Total Cholesterol and Heart Attacks

[Dean Pomerleau]

[Another one for the "non-CR diet and health" forum. If such a forum ever gets created, I promise I'll use my moderator super-powers to move all these threads to the new forum!]

 

Dr. Greger's latest video titled Everything in Moderation? Even Heart Disease? has this interesting graph from [1] of cardiovascular disease and heart attacks as a function of total serum cholesterol level (click to enlarge):

 

 

It shows that 35 percent of heart attacks occur in people with total serum cholesterol between 150 and 200 mg/dL. I had no idea it was that high. And virtually no heart attacks occur in people with cholesterol below 150 mg/dL, which is why many people (including me) have said it makes you virtually "heart attack proof".

 

But then I started thinking, wait a minute. Couldn't this simply be a reflection of population statistics, and not reflect a causal relationship between cholesterol level and heart attacks?

 

To understand this possibility, consider a similar plot of height vs. # of heart attacks. Assuming heart attacks are totally independent of height, you'd still see a similar bell curve of the number of heart attacks plotted against height, for the simple reason that height is distributed along a bell curve. So 50% of heart attacks would occur in men below the median height of 5'10" in the US, and furthermore only a tiny fraction of heart attacks (~3%) would occur in men shorter than 5'2", which is two standard deviations below the median. Does that mean that having a very short stature makes you heart attack proof? Of course not, it just means that there aren't many men shorter than 5'2" to contribute to the heart attack statistics.

 

As an admirer of both Dr. Greger's work, I am sometimes disappointed when he uses potentially misleading statistics like this one to advance his perspective on diet and health (i.e. the value of following a plant-based diet - which I very much agree with).

 

So what is the more accurate picture of the relationship between cholesterol and heart attack risk?

 

Here is a graph, from [2], which BTW has a very good overview of various blood markers, including cholesterol sub-components and their association with CHD:

 

 

As you can see from the graph on the right, CHD mortality rate (as opposed to total # of heart attacks) appears to be pretty asymptotic below 200 mg/dL. It's only when you get up to a total cholesterol of about 225 mg/dL that you see CHD mortality rate rising significantly, above which it goes through the roof. This is what's called evidence-based medicine, and it is why the American Heart Association and European equivalent (the European Societies for Cardiology, Hypertension and Diabetes) recommend keeping total cholesterol below 190-200, rather than necessarily trying to push it below 150 using diet or statins. With the latter, you might end up like this guy  :

 

 

So despite what Dr. Greger suggests, keeping one's total cholesterol below 150 mg/dL, as opposed to somewhere in the range of 150-200 mg/dL, doesn't appear to provide a dramatic benefit in terms of heart attack risk.

 

To be fair, Dr. Greger has another video on the optimal cholesterol level for heart health that does seem to get the science better. It ignores total cholesterol level, and instead looks at all the randomized control trials of cholesterol lowering drugs, which suggest that an LDL level below 70 mg/dL (about 1/2 the average LDL level in US adults, 130 mg/dL) does make one virtually "heart attack proof". But then again, the relevance of results from people who are taking statins, not to mention the relevance for us of statin-induced LDL reduction or other positive effects of statins, make it far from certain that these results apply to people keeping LDL cholesterol low through diet and lifestyle choices.

 

--Dean

 

---------------

[1] Atherosclerosis. 1996 Jul;124 Suppl:S1-9.

Lipids, risk factors and ischaemic heart disease.

Castelli WP(1).

Author information:
(1)Framingham Cardiovascular Institute, MA 01701-9167, USA.

Over 200 risk factors for cardiovascular disease (CVD) have now been identified.
Among these, the three most important are (1) abnormal lipids, including the fact
that there are more than 15 types of cholesterol-containing lipoproteins and four
different types of triglyceride-rich particles, some of which are very
atherogenic, (2) high blood pressure, and (3) cigarette smoking. In addition,
many other factors including diabetes, haemostatic factors such as fibrinogen,
factor VII, plasminogen activator inhibitors, and new factors such as
apolipoprotein E4 and homocysteine, are known to increase the risk of developing
clinical CVD. A low risk for CVD requires that these various factors are present
in the circulation in the correct proportions. Two simple tests for determining
plasma lipid levels can be used to identify those individuals with an atherogenic
lipid profile and who are, therefore, at increased risk for CVD. Firstly, the
ratio of total cholesterol to high density cholesterol (HDL cholesterol) should
be determined, followed by measurement of plasma triglyceride concentrations.
This will allow differentiation of whether the low density lipoproteins (LDL),
HDL cholesterol or triglyceride-rich particles such as the small dense beta-very
low density lipoproteins (VLDL) are the major cause for concern. Once identified,
those individuals with a high lipid risk profile should be treated before, rather
than after, experiencing coronary heart disease (CHD).

