Friday, January 29, 2010

Who pays the piper for arterial stiffness? Now for Table 7...

First the problem: TABLE 7

OK, first the easy bits. Both diets dropped systolic and diastolic blood pressures by the same amount. I'll come back to the pulse pressure (systolic - diastolic) later, but it didn't change by any significant amount either.

The last line, brachial pulse wave velocity, didn't change and was the same on both diets. This is a marker of how stiff the brachial artery is, a muscular artery which doesn't store blood in the same way as the elastic arteries such as the aorta. You can say muscular arteries didn't change with diet or weight loss.

There are then a set of numbers derived from the aortic arterial waveform, this waveform, deep in the aorta, is estimated from a peripheral pulse (illustration stolen from some random Nature paper where folks probably knew what they were talking about):

The time-to-wave reflection is the time from the start of contraction to a very early reflected wave from the periphery. It comes much sooner than the wave described in the previous post and just shows as a "bumping up" of the pressure in the aorta.

The sooner this wave arrives the more rigid the aorta. To find it you look for an inflection point on the upswing of the pulse pressure. It's marked as Tr in the diagram. It's probably similar in the information it carries as aortic pulse wave velocity in the last post but requires much more sophisticated software to extract.

This marker of aortic health improved by twice as much in the low fat diet as the low carbohydrate diet. That's interesting, but note that both groups improved.

The amount that the blood pressure gets "bumped up" by using this wave is the augmentation pressure, recorded as "augmentation" in the table. To get the augmentation index you should just divide the augmentation pressure by the pulse pressure and multiply by 100 to get a percentage. ie how much of your pulse pressure is from augmentation due to early reflection... The numbers don't add up exactly as the machine seems to be doing something slightly different and describing the end result as aortic augmentation index as compared to the usual augmentation index... That's just inside the box of tricks used and I can't tell exactly what they've done.

So, because pulse pressure didn't really change, augmentation and augmenation index should change together. They do, but only approximately. The difference has, again, to be within the machine and how it looks at the waveforms and does its calculations.

What's bad is that, as reported by Hunter, AI got worse in the low carb group and got better in the low fat group. Oh no! So Hunter can say in the discussion:

"It is possible that the high fat content of a low-carbohydrate diet exerts detrimental effects on endothelial function, which raises concerns regarding the long-term safety and efficacy of low-carbohydrate diets"

But when you look at the numbers the low carbohydrate group started with an augmentation of 7.4 mmHg and this increased to 8.4 mmHg.

The low fat group started with a higher value of 9.2 mmHg and this dropped to 8.3 mmHg.

So the low carbohydrate group started 1 mmHg of augmentation below the end result of 8.4 mmHg. The low fat group started at 1mmHg of augmentation above the end result of 8.3mmHg.

I defy anyone to claim 8.4 is different from 8.3 with SDs of 5.4 and 7.8 respectively.

The end values were the same.

So there are two insoluble mysteries. First is how the "aortic" augmentation index, the only value which made p<0.05, is different for the simply calculated augmentation index percentage, which probably didn't reach p=0.04.

The second is how come a group of 12 people can improve one measure of aortic stiffness (time-to-wave reflection) and worsen another (augmentation index), when both parameters are derived from the same 12 cardiovascular systems! Dunno on either of those.

But I would also add that augmentation should never be zero! You're pushing blood down a pipe. Some augmentation is essential and normal and a quick look around pubmed has some poor folks with augmentation indices of >40%, to put things in perspective... It's not like cholesterol (jk), the lower the better blah blah blah !

This comes down to clinical vs statistical significance. Both groups ended up with the same augmentation, neither change was significant, biologically or statistically, but a machine derived variant made p=0.04 in favour of low fat diet, but with dubious biological significance.

There is a huge goldmine of information in the results which need talking about but I think that's enough for now. It's all pro LC and anti LF, as you would expect.


BTW I've just calculated the AI% from changes in pulse-pressure and reported augmentation and, using the simple percentage technique [of AP/PP X 100], the end of study AI% for LC (17.14%) actually ends up slightly lower, compared to the end value for the LF group (17.29%). Hunter no doubt would argue the direction of change being awful despite LC end result beating LF etc etc but still, it's pleasant pedantry to look at the numbers...


caphuff said...

Awesome. Sometimes when I read this blog I feel I've stumbled into some sort of genius olympics where the gold medal goes to the most complete and utter evisceration (with style) of a pubmed report.

In my (unscientific) opinion I would give this one a perfect 10.

Jim Purdy said...

As a lay person, much of this post was over my head.

However, what I do know is that on a high carb diet, I have frequent episodes of very unpleasant tachycardia and chest pain.

On a low carb diet, those problem are greatly reduced.

That's all I need to know. It's low-carb for me, and especially low grains and low cereals and low bread.

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SamAbroad said...

Hi Peter,

Did you see this?

Iron lady indeed!

Bruce said...

This is a superb blog, Peter. What better peer review system for industry funded-propaganda (a.ka. "scienctific studies") than a world-wide network of independent, skeptical scientists? Bravo.

Are you aware of any outcomes studies on low carb diets for secondary prevention of CHD? There are many surrogate studies (i.e. lipid profiles), but I haven't found any outcomes studies (rate of MI, cardiac death, etc.)

Bruce Wilson
Montreal, Canada