.

.
marylin monroe
Showing posts with label health. Show all posts
Showing posts with label health. Show all posts

Intelligent Weight Loss Workouts: 45 Min of HIT'14 = "High Intensity Thinking" Help Resolve HIS New Year's Resolution

High intensity thinking - intelligent weight loss workouts
It's almost 2014! Actually it is already 2014; at least for my friends in the "Far East" (HAPPY NEW YEAR!) and thus almost too late for the annual "I want to lose weight" new year's resolution. Ok, you as a SuppVersity reader should actually know better, but just in case you are still planning to make the weight loss happen solely by increasing your workout volume, I would suggest that you replace some classic HIT training with the revolutionary HIT 2.0 - high intensity thinking regimen (warning: doing this too often may actually build more brain than muscle mass ;-). 

Well,... now that I take a closer look at the results of this recent study from the University of Quebec here,  I have to realize that this will only work if you are a man. But don't worry, I am pretty sure there is something to be learned for the ladies in the last SuppVersity article of 2014, as well ;-)

All jokes aside, your brain is a sucker for energy!

I guess you will be familiar with the over-cited fact that "the human brain is only 2% of the weight of the body, but it consumes about 20% of the total energy we need every day"... I know that's boring, but actually that's quite an important point, because it tells you that your brain is not just a sucker for energy, but also a sucker for new information, which will in turn increase the energy requirements of the insatiable heap of neurons in your skull. Why? Well, our brains need energy to process each and every of these information chunks - max. 30W per opeartion, if the currently heralded estimations are correct. I know that sounds tremendously much, but if we performed only one of these operations per minute, you would hardly burn the energy equivalent of 1/25 of a 70-85% chocolate bar during your high intensity thinking sessions.

Against that background it's all the more impressive that Emilie Pérusse-Lachance and her Canadian colleagues were able to measure a significant increase in energy expenditure, when they had their 35 subjects (22 men and 13 women; aged 24 ± 3 years) read a 10-page text and write a summary of approximately 350 words using a computer in the "mental work condition" of their study.
Figure 1: Energy expenditure in kcal/45min in the control and the mental work condition, left; energy intake during the buffet ca. 15min after the control and mental work condition, right (Pérusse-Lachance. 2013)
If you take a look at the data in Figure 1, you will also notice that the scientists original hypothesis, which was that they would observe a similar hyperphagic (=hunger ➲ increased energy intake) response to in the "mental work" condition as Chaput et al. who conducted two very similar studies in 2007 and 2008.  The actual study outcome does yet tell a different story: While the female study participant did in fact supercompensate for the extra-energy they had to spent, when they were not watching TV and lolling around like in the control condition, the men were probably so immersed in their thoughts that they simply forgot to eat... ok, I guess you already realized that this was an ad-hoc hypothesis to make sure you don't realize that neither I nor the scientists have any clue what the underlying reasons of this sex-difference were.

I would even guess that the women did not even notice that they were overcompensating. If you take a look at the subjective hunger scores that have been assessed by seven visual analogue scale questionnaires the participants had to fill...
  1. at the beginning (T-60/60 minutes before the buffet), 
  2. after the experimental session (T-15/15 minutes before the buffet), and 
  3. after the buffet-type meal (T0, T60, T120, T180, and T240).
...those will tell you that the ladies either claimed to, or actually weren't more hungry than in the control condition. In view of the irrefutable evidence that they still ate more (see Figure 1) this may look awkward. When it's all said and done, these contradictory result does yet only confirm that you cannot trust people, when they tell you "I am never hungry and actually don't eat that much.... I have really NO clue where that belly comes from". This may even be their own perception, but that does not change that it is usually not in line what happens at the buffets, dinner tables and - most importantly - during the snack breaks people take during not after their high intensity thinking regimen all over the world.
Figure 2: Change in energy balance (kcal) in the "exercise" condition in the course of which the subjects walked on a treadmill for 45 min, waited for 15 minutes and were then allowed to avail themselves of as much food as they wanted at the buffet - further evidence that the "exercise just makes you hungry" hypothesis is bunk.
Bottom line: By now you should have realized that this article must not be taken too seriously. Though,... if this type of heavy brain lifting would have women eat 15.3% (=121kcal/day) more and men 16.1% (=267kcal/day) less every day it would probably have a non-negligible impact on your chances of living up to your new year's weight loss resolution in 2014.

But don't worry, ladies. Life is not so unfair as it may seem. All you have to do to achieve an almost level playing field is to convince him that a 45 min walk in the park with you is much more fun than 45 min of high intensity thinking. And if that's  not convincing enough, show him the data in Figure 3 and tell him that real exercise (in the study 45min of paced walking) will help both of you improve your energy balance - his by -31% (-516kcal) and yours by -23% (-184kcal).
References:
  • Chaput, J. P., & Tremblay, A. (2007). Acute effects of knowledge-based work on feeding behavior and energy intake. Physiology & behavior, 90(1), 66-72.
  • Chaput, J. P., Drapeau, V., Poirier, P., Teasdale, N., & Tremblay, A. (2008). Glycemic instability and spontaneous energy intake: association with knowledge-based work. Psychosomatic medicine, 70(7), 797-804.
  • Pérusse-Lachance, E., Brassard, P., Chaput, J. P., Drapeau, V., Teasdale, N., Sénécal, C., & Tremblay, A. (2013). Sex Differences in the Effects of Mental Work and Moderate-Intensity Physical Activity on Energy Intake in Young Adults. ISRN Nutrition, 2013.

A "Question of Faith": Do Multivitamins, Antioxidants and Mineralsupplements Improve Your Quality of Life?

Image 1: Do you believe that you could solve this profound imbalance by randomly adding more people to both sides of the seesaw? No? Well, why are you taking a high-dose multivitamin then?
As the name of this website already implies, I am an outspoken believer in the usefulness of "supplements" (as in "to supplement" = to add to something, where it makes sense). There is however a particular group of "supplements", which is a real thorn in my side... Yes, I am talking about those one-size-fits-it-all-multivitamin-multimineral-multi-whatever products with "high quality ingredients" the ratios of which are based on either the "recommended dietary allowances" of the omniscient USDA (actually a way better name would be "random dietary allowances") or the even more idiotic maxime that "if some is good, then more is probably even better". These days every major supplement company has at least one of these formulas in their line-up and obvoiusly they all will claim that only their product will provide you "with all the vital nutrients you need".

Wtf!? How do those guys know which nutrients I need? 

Even if those formulas were perfectly balanced - which they certainly are not, because we simply don't know what the "perfect balance" is, yet - the chances that anyone of you, my educated, well-nourished whole-food eating readers, has a full-blown, all across the board nutrient deficiency that would be fixed by any of those products are probably one in a million. What is much more likely, though is that you have a small or (oftentimes due to "healthy supplements") profound nutrient imbalance.

Let's say you are an aspiring male fitness athlete and have been taking your ZMA religiously for years. At the same time you have heard that copper is not only bad for you, but that "we all" would get way too much copper in our diet, anyways. So you have been avoiding copper like a plague and ingesting 30mg of zinc from your ZMA everyday... now chances are that you have already set off the natural (and optimal) ratio of copper to zinc in your body. Let's say the optimal ratio was 1:12 (copper to zinc, and again - we do not even know what the optimal ratio would be). With your high zinc and low copper intake you are now at 1:20, i.e. 60% off! Now the nice guy from your local GNC convinces you that it would be prudent to add the brand new "Male Super-Power Vitamin" to you supplement regimen if you wanted to live a long and healthy life. Chances are that the guy who designed that product will also have heard that zinc is good for men and that we all get way too much copper (and even if he knew better, he will be aware that his formula won't sell if it does not follow conventional stupidity... ah, I mean wisdom). So, the product will have 200mcg of copper and 30mg of highly bioavailable zinc - I mean it's a "high quality product"! What is going to happen now? What? Right! The well-formulated product will exasperate you existing imbalance... Your multi does not do that? How come you think so?

