Video Presentation: Recognising & Avoiding The Plagues of 'Broscience'

This month's post is another video. This time, it's one of me delivering a presentation rather than interviewing a fitness industry professional.

The presentation was recorded just over a month ago in London for the ISSN Diploma in Sports & Exercise Nutrition organised by Laurent Bannock of www.guruperformance.com.

Given the caliber of guest speakers, as well as Laurent himself, it was a privilege to talk in front of an audience who share an enthusiasm for nutrition. For anyone looking for an evidence-based qualification to pursue, I'd highly recommend the looking into the course as it perfectly bridges the gap between a degree and becoming a solid practitioner.

In the presentation, I discuss the tools available for recognising and avoiding 'broscience' and talk through some popular examples in the fitness industry, picking them apart from several angles.

Topics include:

1. Biosignature Modulation

2. Carb Back-loading

3. Metabolic damage

4. Pre-bed casein

I hope you enjoy it as much as I did putting it together...

Edit: the video has been removed by the user. Not to worry, here's a link to a PDF version of the slides.

BCAAs for Bodybuilders: Just the Science, Part 4 (Addendum; was Poliquin right all along?)

Just when I thought I was done with the BCAA series after exhausting the scientific literature, I came across some more research that put a spanner in the works. Many of you reading this know I’m not a fan of Poliquin in general, but if he turns out to be right and I’m wrong, I’m willing to change by position, as that is what every good scientist should do. As far as I’m concerned, I’m not interested in being right, but having the right answers. So if I am wrong, I consider it a learning opportunity.

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What is this research?

The research in question is two papers by Bul & Chitè published in an obscure Soviet (now known as Russia) journal in 1941 and 1942, respectively. The reason I missed this research during the time of writing my initial articles, is due to the fact that they can’t be accessed online, and therefore can’t be linked to, unfortunately. However, I was lucky enough to receive an email last week from a subscriber to my blog who kindly emailed me the two articles in full. Since they can’t be accessed online, I’d be happy to send them to whoever wants them, just drop me an email.

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What was found?

Because the papers were published in a Soviet journal, they were written in Russian. Luckily, one of these papers (the 1942 one) has been translated to English so I can only comment on the details of that particular study. In it, Bul & Chitè compared the effects of a BCAA-saline solution (0.2g/kg/h) with a placebo (saline solution), delivered intravenously every hour, for four hours, following a series of intense training drills, on measures of body composition and performance in a cohort of Soviet Special Operatives. Given the invasion of the Soviet Union in 1941 by the Germans, this type of study seems rather timely. After the 12-week trial, the authors observed an increase in muscle mass of 6.3kg and decrease in fat mass of 1.7kg in the experimental group, compared to values of 0.9 and 0.6kg, respectively, in the placebo-control group. To top things off, the experimental group gained an average of 28kg on their back squat and 37kg on their deadlifts, compared to 6 and 8kg, respectively, in the control group. Though I’ve highlighted limitations of such studies before, what makes this study unique is that subjects were consuming a maintenance calorie diet with already sufficient amounts of protein (2.6g/kg of protein). This is significantly more protein that that observed in other investigations, making things very interesting indeed!

Though this study is limited by the method of BCAA delivery (infusion vs. oral ingestion), as BCAA are rapidly digested and appear in the blood stream soon after ingestion, oral ingestion probably would’ve produced similar results. As such, if we take a 75kg individual as an example, it would be the equivalent of ingesting 15g of BCAAs straight after a workout, and an additional 15g every hour, for the next three hours (60g total). Coincidentally, this arrives at a value remarkably similar to that advised by Poliquin. Is this a fluke on Poliquin’s part? Nobody knows, and I’ve never heard of him speak of this research. It would seem however, that with his years of experience in the field, he is able to notice subtle trends regarding the efficacy of various supplementation protocols, which future research would be needed to verify. Because of this, it begs the question: if Poliquin might be right about the BCAAs, what else might he be right about?

Though the authors of the study were unable to explain the mechanism behind their findings, based on advances in the understanding of protein metabolism in the past decade, there seems to be some plausible explanations. Firstly, as BCAAs aren’t bound to the matrix of a whole food protein source, they are rapidly absorbed and create a huge spike in levels of leucine in the blood. During normal situations (i.e. between-meal doing of 6g BCAA as advised by Layne Norton) levels of plasma leucine would quickly return to baseline. However, with the aforementioned higher doses, supraphysiological levels of plasma leuince concentration would be extended for a much longer duration, resulting in a much higher rate of MPS, thus leading to greater muscle growth over time. This is something that is not achievable with a normal protein source given its relatively slower rate of digestion.

