Tag Archives: science

What makes a scientist, a scientist?

As a university professor, I often get asked ‘what is a scientist?’ What do these geeks actually do? Fortunately, I teach a university-level Research Methods course. Thus, I have a forum for giving a somewhat elaborate response to my students. I think what’s confusing to the untrained or novel eye is that social media has witnessed a proliferation of those who claim to be ‘researchers.’ For the purpose of this article, I’ll treat ‘researchers’ and ‘scientists’ synonymously. Nevertheless, I will address the question of what exactly a scientist is. And more specifically, what a professional scientist actually does. Furthermore, I’m writing this from the standpoint of someone trained in the biological sciences because I’m not familiar with the manner in which chemists or physicists conduct ‘science.’ So to my students who have asked this question, I’ve finally put pen to paper, or more precisely, fingers to keyboard, and given you a somewhat limited answer to a rather complex question.

Key Points to Remember

Sitting in your Garanimals® while doing a PubMed search does not make you a scientist.
Being published in a peer-reviewed journal does not make you a scientist (I can see the confusion in many faces now).
Professional scientists are typically involved in a series of steps that are unseen by non-scientists. In the short run, publication is the goal of professional scientists. In the long run, if you want to make a significant impact on our field, you need to conduct original investigations (i.e., generate original data).
Conducting original investigations is the hallmark of ‘doing science.’ If you’ve never done this, then you’re not a scientist. Review papers and meta-analyses are great for giving a ‘snapshot’ of the current state of science in a given field; however, they are not original investigations. They’re summaries of other original investigations (i.e., the work of other scientists).
It is easy to criticize a study. Students in my Research Methods class are often surprised as to the ease of finding limitations in studies published in peer-reviewed journals. However, try being the PI (principal investigator) of a study. When you walk a mile in someone else’s shoes, you’ll realize that banging your keyboard in the comfort of your underwear ain’t nothing like being the PI of a study. It’s the difference between being a movie critic and someone who makes movies.
You can indeed be very good at using the scientific method in your profession (e.g., personal trainer, dietitian, etc.) without being an actual scientist. I wholeheartedly implore everyone in the fitness-nutrition fields to embrace science. It would be like embracing medicine. You don’t have to be an MD to do that.

Let me outline the typical steps that a scientist performs before you, John Q. Public, can sit in your La-Z-Boy chair and leisurely read a peer-reviewed publication. I’m coming from a background of having done both extensive animal (i.e., rodents, birds, etc) and human research.^1-7 The process is similar.

Ideation phase – this is perhaps the most fun. Why? Because it’s free and anyone can do it. In this phase, you basically come up with an experimental idea. Interestingly, these ideas can arise at any time: while sunbathing, working out, or after consuming 6 beers. For instance, my idea of coming up with the initial high protein diet (4.4 g/kg/d) arose from a random conversation with a recreational bodybuilder who admitted to eating boatloads of protein.⁸ I asked myself: “what if we just got trained guys and girls to just eat a lot of protein?” Simple enough, right? Uh no. The hard part comes after this.
Delineating the experimental protocol – now you put the pedal to the metal and write the IRB proposal (Institutional Review Board) and Informed Consent to submit to the university. If you work for a private clinical research organization or CRO, there are external IRBs that you can submit your proposal to. If you don’t like writing, you’ll hate this phase. At my university, it requires that you fill out a 20-page form. Yeah fun. Like stepping on a porcupine. I think pretty much every scientist dislikes this phase. Why? Because the folks who often review your IRB proposal are not experts in your particular field. Thus, the questions you receive regarding your protocol are often bizarre. But this is a hurdle every scientist must jump over before you initiate subject recruitment.
Subject recruitment – after getting IRB approval, which can take anywhere from 1 month (a rarity) to several months (for me, the average length is about 3 months), you subsequently initiate subject recruitment. This is perhaps one of the most misunderstood steps. First of all. It is difficult to recruit subjects for a study. In fact, getting the right subjects for a study is absolutely critical. For example, doing studies on untrained subjects is largely irrelevant to those who work with athletes. Why? Because untrained people respond to pretty much anything you throw at them. Yet many studies published in the sports sciences use untrained subjects. Why? Because the subject pool is enormous. When boneheads on Facebook lament the fact that a study has “only 20 highly trained cyclists (or any athletic group)” (meaning the sample size is ‘too small’ to be meaningful), it clearly underscores how little they know about research in general and subject recruitment specifically. Give me 20 highly trained athletes any day versus 60 untrained slobs.
Data collection – I want to clear one thing up. If a study has 40 subjects for instance, it does not mean you pre- and post-test all 40 of them on the same days. Folks don’t understand why studies often take an inordinately long time. Once you’ve recruited subjects, data collection is typically staggered. Meaning, you get subjects in the lab (or field) when you can. Sometimes pre-testing a group of subjects can cover the span of months. Moreover, data collection requires its own unique set of skills. And like any skill, if you don’t use it, you lose it. Data collection would be akin to swimming in water. Reading about data collection would be like watching someone swim. Guess which is more difficult? The critiques I see on social media often underscore how little folks know about data collection. So unless you’ve actually jumped in the water, you will never truly know what it’s like to collect data. And the studies that are the absolute most difficult to do? Dietary intervention studies (i.e., comparing ketogenic vs. low carb vs. high carb vs. any random diet). I cringe a bit when I read social media critiques of diet studies. If folks only knew how difficult it is to ‘control’ these studies then one might get a better appreciation for these kinds of investigations. And there is a trade-off between control and real-world application. The more tightly a study is ‘controlled’ (e.g., metabolic ward diet studies), the less it resembles what free-living human beings do. The less tightly a study is controlled (i.e., getting highly trained, free-living subjects to comply with an intervention), the more applicability it may have to real life. Clearly both have their pros and cons.
Data analysis – once you’ve collected all your data (the shortest time frame for collecting data that I’ve done was 1 month; the longest was > 1 year), then the fun begins: interpreting the data. This is perhaps one of the more confusing steps for scientists-in-training (i.e., grad students). You can present the same data set to a dozen scientists and you may end up with a dozen different interpretations. In fact, it may be confusing to scientists themselves. Data
interpretation requires that you have a solid background in the basic sciences (e.g., biology, chemistry, physics, math, etc). Furthermore, an extensive knowledge of the existing literature is key. Like any skill, this one requires practice, practice and more practice.
Presentation at a science conference – prior to submitting a study (in the form of a manuscript) for publication in a peer-reviewed science journal, scientists will often present their data at a science conference. For instance, the International Society of Sports Nutrition conference has some of the latest research presented in the form of poster presentations and/or tutorials. If you fear public speaking more than sharks, then perhaps science ain’t the best career for you.
Publication – writing a paper for publication is the ‘last’ step in the process. Though in actuality, each study you do will likely lead to a different experimental question which in turn leads to another investigation. The mark of an excellent scientist isn’t just the ‘answers’ they arrive at, but the questions they generate. I actually enjoy writing. It’s like the icing on the cake. Writing for scientific journals is its own unique skill. There are some individuals
who are amazing writers. Two of the very best I’ve read are Peter Lemon PhD and John Ivy PhD. Meanwhile, others are about as eloquent as a chimpanzee banging on a Mac Pro laptop. Inasmuch as English is now the language of science, English-writing skills are absolutely critical for anyone who wishes to be a published scientist.
Repeat steps 1-7