"Ever since I take my multi, I have not become sick and feel way better!"

Right, you feel better... and you are not alone! In fact many of the 8112 participants in a well-controlled randomized, double-blind, placebo-controlled, primary human intervention trial which was conducted by a group of scientists from Paris (Briancon. 2011), also felt that the capsule with 120 mg vitamin C, 30 mg vitamin E, 6 mg beta-carotene, 100 µg selenium and 20mg zinc, they had been taking for 76 months(!) improved their overall well-being.
Warning! I suggest you don't continue reading the following paragraphs if you do feel that your vitamin product works and do not want to take the risk that it will stop working as soon as you have finished reading this blogpost ;-)
What is pretty strange, though, is that this effect did not depend on whether the subjects actually received the anti-oxidant + mineral combination, or not. Rather, the main determinant of the the results of the health-related quality of life (HRQoL) questionnaire in this sample of healthy French adults was whether the subjects, who, as it is right and proper for a "placebo-controlled" trial, obviously did not know whether they were ingesting a capsule with the active ingredients or the placebo (it had been established in a previous study that the two capsules were indistinguishable; cf. Hercberg. 1998), believed that they were in the active arm of the study (cf. figure 1, believers vs. non-believers):
Figure 1: Perceived effect on global health (VAS) in subjects who had "no idea" whether they received the active or the placebo treatment and subjects who thought they received the active ("believers") or placebo ("non-believers") treatment (data adapted from Briancon. 2011)
What is also interesting, is that women were slightly more susceptible to placebo effect than men (not to the nocebo effect though), although this difference did not reach statistical significance.

Multivitamins are like religion: Believe in it and it works!

A pros pos statistical significance, as far as the "real" markers of health and disease are concerned, the "key message" (I use the words of the scientists ;-) of the SU.VI.MAX was that "long-term supplementation with antioxidant vitamins and minerals has no effect on quality of life" - in other words, although there were not measurable improvements, the study did not provide further evidence for the hypothesis that long term supplementation with anti-oxidant supplements, selenium and vitamin E in particular, had any negative effect on objectively measurable health markers (if you want to read more about the flawed analysis of and biased media reports on the data from the SELECT trial, read my previous blogpost on this issue).
Image 2: Add a body made of animal products to this guy and you have all the nutrients you need ;-)
It should be mentioned here that in a previous analysis of other data from the same cohort, the scientists had found a small, but statistically significant decrease in cancer and all-cause mortality among the male study participants of the active arm of the SU.VI.MAX trial (Hercberg. 2004). So, while the quality of life did not improve, the miserable life of some of the male subjects was at least extended by a few years ;-) All sarcastic jokes aside, even the scientists realize that in the presence of conflicting evidence, the "major implication for public health of the present findings is that a lifelong diet rich enough in vitamins and min-erals may be preferable to supplementation that is likely not to be efficacious and has the potential to be harmful." - sound advice!
Those of you for whom this is not the first visit, here at the SuppVersity, will be aware, that, as a trained scientist, I don't content myself with the conclusions my "colleagues" (from another branch of science) draw. Therefore, I dug a little deeper into the actual data that comes with the study and - alas! - I was able to find a statistically significant (p<0.014) increase in the reported "vitality" among the women who actually received the vitamin + mineral supplement (cf. figure 2):
Figure 2: Real (difference between treatment and placebo) and perceived (difference between "believers" and "non-believers") of antioxidant + mineral supplement (data calculated based on  Briancon. 2011)
What is strange though, is that of all statistically significant differences between women who believed they received the supplement and those who did not, just this one is the least distinct. Moreover, in all the other variables, where there was a statistically significant difference between believers and non-believers, the "real" data (meaning the comparison of subjects who actually received the treatment vs. the placebo group) could not confirm the positive self-assessment of the believers. Among the male subjects, there was even a trend toward reduced quality of life measures in the real data, where the "believers" thought that it was the "supplement" they were taking that soothed their bodily pain, improved their general health or overall physical performance (physical summary scale).

So what? Am I wasting my money?

These additional observations do yet not falsify any of the three main conclusions, Serge Briacon and his five colleagues from Nancy University, the Metz University, the University Paris Descartes, the University hospital of Nancy and the French Department of Public Health draw based on their interpretation of the data:
  1. [t]here is no proof that supplementation with these vitamins and minerals is beneficial in participants whose dietary intakes are already sufficient
     
  2. [t]he perception that supplementation improves general well-being is not supported by this trial.
     
  3. [a] reverse causal pathway may even be advocated (healthier participants may have been more likely to believe they were in the supplement group).
What this means for you is that if your multivitamin "works", chances are that you are doing something right as far as your general lifestyle, your diet and your exercise regimen are concerned. If despite taking your multi religiously, you still feel miserable, you better take a closer look at what your real problems are instead of switching from one band-aid-fits-it-all "solution" to the next one.

Forskolin: Friend or Foe? Stories and Studies About Fat Loss, Lean Gains, Topical Cellulite Treatment, Testosterone, Cancer, Hepatotoxicity, Drug Interactions & More

There is a single human study that would suggest that forskolin would make you get closer to this classic physique w/out tons of salad (who said that's necessary anyway?).
Since Maxim asked in one of his more recent comments about the usefulness and/or downsides of forskolin, I dediced to dedicate this Sunday (finally again?) to answering a user question and am going to briefly sum up some older and the few novel findings on forskolin I am aware of.

For those of you who find that boring: Don't blame Maxim alone, another reason for this decision was that I have seen discussions on forskolin resurface elsewhere on the Internet. By the way, I write re-surfaced, because forskolin has once been hailed as a testbooster and fat loss adjuvant, but as the prices increased and people came out with faked or low-quality products that did not yield results, the market collapsed.

What is forskolin and where does it originate from?

As usually there is more than a single answer to this question. The most straight forward general ones are probably (a) it is a white to white with yellow cast powder, or (b) a labdane diterpenoid with antihypertensive, positive inotropic, platelet aggregation inhibitory and adenylate cyclase activating properties. Moreover, forskolin is able to activate the adenylate cyclase and thus increase the intracellular cyclic AMP levels in most tissues and cells. And hat  it's called forskolin, because it is derived from the Indiant plan Coleus forskohlii is probably something 99% of you knew already.

The reason I suppose that Maxim got interested in it, is that it is commonly used in cell studies to raise the levels of cyclic AMP (cAMP; cf. Alasbahi. 2012) and did a pretty impressive job in the recently discussed PGC-1a study. On the other hand, it did also increase the expression of the aromatase enzyme in the Yang study mentioned in the "Natural Sildenafil & Testosterone Alternative" post on which Maxim replied with the initially mentioned comment.

"Wait, wasn't it supposed to be a testbooster and now it also inhibits myostatin and increases estrogen? What does this stuff not do?" - Well, forskolin is, above all, a cAMP modulator

Forskolins chemical structure. Sometimes it's also referred to as Colforsin; 7-beta-acetoxy-8, 13-epoxy-1-alpha, 6-beta, 9-alpha-trihydroxylabd-14-en-11-one; or Coleonol (img. from Sigma-Aldrich's product database)
I know that sounds confusing, but in essence forskolin does nothing but increasing cAMP levels in almost all types of cells. cAMP a breakdown product of ATP (=> cAMP => AMP) in turn is one of those molecules which exert most their effects as intracellular signal transducer. In that, it is involved in the activation of protein kinases and regulates the effects of adrenaline and glucagon. It also modulates the calcium channels and contributes to growth hormone release; unfortunately, cAMP has also been implicated in the proliferation of not very beneficial cell growth aka cancer. The same ion-flux mediation has recently been implicated in the etiology of ADHD, as well (Arnsten. 2012).

