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
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
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
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.
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 %].
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. read full comment
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 read full comment
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.
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
tight diabetic control (Laura LaValle, 03 February 2009)
I have been closely following the work of Dr. Westman and other researchers looking at low carbohydrate diets for diabetes and weight management. I have been using low carbohydrate diets with great results in clinical practice. I noted some comments by other researchers in an article about this study written by Shelly Wood which appeared in Medscape, notably that we should not be striving for the lowest HbA1 c levels. <br><br>Since the ACCORD trial, medicine has cautioned against the lowering of HbA1c's. A distinction between the ACCORD trial and some other studies looking at tighter control in diabetics, is that the primary intervention used to achieve the control was increased medication and/or insulin. <br><br>While the researchers involved in the ACCORD trial...
read full comment
Updated authors (W. Todd Penberthy, 13 January 2009)
<br>We were most grateful for the opportunity to examine Vaticanol B, a fascinating molecule. <br><br>Tetsuro Ito, Munekazu Iinuma, and Osamu Hori made this possible. Vaticanol B was isolated and prepared as described [1]. <br><br>Accordingly we enthusiastically update the list of authors to properly recognize the contribution of these individuals:<br>Kevin S. Jones, Alexander P. Alimov, Horacio L. Rilo, Tetsuro Ito, Munekazu Iinuma, Osamu Hori, Ronald J. Jandacek, Laura A. Woollett, and W. Todd Penberthy<br><br><br>Sincerely, <br>W. Todd Penberthy <br><br><br>[1] Ito TA, Tanaka T, Iinuma M, Iliya I, Nakaya K, Ali Z, Takahashi Y, Sawa R, Shirataki Y, Muratae J, Darnaedif D: New resveratrol oligomers in the stem...
read full comment
Comment on: Jones et al. Nutrition & Metabolism, 5:23
Dietary protein and bone health (Anssi Manninen, 08 September 2006)
A well-written review Valsamis et al. discussed the pathophysiologic mechanisms of bone disease associated with anti-epileptic use. The authors righly pointed out that low calcium intake and vitamin D deficiency can aggravate adverse bone effects. However, the importance of adequate dietary protein went unrecognized. Like calcium and vitamin D, protein is an critical nutrient for bone health. The old hypothesis that proteins (especially animal proteins) are causally associated with an increased incidence of osteoporotic fractures is simply incorrect [1]. In fact, prospective epidemiologic observations indicate that higher protein intake is associated with increased bone mineral mass and reduced incidence of osteoporotic fractures [1]. In addition, higher protein intake has positive effects...
read full comment
upper protein limit not known (Dan Kampmeier, 11 April 2006)
Manninen claims that there is no scientific evidence supporting the notion that 30% protein intake has any adverse effects on bone health, although his own review (his [1]) of the related acid load hypothesis states that "the epidemiological and clinical data addressing this hypothesis are controversial". I reached the same conclusion, and, given the controversial and often-contradictory results of a large number of studies, was unable to justify a 30% protein intake until further research has fully resolved the question of protein's acid load effects on bone health.The major problem is that most of the studies of this issue have been done in the range of 0.7 to 1.5 g/kg, or about 10 to 20% protein intake, well below the 30% that is in question. This lower range has created a good...
read full comment
Comment on: Gannon et al. Nutrition & Metabolism, 3:16
High-protein intake and bone health (Anssi Manninen, 01 April 2006)
Kampmeier suggested that high-protein intake (30%) may have some adverse effects on bone health. It should be noted, however, that there is no scientific evidence supporting this notion. High protein intake enhances IGF-1, a growth factor that exerts highly positive activity on bone formation. Consequently, high-protein intake is, if anything, protective against loss of bone minerals. For a more detailed reviews, see the papers by Manninen [1] and Bonjour [2]. References1. Manninen AH. High-protein weight loss diets and purported adverse effects: where is the evidence? Sports Nutr Rev J 2004;1(1):45-51.2. Bonjour JP. Dietary protein: an essential nutrient for bone health. J Am Coll Nutr 2005;24:526S-36S.
read full comment
Comment on: Gannon et al. Nutrition & Metabolism, 3:16
personal confirmation of results (Dan Kampmeier, 01 April 2006)
Gannon and Nuttal's study closely reflects my personal experience during the last 3 years. Starting as a prediabetic (FBG > 100), I was able to "cure" this by modifying my diet from about 55% carbs down to 40%, and then 30%, with increases in protein and fat similar to those in their study. One difference, however, is that I experienced significant weight loss without calorie restriction. So they may want to consider that the amount of fat and muscle carried by one's body may be sensitive to the macronutrient ratios, independent of calorie intake.Another issue is whether 30% protein is safe for bone health. My review of the literature led me to conclude that 20% was closer to optimal, with 15% being the minimum for good bone growth, and 30% producing too high an acid load, leading to...
