Artificial Sweeteners Can Promote Glucose Intolerance

The movement away from sugar and towards non-caloric artificial sweeteners (NAS), began over a century ago after recognizing that 1) large amounts of calories could lead to obesity and likely a variety of other health problems, and 2) that large amounts of sugar adversely affected hormone levels (in particular insulin), which could also lead to obesity and a variety of other health problems. Thus, consumers looked to NAS as a way to continue to eat sweet foods and beverages while protecting their health. However, research is beginning to indicate that NAS may not be as harmless as we had hoped.

I posted previously about an interesting study in rats, which examined examined the effects of NAS in diet. The results were fascinating as many of the problems we know to arise from over-consumption of sugar, were also found after consuming the artificial sweetener. If you haven’t read my review, it’s worth a read. Recently, another study was published on NAS, this time by Suez and coworkers. Suez et al., 2014 was conducted in both mice and humans.

The Takehome: Glucose intolerance (high levels of blood sugar), often a precursor to Type 2 Diabetes, has been linked to cardiovascular disease, muscle loss, and a variety of other health problems. In this study, the authors found that the commercial non-caloric artificial sweeteners (NAS) saccharine, sucralose, and aspartame all caused mice to develop glucose intolerance. Further examination of saccharine alone (which had the greatest effect of the three), revealed that this intolerance was associated with a change in gut microbiota (bacteria) populations. Fecal matter with these altered microbiota could be transplanted into healthy mice and cause them to become glucose intolerant. In humans, increased consumption of foods with NAS was correlated (a questionnaire-based study) with impaired glucose tolerance and also an alteration of gut microbiota. Finally, ingesting NAS-continaing foods for 1 week was enough time to show reduced glucose tolerance in some, though not all, humans. In these affected humans, microbiota populations were, as expected, altered, though differently than in mice. Nevertheless, when this fecal material from humans was transplanted into healthy mice, the mice developed glucose intolerance. The results of this study indicate that artificial sweeteners don’t give us a free pass to eat without consequence. Although artificial sweeteners do not raise insulin, there appears to be another route by which they can disrupt blood glucose levels, and that is through modification of the bacterial populations that live in our digestive tract. The bacteria in our digestive tract don’t only affect the processing of sugars and artificial sweeteners as highlighted in this study. In fact, they play many other roles in maintaining our health, so it’s quite possible that consumption of artificial sweeteners may negatively impact our health in even more ways than we have yet to realize.

The Experiment:

  • 10-week (young adult) C57/BL6 mice were given one of three NAS in their drinking water: commercial saccharin, sucralose, or aspartame. Control mice were given either water or water with glucose or sucrose. Note: commercial NAS typically contain large amounts of glucose (~95%) and only small amounts of the artificial sweetener (~5%). The investigators matches these ratios.
  • Fecal mibcrobiota composition was assessed in mice through rRNA gene sequencing.
  • Fecal matter was removed from mice and cultured in tissue culture dishes to examine direct effects of NAS on microbiota growth.
  • The effect of NAS in humans (381 non-diabetic males and females, mean age of 43 years old) was assessed through a food frequency questionnaire.
  • 7 humans (5 males, 2 females) who do not normally consume NAS were given NAS-containing foods (at the FDA’s maximal acceptable daily intake levels) for 1 week, after which glucose intolerance and gut microbiota were assessed.

The Results:

  • After 11 weeks, the three groups that drank commercial NAS all had marked glucose intolerance (higher than normal blood sugar levels).
  • The greatest intolerance was found in mice who consumed commercial saccharine.
  • In mice who were on a high-fat diet (to simulate obesity), glucose intolerance from commercial saccharine ingestion was greater than from glucose ingestion.
  • As with commercial saccharine, a lower dose (FDA acceptable daily intake adjusted to mouse) of pure saccharine, also resulted in glucose intolerance in mice on a high fat diet.
  • Fasting serum insulin levels and insulin tolerance were similar in all mouse groups, regardless of diet.
  • Mice drinking saccharine had a fecal microbiota profile different from their starting profiles and from the profile of all control groups (including a group that drank glucose). Profile differences were present even in mice that were on a high fat diet.
  • Gene pathway analysis indicated that the microbiota profile in saccharine-fed mice had gene profiles for enhanced sugar breakdown/fermentation activity. These profiles were previously associated with obesity in mice and humans; overabundance of Bacteroides and under-abundance of Clostridiales.
  • Fecal matter isolated from mice and treated with pure saccharine yielded similar shifts in the microbiota profile and transplanting this altered fecal material into normal mice resulted in their developing glucose intolerance.
  • In humans, NAS consumption was significantly correlated with higher fasting blood glucose, glycosylated hemoglobin (indicates higher than normal levels of blood glucose), and higher glucose intolerance (as measured by a glucose tolerance test).
  • In humans, NAS consumption was significantly correlated with differences in microbiota profiles.
  • In 7 humans given NAS-containing food for 1 week, all developed a poorer glucose tolerance as compared to before they started consuming NAS-containing foods.
  • Fecal material from humans who consumed NAS-containing food for 1 week and developed impaired glucose tolerance was transplanted into healthy mice and resulted in these mice developing glucose intolerance.

The Limitations:

  • Although very often a good model for humans, mice are not humans, so differences may exist where the initial mouse data is concerned. However, the pairing of human data with mouse data in this study makes this much less of a limitation.
  • After seeing the greatest glucose intolerance effect from saccharine, the authors do not further examine effects/mechanisms in mice using sucralose or aspartame. We therefore do not know if the different sweeteners behave any differently beyond impairing glucose tolerance.
  • Insulin levels appear to be unaffected by NAS (as expected), so the exact mechanism of intolerance remains somewhat unclear. We know gut microbiota are involved, but not exactly how.
  • Food questionnaires are noted for being inaccurate as participant reporting is often inaccurate despite the participants’ best efforts.
  • In humans, the microbiota profile differences resulting from NAS were not identical to those found in mice and were also different human-to-human. This suggests that the effects may vary substantially from person-to-person.
  • The human study where NAS-containing foods were consumed had a very low sample size and an unequal distribution of men and women. This would generally be considered “preliminary” data that could be used to support a larger study.
  • In the human study where NAS-containing foods were consumed, the types of NAS consumed were variable, so any differences among them could not be examined.
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Video Post – Clip from “Health & Fitness During Aging” Seminar at UCONN

Below is a video clip from my recent seminar at UCONN. The audience was older and the seminar therefore dealt with health and fitness during aging. It examined, from a scientific perspective, the theme of death and rebirth at the organ and tissue level and how these processes are influenced by modifiable lifestyle factors such as nutrition (calories, fat, carbohydrates, salt) and activity (walking, running, weight training). For more information on my seminars, click the Seminar tab on the menu.

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Creatine Supplementation Can Boost Testosterone

Creatine is an organic acid naturally found in vertebrate muscles and it is arguably the most extensively studied supplement on the market. A variety of studies indicate that supplementing with creatine can enhance athletic performance, endurance, and muscle growth. A previous post of mine goes deeper into creatine, its mechanism of action, and the studies that support its effectiveness. If you haven’t read it, check it out now. In this post I add another potential role for creatine supplementation as indicated in Arazi et al., 2015: the ability to raise testosterone levels. Testosterone is a hormone, produced largely by the male testes, that plays a major role in building muscle (it is therefore said to be anabolic). As such, this study is of immediate interest to men who are interested in getting bigger or stronger.

The Takehome: Both 5 and 7 days after creatine supplementation, men who were resistance training (lifting weights) had significantly higher testosterone levels than they did at baseline and also higher levels compared to those who did similar weight training, but took a placebo instead of creatine. Creatine supplementation also reduced cortisol levels relative to baseline at 5 and 7 days. High levels of cortisol are “catabolic” in that they can lead to tissue breakdown (muscle loss), inefficient tissue repair, and a variety of other processes that hinder growth and recovery of body tissues. So, while previous literature assumed creatine’s main route of action was through restoration of muscle energy reserves, this study indicates there may also be a systemic response through the upregulation of anabolic hormones (testosterone) and the downregulation of catabolic hormones (cortisol).