If you don’t do the steps outlined above, then you’re not a professional scientist. Anything less than the above dilutes the meaning of the word ‘scientist.’ The fact of the matter is that conducting original investigations is quite difficult. The notion that scientists can “control” all extraneous variables is very much a Sisyphean task.

But what if I’m published in a peer-reviewed science journal? Does that mean I’m a professional scientist? The simple answer to that is ‘no.’ They’ve basically skipped steps #1-7. Keep in mind that for many published papers, students and lab techs are often listed as co-authors. Does that mean they are now ‘scientists?’ Uh no. It’s like calling yourself a medical doctor because you wear a white lab coat, hang a stethoscope around your neck and watch re-runs of Grey’s Anatomy. The most important individuals listed on a scientific paper are the first and last (senior) author. The last author is typically the PI and runs the lab. The first author is often the person who does most of the data collection. Sometimes the PI is also the primary data collector. Not everyone follows this ‘rule’ so to speak. But most do. Either way, research is always a team effort. You need students, lab techs as well as your science colleagues.

You can still use the scientific method even if you’re not a scientist. You don’t have to be a scientist to be able to deftly use the scientific method in your daily life. In fact, you can be one helluva ‘thinker’ (in the scientific sense) and not be a scientist. For instance, personal trainers who use and embrace science and the scientific method are better trainers because of it. Why? Because rather than just being a parrot telling their clients what to do (because that’s what they were told when they were younger), they understand the ‘why’ of their advice. And if they don’t understand the ‘why’ of their advice, they’ll fully admit to not knowing. And that’s fine. The more you learn in this field, the more realize there’s a lot of stuff that you don’t know. The scientific method is the single most powerful way of thinking. Embrace it. Anecdotes are nice. But data trumps anecdotes.

BIO – I live in South Florida with my wife and twin daughters. I teach at Nova Southeastern University. I run the ISSN. I paddle in the ocean. I eat a lot. I have a daily beer or wine and last but not least, I worship the sun.

