On 2015 Oct 12, Simon Young commented:

There are a number of problems in this paper in the interpretation of the results, and in the discussion of the previous research on which this study was based. 1. The paper does not mention that tryptophan is taken up into brain by a transport system that is active towards all the large neutral amino acids (LNAA). The other LNAA compete with tryptophan for uptake into brain. When protein is ingested the plasma level of tryptophan increase, but so do plasma levels of the other LNAA. As a result, ingesting normal dietary proteins, or increasing the protein content of the diet, will not raise brain tryptophan or serotonin synthesis, as discussed in many reviews, e.g. Fernstrom JD, 1994. This has been confirmed in a human study involving CSF measures as an approximation of what happens in the brain Teff KL, 1989. While the paper by Lindseth at al does not describe the diets used, it mentions “A variety of foods containing tryptophan were served, including mozzarella cheese, soy products, pumpkin seeds, and egg whites.” This implies that the variation of the tryptophan content of the two diets was manipulated by altering the protein levels in the diet. Therefore the high tryptophan diet would not have raised brain tryptophan and serotonin synthesis relative to the low tryptophan diet. 2. The authors did not consider what factors other than tryptophan might be responsible for the effects on mood that they report. Given that the low tryptophan diet provided <5 mg/kg body weight/d and the high tryptophan diet provided >10 mg/kg body weight/d presumably the protein content of the diet for the high tryptophan group was at least double that for the low tryptophan group. There is some evidence that protein has a greater satiating effect than the other macronutrients Pesta DH, 2014, so it is possible that the participants were more hungry on the low protein diet causing a lowering of mood. This could explain the better mood during the hight tryptophan diet phase. The researchers make no mention of measuring the hunger of the participants or possible preferences for the different diets. Furthermore, various amino acids are converted to psychoactive compounds including phenylalanine and tyrosine (catecholamines), methionine (S-adenosylmethionine), histidine (histamine) and leucine (glutamate), but the authors considered only the effect of tryptophan. 3. The section of the paper on Implications for Practice mentions that “the benefits of a diet for patients susceptible to affective disorders seem important since tryptophan-dense diets also improved mood and decreased symptoms of depression among depressed individuals in other studies (Badrasawi et al., 2013; Markus et al., 2008; Neumeister et al., 1998)”. The Badrasawi et al study Badrasawi MM, 2013 looked at the effect of a dietary supplement on mood. A comment on that article in PubMed (accessed by the previous link) explains why any effect on mood could not have been due to tryptophan. The Markus et al study Markus CR, 2008 looked at the acute effects of a high tryptophan hydrolyzed protein supplement on mood, and is therefore not relevant to how alterations in habitual food intake might alter mood. The Neumeister et al study Neumeister A, 1998 looked at the effect of acute tryptophan depletion (ATD) on mood in recovered depressed patients. Information on the ATD technique as used by Neumeister et al is available Young SN, 2013. In the control condition participants are given an amino acid mixture that is similar to the amino acid content of human milk, a source that is presumably optimum for human consumption. Because there are more LNAAs in this mixture than tryptophan, it will lower brain tryptophan slightly, but presumably within, or close to, the normal physiological range. The active treatment is the same as the control mixture except that tryptophan is omitted. The mixture induces protein synthesis and as tryptophan is incorporated into protein its level in blood and tissues falls dramatically, e.g. 80% or more decrease. This lowers brain tryptophan and serotonin synthesis greatly. In the Neumeister et al study ATD lowered mood relative to the control condition. However, the relevance of a lowering of mood caused by a large and unphysiological decrease in tryptophan, relative to control treatment that caused a small and probably physiologically relevant decline of tryptophan is not relevant to the possible effects of “tryptophan-dense diets”. Tryptophan in purified form is an antidepressant Shaw K, 2002 and under some circumstances tryptophan in purified form can improve mood in healthy people Young SN, 2013, Young SN, 2002. Markus et al Markus CR, 2008 and others have shown similar effects using proteins that contain unusually high amounts of tryptophan but are present in very small amounts in the diet, such as alpha-lactalbumin. However, as discussed above real foods will not raise brain tryptophan and serotonin even if the intake of tryptophan is elevated. Thus, the rationale for the study is not sound.

