Capsaicin - 2.56mg to Keep Your Metabolism Running on a Diet. Cold Thermogenesis - 5°C for 6kcal/h. Mobile Phones - 0.853 W/kg Pulsed EMR to Mess Up Neurotransmitters

You don't have to worry, the "guidelines" do not require you to perform either your 150 minutes of moderate cardio, or your 75 minutes of vigorous-intensity aerobic activity, and not even your two weekly full-body workouts in these shorts.

24% that's the SuppVersity Figure of the Week and it is actually not so low as I would have expected it to be, after all those 24% describe the ratio of US adults who meet the Physical Activity Guidelines for muscle-strengthening physical activity. Which guideline? Ah, you are the US guys and gals, so you should know that you are advised to

"perform muscle-strengthening activities that are moderate or high intensity and involve all major muscle groups on 2 or more days a week, because these activities provide additional health benefit" (2008 Physical Activity Guidelines for Americans)

Additional benefit? Well, it goes without saying that the 150 minutes of moderate aerobic training and the reduction of salt, as well as the use of healthy vegetable oils are the primary object for every 'true American'.

Not That Hot: Cold Thermogenesis

Figure 1: An avg. effect size of 6kcal/h, non-responders + "negative-responders"; it doesn't work for those past the 30y mark - how on earth is cold thermogenesis going to help us solve the obesity pandemic?

(Chen. 2013) In a single-blind, randomized crossover intervention 24 volunteers (14 men, 10 women) were exposed to a 5°C temperature reduction (from 24°C to 19°C). During that treatment they wre sitting in a whole-room indirect calorimeter to measure their energy expenditure and lay in a positron emission tomography (PET) scanner afterwards (results, see image to the right).

Now, based on previous SuppVersity articles on the matter, you'll know that it is not exactly easy to find people who actually harbor a "significant" (and in this case this means "any at all") amount of metabolically active brown adipose tissue to get the thermogenesis going.

And with 23cm³ and 35cm³ for the men and women participating in the study at hand, the amount of the "good fat" they were carrying around is still pretty stingy. No wonder ...

• there was no thermogenic response in the male participants, but a
• 10% increase in energy expenditure in the female participants

I already see your eyes glow in the cold, ladies, but you crow too soon - those 10% were 6kcal/h, I repeat in full words "six additional calories per hour". Or roughly as much energy as a single set of body weight squats would be burning .

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If you are looking to shed 18% fat in 21 days, increase your health and your physical appearance, turn up the heat during your workouts, clean up your diet and don't move into the fridge (learn more)!

Bottom line: Against the background that there were neither significant changes in the hormonal profile (thyroid, adrenal, etc.) and considering the fact that the effect declined with age and was hardly measurable for 5 and negative (=lower energy expenditure in the cold) for 4 subjects, I stick to previous assessment: cold thermogenesis as a means of "expending more energy to get rid", is about as stupid as the whole concept of expending more energy to lose fat and it certainly does not, as the scientists state "represent a novel environmental strategy in obesity treatment".

If you want a "environmental strategy in obesity treatment", ban all the junkfood, switch off the elevators, hand out bikes and increase the health insurance cost for everyone who refuses to get his or her ass off the couch on a regular bases. Zealous? Unrealistic? Yeah, it is - but not more unrealistic than the hilarious notion that cooling the overweight majority of the inhabitants of the Western Obesity Belt down by 5°C would solve the obesity problem.

Mobile phones mess with neurotransmitter levels

Andreassen et al. have already developed a "Facebook Addiction Scale" and found that Facebook junkies tend to be

neurotic and extraverted, but lack a reasonable amount of conscientiousness (Andreassen. 2012)

(Aboul Ezz. 2013) I am well aware that many of you don't want to hear this and will discard the results researchers from the Cairo University present in their latest paper in the European Review forMedical and Pharmacological Sciences as "just another worthless rodent study" and I freely admit, you may be right.

It is well possible that rodents are more susceptible to the pulsed electromagnetic radiation from mobile phones than humans are, but I gather you will have to agree that the chance that there are still residual effects in human beings is by no means zero... and based on my personal observations, I would even argue that you see certain abnormalities in mobile phone junkies, already. Ok, those could have psychological and behavioral roots, but ...

Before I digress even further into the abyss of the "I cannot live without my mobile" virus that has already befallen many of my real world students, let's rather take a look at the outcome of Aboul Ezz et al.'s latest experiment.