PMID: 8831910

 

-------------------

[2]  The Journal of the International Federation of Clinical Chemistry and Laboratory Medicine Vol 13:2 (2003)

 

THE ROLE OF LIPIDS IN THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY HEART DISEASE: GUIDELINES FOR DIAGNOSIS AND TREATMENT

 

Victor Blaton

 

Department of Clinical Chemistry, Hospital AZ Sint-Jan AV, Brugge,

Belgium

 

pdf: http://www.ifcc.org/ifccfiles/docs/140206200306.pdf

[nicholson]

Hi Dean:

 

More interesting stuff, thank you.  Could you please let us know the units for the Y-axis of the right-hand graph of the Scott Grundy paper?

 

At total cholesterol of 150 the rate seems to be "2". Does that mean that 2% of people at that level of TC are diagnosed with CHD each year?  Or is it 2 per 10,000?  Or what?  And whatever it is, would not that rate vary with age?  Not many five year-olds with TC of 150 have heart attacks but no doubt a few do at age 70?   So what I am saying is I don't understand the data in that graph without more information (please).

 

Similarly with the graph on the left.  When it says "risk ratio" it seems to be saying the risk of death at TC of 300 is four times that at TC of 150.  Is it saying that?  If so it isn't telling us anything about the actual rate at 150, or at 300,  And again, does this apply to any specific age group?   

 

Or am I simply confused?  Probably.

 

Rodney.

[Dean Pomerleau]

Could you please let us know the units for the Y-axis of the right-hand graph of the Scott Grundy paper?

 

Good question Rodney. The graphic as it stands leaves a lot to be desired. Here is a reproduction of the diagram (including caption) from the original Grundy 1998 paper [1]:

 

 

As you can see, the '2' represents two deaths per thousand people among the 350,000 men in the MRFIT trial.

 

The weird thing is that this version of the graphic (which I screen captured from the original text) looks like the risk does in fact start rising pretty quickly above the 150 mg/dL TC level...

 

Similarly with the graph on the left.  When it says "risk ratio" it seems to be saying the risk of death at TC of 300 is four times that at TC of 150.  Is it saying that?  If so it isn't telling us anything about the actual rate at 150, or at 300,

 

Yes - you are interpreting that one correctly. The risk of death for a TC of 300 appears to be 4x that of people with a TC of 150. It isn't giving an absolute risk, but relative risk, as is standard in many such studies. 

 

And again, does this apply to any specific age group?  

 

It applies to the subjects in the three prospective studies that were used to generate the graph, the Framingham Heart study population, the Pooling Project population and the Israeli Prospective Study. See full text of [1] for more details and specific references.

 

--Dean

 

--------------

[1] Circulation. 1998 Apr 21;97(15):1436-9.

Statin trials and goals of cholesterol-lowering therapy.

 

Grundy SM.

 

Full text: http://circ.ahajournals.org/content/97/15/1436.full.pdf

 

Comment in

Circulation. 1999 May 11;99(18):2477.

 

Comment on

Circulation. 1998 Apr 21;97(15):1453-60.

Circulation. 1998 Apr 21;97(15):1440-5.

Circulation. 1998 Apr 21;97(15):1446-52.

 

PMID: 9576422 

[nicholson]

Thanks Dean.  And even the screen shot from the full text seems not to specify if it is 2 per 1000 per year, or 2 per 1000 during their lifetimes.   In the left chart the incidence risk at 300 TC is four times that at 150 TC; in the right chart the difference in risk of mortality appears to be about eight times.

 

Presumably most of the participants were within an age group where CHD deaths occur fairly frequently.  If the sample is mostly people aged from 50 to 80, then two out of one thousand per year would imply sixty per thousand over those 30 years.  That would be 6%.  Which seems a reasonable number I suppose for a TC of 150. (Similar to China and Japan)   And eight times that at a TC of 300?  (Approximately the rate in the US back around the 1950s, IIRC, before the big drop in fat intake).  But it would have been helpful if that had been specified in the labeling of the charts.

