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HIIT-like 400m sprinting is exhausting, but unlike running to exhaustion and medium intensity steady state cardio its not going to mess up your nervous system.

Not one but two recent studies confirm what many of us have experienced first hand: Endurance training - specifically during a cut - is a double-edged sword. On the one hand, its a neat way to augment the energy deficit, when youre dieting and maintain in a eucaloric state, when youre not. On the other hand, however, even moderate endurance training can alter the sympathetic and parasympathetic balance and thus create an imbalance that is characteristic of any form of overtraining.

Speaking of overtraining: As a SuppVersity reader you should actually be aware of the fact that scientists distinguish two different types of overtraining: Sympathetic and parasympathetic overtraining
Due to the fact that the symptoms (see Figure 1) closely resemble those Morbus Basedow (engl. Graves Diseases) and Addisons Disease, respectively, sympathetic and parasympathetic overtraining are also called Basedowoid and Addisinoid overtraining.

Figure 1: Overview of the symptoms of the two major forms of overtraining.

You can see that the symptoms partly overlap. Thats yet not the only problem you have if you want to diagnose the type of overtraining. In many resistance trainees, for example, you find either mixed forms or see a transition from classic sympathetic to parasympathetic overtraining over time (assuming the athlete doesnt do anything to normalize his / her sympathetic nervous system function).
For the average study participant in a recent experiment that was conducted by scientists from the , The 42nd Hospital of PLA, the Xinqiao Hospital and the Chongqing Normal University in China, the duration and intensity of their cardio workouts (running) determined, whether the prescribed workout routines that consisted of ...

• There is such a thing as overtraining, folks | read more

  4 times a week running at 100% of their maximal heart rate until they were exhausted (utmost intensity group)
   
• 30 minutes of running four times per week (moderate intensity group)


• 3 - 5x 1200 m runs per day with a  5-min break every 400 m four times per week (high intensity group)

made them overtrain or not, and whether their para- or sympathetic nervous system was overreacting.

Table 1: Characteristics of study groups at pre and post | Data are means XS± . Pre, pretraining; post, at the end of 8-week training; mid, at the end of 4-week training. Utmost, utmost intensity endurance training; moderate, moderate intensity endurance training; high, high intensity endurance training (Tian. 2014)

The subjects, 72 nonsmoking male students whose characteristics are summarized in Table 1, followed the routine they had been randomized to for 8 weeks. As you can see, there were no statistical significant changes in body composition over the course of the 8-week study. Although, it sould seem that the body fat percentage (I assume BFR is body fat) declined a tad bit more in the high intensity group.
Where the subjects differed, however, was in their response to the specific aerobic exercise programs theyve been assigned to (I will directly quote the results from Tian et al (2014) and briefly comment on each of them):

• Heart rate variability (HRV): No significant changes in HRV parameters were found in all groups at pre and mid. But at post, the moderate intensity group showed more significant increases in RMSSD, PNN50, HF, LF and SDNN (P < 0.05 or 0.01) and much greater reduction in LF/HF than the other two groups (P was 0.033, 0.037 respectively). HFn of the moderate intensity group was significantly higher than that of the utmost intensity group (P = 0.012), while the opposite pattern occurred in LFn and LF/HF of the two groups (P was 0.025, 0.015 respectively).
  
  As you would expect the changes in HRV in the moderate and utmost intensity group reflect increases in parasympathetic and sympathetic nervous system activity, respectively.
• Circadian Changes in Cold Pressor Test (CPT): From pre to post marked differences were not found in SBP and DBP of all groups and their increases. At post HR was much less increased in utmost intensity group during CPT than the other two groups (average P < 0.05).
  
  Next to a high basal heart rate an inhibited increase in heart rate is another characteristic of later stages of sympathetic overtraining.
• Plasma catecholamine (NE & EPI): Norepinephrine (NE) concentration was considerably lower in utmost intensity group than the other two groups (P was 0.001, 0.00 respectively). At post marked inter-group differences were still not found in plasma PEI concentration.
  