The Experiment:

  • 20 active males (mean age of 20 years old).
  • Baseline levels of markers were taken: testosterone, cortisol, heart rate and blood pressure.
  • Participants were given 5g of creatine (or dextrose as placebo) 4 times daily dissolved in grape juice.
  • Creatine or placebo was ingested morning, mid-day, afternoon, and before sleep.
  • 3 sessions of resistance training were given (days 3, 5, 7).
  • 3 sessions were conducted to test for the above-mentioned markers (days 4, 6, 8).

The Results:

  • At both 5 and 7 days, resting testosterone levels in creatine supplemented individuals were significantly higher than their baseline levels.
  • At both 5 and 7 days, resting resting testosterone levels in creatine supplemented individuals were higher than placebo supplemented individuals.
  • At both 5 and 7 days, resting cortisol levels in creatine supplemented individuals were significantly lower than their baseline levels.
  • Blood pressure and heart rate levels were largely unaffected by creatine supplementation.

The Limitations:

  • Only men were used and they were fairly young, an age when testosterone levels are already fairly high to begin with. It is unclear if similar results would be found in women or if the same results would be found in older men.
  • The sample size (10 participants per group) is low.
  • We do not know if the changes in testosterone and cortisol levels will be maintained throughout longer periods of creatine use.
  • The exact form of creatine used (i.e., creatine monohydrate) was not listed in the methods.
  • This is just one study. More studies are needed to confirm these findings.
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A Recap of My Recent Strength Cycle

I recently tested a couple of strength cycle variations and wrote up a recap of how things went on the CrossFit Solace blog. If you are interested in balancing strength cycles and conditioning in your CrossFit training, I encourage you to have a read. To access the article CLICK HERE.

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Refocusing My Efforts – Subscribe to My Newsletter

Since I launched Science for Fitness, the regularity of my posts has been fairly frequent and over the past several months new posts were going live nearly every week. This is a lot of content and I’ve been thinking about how much is too much. I know some of my readers have had a hard time keeping up, so that’s one issue. Another issue is that the posts take time, especially if they are to be accurate and of good quality (and I don’t want to post anything that isn’t). The risk of losing quality when you ramp up the quantity of your material was impressed upon me recently when I came across a review of the Paleo literature. My previous post on this site addressed the problems with this review, so if you haven’t read it, check it out. I don’t want to succumb to the kind of problems this review had.

Another consideration is that I want to refocus my efforts a bit. There is more to Science for Fitness than just my articles. There are of course the clients I train that need my attention, but I also need to spend more time working on seminars that I will be giving, as well as on a book that I am trying to put together. What this means is that the frequency of posts to will drop a bit. You will still see at least 1-2 posts per month, but posting dates will be variable. This means that the best way to keep track of what’s going on is to sign up for my monthly newsletter (on my homepage). This will go out at the beginning of each month and recap everything from the month prior, so you won’t miss a beat.

Thanks for reading,

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Quality vs Quantity: A Paleo Review That Doesn’t Quite Add Up

Not too long ago I came across Led by Dr. Greger, the organization’s goal is to “present you and your doctor with the results of the latest in peer-reviewed nutrition and health research, presented in a way that is easy to understand.” We certainly need more people out there doing this. The videos the organization puts out are very slick (as you will see below in a moment) and it’s a format I’ve been considering adopting for quite some time. However, I soon noticed that videos were being released every other day and they were each discussing the primary literature (scientific studies). It takes time to read and interpret scientific studies. I was puzzled. And then I came across one of the organization’s videos on Paleo research. The video is below, give it a watch:

The video threw me for a loop because it was espousing things I had understood to be different. In short, I felt the data wasn’t being interpreted properly. This happens all the time in the popular media when they summarize science, but here a doctor was interpreting (or at least speaking the interpretation) and citing the actual studies. So, I went through the article piece by piece and here is what I found:

  • At 1:10: Here Holt et al., 1997 is referenced and in the video’s bar graph a serving of meat was shown to increase insulin the most. But this isn’t what the study showed. As seen in Table 4 of the study, the beef insulin came in at 7910 pmol(min/L) and the apple came in at 8919 pmol(min/L). The study showed the apple raised insulin more than the beef.
  • At 1:37: Here a graph is shown indicating that beef causes the same insulin spike as pure sugar (glucose). But the study isn’t cited, so I don’t know where it comes from. But if we look back at the Rabinowitz et al., 1966 paper which is cited in the very beginning of the video, we see a lot of data on this – data that actually looks at the insulin levels after various times post-ingestion. This data does not indicate a similar insulin spike between meat and glucose. In all the graphs shown in Figures 4&5, insulin levels during the 1st two hours after ingestion are greater for glucose than meat (click to see an example here).
  • At 3:37: Bueno et al., 2013 is cited comparing a low-carb diet to a low-fat diet is cited to indicated that dropping carbs does not lower insulin. But this is a Meta Analysis study. It is collating data from many studies and the “low-fat” groups are not necessarily high carb diets and the types of carbohydrates consumed is also not accounted for.
  • At 4:00: The Smith et al., 2014 study is cited to close the video. In the video we are told that the paleo diet worsened LDL cholestrol (“bad cholesterol”) and reduced HDL (“good cholesterol”) in individuals who were exercising (CrossFit). The narrative has now, only at the very end, switched away from insulin, to cholesterol to address an interaction effect with exercise. I’ve posted numerous times about how the cholesterol literature is riddled with problems, so I won’t go into it again. But I will note that this study is problematic for another big reason – the participants didn’t strictly follow a Paleo diet as indicated in the study’s methods. For a write-up on this, check out this blog post by The Russells.

As you can see, the above video is problematic. There is some interesting data in the video, such as the fact that Holt et al., 1997 saw white pasta spike insulin less than meat, and the fact that vegetarians tend to have lower insulin levels (despite eating more carbs than non-vegetarians), but there are many key points that just don’t add up and the viewer is given the impression that the “case is closed” when we are really still putting the pieces together.

I posted several of my above-mentioned corrections to the video in the comments thread (because of course maybe I was missing something), but didn’t get any response. I then suspected that Dr. Greger wasn’t reading all the social media himself and that he probably wasn’t reading the actual studies himself either. It made sense, because for me to really pick apart one study and make sure I get it right, it takes several hours. In this video alone, there were more than 5. He must have been using a team to go through the studies.

It turns out I was right. Earlier this month February Dr. Greger put out a call for “fact checkers” to work freelance for the organization. It’s also revealing that he tested applicants on their fact-checking skills and during the first round everyone was under 80% (out of 100%). has a great mission statement, and many of their videos are great, but interpreting scientific studies is hard, even for the scientists. It’s very demanding and requires a lot of training, thought and focus.

As scientists and doctors we have to remember this and not get caught up in trying to give the public large quantities of information covering all topics all the time. Quality suffers when quantity goes up. Not to mention, our understanding of science (e.g., nutrition, health, fitness), does not change every time a new study comes out. It’s an aggregate of studies over time, shown to be repeatable, that have meaning and putting this message together requires quite an enormous investment of thoughtful consideration.

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Scientists Need to Give Lectures More Like This

Starting Strength Coach Association Series: Exercise Science Presentation 2014, Part II from Starting Strength on Vimeo.

It’s a rare occasion that I see a scientific lecture that excites me and leaves me thoroughly satisfied in the end. The above video is one of those rare occasions. In the above video Starting Strength Coach Dr. Sullivan gives a review of literature on the topic of concurrent training and exercise interference. That is, does endurance training interfere with strength training? His answer to this question is the least interesting part of this lecture. In my opinion, the video excels for a number of other reasons:

  • Dr. Sullivan references specific studies
  • The studies are given a level of scrutiny that matches my own (which is quite rare)
  • Discussion of limitations and weaknesses is bold, colorful, and up-front.

As a scientist I spent nearly two decades attending conferences and listening to lectures. Many of those lectures were topical reviews like Dr. Sullivan’s and yet not one of them was like his. The vast majority of the time, scientists review literature in a positive light. Supporting studies or pieces of data within the studies are chosen and then simply referenced with virtually no consideration of the study as a whole nor the limitations of the study. It’s as if researchers at conferences turn a blind eye to limitations or maybe they just want to be everybody’s friend. Or maybe a bit of both. Yes, Dr. Sullivan’s tone might be a bit too harsh for a conventional scientific meeting, but it was a breath of fresh air for me, and this is a clear indication that a better balance is needed.