References

Vierck J, O’Reilly B, Hossner K, et al.: Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 2000, 24:263-72.
Antonio J and Gonyea WJ: Skeletal muscle fiber hyperplasia. Med Sci Sports Exerc 1993, 25:1333-45.
Bertocci LA, Fleckenstein JL, and Antonio J: Human muscle fatigue after glycogen depletion: A 31p magnetic resonance study. J Appl Physiol (1985) 1992, 73:75-81.
Antonio J, Wilson JD, and George FW: Effects of castration and androgen treatment on androgen-receptor levels in rat skeletal muscles. J Appl Physiol (1985) 1999, 87:2016-9.
Antonio J and Gonyea WJ: Progressive stretch overload of skeletal muscle results in hypertrophy before hyperplasia. J Appl Physiol (1985) 1993, 75:1263-71.
Antonio J and Gonyea WJ: Role of muscle fiber hypertrophy and hyperplasia in intermittently stretched avian muscle. J Appl Physiol (1985) 1993, 74:1893-8.
Antonio J and Gonyea WJ: Muscle fiber splitting in stretch-enlarged avian muscle. Med Sci Sports Exerc 1994, 26:973-7.
Antonio J, Peacock CA, Ellerbroek A, et al.: The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals. J Int Soc Sports Nutr 2014, 11:19.

Hierarchy of Evidence is Wrong

By Jose Antonio PhD FNSCA FISSN.

A pithy summary

The typical ‘Hierarchy of Evidence’ is wrong.
The gold standard in science will always be the randomized controlled trial or RCT (i.e. the original investigation).
If you truly want to change a field, you have to conduct the RCT.
Reviews and meta-analyses exist only because scientists have conducted prior RCTs.
Reviews and meta-analyses do not provide new (i.e. original data) information.
If you’re lazy, read reviews and meta-analyses.
If you’re ambitious, make sure you read RCTs.
If you profess to be a scientist, then there better be RCTs in your CV.
If you’re a Monday morning quarterback, I can’t help you there.
If your mommy didn’t hug you enough as a young lad, so sad.

I’ve seen this pic about as often as I’ve seen sand on a beach. Funny how social media works. One person puts up this pic and before you know, you’ve got your loyal band of merry followers parroting the same old silliness. The speed in which these pics are posted is inversely proportional to amount of thought given to the veracity of the pic. This evidence hierarchy pyramid is at best misleading and at its worst, just downright wrong. Have patience grasshopper; I’ll explain why. First some background. Variations of this pyramid exist with Cochrane Reviews sometimes at the top (i.e., it’s still a Review no matter what adjective you place in front of it). Either way, what is typically grouped at the top of the evidence pyramid are Reviews and Meta-Analyses. Ostensibly that represents the crème de la crème of science. Below that we find Randomized Controlled Trials or RCTs, Cohort/Case Control studies, Case Studies/Reports, Animal Studies, In Vitro data etc.

In the category of Sports Science, this pyramid makes no sense. Why? Because the way to make changes in a field isn’t by writing umpteen review articles and/or meta-analyses. How do you make changes in a field?

If you answered, “you have to generate original data” then go to the head of the class. Original data. That’s right. You have to do the RCT. Or do a cohort/case control study. Though if you’re studying human performance, a cohort study is about as useful as chopsticks in a hot dog eating contest. Even though case studies get the shaft much of time, these too are important. Particularly if case studies involve what you’ve done with hundreds of athletes. Strength coaches who have worked at the collegiate or professional level with perhaps thousands of athletes must be doing something right. Nonetheless, the gold standard is the RCT.

Review papers and meta-analyses are nice and all; I’ve even written a bunch. Heck, I recommend to my students that to get an initial bird’s eye view of a topic, reading review papers and meta-analyses is a great way to start. But the key word is ‘start.’ If all you relied on were reviews, that would be like watching the finish line of the Boston Marathon. You’d have no clue as to what transpired during the first mile, mile 13, or Heartbreak Hill (mile 21). You’d have no clue as to how these runners trained for the marathon. All you’d know is how they finished. That’s a typical review. You get the finish line.

Meta-analyses are even more problematic. You’re basically ‘combining’ studies that may be as disparate as hot dogs and cotton candy. The hope is that you can narrow down a bunch of RCTs into a single number and conclusion. That would be like describing the United States by doing a meta-analysis of the 50 states. It would go something like this:

The USA is 78% white, 13% black and 17% Hispanic with a small minority of Asians, Pacific Islanders etc. The median income is $53,000, the percentage of college grads about 29% and number of those living below poverty about 15%. Get my drift? I won’t list every possible way to describe the USA but let’s just say you can’t ‘meta-analyze it’ in a fashion that makes any sense. Clearly, there are MANY ways to ‘explain’ the USA. There are statistics galore you can use to describe the USA to someone who has never been there. But in the end, it’s a bit like grabbing water. Does anyone actually think living in Oklahoma is anything like Northern California? Is Texas anything like Massachusetts? Is the Sunshine State anything like Iowa? Not only is the racial make-up entirely different between these states, but geography, political leanings, and average income differ. Heck, you could probably divide the USA into 6 different countries. In the state of Florida alone, the Miami area is virtually a different country compared to north Florida. It makes you wonder if you’re in the same state. But I do love South Florida.

So next time you think a meta-analysis is the best arbiter of science, try describing the United States using a meta-analysis. Good luck. (Note: I am a co-author on a caffeine meta-analysis as well as several review papers; so I’m not ‘bashing’ these types of publications for the sake it. I’m trying to get you to think beyond the obvious).