  A reduced catecholamine release is a classic characteristic of long(-er) term sympathetic overtraining - a phenomenon, some people may call "adrenal fatique" that occurs after an initial phase of catecholamine overproduction in sympathetic overtraining.

Overall, the results of the study at hand confirm previous research that found associations between classic "moderate intensity" endurance training and parasympathetic dominance (Yamamoto. 2001; Pichot. 2002; Myslivecek. 2002).

For the utmost intensity group, on the other hand, the scientists diagnosed an "over-excited SN [sympathetic nervous system]" (Tian. 2014), which is in contrast to the medium intensity and high intensity group, where the head-up tilt test did not indicate an "impairing effect on autonomic regulation" (Tian. 2014).
References:

• Myslivecek, P.R., Brown, C.A. and Wolfe, L.A. (2002) Effects of Physical Conditioning on Cardiac Autonomic Function in Healthy Middle-Aged Women. Canadian Journal of Applied Physiology, 27, 1-18. 
• Oosthuyse, T., & Avidon, I. (2014). Changes in substrate utilisation and protein catabolism during multiday cycling in well-trained cyclists. Journal of Sports Sciences, (ahead-of-print), 1-11.
• Pichot, V., Busso, T., Roche, F., Garet, M., Costes, F., Duverney, D., Lacour, J.R. and Barthélémy, J.C. (2002) Autonomic Adaptations to Intensive and Overload Training Periods: A Laboratory Study. Medicine & Science in Sports & Exercise, 34, 1660-1066. 
• Tian, Kaixin, et al. "Effect of Endurance Training on the Autonomic Nervous System Function of Young Male." International Journal of Clinical Medicine 5.19 (2014): 1189.
• Yamamoto, K., Miyachi, M., Saitoh, T., Yoshioka, A. and Onodera, S. (2001) Effects of Endurance Training on Resting and Post-Exercise Cardiac Autonomic Control. Medicine & Science in Sports & Exercise, 33, 1496-1502. 

If you want other to see your pump, you got to be ripped. If not, why care about reductions in BMR?

If you remember my posts about the first generation, arginine-based pre-workout products you will be aware that the only pump they produced was the word "pump" in their name or product description. The reason was and still is simple. The mere provision of l-arginine, which is a precursor to nitric oxide does not lead to an increase in nitric oxide production. Why? Well, think of a building a house: Just buying some concrete wont make you a proud home owner, either ;-)

The bad thing: Arginine didnt work. The good thing: This means it didnt decrease your BMR, either

Against that background its quite astonishing that arginine and citrulline based pre-workout products have dominated the top-seller lists of the big supplement vendors for decades. A fact thats probably partly due to other potential benefits of these amino acids, of which one - you as a SuppVersity reader know that - could be fat loss | learn more about the potential fat loss effects.
With more and more people openly declaring that they would no longer waste money on "good tasting, but expensive and disfunctional products", they industry was yet pressed to develop alternatives. Luckily, our body has two options it can chose from, when producing nitric oxide.

Fortunately, the industry has developed better alternatives...?

You know option #1, the arginine ? nitric oxide pathway, and - with all the hype and hyperbole that surrounded the introduction of the first nitrate supplements - I am pretty sure, you know the other one as well, the nitrate-nitrite ? nitric oxide pathway

Figure 1: The Arginine- and the Nitrate-Nitrite - NO pathway are the yin and yan of nitric oxide production (Lundberg. 2008).

As the illustration (Figure 1) I have "borrowed" from a comment by Jon. O. Lundberg et al. (2008) illustrates quite nicely, the arginine and nitrite nitric oxide pathway are the yin and yan of NO production.

With the "yan", i.e. the nitrate-nitrite ? nitric oxide pathway being a relatively "new kid on the NO block", that recycles (=reduces) inorganic anions nitrate and nitrite to form bioactive NO in blood and tissues during physiological hypoxia.

It goes without saying that there is a bottle neck to this process as well, but the rate limiting availablility of oxygen which hampers the argine-based NO generation by NOS becomes limited as oxygen levels fall is actually a signal for the nitrate–nitrite ? nitric oxide to really kick in.