 

And regarding:  "The weird thing is that this version of the graphic (which I screen captured from the original text) looks like the risk does in fact start rising pretty quickly above the 150 mg/dL TC level...".  It looks to me as if this may be saying that there are people with TC between 150 and 200 who never get far enough along with CHD to become symptomatic and therefore are not classified as 'incident' - not yet - but who suffer a plaque rupture which causes them to be recorded in the data in the mortality chart at right?  This suggests getting really close to a TC of 150 is desirable. 

 

When people put up a chart of patients supposedly: "without heart disease" they do not mean their arteries aren't clogged.  All it really means is that they aren't quite clogged enough yet to have caused the patient to go to the doctor to complain about overt symptoms.  So the ones recorded in the mortality chart between 150 and 200 are those with covert disease.  But I think we know from carotid IMT data that over 90% of people aged 60 have at least some deposition on their arteries. I.E. carotid IMT greater than 0.5. Some US Korean War and Vietnam troops in their teens on autopsy were found to have partially clogged arteries.  It seems that only people on CR have carotid IMTs of 0.5.

 

Rodney.

[Dean Pomerleau]

Rodney,

 

You shouldn't really try to compare the graph on the left with the graph on the right, since they are derived from different populations in different studies.

 

But I agree with you that asymptomatic CVD (i.e. modest plaque buildup in arteries) may be developing in people with total cholesterol between 150 and 200 as they age.

 

Dean

[nicholson]

Hi Dean:

 

I  seem to recall that Bill Clinton didn't have symptoms he considered of interest (breathlessness I believe in his case) until one of his coronary arteries was 95% occluded, and a second 50% occluded.  So I think your "modest plaque buildup" may understate how seriously sick it is possible for an individual to be and still be described as: "free of CHD" in a study control group. 

 

And I believe fatal heart attacks do occur in some people with relatively little plaque, because it is the tendency for plaque to rupture - rather than the amount of it - that matters in such a case.  And it seems some families are more susceptible to plaque rupture than others (Peter Sellers and his son come to mind).  They can experience a fatal cardiovascular event 'out of the blue' (as did Sellers' son) without any previous overt symptoms typical of severely occluded arteries.

 

I mention this because it is likely relevant to the very first graph in your first post in this thread, which compares people with "CHD" and "No CHD".  It would be a lot more instructive, I think, if control groups of this kind contained only people with carotid IMT of less than 0.6.  But where would they find them, except at CRsociety?!

 

Rodney.

[nicholson]

And if we had a forum here specifically reserved for people to brag about how healthy they are, I would certainly hope that a few people with a measured carotid IMT of 0.5 would do so on such a forum.

 

Rodney.

[Dean Pomerleau]

Above I wrote:

 

The weird thing is that this version of the graphic (which I screen captured from the original text) looks like the risk does in fact start rising pretty quickly above the 150 mg/dL TC level...

in reference to the graph on the right of this figure:

: 

 

It was a figure from [1], specifically referenced data from this paper [2] on the MRFIT trial. It followed 356K men aged 35 to 57 years at baseline for a few years, to see how their baseline total cholesterol predicted death from heart disease down the line. Here are the highlights:

 

[T]he age-adjusted risks of CHD death in cholesterol quintiles 2 through 5 (182 to 202, 203 to 220,

221 to 244, and greater than or equal to 245 mg/dL) relative to the lowest

quintile (<182 mg/dL) were 1.29, 1.73, 2.21, and 3.42.

 

These data of high precision

show that the relationship between serum cholesterol and CHD is not a threshold

one, with increased risk confined to the two highest quintiles, but rather is a

continuously graded one that powerfully affects risk for the great majority of

middle-aged American men.

 

So my eyes weren't deceiving me, it appears that there is indeed 30% increased risk of dying from a heart attack with a total cholesterol in the range of 182-202 compared to keeping it below 182 mg/dL . One would presume that the benefit would be even greater if one keeps it below 150 mg/dL.

 

In short, it appears beneficial for reducing heart disease risk to keep total cholesterol well below 200, and this benefit likely extends (rather continuously) down to 150mg/dL. But the original graph Dr. Greger used to argue the point is nonetheless misleading.

 

--Dean

 

--------------

[1] Circulation. 1998 Apr 21;97(15):1436-9.

Statin trials and goals of cholesterol-lowering therapy.

Grundy SM.

 

Full text: http://circ.ahajourn...5/1436.full.pdf

Comment in
Circulation. 1999 May 11;99(18):2477.

Comment on
Circulation. 1998 Apr 21;97(15):1453-60.
Circulation. 1998 Apr 21;97(15):1440-5.
Circulation. 1998 Apr 21;97(15):1446-52.

