Nutrition

November 24, 2013

Nutrient Timing: Don’t Let Confirmation Bias Stand in the Way of Science

Earlier this year, Alan Aragon and I published a review on the efficacy of nutrient timing with respect to enhancing muscular adaptations. The article, titled Nutrient timing revisited: is there a post-exercise anabolic window?, challenged the popular claim that nutrients must be consumed immediately after training to maximize muscular adaptations. For those who want the “consumer friendly” version of the paper, I posted a summary of findings in an earlier blog post; you can read it here.

Recently, Dr. John Ivy took issue with our findings in this review paper published in the American Journal of Lifestyle Medicine. Here is the specific passage where Dr. Ivy references our paper as well as his associated commentary attempting to refute its conclusions:

Whether there is an advantage to nutritional supplementation within the first hour after exercise has been recently challenged. It has been pointed out that the rate of protein synthesis was the same when a supplement composed of 6 g of an essential amino acid (EAA) mixture and 36 g of carbohydrate was provided either 1 or 3 hours after resistance exercise (Rasmussen et al. 2000). It was also reported by Tipton et al. that immediate pre-exercise ingestion of an EAA/carbohydrate solution resulted in a significantly greater and more sustained muscle protein synthesis response compared to its immediate postexercise ingestion. Moreover, the effect of an acute bout of exercise on muscle protein synthesis has been found to last for several days (Chesley et al. 1992; Phillips et al. 1997).

A closer evaluation of these studies, however, shows they do not refute or diminish the importance of supplementation in the first hour postexercise. For one, Fujita et al found that supplementing 1 hour before exercise with an EAA/carbohydrate supplement did not result in enhanced postexercise muscle protein synthesis. Second, Tipton et al later reported no significant difference in net muscle protein synthesis postexercise when 20 g of whey was consumed immediately before versus 1 hour postexercise. Third, when the effect of timing of nutrient supplementation on protein synthesis postexercise is evaluated, the supplement ingested closest in time to the exercise generally has the greatest impact. For example, the increases in muscle protein synthesis reported by Phillips et al at 3, 24, and 48 hours after exercise were 112%, 65%, and 34%, respectively. Finally, there are few studies that actually compare the response of supplementation immediately or within the first 45 minutes postexercise with delaying supplementation for several hours as evaluated by Okamura et al. and Levenhagen et al.. In summary, most acute exercise studies clearly support supplementation soon after exercise for optimal stimulation of protein synthesis and protein accretion.

I’ll start off by saying that I have great professional respect for Dr. Ivy. He is an esteemed professor in the Kinesiology and Health Education department at the University of Texas as well as a renowned nutritional researcher, with a long history of publications in peer-reviewed journals. What’s more, Dr. Ivy literally wrote the textbook on nutrient timing. He has been a staunch proponent of the practice for many years, and frequently lectures on its complexities. But simply because someone is considered an authority on a topic does not mean that he should be above reproach. Science is about evidence. For science to have integrity, we must be willing to challenge popular dogma and test whether it stands up to scrutiny.

In my opinion, the paper by Dr. Ivy falls far short in this regard. Instead, it comes across as a classic example of confirmation bias where evidence is cherry-picked to support a pre-determined opinion. What follows is a point-by-point rebuttal of the points made by Dr. Ivy.

1. First, Fujita et al found that supplementing 1 hour before exercise with an EAA/carbohydrate supplement did not result in enhanced postexercise muscle protein synthesis.

I’ll start with a brief summary of this study: 22 subjects performed a bout of resistance training for the lower body. One group (n=11) consumed a pre-exercise drink containing carbohydrates and protein while the other group (n=11) did not ingest nutrients prior to training. Results showed an increase in post-exercise fractional synthetic rate of ~50% with no significant differences between groups.

On the surface, these findings might seem to support Dr. Ivy’s claim that post-workout nutrition is more imporant than pre-workout nutrition. However, a closer examination reveals otherwise.

First, what Dr. Ivy conveniently failed to point out was this little nugget from the study: “However, the postexercise time course for FSR was different between the two groups in that during exercise the FSR did not decrease below basal values in the EAA + CHO group, and the postexercise increase in FSR was delayed compared with the fasting control group.” Moreover, this is but one study on the topic. Other studies have reported either similar or greater increases in protein synthesis from pre-workout protein consumption versus consuming the same nutrients post-exercise. If you are going to broach the acute response angle, it should be done in the context of the body of literature. At best, an unbiased assessment would say that evidence remains equivocal on the topic.

Perhaps more importantly, Dr. Ivy’s contention here in no way proves the existence of a narrow post-exercise window. Even if post-workout nutrition is more important than pre-workout consumption (which remains debatable), the reference provided does not indicate whether consuming nutrients within 1 hour post-workout would confer any advantages over consuming them say 3 hours post-workout.

2. Second, Tipton et al later reported no significant difference in net muscle protein synthesis postexercise when 20 g of whey was consumed immediately before versus 1 hour postexercise.

I just mentioned this study in Point 1 to counter Dr. Ivy’s claims of a narrow anabolic window of opportunity. In short, the study showed no differences between consuming 20 grams of whey either an hour before or an hour following exercise. How does this support the concept of a narrow anabolic window? If anything, it suggests no benefit to post-exercise nutrient consumption. Dr. Ivy needs to clarify his position here.

3. Third, when the effect of timing of nutrient supplementation on protein synthesis postexercise is evaluated, the supplement ingested closest in time to the exercise generally has the greatest impact. For example, the increases in muscle protein synthesis reported by Phillips et al at 3, 24, and 48 hours after exercise were 112%, 65%, and 34%, respectively.

Again, I am not clear on how the study cited here supports the concept of a narrow post-workout window? The protocol examined protein synthesis at 3, 24, and 48 hours following a bout of resistance training. The response was greater at 3 hours than at 24 or 48 hours. I am at a loss as to the relevance of these findings with respect to immediately consuming nutrients versus delaying consumption for a period of time. Perhaps I’m missing something?

4. Finally, there are few studies that actually compare the response of supplementation immediately or within the first 45 minutes postexercise with delaying supplementation for several hours as evaluated by Okamura et al. and Levenhagen et al..

