Weight Loss Program for Health: childhood obesity

Showing posts with label childhood obesity. Show all posts

Fit Kids = Smart Kids, Creatine & Muscle Repair, Epigenetic Transfer From one Leg to Another. Plus: Fat Effects of Anti-Psychotics, Larger Muscle = Greater CNS Impact, Rhodiola a Natural Opiate, Hawthorn for More & Thicker Hair

It's never too early for your first push-up ;-)

"10" is this week's SuppVersity figure of the week. Ten as in "ten push-ups" which is the mean number of push-ups the 12 year-old boys and girls from the Coe study you can read about in one of the items of today's news mash-up aka "On Short Notice". I am honestly not yet sure what to make of it, it's not as bad as what I had expected based on a couple of observations I have made as of late, but it still goes to show you that you cannot take the most fundamental feats of physical fitness for granted, when it comes to pre-/peri-pubertal kids in today's sedentary society.

Now, while I am still trying to make up my mind I would suggest we take a look at the actual outcomes of the study. The 10 push-ups were after all only part of the subject characteristics and not the reason Coe et al. actually conducted their study.

Fit Kids are smart kids - Strength and cardio both matter!

You can hardly start your career as a physical culturist too early, there are simply way too many benefits from giving your body the nutrients and the exercise it needs and therefore it is actually not surprising that conclusion of a recently published paper in the Journal of Sports Medicine and Physical Fitness reads:

"Students with the highest fitness level performed better on standardized tests and students with the lowest fitness level performed lower in class grades" (Coe. 2012)

Interestingly enough, this effect was associated with both cardiorespiratory fitness and strength, which brings us back to yesterday's news about the PGC-1 alpha isoforms (read the comments as well) and the detailed follow up I just decided to post on the whole matter, tomorrow.

Figure 1: Spearman rank correlations and achievements cores in terms of grades (0:min, 80:max), test scores (% of max) and combined (% of mean of all kids; data based on Coe. 2012)

Since this is the first study of its kind to investigate all five established parameters of health-related fitness (HFR), it should also be mentioned that body composition, flexibility and muscular endurance did not show the same statistically significant correlations the scientists observed for cardiorespiratory endurance and muscle strength in the kids (52% boy, 48% girls; all from the same age group ~12 years). Now, it would be nice if the people who design the curricula would keep that in mind, when they add junk after junk to the syllabus and regard sports and being active as an unnecessary diversion from the constant intellectual drills.

Creatine can do much, but it can't accelerate skeletal muscle repair after a workout

The results of a recent study from the Department of Kinesiology and Physical Education at the Wilfrid Laurier University in Canada (McKinnon. 2012) , in the course of which a total of 27 male (n = 15) and female (n = 12) participants between the ages of 18-24 completed an experimental training protocol with either

2x creatine monohydrate (20g) and a carbohydrate supplement (20g) in order to blend consistency and taste (CREA),
2x 40 g of maltodextrin only in 500mL of water (MALTO), or
no supplementation at all (control)

The supplement was consumed over a 5-day period (check out the "Pharmacokinetics of Creatine" posts and you will learn that this dosage regimen is an unnecessary overkill - even if you insist on "loading") after which the participants participated in a baseline strength test that was followed by a muscle-damaging protocol that consisted of maximal force eccentric contractions:

Suggested read: "Creatine a Proven Non-Anabolic Agent: It's the Increase in Training Intensity that Will Give You the Hypertrophic Edge (read full story)
"Subjects performed 60 maximal eccentric contractions that were divided into 6 sets of 10 repetitions, with a 45 second rest period between repetitions. The velocity of eccentric contractions was varied between sets (2 at 75°/sec, 2 at 90°/sec, and 2 at 120°/sec). This protocol has been used in previous studies and has been shown to be an effective means of inducing skeletal muscle damage (Cooke et al., 2009). The researchers also provided verbal encouragement to the subjects to help maintain maximal effort throughout the protocol." (McKinnon. 2012)

After adequate rest, the first of 5 post-tests was conducted. The results (figure 2) clearly show that despite the overall greater force recovery in the creatine group, the relative rebound after an allegedly higher drop was seen in the MALTO group while it was minimal in the no-supplement group.

Figure 2: Force recovery and muscle soreness at 0h, 24h, 48h, 72h, 96h in the control, maltodextrin and creatine groups subsequent to a 5-day suppelemtation regimen (nothing, 2x 20g crea + 2x20g malto, or 2x40g malto (McKinnon. 2012)

Overall the scientists are yet still right, when they say that "creatine supplementation failed to significantly influence indices elbow flexor muscle damage or rate of muscle recovery following eccentric muscle contractions." After all, there were no statistically significant differences between either the muscle force loss and rate of recovery or muscle soreness (small figure in figure 2) between the groups - and it is unlikely that this would change after the initial 96h of recovery.

Additional suggested reads:

DHEA Blunts Muscle Damage During 5 Days of Combined Endurance, Strength and HIIT Training in Young Men (read more)
Speed Up Your Regeneration and Propel Your Gains by Taking a HOT Bath Bath 2-Days Before Arduous Workouts (read more)
Overtraining, Inflammation, Insufficient Repair: Scientists Shed Some More Light on the Counterproductive Triad of Ups & Downs in Testosterone, IL-6, IL-10, COX II & Co (read more)

Ah, I almost forget to mention, you see that the mean isometric peak torque is not even back up to 100% after 96h, right? Remember that whenever you decide that it would be a good idea to do "yet another set of forced reps". It is possible that the seasoned strength training veteran you are, you recover faster than the subjects in the study at hand who had not trained for at least 4 months, but it stands out of question that eccentric forced reps will increase the time you need to regenerate, let alone to see what we are all striving for, i.e. super-compensation effects (see suggested links on the right for more on "doing too much" and faster recuperation after workouts).

Working out one leg changes genes in the other leg as well

The progress research in the area of epigenetics, i.e. the changes of gene methylation and thus activity in response to nutrition, exercise and other variables you can easily control is actually amazing. With the recent publication of a study into what you may call epi-genetic cross-reactivity further contributing to our insights into the relations of the local and system epigenetic effects of exercise and their respective metabolic downstream effect (Catoire. 2012).

Figure 3: Graphical summary of the study design and selected results (Catoire. 2012)

As you can see in my graphical mini-summary of the study design (top) and outcomes (middle + bottom) in figure 3 there was a whole lot going on... and that despite the fact that I did already spare you a complete page with font 10 lists of genes that changed (you do have the numbers, I guess that shall suffice) and paired them in groups. What's funny is that, when it's all said and done, this does yet again tie in to yesterday's news on PGC-1 alpha 4 - how? Well, let's hear (or read), what the scientists have to say in the discussion of their results:

"Many of the observed exercise-induced changes in gene expression are likely part of an acute stress response related to disturbances in homeostasis elicited by exercise. The most highly induced genes in the exercising leg were all members of the NR4A family, a subgroup of orphan receptors within the nuclear receptor superfamily. NR4A1 and NR4A3 have been reported to be upregulated shortly after acute exercise and during recovery in rat, pig, and human [24], and this upregulation likely occurs locally by contractile stimuli. This finding was confirmed by our study in which we observed an upregulation of NR4As in the exercising, but not in the non-exercising leg. NR4A transcription factors are also known to be induced by adrenaline and noradrenaline. Circulating adrenalin and noradrenalin levels were increased in our study but must exert only a minor effect as NR4As were exclusively induced in the exercising leg,. [...] NR4A1 and 3 are thought to play a key role in regulating energy metabolism and early adaptation. [...] The results may imply that NR4A family might play an important role in the regulation of metabolic responses after exercise." (Catoire. 2012)

The study at hand does thus add yet another puzzle piece to the image of the crossroads of the endocrine (from one tissue to the other) and intracrine (in this case in the exercised muscle) effects of energy and metabolic changes on the one hand and muscular contraction and local stress, on the other hand. As closely interwoven as they are, we are now - thanks to the novel gene essays - able to see through the complex network, understand what exercise does to our physiology and can then, in the next step, come up with ways to modulate these effects for our own benefit.