PMID: 9576422 

 

--------------------

[2] JAMA. 1986 Nov 28;256(20):2823-8.

Is relationship between serum cholesterol and risk of premature death from
coronary heart disease continuous and graded? Findings in 356,222 primary
screenees of the Multiple Risk Factor Intervention Trial (MRFIT).

Stamler J, Wentworth D, Neaton JD.

The 356,222 men aged 35 to 57 years, who were free of a history of
hospitalization for myocardial infarction, screened by the Multiple Risk Factor
Intervention Trial (MRFIT) in its recruitment effort, constitute the largest
cohort with standardized serum cholesterol measurements and long-term mortality
follow-up. For each five-year age group, the relationship between serum
cholesterol and coronary heart disease (CHD) death rate was continuous, graded,
and strong. For the entire group aged 35 to 57 years at entry, the age-adjusted
risks of CHD death in cholesterol quintiles 2 through 5 (182 to 202, 203 to 220,
221 to 244, and greater than or equal to 245 mg/dL [4.71 to 5.22, 5.25 to 5.69,
5.72 to 6.31, and greater than or equal to 6.34 mmol/L]) relative to the lowest
quintile were 1.29, 1.73, 2.21, and 3.42. Of all CHD deaths, 46% were estimated
to be excess deaths attributable to serum cholesterol levels 180 mg/dL or greater
(greater than or equal to 4.65 mmol/L), with almost half the excess deaths in
serum cholesterol quintiles 2 through 4. The pattern of a continuous, graded,
strong relationship between serum cholesterol and six-year age-adjusted CHD death
rate prevailed for nonhypertensive nonsmokers, nonhypertensive smokers,
hypertensive nonsmokers, and hypertensive smokers. These data of high precision
show that the relationship between serum cholesterol and CHD is not a threshold
one, with increased risk confined to the two highest quintiles, but rather is a
continuously graded one that powerfully affects risk for the great majority of
middle-aged American men.

PMID: 3773199

[James Cain]

Dean, I think your logic and height analogy regarding Dr. Greger's graph are on point but somewhat confusing. I think I get what you're trying to say, in which case I think your height analogy is just not coming off as clearly as it could.

 

The graph is showing the cholesterol of those who get CHD and those that don't, and regardless of the actual contribution of cholesterol to CHD this graph is showing that the tail ends don't overlap between having and not having CHD. It is completely logical to say that based on this data nobody with less than 150 mg/dl cholesterol developed CHD, or that only those with 150 mg/dl developed CHD. Dr. Greger (and many others) are statistically correct, but perhaps the statistics aren't showing what we really want to know. As you know, statistics are notoriously misused to make 'factual' statements that aren't actually applicable or contextually relevant.

 

If plasma cholesterol were to have contributed I'd expect not to see a bell curve but increasing risk with increasing cholesterol, which is what I think you're saying by giving the other two graphs as examples.

[nicholson]

I should point out that when I had made my previous comments on this thread I had assumed that the side-by-side charts, shown by Dean three times in previous posts, were the same charts.  Superficially they look the same, but the one on the right in Dean's 15 October 2015 - 11:21 AM  is considerably different from the one on the right in his original post on this thread.

 

To see this most clearly note that in the first post the CHD mortality rate indicated for 250 total cholesterol is - by eye - approximately 5.  But in his post dated '15 October 2015 - 11:21 AM' it is more like 8.5 or 9. 

 

Obviously any conclusions drawn will be different depending on which chart you wish to quote.

 

The three versions of the charts on the left do appear to be very similar/identical.

 

Rodney.

[Dean Pomerleau]

The graph is showing the cholesterol of those who get CHD and those that don't, and regardless of the actual contribution of cholesterol to CHD this graph is showing that the tail ends don't overlap between having and not having CHD. It is completely logical to say that based on this data nobody with less than 150 mg/dl cholesterol developed CHD, or that only those with 150 mg/dl developed CHD. Dr. Greger (and many others) are statistically correct, but perhaps the statistics aren't showing what we really want to know. As you know, statistics are notoriously misused to make 'factual' statements that aren't actually applicable or contextually relevant.