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Other lines of evidence supporting these findings

The knowledge that the Soviets possessed regarding the effects of mega-dosing BCAAs may have translates to other uses, most notably, their domination of the summer Olympic games following WWII. The Olympics were suspended in 1940 and 1944 due to the war, and the Soviet Union didn’t compete in the 1948 games. However, from 1952-2000 (with the exception of 1984 when the Soviet Union boycotted the Los Angeles games), the Soviet Union/Russia have either placed 1^st (1956, 1960, 1972, 1976, 1980, 1984, 1988 & 1992) or 2^nd (1952, 1964, 1968, 1996 & 2000) in the medal table; that includes topping the medals table in six consecutive games!

Though anabolic steroids certainly played a large part of their success, virtually every developed country would have had access to the same drugs, nullifying any potential advantage to be gained from them. As such, it may well have been the inside knowledge of the benefits of BCAAs that were responsible for their Olympic domination.

Further support comes in the form of BCAA supplements. The popularity of BCAAs as a supplement didn’t really being until the early 2000s, so by the time the Athens games were held in 2004 (when athletes from all countries were using them), Russia didn’t have the advantage of BCAA supplementation. So what happened in Athens? Well, Russia placed below 2^nd for the first time in over half a century; this can hardly be written off as coincidence.

Having only been aware of these studies for the past week or so, I though I’d implement BCAA mega-dosing in my current diet and training setup. Though I’ve only been using a protocol that I devised based on the above findings (20g immediately before, 20g during and 20g immediately after training) for just a week (four sessions in total), I’ve already put 25kg on my deadlift and 15kg on my squat. I’ve also gained 2kg in weight with no change in skinfold thickness, indicating it is pretty much all from muscle. For the record, my diet has remained exactly the same, ruling out the possibility of dietary influences.

Additionally, by scouring the fitness/nutrition online forums, I began to notice a trend, in that people who take upwards of 40g BCAA per day seem to benefit in the presence of already sufficient protein. Those who consume more modest amounts tend not to experience such ‘steroid-like’ gains in strength and size unless their protein is lacking.

As a final piece of evidence supporting the validity of the above study, Charles Poliquin and Nick Mitchell (dubbed by Men’s Fitness as “one of the world’s leading body composition experts” and by Time Out as “London’s best personal trainer”) – who both advocate high doses of BCAAs – are very well muscled, as well as having got their clients results following such protocols. One day, with continued use of BCAAs, I'll hopefully reach a similar size as these guys.

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Conclusion

In summary, if you believed a word of what was said in this post then April fools’! If not, then I wasn’t subtle enough (maybe next time). For those that were fooled by the article, it is an important demonstration of how logical sounding arguments can be taken as fact. To give you an idea of how to spot such deceptions in other work, what follows is a list of common logical fallacies that I deliberately committed in order to strengthen my fabricated position:

• I made up research – this one is common, always look out for references linked to PubMed.
• I appealed to coincidence – there are numerous explanations for the success of the Soviets during the summer Olympics.
• I appealed to authority – I backed up this fictitious study with Poliquin’s practise. Since he is held in high esteem (I’m not sure why), people are more likely to believe it. I also put Nick Mitchell’s name in there too for a laugh. Speaking of Mitchell, credentials like “London’s best personal trainer” are at best, comical, and at worst, meaningless.
• I appealed to popularity – stating that everyone on message boards gets results make it seem like it is really popular and really works. Everyone is convinced when “real” people get results, right? (As if humans in controlled trials aren’t “real people”).
• I appealed to personal observation and experience. It must be remembered that the placebo effect is extremely powerful, and if I know what I’m taking, the self-experiment is flawed from the very start due to an expectation bias. Not to mention completely ignoring all the research highlighted in parts 1-3 of my BCAA series.
• In using my personal experience, I also appealed to aesthetics. Saying I got bigger by doing something, or that BCAAs must work because Poloquin and Mitchell use them suggests that only BCAAs are responsible for their physiques as opposed to other 'special supplements'.
• Finally, I also made up physiology in the part about extending supraphysiological rates of MPS and provided no scientific references to support such claims, just links to less than scientific sites such as cutandjacked.com, mensfitness.com and charlespoloquin.com.

BCAAs for Bodybuilders: Just the Science (Part 3)

Firstly, I’d like to apologise for my lack of activity on my blog. I have been extremely busy over the past few weeks and was lucky enough to have Matt Jones of Nutrition Condition to fill my shoes and post a couple of guest articles. As his content has been well received, you can expect to see future posts from him here.

