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marylin monroe
Showing posts with label sleep deprivation. Show all posts
Showing posts with label sleep deprivation. Show all posts

Get Lean & Stay Lean Quickie: OTC Fat Loss Supps Under Scrutiny. Sleepless Yet Lean in India?! Sesamine - Falsely Forgotten? High Carb Nighttime Snacks for Fridge Raiders?

Without an optimized dietary routine, a sound training plan and tons of discipline no fat burner is going to get you abs like these (suggested read: The SBSG Fat Loss Support Routine)
I suppose by today, the last remnants of your turkeys should be gone and you and your relatives ~0.5kg heavier (Hull. 2006). Against that background it appears only logical to turn this week's installment of On Short Notice into another Get Lean & Stay Lean Quickie. Moreover, with the 0.5kg the average American gains in the course of the Thanksgiving holidays, I already have my (or should I say your? Be honest ;-) figure of the week, so that there is actually no reason why we could not dive right into the science of fat loss.

As you are about to see, this installment has more ineffective than effective fat loss treats. Why? Well, maybe due to the fact that it harbors two studies on commercially available supplements? But whom am I telling this... you already know that the main benefits of these so-called "thermogenics" are actually related to their appetite suppressing and stimulating effects, which can help you stick to your diet and workout regimen, and not to their ability to actively "burn" body fat.

Apropos stimulant: Were you aware that there could be methamphetamine in a common ingredient of some thermogenics? No? I'd suggest you check out the last news of this Get Lean & Stay Lean Quickie first, then. If you are not interested in "scandalous" revelations of which you don't even know if they have a bearing on the extracts that are used in your favorite Acacia rigidula supplement (I would actually hope you don't have one, but anyway), you may obviously start at the top, as well:
  • Weight loss stack fails to produce results: Caffeine + BCAA + CLA + Green tea = soy bean oil placebo (Thomas. 2012) At the 9th Annual ISSN Conference and Expo, Daniel Thomas and his co-workers  presented a study in which they investigated the effects an commercially available multi-ingredient dietary supplement containing 99mg of caffeine and a proprietary blend containing 1510 mg of CLA, green tea extract (45% EGCG), L-leucine, L-iso-leucine and L-valine in 22 obese volunteers (placebo arm: age, 34 ± 12; BMI, 34.1 ± 6.1; active arm: age, 36 ± 11.1 years; BMI, 30.0 ± 4.9).

    The supplement / placebo had to be taken with breakfast and lunch (with two pills per serving this would amount to 400mg of caffeine per day and an undisclosed amount of CLA, green tea and BCAAs, of which you can yet probably safely assume that they were underdosed). Body composition and android fat (dual-energy X-ray absorptiometry), waist and hip circumferences, blood pressure and heart rate were measured at baseline and after 8 weeks of supplementation. Aside from taking the supplement the participants were advised to stick to their regular dietary and activity patterns. Against that background it is not exactly surprising that the 'wonder pills' did not bring about any changes in body composition, android fat, waist or hip circumference; and in contrast to the acute effects of the  "hardcore" competition about which you can read in the last post of today's Get Lean & Stay Lean Quickie the product did not even increase the heart rate and blood pressure of the subjects.
  • Blood sugar levels of Indian adolescents are not associated with insufficient sleep and yet not sleeping enough still takes its toll (Patel. 2012) -- You've read more than enough about the importance of sleep on the SuppVersity within the past couple of months (e.g. The SuppVersity Circadian Rythm Series) to be surprised by what Patel et al. conclude in the abstract of  their latest paper:
    "The current study indicates that inadequate sleep duration at night (<7 hrs) does not affect the blood glucose level of the Gujarati Indian adolescents of age group 13-20 years." (Patel. 2012)
    Unfortunately, this is yet again an instance where cursory skimming the abstract provides a  skewed image of the actual study results, which - as you can see in my plot of the actual results - did very well confirm previous observations of the same authors and the findings of the majority of studies which investigated the effects of insufficient sleep on body composition in Western adolescents.

    Figure 1: Body fat (%), fat free mass (FFM) and waist circumference in Indian adolescents (Patel. 2012)
    Statistically significant were the respective differences only in the male part of the study population. That's yet probably just a result of the low number of female participants which was not only significantly smaller (N=95 vs. N=237), but also very unevenly distributed as far as the ratio of female adolescents with adequate (N=90) and inadequate sleep (N=5) are concerned. Against that background you should also exert some caution with respect to the fat free mass values in the N=5 short sleepers. It would probably suffice to have one muscular athlete in this group to skew the whole results.

    Apropos "short sleepers": Can you imagine that only 14% of the male and 5% of the female Indian Gujarati adolescents actually didn't get their share of 7h+ sleep per day!? Makes me wonder about the number of smartphones, Playstations and cable TV channels in the Anand district where the 332 Gujarati adolescent school and and college students came from - the same goes for the respective interactions between nutrient quality, sleep duration and family income.
  • Study shows addition of fish oil accentuates sesamin's 'fat burning effects' (Ide. 2012b) In what could be considered a follow up to the results of a previous study in which Ide et al. were able to show that the addition of arachidonic acid (ARA) to sesamin supplemented chow augmented body fat loss, and increased the expression of enzymes that are involved in the oxidation of fatty acids, Takashe Ide has just published another study, which shows that high dose fish oil (15-20g/kg chow) will illicit similar, if not even more pronounced effects on the expression of Carnitine palmitoyltransferase 2, which is necessary to transports fatty acids into the mitochondria, and the alpha and beta subunit of the trifunctional enzymes that are involved in their subsequent oxidation.