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Low-Bar vs High-Bar Squat

Image from Starting Strength, Rippetoe and Kilgore

I’ve been wanting to write about low-bar and high-bar squats for quite some time and now that I am programming for a large number of individuals, it seems like the time is right. I’ve gotten some questions from my members at CrossFit Solace and they’ve also forwarded me the writings and thoughts of others. Let me begin by saying this topic is not new; there have been many articles written on it, However, I have a few points that I’ve not seen mentioned elsewhere and perhaps more importantly, how I approach the issue is, I think, different.

The Difference in the Squats: There are 3 squats that come into play in this argument: the low-bar squat (pictured above right), the high-bar squat (pictured above middle), and the front squat (above left). The front squat is the squat position needed to rack a bar on your shoulders to complete a Clean in the sport of Weightlifting. Standing up from rock bottom in this vertical torso position emphasizes glute and quadriceps activation. The high-bar squat has the bar resting on the shoulders. The torso is still largely upright and standing up from rock bottom in this position is also largely glute and quadriceps driven. The low-bar squat as you can see above has the hip angle much more closed and the finish position is taught with hip crease just below parallel. The difference here is notable as more leg muscles are being worked with this version of the squat (quadriceps, glutes, hamstrings, adductors, abductors). I don’t really know of anyone that disputes this difference and anyone who has never low-bar squatted can verify for themselves, by seeing where they are sore the day after they first try it.

The Weightlifting Argument: First and foremost, the low-bar vs high-bar argument arose in the context of Weightlifting movements. So let’s stay within this context for a moment. This argument concerns which is “better,” the low-bar squat or the high-bar squat. The front squat is generally left out of the argument because it is a movement that is part of the sport of Weightlifting. You have to do this movement if you want to perform Cleans. So, training it is by definition useful. But for the other versions, you generally only see high-bar squats being used. People often ask why Weightlifting coaches don’t use the low-bar squat. Greg Everett was asked this question and he responded with, “That’s like asking why baseball players don’t use footballs.” In short, he’s saying that the low-bar squat does not have carry over to the functionality of Weightlifting. But this isn’t entirely true:

  • The position of the bar and the back angle for a high-bar squat is not the same as a front squat. It is more similar to a front squat than a low-bar squat, yes, but it is not the same. There is a difference. So, in terms of form, saying the high-bar carries over and the low-bar does not, is a matter of drawing a line. You are of course welcome to do this, but the differences are not black and white.
  • A low-bar squat does in fact have carry over to weightlifting in that is develops strength. Strength is a general adaptation. Just being stronger will make you better at Weightlifting. I have seen this time and time again with my clients and myself. For example, after just a month of low-bar squatting I PR’d my Clean and front squat. Perhaps you can say my PRs would have been better if I high-bar squatted instead, but you can’t say the low-bar had no carry over. It did. This point is an important one. It goes beyond just squatting. Years ago, after 2 months of only upper body strength training (with no technical work), I PR’d my Snatch.
  • The low-bar squat does a better job of strengthening your lower back through isometric contraction than the high-bar does. This is a particularly important adaptation for Weightlifting as most lifters try their best to keep their shoulders over the bar during the first pull. This loads your hamstrings and requires a very strong lower back. Again, I am not saying you can’t train this other ways (heavy Clean pulls work well for this too). I’m just saying that for this adaptation, low-bar squats are more effective than high-bar.
  • One thing I found when returning to performing Cleans after low-bar squatting, was that my legs felt stronger in the transition out of the bottom of the squat to above parallel – they didn’t cave in as much. Your hamstrings, abductors, and adductors are largely “turned off” in the bottom of the low-bar and front squat (or Clean) and they need to kick in at the transition. You can see this by watching a lot of lifters Clean heavy weights. In the video of Ilya below, you’ll see his knees cave in a bit (at about 0:02):

    This is purely personal observation, but I had less knee cave-in at even heavier weights after low-bar squatting. I’m not saying low-bar squatting will prevent this knee movement in Weightlifting, but I suspect it is a very efficient way to strengthen/improve this transition position in the Clean, at least for less advanced athletes.