Today, I aim to tie up the article series looking at BCAA supplementation and its effects on body composition. Before moving onto part 3, I first want to quote the summary from part 2, as it will set the stage for this post:

• The amount of muscle mass a person has depends on the long-term relationship between muscle protein breakdown and synthesis.

• A threshold amount of leucine of 2-3 g (~ roughly 0.05g/kg body weight) is thought to exist, with no apparent further stimulation of MPS with higher intakes.

• This would translate to 25-37.5 g of leucine-rich protein sources.

• Yes, you can absorb more than 30g of protein in one sitting!

• Due to the apparent refractory nature of MPS, it would seem that eating meals spaced every 3/4-6 hours apart would optimise MPS within a 24-hour period.

• However, it appears that there is more to muscle gain than frequently stimulating MPS; the reasons being as follows:

1. A recommendation for higher daily amounts of protein than is likely to ‘max’ out MPS.
2. Concept of the anabolic drive and hidden signaling pathways involved in protein turnover and AA oxidation.
3. Real-world observations of excellent improvements in muscle mass despite theoretically ‘too high/too low’ meal frequencies.

1. Apparent lack of effects on LBM whilst dieting with reduced meal frequencies (i.e. 1-2 meals per day).

• It therefore seems that total protein intake is the most important variable, and how this intake is distributed, impacts body composition to a lesser degree.
• For this reason, I don’t see any reason for meal frequency to be higher than the typical 3-4 meals per day for most people seeking optimal rates of muscle gain.
• Though it is unknown whether moving to the ‘optimal frequency’ would be of benefit, it seems unlikely in the real world; and if so, it may only benefit the elite physique athlete looking for that 1-2% over their competition. Likewise, eating less than twice per day may compromise rates of muscle gain, however, no solid data exist to be make definitive conclusions.

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Whole proteins vs. free form amino acids: between-meal dosing

Having mentioned the practise of consuming free-form amino acids such as leucine and BCAAs on top of an existing sufficiency of protein in part 1, it is now time to get to the main point of this article and discuss the more theoretical uses of BCAAs. Having nicely set the stage by taking a look at the topic of meal frequency, the information that follows will hopefully make a bit more sense.

It was Dr. Layne Norton who originally popularised the notion of consuming free-form amino acids (e.g. BCAA) between meals. In recent years, several others have latched on to this concept and recommended their own protocols, such as dosing leucine between meals, on top of meals, between exercise sets etc.; I’m still waiting for someone to recommend snorting pure leucine!

If you remember from part 2, I talked about the refractory phenomenon associated with MPS, which has been explained by the ‘protein stat hypothesis’. It is argued that because free-form BCAAs aren't protein-bound within the matrix of the food, they are more quickly absorbed than intact proteins such as whey. It is further argued that because of this protein stat hypothesis - which indicates that an extracellular membrane-bound sensor is influenced by relative changes in amino acid concentrations as opposed to absolute concentrations - whole proteins don’t elicit a rapid rise and subsequent fall in amino acid levels, unlike their free-form counterparts. As such, Norton has advised that a BCAA mix containing 2-3g leucine (with our without additional carbohydrates – as the time course of MPS somewhat reflects plasma insulin levels) should be consumed between meals spaced 4-6 hours apart, with the aim of circumventing this refractory phenomenon associated with protein synthesis in response to the first meal. Theoretically, blunting the decrease in MPS (with a BCAA/BCAA-CHO mixture), which may occur a couple hours following the first meal, would lead to increased muscle hypertrophy over time.

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Is there any data to support this theory?

There are two main pieces of data used to support this hypothesis. The first is the already cited amino acid infusion data by Bohe et al. (2001). Secondly, Norton uses the study by Paddon-Jones et al. (2005) to justify his between-meal dosing strategy. In this trial, the authors compared the effects of supplement containing 30g of carbohydrate and 15g of essential amino acids (EAA) ingested between meals (consisting of 23.4g PRO, 126.6g CHO, 4g FAT) spaced five hours apart, with ingesting nothing between meals. The authors found that the supplement group experienced a greater overall anabolic response (nitrogen balance and fractional muscle protein synthesis) compared with the control group. This is all well and good but the problem with these findings are that the supplement group consumed 45g extra EAA (equivalent to 90g of whey or roughly 20g BCAA) and 90g extra carbohydrate than the control group. Furthermore, since total protein intake in the experimental group was 109g compared to 64 in the control group, what we’re actually comparing is an adequate intake (1.25g/kg) with an intake below the RDA of 0.8g/kg (0.74g/kg). As such, it is extremely unsurprising that a sufficient protein intake plus extra carbs is potentially more anabolic than an insufficient protein intake.