Still, it's not all about c-AMP. Probably cAMP unrelated downsides of coleus forkohlii are for example:
  • forskolin induces hepatic CYP2C enzymes and coleus forskohlii extract and thus attenuates the anticoagulant action of warfarin. (Yokotan. 2012) 
  • even more than isolated forskolin, coleus forskohlii  messes with the hepatic enzyme cascade (P450) and has even been shown to be hepatoxic in a study published in the July issue of the Journal of Toxicology (Virgona. 2012)
On the other hand there are a handful of benefits, e.g.
  • Figure 1: Effects of 12 weeks on 2x250mg (10%) forskolin on testosterone (free and total) and lean & fat mass (Godard. 2005)
    In a 2005 study (Godard. 2005), which caused quite a stir in the health and fitness community back then, Godard et al. observed profound beneficial effects of testosterone and body composition (cf. figure 1) after the ingestion of 2x250mg of a 10% standardized forskolin (Forslean).

    Now, the unfortunate truth is that the15 subjects (average age, BMI, and body fat percent were 24.4 +/- 5.9 years, 32.5 +/- 4.1 kg/m2 , and 35.2 +/- 8.3%) who had been randomized to the active arm of the study, and the 15 participants in the placebo arm (28.7 +/- 8.6 years, 32.6 +/- 3.8 kg/m2 , and 35.0 +/- 7.3%) were non-active sedentary overweight/obese (BMI 26 kg/m2 or more) individuals. Add the funding by Sabinsa (Forslean producer) to the equation and decide for yourself how relevant you think the results are going to be for you...
  • In several in-vitro studies, forskolin has been used as a positive control to compare the effects of other compounds on the testosterone release in leydig cells. Lin et al. for example used it in 2001 as a comparison for lactate and found a ~3x increase in testosterone release in incubated leydig cells (Lin. 2001). A similar study by Yu et al. showed that the addition of green tea catechins lead to an additional stimulation of forskolin induced testosterone production in cell cultures (Yu. 2010).
  • Figure 2: Results of 12-week intervention w/ forskolin containing topical cream (Roure. 2011)
    As part of a topical cosmetic slimming product combining tetrahydroxypropyl ethylenediamine, caffeine, carnitine, retinol and, obviously, forskolin it has shown some promise as a topical anti-cellulite and toning agent (Roure. 2011). The clinical study was however financed by Johnson & Johnson and I am not sure how much of the effects were actually brought about by forskolin (the placebo was a basic gel with the same texture containing mainly water, gelifying and preservative systems). So take the data in figure 2 with a grain of salt, ladies - I bet 12 weeks on this product are not going to be exactly inexpensive.
    • The administration of forskolin in conjunction with rutin (the glycoside between the flavonol quercetin and the disaccharide rutinose), vitamin B1 & B2 in a 2010 study by Pescosolido et. al. lead to a significant reduction in intra-ocular pressure in 15 glaucoma patients after 40 days (Pescosolido. 2010). Similar results were observed in a 2012 study for forskolin and rutin alone (Vetrugno. 2012)
    • An in-vitro study by Cristobal et al. provides first evidence for the ability of forskolin to restore PPA2 in acute myeloid leukemia. That would make it a potential candidate for the treatment of this type of cancer, but to my knowledge there is as of yet not even a rodent study that would support these in-vitro results. Moreover, previous studies have suggested that Forskolin may even favor the proliferation of other types of leukemia (Kobayashi. 1994)
        Time to weigh the "established" benefits and downsides

        Figure 3: Effect of different doses of forskolin with and w/out epinephrine on FFA release from rat adipocytes - watch out this is from yet another in-vitro study with rodent cells (Litosch. 1982)
         In view of the fact that the aforementioned study by Godard is the only human study is only backed up by in-vitro data from rodent studies (Litosch. 1982, cf. figure 3), the fat loss benefits are as  Jeukendrup et al. point out in their 2011 review of purported fat burners...
        "[...] promising, there is [yet] only one study at the present time and more work is required before forskolin can be recommended as a fat metabolism-enhancing substance." (Jeukendrup. 2011)
        If you add to this the host of wanted and unwanted, known and unknown side effects that occur in response to the coleus foskohlii induced cytochrome P450 modulation (e.g. the mice in the aforementioned study by Virgona lost some visceral fat, but the costs were increased fat deposition in the liver and elevated transaminase levels).

        With the questionable "fat loss" benefits (remember stress is also a powerful lypolitic and the problem is not to get the fat out of the cell, but rather to burn it), and the almost non-existant human data on the purported testosterone boosting effects, this should be reason enough not to buy more than one bottle for a test-run. After which I highly suggest to do some lab work to see if whatever good or bad you believe you are feeling is an actual boost in T (check T-levels) or hepatic side effects (check ALT, AST & ALP).

        Note (update in response to comments): As far as the hepatoxicity is concerned the suggested dosage of 2x 250mg coleus forskholii most supplements come with may be higher than the medium dose in the study by Virgona, but is still probably "liver save" if you double dose on that, you are however landing in the no-man's land (=not tested for) gray zone between the medium dosage and the "danger zone" of  ~49mg/kg per day (human dose equivalent) that was tested in the study. Don't freak out, if you did that in the past, the levels return to normal afterwards and temporarily elevated ALT + AST or ALP levels do not necessarily mean that your liver is whacked forever ;-)

        References:
        • Alasbahi RH, Melzig MF. Forskolin and derivatives as tools for studying the role of cAMP. Pharmazie. 2012 Jan;67(1):5-13.
        • Arnsten AF, Jin LE. Guanfacine for the treatment of cognitive disorders: a century of discoveries at Yale. Yale J Biol Med. 2012 Mar;85(1):45-58. Epub 2012 Mar 29.
        • Godard MP, Johnson BA, Richmond SR. Body composition and hormonal adaptations associated with forskolin consumption in overweight and obese men. Obes Res. 2005 Aug;13(8):1335-43. 
        • Jeukendrup AE, Randell R. Fat burners: nutrition supplements that increase fat metabolism. Obes Rev. 2011 Oct;12(10):841-51. 
        • Kobayashi K, Nishikawa M, Omay SB, Toyoda H, Deguchi K, Shirakawa S. Forskolin potentiates G-CSF-induced proliferation of a murine myeloblastic leukemia cell line. Leuk Res. 1994 Feb;18(2):111-7.
        • Lin H, Wang SW, Wang RY, Wang PS. Stimulatory effect of lactate on testosterone production by rat Leydig cells. J Cell Biochem. 2001 Jun 26-Jul 25;83(1):147-54.
        • Pescosolido N, Librando A. Oral administration of an association of forskolin, rutin and vitamins B1 and B2 potentiates the hypotonising effects of pharmacological treatments in POAG patients. Clin Ter. 2010;161(3):e81-5. 
        • Roure R, Oddos T, Rossi A, Vial F, Bertin C. Evaluation of the efficacy of a topical cosmetic slimming product combining tetrahydroxypropyl ethylenediamine, caffeine, carnitine, forskolin and retinol, In vitro, ex vivo and in vivo studies. Int J Cosmet Sci. 2011 Dec;33(6):519-26.
        • Vetrugno M, Uva MG, Russo V, Iester M, Ciancaglini M, Brusini P, Centofanti M, Rossetti LM. Oral administration of forskolin and rutin contributes to intraocular pressure control in primary open angle glaucoma patients under maximum tolerated medical therapy. J Ocul Pharmacol Ther. 2012 Oct;28(5):536-41.
        • Virgona N, Taki Y, Yamada S, Umegaki K. Dietary Coleus forskohlii extract generates dose-related hepatotoxicity in mice. J Appl Toxicol. 2012 Jun 22.
        • Yokotani K, Chiba T, Sato Y, Taki Y, Yamada S, Shinozuka K, Murata M, Umegaki K. Hepatic cytochrome P450 mediates interaction between warfarin and Coleus forskohlii extract in vivo and in vitro. J Pharm Pharmacol. 2012 Dec;64(12):1793-801.
        • Yu PL, Pu HF, Chen SY, Wang SW, Wang PS. Effects of catechin, epicatechin and epigallocatechin gallate on testosterone production in rat leydig cells. J Cell Biochem. 2010 May 15;110(2):333-42.