Getting back to RCTs. If you want to truly change a field, you need to do the RCT. RCTs are the bread and butter of science. Without RCTs, there are no reviews or meta-analyses. The field of sports science in particular needs more RCTs. Reviews and meta-analyses exist at the behest of RCTs. So why on Earth would anyone think RCTs are less important than reviews/meta-analyses?

Androgens – Roid Rage Nonsense

Back in the 1970s and 80s, the American College of Sports Medicine (ACSM) published their Position Stands on Anabolic-Androgenic Steroids. [1] Their original Position in 1977 basically stated that anabolic steroids don’t work and are dangerous. Their revised position in 1987 stated they might work but are still dangerous. The funny part about the 1987 revision was they changed their conclusions based on no new data. Yes you read that correctly. Nothing changed in terms of original data. That left my head scratching. Moving on. When I examined the literature way back when (and I read EVERY original paper on this subject), I had a sneaking suspicion that the ACSM was flat-out wrong on both counts. In 1996, I co-authored a review paper stating that “the use of moderate doses of androgens results in side effects that are largely benign and reversible. It is our contention that the incidence of serious health problems associated with the use of androgens by athletes has been overstated.”[2] My review was nice and all, but it really won’t change anyone’s mind. It won’t change a field. So what did change the prevailing view of androgens? If you answered an RCT, you get an “A.”

Dr. Bhasin published the classic paper on androgens in the New England Journal of Medicine.[3] His research team found that “supraphysiologic doses of testosterone, especially when combined with strength training, increase fat-free mass and muscle size and strength in normal men.” So anabolic steroids work and the side effects were…oh wait…they didn’t find any. And they found no changes in mood or behavior. Yep. The myth of ‘roid rage busted. This RCT was the tipping point in the study of androgens.

Creatine – The Tipping Point

Dr. Roger Harris published the seminal paper on creatine.[4] That original investigation and the subsequent economic boom that resulted from the sales of creatine monohydrate has done more to change the sports nutrition industry (business and science) than any single supplement. Creatine gave respect to the supplement industry that otherwise was known more for selling protein powder that tasted like dirty socks soaked in sour milk. The study of creatine has generated 100s of RCTs and has probably been the topic of study for many a Masters and PhD student.

Caffeine – thank Dr. David Costill for this one

The 1978 study published in MSSE gave Dr. Costill more notoriety than his entire body of work (which was a LOT!). He showed that caffeinated coffee improved cycling performance compared to the placebo. Coffee and caffeine lovers rejoiced. Again, it was an RCT that changed the field of caffeine/exercise. There are literally hundreds of studies on caffeine and exercise. You can thank Dr. Costill for that.

The Big Picture

Having written many reviews, they do have their value. Often times reviews, and in particular the ISSN Position Stands, can give you a snapshot of the current science as we know it. Most of us don’t have time to sift through the umpteen studies on a particular subject. Hence, reviews (and meta-analyses) have an important role. Like I said before; it’s a good place to start. In fact, a great review or meta-analysis might generate the questions that will spur scientist(s) into conducting the appropriate RCT. Perhaps the RCT/Cohort/Case Study and the Review/Meta-Analysis categories are like two wheels of a bicycle. Both wheels are important. However, you can’t have the latter without the former.

Thus, don’t delude yourself into thinking that reviews/meta-analyses represent the most important pieces of evidence. They are not. They exist only because hundreds of scientists have done the hard work of performing RCTs. Heck, anyone can write a review. Just sit in your underwear, PubMed search whatever topic you like, and write. Believe me. I done my fair share of underwear-sitting and writing. I kinda like it actually.

Performing an original investigation is the bread and butter of science. Original data gives a field credibility. Imagine if you were to magically delete EVERY study ever done in the world of sports nutrition and strength and conditioning. What would you have left? A bunch of angry trolls fighting online. “One set is better than three sets.” “No 10 sets is better than 3 sets.” “Squeezing my butt is best for the glutes.” “No way Jose. Squats are the best butt exercise.” “Low carb is best.” “No high carb is best.” The endless drivel would be enough to shut down Facebook. And the list goes on and on. How should these disputes be resolved. If you answered ‘science’ than go to the head of the class. Science, particularly original investigations (i.e., RCTs), are the only way to objectively resolve disputes. So unless you’ve actually conducted a study, you’ll honestly have no idea what it’s like. Doing research is a brutal teacher.

I love it when an original investigation is posted on social media. The keyboard warriors, Monday-morning-quarterbacks and University of Google “PhDs” come out in full force with their critiques of the study. “Why is the sample size so small?” “Why’d you use male subjects only and not female?” “This study is invalid because it is sponsored by a private company.” Folks who critique scientific studies (i.e., those whose experience with science is reading Discover magazine and playing “Operation”) are often criticized for their lack of scientific expertise. Hence, they often resort to the intellectually lazy argument of “that’s an ad hominem attack.” Judge the message, not the messenger. Sure in the world of frickin’ Utopia, we have endless hours in the day to vet everything said by everyone. But alas, I don’t live in that world. In the interest of being pragmatic (and so as to not infringe on my beach time), judgements have to be made on the messenger. And guess what. I’ll take the advice of my internal medicine doctor over some dipshit who memorizes the WebMD website. Oops. Is that an ad hominem attack? Ask me if I care. Yes it does matter WHO gives advice. Just because you have fingers, a laptop and can type search words in Google, Wikipedia or any other third party site does not make you an expert. (For an interesting piece on ‘expertise,’ read this: http://thefederalist.com/2014/01/17/the-death-of-expertise/ ).

