminished creatinine clearance in anorexia nervosa: reversal with weight gain. J Clin Pathol. 1985 Jan;38(1):60-3. 
• Böni-Schnetzler M, Hauri C, Zapf J. Leptin is suppressed during infusion of recombinant human insulin-like growth factor I (rhIGF I) in normal rats. Diabetologia. 1999 Feb;42(2):160-6.
• Caspar-Bauguil S, Montastier E, Galinon F, Frisch-Benarous D, Salvayre R, Ritz P. Anorexia nervosa patients display a deficit in membrane long chain poly-unsaturated fatty acids. Clin Nutr. 2013 Jun;31(3):386-90.
• Davee AM, Rosen CJ, Adler RA. Exercise patterns and trabecular bone density in college women. J Bone Miner Res. 1990 Mar;5(3):245-50.
• Di Carlo C, Palomba S, De Fazio M, Gianturco M, Armellino M, Nappi C. Hypogonadotropic hypogonadism in obese women after biliopancreatic diversion. Fertil Steril. 1999 Nov;72(5):905-9.
• Di Luigi L. Does the high performance athlete need hormone replacement? Endocrine Abstracts. 2013; 29: 35.1 
• Foster-Schubert KE, Overduin J, Prudom CE, Liu J, Callahan HS, Gaylinn BD, Thorner MO, Cummings DE. Acyl and total ghrelin are suppressed strongly by ingested proteins, weakly by lipids, and biphasically by carbohydrates. J Clin Endocrinol Metab. 2008 May;93(5):1971-9.
• Figueiro MG, Plitnick B, Rea MS. Light Modulates Leptin and Ghrelin in Sleep-Restricted Adults. International Journal of Endocrinology. 2013, Article ID 530726.
• Golden NH, Meyer W. Nutritional rehabilitation of anorexia nervosa. Goals and dangers. Int J Adolesc Med Health. 2004 Apr-Jun;16(2):131-44.
• Hernández M, Argente J, Navarro A, Caballo N, Barrios V, Hervás F, Polanco I. Growth in malnutrition related to gastrointestinal diseases: coeliac disease. Horm Res. 1992;38 Suppl 1:79-84.
• Hobart J, Smucker D. The Female Athlete Triad. Fam Physician 2000; 61:3357-64,3367. 
• Hoppe C, Mølgaard C, Dalum C, Vaag A, Michaelsen KF. Differential effects of casein versus whey on fasting plasma levels of insulin, IGF-1 and IGF-1/IGFBP-3: results from a randomized 7-day supplementation study in prepubertal boys. Eur J Clin Nutr. 2009 Sep;63(9):1076-83.
• Khan KM, Liu-Ambrose T, Sran MM, Ashe MC, Donaldson MG, Wark JD. New criteria for female athlete triad syndrome? As osteoporosis is rare, should osteopenia be among the criteria for defining the female athlete triad syndrome? Br J Sports Med. 2002 Feb;36(1):10-3. 
• Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007 Jan;8(1):21-34.
• Kratz M, von Eckardstein A, Fobker M, Buyken A, Posny N, Schulte H, Assmann G, Wahrburg U. The impact of dietary fat composition on serum leptin concentrations in healthy nonobese men and women. J Clin Endocrinol Metab. 2002 Nov;87(11):5008-14.
• Lagaly DV, Aad PY, Grado-Ahuir JA, Hulsey LB, Spicer LJ. Role of adiponectin in regulating ovarian theca and granulosa cell function. Mol Cell Endocrinol. 2008 Mar 12;284(1-2):38-45.
• Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8. Erratum in: N Engl J Med 1995 Aug 10;333(6):399.
• Loucks AB, Verdun M, Heath EM. Low energy availability, not stress of exercise, alters LH pulsatility in exercising women. J Appl Physiol. 1998 Jan;84(1):37-46.
• Loucks AB. Energy availability, not body fatness, regulates reproductive function in women. Exerc Sport Sci Rev. 2003 Jul;31(3):144-8.
• Lu M, Tang Q, Olefsky JM, Mellon PL, Webster NJ. Adiponectin activates adenosine monophosphate-activated protein kinase and decreases luteinizing hormone secretion in LbetaT2 gonadotropes. Mol Endocrinol. 2008 Mar;22(3):760-71. Epub 2007 Nov 15.
• Manore MM. Dietary recommendations and athletic menstrual dysfunction. Sports Med. 2002;32(14):887-901. 
• Mikos AE, McDowell BD, Moser DJ, Bayless JD, Bowers WA, Andersen AE, Paulsen JS. Stability of neuropsychological performance in anorexia nervosa. Ann Clin Psychiatry. 2008 Jan-Mar;20(1):9-13.