It’s true that there are a paucity of studies examining the acute response to consuming protein immediately after training versus delaying consumption. My first question thus would be: Given the dearth of such research, how can Dr. Ivy claim there is such overwhelming evidence in favor of nutrient timing if this is indeed what he is using to formulate his opinion?

But let’s overlook this point and explore what research does in fact show. Here Dr. Ivy cites two studies to support his contention. The first one, by Okamura et al. investigated the response to the timed protein feeding after treadmill running in dogs. I’m going to toss this one out as pretty much irrelevant to the topic. It’s an animal study using aerobic training; not exactly indicative of the anabolic response of hard-training lifters. The other study by Levenhagen et al. was a human trial, and it did show that lower body (and whole body) protein synthesis of the legs was increased significantly more when protein was ingested immediately versus 3 hours after exercise. Problem is, the training involved moderate intensity, long duration aerobic exercise. This raises the distinct possibility that results were attributed to greater mitochondrial and/or sarcoplasmic protein fractions as opposed to synthesis of contractile elements. Let’s face it, long duration aerobic exericse is not much of a muscle-building activity. In contrast, Rasmussen et al. investigated the acute impact of protein timing after resistance training–without question a better indicator of synthesis of muscle contractile elements. In this study, no significant differences were seen in the protein synthetic response after consuming nutrients 1 versus 3 hours post-exercise.

5. In summary, most acute exercise studies clearly support supplementation soon after exercise for optimal stimulation of protein synthesis and protein accretion.

Apparently, Dr. Ivy feels he has made a compelling case to substantiate this broad, sweeping statement. As discussed herein, I think not. You be the judge.

By Dr. Ivy’s own admission, there are only a limited number of studies that have investigated the acute response to nutrient timing, and the findings of those that have endeavored to do so are discrepant. If this is indeed the basis for the nutrient timing hypothesis, it’s built on a flimsy house of cards.

Later in his review, Dr. Ivy proceeds to discuss the research looking at chronic muscular adaptations pursuant to nutrient timing. Longitudinal studies would seemingly have greater relevance to practical application, as acute measures of protein synthesis are not necessarily predictive of the long-term hypertrophic responses to resistance training. There actually are a number of studies that have investigated the temporal effects of nutrient provision on muscle hypertrophy following regimented resistive exercise. Alan and I discussed these papers in detail in our review. I won’t rehash the specifics here, but in short some studies show a benefit while others do not. Dr. Ivy curiously chose to extol the virtues of the select few that provided support to his opinion (including a study carried out in rodents and another that inexplicably found no increases in muscle mass when subjects delayed protein consumption a mere two-hours after a training bout over 12 weeks!) while harping on the limitations of those in opposition. Interestingly, he criticizes a study by Verdijk et al. (that failed to show a benefit for nutrient timing) because the dose of protein (20g) was too low while failing to levy the same criticism of a study by Esmarck et al., which showed a benefit to nutrient timing using a protein dose of only 10g! Confirmation bias?

To provide further clarity on the topic, I recently collaborated with Alan and James Krieger to conduct a meta-analysis as to the effects of protein timing on muscular adaptations. We compiled the results of 23 studies on the topic using rigid inclusion/exclusion criteria. In brief, findings showed no differences between immediate versus delayed nutrient consumption with respect to muscle strength or hypertrophy; any benefits from timing were attributed to an increased protein intake as opposed to temporal factors. The meta-analysis will be published soon in the Journal of the International Society of Sports Nutrition. I’ll have lots more to say about the study once it is available in print.

For the record, Alan and I limited the focus of Nutrient timing revisited: is there a post-exercise anabolic window? to hypertrophic adaptations. As we pointed out, there are certainly other areas where timing of meals can be a viable strategy, particularly for athletes who need to train or perform multiple times in the same day. What’s more, there is compelling evidence that resistance exercise sensitizes muscle to the anabolic effects of food. Thus, there is a benefit to consuming nutrients, and protein in particular, following a resistance training bout. The caveat is that you don’t necessarily need to worry about scarfing down nutrients the moment you finish lifting. Our findings suggest that the “window of opportunity” is probably around 4-6 hours following resistance exercise, with the specifics of timing dependent on when you ate your last meal prior to training. Delaying nutrient consumption for many hours after training would seem to be unwise.

In closing, there certainly is a need for more studies on the topic. I am open to changing my opinion should compelling evidence come to light. But based on our extensive review of literature, research supporting a narrow anabolic window is currently lacking.

If Dr. Ivy wishes to debate the topic, I welcome him to rebut my comments. I will gladly publish his response on my blog in its entirety without editing. Let’s put all the information out there so that the general public can form an educated opinion. After all, that is how science ultimately progresses and thrives.

Nutrition

August 24, 2013

High Protein Intake: Myths and Misconceptions About Safety (Part 1)

Read pretty much any academic nutrition text and you’ll get the same-old same-old about high-protein diets being harmful to your health. The concerns center around everything from cardiovascular disease to kidney function to bone resorption. Question is, are these claims grounded in science or are they mostly hyperbole?

We can dismiss the cardiovascular claims offhand as they are based on consumption of ketogenic diets. The issue here is not with protein intake per se but rather with saturated fat. Let’s be clear: you can have a high protein intake without consuming large amounts of dietary fat. They are not necessarily tied to one another. Lean poultry, fish and beef have a low fat content. So any discussion about cardiovascular issues should be relegated to dietary fat consumption irrespective of protein intake (and for the record, there is much dispute as to whether saturated fat actually plays a role in atherosclerosis – but that’s a topic for another day).

That out of the way, I’ll delve into the other areas of contention. In this post I’ll cover the effects of a high protein intake on kidney function. In Part II I’ll explore the impact on bone. Okay, let’s dig in.

