This paper came my way through Luca and THINCS. Free fatty acids are just appalling. Read this paragraph from the discussion section and clutch at your chest:
"... studies have shown that a fat-enriched meal, in contrast to a high carbohydrate meal (HCM), is associated with endothelial activation [30] and may initiate injury to the blood vessel wall [31]. Increased circulating FFA and their derivatives have also been shown to be particularly deleterious on myocardial function during ischemia and reperfusion (for review see Ref. [32]). Indeed, in the ischemic myocardium, long-chain fatty acids accumulate quickly. The rate of fatty-acid uptake and oxidation by the heart is controlled by their availability [33]. Exogenous fatty acids, the main metabolic fuel of the myocardium under aerobic conditions, are detrimental during oxygen deprivation since their presence further augments the accumulation of long-chain acyl esters in the myocytes. The accumulation of lipids and their degradation products may contribute to the progression of injury. Furthermore, during reperfusion, fatty-acid oxidation can quickly recover and become the dominant source of ATP production. A high rate of fatty-acid oxidation contributes to a marked decrease in cardiac efficiency during the ischemia–reperfusion period [34]. We have previously shown that pharmacologically-induced increase in plasma FFA can significantly reduce the ischemic threshold in patients with stable coronary artery disease [35]. Recent studies have shown that FFA may also attenuate endothelium-dependent arterial vasodilatation [17,36] and increase sympathetic drive and alpha 1-adrenergic receptor reactivity and tone [37]. In addition, a HFM leads to an increase in calf vascular resistance [38]. All these data support a role for FFA and triglycerides both in vascular and muscular metabolic regulations."
I have to say that I've been through most of the references cited and many of them are quite hysterical. But that's another matter, maybe another post.
So the people who wrote the above paragraph had the bravery to feed a high fat meal, a high carbohydrate meal or nothing (on different days) to some cardiac patients and then treadmilled them to ST segment depression, ie until myocardial ischaemia set in. Obviously a high fat meal, particularly one based on saturated fat (as the test meal is claimed to have been, you don't get enough detail to tell what they used) should have crippled these people.
It didn't. The high fat meal had absolutely no effect on time to ischaemia.
How do they explain this? Easy, the high fat meal may have been a high fat meal, but it never raised plasma free fatty acids! This is what they say:
"However, this study was targeted to assess the role of a high fat meal and not of high serum FFA concentration; in fact due to the antilypolitic effect of the hyperinsulinemic response to the meal the serum FFA concentration was lower than in the fasting state."
Cunning hey? Just spike the high fat meal with exactly the correct amount of carbohydrate to lower lipolysis derived FFAs by an amount slightly more than the test meal generates and there is no overall change in FFAs (p > 0.05, ns) so no change in time to ischaemia! Beautifully done. But bollocks never the less.
Aside: Weird how you can use insulin to inhibit lipolysis in heart patients, just like treating ketoacidosis. You might almost imagine that insulin has something to do with weight control, I dunno... Back to the bollocks:
The same number of calories consumed as mostly carbohydrate dropped the time to ischaemia from 376 seconds to 297 seconds, p = 0.003, Table 2, line 13. This is despite the fact that carbohydrate meal reduced the Spawn of Satan from 0.89mmol/l to 0.27mmol/l, p = 0.002.
Of course with all that hard evidence about FFAs delaying myocardial recovery you really would expect an accelerated recovery from ST segment depression after the high carbohydrate meal, after all FFAs concentration is only a third of that under fasting conditions. In fact we can see from line 15 that the high carbohydrate meal gave a recovery time 30 seconds slower than after fasting, with all of that Spawn of Satan released from adipocytes due to not eating for a few hours. The high fat meal gave a recovery time which was 30 second faster. The spread in the numbers means that all of these differences are ns. No way can we tell how close p got to that good old 0.05, ns is all we get. But you really do have to wonder about how this fits in with all of those references in the above quote!
These authors do not go so far as to make dietary recommendations for folks with cardiovascular disease eager to spend a few minutes on a treadmill after supper.
Cardiologists back in the 1990s were not so reticent. This paper came out in 1996. It is essentially a poor man's version of the modern epic discussed above, with identical findings. What is the dietary advice if you have angina in Sheffield in 1996? Eat fat or carbohydrate before your jogging?
"It would be difficult to advise patients to take a higher proportion of calories as fat in the diet to minimize these early adverse cardiovascular effects, because of the potential effects of dietary fat on atherosclerosis genesis."
And the solution, just say no!
"...patients with angina should be advised to limit their activities in the early (first 30 min) postprandial period because of the reduction in angina threshold."
So if you are planning some post prandial exercise you can have an extra 79 seconds before myocardial ischaemic sets in by having cream instead of potatoes, but don't. Instead just put your feet up!
Peter