• Miller SM, Kukuljan S, Turner AI, van der Pligt P, Ducher G. Energy deficiency, menstrual disturbances, and low bone mass: what do exercising Australian women know about the female athlete triad? Int J Sport Nutr Exerc Metab. 2013 Apr;22(2):131-8.  
• Modan-Moses D, Stein D, Pariente C, Yaroslavsky A, Ram A, Faigin M, Loewenthal R, Yissachar E, Hemi R, Kanety H. Modulation of adiponectin and leptin during refeeding of female anorexia nervosa patients. J Clin Endocrinol Metab. 2007 May;92(5):1843-7. Epub 2007 Feb 27.
• Mont L, Castro J, Herreros B, Paré C, Azqueta M, Magriña J, Puig J, Toro J, Brugada J. Reversibility of cardiac abnormalities in adolescents with anorexia nervosa after weight recovery. J Am Acad Child Adolesc Psychiatry. 2003 Jul;42(7):808-13.
• Murdolo G, Lucidi P, Di Loreto C, Parlanti N, De Cicco A, Fatone C, Fanelli CG, Bolli GB, Santeusanio F, De Feo P. Insulin is required for prandial ghrelin suppression in humans. Diabetes. 2003 Dec;52(12):2923-7.
• NCAA® Sports Sponsorship and Participation Rates Report • 1981-82 – 2010-11.  
• Orlandi E, Boselli P, Covezzi R, Bonaccorsi G, Guaraldi GP. Reversal of bone marrow hypoplasia in anorexia nervosa: case report. Int J Eat Disord. 2000 May;27(4):480-2.
• Ott V, Fasshauer M, Dalski A, Meier B, Perwitz N, Klein HH, Tschöp M, Klein J. Direct peripheral effects of ghrelin include suppression of adiponectin expression. Horm Metab Res. 2002 Nov-Dec;34(11-12):640-5.
• Otto B, Cuntz U, Fruehauf E, Wawarta R, Folwaczny C, Riepl RL, Heiman ML, Lehnert P, Fichter M, Tschöp M. Weight gain decreases elevated plasma ghrelin concentrations of patients with anorexia nervosa. Eur J Endocrinol. 2001 Nov;145(5):669-73.
• Rguibi M, Belahsen R. Body size preferences and sociocultural influences on attitudes towards obesity among Moroccan Sahraoui women. Body Image. 2006 Dec;3(4):395-400. Epub 2006 Sep 7.
• Rodriguez-Pacheco F, Martinez-Fuentes AJ, Tovar S, Pinilla L, Tena-Sempere M, Dieguez C, Castaño JP, Malagon MM. Regulation of pituitary cell function by adiponectin. Endocrinology. 2007 Jan;148(1):401-10.
• Scacchi M, Ida Pincelli A, Cavagnini F. Nutritional status in the neuroendocrine control of growth hormone secretion: the model of anorexia nervosa. Front Neuroendocrinol. 2003 Jul;24(3):200-24.
• Scheid JL, De Souza MJ. Menstrual irregularities and energy deficiency in physically active women: the role of ghrelin, PYY and adipocytokines. Med Sport Sci. 2010;55:82-102.
• Schtscherbyna A, Barreto T, de Oliveira FP; Luiz RR, de Abreu Soares RR, Gonçalves Ribeiro B. Age of onset training but not body composition is crucial in menstrual dysfunction in adolescent competitive swimmers. Rev Bras Med Esport. May/June 2013; 18(3).
• Steinberg SE, Nasraway S, Peterson L. Reversal of severe serous atrophy of the bone marrow in anorexia nervosa. JPEN J Parenter Enteral Nutr. 1987 Jul-Aug;11(4):422-3.
• Skarda ST, Burge MR. Prospective evaluation of risk factors for exercise-induced hypogonadism in male runners. West J Med. 1998 Jul;169(1):9-12.
• Sundgot-Borgen J. [Physical activity and reproductive health]. Tidsskr Nor Laegeforen. 2000 Nov 20;120(28):3447-51.
• Teufel M, Zipfel S, Herpertz S, Zwaan M. (ed.). Handbuch Essstörungen und Adipositas. Springer Berlin Heidelberg. 2008. 
• Williams NI, Helmreich DL, Parfitt DB, Caston-Balderrama A, Cameron JL. Evidence for a causal role of low energy availability in the induction of menstrual cycle disturbances during strenuous exercise training. J Clin Endocrinol Metab. 2001 Nov;86(11):5184-93.
• Wölfing B, Neumeier M, Buechler C, Aslanidis C, Schölmerich J, Schäffler A. Interfering effects of insulin, growth hormone and glucose on adipokine secretion. Exp Clin Endocrinol Diabetes. 2008 Jan;116(1):47-52.
• Yamanaka A, Beuckmann CT, Willie JT, Hara J, Tsujino N, Mieda M, Tominaga M, Yagami K, Sugiyama F, Goto K, Yanagisawa M, Sakurai T. Hypothalamic orexin neurons regulate arousal according to energy balance in mice. Neuron. 2003 Jun 5;38(5):701-13.