Trying to explain the intricacies of conducting a study would be like dry-land swimming. Sure. I can explain the stroke. I can show you videos of swimming. I’ll even let you look at the water. But unless you jump in the water, you really will have zero idea as to the process of swimming (i.e., research). Unfortunately the ratio of scientist to Monday-morning-quarterback ain’t good. It’s something like for every one genuine scientist, there are probably enough Monday-morning-QBs to fill AT & T Stadium in Dallas Texas.

Summary

I’ve published in the categories of RCTs, Reviews, Meta-Analyses, Case Studies and Animal Research. They are all important though in different ways. Keyboard warriors and Monday morning quarterbacks notwithstanding, if you want to really change a field and I mean really change it, you have to do original research. You can blog until your blue in the face and it won’t change a damn thing. It would be like putting lipstick on pig and entering it in beauty contest. Cheers.

References

1. ACSM Position Stand on Anabolic Steroids: http://journals.lww.com/acsm-msse/Citation/1987/10000/Position_Stand_on_The_Use_of_Anabolic_Androgenic.23.aspx

2. Street C, Antonio J, Cudlipp D: Androgen use by athletes: a reevaluation of the health risks. Can J Appl Physiol 1996, 21:421-440.

3. Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R: The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996, 335:1-7.

4. Harris RC, Soderlund K, Hultman E: Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci (Lond) 1992, 83:367-374.

In Defense of Cortisol

by Jaime Tartar PhD – “If the glove don’t fit, you must acquit.” – Johnnie Cochran – Wacky Attorney

Why Do I Need to Write This? – If Johnnie Cochran was a scientist, he’d certainly acquit cortisol. But before I get ahead of myself, here’s a little background. Just so there’s no confusion, I’m not an expert in exercise science. The extent of my background here is that I jog regularly(ish) and lift weights often enough to psychologically validate my gym membership fees. I’m a Behavioral Neuroscientist which basically means that I like to know how the brain and body influence each other (it’s a good gig if you can get it especially in South Florida). Because much of my background and training has been focused on the neurobiology of stress, I find myself getting eye-twitchy and moaning inwardly quite often. It seems that there are some areas of science where anecdotal ideas and misinformation pervade and no one (in my humble, yet biased, opinion) has been more of a victim to this than my good buddy, cortisol. Facebook anyone? This poor little bugger (aka cortisol) has gotten so beat up and kicked around that he could serve as the protagonist of a Victor Hugo novel. Understanding why cortisol is not “bad” is pretty straightforward. In order to help fix the tarnished reputation of cortisol I would like to consider and correct a few key ideas. Necessarily, this begins with a quick and painless overview of the network in which cortisol acts; actually there are some cool points here that can offer winning facts to pepper into a random conversation.

SUPER QUICK Overview of Cortisol Release with Stress – So here we go; stress responses actually involve two major systems: the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS). The final product from the SNS in response to stress is epinephrine (“adrenaline” if you’re nasty or European). This isn’t his story, though, so we are going to justifiably ignore him and just focus on the HPA system and cortisol for the current tale of woe and strife. While the response to stress through the HPA axis is intricate and complex, a review of the major players will suffice to shed light on why cortisol is an O.K. dude. The first step in the HPA stress response is that perceived or physical stress will induce the release of corticotrophin releasing hormone (CRH) from the hypothalamus in the brain. This guy then tells the pituitary gland to release pituitary adrenocorticotropic hormone (ACTH) into the bloodstream, who then stimulates the release of cortisol from the adrenal cortex (Hellhammer, Wust et al. 2009). The released cortisol does exactly what it is supposed to do to help deal with a stress. In response to stress, cortisol will mobilize energy for muscles, increase energy metabolism, increase cardiovascular tone, turn off nonessential activities, acutely increase immune function, and alter brain functions such as learning and perception processing (Aguilera 2011). However cortisol’s time in the limelight after stress is short-lived. It peaks about 30 minutes after the stressor and then further release is shut off through negative feedback regulation at all levels of the HPA axis and in an area of the brain called the hippocampus- he puts the breaks on the whole system at the level of the hypothalamus (from whence it all began). Cortisol levels are extremely tightly regulated and follow a predicable daily/circadian pattern of release (with the peak in the morning and the trough, or nadir, occurring at night). Although there is cortisol release with stress, the release is adaptive and helps to respond to increased energy demands – this is also why cortisol levels are high in the morning (known as the cortisol awakening response). This surge in a.m. cortisol helps to meet the energy demands needed to get moving and start a new day. In general, based on the negative feedback mechanisms that are in place for cortisol, we can rest assured that, in the absence of clinical disease or chronic stress (these ideas are reviewed at the end), cortisol is doing exactly what it needs to do to keep the body healthy and capable of dealing with a stress. Remember that cortisol reigns only briefly after stress and its actions here are beneficial in helping the body manage a perceived or physical challenge. Based on these ideas we can now clear up the three largest misconceptions of cortisol.