Table 1: While the first six are actually the TOP (=low SAR) phones that are currently on the market, the others are random picks of mine from the data on SARdatabase.com

In the course of the latter, the scientists exposed a group of adult rats to the pulsed electromagnetic radiation of a mobile phone having a power density of 0.02W/cm² and an average specific absorption rate (the notorious SAR-value) of 0.843W/kg for 1h/day (that happens to be a little less of what your neat iPhone5 is pumping into your brain day in and day out) and measured the monoamine levels after one, two and four months, as well as on a follow-up one month after the last exposure and found:

The exposure to EMR resulted in significant changes in DA [dopamine], NE [norepenephrine] and 5-HT [serotinine levels] in the four selected areas of adult rat brain" (Aboul Ezz. 2013)

And the Egyptian researchers add, these chance could well explain the adverse effects that have been reported in conjunction with chronic "low level" exposure to pulsed electromagnetic radiation, which are usually related to memory problems and chronic stress.

What they don't mention in the abstract though is that the changes were not really consistent. It appeared as if there was some cyclicity involved with an initial increase in 5HT, a concomittant decrease in dopamine a newly established "balance" between the two leading to an increase in norepinephrine (=chronic stress) in months four.

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Bottom line: That being said, I can only repeat that even in the absence of direct physiological effects of the EMR exposure, the constant state of "being available" to whoever wants to reach you, as well as the addictive potential of being in contact with all your (often fake) facebook friends alone should be reason enough to re-evaluate your own mobile phone use.

Capsaicin keeps fatty acid oxidation & total energy expenditure up, when you're dieting

No this is not Liza Oz after taking Mehmet's beloved RK supplements - and it is not one of the subjects from the "Kitchen Sink Approach to Fat Loss study"... although, who knows? (learn more about that study)

(Janssens. 2013) Right from the Department of Human Biology, School for Nutrition, Toxicology and Metabolism (NUTRIM) at the Maastricht University in The Netherlands comes a new study that confirms that capsaicin a long-touted "fat burner" and anti-obesity agent  that's also turning up your heat, when you consume hot peppers, will maintain your energy balance and fatty oxidation rates in the normal zone, when you are dieting.

The 15 healthy Caucasian subjects underwent four 36 h sessions in a respiration chamber, which allowed the scientists to accurately measure their energy expenditure, the ratio of glucose / fat oxidation and blood pressure after receiving a dose of 2.56mg (1.03g of red chili pepper worth 39,050 Scoville heat units (SHU)) with every meal.

Now, this wouldn’t be something we have not seen in previous studies, already. With the study at hand, however, the capsaicin intake, was not the only controlled variable. In addition to simply checking what happens, when you consume one serving of capsaicin with each meal, the scientists also assessed the influence of the baseline energy intake of the subjects, with them being randomly assigned to receive adequate amounts of energy (= 100% of the daily energy requirements), or a calorically reduced diet (=75% of the daily energy requirements) during the tests.
 
The first noteworthy observation the scientists made is the adaptiation induced amelioration of the energy deficit. Contrary to what the simply calories in vs. calories out equation would suggest, the participants who received 25% less energy than they would need ended up having an effective energy deficit of only 20.5% - in other words, the missing 4.5% were simply conserved by the dreaded metabolic downregulation that’s one of the most important reasons for weight loss plateaus.

Figure 2: Changes in energy expenditure at rest, during sleep in response to food intake and activity, as well as substrate oxidation in 15 healthy Caucasian subjects (seven women, eight men) during the supplemented (CAP) and non-supplemented (PLA) energy sufficient (100) and restricted (75) conditions (Janssens. 2013).

Now this is where the capsaicin comes into play, as the results of the study at hand clearly demonstrate, the additional provision of 2.56 mg of the hot spice with every meal can negate the reduction in diet-induced thermogenesis and restore the lowered sleeping metabolic rate the 25% caloric reduction has brought about.

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Suggested read for those looking to stacking different ingredients to propel their weight loss efforts: "Forgotten Dieting Aids: Choline, Carnitine, Caffeine and the Anti-Weight-Loss Plateau Effects of Sugar and Phosphates" (read more)

Bottom line: In view of the fact that the capsaicin supplement also increased the fat oxidation during both the calorically reduced and the normal dieting conditions, it may in fact be that we've hot a pretty "hot" fat burner here... unfortunately, just with any other "fat burner", you still got to give your body the chance to actually burn the fat. Without sweat and a slightly reduced energy intake (25% does by the way make a good rule of thumb) this is yet not going to work.

Moreover, it is also questionable, whether the effects will be that noticeable after 1-2 weeks of chronic usage. I'd bet money they will either disappear completely or be drastically reduced, but that would be the topic for another study ;-)

All that's left are... *drumrolls* the Facebook news and an awesome weekend!

You know what's coming now, right? Correct, first I will enumerate a couple of Facebook News you may or may not have seen on the SuppVersity Timline (ha! I did not write "wall", am I now going to be rewarded, Mark Zuckerberg?)