Carbs Past 6PM Reloaded: Circadian Shifts in Leptin and Ghrelin + Rising Adiponectin During the "Carb-Fast" Could Explain the Efficacy of Eating All Carbohydrates at Night

Image 1: Paul Bart (Kevin James) in Mall Cop (Columbia) probably would be better off weight- and health- wise without his Segway, which is by the way among the "50 Worst Gadgets of the Decade" in the Business Insider hall of shame from 2009 (Barret, Brian. 2009)

The SuppVersity was the first place you read about the how "Carbs past 6pm Will Make You Lean" (at least about the non-anecdotal scientific evidence) and for 99% of you, this will probably be the first time you read about the "follow up paper" on the original study, which was originally intended to induce a shift in the circadian pattern of leptin secretion in order to make use of its fat burning effects over night. Exactly this is the focus of a follow up paper that's soon going to be published in Nutrition, Metabolism & Cardiovascular Diseases (Sofer. 2013).

Israeli Police Diet Acadamy Reloaded!

Now the bad news is that the news are only partly new. In other words, the Israeli scientists only reevaluated the original data which was based on 63 overweight police officers who finished the original "don't eat carbs before dinner study."

And if that was not already enough, the complete hormonal profiles which had been collected on days 0, 7, 90 and 180 of the study period were only available for 39 of them.

Figure 1: 24h leptin profile before and after the intervention in the control (left) and experimental (right) group
(graph adapted from Sofer. 2013)

Still, the data in figure 1 does support the original hypothesis that the mechanism due to which the participant on the experimental diets (composition see figure 3 in "Carbohydrates Past 6PM Will Make You ... Lean!") lost ~2% more weight, and ~4% more body fat was in fact a shift in the circadian expression of leptin:

I suggest you go back to the original "Carbs past 6pm Will Make You Lean" post to read up on the details; unless you're a longstanding reader and this reminder is enough for you.

"On day 0 both groups demonstrated typical concave diurnal leptin curves, including a fall throughout the hours of 08:00-16:00, reaching a nadir at the afternoon and a rise from 16:00. On day 180, leptin curves were lower compared to day 0 in both groups. In the experimental group, the curve became more convex with a nadir only in the evening and not in the afternoon (figure 1, right). A significant difference was observed within the experimental group between day 0 and day 180 in the morning and in the evening (p = 0.023 and p = 0.021, respectively). For subjects in the experimental group that had complete data, the change in evening measurements from day 0 to day 180 was significant(p = 0.024). Using these data, the change in evening measurements was significantly greater than the afternoon and the noon change (p = 0.009 and p = 0.014, respectively). In the control group, a significant difference was observed between day 0 and day 180 at noon (p = 0.042). This result was also found for subjects with complete data (p = 0.045)." (Sofer. 2013)

What's also noteworthy is that the sparse information the scientists had on the ghrelin levels of their participants (believe it or not, but the nurse or whoever took the blood samples must have messed up, so that much of the data was lost) would suggests that the "post 6pm group" (=experimental group) were freaking hungry in the evening (see figure 1, right), but this was not the case, contrary to the subjects in the control group which had carbs from AM to PM, they did rather expose an "enhanced daytime satiety" an observation based on which Sofer et al. rigthly state that

"[...] the alteration in ghrelin’s peak from daylight hours to the evening just before dinner was another cause for the elevated daylight hour satiety, improved persistence in the weight loss process and better anthropometric outcomes that were reported [16]." (Sofer. 2013)

Next to with the circadian shifts in leptin and ghrelin levels, the pronounced increase in adiponectin (see figure 2), a reliable marker for an improved glucose tolerance, the "carb binges" which as you will probably remember included desserts such as ice-cream and co (see figure 3 in "Carbohydrates Past 6PM Will Make You ... Lean!"), probably is the third pillar of the superiority of the past-6PM carb regimen over the conventional "eat small amounts of carbs all day" approach  the control group was following.