The claim that a high protein intake is detrimental to the kidneys has been attributed to Dr. Barry Brenner, a physician at Brigham and Women’s Hospital. A little background is in order to understand the purported issues. The metabolism of protein entails a complex sequence of events for proper assimilation to take place. During digestion, protein is broken down into its component parts, the amino acids (via a process called deamination). A byproduct of this occurrence is the production of ammonia, a toxic substance, in the body. Ammonia, in turn, is rapidly converted into the relatively non-toxic substance urea in the liver, which is then transported to the kidneys for excretion. The excretory process initially takes place in an area of the kidneys called the glomerulus, where waste is filtered through a large network of capillaries.

Brenner proposed that the associated urea production from excessive protein intake overloads the glomerulus, thereby causing renal injury and dysfunction. This became known as the “Brenner Hypothesis.” Brenner’s work in the area was published in the prestigious New England Journal of Medicine and the hypothesis subsequently became gospel in academic nutritional circles.

Here’s the rub: Brenner’s hypothesis was based on data from animal studies and those with existing renal disease. And as any good scientist knows, you cannot necessarily extrapolate such results to a healthy population.

An examination of the literature shows that, within wide limits, there is no evidence that a diet high in protein has any detrimental effects on those with normal renal function. Healthy kidneys are readily able to filter out elevated amounts of urea. In a review of research, Martin et al. concluded that “we find no significant evidence for a detrimental effect of high protein intakes on kidney function in healthy persons after centuries of a high protein Western diet.” These findings are consistent with those in a review on the effect of high protein diets in an athletic population. Studies have examined protein intakes in excess of three times the RDA without noting ill-effect. And in case you want to argue that the negative effects of protein intake on renal function take a long time to manifest and thus may not be detectable in shorter-term studies, a recent study by Lowery et al. found no markers of renal damage over a nine-year period in a cohort of healthy resistance trained subjects who consumed an average of 2.5 g/kg/day. It should be noted that increased protein consumption does lead to increases in renal size over time. However, studies show that this is a normal adaptation that has no adverse effects on kidney function.

So how much is too much? It has been postulated by some researchers that an intake greater than ~4 to 5 g/kg/day may exceed the body’s ability to convert the excess nitrogen load to urea for safe excretion. Thus, a 165 pound male would theoretically fall into the safe range at anything up to about 300 g/day; a guy weighing 220 pounds would have an upper limit of ~400 g/day. That’s *a lot* of protein! In actuality, this recommendation is probably a bit conservative. A portion of the protein you consume does not require deamination since it is directly utilized for structural remodeling of bodily tissues as well as production of hormones, enzymes, and other functions. Thus, safe levels of intake conceivably would be somewhat higher than previously thought.

Bottom line: High protein intakes may be detrimental to those with existing renal dysfunction, but there is no evidence that any negative effects are seen in individuals with healthy kidneys. Consumption of up to approximately 4 g/kg/day appears to pose no increased health risk when kidney function is normal. It’s been well-demonstrated that resistance-trained individuals require at least twice the amount of protein compared to non-lifters (although the benefit of consuming more than ~2 g/kg remains questionable from an anabolism standpoint). Moreover, higher protein intakes are beneficial for fat loss, both in terms of promoting satiety as well as reducing muscle catabolism during times of caloric restriction.

Stay tuned for Part II where I’ll discuss the claim that high protein diets are harmful to bone.

Stay Fit!

Brad

Nutrition

April 13, 2013

Q&A: Protein Requirements During Resistance Training

Hi Brad

David,
Denmark

Hi David:

The focus on “ideal bodyweight” is simply a way to qualify that an overweight person does not need extra protein to support growth. As an extreme example, if you weigh 300 pounds at 50% body fat, there is no added benefit to consuming ~300 g/day of protein; the additional intake it’s not going to help you build more muscle. Curiously, however, the literature historically has historically reported protein requirements in terms of bodyweight without standarizing recommendations for percent body fat. Given that body composition of subjects varies from study to study, this makes it somewhat difficult to tease out the true lean tissue requirements for anabolism.

There is compelling evidence that those involved in resistance training need more protein than sedentary couch potatoes. This is not even debatable. So assuming you regularly lift weights (and if not, get with the program!) how much protein should you consume? There are a number of mitigating factors here. First and foremost is caloric intake: a caloric surplus (i.e. taking in more calories than you are expending) will reduce protein requirements, while a caloric deficit (taking in fewer calories than you are expending) will increase protein requirements (Mettler et al. 2010). Moreover, the protein needs for lean individuals in a caloric deficit will be higher than that of those who are overweight.

Gender also has an impact on protein requirements. Specifically, women are better able to preserve lean mass compared to men during times of reduced caloric intake (Lemon, 2000). This appears to be a survival mechanism related to maintenance of reproductive function. Bottom line is that men are more apt to lose muscle while dieting if protein consumption is low.

Of course, genetics will also enter into the equation. Research studies report the mean (i.e. average) value of all subjects in the trial. Some individuals will display greater needs while others not so much. Unless you are tested individually, there is no way to know your exact requirements.

Finally, there is some evidence that highly experienced lifters actually need *less* protein than those in the early stages of training (Phillips et al. 2007). It is theorized that well-trained individuals become more efficient at utilizing dietary proteins for tissue building, thereby reducing requirements. The validity of these findings remain to be determined.

With this as background, my general recommendation as outlined in The MAX Muscle Plan is to consume approximately 1 gram per pound of “ideal” bodyweight, which I subjectively qualify as being around a 10% body fat level. This is slightly above the generally prescribed levels necessary to maintain a non-negative protein balance in resistance-trained individuals (Kersick et al. 2008). My reasoning is to provide a margin of safety. An insurance policy, if you will. IMO, there is a good cost/benefit ratio to such an approach: keeping protein intake a little higher *might* confer an anabolic advantage depending on some of the previously mentioned factors; at worst you’ll simply oxidize the extra protein for energy (assuming total caloric intake remains constant).

And in case anyone thinks that consuming higher protein will damage your kidneys or bones, think again. Provided that you are otherwise healthy, studies show no negative effects on renal function (Martin et al. 2005; Poortmans and Dellalieux, 2000) or bone health (Bonjour, 2005).

Hope this helps. Cheers!