It is clear that this is not going to be easy and the presence of two "mutants" among the 12 relatively old study participants (52 year; "old" only for studies like this, of course!) suggests that any cookie cuter solutions are probably about to fail. I mean, if you have got two guys out of twelve where the overall magnitude of gene expression changes in the exercising and non-exercising leg were very similar, it is more than likely that you would see these and other anomalies very frequently; and each of them would have to be considered if you wanted to design he optimal workout (nutrition and supplementation) regimen for an individual (good news for personal trainers, if you know what you are doing, no sciency compendium is ever going to replace you ;-)

In rehab, doctors and therapists use the neurological stimulation a stiff leg receives, when you move the other while looking into a mirror that fools you into believing that the stiff leg would be moving as well.

In that it does not even really matter, whether the observed anomalies were actually due to genetic differences or, as the scientists suspect simply the result of unconsciously performed isometric contractions in of the non-exercising leg. The ensuing neuronal activation could have brought about similar effects as they are observed (and intended) during mirror therapy (see image on the right), where an involuntary neural stimulation of the muscles in a stiff leg occurs, when the mirror fools you into believing that you actually just moved your stiff leg, or other body part, when it was in fact only the counter-lateral limb that moved (note: one of the latest reviews of the literature says about its efficacy in stroke rehab would facilitate the recovery of "motor function, activities of daily living and pain" and could be recommended "at least as an adjunct to normal rehabilitation for patients after stroke"; cf. Thieme. 2012).

With the effects of neural stimulation, which has already been shown to induce gene expression changes via increased calcium concentrations in the skeletal muscle as well as via other mechanisms (Long. 2007; Kanzleiter. 2009; Chin. 2010, we do thus have a third player in the epigenetic / protein regulatory exercise orchestrate that does now consist of a metabolic, a contractile / stress mediated and a neuronal component. As far as skeletal muscle hypertrophy is concerned, the local expression does still appear to be the major determinant of adaptation and thus growth - to train your left leg only expecting that the other will grow due to "bystander effects" is therefore almost as hilarious as skipping leg day with the lame excuse that your legs would grow from training your biceps ;-)

On ultra short notice

With that I'll call it a day as far as the detailed posts are concerned and invite you to come back tomorrow, when I am going to pick up on this discussion in a detailed post on the Roa study on PGC-1 alpha 4, muscle growth, myofiber composition, strength development, workouts and the whole megillah. For the time being here is a bunch of unsorted other things I considered newsworthy:

Anti-psychotics increase lipid synthesis by depressing it!? What sounds totally counterintuitive, is actually the main message of an editorial to the latest issue of the Journal of Lipid Research, in which Skreede, Steen & Ferno argue that a paper by Canfrán-Duque et al. clearly suggests that the obesity and hypercholesterolemic effects of 2nd generation anti-psychotics such as clozapine, risperidone, and ziprasidone are brought about by the counter-regulatory upregulation of cellular lipogenesis in response to their suppressive effect on cholesterol synthesis. (Skreede. 2012)
The greater the muscle group you work, the larger the impact on the central nervous system will be (Rossmann. 2012) -- In the end everybody will know that intuitive, back and leg days are the hardest and most taxing to the whole system. Based on a trial involving eight young men who performed exhaustive large (cycling – BIKE) and small (knee extensor – KE) muscle mass dynamic exercises at 85% of the modality-specific maximal workload, scientists from Salt Lake City did now provide further experimental evidence that supports the notion that the CNS tolerates a greater magnitude of peripheral fatigue and likely a greater intramuscular metabolic disturbance when the pertinent afferent signaling comes from small vs. large muscle groups .
Rhodiola Rosea turns out to be an opiate (Lee. 2012).-- In a recent study scientists from the Chi-Mei Medical Center in Yong Kang, Tainan City, Taiwan were able to show that the popular but questionable (as far as the significance of its effects are concerned) adaptogen rhodiala decreased the systolic blood pressure of spontaneously hypertensive rats. Intriguingly the effect was blunted by the administration of the selective opioid μ-receptor antagonist, cyprodime, but not by naloxonazine, an antagonist specific to opioid μ1-receptor, which suggests that a direct effect on the opiate receptor. Moreover, the level of mood enhancing and relaxing beta-endorphins rose in both wild type and hypertensive rodents (with the effect being more pronounced in the latter)
Chinese hawthorn for the hair, not the heart (Shin. 2012) -- I guess if you hear hawthorn or Crataegus you will probably think of its purported beneficial effects on heart health. Now if the results from a recent rodent study are applicable to humans, as well, you will soon have to establish a novel neuronal connection between (Chinese) hawthorn and your scalp, or rather the hair on your scalp . With its beneficial effects on the initiation of the anagen phase in mice in teloge and the ensuing increase in skin color, thickness of the hair shafts, and density (number and size) of the hair. Oral C. pinnatifida extract (at a human equivalent dose of ~320mg/day) could soon be all the rage among men and women who fear for their superb head of hair.

I think this is enough for today. There is a life beyond the SuppVersity not for you, of course, but for me - so while you head over to the SuppVersity facebook page for even more news, I am going to enjoy Saturday night ;-)

References:

Canfrán-Duque, A., M. Casado, Ó. Pastor, J. Sánchez-Wandelmer, G. Peña, M. Lerma, P. Mariscal, P. Bracher, M. Lasunción, and R. Busto. Atypical antipsychotics alter cholesterol and fatty acid metabolism in vitro. J Lipid Res. 2012 [in press]
Catoire M, Mensink M, Boekschoten MV, Hangelbroek R, Müller M, et al. Pronounced Effects of Acute Endurance Exercise on Gene Expression in Resting and Exercising Human Skeletal Muscle. PLoS ONE 7. 2012; 11: e51066.
Chin ER. Intracellular Ca2+ signaling in skeletal muscle: decoding a complex message. Exerc Sport Sci Rev. 2010 Apr;38(2):76-85.
Coe DP, Pivarnik JM, Womack CJ, Reeves MJ, Malina RM. Health-related fitness and academic achievement in middle school students. J Sports Med Phys Fitness. 2012 Dec;52(6):654-60.
Kanzleiter T, Wilks D, Preston E, Ye J, Frangioudakis G, Cooney GJ. Regulation of the nuclear hormone receptor nur77 in muscle: influence of exercise-activated pathways in vitro and obesity in vivo. Biochim Biophys Acta. 2009 Aug;1792(8):777-82.
Lee WJ, Chung HH, Cheng YZ, Lin HJ, Cheng JT. Rhodiola-Water Extract Induces β-endorphin Secretion to Lower Blood Pressure in Spontaneously Hypertensive Rats. Phytother Res. 2012 Nov 28.
Long YC, Glund S, Garcia-Roves PM, Zierath JR. Calcineurin regulates skeletal muscle metabolism via coordinated changes in gene expression. J Biol Chem. 2007 Jan 19;282(3):1607-14.
Rossman MJ, Venturelli M, McDaniel J, Amann M, Richardson RS. Muscle mass and peripheral fatigue: a potential role for afferent feedback? Acta Physiol (Oxf). 2012 Dec;206(4):242-50.
Shin HS, Lee JM, Park SY, Yang JE, Kim JH, Yi TH. Hair Growth Activity of Crataegus pinnatifida on C57BL/6 Mouse Model. Phytother Res. 2012 Nov 12.
Skrede J, Steen VM, Ferno J. Antipsychotic-induced increase in lipid biosynthesis: activation through inhibition? Journal of Lipid Research. December 7, 2012 [Epub ahead of print]
Thieme H, Mehrholz J, Pohl M, Behrens J, Dohle C. Mirror therapy for improving motor function after stroke. Cochrane Database Syst Rev. 2012 Mar 14;3:CD008449.

Low Fat Toddler, High Fat Adult?! Intra-Workout Carbs More 'Anabolic' Than Protein!? Iron Prevents Gastric Cancer & Insulin Resistance?! Plus: A Sixpack of Kettlebell Studies

If you want to know exactly how your neighbors or rather your county did, check out the CDC's brand new County Data Interactive Atlas (may take some time to load), select your state and click on your county. Unfortunately, it's not exactly likely that you will be pleasantly surprised after all, places with rates below 6.5% (white on the map) have become rare, while those with 11.2% or more are becoming the norm.

"100%" - In words: One hundred percent, that's the SuppVersity figure of the week and at the same time the rate at which the prevalence of diagnosed diabetes in 14 of the US states grew faster in the years between 1995 and 2000 than previous estimates had predicted. The CDC has published this figure along with more information and the link to their brand new County Data Interactive Atlas in their weekly report on November 15, 2012. The Top 5 offenders on the list that's attached to the report are (1) Oklahoma (226 percent), (2) Kentucky (158 percent), (3) Georgia (145 percent), (4) Alabama (140 percent), and (5) Washington (135 percent).

