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Correction to Table 2 (Krista Varady, 05 December 2014)

Due to data entry errors, the Energy (kcal) values in Table 2 are incorrect. The correct values are as follows: IFCR-L week 10: 1655 kcal, IFCR-L change: -53 kcal.
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Comment on: Kroeger et al. Nutrition & Metabolism, 9:98

“Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review”. The other side of an alleged plagiarism story (Antonino Bianco, 01 October 2014)

“Alcohol consumption and hormonal alterations related to muscle hypertrophy: a review”. The other side of an alleged plagiarism story   On June 6, 2014 the article entitled “Alcohol consumption and hormonalalterations related to muscle hypertrophy: a review” was accepted by the scientific journal “Nutrition and Metabolism”. What a great day for our research team, our review that tried to elucidate the consequences of excessive alcohol consumption was finally on-line. Unfortunately we didn’t know, and could not imagine, that was the beginning of an ordeal of injustice..... please visit the following link  www.fitnessa360.com/2014/09/alcohol-consumption-and-hormonal.html   read full comment

Comment on: Bianco et al. Nutrition & Metabolism, 11:43

Change in author affiliation address. (Andreea Soare, 01 October 2014)

For the author Mario Pianesi the correct affiliation is: International Study Center for Environment, Agriculture, Food, Health and Economics, Via San Nicola 9, 62029 Tolentino, Italy. read full comment

Comment on: Soare et al. Nutrition & Metabolism, 11:39

Question the conclusion not HDL predictive value (eric anderson, 29 November 2013)

1) 30 days is a very short... read full comment

Comment on: Kent et al. Nutrition & Metabolism, 10:58

Response of Jugdaohsingh et al. (Nutrition & Metabolism 2013, 10:65) is not convincing concerning the safety of MMST. (Dirk Vanden Berghe, 29 November 2013)

It is correct that I was involved in clinical and pre-clinical studies on choline-stabilized orthosilicic acid (ch-OSA) and in the galenic formulation of ch-OSA containing food supplements. As indicated in my letter, my work on silicon was partly funded by research funds from the industry. I have received such funds not only from Bio Minerals but also from other companies and only until September 2009 which is more than 4 years ago. Sponsoring of research by the industry is common practice, in fact the study of the authors on MMST was also sponsored by the manufacturer of MMST (LLR-G5... read full comment

Comment on: Jugdaohsingh et al. Nutrition & Metabolism, 10:65

MMST ingestion in humans does not affect urinary volume (Ravin Jugdaohsingh, 25 September 2013)

Dr Exley makes a perfectly valid comment concerning the role of urinary creatinine in studies with spot urines. However, to suggest that our entire study is flawed because this is not reported is as dramatic as it is erroneous. Three of the four major outcomes in our work would not have been informed by urinary creatinine. The fourth- the increase in urinary silicon/MMST concentration following supplementation ¿ could have been. Nonetheless, double-blind, cross-over placebo control confirmed the consistency of inter-individual urinary silicon concentrations when matched for time of day. Our previous data have shown that MMST ingestion in humans does not affect urinary volume. So, as Dr Exley states, a supplement induced change to GFR would be required to misinform this outcome.... read full comment

Comment on: Jugdaohsingh et al. Nutrition & Metabolism, 10:37

Measuring the urinary excretion of silicon (Chris Exley, 27 June 2013)

The data in this paper relating to the urinary excretion of silicon are expressed as mg/L for point samples.

These are meaningless. Either the data should be normalised to account for differences in glomerular filtration rate and expressed per mmol creatinine or 24h urine samples should have been collected so that the data could have been expressed as per 24h.

Unfortunately data expressed in this manner are not only useless in comparisons between groups within the same study (what if MMST affected GFR?) they are also useless as they cannot be used to compare with data for urinary Si excretion in other studies.

This basic error means that this study though potentially very interesting is fundamentally flawed. read full comment

Comment on: Jugdaohsingh et al. Nutrition & Metabolism, 10:37

Erratum (Didier Chapelot, 16 July 2012)

Please note that a reference has been forgotten and wrongly attributed. This is reference [28] in the discussion section (last paragraph). The correct reference is "Lu CL, Zou X, Orr WC, Chen JD: Postprandial changes of sympathovagal balance measured by heart rate variability. Dig Dis Sci 1999, 44:857-861".
Moreover, the symbols of conditions in the figures are not stipulated. So, note that black squares indicate the exercise condition and white squares the rest condition.
Sorry for these errors. read full comment

Comment on: Charlot et al. Nutrition & Metabolism, 8:66

Complex effects of D-lactate (Heikki Savolainen, 04 July 2012)

Dear Editor,

Ling et al. (1) show convincingly that highly oxygen-depedent organs are more prone to the toxic effects of D-lactate than liver.

However, dosing of D-lactate in a liver cell culture has other very interesting effects. Namely, the PI3K/AktPKB/PKC acitivity is decreased which leads to low BAD activity allowing increased apoptosis (2).