Figure 1: 24h Adiponectin profile before and after the intervention in the control (left) and experimental (right) group
(graph adapted from Sofer. 2013)

In conjunction those three made the "impossible possible": Eat all instead of no carbs past 6PM and lose weight! Now the unfortunate truth is that this works well for people with compromised insulin sensitivity and anywhere between 15-20% body fat to shed before they approach the level of leanness (<20%) most of you probably started out with, whether it will work similarly well for significantly leaner, physically active individuals, on the other hand, remains to be seen.

Video 1: I don't want to be a spoil, but the weight loss program of the Stadtwerke Cologne which works by simply skipping dinner (!) and without any caloric restriction got some series attention here in Germany. Why? Well, it simply works... so what does this tell you? Maybe it's more about helping AMPK come to it's own, instead of stuffing yourself with readily available energy 24/7, than about exact timing or meticulously calculating macro compositions?
(click here to watch Quarks & Co.)

Bottom line: Irrespective of my all doubts about the applicability of the very same diet principle in a context, where the goal is to get really ripped and not simply non-obese, the study at hand (and I am referring to the whole experiment, here not just the last paper) does confirm that there is more to dietary success than calories in vs. calories out that having breakfast like a king is not a necessity (nuts + coffee, which was the standard breakfast in the experimental group, or nothing, which is Adelfo Cerame's standard breakfast, work just as well) and that the influence of circadian rhythms goes far beyond our sleep-cycles... which reminds me that I'll do my very best to get into more details on that in the coming episode III of the SuppVersity Circadian Rhythm Series on Sunday. Until then, try not to lose the beat ;-)

References:

• Barret, Brian. The 50 Worst Gadgets Of The Decade. Business Insider. Dec 31, 2009. < http://www.businessinsider.com/the-50-worst-gadgets-of-the-decade-2009-12?op=1 > retrieved on Aug 24, 2013.
• Sofer S, Eliraz A, Kaplan S, Voet H, Fink G, Kima T, Madar Z. Changes in daily leptin, ghrelin and adiponectin profiles following a diet with carbohydrates eaten at dinner in obese subjects. Nutr Metab Cardiovasc Dis. 2013 Aug 14.

Whey or Casein, Pulse or Spread Evenly Across the Day? Does it Even Make a Difference in Terms of Fat Loss and Lean Mass Retention on a Diet? New + Old Empirical Data!

Image 1: Instinctively right? Milk contains soluble (=whey) proteins and casein. Are we overthinking things, when we rip them apart and does it even make a difference? Or is timing all that counts?

It's funny "overthinking", right next to overtraining and overdieting, has become one of the most common problems among the health and fitness enthusiasts who spend equal (or even more) time online as in the gym. "Would it be better if I take my BCAAs at a 3:1:1 or 2:1:1 ratio?", "Does it matter if my protein powder is 10% hydrosolate, 50% isolate and 40% concentrate or has a 30/50/20 ratio?" All that may well make a difference, but let's be honest: Look at the things 80% of these people are eating day in and day out and the way they throw the weights around in the gym and contrast that to a question like "Will my post-workout protein synthesis be 5% greater, when I switch from concentrates to hydrosolates?" ... enough of the ranting, though. After all this post is actually about one of the more sensible among these world-shattering questions:

Q

Will it make a difference, whether I use casein or whey protein on a diet and... what's the significance of having my daily allotment of protein spread evenly across the day vs. mostly (80%) in one sitting, when I am dieting?

In order to find the answer to this question a group of French scientists recruited 41 healthy, but chubby subjects (BMI ~32kg/m²; age ~33y) and put them on a relatively moderate caloric deficit that was calculated based on their basal energy requirement (what you would need lying around all day). In all four arms of the study, the macro-nutrient composition (25% as proteins, 25% as lipids, and 50% as carbohydrates) and energy content per pound of lean body weight (average energy intake 5.87 MJ per day) of the meals, which were prepared according to personalized menus the subjects received from trained dietitians, were identical.