    Figure 2: Effects of Sesamin (SES) + fish oil or arachidonic acid (ARA) on mRNA expression of CPT, trifunctional enzymes alpha & beta, as well as serum lipids in rodents after 15/16 days on respective diets  (Ide. 2012a & 2012b)
    As the data in figure 2 goes to show you, these increases were accompanied physiologically relevant decreases in the concentrations of triglycerides, cholesterol and phospholipids in the blood of the 5-week old male Sprague Dawley rats, Ide used in his latest study. Moreover, the observation that the supplementation regimen enhanced increases in mRNA of the peroxisomal enzymes involved in fatty acid oxidation and
    a membrane protein (peroxin-11α) associated with peroxisomes without affecting enzymes associated with mitochondria and microsomal cytochrome P-450 4a1 expression indicates the "existence of a mechanism independent of PPARα to specifically induce the gene expression of peroxisomal proteins." (Ide. 2012b)  That's an unquestionably interesting observation; also because it could open up new avenues for the development of anti-diabesiety drugs or the identification of herbs and natural "fat burners".
  • More scientific evidence: Eating carbs in the evening does not necessarily make you fat - even if you eat them instead of protein! (Eddy. 2012) While I would still be hesitant to recommend the ingestion of maltodextrin instead of casein or whey protein as a pre-bed snack, the results of a recent study by Eddy et al. clearly show that the sugar load right before bed did not have negative effects on the 59 sedentary, overweight and obese volunteers who were randomly assigned to ingest isocaloric amounts of maltodextrin (PLA), casein (CAS) or whey (WP) max. 30min before bed.
    Carbs Before Bed: What's good for overweight Israeli police cannot be bad for overweight Americans, can it? (photo by Mark Probst)
    "No significant group differences existed at baseline. There were no group x time interactions for RMR, hunger, satiety, desire to eat, fat mass, lean body mass, or weight (P< 0.05), although RMR displayed a trend towards significance with the PLA group decreasing by 74.3 ± 94.5 and WP and CP increasing by 235.73 ± 84.5 and 51.7 ± 79.4kcal/day, respectively (P=0.0559). Significant time effects were measured for satiety (pre: 31.5 ± 2.3, post: 40.6 ± 2.3, P< 0.008) and LBM (pre: 51.8 ± 0.1, post: 52.3 ± 0.1, P< 0.0001)." (Eddy. 2012)
    In view of the fact that it cannot be said if the absence of negative effects on hunger, satiety, desire to eat, fat mass, lean body mass, or weight was related to the obligatory supervised exercise sessions (3x/week; 2 days of resistance exercise and 1 day of high-intensity cardiovascular exercise) all participants had to attend, it does yet remain to be seen if similar results would be observed in obese (or lean?) subjects in the absence of a supervised resistance training and HIIT workouts. That said, as "non-significant" as the previously cited trend in resting metabolic rate ((RMR) may be, the increase in the amount of energy the obese subjects spent sitting around in both protein groups and the contrasting decrease in the maltodextrin group, is something to keep in mind .
    Ok, nighttime snacking increases LDL, but if you measure it in the morning after a high carb + high fat  snack that alone can contribute to the statistically "significant", but physiologically irrelevant LDL increase of 7mg/dL the scientists observed in their 11 healthy participants.
    Midnight snacking (Hibi. 2012): Whether eating right before bed is a good idea at all was not addressed in the study at hand and according to an even more recent paper by Hibi et al., postponing your 10am 192kcal snack (mean protein : fat : carbohydrate ratio of 5:50:45) to 11PM will significantly decrease fat oxidation (daytime snacking: 52.0 ± 13.6 g/d; nighttime snacking: 45.8 ± 14.0 g/d; P = 0.02) and increase total and LDL cholesterol significantly. How bad that actually is, is however likewise questionable, after all the blood glucose and insulin levels, snack and total energy intake, body weight, and energy expenditure of the 11 healthy women (age: 23±1 y; body mass index: 20.6 ± 2.6 kg/m²) who participated in the randomized-crossover trial were not affected by the switch from the daytime to the nighttime snack.
    Irrespective of any trends and non-significant differences, eating a heap of pure sugar (~35g - this is based on the assumption that the amounts were identical to another recent study by the same group which tested the acute effects of carbs and protein, cf. Kinsey. 2012) before going to bed has little to nothing to do with having a whole meal, with or without carbohydrates before bed -- and that this can increase not hamper weight loss, is something you as a SuppVersity reader are well aware of (see "Carbs after 6PM Will Make You Lean" & "Carbs After 6PM Reloaded").
  • Figure 3: According to a somwhat dubious study Acacia rigidula contains more than 44 "toxic amines and alkaloids" (data in ppm; Clement. 1998)
    Hi Tech Pharmaceuticals sponsored trial finds: Fastin RX is better than only two of its ingredients (Jacobs. 2012) -- I guess you won't be surprised to hear that the addition of  methlsynephrine, 1,3 dimethylamylamine ("geranium extract"), yohimbine HCL, naringen and theobromine to caffeine and Acacia rigidula extract potentiates the effects of either 300 mg caffeine (C) or 250 mg Acacia rigidula (AC) alone or in combination, right?

    Fine, 'cause this leaves more room for the important question, whether an additional increase in heart rate of 6.9 and 6.0bpm 2h and 3h after the ingestion of the extended release "fat burner" Fastin RX, a significant increase in systolic blood pressure of 33%, 26% and 19%, as well as increases in diastolic blood pressure that were 16.6%, 2.9% and 15% higher than in the caffeine (only) trial have any bearing on the efficacy of this product, when the 10.1%, 10.0% and 4% greater VO2 consumption (compared to AC and C, only) in the first three hours after the ingestion of the diet pill did no not show any significant main or interaction effects on resting metabolic rate? Probably not? Yeah... I would guess so, as well.
    That's it for today... aside from the advice not to freak out over whatever amount of weight you may have gained in the past couple of days, I shold say: Trust me, it's not worth stressing yourself this is just going to make things worse. Just return to your regular nutritional habits, keep working out and it will be gone in no time. I'd also suggest you check out the latest  SuppVersity Facebook News on
    • Aqueous dried barberry extract as a treat for acne vulgaris (learn more)
    • Zinc + phytoestrogens vs. osteoporosis - a double- yet dull-edged sword  (learn more)
    • Cold-water immersion beats passive recovery and contrast water therapy for recovery after an intense American football training (learn more)
    • Study from the Boston University School of Medicine says: Female adolescents don't eat enough meat. (learn more)
    and the other news I posted today and am going to post in the course of the next 24h. I guess that should suffice to bridge the time until I post tomorrow's full-length SuppVersity article. I'll see you tomorrow, then!

    References:
    • Clement BA, Goff CM, Forbes TDA. Toxic amines and alkaloids from acacia rigidula. Phytochemistry, Volume 49, Issue 5, 5 November 1998, Pages 1377–1380. 
    • Hibi M, Masumoto A, Naito Y, Kiuchi K, Yoshimoto Y, Matsumoto M, Katashima M, Oka J, Ikemoto S. Nighttime snacking reduces whole body fat oxidation and increases LDL cholesterol in healthy young women. Am J Physiol Regul Integr Comp Physiol. 2012 Nov 21.
    • Hull HR, Hester CN, Fields DA. The effect of the holiday season on body weight and composition in college students. Nutr Metab (Lond). 2006 Dec 28;3:44.
    • Ide T, Ono Y, Kawashima H, Kiso Y. Interrelated effects of dihomo-γ-linolenic and arachidonic acids, and sesamin on hepatic fatty acid synthesis and oxidation in rats. Br J Nutr. 2012a Feb 28:1-14.
    • Ide, T. Fish oil at low dietary levels enhances physiological activity of sesamin to increase hepatic fatty acid oxidation in rats. Journal of Clinical Biochemistry and Nutrition. 2012b; 51(3):241–247.
    • Jacobs PL. Acute physiological effects of the commercially available weight loss/energy product, Fastin-XR®, in contrast with the individual effects of caffeine and acacia rigidula. Journal of the International Society of Sports Nutrition 2012, 9(Suppl 1):P10.
    • Kinseyet al.: The effect of acute ingestion of a protein beverage consumed late in the evening on metabolism, appetite, mood state, and blood lipid in overweight and obese adults. Journal of the International Society of Sports Nutrition. 2012; 9(Suppl 1):P16.
    • Patel MC, Shaikh WA, Singh AS. Association of sleep duration with blood glucose level of gujarati indian adolescents. Indian J Physiol Pharmacol 2012; 56(3):229–233.
    • Thomas DD, Rawal S, Kinsey AW, Eddy WE, Fisher N, Spicer MM, Ormsbee MJ. The combination of green tea, caffeine, conjugated linoleic acid and branched chain amino acids have no effect on body composition and abdominal fat changes in overweight and obese men and women. Journal of the International Society of Sports Nutrition. 2012; 9(Suppl 1):P29

    Fragmented Sleep Reduces 24h Fat Oxidation by > 50% - Not Getting a Good Night's Sleep Sets You Up For Obesity.

    Image 1: It looks awkward, but sleep masks
    and ear-plugs are effective, cheap and
    save ways to improve sleep quality
    (image from lackofsleepsymptoms)
    I think you will be familiar with the idea that an insufficient amount of sleep has been found to correlate (! not induce !) with visceral obesity and other negative health markers (e.g. Strian. 2005). Now a study from a the Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht (NUTRIM) at the University of Maastricht in the Netherlands found that not getting a good nights sleep or, in this particular case, waking up every hour, reduces the amount of fat you burn in a period of 24 hours by -52% (Hursel. 2011, cf. figure 1).