read full comment
Comment on: Gannon et al. Nutrition & Metabolism, 3:16
The high-carbohydrate advice has never made sense in the treatment of (ron raab, 01 October 2005)
I am a Vice-President of the International Diabetes Federation (IDF) www.idf.org I have had Type 1 diabetes for the last 48 years since the age of 6. I have adopted the low carbohydrate/low insulin regime as the basis for managing my diabetes. I am writing in a personal capacity and not on behalf of the IDF. The high-carbohydrate advice for diabetes reminds me of the disastrous approach taken by many physicians up until the mid 1980's .... that it was appropriate to have high blood sugars because there was no evidence to the contrary. A much more sensible position was that trying to normalise blood sugars was inherently wise because that is how the normal body functions. The high-carbohydrate advice has never made sense in the treatment of diabetes, and a lot of people suffer...
read full comment
Comment on: Arora et al. Nutrition & Metabolism, 2:16
A few thoughts about Professor Ancel Keys (stephen phinney, 28 February 2005)
Although I was saddened by the news of Ancel Keys' passing last fall, I took the opportunity to reflect upon his long and productive life. My most memorable encounter with Dr. Keys was in the mid-1980's, about the time that the Lipid Research Clinic Coronary Prevention Trial had demonstrated that using cholestyramine to reduce cholesterol significantly reduced coronary mortality. Of course Dr. Keys had set this study in motion two decades earlier when he undertook his Seven Countries Study, which laid the foundation for the diet, cholesterol and heart disease hypothesis. Meeting Dr. Keys by chance in a hallway at the University of Minnesota, he took the opportunity to show me a manuscript that examined long-term mortality risk relative to baseline HDL cholesterol in a cohort of Minnesota...
read full comment
Comment on: VanItallie Nutrition & Metabolism, 2:4
RSS
Latest comments
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 %].
read full comment
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.
read full comment
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
read full comment
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
read full comment
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
tight diabetic control (Laura LaValle, 03 February 2009)
I have been closely following the work of Dr. Westman and other researchers looking at low carbohydrate diets for diabetes and weight management. I have been using low carbohydrate diets with great results in clinical practice. I noted some comments by other researchers in an article about this study written by Shelly Wood which appeared in Medscape, notably that we should not be striving for the lowest HbA1 c levels. <br><br>Since the ACCORD trial, medicine has cautioned against the lowering of HbA1c's. A distinction between the ACCORD trial and some other studies looking at tighter control in diabetics, is that the primary intervention used to achieve the control was increased medication and/or insulin. <br><br>While the researchers involved in the ACCORD trial... read full comment
Comment on: Westman et al. Nutrition & Metabolism, 5:36
Updated authors (W. Todd Penberthy, 13 January 2009)
<br>We were most grateful for the opportunity to examine Vaticanol B, a fascinating molecule. <br><br>Tetsuro Ito, Munekazu Iinuma, and Osamu Hori made this possible. Vaticanol B was isolated and prepared as described [1]. <br><br>Accordingly we enthusiastically update the list of authors to properly recognize the contribution of these individuals:<br>Kevin S. Jones, Alexander P. Alimov, Horacio L. Rilo, Tetsuro Ito, Munekazu Iinuma, Osamu Hori, Ronald J. Jandacek, Laura A. Woollett, and W. Todd Penberthy<br><br><br>Sincerely, <br>W. Todd Penberthy <br><br><br>[1] Ito TA, Tanaka T, Iinuma M, Iliya I, Nakaya K, Ali Z, Takahashi Y, Sawa R, Shirataki Y, Muratae J, Darnaedif D: New resveratrol oligomers in the stem... read full comment
Comment on: Jones et al. Nutrition & Metabolism, 5:23
Dietary protein and bone health (Anssi Manninen, 08 September 2006)
A well-written review Valsamis et al. discussed the pathophysiologic mechanisms of bone disease associated with anti-epileptic use. The authors righly pointed out that low calcium intake and vitamin D deficiency can aggravate adverse bone effects. However, the importance of adequate dietary protein went unrecognized. Like calcium and vitamin D, protein is an critical nutrient for bone health. The old hypothesis that proteins (especially animal proteins) are causally associated with an increased incidence of osteoporotic fractures is simply incorrect [1]. In fact, prospective epidemiologic observations indicate that higher protein intake is associated with increased bone mineral mass and reduced incidence of osteoporotic fractures [1]. In addition, higher protein intake has positive effects... read full comment