Cortisol is not a stress meter – Cortisol levels do not simply rise and fall as the body is stressed. This is subtle, and where some information is misconstrued, because, as reviewed above, cortisol will go up when the body is stressed; however, that is not the same thing as being a direct measure of stress. Cortisol levels do not correspond directly to the type and intensity of stress and there are many individual differences in cortisol release in response to stress. Also, cortisol levels do not go down in the absence of stress. Please re-read that phrase. We reviewed above a typical circadian cortisol pattern. This exists because ACTH is released continuously in pulses throughout the day; the pulses speed up or slow down because they are entrained to circadian processing in the hypothalamus (Veldhuis and Johnson 1991). Negative feedback regulation of the HPA axis ensures that cortisol levels don’t get too high for too long, and when they do, they are shut down with rapid and decisive action. So we can appreciate that there is not signal for “Hey we are not stressed so let’s decrease cortisol!” That’s bonkers and makes no sense since cortisol is an essential hormone in the body. This leads to the second point.

Cortisol is not “bad for you” – it helps keep you alive! – Truly! Natural selection has ensured that in response to a stressor or challenge to homeostasis, cortisol does exactly what it is supposed to do. We all get to be alive today because our ancestors could mount an appropriate stress response. Furthermore, once cortisol is increased in response to stress or a change in homeostasis (e.g. through physical exertion), the changes are short-term. Chronically low cortisol levels can lead to decreased energy, muscle weakness, and low blood sugar. Critically, also, is that cortisol helps to reign in the immune system and helps prevent chronic inflammation and autoimmunity. For example, hyporesponsive HPA activity is seen in autoimmune disorders such as rheumatoid arthritis and chronic fatigue syndrome (Demitrack, Dale et al. 1991, Chikanza, Petrou et al. 1992)

Cortisol isn’t making you fat – Many people associate increased cortisol with weight gain. This viewpoint is prevalent in the fitness world. It’s true that elevated and sustained levels of cortisol levels can increase fat storage; especially in the abdomen and face. However, the key here is sustained elevations. For example we tend to see this body type in those with Cushing’s disease. These are individuals with pathologically high levels of cortisol. Weight gain with exercise is not likely to happen because of cortisol. This is a misconception probably partially based off of misinterpretation of science. For example, one study demonstrated a correlation between cotrisol and weight gain (Epel, Moyer et al. 1999); this does not mean increased cortisol caused increased weight gain (this is why the mantra of every Introduction to Statistics class is “correlation does not imply causation”). Also, based on what we’ve reviewed about short-term cortisol actions, it would not make sense that cortisol “makes you fat” since the major role of cortisol during an intense exercise session is to mobilize energy resources to meet the immediate demands of the body. This primarily involves increased gluconeogenesis (converting glycogen to glucose), higher triglyceride levels, and increased blood flow to the heart and muscles (Majzoub 2006). Stress can cause weight gain; but this is through increased eating behavior not increased cortisol. Cortisol is an easy target, though, because pathologically or sustained levels of cortisol can cause increased fat storage. So the faulty thinking goes like this: exercise increases cortisol and cortisol causes weight gain. This is where that idiotic idea of too much cardio making you fat comes from. This is simply not accurate and a logical fallacy BUT it is an easy way to sell people a bunch of useless cortisol-fighting pills. Do you remember CortiSham? Ooops, I mean CortiSlim. The stuff worked about as well as giving a killer whale a bite of an apple and saying ‘hey Orca, I bet that filled you up.’ Increased eating that happens with chronic stress is complex and not directly due to cortisol levels. It is likely a product of individual differences in physiology, cognitive mechanisms, and a surplus of high calorie choices (Gibson 2006, Torres and Nowson 2007).