James,

 

I agree with you that the fact the "no-CHD" bell curve of cholesterol level in Dr. Greger graphic in my original post, reproduced here:

 

 

is shifted left relative to the "CHD" bell curve indicates that people without CHD generally have lower cholesterol that people with CHD. And I agree that this is suggestive evidence that keeping one's cholesterol low will help one avoid CHD. But if you watch Dr. Greger's video again, you see that the No CHD curve is ignored in the video, and he focuses on the region of the CHD curve below 200 mg/dL, saying:

 

Because we now know that 35% of heart attacks occur in people with total cholesterol levels between 150 and 200, setting a target level of only 200 [rather than a lower value of 150 - DP] guarantees that millions of US citizens will perish of coronary disease.

 

This statement alone is pretty much meaningless - for any normally distributed variable across the population, you'll see a bell curve relationship between that variable and # of heart attacks, even though there may be no causal relationship between that variable and heart attacks. I used height as the example above. But let's instead use something that's modifiable to illustrate my point. 

 

Consider the variable "how many showers have you taken in the last month?". Assuming showers/mth is a gaussian (i.e. bell-shaped) distribution with a peak around 30 in the US (i.e. one shower per day), and assuming showers/mth is independent of CHD, then for some value of showers/mth in the neighborhood of about 10 (I'm guessing) it would be true that 35% of all heart attacks would occur in people who take between 10 and 30 showers/mth. And it would further be true that a very small number of heart attacks would occur in people who take less than 10 showers per month, for the simple reason that very few people in the US take showers that infrequently. Would we therefore be justified in saying:

 

Because we now know that 35% of heart attacks occur in people who take between 10 and 30 showers/mth, setting a target level [i.e. upper limit] of only 30 (rather than 10) showers/mth guarantees that millions of US citizens will perish of coronary disease.

 

and then going on to advocate people take fewer showers to avoid heart attacks, and furthermore that if they take fewer than 10 showers/mth it will make them virtually heart attack proof?  Of course not. Taking showers doesn't cause heart attacks. Heart attacks are rare in people who take fewer than 10 showers/mth because people who take fewer than 10 showers/mth are rare.

 

By the same logic, there could be very few heart attacks in people with TC below 150 mg/dL for the simple reason that people with TC below 150 mg/dL are rare. Now of course we know from other evidence (including the non-CHD curve in the background of this graph, and better the graph on the right I posted above - more on that below), that serum cholesterol level is very likely part of the causal chain leading to heart attacks - so lowering cholesterol is likely a good thing.

 

But the way Dr. Greger argues for lowering the cholesterol target from 200 to 150, by simply pointing to the tail of the CHD curve between 150 and 200 and saying it contains 35% of heart attack cases, is quite misleading. Now I'm sure Dr. Greger was (and is) sincere in his motives, and likely accurate in his assessment (i.e. reducing cholesterol would indeed prevent many heart attacks). But the way he's arguing for it in this video is a classic example of the way people sometimes use statistics to mislead their audience, and so this kind of fallacious argument should be avoided, even if well-intentioned.

 

I should point out that when I had made my previous comments on this thread I had assumed that the side-by-side charts, shown by Dean three times in previous posts, were the same charts.  Superficially they look the same, but the one on the right in Dean's 15 October 2015 - 11:21 AM  is considerably different from the one on the right in his original post on this thread.

 

To see this most clearly note that in the first post the CHD mortality rate indicated for 250 total cholesterol is - by eye - approximately 5.  But in his post dated '15 October 2015 - 11:21 AM' it is more like 8.5 or 9. 

 

Obviously any conclusions drawn will be different depending on which chart you wish to quote.

Rodney,

 

I too am baffled why the first version of the MRFIT "CHD mortality vs. TC" graph that I posted is so different from the (nearly identical) one I posted in my later responses. All I can say is the later version(s) should be the accurate ones, since they were screen captured directly from the original source. The later (accurate) one (reproduced below), shows there is quite a steep rise in mortality risk as cholesterol levels rise from 150 to 200, implying it would indeed be beneficial to advocate for a lower threshold for TC level across the population.

 

 

--Dean

[nicholson]

Hi Dean:

 

Regarding your:  "Because we now know that 35% of heart attacks occur in people who take between 10 and 30 showers/mth, setting a target level [i.e. upper limit] of only 30 (rather than 10) showers/mth guarantees that millions of US citizens will perish of coronary disease."

 

Probably I am confused.  Actually, I am definitely confused.  What I am most confused about is what the data on the Y-axis of the CHD/NO CHD chart represent.  And I mean PRECISELY what do they represent?  There are no Y-axis labels on the chart, which is pretty extraordinary, and makes me wonder if the author was trying to hide something.   Does it really represent just the number of people?  If so then I don't see the point of it.  And second, how are 'CHD' and 'NO CHD' defined (I am still thinking of Bill Clinton not noticing 90% occlusion even when jogging.  Finally, at 95%, he noticed shortness of breath).  If NO CHD simply means no diagnosis of CHD *yet* then I am having difficulty understanding why the chart is worth discussing.