        3g Taurine Improve Post-Workout Glycogen Resynthesis, Protect the Testes of Doping Sinners & Battles Alzheimer's

        Taurine - A useful supplement for chemical, natural athletes and even sedentary slobs who are afraid of diabetes.
        Taurine, or 2-aminoethanesulfonic acid, as Wikipedia says, is an organic acid widely distributed in animal tissues. It is a major constituent of bile and can be found in the large intestine, and accounts for up to 0.1% of total human body weight. That does not sound like much, but taurine has many fundamental biological roles, such as conjugation of bile acids, antioxidation, osmoregulation, membrane stabilization, and modulation of calcium signaling. It is essential for cardiovascular function, and development and function of skeletal muscle, the retina, and the central nervous system and you were thus probably not too surprised, when you've recently read on the SuppVersity Facebook Page that taurine may help with Alzheimer's disease.
        You can learn more about taurine & other amino acids at the SuppVersity

        Taurine Pumps Up Strength & Recovery?

        Taurine Improves Insulin + Glucose Metabolism

        Taurine ➲ 180% Testosterone Increase

        Taurine + BCAA Work Hand in Hand

        43% Reduced Performance W/ BCAAs

        BCAA Neurotransmitter Depletion
        In the corresponding paper that was published only recently in the ScientificReports on Nature.com Kim et al. report that orally administered taurine via drinking water rescued the cognitive deficits in a standard rodent model of Alzheimer's (APP/PS1 mice) and brought them back up to age-matching wild-type mice.
        Figure 1: Improvement in spatial and hippocampal learning behaviours in taurine-treated transgenic mice. 7-month old wild-type (Wt) and agematched APP/PS1 transgenic (Tg) male mice were orally administered water or taurine (1,000 mg/kg/day) for 6 weeks (n 5 8–10 per group). After 6 weeks, behavioural tests were administered to the 8.5-month old mice. (Left) Y-maze. Average alternation (%) of each group of mice was calculated. (Right) Passive avoidance. Average latency time in seconds for each group of mice was measured (Kim. 2014).
        That's unquestionably impressive, but what's more impressive is that this is by far not the first study to report that taurine exhibits a plethora of physiological functions in the central nervous system.
        But taurine gives me diarrhea! If it does try taking it with a meal that will greatly reduce the risk of having to rush to the toilette and should not reduce the physiological benefits significantly. At least for the muscular effects its unlikely that it will matter at all. For the beneficial effects on the brain, it may be necessary to achieve higher serum peak levels. In view of the fact that the rodents in the aforementioned study by Menzie et al. received the taurine in the drinking water, even this is yet unlikely. If the taurine "goes right through", though, it's certainly not going to help you ;-)
        In a recent review in the scientific journal Amino Acids review, Janet Menzie et al. describe the mode of action of taurine and its clinical application in the neurological diseases: Alzheimer’s disease, Parkinson’s disease and Huntington’s disease and conclude that taurine...
        "[...] functions through multiple neuroprotective mechanisms: regulation of cellular osmolarity , anti-oxidant, neuromodulator of GABAergic transmission, maintenance of calcium homeostasis, inhibition of glutamate excitotoxicity, attenuation of endoplasmic reticulum stress, modulation of mitochondrial pore permeability, downregulation of a range of proapoptotic proteins while upregulating anti-apoptotic proteins and downregulation of inflammatory mediators." (Menzie. 2014)
        Moroever, Menzie et al. believe that there is "strong evidence" of the existence of a specific taurine receptor, which is activated exclusively by taurine, but not by structurally similar amino acids such as glutamate, GABA and glycine and could be responsible for many of the beneficial effects taurine exerts in the context of central nervous system disorders. More specifically existing evidence clearly suggests protective effects in Alzheimer’s, Parkinson and Huntington diseases. Three pathologies that share a number of broad mechanisms: Oxidative stress, mitochondrial dysfunction, excitotoxicity, calcium imbalance, inflammatory changes apoptosis - and *tadaa* a reduced level of (Arai. 1985; Alom. 1991; Molina. 1997).

        Enough of the health stuff, what about the post-workout goodness?

        I know, as long as we are healthy we don't really care about debilitating central nervous system disorders... well, ok. I will spare you my moral pointing finger and get straight to the similarly unsurprising results of a recent study from the University of Tokyo. A study which clearly indicates that the provision of taurine after workouts can lead to a significant enhancement of the already elevated glycogen synthesis after your workouts.
        Figure 2: Muscle and liver glycogen and serum free fatty acids (FFA) before and after the workout (Takahashi. 2014).
        In two rodent studies, the Japanese researchers tested whether the oral administered of taurine  at a dosage of 0.5 g/kg body weight (for human beings that's 0.04g/kg or approximately 3g total | the SuppVersity suggested dose from previous articles, by the way) immediately after treadmill running at 25 m/ min for 90 min would alter the metabolic response and glycogen synthesis after workouts when it was (A) administered alone or (B) as part of a glucose solution containing taurine and glucose at a ratio of 1:2 - in this case 0.5g/kg taurine and 1.0g/kg glucose.
        Figure 3: AUC for glucose after for 60min and 120min after the ingestion of the taurine + glucose solution. As the data indicates taurine helped to "clear" the sugar from the blood stream (Takahashi. 2014).
        As the scientists point out, their "results show that post-exercise taurine administration enhances glycogen repletion in skeletal muscle" (Takahashi. 2014). The underling cause, however, is still speculative. Takahashi et al. believe that it is triggered by
        1. Figure 4: Changes in general oxidative damage (TBARs), protein damage and exercise performance in response to taurine vs. placebo vs. bet alanine supplementation; expressed relative to untrained control (Dawson. 2002).
          an acceleration of glucose uptake, and
        2. an increase in fat oxidation
        of which the latter will have a carbohydrate sparing effect and will thus leave a higher amount of carbs for glycogen repletion. In conjunction with previously established benefits of taurine, such as
        • the attenuation of exercise-induced DNA damage during workouts (young men | Zhang. 2004),
        • the amelioration of cytotoxic (cell damaging) effects of exercise (rodents | Dawson. 2002),
        • an increase in exercise performance (specifically endurance ex. | Dawson. 2002; Miyazaki. 2004),
        • additional effects on the benefits of BCAA intake for the delayed-onset muscle soreness and muscle damage induced by high-intensity eccentric exercise (Ra. 2013),
        • an improvement in osmoregulation (water balance) of the muscle (Cuisinier. 2002), and
        • decreases in oxidative stress during eccentric exercises (Silva. 2011)
        The optimal dosing for performance increments, by the way, is between 1.2-6.0g for 2 weeks (other timing has not been tested, so it's possible that one week will suffice, too). That's at least what the only hitherto published study that investigated the effects of different doses of taurine as a means to improve the endurance performance (Miyazaki. 2004). If you want the nutrient partitioning effects, though, you would have to consume CHO + taurine after the workout - 3g of taurine should suffice. Judged by the hitherto published studies this should automatically help you to increase your workout performance after 2 weeks (the beneficial effects will, just as it is the case for creatine, accumulate until the levels are saturated).

        And there are more benefits - health benefits, for juicers and non-juicers

        The former, i.e. the juicers will probably be happy to hear that taurine does not just have liver protective effects (Miyazaki. 2005), but will also reverse the nandrolone decanoate induced perturbations in sperm characteristics, normalize the serum testosterone level, and restore the activities of the key steroidogenic enzymes in rodents that are treated with nandrolone and taurine (at a dosage equivalent to only 1.3g/day | Ahmed. 2014).