So what the hell cortisol – why the bad rep? – Most of the deleterious effects associated with cortisol come about as a result of chronic stress. While the HPA axis is well adapted to respond to threats, it is a reflexive physical response from the body and does not discriminate between real and perceived stress. A threat is a threat and it is was historically not adaptive for the brain to consider if something was really a threat before mounting a stress response. However, this can sometimes present problems to us “modern humans” since most of the things that stress us are not life threatening and are coming at us on a somewhat regular (chronic) basis. Humans living in industrialized nations are not likely starving, threatened by predators or, or battling for mating rights. Though if you went to a local pub you might wonder. However, we’re very good at experiencing chronic perceived emotional (sometimes imagined) chronic stress. In the absence of a disease process (e.g. Cushing’s disease) to cause hypercortisolemia, cortisol levels can become chronically elevated when the HPA axis is dyregulated. While even amidst ongoing chronic stress (the daily life hassles we all experience), the HPA axis does a remarkable job of regulating cortisol. This is pretty amazing given that we do things like respond to an asshole in traffic the way we would a predator 10,000 years ago. And we got plenty of those in South Florida. Believe me. We might mount a stress response to assholes every day, while the predator only occurred once in a while. So, good on you HPA axis- you are doing a damn fine job! But (and this is where the mass hysteria arises) HPA axis dyregulation can come about from chronic stress through several ways. The big one here is unremitting and uncontrollable stress. So in order to really dysregulate the HPA axis, you really need to get in there and be sure that the stress is ongoing and that there is no habituation to the stress. In other words, if someone gets punched in the face regularly and predictably it stops becoming a stressor. So for those of you interested in “death by stress,” recognize that unpredictability and uncontrollability is essential to this. So pushing yourself in exercise won’t likely lead to a breakdown of the HPA axis since you have control and the act is predictable. To really do someone in, you might consider having that person run on a treadmill against his or her will and have the treadmill turn on and off at random times. Sounds like a CrossFit workout. LOL. Okay moving on. With that said, there are still some individuals that have an inability to adjust to regular, ongoing stress. These are what we call “high responders.” They mount a stress response very easily and seem to be in perpetual hypervigilance (I say “they” but I fall directly in this camp – knowledge is not always power?) There is evidence to suggest that these differences in stress sensitivity can be altered through stress in the womb (which changes the HPA axis “set point”) or through innate differences in physiological arousal- but this is an area that is greatly scientifically underexplored. Lastly, chronic stress can cause problems through rumination, or reactivation after stress has ended. If someone gets bitched out at work, that sucks, but since HPA activity is sensitive to psychological and physical insults, dwelling on the event and perpetually “reliving” it can cause a stress activation over and over, long after the actual event has passed. The problem with writing this is that I fear ruminators read it and ruminate on how they ruminate too much! So I suppose the take home message here is that chronic physical or psychological stress can produce chronically high levels of cortisol under very special circumstances. Exposure to chronic or severe stress (perceived or realized) can produce dysregulation of the HPA axis, which is characterized by enduring pathological hyper- or hyposecretion of cortisol.

End on a positive! – Importantly for athletes, chronic stress in the form of endurance or exercise-induced increases in cortisol are not likely pathological or related to negative health consequences (Gerber, Brand et al. 2012). In fact, athletic training is associated with a decreased HPA response to an exercise challenge; it’s all about the habituation (Mastorakos, Pavlatou et al. 2005). Critically, also, is the overwhelming evidence that, despite HPA axis activation, regular exercise can also offer increased emotional well-being and protects against depression and other mood disorders (Galper, Trivedi et al. 2006, Lucas, Mekary et al. 2011, Hogan, Mata et al. 2013).

The bottom line is that exercise does increase cortisol, but these increases are not harmful and work to increase real energy demands on the body. Increased cortisol from exercise is not making anyone fat; that would be like blaming your fork for making you fat. Or chopsticks if you live in China. Instead blame increased eating with increased exercise. Go ahead and work out knowing, with great confidence, that cortisol is not your enemy. Donuts maybe, but not cortisol.

BIO – Jamie Tartar PhD earned her doctorate in the area of behavioral neuroscience from the University of Florida. She did her post-doctoral studies at Harvard Medical School’s Department of Psychiatry (2004-2006) and worked with the United States Army Reserves: Medical Service Corps (1998-2004). She is currently a professor at Nova Southeastern University in the Department of Neuroscience. She loves brain stuff. One of her fellow Nova colleagues, Jose Antonio PhD, suggested this article topic because as he points out, there are too many self-appointed experts who think cortisol is the enemy. But as a smart dude once said: “Wisdom is a weapon, knowledge is the armour, and ignorance is the enemy.” Cortisol ain’t the enemy. Cotton candy maybe, ice cream perhaps, but cortisol? Nah.

Science References For All You Nerds

Aguilera, G. (2011). “HPA axis responsiveness to stress: implications for healthy aging.” Exp Gerontol 46(2-3): 90-95.

Chikanza, I. C., P. Petrou, G. Kingsley, G. Chrousos and G. S. Panayi (1992). “Defective hypothalamic response to immune and inflammatory stimuli in patients with rheumatoid arthritis.” Arthritis & Rheumatism 35(11): 1281-1288.

Demitrack, M. A., J. K. Dale, S. E. Straus, L. Laue, S. J. Listwak, M. J. Kruesi, G. P. Chrousos and P. W. Gold (1991). “Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome.” The Journal of Clinical Endocrinology & Metabolism 73(6): 1224-1234.

Epel, E. E., A. E. Moyer, C. D. Martin, S. Macary, N. Cummings, J. Rodin and M. Rebuffe‐Scrive (1999). “Stress‐Induced Cortisol, Mood, and Fat Distribution in Men.” Obesity Research 7(1): 9-15.