No reason to worry, though, my American friends! According to their own assessment, the CDC and its partners are working on "a variety of initiatives to prevent type 2 diabetes and to reduce complications in those already diagnosed."... you see,all is going to be good! Your well-meaning government is taking care of the problem ;-)

I guess that's enough sarcasm and useless statistics for the day. Let's get down to some serious On Short Notice business, now. And what would be more obvious than to start with something that's probably still not on the radar of the CDC or any its smart partners over at the NIH who are still promoting a high carb + low fat diet to people who can hardly tolerate the amount of carbohydrates in a TicTac. What I am talking about? The predispositioning effects of a fat-deficient toddler diet...

Fat loving toddlers grow up to be leaner adults (Rolland-Cachera. 2012) -- To determine whether nutritional intakes in early life are associated with body composition and hormonal status at 20 years, a group of researchers from the University of Paris analyzed data from 73 subjects, who had been part of a two-decade-long prospective study (ELANCE, Etude Longitudinale Alimentation Nutrition Croissance des Enfants).
Associations of specific factors that increase the risk of being obese in the kindergarten as based on another study that's also been published ahead of print in the online version of Obesity (Flores. 2012):
- born to an obese mother + 240% risk
- gestational diabetes and gestational diabetes + 190%
- drinking tea or coffee between meals before bedtime at 2 years old +230% and drinking sugary beverages at kindergarten age at least weekly + 130%
- Latino or multiracial + 130% race ethnicity
- ever-attending center-based daycare -70%
- eating fruit at least weekly at kindergarten age -70
- maternal history of a prior newborn birth weight greater than or equal to 4000g -90%
If you do have or plan to have kids, you should maybe make a mental note on some of these.
The kids, now all young adults had been examined twice, at the age of 10 months and with 2 years. During the recent followup, the body weight, height, subscapular and triceps skinfold thicknesses, fat mass (FM), fat-free mass (FFM) and serum leptin concentration of the young adults (now twenty years of age) were recorded in order to identify associations between early nutrition and adult body weight.

The adjusted linear regression models Rolland-Cachera and colleagues used to analyze the data actually showed a couple of significant associations, the first one of which, i.e. the fact thatan increase by 100 kcal in energy intake at 2 years was associated with higher subscapular skinfold thickness (β=6.4%, P=0.002) and higher FFM (0.50 kg, 0.06–0.95, P=0.03) at 20 years, seems to stand in line with the hilarious calories-in-vs-calories-out hypothesis. However, these associations could also be related to the fact that early nutrition will program our satiety response, so that those programmed to be "good eaters" by a less nurturing diet in their earliest childhood will remain "good eaters", even when they switch to the energy-laden standard American diet.

Against that background, the second significant association the researchers observed, i.e. the fact that an increase by 1% energy from fat at 2 years was associated with lower subscapular skinfold thickness (−2.3% SF, −4.41 to −0.18, P=0.03), lower FM (−0.31 kg, −0.60 to −0.01, P=0.04) and lower serum leptin concentration (−0.21 μg l−1, −0.39 to −0.03, P=0.02) at 20 years appears to be even more important. After all, it looks like the Rolland-Cachera et al. had found the first relatively convincing evidence (not proof, yet) for the negative metabolic effect of early low fat diets in human beings:
"Low-fat intake in early life was negatively associated with body fat (particularly at the trunk site) and serum leptin concentration at 20 years, suggesting that early low-fat intake could increase the susceptibility to develop overweight and leptin resistance at later ages. These findings substantiate current recommendations against restricting fat intake in early life and open new directions for investigating the origin of obesity." (Rolland-Cachera. 2012)
Now let's just hope that scientists are actually tackling these "new directions" and - more importantly - that the respective results are recognized by the public and incorporated into the "dietary guidelines".

Study suggests: If you could chose only one, your intraworkout nutrition should be a carbohydrate not a protein supplement (Kazemzadeh. 2012) -- This is at least the authors' own interpretation of the results of a recent study that was conducted by three researchers from the Azad University and the Teheran University in Iran.

Figure 1: Changes in hormone levels from pre to post exercise (Kazemzadeh. 2012). If you focus solely on statistical significance you can be likewise mislead as, when you don't even check whether you findings are significant at all.

According to the statistically significant part of the hormonal response of the 18-25-year-old subjects (university students who selected physical training course, but had no prior training experience), the consumption of an intra-workout supplement containing either 10 ml/kg of a 6% glucose solution was in fact "less catabolic" than during the same strength training routine with a 0.2 g/kg protein shake (PRO group) as an intra-workout supplement. On paper that's certainly true: The increased insulin response "enhances removal of amino acids and synthesis of proteins after the resistance exercise, on the one hand, and decreases the activity of proteolytic enzymes" (Kazemzadeh. 2012) and the non-existant increase in cortisol is in fact what scientists have long heralded as the goto indicators of anabolism.

Note: Just as most of these studies the participants did not consume breakfast before the resistance exercise session, which comprised six selected exercises: The bench press, biceps curl with barbell, side stretch, leg press, knee stretch, knee bending. If the study had been conducted after a regular breakfast ~2-3h before the workout, the study could have yielded totally different effects with respect to both, the blunted insulin, as well as the increased cortisol response. On the other hand, the GH spike in the protein group would most certainly have been lower as well. After all, the latter is - as you may have read in the SuppVersity Facebook News earlier today - basically only a means by which your body taps into its fat reservoirs to satisfy his acute energy demands and not strictly a way to protect lean mass (Gahete. 2012).

I do still have serious doubts about the real-world significance of the temporary blunt in cortisol. After all, the immediate post-workout response is, in contrary to sustained elevations of cortisol levels for hours or days after a workout, associated with an increase, not a decrease in skeletal muscle hypertrophy (West. 2012) and in essence nothing else, but a physiological adaptation that's necessary to maintain stable blood glucose levels during strenuous workouts and sooth the early burst of inflammation after a workout. Moreover, despite being only borderline significant, only the protein shake did increase growth hormone (p=0.057), testosterone (p=0.52) and IGF-1 (p=0.51) levels during the workout.

This does not necessarily refute the benefits of carbohydrate supplementation during a workout, but if you insist on maximizing gains (not necessarily all lean I would guess) at all costs, it may be wise to consume a slow digesting protein + some fiber-laden carbs like oats 1-2h before a workout, to sip a light carbohydrate + BCCA drink intra- and wash everything down with another shake w/ whey protein and one or two bananas afterwards instead of just drinking some sugar water while you are lifting.

Iron is a negative predictor of gastric cancer in humans and lowered hemoglobin and hematocrit levels induce insulin in rodents (Cook. 2012; Davis. 2012) -- While the alpha-tocopherol, beta-carotene cancer prevention study was a failure (at least with respect to the expected benefits of the anti-oxidants), there are still a couple of interesting side-findings.

Meat-Ology: The Link Between Red Meat, Cooking Techniques & Prostate Cancer
One of these side-findings pertains to the touted effects of increased iron intake on the etiology of gastric cancer, which is simply not existent. According to Cook et al. there were statistically significant negative associations for ferritin in the 2nd, 3rd quartile (-33% risk and -48% risk, respectively) and a borderline significant risk reduction of -31% for overall gastric cancer in the highest quartile (>241 ng/ml) and statistically nonsignificant decreases in gastric cancer risk for total iron, transferrin saturation and total dietary iron intake per 1,000kcal/day in the 2nd-4th quartiles of the respective serum parameters.

That said, subsequent adjustments for H. pylori and then gastric atrophy did not materially affect a majority of the estimates ...
"[...] the only exception was that the relationship between ferritin and GNCC [Gastric noncardia cancer] was attenuated There was little evidence for direct associations between iron metrics and H. pylori seropositivity or gastric atrophy (low pepsinogen I)—only serum ferritin appeared to share a relationship with these variables, and this relationship was stronger between ferritin and gastric atrophy." (Cook. 2012)
So if "red meat is bad for you" it is probably not the iron content of the meat that is responsible for the observed associations of gastric cancer and high red meat intake in some previous studies (cf. WCR Fund. 2011).