Brad

1. Bonjour JP. Dietary protein: an essential nutrient for bone health. J Am Coll Nutr. 2005 Dec;24(6 Suppl):526S-36S.
2. Kerksick C, Harvey T, Stout J, Campbell B, Wilborn C, Kreider R, Kalman D, Ziegenfuss T, Lopez H, Landis J, Ivy JL, Antonio J. International Society of Sports Nutrition position stand: nutrient timing. J Int Soc Sports Nutr. 2008 Oct 3;5:17
3. Lemon PW. Beyond the zone: protein needs of active individuals. J Am Coll Nutr. 2000 Oct;19(5 Suppl):513S-521S.
4. Martin WF, Armstrong LE, Rodriguez NR. (2005). Dietary protein intake and renal function. Nutr Metab (Lond). 20;2:25
5. Mettler S, Mitchell N, Tipton KD. Increased protein intake reduces lean body mass loss during weight loss in athletes. Med Sci Sports Exerc. 2010 Feb;42(2):326-37
6. Phillips SM, Moore DR, Tang JE. A critical examination of dietary protein requirements, benefits, and excesses in athletes. Int J Sport Nutr Exerc Metab. 2007 Aug;17 Suppl:S58-76.
7. Poortmans JR, Dellalieux O. (2000). Do regular high protein diets have potential health risks on kidney function in athletes? Int J Sport Nutr Exerc Metab. 10(1):28-38

Nutrition

February 15, 2013

Nutrient Timing Revisited: The Anabolic Window of Opportunity

I recently co-authored a review article with my good friend and colleague Alan Aragon titled, “Nutrient Timing Revisited: Is there a post-exercise anabolic window?” I’m happy to say the article was published in the prestigious Journal of the International Society of Sports Nutrition and has received a lot of favorable attention. Here are the highlights:

1) Nutrient timing can be a beneficial strategy for maximizing muscular gains, but the “window of opportunity” is not necessarily as narrow as often believed.

2) Provided that a protein-rich meal is consumed within about 3-4 hours prior to a workout (or possibly even longer, depending on the size of the meal), you don’t have to stress about chowing down a post-workout meal as soon as you finish training. For those who train partially or fully fasted, on the other hand, consuming protein immediately post-workout becomes increasingly more important to promote anaoblism.

2) Although research is somewhat equivocal, it seems prudent to consume high-quality protein (at a dose of ~0.4-0.5 g/kg of lean body mass) both pre- and post-exercise within about 4-6 hours of each other depending on meal size.

3) Contrary to popular belief, consuming post-exercise carbohydrate does not meaningfully enhance anabolism. Moreover, unless you are performing two-a-day workouts involving the same muscle group(s), glycogen replenishment will not be a limiting factor in those who consume sufficient carbohydrate over the course of a given day. So from a muscle-building standpoint, just focus on meeting your daily carb requirement as opposed to worrying about timing issues.

One of the most surprising aspects of writing this paper was the lack of clarity in the current body of research. Alan and I reviewed every direct study conducted on the subject. Not only were results of these studies highly conflicting, but most had confounding issues that obscured the ability to tease out the impact of the effects of consuming nutrients post-workout. I am planning a study in my lab that addresses the gaps in the literature. Hope to begin data collection in the near future. Stay tuned!

In case you want to delve into the heavy science on the topic, here is a link to a PDF of the article:

Nutrient Timing Revisited: Is there a post-exercise anabolic window?

Cheers!

Brad

Nutrition

August 27, 2011

Is Saturated Fat Intake Associated with Heart Disease?

For decades now, physicians and dieticians have warned against the perils of consuming foods high in saturated fat. These recommendations are based on years of epidemiological evidence that saturated fat intake is associated with an increased risk of numerous diseases–particularly cardiovascular disease. The majority of the general public has taken this advice as gospel, demonizing saturated fat as the nutritional enemy.

Recently, however, some researchers have begun to challenge the accepted dogma that saturated fat intake actually increases cardiovascular risk. A recent systematic review by Siri-Tarino and colleagues in the American Journal of Clinical Nutrition sought to investigate the subject. The review used a technique called meta-analysis to investigate the association of saturated fat and cardiovascular disease. In case you don’t know, meta-analysis involves pooling the results from multiple research studies so as to improve statistical power and arrive at a more definitive interpretation of data. The review identified 16 studies that evaluated the association between saturated fat consumption and heart disease and 8 studies that evaluated the association of saturated fat and stroke. After performing statistical analyses, the researchers concluded that “there is insufficient evidence from prospective epidemiologic studies to conclude that dietary saturated fat is associated with an increased risk of coronary heart disease, stroke, or cardiovascular disease.” A pretty definitive statement, wouldn’t you say?

Based on the results of the study, it would seem that previous recommendations have been off-base and that we should feel free to slap the butter on thick and have that extra serving of bacon for breakfast. After all, a systematic review is considered the gold-standard in evidence-based practice. What more info do we need? Well, not so fast…

As is often the case, things aren’t necessarily as simple as they may seem. In the same journal issue, Dr. Jeremiah Stamler provided a detailed critical assessment of the Siri-Tarino et al. study that exposes issues with some of the methodologies of the review. While I don’t necessarily agree with all of Stamler’s points, he nevertheless does make some interesting observations.

First and foremost, there are potential biases in the method of dietary analysis in the studies evaluated by Siri-Tarino et al. Namely, 4 of the studies relied on a single 24-hour dietary recall to determine nutrient intake. This method of data collection is highly subject to recall bias and research shows it “provides a very inadequate estimate of usual intake of individuals”. Interestingly, only 1 of these studies showed an increased relative risk for saturated fat intake with respect to heart disease. On the other hand, of the 5 studies that used dietary history or multiday food records–a more accurate method of determining food intake–all 5 showed an increased relative risk.

Stamler also notes that results of the 11 studies that investigated “hard” fatal coronary heart disease (i.e. deaths from heart attack) showed a significant increase in relative risk from saturated fat intake as opposed to the 5 studies looking at “soft” data (those who experience increased total cardiovascular risk). This suggests that saturated fat intake may have a greater effect on causing cardiovascular fatalities irrespective of increasingly markers of cardiovascular disease. In other words, it is possible that a high saturated fat intake might result in a greater incidence of death from heart disease than lower intakes even if overall risk for disease is not significantly increased (i.e. progression of the disease is worse).