• SuppVersity Highly Suggested Read - Part II of Sean Casey's summary of the ISSN conference | read more...
• Science for Science Sake - In the current scientific environment many scientists turn to biased reporting, intrinsically flawed study design & the like to produce "break through" results that are at best irrelevant, in the worst case threaten the live of participants in follow up studies | learn more... 
• Moderate Drinking Probably Lacks Life-Extending Effects - Sociologists argue: The lifestyle and not the booze of moderate drinkers is what prolongs their lives | learn more...
• Barefoot Running is Good for Your Knees: Take your shoes off to reduce patellofemoral joint stress during running | read more ...
• Can Supplements Precipitate Headaches? At least in a recent study from China the researchers observed correlations between isoflavone-supps in men and B-complex, vitamin C and green algae supplements in women | read more...

And afterwards I am telling you to have a nice weekend and reminding you of the fact that Sunday is no "off day" here at the SuppVersity ... although, for many of you it appears to be, which is why I am actually thinking about dropping the Sunday posts completely. Whatever... enjoy your weekend!

References:

• Aboul Ezz HS, Khadrawy YA, Ahmed NA, Radwan NM, El Bakry MM. The effect of pulsed electromagnetic radiation from mobile phone on the levels of monoamine neurotransmitters in four different areas of rat brain. Eur Rev Med Pharmacol Sci. 2013 Jul;17(13):1782-8.
• Andreassen CS, Torsheim T, Brunborg GS, Pallesen S. Development of a Facebook
  Addiction Scale. Psychol Rep. 2012 Apr;110(2):501-17.
• Chen KY, Brychta RJ, Linderman JD, Smith S, Courville A, Dieckmann W, Herscovitch P, Millo CM, Remaley A, Lee P, Celi FS. Brown fat activation mediates cold-induced thermogenesis in adult humans in response to a mild decrease in ambient temperature. J Clin Endocrinol Metab. 2013 Jul;98(7):E1218-23. 
• Janssens PL, Hursel R, Martens EA, Westerterp-Plantenga MS. Acute effects of capsaicin on energy expenditure and fat oxidation in negative energy balance. PLoS One. 2013 Jul 2;8(7):e67786.
   

Coffee - 3 Cups Per Day Keep Insulin at Bay: You Better Start Today if You Want to Retain Your Insulin Sensitivity, and Stay Cancer & CVD Free Beyond Your Own Centennial!

I am not entirely sure how often I have used the sentence "consistency is key", here at the SuppVersity, but there is no way I don't reiterate it in the context of the never-ending debate over the pros and cons of habitual coffee drinking, once again. While much of the experimental evidence would suggest that coffee, or to be precise, caffeine the major methylxanthine in the brown brew is a bad sympathetic nervous system activator that stresses your body and will deteriorate your glucose and fat metabolism, the majority of the epidemiological evidence points into the exact opposite direction.

A paper that's going to be published in the next issue of AGE the Journal of the American Aging Association could however help not just to bridge the widening gap between the ever-increasing number of epidemiological studies showing between moderate caffeine consumption and metabolic, cardiovascular, neurological, and cellular health (see list at the end of this post) and the conflicting evidence from experiments that investigate the acute response to caffeine ingestion in both caffeine-naive individuals and habitual caffeine consumers.

Consistent caffeine consumption is the key to "chronic health" ;-)

I am pretty sure this study won't close the lit on the never-ending debate about the pros and cons of caffeine consumption - mostly because it's a rodent study, but also in view of the fact that there is no definite border between "habitual consumption" and "chronic abuse", when it comes to a substance the stimulating side-effects of which can keep you functioning (and training!), when your body would otherwise long have called a halt.

Against that background it is important to realize that the rodents in the study at hand were leading a happy, more or less stress-free life. They consumed what you would consider a "healthy" diet for a rodent and had free access to a wheel, the average male and female Wistar who has neither television, nor Internet or a PlayStation in his or her cage, will actually make good use of.

Figure 1: Body weight (in g), visceral fat weight (in g/kg body weight) and skeletal muscle glucose transporter 4 expression (GLUT4 activity relative to glucose breakdown) over the course of 24 months with or without the provision of the human equivalent of caffeine of roughly 3 cups of coffee in the drinking water (data based on Guarino. 2012)

Accordingly, you should not wonder, let alone be disappointed that there is no magical "fat destruction" such as the one we've seen about a months ago in the CLA-study (see "CLA Destroys Body Fat: Effect Borders Pathological Lipodystrophy!"). Remember: Consistency is key! And some of the benefits of today's coffee may not show before you are in your late 70s... but let's get back to the results data from figure 1 and their implications for your current and future health:

Additional observations:

• the decrease in visceral fat mass was not due exclusively to increased lipolysis
• the increase in insulin sensitivity induced by caffeine was not attributable to weight loss, increased NO production, caffeine-mediated antioxidant effects, decreased cortisol levels, or decreased SNS activity
• caffeine intake did not modify blood pressure, endogenous NO production, or antioxidant capacity in aged animals 
• caffeine administration restored Glut4 expression in the elderly group, but it was not able to increase Glut4 expression above amaximal level in the 12Mgroup