Figure 1: It did not make a difference if the protein was ingested either spread equally across the day or as a pulse mostly (80%) in one sitting (top), fat and weight loss after the 6 week study period were virtually identical (data based on Adechian. 2013)

The little information on the exact menu choices the scientists offers includes a list of stable foods, such as various proportions of spinaches, broccoli, lentils, or green beans, butter, bread, fruits, soy yogurt, rice cakes and gingerbread and suggest that we are dealing with the typical "your dietitian recommends diet", here. With one exception, of course, the main protein source of all four experimental diets were dairy proteins (~80g; >80% of total protein). Casein and whey aka "milk soluble protein"* (see red box above), which were to be ingested either spread equally across or in a "pulsed" fashion (see figure 1, left):

*Note: the scientists refer to whey as "milk soluble protein, I stuck to the terminology in the graphs, but in essence these are mainly β-lactoglobulin, α-lactalbumin, as well as serum albumin, immunoglobulins, lactoferrin, and other minor fractions and thus the same you would find in your average whey concentrate which is, as you may have notices "more soluble" than casein (cf. Lacroix. 2006)

• casein spread- subjects consumed ~20g of a casein protein supplement 4x a day
• milk spread - subjects consumed ~20g of milk protein supplement 4x a day
• casein pulse - subjects consumed the lions share, i.e. 80% of their ~80g of casein, as part of their 2nd meal, so that the protein intake over the day was 6.4g / 64g / 3.2g / 6.4g (see figure 1)
• milk pulse - same as above, but with milk instead of casein protein

In view of the overemphasisze nutrient timing has gotten as of late withing the physical culture and the assumption that you would expect to see profound differences based on when you consume how much of fast or slow, high (milk) or average (casein) leucine protein etc., it may be disappointing that the weight loss was absolutely identical in all four arms of the study (-7.5 ± 0.4 kg).

Differences are few and far between: Weight loss, fat loss, muscle loss - NOT different! 

What may yet surprise even you, a seasons SuppVersity veteran, who will probably already have expected the non-significant (in fact non-existent) differences in terms of weight loss, could be surprised that the changes in body composition (see figure 1, bottom), i.e. -5.1 ± 0.2 kg reduction in body fat mass and -2.2 ± 0.2 kg reduction in lean body mass, were identical.

Since the same goes for the changes in the fat "liberating" proteins lipoprotein lipase (LPL) and adipose triacylglycerol lipase (AGTL), the fat "forming" protein fatty acid synthase (FAS), and three of the usual subjects, i.e. leptin, the adipoQ gene which is responsible for encoding adiponectin, of which recent research suggests it may be even more important than leptin for your metabolic health (Li. 2013; Hickman. 2013), and the reduction in the pro-inflammatory monocyte chemotactic protein-1  (MPC-1), the slightly more pronounced meal-induced postprandial protein synthetic response in the casein group at the end of the study period is actually the only difference based on which you could argue for one over the other protein source:

Figure 2: While the changes in LPL, AGTL, FAS, leptin, AdipoQ and MCP expression were identical (left); the post 6-week protein synthetic response to identical meals was slightly more pronounced in the casein group (right), the overall significance of this finding is yet questionable in view of identical lean mass losses - it could yet become important on a diet + exercise regimen as in the Demling study discussed in the bottom line box  (data based on Adechian. 2013).

Whether the measurable advantage of casein during this test (the evaluation was carried out by leucine tracer infusion, by the way) is just an experimental artifact or

Adherence is the key to success: While there was no difference in terms of the hunger the subjects felt when they were on the diet, the fact that only 23 of the initially 41 subjects did make it through the 6- week on ~ 1,500kcal/day is quite telling, also in view of the perceived inability to lose weight - if you can't stick to a by no means crazy caloric restriction for 6 weeks, how can you expect to get lean and stay lean, when the inevitable prerequisite for the latter is that you totally revamp your dietary habits for the rest of your life not just six, eight, or twelve weeks.

• maybe something like "leucine resistance" in response to the higher leucine concentrations after the ingestion of the milk protein supplement in the course of the study period, or
• alternatively, the greater IGF-1 response to casein (cf. Hoppe. 2009, a study which compares whey vs. casein, but would obviously suggest an advantage of casein over milk = whey + casein, as well); unfortunately IGF-1 wasn't measured, but the insulin levels which were minimally higher in the casein group could support that hypothesis,

... is questionable. Since the same is true for the practical relevance of the ~10-13% larger leucine balance during the postprandial phase of the post-diet whole body protein metabolism test in week 6, I would not fret about this difference too much, though.