This indicates that D-lactate can also have other significant metabolic effects e.g. in diabetics who have increased D-lactate burden because of excessive methylglyoxal from glucose (3).

1 Ling et al. Nutrition and Metab 2012; 9: 6

2 Miyamato. J Am Coll Surg 2007; 204: 182

3 Talasniemi et al. Clin Biochem 2008; 41: 1099 read full comment

Comment on: Ling et al. Nutrition & Metabolism, 9:6

Typing error in Flatulence mean figures (Beatriz Sarria;, 04 July 2012)

In table 7, under Flatulence, the mean figures are incorrect: instead of 2.14a of 2.07a and 2.32a they should read 1.42 a, 1.61a and 1.70a, respectively. The p value shown (0.019) corresponds to the correct set of data. read full comment

Comment on: Sarriá et al. Nutrition & Metabolism, 9:33

2012 follow-up of case? (Hans Krause, 04 July 2012)

It would be interesting to know the follow-up on this case, now 2 years later. How has the patient fared since this article was written? read full comment

Comment on: Zuccoli et al. Nutrition & Metabolism, 7:33

KD diet composition (Jeff Kiefer, 21 June 2011)

I can't help but to think that the results may be more impressive if not based on the formulated diet that was used in this study. Crisco is anything but a natural and healthy oil and would compromise a number of confounding variables. Something such as a more natural sat. fat source, say coconut oil might be preferable. Additionally, it would certainly be more ketogenic. Think long term such supplementation in human subjects would be preferable to crisco. read full comment

Comment on: Stafford et al. Nutrition & Metabolism, 7:74

CYP1A2*1F is not a 'rapid metabolizer' phenotype (Vidya Perera, 21 June 2011)

The authors of this study conclude that bone mineral density (BMD) was lower in people who reported having high coffee consumption and also had rapid metabolism of caffeine (defined as having a particular CYP1A2 genotype), indicating `this group' of coffee consumers might be at special risk of bone loss and its associated clinical consequences. However, it is our view that this study does not take into account two critical factors related to CYP1A2 activity that influence the conclusions drawn. Firstly, the CYP1A2 polymorphism (-163 C>A) is associated with higher inducibility only in people who are cigarette smokers and secondly, environmental factors play a major and significant role in determining CYP1A2... read full comment

Comment on: Hallström et al. Nutrition & Metabolism, 7:12

Error correction of genotype name in Table 2 and Table 3 (Oh Yoen Kim, 21 June 2011)

"FEN1-10154G>T " was duplicated In Table 2 and Table 3. The second one should be changed to "FADS3 rs1000778"

[ Table 2 ]
second "FEN1-10154G>T " [GG (n=259), GT+TT (n=308)] should be changed to FADS3 rs1000778 [CC (n=280), CT+TT(n=287)]

[ Table 3 ]
second "FEN1-10154G>T " [GG (n=259), GT+TT (n=308)] should be changed to FADS3 rs1000778 [CC (n=280), C carrier (n=287)] read full comment

Comment on: Kim et al. Nutrition & Metabolism, 8:24

Protein and ageing (eric anderson, 26 January 2011)

I would like to see a folow up to look at protein levels of 6.25, 7.5, 8.75 and 16% of calories from protein on older pigs (75% of average lifespan) to see the effect of the change in diet and the pig longevity. read full comment

Comment on: Zhao et al. Nutrition & Metabolism, 7:6

I believe you mean (Laura Buti, 26 January 2011)

(from page 2)
"Whey proteins also modulate several hormones that influence body
composition. Short term acute studies with whey proteins corroborate
the body composition changes seen with longer term feeding studies.
Whey protein isolate (75 grams per dose) was evaluated [12] for its
impact on obesity-related hormones in an acute (5 hour) protein
ingestion in overweight and obese women with polycystic ovary syndrome
(PCOS). The acute hormonal response showed significantly lower
hyperinsulinemia (less lipogenesis), lower cortisol levels (lean
muscle preservation) and increased ghrelin release (satiety
enhancement)."

The last line in the paragraph is inaccurate, as even the most amateur
nutrition student can tell... read full comment

Comment on: Frestedt et al. Nutrition & Metabolism, 5:8

Diet-Induced Thermogenesis (Frank Dobner, 02 July 2010)

I have thought about thermogenesis many times since I first learned about it. Not being a medical practitioner, I have a question about this I would like pose.

Many people of the world are being encouraged to eat smaller and few meals on the basis that it will encourage diet-induced thermogenesis. However, if this thermogenesis is a function of simply how much is eaten in a day, why would it matter if you ate once or six times?

Your contribution to this question would be very appreciated.