So what do we make of this data? Do we believe the results of the systematic review–a gold standard in evidence-based practice–that saturated fat intake is benign? Or do we dismiss it because of its inherent limitations? My view on the subject is somewhere in the middle. People are often all-too-quick to pounce on new research as the be-all, end-all on a particular topic. This is invariably a mistake and it certainly would be here. Research will always have inherent limitations and biases; this is the nature of the beast. Still and all, we must be open to new information and not rigidly adhere to previously held beliefs. As such, we must sift through the evidence and then use logical reasoning to try to make sense of what we know.

There is very good evidence that saturated fat intake increases cholesterol production, including increased LDL levels (the so-called “bad” cholesterol). However, recent research indicates that LDL levels may not be as important as once thought in promoting atherosclerosis. Rather, it is suggested that the size of the LDL particles are more indicative of cardiovascular risk, with the smaller, denser particles being atherogenic and the “large, fluffy” particles being benign. While this hypothesis is interesting, it remains largely untested in controlled research. We simply don’t know as much as we previously thought on the topic and more research is needed to draw firm conclusions.

There is emerging evidence that chronic inflammation is involved in the development of cardiovascular disease. It is therefore possible that the combination of high inflammatory markers and a high saturated fat intake may exacerbate plaque build up in the arteries and ultimately lead to an increased risk of a cardiovascular event. Again, while this hypothesis is interesting, it requires further research.

Considering the best available evidence, my advice is that you are probably better off limiting saturated fat consumption. If nothing else, saturated fat intake does little if anything for biological function (it does have a positive effect on HDL and testosterone, but so do the more biologically active monounsaturated fats). Moreover, emerging research suggests that replacing saturated fat with unsaturated fat can reduce cardiovascular risk. Given that omega-6 fats are pro-inflammatory, you’re best bet is to focus on monounsaturated fats (like those found in avocado, olive oil, almonds, etc) and omega-3s (like those found in cold water fish such as salmon, sardines, etc). This is considered to be one of the key components of the cardioprotective effects of the Mediterranean Diet. The omega-3 fats, in particular, have been shown to be heart-healthy (as well as potentially conferring many other health benefits for virtually every organ system in the body).

On the other hand, you don’t need to be anal about counting every gram of saturated fat consumed. For the majority of people, having a modest amount of saturated fat in your diet is not likely to have a significant effect on cardiovascular risk. Nutrition is highly individualized and it may well be that some people are more susceptible to negative effects from saturated fat intake than others. Hopefully the day is approaching when we will be able to customize nutritional regimens based on an assay of our individual genetic code. Until then, a balanced approach is warranted.

Stay Fit!

Brad

Nutrition

June 19, 2011

High Protein Diets and Kidney Function

A recent New York Times article took to task the all-too-often-expressed claim that high protein diets are bad for the kidneys. After citing some of the relevant research on the topic, the article goes on to conclude: “…studies show that in healthy adults, increased protein intake does not put excess strain on the kidneys.” Hooray for the New York Times for finally acknowledging what those of us who keep abreast of research have known for years! The real question is, What took so long?

The myth that protein is detrimental to the kidneys dates back to the early 1980’s when Dr. Barry Brenner, a nephrologist at Brigham and Women’s Hospital, published several research papers linking high protein diets to the progression of renal disease (1). In short, Brenner claimed that a high protein intake increased glomerular filtration rate (i.e. the volume of fluid filtered in the kidneys), ultimately leading to renal dysfunction. This came to be known as the “Brenner Hypothesis” and was adopted as gospel by a large segment of the nutritional community. To this day, most college nutritional texts continue to espouse the dangers of a high protein consumption on the kidneys.

The problem with the Brenner Hypothesis is that it was based almost entirely on data from animal subjects and those with existing kidney disease. Extrapolating results from such populations to healthy humans is a classic case of improperly generalizing findings. Research 101 dictates that external validity (i.e. generalizability) is limited to the population studied. That’s certainly the case here.

As noted in the New York Times article, research on healthy individuals has continually failed to find any negative correlation between protein intake and kidney problems. While a higher protein consumption does lead to changes in renal size and GFR, these have proven to be normal adaptations with no adverse effects on kidney health (2). And this is not a case of cherry picking studies; results have held true in multiple research trials across a wide variety of demographic groups including athletes, the elderly, and the obese.

In fairness, it should be noted that studies on the topic have been limited to examining an intake of under 3 grams/kg of protein a day. Thus, it is not known if intakes above this amount might cause detrimental effects. However, 3 grams/kg/day is a substantial amount of protein, equating to a daily intake of about 250 grams of protein for a 180 pound guy. What’s more, there’s a large body of anecdotal evidence from athletes who consume extremely high protein diets (sometimes in excess of two times body weight) without displaying associated kidney issues. This would seem to indicate that higher intakes are not an issue but further research is needed for confirmation.

In sum, it’s about time to put to rest the myth that a high protein intake will harm your kidneys. Given that higher protein diets have been shown to be metabolically advantageous for those who are trying to lose weight and/or maintain a healthy body weight, we should be encouraging people to adopt such nutritional practices, not scaring them off with baseless claims.

Stay Fit!

Brad

1) Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease. N Engl J Med. 1982 Sep 9;307(11):652-9

2) Skov AR, Toubro S, Bülow J, Krabbe K, Parving HH, Astrup A. Changes in renal function during weight loss induced by high vs low-protein low-fat diets in overweight subjects. Int J Obes Relat Metab Disord. 1999 Nov;23(11):1170-7

Nutrition

May 28, 2011

Review of Alan Aragon’s Research Review

In case you don’t know, Alan Aragon is a popular expert on nutrition in general, and sports nutrition, in particular. I’ve seen several of Alan’s articles over the years on various internet sites (including one I mentioned in a recent post on How Many Meals A Day Should You Eat) and have always been impressed with his evidence-based approach. Recently I became aware that he publishes a monthly e-zine called, not surprisingly, Alan Aragon’s Research Review (AARR). I subsequently received a copy of the latest issue of AARR, for reasons which I will describe shortly. After reading through the publication, I thought I would share my views on it.

