Re: Cholesterol's Function?

From: Mirek Fidler (cxl_at_volny.cz)
Date: 03/28/05 

Date: Mon, 28 Mar 2005 22:02:05 +0200

>>If he is 50 years old, non-smoker, no DM, BP < 120, his profile
>>indicates same risk (2%) as e.g. one with HDL 50, LDL 120, TG 120 (which
>>would be considered absolutely OK without further risk factors).
>
>
> Not in all cases. Keep in mind that they are "independant" risk factors
> which mean that they are independant of each and every other lipid analytes.
> HDL is independant of LDL and vice versa.

No. That is what I want to say. It is not independent.

> Each is assigned as a risk factor. If you want to claim all of them in a
> whole places the individual in question at lower risk then you are cheating
> the concept of independance.

There is none.

Even if LDL causes CAD, exact mechanism is unknown. In that situation,
all you have is raw statistic data. Those data clearly indicate that
what really matters is balance, not absolute values. You have profiles
indicating high risks and profiles indicating low risks.

>>This specific profile is low-risk (that is, less than 10% for 10 years
>>prediction) both for male and female for all ages.
>>
>>Of course, little we know about other risk factors (but based on low TG
>> DM or MetS diagnosis is unlikely). Anyway given this profile alone,
>>risk is definitely low (<10% is considered low AFAIK).
>>
>>Mirek
>
>
> Too early to make that assessment without more input. Those are numbers

I am not makeing assessment, (BTW, I am not qualified to do that, I take
this as informal chat about lipid issues over usenet), I was just
commenting lipid profile :)

> acceptable to the conventional testing done. I understand that but there is
> a reason why this person started out with a high glycohemoglobin of 6.1
> which is borderline abnormal. I believe that is A1C and not 1AC.

You are right here. I did not liked his A1C too. Seems he started some
kind of life-style modification in 2003....

> Keep in mind that some individuals can have a normal lipid profile by
> conventional lipid profiles that don't fractionate the LDL and be dead the
> next day. A genetically inherited LDL very atherogenic light form.

Well, now you are going deeper and that is good. Anyway, that is exactly
  what I wanted to show you. In fact, there seems to be well established
inverse correlation between LDL particle size and TG.

That is in good accordance with large statical volumes that not
surprisingly show high risks for profiles estimated to indicate small
LDL particles.

> There are other risk factors not mentioned such as CRP and homocysteine and
> these are non lipid factors or factors not measured in the lipid profiles.

Sure there are. All should be accounted for. And do not forget about
family history, BMI and age, later being the most predictive risk factor
of all :)

> No mention here so again it is too early to say the individual as a whole is
> at risk or not.

That is not what I said. I was speaking about his lipid profile, nothing
more, nothing less.

> Statistics based on the relative risks of the conventional risk factors
> within this profile it is relatively low.
> He might be one of the 10% that will die which be might acceptable in terms

2% for CAD event if he has no other risk factors. Not 10%.

> of general health policy and resources but if the other 10% can be detected
> and treated properly then you can cut the odds down even more.

The question is how much improvement can be achieved here when "treated
properly". Statins show reduction od CAD events by 30% AFAIK in high
rist patients (correct me if I am wrong). So you could reduce risk to
about 1.4%. In other words, his chance of being CAD free would increase
from 98% to 98.6%. (All that in case there are no other risk factors, so
those 2% are final).

Mirek

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