• the rodents were kept on a normal diet, a healthy body weight is thus only a sign of overall metabolic health (remember: skinnier does not equal healthier!),
• the 42% lower visceral fat levels in what would be middle aged rodents (12 months) is one of the most significant predictors of healthy aging (optimal brain and metabolic health + no cancer), and
• the maintenance of skeletal muscle GLUT4 expression is of fundamental importance to ward of those increasingly common "age-related" diseases of which we already know that they are at least precipitated by insulin resistance and high glucose levels, such as Alzheimer's and "regular" dementia (e.g. Rönnemaa. 2008; Accardi. 2012; Williamson. 2012)

Against the background of the previously mentioned conflict between experimental (caffeine induces stress and thwarts glucose and fatty acid metabolism) and epidemiological (caffeine correlates with metabolic health) evidence it is also important to mention that these beneficial effects were not negated by the dreaded stress-induced increases in non-esterified fatty acids (NEFA), which is the most commonly heard argument of the opponents of caffeine / coffee consumption. On the contrary, the ...

"[...] increase in insulin sensitivity induced by caffeine was not attributable to weight loss, increased NO production, caffeine-mediated antioxidant effects, decreased cortisol levels, or decreased SNS activity [so that caffeine effectively] restored [otherwise elevated] circulating NEFA in aged animals to values observed in young 3 M control rats." (Guarino. 2012)

In the absence of increased NEFA levels, an increased sympathetic tone (=higher catecholamine and cortisol levels) and in the presence of optimal GLUT-4 expression and low visceral fat levels in the young and middle aged rodents, there is actually no reason why we would see any of the putative negative effects on glucose metabolism of about which you will probably have read and heard numerous times in the laypress.

Figure 2: Glucose clearance during ITT (in % glucose/min), basal plasma and insulin levels (in mM) over the course of 24 months (basically one rodent lifespan) with or without the provision of the human equivalent of caffeine of roughly 3 cups of coffee in the drinking water (data based on Guarino. 2012)

And, as a matter of fact, the data in figure 2 does confirm just that: The chronic administration of caffeine at a dosage of which the researchers state, that it will generate plasma caffeine levels "comparable to those in moderate to low consumers of caffeinated beverages" (Guarino. 2012), i.e. people who drink about 3 cups of the delicious brew per day (300-500mg caffeine; Gasio. 2002), is probably one of the most delicious and convenient ways to ward off age-related declines in glucose tolerance... this does yet not mean that drinking coffee (let alone Coke or energy drinks) could make up for a sedentary lifestyle and (ab-)using caffeine pills and stims to keep functioning will probably even have the opposite effects.

Glucose management figures everywhere and so does coffee!

Did you know that the data from a recently published trial suggests that "14-day caffeine supplementation [at 5mg/kg body weight] can probably decrease exercise-induced inflammatory response (CRP elevation and Leukocytosis) following 30 min downhill running in male non-athletes" (Jafari. 2012)? That's actually pretty intruiging, as it shows that the already mentioned differences between the chronic and acute effects of trimethylxanthie aka caffeine are not restricted to its effect on overall and metabolic health, especially as, caffeine has hitherto not exactly been known as a an ergogenic the effects of which build up over time... in fact, rather the opposite is usually assumed, although the evidence for the decline of the ergogenic (not the stimulant!) effects of caffeine are still inconclusive.

In view of the major role of glucose management in all sorts of the metabolic, endocrine and neurcrine diseases, it is thus no wonder that study after study finds beneficial effects of moderate caffeine consumption on...

• risk of heart failure (Mostofsky. 2012)
• perceptibility to arrhythmia (Klatsky. 2011)
• venous thromboembolism (Enga. 2011)
• general cardiovascular disease (Bøhn. 2012)
• dementia & Parkison's (Cao. 2012; Campdelacreu. 2012)
• diabesity (Hjellvik. 2011; Matsuura. 2012)
• pancreatic cancer (Dong. 2011), as well as 
• bladder, breast, buccal and pharyngeal cancer (Yu. 2011) 
• colorectal, endometrial, esophageal cancer (Yu. 2011) 
• hepatocellular, leukemic, and prostate cancers (Yu. 2011)

And though, I could certainly extend this list by a dozen or so references for each item and half a dozen additional items, I guess I'd rather end today's blogpost on the note that coffee (and tea) contain way more than just caffeine. I would therefore suggest you don't rely on caffeine alone, but rather grab yourself an old-fashioned black cup of coffee (ad some creme if you can't stand it black, or coconut oil, if you like that better) and the time it takes to savor the aroma and taste of it... I can guarantee: That will exponentiation its health effects and will allow you to catch up on the 5 minutes you may have lost in no time.