There is more yin and yan, here

If you take a closer look at the results of a study in the America Journal of Clinical Nutrition (Figure 2), you will yet have to realize that there is "more yin and yan", here than youd probably hope for. According to the data scientists from the venerable Karolinska Institutet in Stockholm, Sweden, present in their paper, "[d]ietary inorganic nitrate reduces the RMR." (Larsen. 2014)

Figure 2: VO2 consumption (marker of fatty acid oxidation) and basal metabolic rate (BMR) relative to means (left), thyroid hormone (T3, T4) levels after 3-d dietary intervention with sodium nitrate (Larsen. 2014)

Whut? Yes, you read Larsen et al. right: In their randomized, double-blind, crossover study, in the course of which the Swedish scientists measured the resting metabolic rate (RMR) of 13 perfectly healthy 18–49 y olds (17 women) via indirect calorimetry after a 3-d dietary intervention with sodium nitrate (NaNO3 @ 0.1mmol/kg body weight) or a placebo (NaCl), Larsen, Schiffer, Ekblom et al. observed a statistically and (probably) physiologically significant reduction BMR reduction of 4.2% which correlated strongly to the degree of nitrate accumulation in saliva (r²= 0.71) and fits in nicely with the reduced O2 consumption of which Bailey et al. were the first to observe it in response to nitrate supplementation during exercise (Bailey. 2009).

Interestingly, these effects were not - as you may have been speculated - brought about by changes in thyroid hormone status. And the subjects insulin sensitivity, glucose uptake, plasma concentration of isoprostanes, as well as their total antioxidant capacity were unaffected, as well.
Reference:

• Bailey, Stephen J., et al. "Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans." Journal of Applied Physiology 107.4 (2009): 1144-1155.
• Hotta, Yuji, et al. "Oral l?citrulline supplementation improves erectile function and penile structure in castrated rats." International Journal of Urology (2014).
• Larsen, Filip J., et al. "Dietary inorganic nitrate improves mitochondrial efficiency in humans." Cell metabolism 13.2 (2011): 149-159.
• Lundberg, Jon O., Eddie Weitzberg, and Mark T. Gladwin. "The nitrate–nitrite–nitric oxide pathway in physiology and therapeutics." Nature Reviews Drug Discovery 7.2 (2008): 156-167.
• Neuzillet, Y., et al. "A randomized, double?blind, crossover, placebo?controlled comparative clinical trial of arginine aspartate plus adenosine monophosphate for the intermittent treatment of male erectile dysfunction." Andrology 1.2 (2013): 223-228.

If we go by the convincing results of the study at hand, the fasted cardio myth is obviously busted.

Sometimes the day youve been waiting for comes faster than youd thought... no, I am not talking about a teens eighteens birthday or Christmas (reminds me, I still have to buy a ton of presents), but rather of the recently hinted at "fasted cardio study" by Brad Jon Schoenfeld, Alan Albert Aragon, Colin D Wilborn, James W Krieger and Gul T Sonmez.

The study of which I wrote only 2 days ago in my article about the 50% increase in fatty acid oxidation in fasted vs. fed morning cardio (learn more). And it is in fact the study which may finally solve the "Is fasted cardio good for your weight loss?"-question.

In contrast to the previously discussed paper, Schoenfeld et al. who started with the common hypothesis that "performing aerobic exercise after an overnight fast accelerates the loss of body fat" (Schoenfeld. 2014), did not content themselves with measures of acute fatty acid oxidation. What they did was a study to investigate the actual changes in fat mass and fat-free mass following four weeks of volume-equated fasted versus fed aerobic exercise in young women adhering to a hypocaloric diet.
Needless to say that this study has the potentially to give us reliable insights with respect to the previously formulated question, because their subjects, twenty healthy young female volunteers were randomly assigned to 1 of 2 experimental groups,

• a fasted training (FASTED) group that performed exercise after an overnight fast (n =10) or
• a post-prandial training (FED) group that consumed a meal prior to exercise (n =10)

not for one or two testing days, but for 4 weeks! The training itself consisted of 1 hour of steady-state aerobic exercise on a regular treadmill (0% incline) and was performed for 3 days per week for the previously mentioned total study duration of 4 weeks.