    Other than in the initially mentioned epidemiological guesswork ... ah pardon, correlation studies, Hursel et al. had their 15 healthy male volunteers report to the laboratory twice (>2 weeks between the sessions of the randomized, single-blind cross-over study). During each visit, the subjects stayed for 48 h in a respiration chamber, where energy expenditure, physical activity (radar), and substrate oxidation were meticulously measured. On both occasions, the subjects had fixed bedtimes (lights out: 11:00pm; lights on: 7:40am) resulting in 8 h sleeping time per night. On one of the occasions, however, the scientists used induced sleep-fragmentation by the means of "approximately hourly wake-up calls" the subjects had to respond to by turning off their alarm after 2 min.
    Figure 1: Relative differences in carbohydrate and fat oxidation, as well as respiratory quotient (higher quotient = more carbohydrate dependent) in 15 healthy men as a consequence of interrupted sleep (data calculated based on Hursel. 2011)
    Diet-wise, the subjects who had been asked to abstain from strenuous exercise and to sleep for 8 h during the nights before their visit at the lab, were fed a standardized (protein:carbohydrate:fat ratio 12:55:33) diet consisting of "normal, everyday food products" two days before and in the course of their stay in a respiration chamber. The use of the latter, by the way, facilitated pretty exact measurements of the subjects energy expenditure and substrate oxidation (cf. figure 2).
    Figure 2: Relative changes in total, resting (REE) and sleeping energy-expenditure (SEE), as well as absolute changes in activity induced energy expenditure (AEE) and overall caloric balance (data calculated based on Hursel. 2011)
    As the data in figure 2 shows there was no statistically significant difference with respect to the overall calorie balances of the subjects (+0.41MJ/day to +0.41 MJ/day in the normal vs. the interrupted sleep group, respectively). While this appears counterintuitive as the recorded physical activity of the sleep-disturbed subjects had eventually increased, Hursel et al. point out that because of their study design, ...
    we showed an initial increase in physical activity and AEE as an effect of sleep fragmentation, mainly because the subjects had to turn off their alarm clock 7 times during the night. However, the resulting increased exhaustion and sleepiness during the subsequent day might eventually counter-balance physical activity and AEE.
    They go on to point out that the increased activity goes hand in hand with the increase in carbohydrate oxidation, the depletion of glycogen stores and the (this is my assumption) stress-related -52% decrease in fatty acid oxidation (cf. figure 1).

    The real-world results of this unhealthy combination of non-regenerative sleep, daytime exhaustion and sleepiness and the accompanying abstract metabolic shifts are cognitive problems, a lack of motivation (esp. to work out or do any physical work), carb-cravings, snack-attacks & co... In your efforts to (re-)feed a body that is unable to access his well-stocked fat reserves, you end up overcompensate the initially increased energy expenditure, constantly provoking insulin spikes which totally blunt fat oxidation, trigger temporary hyperglycemia (if you are not already diabetic) and induce further snack-attacks. Thus, you are triggering a down-ward spiral that is especially hard to escape from, if your body does not get the chance to reset his insulin and stress levels in the course of a good nights sleep - keep that in mind before you place your cell-phone next to your pillow in order to "keep in touch" with your (facebook-)friends 24/7, as a very recent study published in the journal SLEEP showed that "mobile phone use for calling and for sending text messages after lights out was associated with sleep disturbances independent of covariates and independent of each other" (Munezawa. 2011).

    Caffeine Works - Study Leaves No Doubt About It! Approx. 400mg of Caffeine Get You Going, Even After 32h Without Sleep - So Why Doesn't It Work for You Anymore?

    The answer to post-positioned question in the headline of today's SuppVersity article is not easy to find. Therefore I will start with the facts. Facts, researchers from the University of Sfax present in their latest paper in the peer-reviewed scientific journal Psychology & Behavior; facts that leave little doubt that 5 mg/kg of caffeine could counteract the negative effect of 36 h of total-sleep deprivation on physical and cognitive performances, if your body would still react to stimulus - in other words: If your body still reacted like the bodies of the 13 healthy male habitual caffeine-not-abusing physical education students (age: 21.1 ± 1.1 years; body mass: 77.1 ± 7.2 kg; height: 1.77 ± 0.06 m) who volunteered to participate in the present study, it would get you going - seriously!

    The students had exactly the same time schedule at the university from sunrise to sunset under the control of the experimental team. Participants had taken part in various recreational low-intensity physical activities such us walking, jogging, or aerobics in our university.
    No time to sleep, do your "cardio" HIIT style instead of steady state for hours

    Never Train To Burn Calories!

    Tabata = 14.2kcal /min ≠ Fat Loss

    30s Intervals + 2:1 Work/Rec.

    Making HIIT a Hit Part I/II

    Making HIIT a Hit Part II/II

    Triple Your Energy Exp.
    The participants were prescribed with standard isocaloric meals to consume, with breakfast at 07:30 h, lunch at 12:00 h, and dinner at 20:00 h. Only water was allowed ad libitum between meals. They were requested to maintain their habitual physical activity throughout the experimental period and to avoid strenuous activity before each test session. The overall daily energy intake goal was set at 10.5 MJ (2500 kcal) per capita/day.
    Figure 1: Caffeine affects both body temperature and physical performance during sleep deprivation (Souissi. 2014)
    During the experimental period, medications, which are expected to affect physical performance, were prohibited, more importantly, though:
    "Participants were selected according to their usual consumption of caffeine and on the basis of their answers to the Horne and Ösberg Self-Assessment Questionnaire (Horne. 1979) (i.e., to have a group without “extreme type” (i.e., participants were selected as “neither type”)). This second criterion resulted in a sample of participants who shared the same timing in terms of rising times (06:30 ± 00:30 h) and bedtimes (23:00 ± 00:30 h). Participants reported no sleep disorder, are non-smokers, and do not consume caffeine or any alcoholic beverages."
    After four consecutive nights of sleep in the laboratory (sleep adaptation: between 22:30 and 07:00 h), in a randomized order, participants performed four test sessions: after placebo or 5 mg/kg of caffeine ingestion during a baseline night (RN) or a night of 36 h of total sleep deprivation (TSD).
    Does this look remotely familiar? If it does, you are already "tolerant".
    Is caffeine tolerance even real? Scientists say: Yes! In 1992 Suzette M. Evans and Roland R. Griffiths conducted a study with 32 "healthy subjects with histories of moderate caffeine consumption" who had to abstain from their favorite beverage throughout the study (Evans. 1992). The subjects were stratified into two groups based on several factors including caffeine preference, which was assessed using a caffeine versus placebo choice procedure. Subsequently, subjects received either caffeine (300 mg t.i.d.) or placebo (placebo t.i.d.) for 18 consecutive days, and thereafter were exposed again to a caffeine versus placebo choice procedure. And the result?

    "The study documented tolerance development to the subjective effects of caffeine: after chronic dosing, administration of caffeine produced significant subjective effects in the chronic placebo group but not in the chronic caffeine group." The study also provided indirect evidence for tolerance development: during chronic dosing, the chronic caffeine and placebo groups did not differ meaningfully on ratings of mood and subjective effect. That's important, because it means that not all benefits are lost; plus, it explains why you still don't quit drinking your coffee ;-)
    During the run-in, participants were synchronized with a nocturnal sleep from 22:30 to 07:00 h. During the TSD-phase, they were not allowed to sleep and were kept awake by passive means such us watching TV.
    Figure 2: Caffeine boosts cognitive performance during sleep deprivation (Souissi. 2014)
    During each test session, after 10 min of rest in a sitting position, participants ingested the caffeine or the placebo dose; then they had to remain in a sitting position for 60 min. After the 60 min, they performed
    • the reaction time, 
    • the squat jump (SJ), and 
    • the Wingate tests at 18:00 h with 15 min of recovery in-between 
    All test sessions took place in similar conditions of temperature and relative humidity (27–28 °C and 63–66%, respectively).  The physical tests were complemented by a simple choice-reaction test and a profile of mood state evaluation - which yielded an impressive reduction of the depression and confusion the subjects felt after the 32h without sleep (see Figure 3)
    Figure 3: Results of the profile of mood test w/ & w/out caffeine before and after TSD (Souissi. 2014)
    In conjunction with the increase in vigor, decrease in anxiety and fatigue this alone would warrant the use, but not abuse of caffeine after sleepless nights. The latter, i.e. habituation to high doses of caffeine as they are really common in the pre-workout guzzling world of physical culturists, could potentially nullify the results.
    So what? To withdraw, or not? In my humble opinion, caffeine junkies like us just have to live with the fact that the psychological and physiolo- gical effects even high doses of caffeine have are negligible. Caffeine or rather coffee is healthy, but it's only healthy if you consume it regularly; and the lack of effects on the central nervous system in the "habitual consumer" will actually protect your nervous and cardiovascular system. So, just stick to whatever you can still get out of caffeine, but do never increase your intake beyond 800mg per day on a chronic basis - if even that does no longer effect you, you've been overtraining + abusing for years.
    Bottom line: We all know that caffeine works. At least for those 95% of us who don't belong to the caffeine hypermetabolizer, there is this memory somewhere deep inside our heads. A memory of our first "high dose caffeine, tear down the gym"-experience. It's a memory that's burried deep below memories of years of daily caffeine abuse and the knowledge that the only way to get anywhere close to the caffeine naive state we were in back in the day is withdrawal...