References:

• Accardi G, Caruso C, Colonna-Romano G, Camarda C, Monastero R, Candore G. Can Alzheimer disease be a form of type 3 diabetes? Rejuvenation Res. 2012 Apr;15(2):217-21.
• Bøhn SK, Ward NC, Hodgson JM, Croft KD. Effects of tea and coffee on cardiovascular disease risk. Food Funct. 2012 Jun;3(6):575-91.
• Campdelacreu J. Parkinson disease and Alzheimer disease: environmental risk factors. Neurologia. 2012 Jun 13.
• Cao C, Loewenstein DA, Lin X, Zhang C, Wang L, Duara R, Wu Y, Giannini A, Bai G, Cai J, Greig M, Schofield E, Ashok R, Small B, Potter H, Arendash GW. High Blood caffeine levels in MCI linked to lack of progression to dementia. J Alzheimers Dis. 2012;30(3):559-72.
• Dong J, Zou J, Yu XF. Coffee drinking and pancreatic cancer risk: a meta-analysis of cohort studies. World J Gastroenterol. 2011 Mar 7;17(9):1204-10.
• Enga KF, Braekkan SK, Hansen-Krone IJ, Wilsgaard T, Hansen JB. Coffee consumption and the risk of venous thromboembolism: the Tromsø study. J Thromb Haemost. 2011 Jul;9(7):1334-9.
• Gasior M, Jaszyna M,Munzar P,Witkin JM, Goldberg SR. Caffeine potentiates the discriminative-stimulus effects of nicotine in rats. Psychopharmacology (Berl). 2002; 162:385–395 
• Guarino MP, Ribeiro MJ, Sacramento JF, Conde SV. Chronic caffeine intake reverses age-induced insulin resistance in the rat: effect on skeletal muscle Glut4 transporters and AMPK activity. Age (Dordr). 2012 Sep 14.
• Hjellvik V, Tverdal A, Strøm H. Boiled coffee intake and subsequent risk for type 2 diabetes. Epidemiology. 2011 May;22(3):418-21.
• Jafari A, Kherad N, Melekirad AA. Effect of short-term caffeine supplementation on downhill running induced inflammatory response in non-athletes. Journal of Cell. Winter 2012; 2(4):377-385
• Klatsky AL, Hasan AS, Armstrong MA, Udaltsova N, Morton C. Coffee, caffeine, and risk of hospitalization for arrhythmias. Perm J. 2011 Summer;15(3):19-25.
• Matsuura H, Mure K, Nishio N, Kitano N, Nagai N, Takeshita T. Relationship between coffee consumption and prevalence of metabolic syndrome among Japanese civil servants. J Epidemiol. 2012;22(2):160-6.
• Mostofsky E, Rice MS, Levitan EB, Mittleman MA. Habitual coffee consumption and risk of heart failure: a dose-response meta-analysis. Circ Heart Fail. 2012 Jul 1;5(4):401-5. Epub 2012 Jun 26.
• Nature.com Reviews. Heart failure: Moderate coffee consumption linked with reduced risk of HF. Nat Rev Cardiol. 2012 Jul 17;9(9):492.
• Rönnemaa E, Zethelius B, Sundelöf J, Sundström J, Degerman-Gunnarsson M, Berne C, Lannfelt L, Kilander L. Impaired insulin secretion increases the risk of Alzheimer disease. Neurology. 2008 Sep 30;71(14):1065-71.
• Williamson R, McNeilly A, Sutherland C. Insulin resistance in the brain: An old-age or new-age problem? Biochem Pharmacol. 2012 Sep 15;84(6):737-45.
• Yu X, Bao Z, Zou J, Dong J. Coffee consumption and risk of cancers: a meta-analysis of cohort studies. BMC Cancer. 2011 Mar 15;11:96.

Cold Thermogenesis - A Safe Ephedra Alternative? 70kcal Increase in 24h Energy Expenditure is Negligible, 50% Lower Than Ephedrine - Not Worth the Torture, Bro!

Image 1 (odditycentral): Jin Songhao, one of China’s most seasoned icemen and not exactly as lean as you may expect based on what you currently read around the blogosphere, managed to beat the previous world record for the longest ice bath - 120min! Congrats, Jin!

Ephedrine for years the go-to OTC fat burner for physique athletes and average Joe's and Jane's alike is no longer (officially) available: No matter how bold the label claims about X mg of "ephedra extract" may be - NONE(!) of the currently available "ephedra based" over-the-counter (OTC) fat-burners contains significant amounts of the active alkaloids, which made the old Mua huang based herbal ephedra products so effective. Against that background, dieters are constantly on the look-out for novel "gimmicks" to help them finally get rid of those annoying love-handles. One of those gimmicks, which has caught quite some attention as of late, is called "cold thermogenesis" and revolves around the idea that our bodies should consume more energy to keep a normal body temperature in a cold, compared to a normal temperature environment.