The Weightlifting Argument Wrap-Up: As you can see, I in no way tried to discredit the high-bar squat. It’s a great exercise and more similar to the front squat than the low-bar, but the Weightlifting argument really needs to be about strength. It can’t be about technique carry over, because if you are training Weightlifting you will always still be training the front squat and the Clean. You will have plenty of technique work for that upright vertical torso position. And along these lines, there are Weightlifting coaches, like Mike Burgener, who don’t use either the low-bar or high-bar squat – they just use front squats and Clean pulls. So, if you’re incorporating any squat that is not a front squat, you’re really doing so to build strength. Strength is paramount in Weightlifting, and low-bar squats build strength exceedingly well. Might high-bar squats do it better, possibly, but that’s a harder argument to make as so few Weightlifters have low-bar squats as a staple of their routine.

The CrossFit Argument: This section is why I really wanted to write this article. I think the major problem with the low-bar vs high-bar argument is that it has morphed from being just an argument about training Weightlifters to an argument for and against the lift regardless of the situation. More specifically, you are now seeing CrossFit coaches saying the low-bar squat is not appropriate because it does not carry over to the functionality of Weightlifting. But a CrossFit coach is not a Weightlifting coach. In response to this, writers have said, yes, but there are so many Weightlifting movements in CrossFit, that you should focus on the lifts that carry over best to these movements. By analogy, if you don’t train with emphasis for this carry over, you’re leaving a lot on the table. Well, I don’t see this as entirely accurate. My points in the Weightlifting argument above are relevant in response, but here are a few other key points:

  • CrossFit having a lot of Weightlifting is relative. It certainly can. If you follow Outlaw CrossFit, then there will be a ton of Weightlifting. Outlaw has basically morphed into a Weightlifting program where its followers also do some CrossFit (see Outlaw Way). However, performing Weightlifting every day is not CrossFit as it was originally designed, nor is it how it is taught and programmed now by HQ. Don’t get me wrong, I’m a huge fan of Outlaw and I program a lot more Weightlifting than traditional CrossFit would suggest. But this is because the lifts are very technical and require lots of practice (and because they are fun). It is not because CrossFit is now largely Weightlifting.
  • A CrossFit coach saying a low-bar squat has no carry over to Weightlifting is an even weaker argument. It fails on the general strength point I noted above in the previous section. The hardest thing for CrossFitters to develop, and what takes the longest to achieve, is strength. If they can get stronger, it will carry over to many of the CrossFit movements and their overall performance. Strength aside, the carry over argument fails because we don’t always use perfect carry over in CrossFit. If we wanted perfect carry over we would never let people learn handstand push-ups against a wall first as this doesn’t have good carry over to a proper, stacked freestanding handstand/handstand walk. Different motor patterns have to be trained for these, and they are. But that is what CrossFit is all about. It’s about being very good at many different things. It’s about being a master of many different movement patterns. Saying you won’t train the low-bar squat because the movement pattern is different than a Clean, is like saying you won’t train the Push Press because the movement pattern is different than the Split Jerk. But of course, most coaches in fact do train both.
  • As a CrossFit Coach you are going to have a wide mix of clients with varying skill and strength levels. I have found that the “knees caving in” phenomenon at the bottom of the squat can be a result of very weak abductors and adductors. Cuing “knees out”, often isn’t enough. I’ve found that even in relatively strong squatters, this can be a problem and that cycling in some low-bar squatting solves the problem nicely.
  • High-bar squatting actually leaves a fair bit on the table for a CrossFitter. In particular, hamstring strength. Ask a typical CrossFitter to perform a Glute Ham Raise with no bend in their hip. Odds are they won’t be able to do it. Low-bar squats help build your hamstring strength.
  • As a CrossFit Coach you are going to have clients that will want to be competitive and compete in either the Open or higher levels. As soon as this comes into play, they are going to want to be as efficient as possible in performing movements such as the squat. A full depth squat as trained in the front squat or high-bar squat is not always advantageous when the workout requires certain weighted movements (i.e., overhead squats). The range of motion requirement is hip crease below parallel, not all the way down, and this will get the reps completed faster. When does this movement pattern get trained? Almost never, and it’s hard to hit just right if you’ve never trained it. But if you have experience low-bar squatting, you will know where to stop intuitively.