    Yeah, I know that's hard to imagine and actually, there is no evidence that would suggest that withdrawal and resensitization would be necessary to get the dozens of health benefits I have written about in the past. In fact, you could rather argue that 400mg+ doses of caffeine are going to have a negative effect on your health, as long as they still 'cause an increase in Central Nervous System (CNS) activity as it was observed in the study at hand. I mean, what would you expect the health consequences of having one of these "high dose caffeine, tear down the gym"-experiences every (other) day? This can hardly be good for your heart and brain, can it?
    References:
    • Evans, Suzette M., and Roland R. Griffiths. "Caffeine tolerance and choice in humans." Psychopharmacology 108.1-2 (1992): 51-59.
    • Horne, John A., and Olov Ostberg. "A self-assessment questionnaire to determine morningness-eveningness in human circadian rhythms." International journal of chronobiology 4.2 (1976): 97. 
    • Souissi, Makram  et al."The effects of caffeine ingestion on the reaction time and short-term maximal performance after 36h of sleep deprivation." Physiology & Behavior 131 (2014): 1-6.

    You Cannot Sleep Before an Important Event? Take High Dose Creatine or Low Dose Caffeine to Battle Fatigue Induced Decrement in Skill Performance and Increase Testosterone.

    Image 1: LG's Anadraulic State is only
    one example for some of the 2nd generation
    pre-workout products with deliberately lowered
    amounts of caffeine and increased amounts of
    creatine & other ergogenics in it.
    You know it, you love it: Creatine Monohydrate - the godfather of dietary supplements; but did you know that Creatine supplementation at 50 or 100mg/kg body weight is as effective as low (1mg/kg) or high dose (5mg/kg) caffeine in preventing the decrease in athletic skill performance after sleep deprivation?

    On ten separate occasions, Cook et al. (Cook. 2011) had ten elite rugby players complete 10 trials on a simple rugby passing skill test (20 repeats per trial). On five of these occasions the players had slept their usual 7-9h on the other five occasions, however, they only slept 3-5h before reporting to the laboratory. While the 2-6h of sleep they were lacking "resulted in a significant fall in skill performance accuracy on both the dominant and non-dominant passing sides (p < 0.001)" in the placebo supplemented players, the sleep deprived athletes who consumed either creatine (50 or 100mg/kg) or caffeine (1 or 5 mg/kg) 1.5h before the test performed just as well as they did in the non-sleep-deprived trials:
    No fall in skill performance was seen with caffeine doses of 1 or 5 mg/kg, and the two doses were not significantly different in effect. Similarly, no deficit was seen with creatine administration at 50 or 100 mg/kg and the performance effects were not significantly different.
    Interesting side-effects, the scientists observed was the increase in testosterone [roughly 32% in sleep deprived and roughly 22% in fresh athletes], the higher dose of creatine supplementation brought about and the increase in cortisol from high dose caffeine:
    Salivary testosterone was not affected by sleep deprivation, but trended higher with the 100 mg/kg creatine dose, compared to the placebo treatment (p = 0.067). Salivary cortisol was elevated (p = 0.001) with the 5 mg/kg dose of caffeine (vs. placebo).
    So, if you got to chose, you probably better use a higher dose of creatine and drink a small cup of coffee than taking one of the highly stimulating preworkout products with loads of caffeine and only small doses of creatine, to optimize athletic performance and your testosterone to cortisol ratio.

    Coffee - The Good, The Bad & The Interesting: 2-4 Cups of Coffee for Adiponectin. Roasted Filtered Coffee & High LDL!? The Optimal Caffeine / Taurine Ratios & the Buzz

    The insights may be based on data from a fruit flies, but the the differential effects of high vs. low taurine / caffeine ratios on wake-, respectively sleepfulness concur with my own N=1 experience.
    It's been a while since we've had a cup of the former Brew of the King's together. Therefore it occured to me that it would be high time to brew not just but three refreshing cups of hot coffee... ah coffee / caffeine news for us.

    If you feel that's way too much, you may avoid one of them, but the way I know the average (=extraordinary ;-) SuppVersity reader, you will have downed them in less than 2 minutes, anyway and if you are lean and healthy the average effect is, as the first and good news is going to tell you will have little but beneficial effects on your ability to keep just that.

    Too late? I mean, you're afraid it could keep you up, then I suggest you start with #3 of today's coffee-potspourri and learn how taurine could help you sleep like a baby despite the energizing effects of caffeine.

    And if you are one of the healthy skeptics out there, who are (rightly so) unwilling to believe that even something as delightful as coffee could have exclusively beneficial effects, you may like the taste of the 2nd cup from today's coffee party best.



    The Good: "Habitual moderate coffee consumption shows significant inverse associations with MetS-related biomarkers possibly involving adiponectin, which is inversely related to visceral fat accumulation. " (Mure. 2013)

    According to a recent study from the Wakayama Medical University School of Medicine in Japan (this is actually important, because much of the previous epidemiological data on the beneficial effects of coffee consumption comes from the Western world), two distinct models of multivariate regression analyses yielded almost identically beneficial inverse associations with visceral fat mass, visceral to subcutaneous fat mass (p<0.0001; no typo!) for those 330 study participants (average age 36–61 y) who consumed either 1-3 (low) or 4+ cups of coffee on a daily basis.
    Figure 1: Association of coffee consumption with adiponectin levels according to their MetS risk factors; according to model 2, i.e. adjusted for age, BMI, alcohol drinking, smoking, and walking status (Mure. 2013)
    Moreover, Kanae Murae and colleagues observed a favorable tendency toward these associations with total adiponectin and high molecular weight adiponectin levels in (P<0.06 bzw. p<0.07) in the moderate coffee consumers (just a reminder: 4 cups + was still considered "moderate" in the study at hand).

    Practically relevant specifically for the healthy folks among us

    Interestingly, these associations became statistically significant in those participants who did not already suffer from metabolic syndrome and are thus particularly relevant for the average non-obese, non-metabolically deranged physical culturist who's trying to stay just that: Lean & healthy.

    Testosterone booster in men and estrogen amplifier in women? As if there were not already enough good reasons to get your daily dose of the 'kingly' brew - suggested read: "Can 5 Cups of Coffee Boost Testosterone to Estrogen Ratio in Overweight Men Transiently by Almost 200%?" (read more)
    For participants with risk metabolic syndrome risk scores >2, on the other hand, did not benefit from either the "low", nor the "moderate" ingestion of caffeine and - I can tell you that without even needing a study to prove it - certainly not benefit from ingesting even more coffee. Why is that? Well, think about what coffee does: It squeezes the fat out of the cell and reduces it's reuptake and de novo genesis by temporarily reducing glucose sensitivity. Since the latter effect is mainly a function of the increased amount of free fatty acids and triglycerides in the blood stream, which is in turn driven by the caffeine induced increase in catecholamines and lipolysis, the same thing that will be beneficial for lean, active people with low baseline FFA and triglyceride levels and the ability to burn those fats in the mitochondria of their muscle while they work out (and even while they sit around), will compromise the glucose and fatty acid metabolism of an obese, sedentary person even more. 