Maybe, just maybe, the adipocyte morphology could make a difference

What I would consider significant, though it did not reach that status (probably due to the low number of participant that actually made it to the end of the study, see red box on the right), is the slight but in my eyes potentially important superiority of the equally spread protein ingestion in terms with respect to the before vs. after adipocyte diameter in the casein group:

Figure 3: The difference did not reach statistical significance, but if we take for granted that greater reductions in adopcyte sizes are associated with healthier metabolic profiles, you would be better advised to take your casein protein equally spaced across (15% reduction in adipocyte size vs. 7%, only, for pulsed casein intake) the day... for whey, aka "milk soluble protein", on the other hand it does not seem to matter (data calculated base on Adechian. 2013)

Now, even if we assume that this made a difference and a greater reduction in adipocyte size was a significant advantage, which it probably is from a health perspective, as Skurk et al. state that there is

"[...] a differential expression of pro- and antiinflammatory factors with increasing adipocyte size resulting in a shift toward dominance of proinflammatory adipokines largely as a result of a dysregulation of hypertrophic, very large cells." (Skurk. 2006)

and a recently conducted human trial, by Rizkalla et al. the main message this study should be sending out is not that it does not make a difference whether you use casein or milk protein as your main protein source on a diet, but that a high protein diet with a mediocre caloric reduction of ~20-25% and supplemented with high quality dairy protein (whey or casein) works: After all, more than -1kg of weight loss per week, 68% of the weight loss from fat in the absence of exercise is more than your average celebrity XYZ diet will do for you ;-)

Whey or casein? It's high cysteine content that can help to replenish your glutathione (=the master antioxidant) pools would be another factor that speaks in favor of whey. Whether normal-weight individuals on an already optimized dietary regimen would benefit to the same extend as the obese young men in the 6-week whey supplementation trial, Vatani et al. describe in the August issue of Appetite, is however questionable. After all, the increases in HDL the total antioxidant capacity and glutathione is as questionable as any possible negative influence of the starchy placebo the researchers used in that study (some of you may have seen the link on the SuppVersity Facebook Wall, already).

Figure 4: Fat loss and lean mass gains in formerly overweight police officers after 12 weeks of training and dieting with or without casein / whey hydrosolate (Demling. 2000)

Moreover, one of the few long-term (=non acute protein synthesis) studies investigating the differential effects of concomitant whey vs. casein hydrosolate protein supplementation, found statistically significant higher body fat reductions and lean mass gains in those 33-34 year-old police officers who supplemented their 12-week diet + strength training regimen with 2x37g of casein hydrosolate (8h apart; for the exact data see figure 4; Demling. 2000).

Note: since both the whey (Pro-Score Champion Nutrition) and the casein protein (MET-Rx USA) in this study were hydrosolates the differences in lean mass gains and fat loss are depend primarily on the amino acid composition of the proteins, and not, as it would be with micelle casein vs. whey, the absorption kinetics!

Bottom Line: Against that background the study at hand supports previous findings of the importance of a threshold intake of protein. Interestingly, it did not confirm the notion that this threshold intake should be spread equally across the day, which is something most commenters (me included) read into the seminal paper by Loenneke et al., which found a statistically significant negative correlation not between total protein intake, but between the number of meals with 10g or more essential amino acids in them and abdominal obesity (Loenneke. 2013). So, does timing matter, or does it not? 

1. It does matter, when you work out, there is ample evidence to support that the ingestion of protein in the vicinity of the workout cannot just amplify the protein synthetic response but will also results in an increase in real world muscle gains.
2. It appears that it does not matter, when you are dieting (only), though; not just the study at hand, but also the success many people report on intermittent fasting regimen, would support the notion that the more sustained anabolism you may be able to achieve by ingesting say 4x25g of protein instead of 1x80 + 2x10g has, compared to the total amount of protein you eat, relatively little influence on the conservation of lean body mass, when you are dieting.