According to Alan’s website, AARR is “is an unbiased monthly critical analysis and application of the latest research pertaining to nutrition, exercise, and supplementation. This journal is designed to help the reader develop a solid understanding of important topics in fitness that are widely misunderstood. Overall, the goal is to provide a unique science & practice-based, multi-topic, bias-free, commercial-free, in-depth, ongoing resource of information.” Pretty lofty goals. Question is, does it deliver as promised?

Each issue of AARR apparently follows a similar format. It begins with an “Editors Cut.” Here Alan dissects a recently published peer-reviewed article. It is an in depth critical analysis where the respective article’s strengths and weaknesses are discussed at length (spanning several pages). The segment concludes with Alan providing his opinion of the article’s validity as well as commenting on any relevant practical applications. Alan is frank in his analysis; he says what he feels.

Of note, the subject of “Editors Cut” in the issue I received was actually an article of mine, recently published in the Strength and Conditioning Journal. He was nice enough to send along a copy so I could see his commentary on my article. He invited me to submit a rebuttal to his criticisms, if I so desired. I did. The gesture was appreciated.

Next up are several shorter reviews of published articles (usually one page in length). These reviews are segmented into three categories: Nutrition and Exercise, Supplementation, and a “Less Recent Gem” which, as the name implies, looks at an article published in the distant past. Although Alan does not go into the detail that he does in the “Editors Cut” section, the reviews are nevertheless quite detailed. He delves into the strengths and weaknesses of each study and makes practical applications where relevant.

The last article in AARR is called “In the Lay Press.” This segment evaluates a non-refereed consumer-oriented article with the same scrutiny afforded peer-reviewed publications. This is especially apt given the pomp and hype surrounding so many articles appearing on the web and in the muscle rags. Given the lack of peer-review in these articles, there is a lot more for Alan to pick apart…and he does so without pulling any punches.

What is my overall impression of AARR? Plain and simple, it’s one of the most definitive resources on nutrition that I’ve seen. Alan is extremely knowledgeable about the subject and obviously keeps up with current research (which sadly is rare, even amongst many nutritional professors). What’s more, Alan understands how to critically evaluate research studies with respect to internal and external validity, providing appropriate recommendations on their relevance. Just as importantly, he provides information in a completely unbiased manner without allegiances to any food or supplement industry companies (as is the case with many so-called “experts in the field). The content is good, the writing is good, and the recommendations are solid. It’s a winning combination.

As for my article, his review was very balanced and fair. He actually pointed out several things that, in retrospect, I should have clarified to a greater extent. It would have strengthened the article. I could have quibbled over a few of his criticisms, but these would have debatable points. Most importantly, I learned from the experience, which is what science is all about.

In conclusion, I would highly recommend AARR for anyone who wants the straight facts about nutrition, particularly as it relates to those involved in exercise programs. You can view a sample copy here and see for yourself if it is worth the investment.

Stay Fit!

Brad

DISCLAIMER: I am not affiliated with AARR and, as is my policy, receive no compensation of any kind from its sale or proceeds.

Nutrition

May 22, 2011

The Truth About Fructose

Fructose is a simple sugar (a monosaccharide, in technical terms) that has been the subject of a great deal of recent nutritional controversy. Alarmist websites, Youtube videos, and even some peer-reviewed research papers have railed against the consumption of fructose, linking it with obesity and the onset of disease. A popular “health guru” has gone as far to call it the “worst of the worst,” and has suggested that fruit intake be severely curtailed (fructose is found in fruit). Are these claims warranted?

To help clear up the confusion, I consulted with nutrition expert James Krieger. I’ve known James for about a decade, and have found him to be one of the most astute fitness pros around (you might remember that I wrote a post overviewing his meta-analysis about Single vs. Multiple Sets). Here he sets the record straight on what is often a misunderstood topic. I’m sure you’ll find his comments of great interest.

BJS: Thanks for agreeing to do this interview, James. Let’s first start off by telling us about your background.

JK: I am the founder of Weightology, LLC, a website dedicated to providing honest, accurate, evidence-based information on weight management. I have a Master’s degree in nutrition from the University of Florida, and a second Master’s degree in Exercise Science from Washington State University. I am the former research director for a corporate weight management program that treated over 400 people per year, with an average weight loss of 40 pounds in 3 months. My research papers have been published in journals such as the American Journal of Clinical Nutrition and the Journal of Applied Physiology. I am also the editor of Journal of Pure Power, an online magazine that delivers scientific information on training and nutrition to athletes and coaches.

BJS: Fructose consumption is a controversial subject these days. How does fructose differ from other simple sugars?

JK: Fructose is much sweeter than other sugars. There are also differences in the way your body metabolizes fructose compared to other sugars. Fructose doesn’t go straight to your bloodstream; instead, it is metabolized by the liver first. The liver can take the fructose, convert it to glucose, and then release that glucose into the blood. It can also take that fructose and store it as glycogen. Finally, it can convert the fructose to fat. It is this conversion to fat that causes a lot of confusion and alarmism.

BJS: There are studies showing that fructose can have a detrimental effect on various markers of health. What’s your take on this?

JK: There certainly are studies showing that fructose can have this detrimental effect. However, these studies have used extremely high doses of fructose. Unfortunately, people have taken this information to the extreme and have concluded that, since high amounts of fructose can be a problem, then any fructose must be a problem. This is simply not the case.

Do we consume too much fructose in our society? Certainly, but we consume too much of everything else too. It is a mistake to try to point the finger at one thing. Anything consumed in excess can be problematic.

BJS: What about the theory that fructose has a greater propensity to be converted into body fat?

JK: This theory unfortunately takes fructose metabolism out of context, and fails to address the bigger picture. People think this because fructose bypasses an important enzyme in the liver, and thus think it is easier to convert the fructose to fat. The problem with this line of thinking is that it fails to address the fact that fructose metabolism changes depending upon the energy state of the body. If you are in an energy deficit, the fructose will not have a greater propensity to be converted to body fat. Rather, it will be directed towards storage as glycogen, or conversion to glucose for energy.