    Bottom line: In the end, it does all come down to the old adage of "Just because it's good for your neighbor, it must not necessarily be good for you as well!" In many previously discussed cases, this was the case for stuff that's highly beneficial for your obese neighbor, but in this case, it's the other way around: If Mr. Average Overweight American from next door mirrored your "moderate" coffee consumption (personally I can only repeat my previous recommendaton to stay below the 400mg/day margin, to play it save), he will - at best - experience no effects at all. In the worst case, it will exasperate his already existing insulin resistance and precipitate him to further metabolic derangements.



    Does it take 5 cups of coffee to battle breast cancer? (learn more)
    The Bad: "Moderate paper-filtered coffee consumption may have an undesirable effect on plasma cholesterol and inflammation biomarkers in healthy individuals regardless of its antioxidant content." (Corréa. 2013)

    Where there is light, there must be shadow. Some shadow, namely the non-existence of the beneficial association between low to moderate habitual caffeine consumption and total, as well as high molecular weight adiponectin levels, has already been mentioned in the Mure study. A recently published study from the Universityof Sao Paulo does yet suggest that there may even be real downsides attached to the consumption of coffee... paper filtered coffee that is to say.

    While the actual intention of the randomized cross-over study Corréa et al conducted was to compare the effects of ingesting medium light roast (MLR) or medium roast (MR) filtered coffee on plasma lipids, total homocysteine (tHcy), endothelial dysfunction–related inflammation biomarkers, glycemic biomarkers, and
    BP in healthy volunteers, the average medical practitioner will certainly jump on the results to rant against coffee as the biggest evil... well, next to saturated fats obviously ;-)
    Figure 2: Relative changes in lipid profile and selected markers of inflammation in response to light (MLR) or medium (MR) roast filtered-coffee; data expressed relative to baseline (Corréa. 2013)
    I guess, at least after taking a peak at the data I've plotted for you in figure 2 you will see where this is heading - the nightmare of every GP: "An increase in LDL cholestrol!" Right there and independent of whether the coffee had peen roasted only lightly or at a medium heat. "Let's ignore all the rest and get the statins ready!" ;-)

    Bottom line: Even if we consider increasing cholesterol levels as being a sign of impeding heart disease, the mere fact that the "healthy participants" had a mean of "only" 27.0 +/- 3.8kg/m² and body fat levels of 29.1% and 37.5% in the male and female participants, respectively, would warrant another reiteration of the "obese neighbor" mantra... and let's be honest, you don't really believe that the subjects in the dozens of epidemiological studies indicating that regular caffeine consumption has beneficial effects on heart health drank only true Italian espresso, do you? And even if they did - the study at hand does not imply that this would not entail similar increases in in cholesterol and inflammation in the not so skinny, but certainly pretty fat participants of the study at hand, right?



    The Interesting: A high taurine:caffeine ratio promotes sleep, while a low ratio of taurine:caffeine inhibits sleep to a greater extent than the equivalent amount of caffeine alone (Lin. 2010)

    While the results are not new - the pertaining study by Lin et al. is from 2010 - I am pretty sure that few of you will have heard about it. On the other hand, I bet that you may have been asking yourselves, why Red Bull & Co. contain an agent that is a mild GABA agonist - shouldn't that make you sleepy instead of spiking you up? Or is it rather like the "energy drink" producers say that it "mitigates" or even "promotes" the energizing effects of caffeine?

    If we assume that human beings work anywhere similar like fruit flies (which is obviously hilarious, but not 100% unlikely, if we put an emphasis on "anywhere", here), then the data Lin et al. collected at the University of Pennsylvania, would suggest that the net result only depends on the dosage. If the ratio of taurine to caffeine is high the net effect will be sedative.
    Figure 3: Effects of caffeine, taurine and their combination in different amounts and ratios on sleep per hour and locomotor activity per 30min in fruits flies; data expressed relative to untreated control (Lin. 2010)
    If, on the other hand, the ratio of taurine to caffeine is low, the aforementioned money printing business men would be right. The unfortunate news, is yet that an increase in locomotor activity in the presence of a decrease of total sleep quantity does, as the researchers themselves point out precipitate "sleep deprivation and subsequent attention deficit in the long run". Whether that in turn can, or I'd better say, should be countered by taking even more taurine to "shut you down" after the spike is questionable and would in the end lead to the usual broscientific vicious circle of using supplement B to counter the side effects of supplement A... I mean, what's supplement C gonna be then? You can't seriously assume that B won't have side effects, as well, right?

    Bottom line: While it would obviously be hilarious to assume that the exact same ratio that works for the fruit flies will work for human beings as well, it is certainly enlightening to see that (a) a ratio dependent does in fact exist and (b) that the "optimal" ratio of 12.5 units per taurine per unit of caffeine happens to be present in Red Bull, as well - and that despite it appears that the Carolina and Pennsylvania State scientists are among the few people who are not yet on the payroll of the omnipresent red bulls.


    References:
    • Corrêa TA, Rogero MM, Mioto BM, Tarasoutchi D, Tuda VL, César LA, Torres EA. Paper-filtered coffee increases cholesterol and inflammation biomarkers independent of roasting degree: A clinical trial. Nutrition. 2013 Mar 16.
    • Lin FJ, Pierce MM, Sehgal A, Wu T, Skipper DC, Chabba R. Effect of taurine and caffeine on sleep-wake activity in Drosophila melanogaster. Nat Sci Sleep. 2010 Sep 24;2:221-31.
    • Mure K, Maeda S, Mukoubayashi C, Mugitani K, Iwane M, Kinoshita F, Mohara O, Takeshita T. Habitual coffee consumption inversely associated with metabolic syndrome-related biomarkers involving adiponectin. Nutrition. 2013 Apr 16. 

    Sleep Quickie: Sleep Restriction ➲ Blood Amino Acid Levels ↑, Glucose Levels ↓ ✰ Food ↻ Sleep & Exercise Interactions ✰ Melatonin, A Safe Sleep Aid W/ Anti-Alzheimer's Effects

    The healthy lifestyle rhythm: "Sleep, eat, train, live, sleep,..." × 365 days/year
    If you were expecting any obscenities in today's "Sleep Quickie", you will probably be disappointed to hear that this article is solely about sleep, metabolism and melatonin and how all that relates to "shutting your eyes and disappearing into the land of dreams".

    This means that it won't touch on the 19% increase in copulatory efficiency and the other "significantly facilitated" aspects of sexual activity (mounting latency -80%, ejaculatory latency -63%, etc.) scientists from the University of British Columbia observed in melatonin treated (4 mg/L of drinking water) Long-Evans rats (Brotto. 2002).

    Rather than that we are going to focus on the non X-rated semantics of "to sleep", its health effects and the role of melatonin in sleep, health and disease. So, let's see what we've got in stock for you:
    • Profound effects of sleep restriction on the human plasma metabolome (Bell. 2014) -- In spite of the the fact that it is well established that short sleep durations and/or poor sleep quality induce changes in our energy and substrate metabolism (Penev. 2012) that increase your risk of developing diabesity (Cappuccio. 2010), we know very little about the biochemical signatures involved in the pathogenesis of type 2 diabetes[5–9].