Comment on: Valsamis et al. Nutrition & Metabolism, 3:36
upper protein limit not known (Dan Kampmeier, 11 April 2006)
Manninen claims that there is no scientific evidence supporting the notion that 30% protein intake has any adverse effects on bone health, although his own review (his [1]) of the related acid load hypothesis states that "the epidemiological and clinical data addressing this hypothesis are controversial". I reached the same conclusion, and, given the controversial and often-contradictory results of a large number of studies, was unable to justify a 30% protein intake until further research has fully resolved the question of protein's acid load effects on bone health.The major problem is that most of the studies of this issue have been done in the range of 0.7 to 1.5 g/kg, or about 10 to 20% protein intake, well below the 30% that is in question. This lower range has created a good... read full comment
Comment on: Gannon et al. Nutrition & Metabolism, 3:16
High-protein intake and bone health (Anssi Manninen, 01 April 2006)
Kampmeier suggested that high-protein intake (30%) may have some adverse effects on bone health. It should be noted, however, that there is no scientific evidence supporting this notion. High protein intake enhances IGF-1, a growth factor that exerts highly positive activity on bone formation. Consequently, high-protein intake is, if anything, protective against loss of bone minerals. For a more detailed reviews, see the papers by Manninen [1] and Bonjour [2]. References1. Manninen AH. High-protein weight loss diets and purported adverse effects: where is the evidence? Sports Nutr Rev J 2004;1(1):45-51.2. Bonjour JP. Dietary protein: an essential nutrient for bone health. J Am Coll Nutr 2005;24:526S-36S. read full comment
Comment on: Gannon et al. Nutrition & Metabolism, 3:16
personal confirmation of results (Dan Kampmeier, 01 April 2006)
Gannon and Nuttal's study closely reflects my personal experience during the last 3 years. Starting as a prediabetic (FBG > 100), I was able to "cure" this by modifying my diet from about 55% carbs down to 40%, and then 30%, with increases in protein and fat similar to those in their study. One difference, however, is that I experienced significant weight loss without calorie restriction. So they may want to consider that the amount of fat and muscle carried by one's body may be sensitive to the macronutrient ratios, independent of calorie intake.Another issue is whether 30% protein is safe for bone health. My review of the literature led me to conclude that 20% was closer to optimal, with 15% being the minimum for good bone growth, and 30% producing too high an acid load, leading to... read full comment
Comment on: Gannon et al. Nutrition & Metabolism, 3:16
The high-carbohydrate advice has never made sense in the treatment of (ron raab, 01 October 2005)
I am a Vice-President of the International Diabetes Federation (IDF) www.idf.org I have had Type 1 diabetes for the last 48 years since the age of 6. I have adopted the low carbohydrate/low insulin regime as the basis for managing my diabetes. I am writing in a personal capacity and not on behalf of the IDF. The high-carbohydrate advice for diabetes reminds me of the disastrous approach taken by many physicians up until the mid 1980's .... that it was appropriate to have high blood sugars because there was no evidence to the contrary. A much more sensible position was that trying to normalise blood sugars was inherently wise because that is how the normal body functions. The high-carbohydrate advice has never made sense in the treatment of diabetes, and a lot of people suffer... read full comment
Comment on: Arora et al. Nutrition & Metabolism, 2:16
A few thoughts about Professor Ancel Keys (stephen phinney, 28 February 2005)
Although I was saddened by the news of Ancel Keys' passing last fall, I took the opportunity to reflect upon his long and productive life. My most memorable encounter with Dr. Keys was in the mid-1980's, about the time that the Lipid Research Clinic Coronary Prevention Trial had demonstrated that using cholestyramine to reduce cholesterol significantly reduced coronary mortality. Of course Dr. Keys had set this study in motion two decades earlier when he undertook his Seven Countries Study, which laid the foundation for the diet, cholesterol and heart disease hypothesis. Meeting Dr. Keys by chance in a hallway at the University of Minnesota, he took the opportunity to show me a manuscript that examined long-term mortality risk relative to baseline HDL cholesterol in a cohort of Minnesota... read full comment
Comment on: VanItallie Nutrition & Metabolism, 2:4