And with respect to its effect on glucose metabolism, a recent rodent study has just shown that a reduction in hemoglobin and hematocrit due to a lack of dietary iron does actually impair, not improve glucose management in otherwise healthy rodents fed an iron-deficient diet:
Figure 2: Blood glucose, insulin and triglyceride on iron sufficient / deficient high sugar (AIN-76) or high starch (AIN-93) died (Davis. 2012)
"Hemoglobin and hematocrit were significantly reduced in both ID groups compared to the C and PF groups. Similarly, animals in the both ID groups exhibited elevated steady-state levels of blood glucose and insulin [...]

[Moreover, hepetic]epatic gene expression analyses revealed a ~4- and 3-fold increase in the expression of glucokinase and pyruvate dehydrogenase kinase-4 mRNA, respectively, in the ID group on either diet compared to their respective PF [pairfed on iron sufficient diets] counterparts" (Davis. 2012)
The accompanying negative effects on triglycerides and fatty acid synthesis and storage Davis et al. observed were yet exclusive to the animals who received a high succrose iron-deficient diet.
Vitamin C, D & E in health not disease - Only alpha-tocopherol shows negative correlation with markers of inflammation (Garcia-Bailo. 2012)-- A very recent study that has been conducted by researchers from the University of Toronto and the University of Guelph did not find any relation between the novel and the old savior of the human race, i.e. vitamin D and C, respectively and expression of inflammatory cytokines.

Suggested read: "Are Vitamin Supplements Bad For Me (1/2)? The wrong Vitamin E Supplements Increase Cancer Risk."
Plain Vitamin E in its alpha-tocopherol form, which has almost been written off after the selenium + E (and E only) cancer trials, on the other hand, showed statistically significant correlations with interferon-gamma and RANTES, a pro-inflammatory cytokine that is also known as CCL5 and the acronym for "egulated and normal T cell expressed and secreted" plays an important role in various immune processes, such as recruitment of leukocytes to sites of inflammation and mediating T cell and monocyte traffic. In view of the fact that this cytokine has also been shown to increase angiogenesis and is generally elevated in several inflammatory conditions, including atherosclerosis, these results would suggest that keeping an eye on your E-levels is about as, if not more important for young healthy individuals than vitamin C and D.

If you also consider the fact that IL-1RA (by the way not necessarily inflammatory), interferon gamma, IP-10, PDGF-bb and RANTES were the only out of 27 cytokines the researchers initially measured with high enough concentrations to be detect accurately in the 1007 subjects with a BMI of ~23 and a weekly activity level of ~7Met, these results do also provide substantial evidence that it would probably be worth spending more money on studies that investigate what it is that makes normal people healthy, instead of spending bazillions of dollars into the 1001st study on how people with XYZ (pt your favorite disease here) have low vitamin D levels *yawn*.

Check out the Website of the Reigning Canadian Kettlebell Biathlon Champion, Ameer Rosic for some workout videos

A sixpack of kettlebell studies to remind trainers and trainees, alike, that there are more things you can lift than just dumbbells and barbells (various authors) -- I have never gotten hooked to kettlebells myself and would never agree to exchange my barbells and dumbbells for the finest set of kettlebells for more than one week, but if you take a look at some of the studies that have been published in the past 12 months or so, there is sufficient evidence to suggest that the incorporation of kettlebell workouts into your routine, as a means to provide new muscular and metabolic stimuli, could yield highly beneficial results:

Kettlebell swings restore and enhance back health and function (McGill. 2012) On the basis of electromyography, ground reaction forces (GRFs), and 3D kinematic data the researchers determined that kettlebell swings create a "hip-hinge squat pattern characterized by rapid muscle activation-relaxation cycles of substantial magnitudes (∼50% of a maximal voluntary contraction [MVC] for the low back extensors and 80% MVC for the gluteal muscles with a 16-kg kettlebell) resulting in about 3,200 N of low back compression." The way the swings activate the abs and the unique loading patterns of the posterior shear of the L4 vertebra on L5, which is opposite in polarity to a traditional lift could make it a valuable tool in re- and prehab.	Kettlebell swing training improves maximal and explosive strength (Lake 2012) 21 healthy men were randomly assigned to either a kettlebell (KB) or jump squat (JS) training twice a week. The KB group performed 12-minute bouts of KB exercise (12 rounds of 30-second exercise, 30-second rest with 12 kg if lower than 70 kg or 16 kg if higher 70 kg). The JS group performed at least 4 sets of 3 JS with the load that maximized peak power—Training volume was altered to accommodate different training loads and ranged from 4 sets of 3 with the heaviest load (60% 1RM) to 8 sets of 6 with the lightest load (0% 1RM). The increase in maximum strength of 9.8%, as well as explosive strength (+19.8%) were identical in both groups
Kettlebell training has "has potential for improving some components of MetS in middle-aged women." (Moreno. 2011): While the changes the author of the thesis observed in response to 10 weeks twice weekly kettlebell training did not reach statistically significance (probably due to the low subject size of N=6 physically inactive women, mean age (mean age 48.8y, BMI 31.8) the trends in " fasting glucose and body fat were encouraging and suggest that kettlebell training has potential for improving some components of MetS in middle-aged women."	Kettle bell workouts can decrease blood pressure (Douglass. 2012): Eight resistance trained pre-hypertensive and HTN males saw statistically and more importantly clinically significant declines in blood pressure (to normal levels!) in the course of a randomized cross-over designed study which included 12 minutes of continuous two-handed swings (THS), three sets of a 6 exercise circuit (CIR), and a resting control (CON).
Kettlebell training can improve strength, power and and endurance (Mannocia. 2012): 23 subjects (age 18-72 years) were required to perform a10-week kettlebell training program that took place in a group setting two times per week. Post hoc pairwise comparisons of assessments barbell clean and jerk, barbell bench press, maximal vertical jump, and 450 back extensions performance revealed significant time x group interaction and a main effect (p < 0.05) for the bench press, a trend toward a time x group interaction and a significant main effect for clean and jerk. These observations suggest "that kettlebells may be an effective alternative tool to improve performance in weight- and powerlifting".	10 min of treadmill running may burn more more energy, than a short 10-min kettlebell drill, but pro-anabolic & strength edurance effects speak in favor of 'the bells' (McGill. 2012): Only those who still believe in santa... ah, I mean the calories in vs. out theory of weight loss, will probably care, whether they are burning 12.5 or 17.1kcal/min and therefore this "advantage" would hardly be important even if the participants had not been sprinting part of their 10min on the treadmill just to make sure to achieve the prescriped (identical) rates of perceived exertion. And as usual, there is no reason, why you could not switch back and forth from one "drill" to another.

That's it once more for this week's installment of pretty longish short news. I hope you liked one or another and will see you tomorrow for some more information on the latest and greatest from the world of exercise and nutrition sciences. And just in case you have not seen those already, I guess there are a handful of news on facebook you may be interested in:

If you just skip the hookers and the transdermal cocaine and take a regular bath, this may speed up your regeneration and propel your gains - if timepoint and temperature are spot on!
Transdermal 'cocaine' in "bath salt" - 3,4-methylenedioxypyrovalerone (MDPV) in OTC "bath salt" is 10x more potent than cocaine and unquestionably hazardous
The anti-cancer effect of 'active vitamin B6' - High levels of pyridoxal 5'-phosphate, the active form of vitamin B6 appear to have protective effects against breast cancer... or is it exactly the other way around?
Bisphenol A is a local fat synthesizer - Study shows how Bisphenol A increases obesity: it ramps up the local cortisol production in adipose tissue and thus 'helps' you stash away more body fat

As usual there is more on facebook and further news to come, but I guess you got other things to do on a Saturday than reading SuppVersity posts all day ;-)

References:

Cook MB, Kamangar F, Weinstein SJ, Albanes D, Virtamo J, Taylor PR, Abnet CC, Wood RJ, Petty G, Cross AJ, Dawsey SM. Iron in relation to gastric cancer in the alpha-tocopherol, Beta-carotene cancer prevention study. Cancer Epidemiol Biomarkers Prev. 2012 Nov;21(11):2033-42.
Davis MR, Hester KK, Shawron KM, Lucas EA, Smith BJ, Clarke SL. Comparisons of the iron deficient metabolic response in rats fed either an AIN-76 or AIN-93 based diet. Nutr Metab (Lond). 2012 Oct 30;9(1):95.
Douglass, MJ. The blood pressure response of two popular kettlebell routines. M.S. thesis in Kinesiology (Exercise Science). California State University, Sacramento, 2012.
Flores G, Lin H. Factors predicting severe childhood obesity in kindergarteners. Int J Obes (Lond). 2012 Nov 13.
Gahete MD, Córdoba-Chacón J, Luque RM, Kineman RD. The Rise in Growth Hormone during Starvation Does Not Serve to Maintain Glucose Levels or Lean Mass but Is Required for Appropriate Adipose Tissue Response in Female Mice. Endocrinology. 2012 Nov 13.
García-Bailo B, Roke K, Mutch DM, El-Sohemy A, Badawi A.Association between circulating ascorbic acid, alpha-tocopherol, 25-hydroxyvitamin D, and plasma cytokine concentrations in young adults: a cross-sectional study. Nutrition & Metabolism 2012, 9:102.
Hulsey CR, Soto DT, Koch AJ, Mayhew JL. Comparison of kettlebell swings and treadmill running at equivalent rating of perceived exertion values. J Strength Cond Res. 2012 May;26(5):1203-7.
Kazemzadeh Y, Gaeini A, Abasrashid N. Comparison of the Effect of Consuming Carbohydrate or Protein during Exercise on Hormonal Response. Zahedan Journal of Research in Medical Sciences. 2013; 15(2): 90-93.
Lake JP, Lauder MA. Kettlebell swing training improves maximal and explosive strength. J Strength Cond Res. 2012 Aug;26(8):2228-33.
Moreno KIK. Effects of kettlebell training on metabolic syndrome in women. M.A. Thesis, San Jose State University, 2011, 138 pages.
McGill SM, Marshall LW. Kettlebell swing, snatch, and bottoms-up carry: back
and hip muscle activation, motion, and low back loads. J Strength Cond Res. 2012
Jan;26(1):16-27.
Manocchia P, Spierer DK, Lufkin AK, Minichiello J, Castro J. Transference of kettlebell training to strength, power and endurance. J Strength Cond Res. 2012 May 3.
Rolland-Cachera MF, Maillot M, Deheeger M, Souberbielle JC, Péneau S, Hercberg S. Association of nutrition in early life with body fat and serum leptin at adult age. Int J Obes (Lond). 2012 Nov 13.
WorldCancer Research Fund/American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: a global perspective. Washington, DC: AICR; 2007.
West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2012 Jul;112(7):2693-702.

On Short Notice: 250% More Testosterone From Oleuropein in Olive Oil? Obese Kids, TV, Twinkies & Tortilla Chips, Vitamin D Supplementation That Works, Coffee, Green or Gomchui Tea as Fat Blocking Orlistat Alternative and More!

Image 1: A tablespoon of olive oil is probably not enough to boost your testosterone levels, right? Probably not, at least not by 250%, I should say.

Another Saturday, time is flying by and we have no time to waste, because YOU will have to dig trough a whole host of pretty long and (hopefully) interesting "On Short Notice" news, today! So let's get to business and start out with the surprising testosterone boosting corticosteroid normalizing effects of a bitter phenol in extra virgin olive oil most of you will probably be consuming on a daily basis without even knowing its name - Oleuropein. When we are through with the human equivalent dosage calculations the scientists obviously forgot to do, we will make a detour to one of those problems that are particularly dear to my heart, childhood obesity and how watching TV and eating fatty and sugary foods make a dynamic duo that can increase your (grand-)son's, (grand-)daughter's, nephew's and niece's risk to become obese by up to 30%. We will then use our flux-compensator (edit: I used the term that's used in the German version, i.e. "flux compensator" before, but edited it after Gary pointed out that the DeLorian in the original US version had a "flux capacitor" and a brief "research" made it obvious that this is a mistake of whoever translated the term for the original Back to the Future movies) and jump forward in time and see that your hopefully by the non-obese daughters and nieces can reduce their risk of visceral obesity and thus increased mortality even if the just wash the dishes, take the dog for a walk and use the stairs instead of the elevator.

Before we are eventually going to have a cup of gomchui tea, to evaluate if we can stand the taste so that we could ingest the 2-3 servings it would probably take to negate the negative effects of an occasional fatty slip on our diet, I will yet invite you to take yet a look at two studies from Saudi-Arabia, in which the researchers showed quite convincingly that vitamin D can actually have all those magical anti-obesity effects that it is hailed for, if... yeah, if you put the active calcitriol instead of its precursor cholicalciferol into the fatty chow of rodents. Sounds good? Well let's go, then!

Figure 1: While the results of the study, as well as the implications are impressive, the statement that one would get the respective human equivalent dose from "normal dietary intakes" is questionable, to say the least (see text for details) - and still the results of the study at hand only add to the nutritional value of the "liquid gold of the Mediterranean" with its proven antioxidant, antiinflammatory, antiageing, anti-viral, anti-microbial, anti-cancer, anti-aetherogenic and skin protectant effects (cf. Omar. 2010)

Olive oil contains natural anabolic... well, sort of; at least according to research from the Laboratory of Nutrition Chemistry at Kobe Women's University in Japan, oleuropein, a phenolic compound in extra virgin olive oil did calm down the potentially catabolic corticosteroid overactivity in male rats fed a high protein (40%; from casein) diet (Oi-Kano. 2012). Allegedly, this alone does not yet make it an "anabolic", but with it's concomitant, but highly protein-dependent effect on the testosterone production in the testes of the male Sprague Dawley rats (see figure 1 - top, right), the ameliorative effect on the high corticosteroid expression on the high protein diet (+100% serum corticosteroids in the 40% vs.10% casein group w/out supplementation) and the consequently increased nitrogen balance (=higher net retention of protein) oleuropein aglycone does have much more of a natural anabolic than 99.9% of the expensive testosterone boosters out there.

The increased secretion of noradrenaline and adrenaline (see figure 1 - top, right), as well as the downstream effect on the expression of uncoupling protein UCP-1 in BAT and the subsequent increase on thermogenesis should contribute to the "body recompositioning" effect of oleuropein, of which Oi-Kano et al. state that they will be particularly pronounced on a "high-fat diet, i.e., 30% fat diet" (Oi-Kano. 2012).

The fact that humans have hardly any BAT is yet not the only problem, when it comes to the real-world significance of these results. With 10.3mg per rodent per day, i.e. 41mg/kg per day (human equivalent dose 6.68mg/kg), the "effective dose" of regular extra virgin olive oil would be unrealistically high, even if we base our estimate on the same (unpublished) data Oi-Kano et al. use in the discussion of their results and assume that there are 104 mg/kg oleuropein aglycone in extra virgin olive oil. The scientists do yet obviously believe that 5L of olive oil (80kg x 6.67mg/kg body weight divided by 104mg/L olive oil) would be a "normal dietary intake of extra virgin olive oil" - a statement that sounds even more laughable, when we use data from a study by Owen et al. which found that the oleuropein content of extra virgin olive oil ranges from 2.3 to 9.0mg/L (Owen. 2000), with higher levels of oleuropein in bitterer EVOOs (Gutiérrez-Rosales. 2003), or base our estimates on another study from Oi-Kano et al. in which they measured an oleuropein aglycone content of ~19mg/kg extra virgin olive oil (actually we would even hate to make up for the lower density of olive oil and divide that by 0.91 to convert it mg/L). And let's be honest in view of the sheer amount of studies investigating the beneficial effects of extra virgin olive oil in animals and humans, I doubt that a +250% testosterone boosting effect of "normal dietary intakes of extra virgin olive oil" could actually have remained unnoticed...