      How bad is bad sleep? That's a pretty good question and if we put faith in the latest meta-analyses by researchers from the University of Warwick and the University of Naples Medical School, it's pretty bad - at least that's what I would call something that is associated with increases in ...
      • diabetes - 28% increased risk with sleep duration ≤5–6 h/night, 48% increased risk with difficulty in initiating sleep, and 84% increased risk with difficulty maintaining sleep (Cappuccio. 2010),
      • cardiovascular disease - 48% increased risk of developing or dying of CHD with short sleep durations (≤5–6 h/night), and 38% increased risk of coronary heart disease , 65% increased risk of stroke, and 41% increased risk of for any form of CVD with long duration (>8h/night) sleep (Cappuccio. 2011),
      • all-cause mortality - 12% higher all-cause mortality risk for short duration of sleep (≤5–6 h/night), +30% all-cause mortality risk with long-duration sleep (>8h/night) (Cappuccio. 2012)
      Looks pretty bad, right? That's just what I said.
      Bell et al. did thus decide to use a metabolomic profiling approach to assess the impact of recurrent sleep restriction on human intermediary metabolism to identify biochemical signatures that may reflect the effects of sleep curtailment on metabolic risk. To this ends, each study participant completed two 8-night inpatient sessions with restricted (5.5-h time-in-bed) vs. adequate (8.5-h time-in-bed) sleep opportunity while daily food intake and physical activity were carefully controlled.

      The subsequent combination analysis of 362 biochemicals in fasting plasma samples that were collected from study participants the morning after each 8-night sleep treatment revealed that..
      1. the relative concentrations of 12 amino acids and related metabolites were increased when sleep was curtailed
      2. sleep restriction also induced elevations in several fatty acid, bile acid, steroid hormone, and tricarboxylic acid cycle intermediates, and surprisingly
      3. the circulating levels of glucose, some monosaccharides, gluconate, andfive-carbon sugar alcohols tended to decline when sleep was reduced.
      According to the researchers the elevation in plasma amino acids (~6-70%), specifically isoleucine, tryptophan, phenyllactate, a byproduct of the phenylalanine metabalism,  glutaroyl carnitine, byproduct of the lysine metabolism, histidine and threonine. If these changes are corollary or causally involved in the increased diabesity risk we see in sleep deprived indiviudals is yet something the researchers cannot tell us, yet.

      Incidentally, the same is true for the answer to the question whether similar changes would have been observed if the hitherto healthy, lean subjects didn't have a parenteral  history of type 2 diabetes. The Bell study must therefore be seen as a first in a series of studies that could broaden our insights into the role of abnormal sleeping patterns in the etiology of type II diabetes and other metabolic disease.
    • Food ↻ sleep interactions and their potential role in the etiology of diabesity (Chaput. 2013) -- The insights we may gain from the previously discussed study by Bell et al. may give some indication of whether or not the increase in energy intake that's so characteristic for sleep deprived human beings is a crucial, necessary or conditional contributer to the increased diabetes and obesity (=diabesity) risk in this population. 

      Figure 1: Potential mechanisms by which insufficient sleep may facilitate the ingestion of calories (Chaput. 2013)
      In his recent paper in Physiology & Behavior Jean-Philippe Chaput aptly illustrated the six pillars on which this increase in energy intake is based (see Figure 1). Chaput does yet also point out that the ingestion of certain foods / food types, especially those which impact the availability of tryptophan could ameliorate these effects that are mediated by their beneficial effects on (Peuhkuri. 2012) and cites examples such as cow's milk that has has traditionally been considered a tranquilizing beverage with sleep-inducing capacity in many Western countries (an effect that could not be confirmed in scientific studies, cf. Valtonen. 2005; Yamamura. 2007).

      Other examples of sleep-promoting foods include herbal products (e.g. chamomile
      tea) and certain fruits (e.g. tart cherries or kiwifruits), but again, robust scientific evidence supporting this is, in many cases, nonexistent (Pehkuri. 2012). And with respect to tryptophan, which is a precursor to the neurotransmitter serotonin and the neuro-secretory hormone melatonin, have only been confirmed in studies using pharmacological doses way above the maximal amount you could get from food. 
    • Can exercise attenuate the metabolic effects of dim light at night? (Fonken. 2013) -- You will be aware that going to bed right after an intense HIIT session is beside the point. Your chances of falling to and gettins some restful sleep don't border zero, they are zero. Against that background it may initially sound surprising that researchers from the Department of Neuroscience at the Ohio State University have recently argued that exercise could exert at least part of its beneficial anti-obesity effects by strengthening and realigning the circadian rhythm.

      To test this hypothesis Fonken et al. maintained four groups of mice in either dark (LD) or dim (dLAN) nights and provided them with either a functional or a locked running wheel or a locked wheel. As it turned out, "[m]ice exposed to dim, rather than dark, nights increased weight gain." If the mice had access to a functional running wheel, however, the dim light at night hat no effect on their body mass.

      This sounds fantastic. Unfortunately, the effect was not brought about by a preventive effect exercise may have on the dim-light-induced defect of the animals circadian system. It was brought about by an increase in energy consumption by the means of which the rodents compensated for the increases in daytime food intake.
    • Melatonin supplements work and won't lose efficacy over time (Ferracioli-Oda. 2013) -- In view of the fact that the classics, i.e. milk and camomile tea obviously don't do much to improve your sleep quality (see previous paragraph), it's all the more important to emphasize that Eduardo Ferracioli-Oda, Ahmad Qawasmi, and Michael H. Bloch's meta-regression analysis that examined the influence of dose and duration of melatonin on reported efficacy yielded results all the melatonin lovers out there will certainly appreciate.

      Figure 2: Restoring reduced melatonin levels (A,B,C) to youthful levels by supplementation (1-3) counters the build-up of ameloid plaque (➲Alzheimer's; cf. Lahiri. 2004).
      The Yale scientists analyzed data from 1683 subjects (19 trials) and were able to demonstrate that the supplemental provision of melatonin ...
      1. reduces sleep latency by t = 7.06 min
      2. increases total sleep time by t = 8.25 min
      3. promotes overall sleep quality (+22%)
      In that, it's quite amazing that the efficiency increases in a both dose- and time-dependent manner. In other words, the ability of melatonin to decrease sleep latency and increase your total sleep time increases the more you take and the longer you stay on a supplementation regimen that mimics the natural diurnal melatonin rhythm.

      The often-heard hypothesis that you could build up a tolerance over time is thus not supported by scientific evidence. And dependence, as it is common with benzodiazepines is not an issue (Srinivasan. 2011)
    In view of the age-related decline in melatonin production (39% reduction in 51-55 year-olds, 62% reduction in 82-86 year-olds; cf. Bubenik. 2011), it may be worth supplementing for anyone over 60 years - if not to improve sleep quality and duration then for the anti-Alzheimer's effects (Lahiri. 2004; Lin. 2013)
    Bottom line: You better make sure you get enough quality sleep, if you don't want to jeopardize your health. If you manage to go to bed "early" every day you will see that after 1-2 weeks you won't even need an alarm clock to get up on 6am, when you went to bed shortly before 10pm the night before... well, assuming that you didn't work out at past 6pm, didn't expose yourself to bright or even worse bright blue light from laptop, iPad or LED TV past 8pm and use ear-plugs to block out all shatter, noise or whatever may wake you up when before 6pm.