How is that different from a "thermogenic fat burner"

The most obvious difference between cold thermogenesis and "thermogenic fat burners" is actually so straight forward that I hardly dare stating that the former is induced by exposing yourself to low(er than normal) temperatures, while the promise of the latter is that the various ingredients of currently or formerly available OTC "fat burners" will induce a thermogenic response, irrespective of the current ambient temperature.

Figure 1: Antropomorphic data of the study participants (Cypess. 2012)

The results of a recently published study from the the Boston Harvard Medical School does yet provide somewhat more sophisticated insights into the differences between cold exposure and a sympathomimetic (i.e. an activator of the sympathetic nervous system), such as ephedrine. On three separate, independent study visits that took place in random order the ten healthy volunteers (age 27.1 years) who participated in the study (see figure 1 for DEXA based anthropometric data) and had been fasting since 12am the day before were exposed to one of the following "stimuli":

• ephedrine - a single intramuscular dose of 1mg/kg ephedrine
• saline control - an equal volume of saline
• cold exposure - in a surgeon’s cooling vest (Polar Products) w/ water temperature 14 °C

60min after the injection of ephedrine, saline, or the initiation of cold exposure, the change in metabolic rate was measured and blood was drawn to determine several metabolic and endocrine markers. Another 60min later, PET-CT scanner images (cf. figure 2, right) to quantify BAT mass and activity were taken. Since the participants obviously had to get rid of their cooling vests for this procedure, the total cold exposure time was limited to 120min, so that it is questionable how valid the 24h energy expenditure calculation (cf. figure 3) actually is. After all, it is not very likely that the norepinephrine levels would constantly stay at 200% over baseline (cf. figure 2).

Figure 2: Metabolic and endocrine effects (expressed relative to saline) of ephedrine injection and cold exposure (main image); CT scans with green arrows in the combined scans indicating  the principal cervical, supraclavicular,
and thoracic depots of BAT (Cypess. 2012)

As far as the acute phase is concerned, it is yet quite obvious that both cold exposure and ephedrine elicited statistically significant effects on various metabolic and endocrine parameters. The exact nature and the purported mechanism that is responsible for these metabolic and endocrine effects are however very different for both treatments:

• while ephedrine lead to an increase in blood glucose (probably subsequent to increased glyconeogenesis), cold exposure did not 
• while ephedrine lead to significant increases in lactic acid levels (corresponding to increases in glucose + glucose oxidation), cold exposure did not
• while ephedrine lead to profound increases in β-hydroxybutyrate (increased ketone productions from fat), cold exposure did not
• while ephedrine increased serum non-esterified fatty acid (NEFA) concentrations (due to increased lipolysis), cold exposure did not
• while ephedrine elevated insulin production (probably due to stress induced insulin resistance), cold exposure did not (p = 0.29)
• while ephedrine lead to highly significant (p < 0.001) increases in C-reactive peptide, cold exposure elicited "only" significant elevations (p = 0.005)
• while ephedrine produced already highly significant increases in noripenephrine levels, those were even more pronounced upon cold exposure
• while ephedrine lead to statistical significant increases in thyroid hormone Total T3 (+14%, p = 0.026) and Free T4 (+19%, p = 0.014), cold exposure did not
• while ephedrine lead to a profound (-22%) and statistical significant (p = 0.007) drop in ghrelin ("hunger hormone" and metabolic regulator), cold exposure did not

In conjunction with the combined CT scans from figure 2 these differences clearly indicate that contrary to ephedrine, which is a mere sympathomimetic (put simply a potent "stim" ;-) without depot-specific (here brown adipose tissue) thermogenic effects, mild cold exposure (remember: those were no ice-baths!) has the ability to stimulate brown adipose tissue (BAT) energy expenditure without significant systemic effects on heart rate or thyroid hormone metabolism.

What does that mean? Is GNC soon going to carry cooling vests instead of fat burner pills?

If you read the scientists' rave conclusion that "[i]n contrast to ephedrine [...] mild cold exposure stimulates a specific response by the SNS [sympathetic nervous system] to activate BAT and increase energy expenditure with few other metabolic effects" and their subsequent reference to the "obesity and diabetes pandemics" and the demand for "safe and novel treatments" of the latter, it is quite understandable that people who are referred by their gurus to "scientific evidence" like this are willing to believe that "cold thermogenesis" would help them to finally get rid of their beer-, burger- and burrito-bellies.