Ultimately, the practise of ingesting BCAAs between meals is largely based on amino acid infusion data - that doesn’t accurately represent oral protein ingestion – and a heavily flawed piece of research by Paddon-Jones et al. (2005). As such, between-meal dosing is an extremely optimistic strategy, based on questionable theoretical evidence. For such a strategy to prove its worth, I’d like to see a between-meal dosing strategy set up around a sufficient protein intake, in trained individuals undergoing a structured resistance programme with body composition endpoints. Will we ever see this data? I doubt it, but I can always dream! But unless it happens, I wouldn’t recommend it to my clients.

Moreover, as discussed in my last article, given the apparent lack of difference in body composition with a decent protein intake spread over 3-4 meals compared with six meals, it is highly unlikely that a slight extension of MPS with a given meal will make any meaningful differences in terms of muscle mass accrual; it almost certainly wouldn’t make a difference in terms of maintenance of muscle mass.

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BCAAs and fat loss?

As you recall from part 2, reducing meal frequency doesn’t seem to affect muscle mass retention as long as sufficient protein is being consumed. This is why intermittent fasting (LeanGains style) works very well for those looking to lose fat and retain muscle. In fact, an interesting review by Varaday (2011) concluded that intermittent calorie restriction (ICR) is just as effective as daily calorie restriction (DCR) at promoting fat and weight loss, though ICR may be more effective for retaining lean mass. However, before the intermittent fasting crowd gets too excited, it is worth remembering that the majority of the ICR studies used bioelectrical impedance (BIA) as a measure of body composition. Anyone familiar with BIA knows that it’s inaccurate at the best of times.

Therefore, it appears that an optimal meal frequency whilst dieting is the one you can best stick to. Because of this, attempting to increase the number of stimulations in MPS, or extend this process, during dieting seems a futile one.

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What about their caloric efficiency?

Given that BCAAs are the only amino acids that stimulate protein synthesis, another rationale for the use of BCAAs whilst dieting is due to their greater caloric economy in comparison to whole protein sources. In other words, if your aim were to get 3g of leucine in a given meal, ingesting whole protein food such as whey would require about 25g (100kcal), whereas 6g (24kcal) of BCAAs would provide the same amount of leucine.

By the same logic, if things were only as simple as getting enough leucine to max out MPS at each meal (~4-6g of most brands of BCAAs), we would theoretically only need 24-36g of BCAAs per day to cover protein requirements. However, it’s no use having leucine to initiate protein synthesis if there is no protein (i.e. other amino acids) to actually carry on this process. What will basically happen is that things will short circuit, meaning that MPS may begin but then stop soon after. A quote from a review by Balage & Dardevet (2010) on the topic sums this up nicely:

“There is some evidence that long-term leucine availability is sufficient to improve muscle mass or performance during exercise training. However, it needs to be associated with other amino acids to be efficient (for example, through leucine-rich proteins).”

This wouldn’t seem to be a problem for the between-meal dosing of BCAAs since there are already other amino acids in circulation. The aim of this strategy isn't to stimulate MPS using BCAAs by themselves; rather, it is to extend MPS.

However, like a complete protein, it also appears that an EAA mixture may optimise MPS. As such, consuming sufficient whole protein the majority of the time and then replacing around-workout whey protein with BCAAs may also have the intended benefit (i.e. optimal MPS stimulation) but with greater caloric efficiency. For example, whey contains roughly 25% BCAA, so assuming someone consumes 30g of whey protein pre and post training, this would amount to 60g of whey (240kcal), whereas isolated BCAAs will account for 15g total (60 kcal), a saving of 180kcal per workout day. If this person trained four times per week, this would be a saving of 720kcal per week, just over 100 kcal per day.