    If all these tips don't help you sleep and/ or you have 5 or 6 decades of extra years under your belt, it may be worth investing in a bottle of 3-10mg melatonin capsules. Avoid the slow-release preparations (unless you like being drowsy the next morning) and take them 1h before you go to bed.
    References:
    • Bell, Lauren N., et al. "Effects of sleep restriction on the human plasma metabolome." Physiology & behavior 122 (2013): 25-31.
    • Brotto, Lori A., and Boris B. Gorzalka. "Melatonin enhances sexual behavior in the male rat." Physiology & behavior 68.4 (2000): 483-486.
    • Bubenik, G. A., and S. J. Konturek. "Melatonin and aging: prospects for human treatment." Journal of Physiology and Pharmacology 62.1 (2011): 13.
    • Cappuccio, Francesco P., et al. "Quantity and Quality of Sleep and Incidence of Type 2 Diabetes A systematic review and meta-analysis." Diabetes Care 33.2 (2010): 414-420.
    • Cappuccio, Francesco P., et al. "Sleep duration and all-cause mortality: a systematic review and meta-analysis of prospective studies." Sleep 33.5 (2010): 585.
    • Cappuccio, Francesco P., et al. "Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies." European Heart Journal 32.12 (2011): 1484-1492. 
    • Fonken, Laura K., et al. "Exercise attenuates the metabolic effects of dim light at night." Physiology & behavior 124 (2014): 33-36.
    • Lahiri, Debomoy K., et al. "Dietary supplementation with melatonin reduces levels of amyloid beta‐peptides in the murine cerebral cortex." Journal of pineal research 36.4 (2004): 224-231. 
    • Lin, Li, et al. "Melatonin in Alzheimer’s Disease." International journal of molecular sciences 14.7 (2013): 14575-14593.
    • Peuhkuri, Katri, Nora Sihvola, and Riitta Korpela. "Diet promotes sleep duration and quality." Nutrition Research 32.5 (2012): 309-319.
    • Penev, P. D. "Update on energy homeostasis and insufficient sleep." Journal of Clinical Endocrinology & Metabolism 97.6 (2012): 1792-1801. 
    • Srinivasan, Venkatramanujan, et al. "Melatonin agonists in primary insomnia and depression-associated insomnia: Are they superior to sedative-hypnotics?." Progress in Neuro-Psychopharmacology and Biological Psychiatry 35.4 (2011): 913-923.
    • Valtonen, M., et al. "Effect of melatonin-rich night-time milk on sleep and activity in elderly institutionalized subjects." Nordic Journal of Psychiatry 59.3 (2005): 217-221.
    • Yamamura, S., et al. "The effect of Lactobacillus helveticus fermented milk on sleep and health perception in elderly subjects." European journal of clinical nutrition 63.1 (2007): 100-105.

    90 Min Sleep Restriction - How Bad is It Really? Changes in Insulin Resistance Last For One Week - Until the System Adapts. Plus: Subjects Even Reduce Weight & Waistline

    In general it's certainly a good idea to rise, when the cock crows on the dung heap, but what if that means you miss 90 min of your precious sleep?
    "Tell me how and how long you slept last night and I'll tell you something about your chances of getting / staying lean and healthy!" It sounds more straight forward than the stupid AM vs. PM system you, my American friends, are still sticking to: If you consistently miss just one hour of sleep, you are messing with your insulin sensitivity, body weight and your plasma concentrations of leptin. But is this actually accurate and "how much messing" does it actually take? A close analysis of a recent study by a group of researchers from University of Surrey in Guildford, UK (Robertson. 2013), does at least raise some questions in how far smaller deviations from your usual 24/7 x 365 consistency will mess with your physique and health.

    Can you "wake your way" towards obesity?

    "Mild sleep restriction" is what scientists call it, when you miss 'only' one hour of your regular 7-8h of sleep every night and "mild sleep restriction" is also what the 19 healthy young normalweight men in the Robertson study have been exposed to over a three-week period.
    Just in case you have forgotten about it, you can do the Munich Chronotype test for free (including personal evaluation) right at the website of the University of Munich (click here to be redirected)
    Healthy male students, aged 20–30years, BMI 19–26kg/m² were recruited for this randomized–controlled sleep intervention study [...] those with a self-reported sleep length of 7.0–7.5h were invited for more detailed screening.[...] According to self-report, volunteers were not taking prescription or over the counter medication and had a stable weight for >3months. Specific exclusion criteria also included (i) shift-work and travel beyond 2 time zones in the preceding 2months, (ii) high intake of caffeine and alcohol, (iii) extreme morning or evening preference assessed with the Munich Chronotype and Horne Östberg Questionnaire, (iv) a self-reported sleep problem (Pittsburgh Sleep Quality Index global score≥6) and (v) daytime naps in the preceding 4weeks.
    Before the actual study began, the habitual sleep patterns were assessed by actigraphy and sleep diary information collected during a two week baseline period. The subjects were then  randomized to either the
    • restricted group spending their regular time-in-bed minus 1.5h per night, or the
    • habitual group who simply followed their habitual sleeping patterns
    The participants had to fill out sleep logs in order to assure compliance. Moreover, participants were instructed not to take naps during the day . The actual acquisition of the weight, blood pressure and adiposity data, as well as the leptin and adiponectin levels, and information about  arterial stiffness took place after a 12h overnight fast, at the Centre for Endocrinology Diabetes and Research (the oral glucose tolerance used to evaluate the effects of sleep deprivation on insulin sensitivity took place at the CEDAR, as well). The procedure was conducted four times, initially following the 2-week baseline period and in weekly intervals for the 3 weeks of the intervention, thereafter.
    Figure 1: Relative changes of insulin sensitivity (HOMA-IR), fasting blood glucose and adiponectin levels in the course of the three-week study period (Robertson. 2013)
    If you simply went by the absolute data and the short but concise summary of the main results the researchers provide in the abstract it would in fact seem as if the provocative statement I at the very beginning of this article would be spot on and you would add a pound of fat to your frame and lose a full week of your precious life-time with each minute of sleep you are missing. If you put things into perspective by calculating the relative changes, you cannot but realize that sleeping 90min less may not be ideal, but it's "medium term"  effects are probably overrated.
    Figure 2: Illustrated and annotated version of the graph depicting the change in insulin sensitivity in the habitual (open circles) and sleep restricted (closed circles) group (Robertson. 2013)
    In fact, the plot of the changes in insulin sensitivity in figure 2 clearly suggests that there is something like an adaptation process that compensates for the initial reduction in insulin sensitivity once a new 'sleep steady state' is achieved. In the absence of data from the following weeks, we cannot however exclude that the in an even longer-term scenario the reduction of sleep duration from below the 5h mark would not have had a negative impact on the overall and metabolic health of the subjects. In this context, Robertson et al. point out that
    "[...] some of the effects of sleep restriction appear transient, i.e. we have beenunable to confirm a change in insulin sensitivity beyond one week of sleep restriction [and that t]he data clearly indicate that the effects of a reduction in sleep duration may change in the course of the exposure to sleep reduction, [which renders any] extrapolation from single visit laboratory studies to epidemiological data problematic." (Roberston. 2013)
    If we would yet discard the epidemiological findings and simply ignore the constant increase in fasting blood glucose and rely on the fact that the insulin tolerance returned to baseline after an initial drop, we could even (ab-)use the data from the study at hand to argue in favor of sleep "deprivation" (I am deliberately using quotation marks, because the previously mentioned adapation process would suggest that the subjects were not actually "deprived") as a means to reduce the obesity epidemic. After all the subjects in the sleep restricted group did lose some body weight and reduced their adiposity index, the waist equivalent to the BMI (higher values = higher ratio of waist to body height), by meager, but at least measurable 0.8%.
    Believe me: Fridge raiding is your least problem if you don't sleep at night. If you want to know more about the profound metabolic, psychological and even carcinogenic effects of having or not having a regular sleeping rhythm, why a dark room is important and more, read up on the Circadian Rhythm Series
    Sleep does not necessary equal sleep: It should also be mentioned that "sleep" data we are talking about is actually data spent in bed and if you take a look at the sleep latency, you will realize that the subjects in the restricted group made up for 4-8 minutes of their 90min sleep debt by simply falling asleep more readily. Another factor to keep in mind is that, at least in my humble opinion, the actual sleep duration of the young men who participated in the study was to low to begin with. This is just my personal N=1 experience, but whenever the demands of life (or my own stupidity) forced me onto a <7h sleeping schedule, I ended up gaining body fat - not necessarily weight, but fat. So if there is something like a "break even" and the subjects were below that already, the effects could be much more pronounced in someone like you, who is (hopefully) getting is 7h of sleep in a pitch black, quiet room every night.
    And what's more, in the correlation analysis the scientists conducted, the only parameter with a statistically singnificant correlation with sleep duration was - you won't guess that - body weight! With a positive correlation of +0.271 indicating that shorter sleep durations exhibited - at least in the study at hand - statistically significant correlations with decreases in body weight.

    So what? You cannot 'wake yourself lean', can you?