"Subjects performed a warm-up for the first 5 minutes at an intensity equating to 50% of maximal heart rate (MHR), determined by the formula 220 - age, then increased intensity to 70% MHR for the next 50 minutes, and finished with a 5 minute cool down at 50% MHR. Heart rate monitors (model F7U, Polar Electro Inc, Lake Success, NY) were used to ensure that exercise remained at the appropriate intensity." (Schoenfeld. 2014)

To ensure that (a) the subjects actually trained and they would (b) only do the prescribed standardized volume of exercise, all training sessions were supervised by research assistants who were upper level undergraduate students in exercise science and the subjects were instructed to refrain from performing any additional structured exercise for the duration of the study.
Subjects were provided with customized dietary plans designed to induce a caloric deficit. In that, their total caloric intake was calculated on the basis of the Mifflin-St. Jeor Equation, which yields adequate, but obviously not 100% precise measurements of the resting metabolic rate (max. 10% off in non-obese adults according to Frankenfield. 2005). Since the same method was used for both groups, any possible inaccuracies, due to which the real caloric deficit among the women may not be identical to the calculated one, should carry no real weight, though. And we can simply assume that all women were in the same ~500kcal/day energy deficit the researchers thought to create.

Figure 1: Nutrient composition and total energy intake of the subjects in both groups (Schoenfeld. 2014)

In addition to their regular diet, the adherence to which was monitored on a regular basis, the subjects received a meal replacement shake either

• immediately prior to exercise for the FED group or
• immediately following exercise for the FASTED group,

with this nutritional provision carried out under the supervision of a research assistant. The "Pursuit Recovery" (Dymatize Nutrition, TX) shake you could also buy at your local GNC contains 250 calories, total, and 40 g carbohydrate (from maltodextrin and organic cane sugar), 20 g protein (from whey protein isolate + added leucine), and 0.5 g fat (residues).

Lets  take a look at the results now

As you can see in Figure 2, both groups showed a significant loss of weight (P =0.0005) and fat mass (P =0.02) from baseline, but no significant between-group differences were noted in any outcome measure (which means, that all the differences you see are "random").

Figure 2: Pre- vs. Post-study body composition measures (Schoenfeld. 2014)

As Schoenfeld et al. rightly point out, their findings clearly "indicate that body composition changes associated with aerobic exercise in conjunction with a hypocaloric diet are similar regardless whether or not an individual is fasted prior to training" (Schoenfeld. 2014) - in other words, in this pretty realistic scenario (I hope nobody starves himself after a 1h morning cardio session for another 4-8h) the myth that morning cardio on an empty stomach would accelerate fat loss is thus busted.
References:

• Frankenfield, David, Lori Roth-Yousey, and Charlene Compher. "Comparison of predictive equations for resting metabolic rate in healthy nonobese and obese adults: a systematic review." Journal of the American Dietetic Association 105.5 (2005): 775-789.
• Van Proeyen, Karen, et al. "Training in the fasted state improves glucose tolerance during fat-rich diet." The Journal of physiology 588.21 (2010): 4289-4302. 
• Schoenfeld, Brad, et al. "Body composition changes associated with fasted versus non-fasted aerobic exercise." Journal of the International Society of Sports Nutrition 11.54 (2014)

Can you hit the fat hard with choline?

I want to be honest with you. I am a huge fan of choline and truly believe that it is hugely under-appreciated, but the prominent relative (not absolute) increase in body fat loss in study at hand must be interpreted with caution - no matter how statistically significant the "choline advantage" may be.