The CrossFit Argument Wrap-Up: The CrossFit argument against low-bar squatting is a very weak one. By definition CrossFitters should be above average in a wide array of skill sets and motor patterns. This is the essence of CrossFit. Why the argument even arises is because CrossFit Coaches are doubling as Weightlifting Coaches these days. I think this has been great for CrossFit and the sport of Weightlifting (I am a Weightlifting Coach as well as a CrossFit coach). But not every CrossFitter wants to be a Weightlifter. So, if low-bar squats are being programmed for CrossFit in addition to other key movements (e.g., Clean, front squat and possibly low-bar squats), you’re getting the best of all worlds. And this is why I rotate low-bar squats into my programming. In a Barbell Club class, which focuses solely on Weightlifting, the decision to use low-bar squats is more complicated for the reasons discussed above in the Weightlifting section. For our class, I do not program in low-bar squats (or any other pure strength developer) as we offer a separate strength class and the time is better spent training Weightlifting technique. But again, this decision depends on your class structure and demographic.

So, next time this argument arises, you have a different perspective on why low-bar squats might be incorporated in training. And most importantly, you will have an appreciation for how the argument against low-bar squats must be placed in a specific context. Who you are training, (age, experience, individual movement patterns/deficiencies) and the goal of the training (strength, technique, etc.) must be considered. There is no one-size fits all answer to training.

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10 Science-Backed Tips to Help Prevent Hip Fractures

My latest article appears as a guest post on The article presents 10 tips that may help prevent hip fracture and gives scientific studies in support of each. Click here to read the article.

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The Importance of Proper Dosing

When I review scientific studies on this website, I always end my review with a “limitations” section. The section is a list of factors or issues that may limit the reproducibility of the study (i.e., self-reporting for food intake), limit who the study is relevant to (e.g., men, women), and so on. When dealing with studies of chemical compounds or drugs, dosing is a very important variable and must be taken into account. I haven’t reviewed a lot of studies where this was an issue, but there were two instances I wanted to point out as they slipped under the radar.

The first pertains to my previous post, “No, a Glass of Wine Does not Equal 1 Hour of Exercise.” This study was overinterpreted by the media, but in my discussion, I left dosing off my limitations list. One of my readers noted that the dose of resveratrol (the compound of interest found in wine) administered to the rats was 4g/kg of body weight. If we take the average rat to weight 300 g (.3kg), then rats were getting about 1.2g of resveratrol. For humans, if they drink a medium sized glass of wine, they are consuming about 0.175 liters of wine. If we are generous and say that the amount of resveratrol in a liter of wine is 7 mg (0.007 g), then one glass of wine gives a human a dose of 1.2x10e-6 (or 0.0000012 g). You can see here that by drinking a glass of wine you are getting nowhere near the amount of resveratrol the rats were getting. In comparison to a human drinking a glass of wine, the rats were overdosed. This is not a fair comparison.

The other instance arose in the article I wrote for entitled, “5 Supplements That Science Recommends for Fitness.” In the article I noted that science backed the use of caffeine to improve performance, which it does. But the original version of the post didn’t have any mention of dosing. Of course the articles I cited in the article give the dosings used (3-4mg/kg body weight), but most readers likely wouldn’t look for that. This equates to around 320 mg for a 180lb person. Most caffeine supplements on the market are pills of 300 mg or less and suggest taking only 1 tablet, so this is in line with the studies. But caffeine is a stimulant. What if you took more than this amount? Well, it turns out this is exactly what a number of teenagers have been doing and a number of them have died. It appears they were using caffeine as a supplement, but taking it in powdered form. In this form, measurement was up to them and made in teaspoons – and 1 teaspoon is about 5 grams. This is over 15 times the amount of caffeine adults were given in the studies I cited. You can see how this might be a recipe for disaster.

The limitations of studies are extremely important. Virtually every study has one or more limitations that make the findings impossible to directly apply to human health and fitness without additional studies to support their claims. Dosing is a common limitation in studies of chemical compounds and supplements, so keep this in mind the next time you read a headline that seems too good to be true…it probably is.

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