And as far as the choice between casein and milk soluble protein, aka whey (see first red box), is concerned (see box on the right, as well), it would appear prudent to assume that a combination of both - just like nature intended it - would be the best choice as a "standalone" protein source (cf. "Whey and Casein Work Hand in Hand for Protein Anabolism, but Scientists Overlook Fat, When They Reassemble Milk"), while the higher leucine content and faster digestibility render whey the better candidate for classic "supplementation", as in having an additional shake before you start preparing your whole-foods post-workout meal, which should - and I hope it's not really necessary that I say that - obviously include a significant amount of protein (fish, eggs, meats, and if you will even more dairy ;-), as well. The usefulness (again, not necessarily the superiority!)  of slow digesting protein is something you should be aware of, anyway, right? If not re-read the "3.2kg of Lean Mass Over Night W/ 40g of Slow Digesting Protein 30min Before Bed!?" post from February 22, 2013.

References:

• Adechian S, Balage M, Remond D, Migné C, Quignard-Boulange A, Marset-Baglieri A, Rousset S, Boirie Y, Gaudichon C, Dardevet D, Mosoni L. Protein feeding pattern, casein feeding or milk soluble protein feeding did not change the evolution of body composition during a short-term weight loss program. Am J Physiol Endocrinol Metab. 2013 Aug 14.
• Demling RH, DeSanti L. Effect of a hypocaloric diet, increased protein intake and resistance training on lean mass gains and fat mass loss in overweight police officers. Ann Nutr Metab. 2000;44(1):21-9.
• Hickman IJ, Whitehead JP. Structure, signalling and physiologic role of adiponectin - dietary and exercise-related variations. Curr Med Chem. 2013 Aug 9.
• Hoppe C, Mølgaard C, Dalum C, Vaag A, Michaelsen KF. Differential effects of casein versus whey on fasting plasma levels of insulin, IGF-1 and IGF-1/IGFBP-3: results from a randomized 7-day supplementation study in prepubertal boys. Eur J Clin Nutr. 2009 Sep;63(9):1076-83. 
• Lacroix M, Bos C, Léonil J, Airinei G, Luengo C, Daré S, Benamouzig R, Fouillet H, Fauquant J, Tomé D, Gaudichon C. Compared with casein or total milk protein, digestion of milk soluble proteins is too rapid to sustain the anabolic postprandial amino acid requirement. Am J Clin Nutr. 2006 Nov;84(5):1070-9.
• Li FY, Lam KS, Xu A. Therapeutic perspectives for adiponectin: an update. Curr Med Chem. 2013 Aug 9.
• Loenneke JP, Wilson JM, Manninen AH, Wray ME, Barnes JT, Pujol TJ. Quality protein intake is inversely related with abdominal fat. Nutr Metab (Lond). 2013 Jan 27;9(1):5. 
• Rizkalla SW, Prifti E, Cotillard A, Pelloux V, Rouault C, Allouche R, Laromiguière M, Kong L, Darakhshan F, Massiera F, Clement K. Differential effects of macronutrient content in 2 energy-restricted diets on cardiovascular risk factors and adipose tissue cell size in moderately obese individuals: a randomized controlled trial. Am J Clin Nutr. 2013 Jan;95(1):49-63.
• Skurk T, Alberti-Huber C, Herder C, Hauner H. Relationship between adipocyte size and adipokine expression and secretion. J Clin Endocrinol Metab. 2007 Mar;92(3):1023-33.
• Vatani DS, Golzar FA. Changes in Antioxidant Status and Cardiovascular Risk Factors of Overweight Young Men after Six Weeks Supplementation of Whey Protein Isolate and Resistance Training. Appetite. 2013 Aug 10.

Epigallocatechin Gallate (EGCG), Capsaicins, Piperine & Carnitine: Rather a Health Than a Fat Loss Stack?

That's not what the ultimate weight loss diet looks like. The pill remains a supplement, i.e. something to supplement (and support) your dietary and exercise efforts, nothing more, but - as long as you pick the right one for your type and goal - also nothing less (photo ehow.com)

Let me first remind you of the fact that something that works in your obese neighbor does not necessarily work as effectively in someone like yourself, a devoted physical culturist who is only a couple of steps away from the six pack he has always been dreaming of. Let me also emphasize the fact that taking the supplement alone, i.e without the -600kcal reduction in energy intake all of the 86 overweight subjects (healthy males and females aged 25–45 years, with a body mass index greater than 25 kg/m² less than 35 kg/m²) had to stick to, there probably wouldn't have been any weight loss at all. And lastly, let me also formulate the hypothesis that the various health benefits, such as the increases in insulin sensitivity, the improvements in the leptin/adiponectin ratio or the decreasing LDL levels would probably have been less pronounced without the game-changing reduction in energy intake.