    No, probably not. The evidence from epidemiological studies is too overwhelming to throw the insufficient sleep = diabesity hypothesis over board. On the other hand, the results of the study at hand are interesting, as they clearly suggest that (a) our bodies are able to adapt to a news steady state within a certain window of suboptimal to optimal sleeping time and (b) that the short term effects of what I would like to identify as an actue stressor, namely 1-2 weeks of reduced sleep will lead to similarly transient weight loss.

    Previous study showed: When you are dieting 40min extra sleep can help you 1lbs extra fat (read more).
    increases in cortisol levels do the exact same thing. In the short run, they will spike you up (Lance Armstrong has admitted using corticosteroids to outperform the competition only days ago). Used intermediately, they will begin to gnaw on your body fat and muscles and in the long run they will totally mess up your metabolism (this assumes chronic low level exposure). To cut a long story short: The study at hand clearly suggests that someone without pre-existing health problems, a young man or woman in the prime of your life, won't risk becoming diabetic during the exam preparations or during any other period in his / her life, where he / she has to reduce the habitual and natural sleep durations by 90min for a <1 month in order to cope with external circumstances he or she has no bearing on.

    Bottom line: Now, does this mean that we have been overrating the importance of sleep hygiene before? Certainly not. What we may have underestimated, however, are short-term compensatory effects which allow for a brief, but non-negligible time window, in which neither the acute very short-term effects - nor the chronic (very) long-term effects of sleep deprivation will harm you. And though we don't know anything about the size of this window, one thing appears to be certain: It's large enough for exam preparations, but not for years of drinking, partying and doing all sorts of things but sleeping ;-)

    References
    • Robertson MD, Russell-Jones D, Umpleby AM, Dijk DJ. Effects of three weeks of mild sleep restriction implemented in the home environment on multiple metabolic and endocrine markers in healthy young men. Metabolism. 2012 Sep 15.

    10h of Catch-Up Sleep Can Ameliorate the Negative Effects of Sleep Restriction on Insulin Sensitivity in Healthy Men

    Can you partly redeem your sleep dept on the weekend? First study to investigate this question in clinical trial suggests: Yes you can! At least to a certain extent.
    In today's installment of the short news I am going to take a closer look at the surprising results of a recent study from the University of Sydney (Killick. 2015). A study which may offer some relief to those of you who are for one reason or another not getting enough sleep on a regular basis.

    If that sounds like you, you may be interested to hear what happened to the healthy male 18-50-year old subjects in the latest study from the University of Sydney. A study the objective of which was to determine whether the ill effects of acute sleep restrictions on insulin sensitivity in healthy individuals could be leveled by recovery or a few nights spend on "catch-up sleep" (10h per night).
    Learn more about the health effects of correct / messed up circadian rhythms

    Sunlight, Bluelight, Backlight and Your Clock

    Sunlight a La Carte: "Hack" Your Rhythm
    Breaking the Fast to Synchronize the Clock

    Fasting (Re-)Sets the Peripheral Clock

    Vitamin A & Caffeine Set the Clock

    Pre-Workout Supps Could Ruin Your Sleep
    To this ends, the participants underwent 2 out of 2 or 3 potential study conditions, in a randomised order, two period crossover design. The three potential study conditions were 3 weekend nights (Friday night to Monday morning) of (A) 10h time in bed (TIB) each night, (B) 6h TIB each night or (C) 10h TIB with slow-wave-sleep (SWS) suppression by acoustic stimuli (10h↓SWS) each night. Those aged ≤35 years (group 1) could be randomised to any 2 of the 3 conditions. Those >35 years (group 2) could only be randomised to Condition A (6h TIB) or Condition B (10h TIB). Men >35 years were not randomised to Condition C (10h↓SWS) because SWS is already reduced in this age group.
    "All participants underwent 2 out of 2 or 3 potential study conditions, in a randomised order, two period crossover design. The three potential study conditions were 3 weekend nights (Friday night to Monday morning) of: (A) 10h time in bed (TIB) each night, (B) 6h TIB each night or (C) 10h TIB with SWS suppression by acoustic stimuli (10h↓SWS) each night-Figure 1. Those aged ≤35 years (group 1) could be randomised to any 2 of the 3 conditions. Those >35 years (group 2) could only be randomised to Condition A (6h TIB) or Condition B (10h TIB). Men >35 years were not randomised to Condition C (10h↓SWS) because SWS is already reduced in this age group. Two separate randomisation lists for young and older men were computer-generated in blocks of 4. There was a minimum of 3 weeks wash-out between each study visit" (Killick. 2015).
    The time of lights out was calculated by the subjects' individual screening actigraphy. Subjects were only told of their lights-off time immediately prior to bed on the first evening.
    What if you can't sleep for 10h? The average effective sleeping time in the study was "only" ~9h. Since the subjects were instructed to stay in bed for a total of 10h they did however at least rest for 10h. It can thus be expected that you can achieve similar results if you "try your best" to sleep as long as possible and rest for the remaining hours. That being said without sleeping in a pitch black room and/or with blindfolds and earplugs only teenagers and adult drunkards will be able to effectively SLEEP for 10h, I suppose.
    They were instructed that if they woke prior to lights on, they should remain in bed attempting further sleep until the lights were switched on.
    Figure 1: Overview of the study design from the original publication (Killick. 2015).
    The parameters the scientists investigated (a) the main outcome, insulin sensitivity that was measured in the morning following the 3rd intervention night by minimal modelling of 19 samples collected during a 2 hour oral glucose tolerance test, as well as (b) auxiliary outcomes, namely glucose, insulin, c-peptide, leptin, peptide YY, ghrelin, cortisol, testosterone and luteinising hormone (LH) which were measured in the fasted state on a daily basis.
    Figure 2: Insulin sensitivity, glucose uptake, glucose & insulin AUC after meals (Killicks. 2015).
    Much to my own surprise, the researchers found that 3 nights of catch up sleep lead to significant increases in insulin sensitivity compared to sustained sleep restriction. That's still not optimal, but the results clearly indicate that getting enough sleep on the weekend could ameliorate, but not abolish the detrimental effects of sleep restriction from Monday to Friday.

    This conclusion is supported by the changes of the previously mentioned auxiliary variables: Fasting insulin, c-peptide, HOMA-IR, HOMA-β, leptin and PYY all decreased with ‘catch-up’ sleep, while the marker of insulin sensitivity QUICKI and the proanabolic male hormone testosterone increased. The attempt to decreases slow-wave-sleep via acoustic stimuli, on the other hand did not have significant effect on the insulin sensitivity of the subject.
    Figure 3: The ill effects of sub-chronic (=days of) sleep restriction are undebatable. The increase in fasting insulin, HOMA-IR and QUICKI insulin sensitivity in the fasted state can however be ameliorated if you manage to get enough sleep on the weekend or the days after party nights / nights at the office, clinic or the lab (Killicks. 2015).
    Bottom line: While the study at hand demonstrates that "catch up sleep", i.e. sleeping longer (10h) on the weekends in order to compensate for a lack of sleep (6h) reduces the impact of sleep reduction on insulin sensitivity, two things should be noted: (A) An amelioration is not a negation. In other words: Just because you get more than enough sleep on the weekend you will not avoid the negative impact of sleeping only 6h instead of the recommended 7-8h everyday. (B) A closer look at the data does yet also reveal that in the short runhealthy individuals are still able to keep their postprandial glucose levels (Figure 3, left / bottom) steady even if they don't get enough sleep.

    Practically speaking, we can thus conclude: (1) An extended night of quality sleep may ameliorate the negative effects of the last party nights; (2) the acute effects of sleep restrictions won't turn you into a type II diabetic; (3) the chronic effects of sleep restriction should still not be underrated | Comment on Facebook!
    References:

    • Killick, Roo, et al. "Metabolic and hormonal effects of ‘catch‐up’sleep in men with chronic, repetitive, lifestyle‐driven sleep restriction." Clinical Endocrinology (2015).