The other problem with this line of thinking is people confuse triglycerides with body fat. If fructose is converted to fat in the liver, it doesn’t mean the fat ends up as body fat. In fact, there is some evidence that fructose is less likely to be converted to body fat. We also have to remember that any fat formed from fructose in the liver can be burned and used for energy. Again, we have to look at the big picture.

BJS: Fruits contain fructose. Should people limit their intake of fruits if they want to lose weight?

JK: As long as you are in an energy deficit, you will lose weight. It doesn’t matter how much fructose you consume. There is no valid scientific reason to limit intake of fruit. Fruit can actually be very beneficial for weight loss because of its fiber content, which makes you feel fuller. It is also low in energy density, and there is a lot of research showing that eating foods that are low in energy density helps promote weight loss.

In the weight management program that I did research for, our clients started the program on high protein shakes sweetened with fructose, and mixed with berries. Our clients were getting a lot of fructose in the diet from the combination of shakes and berries. Yet, they lost tremendous amounts of weight.

BJS: High fructose corn syrup (HFCS) is used in many food products. Is HFCS worse for you than sugar?

JK: There is little difference in the composition of sugar and high fructose corn syrup. Both contain similar amounts of fructose. The only reason manufacturers choose HFCS over regular sugar is because HFCS is cheaper.

When you look at all of the studies that compare sucrose (table sugar) metabolism to HFCS metabolism, they are identical as far as your body is concerned.

BJS: How do you explain the studies showing that obesity rates skyrocketed after the introduction of HFCS?

JK: This research suffers from a fallacy known as post hoc, ergo propter hoc (after this, therefore because of this). Just because event B happens after event A, doesn’t mean event A caused event B. Obesity also skyrocketed after the introduction of microwave ovens and VCR’s, but that doesn’t mean microwave ovens and VCR’s cause obesity!

BJS: What about the fact that HFCS isn’t “natural.” Should this matter?

JK: There is no evidence that products that are “natural” are any healthier or safer than products that are not “natural.” For example, there are many natural substances out there that are poisonous or carcinogenic to the human body. Calamus oil, which was a natural food additive before it was banned in 1968, is a carcinogen.

In fact, I often ask people to define what they mean by “natural” and they struggle to do so. If you think about it, there is really no clear cut way to determine what is natural or artificial. For example, aspartame is actually made up of natural ingredients (aspartic acid, phenylalanine, and methanol). So why would we call aspartame artificial? Also, we call Stevia natural, but that doesn’t make sense because it requires human intervention to extract it from the stevia herb.

BJS: Anything else you’d like to add on the topic?

JK: I would say that people do not need to worry about moderate fructose consumption. Basically, the idea of “everything in moderation” applies to fructose just like anything else. Thanks for the opportunity to interview!

Check out James’ website at: weightology.net

Check out the Journal of Pure Power at: Journal of Pure Power

Nutrition

May 20, 2011

How Many Meals a Day Should You Eat?

I recently wrote about the lack of scientific support for the theory that you should reduce carbs at night . In the same spirit (and by popular request), I thought I’d take the time to tackle another common nutritional theory. Namely, the claim that eating small, frequent meals stokes your metabolism.

I’m sure you’ve heard this one before. Bodybuilders and nutritionists have long preached that spacing out food consumption over five to six small meals a day is optimal for losing body fat. For years I too adhered to this belief. A wealth of emerging research, however, changed my viewpoint.

The strategy to eat small, frequent meals is based on the belief that when you go without eating for more than a few hours, your body senses deprivation and shifts into a “starvation mode.” Part of the starvation response is to decrease resting energy expenditure. In effect, the body slows down its metabolic rate to conserve energy. It’s a logical theory but alas it doesn’t seem to translate into practice, at least in the short-term (i.e. over about a 24 hour period or so). As such, the vast majority of studies examining metabolic rate have failed to show a clear advantage for increasing meal frequency.

On a similar note, the thought that frequent eating enhances the thermic effect of food (TEF)–a measure of the energy expended during digestion–is also flawed. A simple example should make this readily apparent. Let’s say you eat an 1800 calorie diet that averages a 10% TEF. If you space out meals equally so that you eat six times a day, the TEF would look like this:

Meal 1: 300 x .10 = 30
Meal 2: 300 x .10 = 30
Meal 3: 300 x .10 = 30
Meal 4: 300 x .10 = 30
Meal 5: 300 x .10 = 30
Meal 6: 300 x .10 = 30

Add up the numbers and total expenditure through the TEF will be 180 calories. Now let’s look at the same scenario except eating three times a day rather than six:

Meal 1: 600 x .10 = 60
Meal 2: 600 x .10 = 60
Meal 3: 600 x .10 = 60

Do the math and you’ll see it’s the same 180 calories expended through the TEF. This holds true regardless of how many times a day you eat.

Okay, so perhaps you want to focus on the benefits of more frequent meals on appetite. This is supposedly related to the effect of eating frequency on hormones. For one, it is claimed that large meals cause insulin spikes, which switch on various mechanisms that increase fat storage. The spikes then lead to a crash, where there is a tendency toward hypoglycemia (low blood sugar). Hunger pangs ensue and you invariably end up binging out. For another, an absence of frequent food is thought to increase the secretion of a gut hormone called ghrelin. Ghrelin is referred to as the “hunger hormone.” It exerts its effects by slowing down fat utilization and increasing appetite. Without consistent food consumption, ghrelin levels supposedly remain elevated for extended periods of time, increasing the urge to eat.

Frequent meals are purported to counteract these negative effects on hormones. Blood sugar is supposedly better regulated and, because there is an almost constant flow of food into the stomach, the hunger-inducing effects of ghrelin are suppressed, reducing the urge to binge out. Sounds logical, right? Sorry, another instance where logic and reality don’t mesh. Recent studies by Leidy et al. (1, 2) found no difference in appetite in those who consume six meals compared to three. Interesting, the researchers actually showed an increased satiety when the three-meal-a-day group followed a higher protein diet! On the other hand, consuming fewer than three meals a day does seem to have a negative effect on appetite (3), suggesting that this may be the minimum number of daily meals that need to be consumed from an appetite-control standpoint.