        In spite of the fact that the administration of taurine did also prevent the nandrolone decanoate-induced testicular toxicity and DNA damage by virtue of its antioxidant, anti-inflammatory, and anti-apoptotic effects, I would like to point out that this article is not intended as an incentive for nandrolone doping.
        While taurine is not made from the sperm of Belgian Blues it may still boost your testosterone levels - whether that's going to be by 140% as in this study is questionable, though.
        From performance to health doping: If you are not into "natural performance enhances" and don't care about the direct performance increases, reduced oxidative damage and increases in glycogen repletion during workouts. I would recommend you reread the previous SuppVersity article about the testosterone boosting effects of taurine, it's ability to improve your strength and recovery during and after resistance training sessions, as well as it's ability to improve your glucose metabolism (Franconi. 2006; Carneiro. 2009), to increase your glucose sensitivity (Han. 2004; Nakaya. 2000), to prevent insulin resistance in hyperglycemic states (Haber. 2003), to prevent the development of hypertension as a result of fructose overfeeding (Rahman. 2011), to prevent the cardiac damage due to iron overload (Oudit. 2004), to protect you from the kidney damaging assault of chemotherapy (Saad. 2010), and god knows which benefits I have simply forgotten in the aforementioned list | Comment of Facebook!
        References:
        • Ahmed, Maha AE. "Amelioration of Nandrolone Decanoate-Induced Testicular and Sperm Toxicity in Rats by Taurine: Effects on Steroidogenesis, Redox and Inflammatory Cascades, and Intrinsic Apoptotic Pathway." Toxicology and Applied Pharmacology (2014).
        • Alom, J., et al. "Cerebrospinal fluid taurine in Alzheimer's disease." Annals of neurology 30.5 (1991): 735-735.
        • Arai, Heii, et al. "A preliminary study of free amino acids in the postmorten temporal cortex from Alzheimer-type dementia patients." Neurobiology of aging 5.4 (1985): 319-321. 
        • Carneiro, Everardo M., et al. "Taurine supplementation modulates glucose homeostasis and islet function." The Journal of nutritional biochemistry 20.7 (2009): 503-511.
        • Cuisinier, Claire, et al. "Role of taurine in osmoregulation during endurance exercise." European journal of applied physiology 87.6 (2002): 489-495.
        • Dawson Jr, R., et al. "The cytoprotective role of taurine in exercise-induced muscle injury." Amino acids 22.4 (2002): 309-324. 
        • Franconi, Flavia, et al. "Taurine supplementation and diabetes mellitus." Current Opinion in Clinical Nutrition & Metabolic Care 9.1 (2006): 32-36.
        • Haber, C. Andrew, et al. "N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress." American Journal of Physiology-Endocrinology and Metabolism 285.4 (2003): E744-E753.
        • Han, Jin, et al. "Taurine increases glucose sensitivity of UCP2-overexpressing β-cells by ameliorating mitochondrial metabolism." American Journal of Physiology-Endocrinology and Metabolism 287.5 (2004): E1008-E1018. 
        • Kim, Hye Yun, et al. "Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease." Scientific Reports 4 (2014).
        • Menzie, Janet, et al. "Taurine and central nervous system disorders." Amino acids 46.1 (2014): 31-46.
        • Miyazaki, T., et al. "Optimal and effective oral dose of taurine to prolong exercise performance in rat." Amino Acids 27.3-4 (2004): 291-298.
        • Miyazaki, Teruo, et al. "Taurine inhibits oxidative damage and prevents fibrosis in carbon tetrachloride-induced hepatic fibrosis." Journal of hepatology 43.1 (2005): 117-125.
        • Molina, José A., et al. "Decreased cerebrospinal fluid levels of neutral and basic amino acids in patients with Parkinson's disease." Journal of the neurological sciences 150.2 (1997): 123-127.
        • Nakaya, Yutaka, et al. "Taurine improves insulin sensitivity in the Otsuka Long-Evans Tokushima Fatty rat, a model of spontaneous type 2 diabetes." The American journal of clinical nutrition 71.1 (2000): 54-58.
        • Oudit, Gavin Y., et al. "Taurine supplementation reduces oxidative stress and improves cardiovascular function in an iron-overload murine model." Circulation 109.15 (2004): 1877-1885.
        • Rahman, Mizanur M., et al. "Taurine prevents hypertension and increases exercise capacity in rats with fructose-induced hypertension." American journal of hypertension 24.5 (2011): 574-581.
        • Saad, Sherif Y., and Ammar C. Al-Rikabi. "Protection effects of taurine supplementation against cisplatin-induced nephrotoxicity in rats." Chemotherapy 48.1 (2010): 42-48.
        • Silva, Luciano A., et al. "Taurine supplementation decreases oxidative stress in skeletal muscle after eccentric exercise." Cell biochemistry and function 29.1 (2011): 43-49. 
        • Takahashi, Yumiko, et al. "Post-exercise taurine administration enhances glycogen repletion in tibialis anterior muscle." The Journal of Physical Fitness and Sports Medicine 3.5 (2014): 531-537.
        • Zhang, M., et al. "Role of taurine supplementation to prevent exercise-induced oxidative stress in healthy young men." Amino acids 26.2 (2004): 203-207.

        Yohimbine & Berberine Protect From Death Due to LPS Intoxication; BCAAs Inhibit Serotonin Metabolism & Cause Anxiety, Tryptophan but not SSRIs Help; Sweet Tea Leaves Are PPAR-G Antagonists & Battle High Lipid + Leptin Levels

        Skip the fireworks invest the money in some quality ingredients for a fondue or whatever you like and invest the (often non-negligible) rest of the money in a gym membership for the next year.
        Actually my figure of the week is 115,000,000 EUR (~152,000,000 US Dollar), which is the sum my fellow country men and women are about to waste on pyrotechnics this year. And a scientifically unconfirmed addition based on my personal observation: 90% of the worst offenders as far as spending money for fireworks goes are at least overweight. Would be interesting to see, if the use of pyrotechnics on New Years Eve is directly associated with fat mass...

        I mean, it could be that they spent so much money on their fireworks that they feel they can only afford the junkfood of which everybody and his/her mama still tend to believe that it would be cheaper than buying fresh products and preparing your own food from those.

        Ah, I am ranting. That's usually Carl Lanore's task, so I will better go on with the items I have compiled for the today's last installment of On Short Notice in the year 2012:
         
        • Berberine + yohimbine - a synergistic duo to prevent LPS toxicity (Li. 2012) -- With all the recent hoopla about the gut microbiome, I suppose that I don't have to tell you what the acronym LPS stands for, right? Hmm... just to make sure it stands for lipopolysaccharide endotoxins which are produced by gram negative bacteria in your gut and are so "toxic" (in fact they cause profound inflammation) that they can be lethal at higher doses.

          Figure 1: Survival rates (%) after ALB/c mice LPS injection (Li. 2012)
          A group of Chinese scientists have now found that aside from berberine the anti-inflammatory effects of which have been known for quite some time now, yohimbine administered in a daily dose of 2mg/kg (human equivalent 0.16mg/kg) does add to the survival rate of berberine treated rodents (human equivalent 4mg/kg) that were injected intragastrically (so not directly into the blood) with a potentially lethal dosage of 20mg/kg LPS. What's more, taken on its own yohimbine is even more potent than the alkaloid that's found in such plants as Berberis aquifolium, Oregon grape, Berberis vulgaris, Berberis aristata, Hydrastis canadensis (goldenseal), Phellodendron amurense, Coptis chinensis and Tinospora cordifolia.