However, I honestly can’t see why someone would want to save calories by reducing protein intake in the first place, never mind go to all that effort just to save themselves 100kcal per day. The same reduction could be achieved by sticking with whey and reducing fat by 11g or carbohydrate by 25g per day, or a combination of the two. Not only will this save you money, you’ll get as much BCAA as well as all the other essential and non-essential amino acids (which may impart added benefit). You’ll also get the

potentially therapeutic compounds contained in whey such as immunoglobins and lactoferrin, as well potentially anabolic properties of whey independent of its constituent amino acids. Finally, you’ll likely experience greater satiety with whey compared to isolated BCAAs (something that would benefit dieters). In clinical research, BCAAs have been used to stimulate appetite in populations at risk for muscle wasting. The mechanism to explain why this is the case involves BCAAs competing with tryptophan for entry into the brain, thereby reducing the production of a satiating neurotransmitter, serotonin.  As such, it is ironic that the same supplement many take for dieting purposes may actually make dieting a more difficult experience than it needs to be. Conversely, the satiating effects of whey protein are well documented.

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Conclusions & Practical Recommendations

In summary, form part 1 of this article series, I discussed BCAA supplementation on top of a pre-existing sufficiency of protein and came to the conclusion that BCAAs would seem to make little, if any, difference in terms of muscle gain. In part 2, the stage was set for the current article in where I discussed the issue of meal frequency, the conclusion of which is outlined at the beginning of this article.

In this final instalment, we dug deeper into the more theoretical arguments for BCCA supplementation. Specifically,  the claims behind the between-meal dosing of BCAAs and how this might positively impact on muscle hypertrophy were examined, as well as their potential benefits whilst dieting.

The protocol advised by Layne Norton involves using doses of BCAAs likely to maximally stimulate MPS (~4-6g) in between meals spaced 4-6 hours apart. However, this strategy is largely based on amino acid infusion data and a deeply flawed study with highly predictable findings. Therefore, the practise of between-meal BCAA doing is essentially a hypothesis (that extending MPS slightly will lead to greater gains in strength/hypertrophy over time) based on a hypothesis (that such dosing protocols will actually extend MPS  under more realistic dietary conditions) based on a hypothesis (that the protein stat hypothesis holds true), thus extremely optimistic.

In terms of muscle retention whilst dieting, the frequency of protein ingestion doesn’t seem to make a difference as long as sufficient total protein is being consumed, meaning that between-meal dosing is irrelevant under dieting scenarios, at least in terms of optimising MPS on a meal-per-meal basis. As such, the caloric economy of BCAAs is their main attraction for dieters. However, at best, this tactic will save you a few calories, possibly at the expense of hunger, other beneficial properties associated with complete protein sources and money. It is much less hassle, cheaper, and potentially more beneficial to cut calories from either fat or carbohydrate.

Layne Norton may indeed be ahead of the game when it comes to his suggested BCAA protocol taken between meals separated by 4-6 hours. However, when compared to a sufficient protein intake (2.5-3g/kg) spread over the typical 3-4 meals (as suggested in part 2), I can’t see how this tactic could be much more beneficial, if at all. To quote Alan Aragon speaking about Layne Norton about the very topic:

“it’s crucial to realize that [Layne’s BCAA protocol] might be miniscule and not worth the effort or expense for non-competitive populations. In repeated personal communication, he has admitted to me that this tactic is done in attempt to clinch a very small edge to win. As a top-level, drug-free competitor, it’s justifiable to exploit all hypothetical nutritional means within reason in order to conjure the last bit of potential.”

As such, unless you are a physique competitor in search of that extra 1-2% (if it exists), it may be feasible to experiment with such tactics in the effort to gain an advantage. For the rest of us (>99.99 of people) looking to get in better shape, I see little point in supplementing with BCAAs. Instead, I’d urge you to save your money and invest in what delivers. That is, consume a sufficient amount (2.5-3g/kg) of high quality protein that will put you in good stead for making solid gains in the gym, whilst constantly hitting other macronutrient targets across a range of minimally processed foods. From there spread this intake evenly over the typical 3-4 meals, with two of these protein-containing meals placed within windows 90-120 minutes prior to and after weight training. If you have difficulty in reaching such intakes with solid proteins, opt for a decent whey protein concentrate or isolate in order to make up the difference. Speaking of weight training, focus on adding manageable weight in the main compound movements. Not only will this save you money, you will surpass the vast majority of people who use isolated BCAA supplements.

Guest Post: The nuts and bolts of nutrition and neurotransmission (by Matt Jones)

‘Neurotransmitter’ appears to be the buzz word of the moment; the belief being that nutrition can have a significant affect on the appearance of blood and brain neurotransmitters themselves, a substantial body of evidence supports this notion (Wurtman & Fernstrom, 1974; Growdon & Wurtman, 1977, 1980; Gelenberg, Wojcik & Growdon, 1980). Such evidence has given rise to a spate of theories, generally all of the ‘Broscience’ ilk, a number of which originate from Charles Poliquin’s ideologies. The Meat & Nut breakfast is his most infamous nutrition and neurotransmission tale. While I personally also see the benefits of the inclusion of meat and nuts at breakfast, Poliquin has vastly over exaggerated the impact this meal has on your brain neurotransmitters and thus the subsequent actions and emotions. Here we’ll critique the current evidence regarding nutrition and neurotransmission and hopefully dispel any of the Poliquin myths along the way.

