Friday, April 09, 2010

For the low fat brigade

Still no significant net time and this is not likely to change in the next few weeks, sorry for emails being ignored....

In the mean time folks might enjoy this from Dr Volek. It didn't seem to make headline news, can't imagine why.

Personally I would be loathe to take dietary advice from an AHA cardiologist who stands to benefit from my having a heart attack. They are unlikely to be completely honest.

Peter

12 comments:

David Moss said...

"hypocaloric diets (approximately 1500 kcal)"

So about 1000 calories short then... one wonders why you rarely see these short term studies feeding people their full calories needs on high carb.

This study basically works out at at 75% fat diet versus a 54% fat diet then (and still with impressive superiority for the really high fat).

jandro said...

DM, I think you are mistaken. The low fat diet only has 24% of the calories as fat, not 56% (it has 56% of the calories as carbs). Just pointing that out.

Vladimir Heiskanen (Valtsu) said...

In the case you have not seen this one yet:

http://www.ajcn.org/cgi/content/full/80/5/1175

"a higher saturated fat intake was associated with a smaller decline in mean minimal coronary diameter (P = 0.001) and less progression of coronary stenosis (P = 0.002) during follow-up."

"Carbohydrate intake was positively associated with atherosclerotic progression (P = 0.001), particularly when the glycemic index was high."

"Polyunsaturated fat intake was positively associated with progression when replacing other fats (P = 0.04) but not when replacing carbohydrate or protein."

Richard A. said...

Here is another not-pc study --

http://www.ncbi.nlm.nih.gov/pubmed/19892353

Low-carbohydrate diets reduce lipid accumulation and arterial inflammation in guinea pigs fed a high-cholesterol diet.

John said...

Incorrect cardiologists would annoy me much less if the majority weren't so arrogant.

David said...

Interesting, but the fact that they used a high-fat meal as the test meal after which they evaluated FMD in both the low-fat diet and low-carb diet groups seems unfortunate. I'd be more interested in seeing effects on FMD of a low-fat meal in the low-fat dieg group compared to effects on FMD of a high-fat meal in the low-carb diet group. Seems much more relevant. Also, the baseline FMD in low-fat diet group appears much higher than the post-12-week FMD in the low-carb group. Wonder how or what they were eating before?

blogblog said...

Cardiologists always ignore the fact that athersclerosis doesn't occur in carnivores but is common in both herbivores and omnivores. This inconvenient fact, of course, totally destroys the entire saturated fat-CHD hypothesis

Unknown said...

jandro, DM has it right. The participants were on a hypocaloric diet. Assuming 2500 kcal is the average energetic requirement and missing energy is derived solely from fat, participants in both studies derived 1000 kcal per day from their own fat which makes both diets high in fat.
1000/2500 + 24*1500/2500 = 54.4% 1000/2500 + 59*1500/2500 = 75.4%

donny said...

"After 12 weeks, peak flow-mediated dilation at 3 hours increased from 5.1% to 6.5% in the CRD group and decreased from 7.9% to 5.2% in the LFD group (P = .004)."

This is a little confusing, it sounds like day 1 flow mediated dilation is being compared to 3 hours after a fat load twelve weeks later.

"Here, we extend our work and address these concerns by measuring fasting and postprandial vascular function in 40 overweight men and women"

This, from earlier in the abstract, makes things a little clearer. It's fasting vs postprandial, all at the end of twelve weeks.

I wonder whether measuring peak flow-mediated dilation at fasting has an effect on dilation three hours after a fat load? Things controlled by hormones tend to have an effect on hormones. The group exhibiting the greatest dilation while fasting is likely to have had the strongest response, so if something were down-regulated as a result of the measurement itself (or if something were "used up," if the ability to produce nitric oxide was compromised, for instance), then a decrease in fmd might be more likely in this group.

williebr said...

Even with no time peter, this is still very interesting.

Thanks.

Pasi said...

Hi Peter,

Volek et al. noticed that restricted carbs led to increased secretion of IL-6 from the muscles. That is no surprice because muscles with low glycogen content secrete more IL-6 under workload.

It is well known that IL-6 has positive anti-inflammatory effects when increased after exercise.

I feel little concerned if carb restriction might eventually lead to the increased plasma IL-6 for a longer time because IL-6 is also a mediator of chronic inflammation.

Short term high IL-6 with proper rest after exercise has positive effect all over the body but chronic elevated IL-6 may lead to health problems or atleast is related to them.

jandro said...

Thanks for the clarification Adrian, I thought (s)he was referring to the food subjects ate rather than the chemicals their body consumed.

westie, like you, I am a little worried about it. IL-6 is chronically high in diabetics, cancer patients, etc

http://www.ncbi.nlm.nih.gov/pubmed/17684929

http://www.ncbi.nlm.nih.gov/pubmed/16306329

I think it is different when you exercise since it is not chronically elevated. Anyone knows how many grams of carb it takes to avoid this effect? I would assume it wouldn't be that many.