Before we can get to said "cautious interpretation", lets briefly take a look at what exactly Gehan Elsawy, Osama Abdelrahman, and Amr Hamza from the Zagazig University and the Mansoura University in Egypt did to produce a 100% increase in body fat loss in their 22 female study participants (15 taekwondo and 7 judo athletes).
The idea was to clarify the magnitude of rapid body mass reduction among Egyptian judokas, in order to identify the scientific basis and justification for such practices. In that, the researchers were particularly interested in the effects of choline supplementation on bodymass reduction and leptin levels among their females taekwondo and judo athletes.

The athletes were divided into two groups, according to their body mass; the experimental group contained ten female athletes, and the control group twelve female athletes. At the time of enrollment, all the subjects were healthy, according to a medical information questionnaire, and none of the subjects had any specific dietary restrictions. Exclusion criteria included the use of any medication or supplement during the previous six months.

2.0g per day divided in two 1.0g doses of choline did the trick

For one week prior to a competition, the athletes in the experimental group took choline tablets (1.0 g) twice daily with a meal, equaling a total daily dose of 2.0 g (the scientists dont provide any information on the form of choline, they used, but their references suggest that it was PS, i.e. phosphatidylcholine). The control group received a placebo, and they participated in usual training (with 75% training intensity) at the same time as the choline group four times per week.

"According to Anni et al. (2011), choline supplementation appears to be safe and the authors recommend taking approximately 2.5 g one hour before a prolonged exercise session. The effective dose in sport studies is 0.2 g phosphatidylcholine 90% per kg of the body mass, which equals 2.1 g of choline for an 80-kg athlete. There is no requirement for a loading or maintenance phase and choline supplementation up to one hour before exercise has been shown to be effective in reducing fatigue." (Elsawy. 2014)

There was no standardized diet, there were no diet logs and there was no recording of training intensity and volume.
Things that were assessed are body weight, body fat (see red box above), serum and urinary choline, as well as back and leg strength.

Figure 1: Changes in leptin, plasma choline, body fat (%), BMI, leg & back strength within the last week of precompetition dieting with or without the addition of 2g of choline (undisclosed form) in a recent study by Elsawy et al. (2014).

Statistically significant differences were observed for plasma choline (obviously), leptin and the change in body fat (-1% vs. -2% in the choline group). It would be nice if we also knew if this affected the food and/or water intake and/or if we had confirmation from DEXA and caliper data that the body fat difference was more than just body impedance b*s* - unfortunately, none of these data are available.
References:

• Elsawy et al. "Effect of Choline Supplementation on Rapid Weight Loss and Biochemical Variables Among Female Taekwondo and Judo Athletes." Journal of Human Kinetics volume 40/2014, 77-82.
• Hanin I, Ansell GB. "Lecithin: Technological, Biological, and Therapeutic Aspects". Plenum Press, NY, 180-181; 1987.
• Slater, Gary. "Assessing Body Composition of Athletes." Sports Nutrition for Paralympic Athletes (2014): 189.
• Wurtman RJ, Hirsch MJ, Growdon JH. "Lecithin consumption raises serum-free-choline levels." Lancet, 1977; 2: 68-69

Shouldnt it be obvious that the "happy medium" must be the solution, when high protein leads to brittle bones, and low protein to frail muscle? Sure! But where is this "happy medium"?

Some of you may remember my recent Facebook post "High Protein Diet in the Firing Line. Rodent Study Says: Kidneys Are at Risk". It was based on a press release you could read on all the major science-news outlets on the Internet; a press release that will give the average reader the impression that the corresponding study by Aparicio et al. would "prove" that high protein diets will ruin your kidneys and eventually jeopardize your health (read more).

Another paper (Cao. 2014), Jose Antonio, the CEO of the ISSN and the editor of the ISSNs journal posted on Facebook yesterday, didnt get as much media attention, though.

No wonder, the message of this study is after all not in line with one of the fundamental arguments you will hear, whenever you question the allegedly necessary restriction of total protein intake to 0.8g/kg, maximally 1.2g/kg protein per kilogram body weight day in the current nutritional guidelines:

"[...S]hort-term consumption of high-protein diets does not disrupt calcium homeostasis and is not detrimental to skeletal integrity."