But what about body fat? Surely eating more frequently has to increase fat loss by some mechanism. Not! Provided calories are controlled, fat loss is similar between three-meals-a-day versus six-meals-a-day (4) A recent review paper (5) actually found that intermittent fasting–where people abstain from eating for upwards of 24 hours at a time–was equally as effective as caloric restriction in promoting weight loss. Read this again. The fasted subjects didn’t eat for an entire day at a time and still lost weight to a similar degree as those who ate daily meals. Apparently the starvation response is a lot more complex than some will have you believe.

A recent position statement by the International Society of Sports Nutrition covered the subject of meal frequency in detail. I’d highly recommend that you check out Alan Aragon’s critique of this paper for an in depth analysis.

In sum, current evidence doesn’t support the contention that eating more frequently enhances fat loss. Provided you eat a minimum of three meals a day, there does not seem to be any difference if frequency is increased beyond this number. Now this doesn’t mean that eating more frequent meals is a bad thing. I actually prefer a “grazing” schedule and have found it to be an effective eating strategy for my lifestyle. This is a personal choice that works for me. Others might find eating three times a day to be more appropriate.

The most important important factor here seems to be maintaining a regimented eating program–those who keep to a schedule see better results than those who don’t. It also should be pointed out that the majority of research studies have evaluated overweight subjects. Might more frequent meals help to strip away that last pound or two of body fat in otherwise lean individuals? As they say, further research is needed…

Stay Fit!

Brad

1) Leidy HJ, Tang M, Armstrong CL, Martin CB, Campbell WW. The effects of consuming frequent, higher protein meals on appetite and satiety during weight loss in overweight/obese men. Obesity (Silver Spring). 2011 Apr;19(4):818-24. PMID:

2) Leidy HJ, Armstrong CL, Tang M, Mattes RD, Campbell WW. The influence of higher protein intake and greater eating frequency on appetite control in overweight and obese men. Obesity (Silver Spring). 2010 Sep;18(9):1725-32.

3) Leidy HJ, Campbell WW. The effect of eating frequency on appetite control and food intake: brief synopsis of controlled feeding studies. J Nutr. 2011 Jan;141(1):154-7.

4) Cameron JD, Cyr MJ, Doucet E. Increased meal frequency does not promote greater weight loss in subjects who were prescribed an 8-week equi-energetic energy-restricted diet. Br J Nutr. 2010 Apr;103(8):1098-101.

5) Varady KA. Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? Obes Rev. 2011 Mar 17.

Nutrition

April 28, 2011

Should You Reduce Carbs at Night?

Bodybuilding lore has long preached that you should reduce carb intake in the evening. This is based on the theory that starches are more readily transformed to fat when eaten before bedtime. The reason goes something like this: The primary function of carbohydrates is to supply short-term energy for your daily activities. If carbs are not used immediately for fuel, they have two possible fates; they either are stored as glycogen in your liver and muscles or are indirectly (or in some cases directly) converted into fatty acids and stored in adipose tissue as body fat . Since activity levels usually are lowest during the evening hours, there is a diminished use of carbs for fuel. This would seem to set up an environment where the body is more inclined to convert carbs into fat. Sounds logical, right?

In the past, I had given the theory some credence based on the diurnal nature of insulin sensitivity. For reasons that aren’t entirely clear, insulin sensitivity is highest in the morning (1, 2). Hypothetically, this means your body is better able to assimilate carbs at this time, thereby keeping blood sugar levels stable. As the day wears on, insulin sensitivity gradually diminishes and, by evening, it’s at its nadir. Hence, carbs eaten at night would evoke a greater insulin response, fueling the processes that facilitate fat storage and suppress fat burning.

In addition, there is some research showing that consuming starches at night has a carry over effect to the next day. Specifically, eating a carbohydrate-rich dinner was found to increase the insulin response of the following morning’s meal (3). So not only are insulin levels elevated after dinner, but they apparently remain that way through breakfast if carbs are consumed in the evening.

While all this makes theoretical sense, it doesn’t seem to translate into practice. There is scant evidence that reducing carb intake in the evening has any negative effect on body composition. In fact, a recent study (4) suggests that evening carb intake may even have a beneficial impact! The study evaluated 78 obese police officers randomly assigning them to either an experimental diet where carbs were eaten mostly at dinner or a control group where carbs were spread out over the day. The study lasted 6 months–a good length of time to determine nutrition-related changes. The results? The subjects who ate most of their carbs at night displayed a greater weight loss, reduced abdominal circumference, and lower body fat compared to controls. The carbs-at-night group also had better satiety (as determined by lower hunger scores) and showed greater improvements in a variety of other metabolic parameters. The authors went on to conclude that “a simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared to a conventional weight loss diet in individuals suffering from obesity.” Whether these results will apply to leaner individuals who want to diet down to very low body fat levels isn’t clear, but it at least raises the possibility of a potential benefit.

Take home message: Theory doesn’t necessarily translate into practice. Just because something seems to make intuitive sense doesn’t mean it will work in the real world. It’s yet another reason to make sure you stay abreast of current research and use it to shape your approach to fitness.

Stay Fit!

Brad

1) Lee A, et al, Diurnal variation in glucose tolerance. Cyclic suppression of insulin action and insulin secretion in normal-weight, but not obese, subjects. Diabetes. 1992 Jun;41(6):742-9.

2) Morgan LM, et al, Diurnal variations in peripheral insulin resistance and plasma non-esterified fatty acid concentrations: a possible link? Ann Clin Biochem. 1999 Jul;36 ( Pt 4):447-50.

3) Wolever TM , et al, Second-meal effect: low-glycemic-index foods eaten at dinner improve subsequent breakfast glycemic response. Am J Clin Nutr 1988 Oct;48(4):1041-7

4) Sofer S, Eliraz A, Kaplan S, Voet H, Fink G, Kima T, Madar Z. Greater Weight Loss and Hormonal Changes After 6 Months Diet With Carbohydrates Eaten Mostly at Dinner. Obesity (Silver Spring). 2011 Apr 7. [Epub ahead of print]