          The mechanism is mediated by the prevention of liver injury, an upregulating of IL-10 production (an anti-inflammatory cytokine), and related anti-inflammatory effects resulting from the suppression of phosphorylation of IkBa, JNK, ERK and IRF3 in macrophages.

        • Chronic 9-week high BCAA diet impairs brain tryptophan levels and causes anxiety (Coppola. 2012) -- Scientists from the Duke University took another look at the BCAA-tryptophan depression connection, you may have read about in the context of my "Sugar Addicted or Just Stressed Out?" post from January 3, 2012.

          According to the results Anna Coppola and her colleagues are about to publish in the American Journal of Physiology  - Endocrinololgy and Metabolism the provision of a BCAA-enriched diet for 9 weeks leads to both reductions in brain tryptophan levels and an increased turnover of serotonin (5-HT) in rodent brains:
          Figure 2: Composition of low fat  (LF) and high fat (HF) diets with or without added BCAAs (left); effects on the ratio of tryptophan  to the molar sum of large neutral amino acids with and without supplemental  tryptophan in the drinking water and 5HT turnover in the brain (no supplemental trp, right; Coppola. 2012)
          Both groups (BCAA and non-BCAA) consumed about identical amounts of food as the rodents in the complementary (LF or HF) groups, which confirms that the BCAA content did not modify the taste of the chow or rendered it unpalatable (cannot have been cheap bulk powder then ;-). The reduction in both the availability of tryptophan as well as the increase in serotonin (5-HT) turnover in the brain must in fact have been a consequence of the added BCAAs and are most likely the root of the disrupted transport of tryptophan across the BBB in rats, leading to reduced exploratory behavior of rats in EPM testing, a sign of increased anxiety.
          "Recent studies demonstrating a strong  association between BCAA levels, obesity, and obesity-related metabolic disorders, when linked to the findings reported here, may help to explain the strong association between obesity and behavioral abnormalities, including depression and anxiety." (Coppola. 2012)
          As the slight differences between the high an low carb diets show, other nutrients can influence serotonin as well (read more)
          In this regard it is important to point out that these negative side effects were mostly reversible by the provision of 15 mg/100 ml tryptophan in the drinking water of the rodents, but were not alleviated by  the administration of the common serotonine reuptake inhibitor fluoxetine (at 10 mg/kg/day for four weeks).

          Bottom line: Isolation is not what you want if what your body has been build for is complex food. And while the single serving of BCAAs you may gulp down during or right before a workout, on the other hand, probably isn't going to harm you. The "I need BCAAs every 30min" approach to gaining muscle mass, may well turn you into a psychotic wrack if you follow it day in and day out for months or years - at least without chronically adding some l-tryptophan to the equation.

        • Sweet tea leaves protect against obesity: Once more via PPAR-gamma blockade (Zhou. 2012) -- Actually this is probably not news to anyone out there with a degree in Traditional Chinese medicine. After all, Lithocarpus polystachyus Rehd.(Sweet Tea) is Chinese folkloric medicine that has always been used to treat obesity, diabetes, and hypertension in South China:
          "Previous experiments revealed that it contains plentiful bioactive flavonoids and polyphenolic compounds, e.g. phlorizin, trilobatin, 3-hydroxy-phlorizin, etc. These components have extensive pharmacological activities, such as anti-diabetes, memory improvement, anti-aging, inhibition of lipid peroxidation and the growth of human colon cancer cells, and so on." (Zhang. 2012)
          From a "scientific" perspective, however, the efficacy of this herbal medicine as an obesity treatment had still to be elucidated.
          Figure 4: Effects of oral gavage of 75 mg, 150 mg and 300 mg/kg of body weight/day of sweet tea extract or placebo (DIO) in conjunction with the 8 weeks on a obesogenic diet (Zhang. 2012)
          In this context it is yet worth mentioning that this study demonstrated for the first time that the aqueous dry leaves extract of Lithocarpus polystachyus Rehd. can potently reduce the worst metabolic side effects of obesity, such as the hypolipidemia, hypoleptinaemia and the degree of insulin resistance (FINS, HOMA-IR, cf. figure 3) what it does not answer, however, is whether the decline in PPAR-gamma is tissue specific, what exactly is behind the profound decline in leptin levels and whether or not lean rodents, let alone humans, who don't consume an obesogenic diet will see anywhere similar benefits.

          In other words, this is research in progress, but I suppose something you are going to hear more about at the Supppversity in 2013.
        * * * * * *

        Apropos hearing or rather reading more, I guess you will realize that you have reached the end of today's installment of On Short Notice which means that you will have to progress to the SuppVersity Facebook Wall if you want a second serving of news on...
        • The history of vitamin A as a light sensor and beyond - actually a free full-text I guess those of you who like to "think paleo" may enjoy (read more)
        • A paper on "good" and "bad" inflammation, where the author points out that soothing inflammation too much can lead to a reduction in energy expenditure and may therefore not be the king's road to getting rid of the last blubber (read more)
        • The food-hitlist of young Americans - Featuring sugar, sugary drinks, sugary bakery, sugary ... as their main energy and carbohydrate sources... (read more)
        • Problems with synthroid and generics that have surfaced in a recent study on their efficacy in the treatment of congenital hypothyrodism (read more)
        as well as a handful of other news, which are already there or are going to be posted within the next hours. Have a great weekend, everyone! 

        References
        • Coppola A, Wenner BR, Ilkayeva O, Stevens RD, Maggioni M, Slotkin TA, Levin ED, Newgard CB. Branched-chain amino acids alter neurobehavioral function in rats. Am J Physiol Endocrinol Metab. 2012 Dec 18.
        • Li H, Wang Y, Zhang H, Jia B, Wang D, et al. Yohimbine Enhances Protection of Berberine against LPS-Induced Mouse Lethality through Multiple Mechanisms. PLoS ONE. 2012; 7(12): e52863. 
        • Zhou CJ, Huang S, Liu JQ, Qiu SQ, Xie FY, Song HP, Li YS, Hou SZ, Lai XP. Sweet tea leaves extract improves leptin resistance in diet-induced obese rats. J Ethnopharmacol. 2013 Jan 9;145(1):386-92.

        The Overfeeding Overview: High Fat, Carb, Protein, MCTs, Leptin, Testosterone, T3 & Reverse T3 - Get an Overview of the Consequences of Short- & Long-Term Overfeeding

        High fat + high carbohydrate foods like mini doughnuts are exactly what you should not eat on a refeed day, let alone during weeks of bulking.
        Do you want to know what happens during days and weeks of gluttony? How the effects "bulking" will have on your body weight and composition, depending on where those extra calories come from? Have you wondered what the optimal nutrient composition on refeed days may look like. And are you concerned about the potential the health consequences of bulking?

        Yes? In this case, I would suggest you take a closer look at the following overview of the research. An overview that is probably not complete, but it should suffice to provide preliminary answers to the aforementioned questions.
        Learn more about the effects of your diet on your health at the SuppVersity

        Only Whey, Not Soy Works for Wheytloss

        Taste Matters - Role of the Taste Receptors
        Dairy Protein Satiety Shoot-Out: Casein vs. Whey

        How Much Carbs Before Fat is Unhealthy?

        5 Tips to Improve & Maintain Insulin Sensitivity

        Carbohydrate Shortage in Paleo Land
        • The amount of weight you gain depends on your genes: They are not the only determinant. That's for sure. A 1990 study by Bouchard et al. still leaves no doubt that your genes are one of the most important determinants of the quantity of weight you gain.