It also remains to be seen if olive leaf extracts provide a better alternative. In 2008, Jemai et al. report that the Chemlali olive leaves they used in their rodent study, yielded 4.32 g oleuropein and 3.82g oleuropein aglycone per 100g dried leaves (Jemai. 2008). In view of the fact that the yield will necessarily depend on both the cultivar an the extraction method, you should thus make sure that any extract you buy has a standardized content of oleuropein / oleuropein aglycone. Moreover, if you are mainly interested in the better-established antioxidant, antiinflammatory, antiageing, anti-viral, anti-microbial, anti-cancer, anti-atherogenic and skin protectant effects of olive oil (cf. Omar. 2010), 5L /day are not necessary, anyway ;-)

Figure 2: Vicious cycle of childhood obesity (top); childhood obesity trends - state rates (data according to Childhood Obesity Action Network. 2009)
In children under the age of 10 television watching increases risk of obesity by +30% This is the alarming result of a subgroup analysis (N = 1,696 schoolchildren) from the IDEFICS study, a large scale epidemiological study that involved a total of 15,144 children aged 2-9y from Italy, Estonia, Cyprus, Belgium, Sweden, Germany, Hungary, and Spain. Contrary to comparable analyses, which tend to simply correlate obesity data with data from a questionnaires on the total daily or weekly TV consumption, the Lissner study had a more sophisticated approach towards "TV watching" which included (a) the kids habitual television exposure time, (b) television viewing during meals, and (c) whether or not the children had a televisions in their bedrooms.
After correlating these data with additional information about taste preferences, Lissner et al. found that all three aforementioned parameters, i.e. total TV consumption, watching TV during meals and having a TV in their room, were associated with profound (21-30%) increases in obesity risk.
The actual novelty of these results is yet that all these TV watching behavior correlated (in most cases monotonously) with the propensity to eat sugary and/or fatty foods - and that despite the fact that the same kids who were eating nothing but chips and dingdongs, when they were sitting in front of the boob tube did not show similar preferences for fatty and sweet in the contextual different testing sessions all 1,696 kids had undergone.
Figure 3: A few steps a day can go a long way (based on Ayabe. 2012)
Frequent everyday activity prevents visceral fat gain This is the result of a study which investigated the relationship between the frequency of everyday physical activity and visceral adipose tissue mass in 42 Japanese women, aged between 40 to 60 years (Ayabe. 2012). A brief look at the figure on the right will suffice to see that the problem of our society (and the US society probably even more than the European or Japanese) is not necessarily too little exercise, but much more fundamentally no movement at all during our everyday lives. I mean, 2 of the women did not even have 1 bout of 1-min moderate physical activity, 9 did not move for 3 min a day - is it a wonder we are having serious problems, then?
Tip: Take a WALK! The results of another recently conducted study, which found that 30 min of brisk walking at approximately 60% of maximum heart rate after a meal reduce post-prandial lipidemia in healthy normolipidemic men, only corroborates the importance of daily physical activity (standing for 45min did not make a difference, btw; cf. Miyashita. 2012). While we do have the stress right after launch, we don't have the "exercise" that would historically be associated with the latter - and as of late this is not just the case for white collar workers like me ;-)

Active vitamin D does what vitamin D3 doesn't do, ameliorate the oxidative damage due to high fat diets. While the few vitamin D3 supplementation trials in rodents and humans were real non-starters, when it came to the purported effects of "everyone's darling vitamin" against diet induced obesity, diabetes, inflammation, etc. a group of Saudi Arabian researchers has just published the second of two papers within the past two months which deal with the effects of active vitamin D, aka calcitriol, on the diet induced damage in muscle and liver tissue (Alkharfy. 2012).

Figure 4 (Zhu. 2012): Vitamin D3 is converted to the active metabolite 1,25(OH)2D3 by sequential 25-hydroxylation and 1a-hydroxylation. If this conversion does not take place (for possible reasons see text) , though, it could be that you don't see any benefits even from exorbitantly high amounts of supplemental vitamin D3

In the July issue of Molecules, the scientists had already presented data on the preventive effect calcitriol had on the myocyte damage (weak, pre-degenerate mitochondria, loss of connections among myofibrils) they observed in the muscle fibers of mice who had been fed a high fat diet for 12 weeks. Now, roughly a month later, the researchers from the King Saud University in Riyadh, Saudi Arabia, report similar beneficial effects on weight-related systemic inflammation and ultrastructural changes of the liver during a 16-week rodent study. Compared to the non-supplemented mice, the mice on the calcitriol enriched high fat diet had reduced concentrations of TNF-α, CRP and IL-6 (p < 0.05) and a way higher insulin sensitivity (C-peptide and insulin levels of 539.4 ng/ml versus 718.9 ng/ml and 0.77 ng/ml versus 1.7 ng/ml, respectively; p <0.05). Moreover, the potentially toxic calcitriol protected the liver of the mice from the marked accumulation of fat droplets Alkharfy et al. observed in 60-70% of the hepatocytes of the mice that were fed the non-supplemented high fat diet.

The profound weight loss the animals in the HFD + calcitriol trials experienced in both trials (even the LFD control did gain some weight!), should yet remind you that there is a good reason that you can't buy calcitriol over-the-counter at your local GNC and better don't reach out to whatever other sources you may just have been thinking about!

That said, it is still remarkable that in a mouse model of prostate and breast cancer, dietary vitamin D3 (cholecalciferol) and thrice weekly injections of calcitriol worked equally well (Swami. 2012), while the cholecalciferol from your average vitamin D supplement sucks, when it comes to the metabolic effects everyone is promising you, you would see if you just bumped your 25-OHD levels to whatever novel heights. At least in the case of the obese rodents, a possible reason could simply be that obesity prevents it's conversion. That this appears to be the case is something we have already discussed in the context of the defect in the enzymatic cascade in obese patients in a previous installment of "On Short Notice". And if it's not obesity that hinders vitamin D from doing its purported job, you still got my hypothetical rants about the exuberant phosphate intake from the average western diet and its negative impact on the conversion of cholecalciferol to calcitriol (see "Hypothesis: Does Vitamin D 'Deficiency' Protect Us From Phosphorus Overload?")

Figure 5: ECGC may be more potent in the in-vitro essay (left, background; anti-lipase effect rel. to Orlistat), its susceptibility to digestion (bottom, right) renders it yet ineffective as a "fat blocker" (left, foreground; FFA during simulated digestion). Appropr. dosed (1-3 serv./day), coffee and gomchui tea thus appear to be better suited to reduce fat digestion and absorption (Cha. 2012).

With di-O-caffeoylquinic acid, Gomchui (Ligularia fischeri) Tea easily outperforms coffee and green tea as an inhibitor of fatty acid breakdown in the stomach - what could in fact turn against you on an already fat-deficient (yeah, there is such a thing!) diet, could be a useful tool for the transient phase from diet-induced obesity to natural leanness on a totally revamped diet + exercise regimen, as well as the occasional "binge", you may planning to have if you are already following a healthy whole foods diet.

Published in the July issue of the Journal of Agriculture and Food Chemistry a recent the study by Cha, Song, Kim and Pan shows quite conclusively that a tea that's brewed from Lingularia fischeri (gomchui) can decrease the activity of the fat-digesting enzymes in your gut and thus minimize the energy influx from free fatty acids.

What's also intriguing about this research is that green tea, despite having the highest content of EGCG and thus theoretically the most potent lipase inhibitor of all the three beverages (green tea, coffee and gomchui tea) had - as soon as a certain dosage threshold of 2-3 servings was achieved, the least effect on on lipase activity in the digestion model the scientists used. If your goal is to ameliorate the potential weight gain right after a binge, gomchui or even a strong black coffee would probably be better choices than a cup of green tea.

Figure 6: The effect green tea extracts have on the synthesis (FAS), transport (CPT II) and oxidation (ACO) of fatty acids in the liver, depend on both EGCG and caffeine (Suigiura. 2012)

In this context, it is also worth mentioning that a related study by Sugiura et al. that has been published in the Journal of Obesity found that the inhibitory effects of EGCG on FAS (fatty acid synthase, i.e. the exact opposite of lipase) expression in the liver, reach statistical significance only in the presence of caffeine (Sugiura . 2012).

This would render the use of decaffeinated green tea extracts for weight-loss purposes at least less effective than the consumption of real green tea. You could probably still grasp the beneficial downstream effects of the anti-inflammatory effects of EGCG, but would miss out on the "fat burning" and "anti-fat depositioning" effects (esp. in the liver), as those are obviously reliant on the simultaneous presence of caffeine. Needless to tell you that this is exactly the way nature has intended it, right? I guess it's about time to have a cup of good tea now... or maybe coffee - or Gomchui?

That's it already for today, but never mind, there will be more. In the next installmenta of "On Short Notice", my daily news-updates on the SuppVersity Facebook Wall (today with news on the muscle building effects of cortisol + IGF1 and more) and - from now on - every Thursday on Super Human Radio (click here to download the first installment of the thursdaily "Super Human Radio + SuppVersity Joint Research Update"). And aside from that there are of course your daily "regular" SuppVersity News!