On 2015 Oct 12, Simon Young commented:

There are a number of problems in this paper in the interpretation of the results, and in the discussion of the previous research on which this study was based. 1. The paper does not mention that tryptophan is taken up into brain by a transport system that is active towards all the large neutral amino acids (LNAA). The other LNAA compete with tryptophan for uptake into brain. When protein is ingested the plasma level of tryptophan increase, but so do plasma levels of the other LNAA. As a result, ingesting normal dietary proteins, or increasing the protein content of the diet, will not raise brain tryptophan or serotonin synthesis, as discussed in many reviews, e.g. Fernstrom JD, 1994. This has been confirmed in a human study involving CSF measures as an approximation of what happens in the brain Teff KL, 1989. While the paper by Lindseth at al does not describe the diets used, it mentions “A variety of foods containing tryptophan were served, including mozzarella cheese, soy products, pumpkin seeds, and egg whites.” This implies that the variation of the tryptophan content of the two diets was manipulated by altering the protein levels in the diet. Therefore the high tryptophan diet would not have raised brain tryptophan and serotonin synthesis relative to the low tryptophan diet. 2. The authors did not consider what factors other than tryptophan might be responsible for the effects on mood that they report. Given that the low tryptophan diet provided <5 mg/kg body weight/d and the high tryptophan diet provided >10 mg/kg body weight/d presumably the protein content of the diet for the high tryptophan group was at least double that for the low tryptophan group. There is some evidence that protein has a greater satiating effect than the other macronutrients Pesta DH, 2014, so it is possible that the participants were more hungry on the low protein diet causing a lowering of mood. This could explain the better mood during the hight tryptophan diet phase. The researchers make no mention of measuring the hunger of the participants or possible preferences for the different diets. Furthermore, various amino acids are converted to psychoactive compounds including phenylalanine and tyrosine (catecholamines), methionine (S-adenosylmethionine), histidine (histamine) and leucine (glutamate), but the authors considered only the effect of tryptophan. 3. The section of the paper on Implications for Practice mentions that “the benefits of a diet for patients susceptible to affective disorders seem important since tryptophan-dense diets also improved mood and decreased symptoms of depression among depressed individuals in other studies (Badrasawi et al., 2013; Markus et al., 2008; Neumeister et al., 1998)”. The Badrasawi et al study Badrasawi MM, 2013 looked at the effect of a dietary supplement on mood. A comment on that article in PubMed (accessed by the previous link) explains why any effect on mood could not have been due to tryptophan. The Markus et al study Markus CR, 2008 looked at the acute effects of a high tryptophan hydrolyzed protein supplement on mood, and is therefore not relevant to how alterations in habitual food intake might alter mood. The Neumeister et al study Neumeister A, 1998 looked at the effect of acute tryptophan depletion (ATD) on mood in recovered depressed patients. Information on the ATD technique as used by Neumeister et al is available Young SN, 2013. In the control condition participants are given an amino acid mixture that is similar to the amino acid content of human milk, a source that is presumably optimum for human consumption. Because there are more LNAAs in this mixture than tryptophan, it will lower brain tryptophan slightly, but presumably within, or close to, the normal physiological range. The active treatment is the same as the control mixture except that tryptophan is omitted. The mixture induces protein synthesis and as tryptophan is incorporated into protein its level in blood and tissues falls dramatically, e.g. 80% or more decrease. This lowers brain tryptophan and serotonin synthesis greatly. In the Neumeister et al study ATD lowered mood relative to the control condition. However, the relevance of a lowering of mood caused by a large and unphysiological decrease in tryptophan, relative to control treatment that caused a small and probably physiologically relevant decline of tryptophan is not relevant to the possible effects of “tryptophan-dense diets”. Tryptophan in purified form is an antidepressant Shaw K, 2002 and under some circumstances tryptophan in purified form can improve mood in healthy people Young SN, 2013, Young SN, 2002. Markus et al Markus CR, 2008 and others have shown similar effects using proteins that contain unusually high amounts of tryptophan but are present in very small amounts in the diet, such as alpha-lactalbumin. However, as discussed above real foods will not raise brain tryptophan and serotonin even if the intake of tryptophan is elevated. Thus, the rationale for the study is not sound.