Simple Truth: The right diet, not the right supplements is the key factor in losing body fat

Apropos reduction in energy intake, one of the most underrated but practically highly relevant beneficial effects the administration of the epigallocatechin gallate (EGCG from green tea), capsaicins, piperine, L-carnitine and a few minor ingredients (see figure 1, left) probably brought about certainly were the psychological benefits, such as the 3.3 pts decrease on the Beck depression inventory (BDI-II), since the ability and will to adhere to a diet - whether this may be for 8 weeks as in the study at hand or (preferably) for life - obviously hinges on the question: "Can you stick to it?"

Figure 1: Energy content (primary axis in kcal) and macronutrient composition (secondary axis in g) and ingredients of the of the weight loss supplement (Rondanelli. 2013)

That said, the diet composition in figure 1 (left) certainly raises another question: "Would it even be wise to adhere to this diet for longer than 8 weeks?" I mean it stands out of question that living on a caloric deficit for the rest of your life is not an option. If you look a the macronutrient composition of the diet, on the other hand, my personal  prognosis is that this program will not yield long-term success. Not because it's high in carbs, but because it is too low in protein and lacks an exercise component - typical mainstream dieting = typical mainstream failure - with or without "bioactive food ingredients" (Rondanelli. 2013).

Fat loss or anti-diabesity stack? That is the question!

The combination of a lack of exercise stimuli and a relatively low dietary protein intake (certainly below the threshold limit of 10g+ of EAA per meal) is probably also the main reason for the slight loss in lean muscle tissue, a phenomenon  - and that's interesting, although the difference did not reach statistical significance - occured only in the supplemented  group.

Figure 2: Changes in body composition (left) and selected markers of glucose management and fatty acid metabolism, adipokine expression and inflammation (Rondelli. 2013)

Now, there are obviously dozens of potential reasons for the minimal muscle loss in the supplement group. In my humble opinion the most likely explanation does yet relate to the very same increase in resting energy expenditure (+120.6kcal/day) that's (alongside the metabolic improvements, cf. figure 2, left) behind the additional 600g of body fat, the subjects in the supplement group shed in the course of the 8-week dietary intervention.

"600g in 8 weeks? Are you kiddin' me?"

Yep, you read me right, 600grams is all the supplement yielded as far as additional fat loss is concerned. That, plus the fact that neither this, nor any of the differences in between the changes in anthropometric data reached significance does tell you something about the actual weight loss effects even obese and insulin resistant subjects can expect from taking an epigallocatechin gallate (EGCG from green tea), capsaicins, piperine and L-carnitine based dietary supplement.

What? That's pathetic? Well, it would be if these changes were not accompanied by way more important and statistically significant different effects on the insulin sensitivity of the 41 overweight subjects in the supplement group who completed the study.

As far as the inhibition of diet induced weight gain and insulin resistance are concerned, there is no synergism of green tea and the L. plantarum, a probiotic. Green tea does the job, the bacteria stand by and watch in awe (read more)

Bottom line: As I've pointed out numerous times before. There are a different types of weight loss adjuvants, with one of the most general, if you will "fundamental" distinctions between (a) those weight loss supplements that have a more or less pronounced direct effect on the energy balance (=carb/fat blocker, beta-agonists, thyroid mimetics, appetite suppressants etc.) and (b) their healthier cousins that promote your weight loss efforts by ironing out acquired metabolic obstacles, such as leptin and insulin resistance. And though you could certainly make a point that green tea exhibits some features of both categories, the overall stack used in this study belongs to the second category and it's efficacy is therefore going to drop the healthier (=less inflamed, insulin & leptin sensitive) you are, when you start dieting.

You may want to keep that, as well as the (un-)fortunate truth that there simply is no "fat burner pill" on the market that will do the allegedly hard dieting and exercising for you, in mind, whenever you pass by the storeboard with the virtual or real shelves of a supplement store and are tempted to invest 50$ or so into yet another "next generation fat burner"... without having a diet and workout plan and the will to stick to it, you can just as well save the 50$.

References:

• Rondanelli M, Opizzi A, Perna S, Faliva M, Solerte SB, Fioravanti M, Klersy C, Edda C, Maddalena P, Luciano S, Paola C, Emanuela C, Claudia S, Donini LM. Improvement in insulin resistance and favourable changes in plasma inflammatory adipokines after weight loss associated with two months' consumption of a combination of bioactive food ingredients in overweight subjects. Endocrine. 2013 Dec 28. [Epub ahead of print]