Galper, D. I., M. H. Trivedi, C. E. Barlow, A. L. Dunn and J. B. Kampert (2006). “Inverse association between physical inactivity and mental health in men and women.” Medicine and Science in Sports and Exercise 38(1): 173.

Gerber, M., S. Brand, M. Lindwall, C. Elliot, N. Kalak, C. Herrmann, U. Pühse and I. H. Jonsdottir (2012). “Concerns regarding hair cortisol as a biomarker of chronic stress in exercise and sport science.” Journal of sports science & medicine 11(4): 571.

Gibson, E. L. (2006). “Emotional influences on food choice: sensory, physiological and psychological pathways.” Physiology & behavior 89(1): 53-61.

Hellhammer, D. H., S. Wust and B. M. Kudielka (2009). “Salivary cortisol as a biomarker in stress research.” Psychoneuroendocrinology 34(2): 163-171.

Hogan, C. L., J. Mata and L. L. Carstensen (2013). “Exercise holds immediate benefits for affect and cognition in younger and older adults.” Psychology and aging 28(2): 587.

Lucas, M., R. Mekary, A. Pan, F. Mirzaei, É. J. O’Reilly, W. C. Willett, K. Koenen, O. I. Okereke and A. Ascherio (2011). “Relation between clinical depression risk and physical activity and time spent watching television in older women: a 10-year prospective follow-up study.” American journal of epidemiology 174(9): 1017-1027.

Majzoub, J. A. (2006). “Corticotropin-releasing hormone physiology.” European Journal of Endocrinology 155(suppl 1): S71-S76.

Mastorakos, G., M. Pavlatou, E. Diamanti-Kandarakis and G. P. Chrousos (2005). “Exercise and the stress system.” Hormones (Athens) 4(2): 73-89.

Torres, S. J. and C. A. Nowson (2007). “Relationship between stress, eating behavior, and obesity.” Nutrition 23(11): 887-894.

Veldhuis, J. D. and M. L. Johnson (1991). “Deconvolution analysis of hormone data.” Methods in enzymology 210: 539-575.

Energy Drink Dumba$$es

By Jose Antonio PhD FISSN, FNSCA, CSCS. There are some things that are just annoying. Stepping on chewing gum. Emails from Nigeria asking for $1,000 so they can transfer a $1,000,000 to your bank (Really? What dope falls for this?). Hitting every red light as you make your way home. Celebrity confessions. Having to actually watch a TV show with the commercials (thank god for TiVo!). And reading the numbskull articles written by the mainstream press on pretty much all things related to sports nutrition. Runner’s World, a magazine that I actually enjoy reading (yeah, don’t tell anyone), posted on their website an article entitled “Sports Nutrition Group Doubts Claims of Energy Drink Makers.” http://www.runnersworld.com/drinks-hydration/sport-nutrition-group-doubts-claims-energy-drink-makers I’m thinking; hey, I wonder who that group is. Inquiring minds need to know. And guess what, it’s the International Society of Sports Nutrition! The ISSN is the leading academic society that studies sports nutrition and supplements and I’m the head honcho. I’ll at least give Runner’s World credit for citing the Position Paper that we recently published. But that’s pretty much where the credit ends.

The Runner’s World interpretation of our article is so wrong. Why? Because my colleagues and I wrote the dang thing. I think we’d know BETTER than anyone what the correct interpretation is! To wit: Here’s the headline – “Sports Nutrition Group Doubts the Claims of Energy Drink Makers.” Uh no. In fact, if you read #3 of the Position Paper’s abstract it says the following: “Consuming ED 10-60 minutes before exercise can improve mental focus, alertness, anaerobic performance, and/or endurance performance.” That my friends is THE most important point. The drinks work! We can argue over the why and whether it’s the ingredients or combination thereof, but the bottom line is that as an ergogenic aid, the stuff will help you perform better.

And then we have the Dawn Report which states that the number of emergency room visits involving energy drinks has increased. The implication is that energy drinks must be hurting thousands of people, right? Well as they say in Alabama, shitfire Bubba, that ain’t no proof!

http://www.samhsa.gov/data/2k13/DAWN126/sr126-energy-drinks-use.htm Since when did emergency room visits become a substitute for scientific studies? Did I miss something in my years of studying the frickin’ scientific method? To fall for the moronic trap that sensational headlines are a substitute for honest-to-goodness critical thinking would be like judging a fish by its ability to climb trees. As I tell my super-smart students at Nova Southeastern University in beautiful South Florida, read the data. Read the science. Whenever you see headlines such as this, instead of believing it hook, line and sinker, instead immerse yourself in the actual studies and decide for yourself. Because one day you’ll write a scientific paper and then some journalist with about as much science training as your pet Beagle will tell you how it should be interpreted. Ok enough of this. Time to consume copious quantities of caffeine-filled java.

Reference: The 2013 International Society of Sports Nutrition position stand: energy drinks http://www.jissn.com/content/10/1/1