Thats not what you will learn at med-school and it is certainly not in line with the hysteria about protein intakes that are 2x or even 3x higher than the 0.8g protein per kilogram body weight we are supposed to consume. Apropos RDA, the subjects in the control group of the said study by Jay J Cao et al. consumed a diet that contained exactly those 0.8g/kg body weight thats supposed to be good for us. The 21 human guinea pigs in the treatment groups, on the other hand, consumed 2x and 3x more than the average dietitian would recommend and they did so for 31 days (Cao. 2014).

Figure 1: Protein intake (in g/day; left), mineral intake (in mg/day; middle)  and calculated renal acid load (in mEq; right) of 49 normal weight, healthy men (n=32) and women (n=7) who consumed normal (0.8g/day), high (1.6g/kg per day) and very high protein (2.4g/kg per day) energy restricted (40%) diets for 4 weeks (Cao 2014)

If you take a look at the PRAL values in Figure 1, you can see that math (not bio- or physiology!) tells us that this reckless practice could compromises the acid-base balance of the healthy, normal-weight subjects, whose energy restricted diets were modeled on the increasingly popular high protein weight loss diets.

Equations vs. experiments | PRAL vs. urinary calclium loss | theory vs. practive

The urinary analysis the scientists conducted does yet speak a very different language. There is, as the scientists emphasize in the discussion of the results no evidence that

Suppversity Suggested Read: "High protein diet = high protein loss" | more

"habitual consumption of dietary protein at levels above the RDA [would] significantly alter urinary calcium excretion, dietary calcium retention, or markers of bone turnover or BMD, despite increased urinary acidity. These results indicate that diets that are 2 or 3 times the RDA for protein are not detrimental to calcium homeostasis when calcium and vitamin D are consumed at recommended intake"

In that I would like to emphasis the importance of adequate calcium (min. 800mg/day) and vitamin D intakes (800-1000IU/day) and the fallacy of the word "habitual". The study at hand did not test the effects of "habitual" high protein consumption. It tested the effects of short-term (28 days) high protein consumption in a low calorie scenario, which is by definition less prone to produce adverse inflammatory and thus potentially pro-osteoporotic side effects (Mundy. 2007).

Not eating enough protein could increase bone loss, when youre dieting

In view of the fact that the evidence I am about to cite, stems from rodent model of postmenopausal bone metabolism, I deliberately used the word could in the headline of this paragraph. And still, the way in which the low protein diet  "negatively impacted bone mass and magnified the detrimental effects of vitD and/or estrogen deficiencies" (Marotte. 2013) in the pertinent study from the Buenos Aires University is particularly disturbing.
The (postmenopausal) women the scientists try to model with their ovariectomized rats (=rats whose ovaries have been removes) are after all one of the many patient groups who are advised to carefully control their protein intake to make sure that the additional acid load will not compromise their bone health even further and that in spite of the fact that there is ample evidence that the current RDA for protein is inadequate to maintain optimal health, particularly when the total energy intake is restricted and especially in populations who are susceptible to bone loss (Kerstetter. 2005; Chernoff. 2004).

Figure 2: We know for quite some time not that low protein diets decrease the absorp- tion of protein (Kerstteter. 2005). Its not certain if this is "just" a homeastatic me- chanism to stabilize the net/acid balance.

In their 2005 study, Kerstetter et al. were in fact able to show that protein intakes that are 2.6x higher than the RDA increase the effective absorption of calcium from the diet (see Figure 2).

This increase stands in contrast to the significant decrease in calcium absorption the researchers observed in the healthy young (age: 26y) women in the low protein arm (0.7g protein per kg body weight) of the study and should remind us that a reduction in protein intake is not going to stop the insidious loss of bone thats caused by the triage of low estrogen, no exercise and a diet that may be low in protein, but high in acid producing grains (Remer. 1995) and devoid of alkaline fruit and vegetables.

I could now go more into details, but I will just leave you with the notion that the "paleo diet" is, despite its high meat content, among the most kidney-, and above all bone-friendly diets we know. In fact, its fruit and vegetables content yield a net alkaline renal load, and will lead to significant improvements in urinary calcium excretion rates (Appelet. 1997; Frassetto. 2013).   