References:

Alkharfy KM, Al-Daghri NM, Ahmed M, Yakout SM. Effects of vitamin d treatment on skeletal muscle histology and ultrastructural changes in a rodent model. Molecules. 2012 Jul 31;17(8):9081-9.
Alkharfy KM, Al-Daghri NM, Yakout SM, Ahmed M. Calcitriol Attenuates Weight-Related Systemic Inflammation and Ultrastructural Changes of the Liver in a Rodent Model. Basic Clin Pharmacol Toxicol. 2012 Aug 21.
Ayabe M, Kumahara H, Morimura K, Sakane N, Ishii K, Tanaka H. Accumulation of Short Bouts of Non-Exercise Daily Physical Activity is Associated with Lower Visceral Fat in Japanese Female Adults. Int J Sports Med. 2012 Aug 17.
Cha KH, Song DG, Kim SM, Pan CH. Inhibition of Gastrointestinal Lipolysis by Green Tea, Coffee, and Gomchui ( Ligularia fischeri ) Tea Polyphenols during Simulated Digestion. J Agric Food Chem. 2012 Jul 25;60(29):7152-7.
Childhood Obesity Action Network. State Obesity Profiles, 2009. National Initiative for Children's Healthcare Quality, Child Policy Research Center, and Child and Adolescent Health Measurement Initiative. Retrieved 06/02/2010 from http://wwww.nschdata.org/content/07obesityreportcards.aspx.
Gutiérrez-Rosales F, Ríos JJ, Gómez-Rey ML. Main polyphenols in the bitter taste of virgin olive oil. Structural confirmation by on-line high-performance liquid chromatography electrospray ionization mass spectrometry. J Agric Food Chem. 2003 Sep 24;51(20):6021-5.
Jemai H, Bouaziz M, Fki I, El Feki A, Sayadi S. Hypolipidimic and antioxidant activities of oleuropein and its hydrolysis derivative-rich extracts from Chemlali olive leaves. Chem Biol Interact. 2008 Nov 25;176(2-3):88-98. Epub 2008 Sep 7.
Lissner L, Lanfer A, Gwozdz W, Olafsdottir S, Eiben G, Moreno LA, Santaliestra-Pasías AM, Kovács E, Barba G, Loit HM, Kourides Y, Pala V, Pohlabeln H, De Henauw S, Buchecker K, Ahrens W, Reisch L. Television habits in relation to overweight, diet and taste preferences in European children: the IDEFICS study. Eur J Epidemiol. 2012 Aug 22.
Oi-Kano Y, Kawada T,Watanabe T, Koyama F,Watanabe K, Senbongi R, et al. Extra virgin olive oil increases uncoupling protein 1 content in brown adipose tissue and enhances noradrenaline and adrenaline secretion in rats. J Nutr Biochem. 2007;18:685–92.
Oi-Kano Y, Kawada T, Watanabe T, Koyama F, Watanabe K, Senbongi R, Iwai K. Oleuropein supplementation increases urinary noradrenaline and testicular testosterone levels and decreases plasma corticosterone level in rats fed high-protein diet. J Nutr Biochem. 2012 Aug 15.
Omar SH. Oleuropein in olive and its pharmacological effects. Sci Pharm. 2010;78(2):133-54. Epub 2010 Apr 23.
Owen RW, Giacosa A, Hull WE, Haubner R, Spiegelhalder B, Bartsh H. The antioxidant/anticancer potential of phenolic compounds isolated from olive oil, Europ. J. Cancer. 2000; 36:1235–1247.
Sugiura C, Nishimatsu S, Moriyama T, Ozasa S, Kawada T, Sayama K. Catechins and Caffeine Inhibit Fat Accumulation in Mice through the Improvement of Hepatic Lipid Metabolism. J Obes. 2012;2012:520510.
Zhu J, DeLuca HF. Vitamin D 25-hydroxylase - Four decades of searching, are we there yet? Arch Biochem Biophys. 2012 Jul 1;523(1):30-6

Weightloss Threesome: TV or Sleep, Black Pepper, Ginger, Horseradish or Mustard, PolyGlycopleX (PGX) or Psyllium?

Image 1: True or false - Is three really better than two?

Since the On Short Notice columns turns out to be a major success, I decided that I could put out studies in packages of shorter items, on a more regular basis - at least if I stumble across pairs such as those in today's Fat Loss Threesome and have time to compile them in to a comprehensive blogpost. But enough of the prelude, let's get right to our threesome: Television or Sleep, Black Pepper, Ginger, Horseradish or Mustard, PolyGlycopleX (PGX) or Psyllium - What do you think, which of these is will spice up, which will water down your weight loss efforts; and for the bros out there: Can you stack all of them or do they have to be cycled?

TV Watching and Insufficient Sleep - A Dynamic Duo for (Childhood-)Diabesity

Image 2: Watching TV eating junk is only part of the equation; what's missing here is the lack of sleep kids don't get, when they watch TV canned with coke and energy drinks all night.

Facebook friends and followers of the SuppVersity Facebook Channel may be familiar with at least some of the recent articles on the negative impact of TV watching alone and in conjunction with sleep deprivation on the body composition and metabolic health of our children. My personal favorite in this regard is a letter to the editor of the British Journal of Nutrition, in which Travis John Saunders and Jean-Philippe Chaput argue that obesity prevention could be as simple as turning off the television and having a nap (Saunders. 2012). The authors reference a whole host of studies to support their hypothesis that TV consumption and the associated lack of sleep esp. during the early hours of the night contribute to the rise of the obesity epidemic:

TV viewing burns energy at a slower rate than most other waking activities and yet still most available evidence suggests that it may be energy intake, rather than expenditure, which leads the scientifically established association between screen time and weight gain, Saunders and Chaput ascribe to several confounding factors such as
TV viewing provides opportunities for snacking & food eaten in front of the TV is generally high in calories and low in nutrients (Thorp. 2011)
TV commercials reinforce the unhealthy dietary habits
Sleeping also burns less energy than regular waking activities, but reducing sleep time usually increases, not decreases weight gain, due to
increased consumption of high energy, specifically high sugar foods to compensate for the lack of energy (cf. "Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g!")
decreased energy expenditure through fatigue-related reductions in physical activity and lower basal metabolic rates

"Pah, that's guesswork!" If that's what you think, when you hear about Saunders' & Chaput's hypothesis, you may want to take a look at another recently published study by Calamaro et al. who report that (1) children who consume caffeinated beverages (not even directly before bed) get 15min less sleep and (2) children with 3 technology items in their room got 45min less sleep (Calamaro. 2012). Significant correlations with BMI were yet present for the intake of caffeinated softdrinks, only!

In other words, although both are characterized by physical inactivity TV watching and sleep "exert opposing influences on energy balance and body weight" - an observation which leads the authors to humorously conclude that

Reducing TV viewing and/or getting adequate sleep require little in the way of resources or expertise, and may therefore be more sustainable than more traditional interventions focused on diet and exercise. If having a good night's sleep truly is better for your weight than watching TV, this would be a lifestyle modification which may be substantially easier to implement than adopting a new diet or exercise routine. This change of focus is certainly worth consideration, right after a short nap. (Saunders. 2012)

Assuming that you did not already take your nap or have exceeded your daily combined TV + Internet screen time, you will probably also be interested to hear that another recently published paper by Caroline Fitzgerald et al. reports that "a child who watches 18 hours of television (per week) at 4.5 years of age will by the age of 10 have an extra 7.6 milllimetres of waist because of his or her habits" (Fitzgerald. 2012). Does not sound much, but you know how things go, proper with 5, chubby with 10, obese with 20 and dead before 40... you don't really think your kid could have invested those 3.5 years(!) of he would have been sitting in front of his television screen into more productive, more healthy and more sustainable hobbies, do you?

Implications: The best way to avoid TV & sleep related weight gain and / or propel your weight loss is to start planning your screen time instead of simply planting your (fat?) ass on the sofa, whenever you have a minute to spare.

Go to one of the free online TV magazines and create a schedule pick only those shows you really feel you have to see and try to reduce your screen time by 20min every week.
Never eat in front of the television spontaneously, if you have a planned, healthy meal, make sure you don't have more on your plate than you plan to eat(!), and don't have anyone tell you cannot enjoy the SuperBowl or the latest Hollywood blockbuster without chips, popcorn and a soft-drink.
Get yourself a time-limit switch program it so that it the TV has no power, after 9PM, which is when you will be grabbing your new blindfolds and earplugs and head to bed, weeknights.