Figure 3: Increase in 24h energy expenditure (kcal/day, left) and detectable BAT volume (right; Cypess. 2012)

If you do yet take a look at the actual metabolic effects (cf. figure 3) the 2x more pronounced effect of ephedrine on 24h energy expenditure (+140kcal/day vs. 70kcal) confirms what my previous overview of the metabolic and endocrine effects of ephedrine and cold exposure already suggested: Ephedrine does not simply have more "side effects" it is also more effective.

Figure 4: Activity of BAT activity in relation to body fat levels (van Marken Lichtenbelt. 2009)

Important:  One thing the scientists wink at in both the abstract as well as the conclusion are the profound inter-individual differences in terms of detectable BAT volume and activity. While the median volume of detectable brown adipose tissue in men and women was 22mL and 20mL, respectively, there was one female subject with a BAT mass of 190mL (85x over median!), one with 7ml and one woman without any detectable brown adipose tissue. Similarly, the BAT mass in the men ranged from 46mL to 12mL. Both the existence of individuals without any significant amounts of metabolically active body fat, as well as the observation of high inter-personal variability in the study at hand stand in line with previous results of Saito et al. who found a ratio of 15/32 (45%) non-responders in young (23-35y) and 22/24 (92%!) in older (38-65y) subjects (Saito. 2009). And as if that alone would not render the practical value of cold exposure as a means to battle the "obesity and diabetes pandemic" questionably enough, van Marken Lichtenbelt et al. report that exactly those people for whom ephedrine and other sympathomimetics such as sibutramine would actually pose a non-negligible health risk, i.e. obese and metabolically deranged people, don't just have 40% less brown adipose tissue, but also a -76% reduced BAT activity (van Marken Lichtenbelt. 2009; cf. figure 4). The implications of these findings should be obvious: It is a) by no means certain that sitting in a non-heated room, let alone an ice-bath, is not just going to give you a cold, but even if it works it is b) probably not going to make a difference for those people who need it most - I mean, let's do the math: "70kcal/day minus 76% of the former equals 16.8kcal per day"!

That being said, even the profoundly greater total increase in energy expenditure in the ephedrine group is of a "magnitude" (I would write "minitude" if such a word existed) that would be completely negligible if it were not for the bad and "dangerous" sympathostimulating side effects (Andraws. 2005), which will allow you to train longer, to diet harder (Astrup et al. ascribe 75% of the weight loss effect due to the ingestion of the infamous ECA stack to anorexia, i.e. loss of appetite; cf. Astrup. 1992) than any ice-filled bathtub in the world will ever do.

Skip on ice-baths, stop winning about the ephedra ban. Get your diet & workouts in check!

Image 2: I don't think Francine Sablan, IFBB Figure Pro and like Adelfo one of Myotropics' sponsored athletes, uses the air-conditioning, let alone a funky cooling vest or ice-baths to propel her fat loss. And why would she? She loves working out and she has her diet in check ;-)

I know this is not going to be a popular conclusion, but believe me, the additional +70kcal/day you could expend in the cold, if you are one of the lucky non-obese "responders" (see red box above), won't make you lose a single pound. Even the "good old" ECA stack (remember: the Cypess study used intravenously administered ephedrine; hence, the effect sizes are directly comparable with pertinent studies from the late 1980s and 1990s using orally administered herbals) worked its fat burning magic only, when it was combined with a comprehensive diet and exercise protocol - and in those scenarios it was mostly the influence of its sympathostimulating activity on your ability to adhere to your diet and to endure the hardships of strenuous workouts and not its often-touted and largely overestimated "thermogenic" effects (cf. Astrup. 1985; Astrup. 1992) that were mostly responsible for the larger-than-life results, people are still raving about.

References:

1. Andraws R, Chawla P, Brown DL. Cardiovascular effects of ephedra alkaloids: a comprehensive review. Prog Cardiovasc Dis. 2005 Jan-Feb;47(4):217-25. 
2. Astrup A, Bülow J, Madsen J, Christensen NJ. Contribution of BAT and skeletal muscle to thermogenesis induced by ephedrine in man. Am J Physiol. 1985 May;248(5 Pt 1):E507-15.
3. Astrup A, Toubro S, Christensen NJ, Quaade F. Pharmacology of thermogenic drugs. Am J Clin Nutr. 1992 Jan;55(1 Suppl):246S-248S.
4. Cypess AM, Chen YC, Sze C, Wang K, English J, Chan O, Holman AR, Tal I, Palmer MR, Kolodny GM, Kahn CR. Cold but not sympathomimetics activates human brown adipose tissue in vivo. Proc Natl Acad Sci U S A. 2012 Jun 4. 
5. van Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, Drossaerts JM, Kemerink GJ, Bouvy ND, Schrauwen P, Teule GJ. Cold-activated brown adipose tissue in healthy men. N Engl J Med. 2009 Apr 9;360(15):1500-8. Erratum in: N Engl J Med. 2009 Apr 30;360(18):1917.
6. Saito M, Okamatsu-Ogura Y, Matsushita M, Watanabe K, Yoneshiro T, Nio-Kobayashi J, Iwanaga T, Miyagawa M, Kameya T, Nakada K, Kawai Y, Tsujisaki M. High incidence of metabolically active brown adipose tissue in healthy adult humans: effects of cold exposure and adiposity. Diabetes. 2009 Jul;58(7):1526-31. Epub 2009 Apr 28.

