Wednesday, January 31, 2007

2006 in Metabolic and Coronary Risk Factors

The year 2006 has seen a tremendous amount of basic science work done on atherosclerosis. The role of cholesterol especially LDL-cholesterol is well established, with no controversy. With that, the basic science work has moved on to identifying the inflammatory molecules associated with initiating and propagating the process of atherosclerosis, especially those molecules that cause stable plaque to become vulnerable. V-cam, and i-cam, with interleukin 6, have been well studied and seem to correlate well with inflammation in the plaque and also making the plaque vulnerable.

What is important is that these molecules, initially only measured at research labs, now can be measured commercially. LDL-cholesterol itself is a derived index, but much work is being done to allow for LDL-C to be measured with commercial kits. CRP measurements are now available commercially, and sometimes misused.

The metabolic risk factor that seemed to be reviewed is the role of homocysteine. The epidemiological data correlating homocysteinemia with atherosclerosis is established, though weak. The pathogenic role is poorly understood, and many controlled trials to see if folic acid improves cardiac outcomes, have proven controversial. Some trials were mildly positive but some trials were obviously negative.

Perhaps the greatest let down was the voluntary withdrawal of torcetrapib by Pfizer after initial results showed that torcetrapid seemed to be associated with some small rise in BP. Then the bigger blow came, when it was shown thet the use of torcetrapib may be associated with a higher incidence of adverse cardiac events. Pfizer quickly terminated the study and withdrew torcetrapib.

I must admit that I was one of those who believed that torcetrapib, by increasing HDL-C, will cause plaque regression . Well, I was wrong. I am still certain that torcetrapib will regress plaques, but surely if it also increase cardiac events, that is not acceptable. It would appear that there may be different types of HDL-C, the natural occurring one (relatively devoid of cholesterol, taking part in the reversed cholesterol transport), and the HDL-C raised by torcetrapib, which were mainly large HDL-C molecules full of laden cholesterol.

Much work was also done, in 2006, on the role of nutriceuticals, in preventing CAD. I was impressed with the data on walnuts taken post lipid meals and their ability to lower V-cam and i-cam levels in the serum, thus making walnut effective agents to stabilise plaques, especially after a high lipid meal.

2006 also saw the banning of transFat in fast foods in New York. The Health Authorities in New York believed that transFat used in fast food were resposible for the rising obesity seen in the young and also their role in promoting CAD. The data here is also not so straight forward. But the USA authorities requirement for food constituents to be displayed in the food packaging should be good in allowing the public to know the amount of calories, fats, proteins and salt in the food. That should be good as we try to fight obesity, which seemed to have increase to almost epidermic proportion.

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