Tweet
Re: Low Carb Diets damage arteries?
I mentioned the endothelium in my previous post. The endothelium is one big cell that forms the inner lining of an artery. This big cell can cause the artery to dilate, constrict and it even has regenerative properties. Most cardiovascular diseases are due to damage to the endotheliums of heart (coronary) arteries.
Under normal conditions, a healthy endothelium will cause the artery to dilate as the blood flow through it (the artery) increases. This "normal" response can be influenced by certain drugs or substances (incl. meals), or the response can change depending on the health of the endothelium.
To measure this response, scientists came up with the so-called flow-mediated vasodilation (FMD). By restricting blood flow through an artery (using a cuff, for humans) and then releasing the pressure, the blood will rush through the artery. Therefore, a healthy endothelium should dilate the artery. By comparing the initial size (diameter) of the artery (measured using ultrasounds) with the "after" size, scientists can tell how healthy/damaged the endothelium is or how a certain meal/diet affects its response.
There are two kind of studies that are done to observe endothelium's response. (1) Longer term studies (a few weeks or more) that look how a diet affects the response. (2) Short term studies, where measurements are taken after different meals and all types of meals (high carb, low carb, high fat, low fat, etc.) are consumed by all subjects (to minimize biases caused by an individual's response to a particular meal type).
An example for (1) is the study on mice posted by Brian, but that study doesn't look at the effect dietary fat has on FMD. Because the only macronutrients that changed from the "Western" diet to the LCHP diet were protein and carbohydrate, any of them (or none at all, for humans) could decrease FMD... although it's impossible to say exactly which does what. The researchers hypothesized that one of the reasons for the difference between the damage to the arteries caused by the "Western" diet and that caused by the LCHP diet is a decrease in FMD (examined in wild mice, so the kind that was not genetically modified) on the LCHP diet.
There are a few (referenced!) studies looking at FMD changes in obese individuals. These studies compare a low-fat high-carbohydrate diet and a high-fat low-carbohydrate ("Atkins-style") diet.
One such study was published last year in Hypertension by Phillips et al. Their experiment lasted 6 weeks. During these 6 weeks, they compared the effect on FMD of the American Heart Association (AHA) diet (30% fat; and to put things in context, Hypertension is AHA's journal) and of the "Atkins Diet". I'm writing "Atkins Diet" in quotes, because if any of those "Atkineers" (or any of the researchers, for that matter) would have been members at ADBB, I would have told them to read/re-read the book.
So for the first 4 weeks of the diet, "Atkineers" were on a "weight reduction plan", where they had an estimated daily caloric deficit of 750 kcal and a carbohydrate (net?) intake of 20 g. In the last 2 weeks, they were on a "weight maintenance plan" --- the carb level stayed the same, 20 g, but Calories increased by 750 kcal (no caloric deficit). We are not told what foods were eaten during these 6 weeks (did they change in the last 2 weeks?); the only thing that is mentioned is that the LC diet was "supplemented with protein and fat content according to the Atkins' diet recommendation (DANDR 2002)" and that fat intake was in the range 55-65%. Both groups (HC and LC) had 10 subjects. Measurements at the end of the 6 weeks showed that subjects who followed the low-fat diet had a 34% improvement in brachial FMD, while those who followed the low-carb diet has their brachial FMD reduced by 14%. All subjects were overweight or obese, with BMIs in the range 29-39.
A similar comparison was published in the same year by Keogh et al. in the British Journal of Nutrition. Keogh at el.'s study had 99 subjects (52 on a LC diet and 47 on a HC diet) with BMIs between 27 and 44, all having abdominal obesity. These are the two isocaloric diets used: AJCN -- Keogh et al. 87 (3): 567 Table 1. The LC diet consisted of 61% fat (20% saturated), 35% protein and 4% carbohydrate, while the HC diet was 30% fat (less than 8% saturated), 24% protein, 46% carbohydrate. The study lasted 8 weeks. Among a bunch of other things, and opposite to the results of Phillips et al., Keogh et al. found that
There are more studies out there if you're interested, but the others I found are either not relevant for Atkineers (are low-carb, high-protein), or don't have enough participants, or use different (less accurate) methods and can't be compared, or have very different accuracies/powers. I just picked the one that received the most media attention and used an "Atkins-style" diet (the first one) and the one that had most participants and looked at a high-fat, low-carb diet similar to OWL Rung 3 of Atkins (the second). The two studies above both have the same power.
In the mice study posted by Brian, the authors say that another possible cause for atherosclerosis is a decrease in the number of endothelial progenitor cells. I'm not sure if this can be measured (legally, i.e. without killing anyone
) in humans and it's not clear to me if the two parameters (EPC count and FMD) are completely independent of each other (anyone knows?). In any case, since FMD measurements give different results in different human studies and the role diet plays is not yet understood, I would also be reluctant to extrapolate the result concerning the EPC count from mice to humans. Currently, there is no unambiguous proof that Atkins or an Atkins-style diet causes heart disease based on FMD (and definitely not based on serum lipid components). From what I read, it seems to me things other than simple macronutrient ratios also play an important role in the FMD.