          In said study the researchers from the Laval University fed 24 sedentary young male twins 1,000kcal extra for six out of seven days of the week. In that the study is not the first to investigate the effects of overfeeding on weight gain in twins. It is yet the first and only one that did this over a period of 100 days and thus with a total energy excess of 84,000 kcal on a diet that contained 50 percent carbohydrate, 35 percent fat, and 15 percent protein.
          Figure 1: Comparison of the weight (left) and visceral fat (right) gains in twin pairs; high correlations were observed for both, but the correlation was significantly more pronounced for the unhealthy visceral fat than it was for the mere body weight (Bouchard. 1990).
          The data in Figure 1 does probably not need any extra explanations. In view of the fact that similar results have also been observed in previous studies like Poehlman et al. (1986), it should be obvious that the difference between the weight (left) and visceral fat (right) two identical twins gained was significantly smaller the difference between one twin from pair A and one twin from pair B. The statistical analysis of body fat and waist circumference data revealed similar correlations which were most significant for the visceral fat mass and the waist hip sizes, i.e. those quantities that predict the ill health effects of weight gain best.

          According to Ukkola, et al. (2001), the genetic differences may partly be mediated by differences in the genetic make-up of ones beta-2 adrenoreceptors with specific variants being associated with greater increases in insulin resistance, body weight and subcutaneous fatness. Other candidates are the cholesterol ester transfer protein (CETP) gene which appears to affect adiposity in response to long-term overfeeding (Terán-García. 2008). Other scientists use similar genetic polymorphisms to explain a general resistance to weight gain during overfeeding via genetically determined variations in nonexercise activity thermogenesis (Vanltallie. 2001).
        • Overfeeding fat, carbohydrate or protein, does it make a difference? Studies that compare isocaloric overfeeding are quasi non-existent. What we do have are studies like the one by Horton et al. (1995) that compared high fat vs. high carbohydrate diets (see Figure 2 for macronutrient composition), where the additional energy came from fat or carbohydrates.

          In the Horton study this was a 50% extra that was added in form of fat or carbohydrates on top of the baseline diets of the normal-weight and obese subjects. A 50% extra that lead to significant weight gain.
          Figure 3: Weight gain (left) and increase in energy expenditure (right) in obese and lean subjects in response to carbohydrate and fat overfeeding (Horton. 1995).
          As you can see in Figure 3, both diets led to a rapid increase in body weight, but the trajectory was different. The main and maybe practically relevant difference, though, was that the rapid increase in water and glycogen in the high carbohydrate group was less resilient weight loss in the post-overfeeding period.
        No! Carbs are not necessarily more fattening in the obese. It's a commonly held prejudice that carbohydrates are more readily coverted to fat and stored in the obese, but a study by Minehira et al. that investigated just this found that there was not just no difference in de novo lipogenesis with carbohydrate overfeeding between lean and obese individuals, there was also no increase in de novo lipogenesis, at all, when the when the obese subjects were overfed with a high carbohydrate diet for one day (Minehira. 2004).
        • Figure 4: Proportion of the energy that was stored as body fat (Horton. 1995).
          If we take a look at the proportion of energy that was stored as body fat in Figure 4, it is obvious why the fat gains lasted longer than the carbohydrate gains. Why? Well, simply because the 14-day overfeeding on fat lead to a significantly higher relative increase in body fat.

          Last but not least, it may also be worth mentioning that the the fat gain in the obese group was 89% and 57% higher in the carbohydrate and fat overfeeding group, respectively. An intriguing result that appears to stand in line with dieting studies, where high fat diets are superior to high carbohydrate diets in the obese, but not in lean individuals.

          What was not different for obese and lean individuals, though, was the the fact that the carbohydrate overfeeding lead to higher gains in lean mass than the fat overfeeding. A result that should remind you of a previously reported study here at the SuppVersity, in which a no fat bulk lead to significantly greater muscle and significantly lower fat gains than a low fat bulk (see "If You Go "High Carb", You Better Go Really High!" | more). Overall, "bulking", i.e. eating more than you need on any mixed diet, has repeatedly been shown to produce significant increases plasma Somatomedin-C/Insulin-like Growth Factor (SM-C/IGF-l) and testosterone concentrations as well as insulin, of which Forbes et al. speculate that they promote the lean mass increases that are particularly pronounced when overfeeding is combined with resistance training.

          In a more nutrient-type specific study b by Dirlewanger that did not focus on the weight gain or anabolism, but on the leptin response and the increase in resting energy expenditure the subjects experienced a significant increase in leptin (+28%) and resting energy only in the high carbohydrate, yet not in the fat overfeeding arm of their study in young, lean individuals (Dirlewanger. 2000). Other studies, without clear distinction between high carb and high fat overfeeding, indicate that fast food like burgers or fries is an effective short-term leptin stimulator, too - at least if it's consumed in a single binge (Kolaczynski,. 1996).
          Figure 5: Energy partitioning in young men upon overfeeding with ~5,000kcal per day - mostly carbohydrates, i.e. 1% protein, 3% fat, and 86% carbohydrate (Acheson. 1988).
          In the short run, like on refeed days, for example, carbohydrate overfeeding has another advantage over fat overfeeding, because it takes roughly 500g of carbohydrates (that's 2,000kcal) before even a single gram of those carbs is converted to fat and potentially, but not necessarily stored as body fat (Acheson. 1988) - at "only" 400kcal extra from carbs for one day there was no net lipogenesis at all (see Figure 5). This result is corroborated by data from McDevitt et al. (2000) who observed that the fat gain with fat overfeeding starts with day 1, while there is a time gap in the increase in body fat with carbohydrate overfeeding (McDevitt. 2000).
        If you consume sugar on a refeed, should you prefer glucose, sucrose of fructose? In view of the fact that I don't suggest you refeed more than 1-2 days and considering the fact that you want to get the majority of your carbs from starches on a true bulks, it does not really matter. In fact, studies show no difference in de novo lipogenesis in 96h overfeeding studies between pure glucose and sucrose, which is a 1:1 combination of fructose or fructose in two studies in lean and obese women by (McDevitt. 2000 & 2001). In the long run, consuming amounts of fructose you could only get by drinking a couple of bottles of coke everyday, will yet not be favorable for your health - even if taking fish oil can blunt the increase in hepatic de novo lipogenesis, it won't blunt the insulin resistance (Faeh. 2005).
        • Figure 6: Schematic representation of the main lipid metabolic pathways affected in skeletal muscle during 4 weeks of fat overfeeding. Genes indicated in white boxes were down-regulated during the dietary study, whereas genes indicated in gray boxes were up-regulated (Meugnier. 2007).
          Fat overfeeding, on the other hand, has been show to favor fat storage not just because the dietary fat can be stored without being converted to triglycerides, but also because metabolic and genomic investigations show that the lipid oxidation rate tends to decrease, and 55 genes in the skeletal muscle were modified.

          Modifications of which Meugnier et al. show that they stimulate the synthesis of triacylglycerol, inhibit lipolysis and reduce the oxidation of fatty acid oxidation, while promoting the development of adipocytes with an excess of only ~550kcal/day from fat per day (see Figure 6).