Date Palm (Phoenix dactylifera) as a Natural Test Booster and Ergogenic

A very recent study (Saddiq. 2010) published in the Journal of the International Society for Horticultural Science found that the seeds of Phoenix dactylifera can raise testosterone, norepenephrine (NE), dopamine (DA) and GABA levels and may counteract the negative effect of prednisolone administration in rats.

[...] the daily oral administration of pits of date palm caused the maximal increase in NE, DA and GABA content that was found in the brain stem after 2 weeks. The daily oral administration of methylprednisolone caused a decrease in NE, DA and GABA content found in the brain stem after 2 weeks. Moreover, the daily oral administration of pits of date palm and methylprednisolone caused an increase in NE content found in the brain stem after 2 weeks. The daily oral administration of pits of date palm and methylprednisolone caused a significant increase in testosterone level in serum blood of male albino rats.

While all this sounds promising, further studies would have to clarify whether it needs the cortisol-like effects of prednisone for the testosterone-boosting effect of the date seeds to take place or whether taking adequate amounts of pits of date palm would provoke similar (or even superior) increases in testosterone in rats and, most importantly, in men. Be that as it may, even the increase in neurotransmitters (NE, DA, GABA) certainly could provide real-world benefits for athletes, as well as people suffering from fatigue.

Pseudo-Ephedrine Improves Cycling Performance in Trained Athletes

As Wikipedia knows, other than its banned brother "real" ephedrine, "pseudoephedrine sulfate are found in many over-the-counter preparations either as a single ingredient or, more commonly, in combination with antihistamines, guaifenesin, dextromethorphan, paracetamol (acetaminophen), and/or NSAIDs." With these medications being readily available from the average Athlete's poison cabinet, it might be of particular interest, that Pritchard-Peschek et al. (Pritchard-Peschek. 2010) found that ingestion of 180 mg of pseudoephedrine (PSE) had immediate positive effects on cycling time-trial (TT) performance in six well-trained male cyclists and triathletes (age 33 ± 2 yr, mass 81 ± 8 kg, height 182.0 ± 6.7 cm, VO2max 56.8 ± 6.8 ml · kg–1 · min–1; M ± SD):

PSE improved cycling TT performance by 5.1% (95% CI 0–10%) compared with PLA (28:58.9 ± 4:26.5 and 30:31.7 ± 4:36.7 min, respectively). There was a significant Treatment × Time interaction (p = .04) for NE, with NE increasing during the PSE trial only. Similarly, blood glucose also showed a trend (p = .06) for increased levels postexercise in the PSE trial.

Apart from its positive effect on exercise performance, the increase in norepinephrine will also effect substrate metabolism by freeing fatty acids for the use as substrate for muscle activity. In that sense, pseudoephedrine appears to work similar to its brother ephedrine. Whether it would be a good weight loss tool, would yet still have to be investigated.

Decreased Catecholamine Release in Obese Individuals: Another Weight Loss Obstacle

Jabbour et. al. (Jabbour. 2010) found that the exercise induced stress response in obese individuals is significantly reduced. The amount of catecholamines released in the course of 6 x 6sec maximal sprints with 2 min of passive rest between each repetition, was significantly lower in the 11 normal-weight adolescent boys compared to their 9 obese (body fat: 31.0 +/- 3.0%) and 11 overweight (body fat: 24.0 +/- 1.9%) age-mates:

Maximal epinephrine concentration was significantly (p<0.05) higher in lean vs. obese and was negatively correlated to body fat percentage (r=-0.60, p<0.05). Maximal norepinephrine values were higher in lean vs. overweight and obese and a negative relationship was found between maximal norepinephrine concentration and body fat percentage (r=-0.60, p<0.05). Maximal lactate concentration was higher in lean vs. overweight and obese (14.7 +/- 3.3, 10.4 +/- 2.7 and 10.2 +/- 2.5 mmol.l-1 in lean, overweight and obese respectively).

In view of the fact that both, epinephrine as well as its precursor, norepinephrine, are well known antagonists of alpha- and beta-receptors, which - apart from their vasoconstrictive properties - also elevate the blood sugar level by increasing hydrolysis of glycogen to glucose in the liver, and at the same time initiating the breakdown of lipids in adipocytes, this may well be another reason for obese people having an extra hard time to get rid of their extra pounds.