Science talk, a neurotransmitter is a chemical signal which allows transmission of signals from one neuron to another, across a synapse; in English that basically means it’s a vehicle which allows messages to be transported from one nerve to another. Neurotransmissions allow, and control muscle fibre contraction, bodily actions, emotions and feelings. The most significant neurotransmitters in the human body are acetylcholine, norepinepherine, dopamine, GABA, glutamate, serotonin and endorphin.

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Neurotransmitters and cognitive function

Serotonin is a known sleep inducing agent (Hartman & Spinweber, 1979), and human research has suggested serotonin reduces subjective alertness, objective performance, and increases feelings of relaxation and lethargy (Spring, 1984). Dopamine on the other hand is associated with pleasurable reward, behaviour, cognition, mood, memory, movement, attention and learning. Acetylcholine has a number of physiological functions, and is a widely distributed excitatory neurotransmitter that in the central nervous system is involved in wakefulness, attentiveness and memory. Interestingly, Alzheimers disease is characterised by a significant reduction in acetylcholine concentration and function (Francis, 2005), highlighting its importance in human performance.

Neurotransmitters and nutrition

The primary neurotransmitters are synthesized from the amino acids, tyrosine and tryptophan. The rates at which these neurotransmitters are synthesized depends upon the availability of the amino acid precursor; where tryptophan is the precursor of serotonin, and tyrosine is the precursor of dopamine and norepinepherine (Wurtman et al. 1980); this link was made in the 70’s and early 80’s when evidence from rat studies became available. The administration of a single dose of tryptophan elevated brain tryptophan levels, and thus the levels of serotonin and its major metabolite 5-hydroxyindole acetic acid (5-HTP). The administration of tyrosine similarly elevated brain tyrosine levels, and thus catecholamine synthesis increased in the central nervous system (CNS), while the consumption of lecithin or choline (found in fat) increases brain choline levels and neuronal acetylcholine synthesis (Wurtman & Fernstrom, 1975).

Most of these studies were on rats, using a single dose of the precursor, although similar effects have been seen following the consumption of dietary sources. The consumption of a single protein-free high-carbohydrate meal elevated brain tryptophan levels. Similarly the consumption of a single 40% protein meal accelerated brain catecholamine synthesis through increased availability of tyrosine (Wurtman & Fernstrom, 1975). A minimal change of delta 0.07 in the tryptophan to large neutral amino acid ratio is required to influence mood following protein consumption, so a considerable shift in the ratio is required to have an effect on subsequent cognition (Fernstrom, 1994).

These early observations clearly demonstrate that serotonin and catecholamine neurotransmitters are under specific dietary control, so in that regards Poliquin is correct. The acute effects of a high-carbohydrate protein-free meal, typical of most children’s and a vast majority of westerner societies breakfast (think cereals) do induce marked increases in serotonin synthesis, and thus may result in increased feelings of lethargy; however, is the absolute avoidance of carbohydrate justifiable based on the current evidence?

It appears not. Interestingly, the addition of protein to that otherwise protein-free high-carbohydrate meal suppressed the increases in brain tryptophan and serotonin (Wurtman & Fernstrom, 1975), because protein contributes to the blood plasma considerably larger amounts of the other neutral amino acids (e.g., BCAA’s, phenylalanine) than of tryptophan. Tryptophan and other large neutral amino acids, most notably the BCAA’s leucine, isoleucine and valine share and compete for uptake along the specific transport mechanism across the blood brain barrier (Maughan, 2000). Therefore brain 5-HTP synthesis will increase when there is an increase in the ratio of free tryptophan to BCAA’s in the blood (Chaouloff et al. 1986), thus explaining why the addition of protein to an otherwise protein-free high-carbohydrate meal can suppress serotonin synthesis.