? Note: If you want more about the "Paleo connection" - let me know this (best on Facebook) and what you would be most interested in and I will address that in a future SuppVersity article.

References

• Aparicio, V. A., et al. "High-protein diets and renal status in rats." Nutrición hospitalaria: Organo oficial de la Sociedad española de nutrición parenteral y enteral 28.1 (2013): 232-237.
• Appel, Lawrence J., et al. "A clinical trial of the effects of dietary patterns on blood pressure." New England Journal of Medicine 336.16 (1997): 1117-1124. 
• Cao, Jay J., et al. "Calcium homeostasis and bone metabolic responses to high-protein diets during energy deficit in healthy young adults: a randomized controlled trial." The American journal of clinical nutrition 99.2 (2014): 400-407.
• Chernoff, Ronni. "Protein and older adults." Journal of the American College of Nutrition 23.sup6 (2004): 627S-630S. 
• Frassetto, L. A., et al. "Established dietary estimates of net acid production do not predict measured net acid excretion in patients with Type 2 diabetes on Paleolithic–Hunter–Gatherer-type diets." European journal of clinical nutrition 67.9 (2013): 899-903.
• Kerstetter, Jane E., et al. "The impact of dietary protein on calcium absorption and kinetic measures of bone turnover in women." Journal of Clinical Endocrinology & Metabolism 90.1 (2005): 26-31.
• Mundy, Gregory R. "Osteoporosis and inflammation." Nutrition reviews 65.s3 (2007): S147-S151.
• Remer, Thomas, and Friedrich Manz. "Potential renal acid load of foods and its influence on urine pH." Journal of the American Dietetic Association 95.7 (1995): 791-797.

Trp and its metabolite 5-HTP may be particularly useful for female sugar cravings and binges.

Can l-tryptophan help you lose body fat? If you look at the results of the latest study from the University for Health Sciences, Medical Informatics and Technology it would seem that the answer to this question may be "Possibly, yes, but..." Before we come to the implications I would yet like to take a closer look at said study which shows that a lack of tryptophan (Trp) during diets does not just affect the biosynthesis of serotonin, but may also be associated with increased susceptibility for mood disturbances and carbohydrate craving. Accordingly, "strategies to supplement Trp while dieting could be highly useful in treating uncontrolled weight gain or in preventing neuropsychiatric symptoms" (Strasser. 2014).
As Strasser et al. point out, both overweight and obesity go hand in hand with significant increases in low-grade inflammation. The latter is not just the reason that obesity increases the risk of cardiovascular disease, though. Recent evidence suggests that it is also associated with errors in the kynurenine (Kyn) pathway, in which tryptophan is broken down to kynurenine which in turn has been associated with increased risk of depressive symptoms, cognitive deficits in schizophrenia, Alzheimers and, as mentioned before, cardiovascular disease. Weight loss, on the other hand,

"[...] has been shown to improve or prevent many of the aforementioned conditions. Bariatric surgical intervention in patients with adiposity was found not to improve tryptophan breakdown rates and other signs of immune activation and inflammation [4], whereas caloric restriction is known to be a strong activator of protective metabolic pathways, thereby leading to lower blood pressure, improved blood lipids, and reduced inflammatory markers, including CRP [9]. Still, little is known about the effects of an extreme short-term hypocaloric diet on Trp metabolism and changes in inflammatory biomarkers" (Strasser. 2014).

The study Barbara Strasser, Ken Berger and Dietmar Fuchs conducted was thus designed to assess the effect of a 2-week caloric restriction weight loss diet on Trp breakdown, leptin, and inflammatory biomarkers in over weight adults.
The scientists randomized 27 overweight and 11 obese participants (22 men and 16 women, mean age 52.8 ± 9.1 years) from the health center Lanserhof, Innsbruck–Lans, into two diet groups:

• a very low kcal diet group (VLCD; Ø 600 kcal/ day) and 
• a low kcal diet group (LCD; Ø 1,200 kcal/day). 