Frank Dobner
Male Weight Loss Now read full comment

Comment on: Westerterp Nutrition & Metabolism, 1:5

Nutrition ratio/description mismatch or error (gamma sync, 02 July 2010)

The article describes the diets as:
high carbohydrate, high energy diet (HED) + exercise (2,600; 55:15:30%);

very low carbohydrate, high protein (VLCHP) + exercise (1,200; 63:7:30%),

low carbohydrate, moderate protein (LCMP) + exercise (1,200: 50:20:30%),

high carbohydrate, low protein (HCLP) + exercise group (1,200: 55:15:30%)

And further says the nn:nn:nn numbers are % carbohydrate: protein: fat

But, the descriptions do not match the ratios. The "Very Low carbohydrate" diet is 63% carbohydrate, which is the highest carb of all of the choices.

As this is the diet which has the most significant weight loss result, it is odd that the name and the proportions are in direct opposition.

None of... read full comment

Comment on: Kerksick et al. Nutrition & Metabolism, 6:23

Diet composition stats typos? (Beth Mazur, 02 July 2010)

Are the carb and protein percentages of the diets swapped? Abstract says that diet composition stats are presented as (kcals; % carbohydrate: protein: fat). Yet the very low carbohydrate, high protein diet (VLCHP) is presented as [1,200 kcals; 63:7:30 %]. And the low carbohydrate, moderate protein diet (LCMP)is presented as [1,200 kcals; 50:20:30 %].

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Comment on: Kerksick et al. Nutrition & Metabolism, 6:23

Thanks for the correction (Anssi Manninen, 02 July 2010)

Dear Sir,

Thanks for the correction. Indeed, the right reference number for "The most sophisticated study to date demonstrated.." is 14, not 13.
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Comment on: Manninen Nutrition & Metabolism, 6:38

Erroneous omission in table 1 (Mario Ciampolini, 02 July 2010)

In table 1, weight of trained subjects significantly decreased after training (P < 0.001), and the decrease was significantly wider than in control subjects (P < 0.01). Thus read weight in last column of table 1 as 72.2±10.1**,a***,b
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Comment on: Ciampolini et al. Nutrition & Metabolism, 7:4

Pantothenic acid is a sulfur containing vitamin (David Figenschou, 02 July 2010)

Thank you for the stimulating overview on sulfur requirements and the possibility of its widepsread dietary inadequacy.

If I am not mistaken you are in error when you state:
"From the standpoint of the diet, methionine alone is capable of providing all the necessary body sulfur, with the exception of the two sulfur-containing vitamins, thiamin and biotin."
Pantothenic acid is also a sulfur containing vitamin which cannot be made from methionine in humans, and therefore must be supplied by the diet.

Also there seem to be contradictory statements about the cysteine/methionine ratios found in various foods:-

"In general the ratio of cysteine/methionine is close to one for poultry and red meat protein, and to 0.7 for fish. Dairy... read full comment

Comment on: Nimni et al. Nutrition & Metabolism, 4:24

Wrong citation (Markus Auer, 03 April 2010)

Hello,

I just discovered a wrong query in your article:

"The most sophisticated study to date demonstrated that a 35 g dose of rapidly absorbed casein hydrolysate is ~30% more effective in stimulating skeletal muscle protein synthesis than intact casein when measured over the 6 h period [13]."

Study #13 is not the right one, #14 would be good instead.

Thanks and bye

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Comment on: Manninen Nutrition & Metabolism, 6:38

A couple of basic errors (John Richards, 11 January 2010)

You seem to have not quite grasped a couple of basic points about the science in paragraph 6.
For one thing, type II diabetes is not a disorder of insulin production but of insulin response - the pancreas is still producing insulin, but for some reason the body's tissues don't react to it as much as they used to.
Secondly, references 5 and 6 are not, as you imply, randomised control trials. One is a meta-analysis of 13 cohort studies and one is a cohort study itself. This is stated quite clearly in the abstracts.
Third, while poor glycaemic control and post-prandial hyperglycaemia were cited as independent risk factors for all-cause mortality, they were not cited as risk factors specifically for cardiovascular disease.
I'm sure you'll... read full comment

Comment on: Arora et al. Nutrition & Metabolism, 1:14

Tea intake and the possibility of adipose tissue remodeling (Rosário Monteiro, 14 May 2009)

This report raises interesting questions, but some aspects deserve further discussion. While stimulation of lipolysis by white tea may confer interest to this product as a helper in a strategy to lose weight, its anti-adipogenic effects may constitute, instead, a subject of concern. In an obesogenic context, reducing adipocyte number should not be an aim [1]. Instead, increasing the capacity of the adipose tissue to accommodate energy surplus, namely through the stimulation of adipocyte differentiation, might be more beneficial, as it will preclude fat from accumulating in other places, such as the liver, and adipocytes from becoming too big. In this regard, large adipocytes are known to be associated with increased plasma inflammatory cytokines [2, 3], this cellular phenotype being... read full comment

Comment on: Söhle et al. Nutrition & Metabolism, 6:20