Just to confirm, this theory has also been confirmed in humans. Using 20 men, Lieberman et al. (1985) administered single oral doses of tryptophan (50 mg/kg) and tyrosine (100 mg/kg) in a double-blind, crossover study. Tryptophan increased subjective fatigue and decreased self-ratings of vigour and alertness, but did not impair performance on any of the tests. Tyrosine produced no effects in our young population compared with placebo, but did decrease reaction time relative to tryptophan. The authors concluded that tryptophan has significant sedative-like properties, but unlike other sedatives may not impair performance in a series of cognitive tests. Now being critical, it’s extremely unlikely – probably impossible in fact – you’d ever consume 50 mg/kg tryptophan in a single dose from a dietary source, thus wouldn’t necessarily have to worry about the negative mental effects of tryptophan consumption.

So Poliquin, who strongly advocates the avoidance of carbohydrate at breakfast time has no science to back up such claims. The truth is the brain neurotransmitters are influenced by the ratio of free tryptophan to large neutral BCAA’s (Fischer et al. 2002), so a mixed meal that will maintain a balance in that ratio is adequate. Further an increase in the ratio of free tryptophan to large neutral amino acids following a high-carbohydrate meal is reversible through the addition of a protein to that meal.

An intricate study by Fischer et al. (2002) examined the cognitive effects of isoenergetic meals consisting of three carbohydrate ratios, a carbohydrate rich meal (4:1), a balanced meal (1:1), and a protein rich meal (1:4) in 15 healthy subjects. Not surprising, attention and decision times were improved in the first hour with the high carbohydrate meal, owing to the greater rise in glucose metabolism. But during the first hour it was both the balanced and higher protein meals that resulted in improved performance. Further, overall reaction times in a central task were fastest after the balanced or high protein meal, thus suggesting a high protein meal or a balanced meal seems to result in better overall cognitive performance. Although the results also revealed participants subjective measures of ‘tasty’ and ‘pleasant’ were greater in the balanced meal than in the high protein meal, which suggests this would be the most effective in a practical sense.

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The mechanisms

Now, from reading the above it may appear that carbohydrates contain significant amounts of tryptophan, thus increase free tryptophan concentrations after ingestion, thus increasing tryptophan uptake and stimulating serotonin synthesis. However, this is not the case. For the sake of dispelling Poliquins breakfast argument let’s take oats for example, the amino acid profile of 100g oats indicates a tryptophan concentration of 234 mg, compared to 694 mg isoleucine, 1284 mg leucine, and 937 mg valine, which collectively make up the BCAA’s. So a high carbohydrate breakfast doesn’t contain that much tryptophan and yet accelerates serotonin synthesis through an increase in tryptophan uptake by the brain, how does that work?

Although the carbohydrate meal itself doesn’t contain much tryptophan, the insulin that is secreted following the carbohydrate meal results in a decrease in plasma levels of the large neutral amino acids (tyrosine, phenylalanine, BCAA’s and methionine) that would ordinarily compete with tryptophan for uptake by the brain. Tryptophan then crosses the blood-brain barrier and is converted to serotonin (Spring, 1984).

So it’s not actually the carbohydrate that causes the problem, it’s the insulin response to that carbohydrate that is the issue.

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Innovative idea

The following is a novel thought that stemmed from logic and my intuition: looking at the insulin index created by Holt et al. (1997) beef, the food advocated by Poliquin in his infamous meat and nut breakfast comes in at an insulin area under the curve of 7910 ± 2193 pmol.min.L and grain bread, a food demonized by Poliquin in fear of it frying your brain cells comes in at 6659 ± 837 pmol.min.L. The insulin index clearly indicates beef is more insulinogenic than most forms of carbohydrate, therefore suggesting that the net effect in regards neurotransmitter synthesis of a high-protein carbohydrate-free meal may be similar to that of a mixed meal. The greater insulin response to beef consumption will lead to a reduction in the BCAA’s and other neutral amino acids, leaving free tryptophan to be taken up by the brain; interestingly 100g steak contains more tryptophan than the same portion of oats (288 mg).

Logic and intuition suggests this could be true, although a number of rat studies have disproved the hypothesis, where Rouch et al. (1998) revealed a high protein diet significantly reduced serotonin concentrations for 2-hours, Wurtman & Fernstrom (1975) reported similar findings. Interestingly, the reduction in serotonin following protein feeding is thought to be among the reasons why protein is more satiating that carbohydrate.