Only healthy subjects with BMI [25 kg/m²] between the ages of 35 and 70 years were accepted for the study. A physician performed physical examinations on all subjects before the study. Subjects were excluded if they consume any anti-inflammatory drugs (e.g., ibuprofen or aspirin) or supplements (such as antioxidants or fish-oil capsules). None from either group was involved in regular training programs.

Figure 1: Changes in body composition pre- vs. post (Strasser. 2015).

As the measurements of body composition, which were just like the energy intake and biologic markers conducted in all subjects before and after the 2-week energy restriction intervention period, indicate, both diets lead to significant reductions in body mass - and that almost exclusively in form of body fat.

Table 1: Biologic markers before and after a 2-week very low kcal diet (VLCD) or low kcal die (LCD) in 38 overweight subjects (mean ± SD)

"Data for biologic markers are shown in Table [1]. Fasting blood glucose declined significantly (P < 0.05) in the LCD group with no significant changes in insulin sensitivity in both groups after 2 weeks of caloric restriction. Weight loss diet lowered leptin levels in both groups, although not reaching the level of significance. Inflammatory biomarkers were not significantly altered during the trial, although there was a tendency toward an increase in IL-6 and TNF-a in the LCD group" (Strasser. 2015).

In contrast to what the researchers expected, both the Trp and Kyn concentrations decreased significantly by 21 and 16 % for VLCD and by 15 and 17 % for the LCD group, respectively, with no significant difference between groups. Practically speaking, this means that the ratio of Kyn/Trp concentrations did not change significantly in both groups.
A significant reduction in Phe concentrations was only seen after VLCD. Neopterin and Tyr levels remained unchanged during the trial. Which leaves us with only one significant finding:

"Trp concentrations decreased significantly with a caloric restriction weight loss diet, and lowest Trp concentrations were observed in the group of individuals with the lowest calorie intake." (Strasser. 2015)

This reduction in Trp levels may well induce a disturbance in the biosynthesis of neurotransmitter 5-hydroxytryptamine (5-HT | Anderson. 1990), and appears to be associated with an increased susceptibility for depression (Widnet. 2002; Raison. 2009). Strasser et al. highlight:

Figure 2: The consumption of tryptophan-free amino acid supplements leads to highly significant increases in hunger ratings in healthy female subjects (Rieber. 2010).

"Because Trp is precursor in various biochemical pathways, e.g., it is hydroxylated by tryptophan-5-hydroxylase (T5H) into the intermediate product 5-hydroxy-tryptophan, which by decarboxylation is further converted to neurotransmitter 5-HT (serotonin), and because substrate saturation of T5H is only about 50 % (Dantzer. 2011), changes in plasma Trp levels may have an immediate impact on brain serotonin levels" (Strasser. 2014).

Experiments in which Trp was acutely depleted (in many studies by administering BCAAs | see red boy) support this assumption. Young et al. (2013), for example, confirmed that the acute depletion of tryptophan will lead to low serotonin and subsequently lower mood and increased aggression, although results vary somewhat between studies with similar participants.

Figure 3: Correlations between changes in tryp:LNAA ratio and appetite ratings (Gendall. 2000).

For the link to obesity, though, the correlation (r-values in Figure 3) between high Trp:LNAA (BCAAs, tyrosine, phenlylanine) and a reduction carbohydrate cravings, general hunger and binge eating is yet way more important - and that specifically for women, who appear more vulnerable than men both to the diet-induced reductions in Trp and to its consequences for brain serotonin function (Anderson. 1990).

Ah, and in case you are asking yourself why carbohydrate / sugar binges are a common consequence of low tryptophane:LNAA ratios, its important to know that increases in glucose and insulin in response to high carbohydrate meals will trigger an increase in brain tryptophan and serotonin synthesis (Benton. 2002). This is why the effects of low tryptophan or high LNAA (BCAA, tyrosine, phenylalanine) levels are more pronounced if you avoid dietary carbohydrates.
References:

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