I mentioned the endothelium in my previous post. The endothelium is one big cell that forms the inner lining of an artery. This big cell can cause the artery to dilate, constrict and it even has regenerative properties. Most cardiovascular diseases are due to damage to the endotheliums of heart (coronary) arteries.
Under normal conditions, a healthy endothelium will cause the artery to dilate as the blood flow through it (the artery) increases. This "normal" response can be influenced by certain drugs or substances (incl. meals), or the response can change depending on the health of the endothelium.
To measure this response, scientists came up with the so-called flow-mediated vasodilation (FMD). By restricting blood flow through an artery (using a cuff, for humans) and then releasing the pressure, the blood will rush through the artery. Therefore, a healthy endothelium should dilate the artery. By comparing the initial size (diameter) of the artery (measured using ultrasounds) with the "after" size, scientists can tell how healthy/damaged the endothelium is or how a certain meal/diet affects its response.
There are two kind of studies that are done to observe endothelium's response. (1) Longer term studies (a few weeks or more) that look how a diet affects the response. (2) Short term studies, where measurements are taken after different meals and all types of meals (high carb, low carb, high fat, low fat, etc.) are consumed by all subjects (to minimize biases caused by an individual's response to a particular meal type).
An example for (1) is the study on mice posted by Brian, but that study doesn't look at the effect dietary fat has on FMD. Because the only macronutrients that changed from the "Western" diet to the LCHP diet were protein and carbohydrate, any of them (or none at all, for humans) could decrease FMD... although it's impossible to say exactly which does what. The researchers hypothesized that one of the reasons for the difference between the damage to the arteries caused by the "Western" diet and that caused by the LCHP diet is a decrease in FMD (examined in wild mice, so the kind that was not genetically modified) on the LCHP diet.
There are a few (referenced!) studies looking at FMD changes in obese individuals. These studies compare a low-fat high-carbohydrate diet and a high-fat low-carbohydrate ("Atkins-style") diet.
One such study was published last year in Hypertension by Phillips et al. Their experiment lasted 6 weeks. During these 6 weeks, they compared the effect on FMD of the American Heart Association (AHA) diet (30% fat; and to put things in context, Hypertension is AHA's journal) and of the "Atkins Diet". I'm writing "Atkins Diet" in quotes, because if any of those "Atkineers" (or any of the researchers, for that matter) would have been members at ADBB, I would have told them to read/re-read the book.
So for the first 4 weeks of the diet, "Atkineers" were on a "weight reduction plan", where they had an estimated daily caloric deficit of 750 kcal and a carbohydrate (net?) intake of 20 g. In the last 2 weeks, they were on a "weight maintenance plan" --- the carb level stayed the same, 20 g, but Calories increased by 750 kcal (no caloric deficit). We are not told what foods were eaten during these 6 weeks (did they change in the last 2 weeks?); the only thing that is mentioned is that the LC diet was "supplemented with protein and fat content according to the Atkins' diet recommendation (DANDR 2002)" and that fat intake was in the range 55-65%. Both groups (HC and LC) had 10 subjects. Measurements at the end of the 6 weeks showed that subjects who followed the low-fat diet had a 34% improvement in brachial FMD, while those who followed the low-carb diet has their brachial FMD reduced by 14%. All subjects were overweight or obese, with BMIs in the range 29-39.A similar comparison was published in the same year by Keogh et al. in the British Journal of Nutrition. Keogh at el.'s study had 99 subjects (52 on a LC diet and 47 on a HC diet) with BMIs between 27 and 44, all having abdominal obesity. These are the two isocaloric diets used: AJCN -- Keogh et al. 87 (3): 567 Table 1. The LC diet consisted of 61% fat (20% saturated), 35% protein and 4% carbohydrate, while the HC diet was 30% fat (less than 8% saturated), 24% protein, 46% carbohydrate. The study lasted 8 weeks. Among a bunch of other things, and opposite to the results of Phillips et al., Keogh et al. found that
[...] weight loss with an LC did not impair FMD or have any adverse effects on other measures of endothelial function. A number of markers of endothelial function (eg, E- and P selectin, ICAM-1, tPA, and PAI-I) were improved as a result of weight loss with the LC. To our knowledge this has not been reported previously.
In the mice study posted by Brian, the authors say that another possible cause for atherosclerosis is a decrease in the number of endothelial progenitor cells. I'm not sure if this can be measured (legally, i.e. without killing anyone
) in humans and it's not clear to me if the two parameters (EPC count and FMD) are completely independent of each other (anyone knows?). In any case, since FMD measurements give different results in different human studies and the role diet plays is not yet understood, I would also be reluctant to extrapolate the result concerning the EPC count from mice to humans. Currently, there is no unambiguous proof that Atkins or an Atkins-style diet causes heart disease based on FMD (and definitely not based on serum lipid components). From what I read, it seems to me things other than simple macronutrient ratios also play an important role in the FMD.
Comment