Finally, Poliquins suggestion that the first meal of the day dictates that whole days brain neurotransmitters. We’ll start with a rat study from 1995; Fernstrom & Fernstrom studied the brain tryptophan concentrations and serotonin synthesis rates of fasted rats fed a high-carbohydrate meal followed 2-hours later by a protein-containing meal. They demonstrated that when the high-carbohydrate meal was fed first, brain tryptophan concentrations increased as did serotonin synthesis, and these changes were reversed at 4-hours if the second meal contained protein. Interestingly they go on to conclude, and I quote: “brain tryptophan concentrations and serotonin synthesis are thus responsive to the sequential ingestion of protein and carbohydrate meals if there is a sufficient interval between meals”. Similarly, Rouch et al. (2003) reported the plasma ratio of free tryptophan to large neutral amino acids was increased by a carbohydrate meal, and remained high for 2-hours, a subsequent casein (protein) meal reversed this change. Interestingly, a first casein meal reduced the ratio, and was not increased again by a subsequent carbohydrate meal. These findings actually favour Poliquins suggestions, although the weight of the evidence doesn’t, again supporting my belief of a mixed meal consumption.

From a human perspective the reversible nature of neurotransmitter synthesis is supported by the central fatigue hypothesis, which predicts that the ingestion of BCAA’s during exercise will raise plasma BCAA concentration and hence reduce transport of free tryptophan into the brain; subsequently reducing the formation of serotonin and alleviating sensations of fatigue and therefore improve endurance performance (Gleeson et al. 2005). This hypothesis lacks support, although does highlight the obvious reversible nature of neurotransmitter synthesis.

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Conclusion and recommendations

My recommendation based on this evidence is that a single macronutrient meal can have a significant impact on the brain neurotransmitters, where a protein-free high-carbohydrate meal can increase serotonin synthesis, and thus increase feelings of fatigue just as Poliquin suggests. Although alternatively, a high-protein high-fat carbohydrate-free meal can increase catecholamine synthesis. Granted you would favour catecholamine synthesis, but with your daily macronutrient requirements in mind, combined with the fact that eating single macronutrient meals would be extremely tasteless and boring it would be more appropriate to consume mixed meals than to focus on meals free from certain macronutrients in fear of a surge of sleep inducing neurotransmitters.

In conclusion the promotion of carbohydrate free, high-protein breakfasts is largely unsubstantiated. A mixed meal consisting of meat, carbohydrate (both starchy and fibrous) and fat (possibly nuts) is adequate, and in a practical sense is optimal.

References

Chaouloff et al. (1986) http://www.ncbi.nlm.nih.gov/pubmed/3083049

Fernstrom & Fernstrom (1995) http://ajcn.nutrition.org/content/61/2/312.short

Fernstrom et al. (1994) http://www.ncbi.nlm.nih.gov/pubmed/7903674

Fischer et al. (2002) http://www.ncbi.nlm.nih.gov/pubmed/11897269

Francis (2005) http://europepmc.org/abstract/MED/16273023

Gelenberg et al. (1980) http://www.ncbi.nlm.nih.gov/pubmed/6443584

Gleeson et al. (2005) http://jn.nutrition.org/content/135/6/1591S.abstract

Growdon & Wurtman (1977) http://www.ncbi.nlm.nih.gov/pubmed/14577

Hartman & Spinweber (1979) http://www.ncbi.nlm.nih.gov/pubmed/469515

Holt et al. (1997) http://ajcn.nutrition.org/content/66/5/1264.full.pdf

Lieberman et al. (1985) http://ajcn.nutrition.org/content/42/2/366.full.pdf

Maughan (2000) http://www.bentrem.sycks.net/NutritionInSport-Ronald-J-Maughan.pdf

Rouch et al. (1998) http://www.sciencedirect.com/science/article/pii/S0031938498002042

Rouch et al. (2003) http://www.ncbi.nlm.nih.gov/pubmed/12722987

Spring et al. (1984) http://www.ncbi.nlm.nih.gov/pubmed/6400041

Wurtman, R., & Fernstrom, J. (1974). Nutrition and the Brain. Scientific American, 230, 84- 91.

Wurtman & Fernstrom (1975) http://ajcn.nutrition.org/content/28/6/638.abstract

Wurtman et al. (1980) http://www.ncbi.nlm.nih.gov/pubmed/6115400

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Bio: Matt holds a BSc (Honours) degree in Sport & Exercise Science, an MSc in Nutrition Science. Through his own Performance Nutrition business, Nutrition Condition, he delivers frequent Health & Wellbeing Workshops to corporate and personal clients advising on how best to develop a sound, scientifically structured nutrition programme free from fads and marketing bias. Nutrition Condition also delivers Performance Nutrition services to professional athletes.

Matt can be contacted on matt@nutritioncondition.com or at www.nutritioncondition.co.uk

For regular updates follow Matt on Twitter @mattNCUK.