          Another potential explanation is the change in thyroid hormones, of which the data in Figure 7 from an overfeeding study by Danforth Jr., et al. (1979) tells you that the high protein overfeeding despite a 29.8% lower total energy intake triggered the most, the carbohydrate diet the 2nd most favorable (=in favor of greater energy expenditure) effects on the thyroid hormone.
          Figure 7: Effects of overfeeding with carbohydrates, fats, and protein on thyroid hormones (Danforth, Jr. 1979).
          Accordingly, high protein diets, of which we know for sure that they are the most satiating hypercaloric diets (followed by high carb and high fat | Johnstone. 1996) and have the highest thermogenic effect (see Figure 8) and can help dieters avoid the yoyo effect after a diet (Lejeune. 2005), should have the least negative impact on your physique.
          Figure 8: Estimates thermic effect of carbohydrates fats, protein, and alcohol in % energy of the energy that's ingested in form of the respective nutrients (Joosen. 2006).
          And in fact, Jose Antonio et al. (2014) have recently been able to show that a diet that contains fivefold more protein than the FDA recommends (4.4g/kg | 307g/day) is not just benign but will, in conjunction with exercise, will have significant beneficial effects on the physique of healthy resistant trained men (learn more). Furthermore studies indicate that a high protein content may also ameliorate negative effects such as an increase in intrahepatocellular lipid deposition in humans (Bortolotti. 2009).
        Beware of bulking the way you did in your twenties! It's almost certainly going to make you fat, because studies indicate that age correlates with a decreased increase in energy expenditure in response to overfeeding (Roberts. 1996). Since the difference is particularly pronounced on day 1 of the respective overfeeding period (see Figure on the left), I would also refrain from excessive "refeed days" if I were 60+ years old, like the subjects in the study by Roberts et al. from which I grabbed the graph that displays the energy expenditure on a diet that contained 956kcal extra per day (phase II in this study).
        • Classic overfeeding studies with protein as a single nutrient are yet unfortunately rare. Even less, namely nothing, is known about the effects of ketogenic diets, which is why it's at the moment impossible to tell whether a hypercaloric high fat diet that is devoid of carbs and low enough in protein to actually induce ketosis will have the same negative effects as a high fat diet that still contains 15-30% carbohydrates and some protein.
          Based on the studies we have, it's yet quite certain that the combination of some carbs and a high amount of fat is the most obesogenic variety of "bulking" you could possibly select. Therefore - with the exception of ketogenic diets, where corresponding data is still missing, the rule of thumb is: The more fat in the diet, the more rapid the body fat, but not necessarily the body weight gain.
        • MCT overfeeding is less obesogenic - The reason that rodents that are overfed with medium-chain triglycerides (Geliebter. 1983) and assumable human beings store less fat than on long-chain triglycerides as you will find them in your bacon, sausages, dairy & co is an increase in thermogenesis that has been observed in both rodent and human studies.
          Figure 10: Metabolic rate in healthy men after the ingestion of isocaloric fat meals containing MCTs or long chain triglycerides (Hill. 1989).
          As you can see in Figure 10, this effect does not diminish over time - at least, when only the effect of the infusion of MCTs versus long-chain fatty acids is concerned. In view of the rodent study by Geliebter et al. (1983) and the results of the study by Hill et al. (1989), it appears to be quite obvious that MCTs constitute a valuable addition to hypercaloric diets. The often-heard claim that they cannot be stored as fat is yet misleading - even if they are oxidized in the liver, the increase in available energy will increase the storage of energy from other nutrients. The dream of eating as much as you want without gaining weight does therefore remain a dream - at least for all of us who don't harbor a gene defect that blunts the storage of fat.

          Still, in theory it would appear as if using MCTs in a dieting context makes sense. In reality, studies have shown that using MCTs as a major source of your dietary fats does not lead to significant long-term improvements in  fat or general weight loss - even if 27% of an 800kcal/day starvation diet were pure MCT oil (Yost. 1989).

        Fivefold More Than the FDA Allows: Extreme High Protein Diet (4.4g/kg | 307g/day) Benign & Non-Obesogenic. Plus: Macronutrient Prescription & Changes in Food Quality | more
        Alright, so what's the bottom line, then? I guess, in view of the fact that we still have few studies on high protein overfeeding and no studies on overfeeding on ketogenic diet, a conclusive bottom line cannot be reached, yet. What appears to be true, though is that a diet containing some carbohydrates and a large amounts of fat is the worst choice you can make, when you are bulking.

        A protein and a high(er) carbohydrate, as well as a correspondingly low(er) fat content on the other hand, appear to be the way to go at least in the short run. In the long(er) run, on the other hand, the differences between higher fat and higher carbohydrate overfeeding appears to disappear - albeit with a small, but potentially practically significant difference in terms of the amount of body fat you will gain (see Figure 4) | Comment on Facebook!
        References:
        • Acheson, K. J., et al. "Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man." The American journal of clinical nutrition 48.2 (1988): 240-247. 
        • Antonio, Jose, et al. "The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals." Journal of the International Society of Sports Nutrition 11.1 (2014): 19.
        • Bouchard, Claude, et al. "The response to long-term overfeeding in identical twins." New England Journal of Medicine 322.21 (1990): 1477-1482. 
        • Danforth Jr, E., et al. "Dietary-induced alterations in thyroid hormone metabolism during overnutrition." Journal of Clinical Investigation 64.5 (1979): 1336.
        • Dirlewanger, M., et al. "Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 24.11 (2000): 1413-1418.
        • Faeh, David, et al. "Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men." Diabetes 54.7 (2005): 1907-1913.
        • Forbes, Gilbert B., et al. "Hormonal response to overfeeding." The American journal of clinical nutrition 49.4 (1989): 608-611.
        • Geliebter, Ae al, et al. "Overfeeding with medium-chain triglyceride diet results in diminished deposition of fat." The American journal of clinical nutrition 37.1 (1983): 1-4.
        • Hill, James O., et al. "Thermogenesis in humans during overfeeding with medium-chain triglycerides." Metabolism 38.7 (1989): 641-648.
        • Horton, Tracy J., et al. "Fat and carbohydrate overfeeding in humans: different effects on energy storage." The American journal of clinical nutrition 62.1 (1995): 19-29. 
        • Johnstone, A. M., R. J. Stubbs, and C. G. Harbron. "Effect of overfeeding macronutrients on day-to-day food intake in man." European journal of clinical nutrition 50.7 (1996): 418-430. 
        • Joosen, A. M., and Klaas R. Westerterp. "Energy expenditure during overfeeding." Nutr Metab (Lond) 3 (2006): 25.
        • Kolaczynski, JERZY W., et al. "Response of leptin to short-term and prolonged overfeeding in humans." The Journal of Clinical Endocrinology & Metabolism 81.11 (1996): 4162-4165.
        • Lejeune, Manuela PGM, Eva MR Kovacs, and Margriet S. Westerterp-Plantenga. "Additional protein intake limits weight regain after weight loss in humans." British Journal of Nutrition 93.02 (2005): 281-289.
        • McDevitt, Regina M., et al. "Macronutrient disposal during controlled overfeeding with glucose, fructose, sucrose, or fat in lean and obese women." The American journal of clinical nutrition 72.2 (2000): 369-377.
        • McDevitt, Regina M., et al. "De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women." The American journal of clinical nutrition 74.6 (2001): 737-746.
        • Meugnier, Emmanuelle, et al. "Changes in gene expression in skeletal muscle in response to fat overfeeding in lean men." Obesity 15.11 (2007): 2583-2594. 
        • Minehira, K., et al. "Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans." International journal of obesity 28.10 (2004): 1291-1298.
        • Poehlman, Eric T., et al. "Genotype-controlled changes in body composition and fat morphology following overfeeding in twins." The American journal of clinical nutrition 43.5 (1986): 723-731. 
        • Roberts, Susan B., et al. "Effects of age on energy expenditure and substrate oxidation during experimental overfeeding in healthy men." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 51.2 (1996): B148-B157.
        • Terán-García, Margarita, et al. "Effects of cholesterol ester transfer protein (CETP) gene on adiposity in response to long-term overfeeding." Atherosclerosis 196.1 (2008): 455-460.
        • Ukkola, Olavi, A. Tremblay, and C. Bouchard. "Beta-2 adrenergic receptor variants are associated with subcutaneous fat accumulation in response to long-term overfeeding." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 25.11 (2001): 1604-1608.
        • Vanltallie, Theodore B. "Resistance to weight gain during overfeeding: a NEAT explanation." Nutrition reviews 59.2 (2001): 48-51.
        • Yost, Trudy J., and R. H. Eckel. "Hypocaloric feeding in obese women: metabolic effects of medium-chain triglyceride substitution." The American journal of clinical nutrition 49.2 (1989): 326-330.