If you stick to those simple rules and use your iPhone or iPad only for your obligatory daily class at the SuppVersity you will not just improve your physique, you will also live a couple of extra years! After all, scientists from the University of Queensland calculated in 2011 that "every single hour of TV [i.e. one hour per day] viewed after the age of 25 reduces the viewer's life expectancy by 21.8 min" (Veermann. 2011)!

Mustard, Horseradish, Black pepper & Ginger - Useless Thermogenics

Image 3: Although it's more effective than horseradish, black pepper or ginger It would probably take more hot mustard than your tummy can handle to get ripped to the shreds.

If you are already not watching TV and getting enough sleep (see above) and still don't look as lean and jacked as you would like to, a group of Danish researchers has some suggestions on which supplements you should not waste any money on (Gregersen. 2012): Mustard, horseradish, black pepper and ginger! While the latter two did not exert any measurable effects on either diet induced thermogenesis or energy intake (obviously the intention was to reduce the latter), when they were administered at oral dosages of 1.3 g and 20g, respectively, the addition of 8.3g of horseradish or 21g of mustard to standardized brunch meal did at least have some effects on the 22 young (age 25y), normal-weight (BMI 21.8kg/m²) men in the randomized cross-over study by Gregersen et al.:

8.5g of horseradish decreased the postprandial heart rate and increased the blood pressure to a statistically significantdegree, while
20g of mustard increased the thermogenic response to the testmeal by 14%

Now, while the former sounds dangerous and the latter as if "Mustard-o-burn (TM)" was just around the corner, none of these statistically significant effects were physiologically relevant. After all, it would take roughly 1 years to shed an additional lbs of body weight from the +14% increased diet induced thermogenesis from mustard (even if that lasted 24/7), because +14% added to 13kcal/h are only 1.82kcal/h. Even if we assume that you eat 5 meals a day this would hardly amount to more than 10kcal/day or 1.5min of light jogging... but hey, we all know how futile calculations like these are - no? Well, then you should check out my "Busting the 3,500kcal Equals 1 Lbs of Fat Loss" post!

Implications: If anything the use of tons of spices will render your food so unpalatable that you will simply eat less. Aside from those anorexic effects the use of copious amounts of spices, as they would obviously be necessary to illicit significant thermogenic effects, will probably produce more negative than positive (side) effects and could thus even contradict the established beneficial effects of having a "normal" (=tasty) amount of spices in your diet (Kochhar. 2008).

And in case you still insist on "spicing" up your fat loss regimen beyond the reasonable level your taste buds (and gastrointestinal mucosa; cf. Jensen-Jarolim. 1998) can handle, the topical route as in "Topical Fat Loss: Capsaicin Cream Blunts Weight Gain in Rodent Model and Increases Leptin, Adiponectin, Lipolysis and Fatty Acid Oxidation in Visceral Fat Depots" could in fact be worth a try.

Viscous Weight Loss Alternatives: Psyllium Seed Gum and PGX^(R)

Now it would be unfair if I left you with "nothing" else but the advice to switch of the TV, get more sleep and refrain from spicy food (unless you eat it simply 'cause you like it). Luckily, there are yet two additional hitherto unpublished FirstView Articles in the queue of the British Journal of Nutrition which do suggest that dietary fibre, viscous dietary fiber, to be precise could make a valuable addition to your no-TV + lots of sleep regimen.

Figure 1: GI (measured according to ISO 26 642-2010) with and without addition of PGX viscous fiber supplement in 2x250ml water to the 50g carbohydrate meal (Brand-Miller. 2012)

When you ingest it prior to bread, rice, boiled potatoes, french fries cornflakes or instant outs (GI range 65-84) it, a novel dietary fiber supplement that goes by the ingenious brandname PolyGlycopleX
(PGX) leads to dose dependent reduction in the GI of a subsequent carbohydrate meals of 16.5% and 31% for the 2.5g and 5g dose of PGX, respectively - or, physiologically speaking, a 15-33% reduction in blood glucose elevations in the 120min after the consumption of the test meals.

Now that certainly does not sound earth-shattering, but a previous human study has already established that the reduced postprandial glycemia goes hand in hand with increases in PYY expression (Reimer. 2010) and reduced food intake on subsequent meals (Vuskan. 2009). Moreover, earlier rodent studies have established that PGX can improve glycaemic control and protein glycation (Grover. 2011), most probably due to the far-reaching metabolic effects of increased glucagon-like peptide 1 (GLP-1; read more about this incretin hormone in "Eat More, Burn More and Lose Fat Like on Crack with GLP-1!?") levels.

Will eating 25g of psyllium /day reprogram your genes to burn not store fat?

What's even better though is that the last FirstView Article in today's fat SuppVersity news clearly suggests that you don't have to buy InoviBiologic's patented purified polysaccharide supplement that is extracted from konjac, sodium alginate and xanthan gum by the means of a proprietary process the company calls EnviroSimplex^®, to benefit from those health and weight loss effects. If the results Togawa et al. observed in their C57BL/6J who were kept on high-fat (40%) diets with or without the addition of 5% psyllium (as psyllium seed gum, PG-200) for 10 weeks translate to humans, the only reason I could see to spend the extra money would be the whopping dose of ~25g/day (0.32g/kg body weight; learn how to calculate Human Equivalent Doses).

Figure 2: Visceral fat mass and parameters of glucose and lipid metabolism after 10 weeks on the low fat control vs. the supplemented or unsupplemented high fat diet (data expressed relative to control; Togawa. 2012)

If the results do translate to human beings, you can stomach this amount of fiber without negative side effects and are still able to consume adequate amounts of "real" food, though, the data in figure 2 will probably have you hack "psyllium fibre buys" into google in no time. After all, the profound upregulation of genes involved in fatty acid oxidation and lipid transport Naoyuki Togawa and his colleagues from the Yokohama Corporate Research Laboratories and the Laboratory of Food and Nutrition, Graduate School of Horticulture at the Chiba University in Chiba, Japan, detected in fat and skeletal muscle tissue of their lab animals were not just statistically, but also physiologically significant. So significant, in fact, that the mice who consumed ~148g of the psyllium enhanced high-fat diet before they were euthanized at the end of the 10-week study period did not just gain 10% less body weight than their unsupplemented peers, they also had lower cholesterol, lower triglyceride and above all lower visceral body fat masses than the "control" animals on the supposedly healthy low-fat diet.

Image 4: Fiber or no fiber - those abs want to be worked out.

Implications: While ginger, pepper, horseradish and cool are still "hot", dietary fiber is (pun intended) somewhat poopooed upon by many of the "everything mainstream must be wrong" nutrition gurus and fitness enthusiasts. From a scientific perspective, however, it does make more sense to spice your meals up with fiber than with spices that burn away your intestinal mucosa and turn your gut into an open barndoor (cf. Jensen-Jarolim. 1998) for all sorts of things you should better leave where a huge amount of the fiber will go - in the toilet bowl.

That being said, we need further studies to elucidate if and at which dosages similar epigenetic changes as they were observed by Togawa et al. occur in human beings before making any definite recommendations. For the time being, I will simply repeat my advice to

fill yourself up with fiber-laden veggies and consume a balanced (!) amount of saturated, mono- and polyunsaturated fats from whole foods,
aim for a mild energy deficit (~20%) and a reasonable carbohydrate intake of roughly 700-900g per week; either by low-carbing + refeeding (e.g. 6x 50-75g + 1x 250-400) or a constantly low intake of preferably low(er) GI carbs (don't count carbs from green veggies and co!)
eat at least 20-25g of a complete protein (count only meats, fish, eggs and dairy) with every meal and supplement with protein powders / bars, whenever you have no whole food source with 10+g of EAAs in it at hand
follow a sound workout regimen (e.g the "Fat Loss Support Routine" from the Step By Step Guide), don't do hours of "cardio" in the non-existent fat burning zone and cherish the fat-burning effects of glycogen depleting strength and HIIT workouts without overtaxing your central nervous system

If you follow 1-4 on 330 of 365 days of the next year you even the ugliest blubber that may still be covering your abs should disappear - and guess what!? All that without patented or non-patented viscous fiber supplements ;-)