  

And if it is just the number of people already diagnosed, and not yet diagnosed with CHD surely those data will vary dramatically by age so what age group is the chart talking about?  As you realize, not many people have been diagnosed with CVD at age 50, but plenty have by age 80.

 

Clarification of the Y-axis label would be very helpful in improving my understanding of this, and may cause me to retract some of my earlier comments, too!

 

Rodney.

[Dean Pomerleau]

Rodney,

 

The Y-axis of the bell curves graph in question is # of heart attacks. So what each bell curve represents is the number of people who have a heart attack with various levels of serum total cholesterol.

 

> Does it really represent just the number of people? If so then I

> don't see the point of it.

 

No, it represents # of people who had heart attacks. I suspect the original point the author was trying to make had to do with the shifting of the "No CHD" curve to the left of the "CHD" curve, suggestion lower risk of heart attacks with lower cholesterol.

 

But even with the fact that it represents # of people having heart attacks with a given cholesterol level, it was still misleading for Dr. Greger to use it in the way he did, as I hope my "showers/mth" analogy shows.

 

--Dean

[nicholson]

Thank you Dean:

 

That is stunning.  Because, if true, the chart supposedly shows that, at any level of TC at or below 235, MORE PEOPLE "WITHOUT HEART DISEASE" HAVE HEART ATTACKS THAN THOSE "WITH HEART DISEASE"!

 

If people don't have heart problems how can they possibly have a heart attack?

 

Presumably the explanation is what I have noted several times previously.  The definition of "no heart disease" is simply ludicrous.  Ninety percent occlusion of a coronary artery (Clinton several months before he experienced shortness of breath) is supposed to be "NO CHD" because the patient hasn't *yet* gone to the doctor to complain that he has severe pain in his left arm, or that he can't breathe!

 

I suspect the real explanation of those curves is this:  Heart attacks are caused by rupture of plaque which often will occur with only moderate - asymptomatic - amounts of plaque build up.  If the patient has managed to avoid heart attack through the 'moderate plaque/rupture risk' stage then when his arteries are 60% 70% 80% occluded he is past much of the risk, and when he gets to 95% occlusion he eventually is diagnosed with blockage.  

 

But the chief lesson I get out of this (again) is the sheer meaninglessness of what is frequently defined as "free of CVD" in control groups.  As currently defined most of the time, anyone not complaining of severe pain in their left arm seems to be defined as "free of CHD" even if tomorrow he is going to drop dead as a result of massively clogged arteries.  In other words the definition of "free of CHD" means very close to nothing.  And any conclusions drawn from such 'analysis' are probably not worth wasting time on.  imo.

 

As is very well known here, one far superior - and inexpensive, and non-invasive - criterion of 'NO CHD' would be carotid IMT or 0.5 or less.  There may be a better one.  But, surely, effectively 'not yet complained of severe chest pain' is just plain stupid.  Calling it 'not yet *diagnosed* with CHD, but arteries probably clogged' would be a more accurate descriptor than 'NO CHD'.  But the change would hardly make the data any more meaningful.

 

And still there is the question of the huge changes the data would show in a chart of this type with patient age.

 

I welcome correction if someone thinks I am missing something.

 

Rodney.

[nicholson]

And further, that the occurrence of some heart attacks at TC levels above 150 indicates that arterial deposits accumulate at any level above 150: only very slowly at 160, but much more rapidly at 300.   So perhaps if your TC is 160 then you will find you have symptoms appear at age 100 (unless you are unlucky to get a plaque rupture sooner).  At TC of 300 the accumulation is fast enough to produce overt symptoms by age 60 (unless a plaque rupture occurs sooner).

 

And genetic susceptibility will add to this by being, almost certainly, a factor in plaque rupture and perhaps the rate of accumulation of deposits also?

 

IMO, what we learn from this is to get TC down to 150.  First by CR.  And if that doesn't get it low enough then by progressively reducing fat intake, first by eliminating obvious sources of saturated fat and, if TC remains above 150, other fat types also.  As previously discussed, long ago, I would include monounsaturated fats in the same category as saturated.  But that is not conclusively proven.

 

Of course I realize none of the above is 'original' in any way.

 

Rodney.

[Dean Pomerleau]

Rodney,

 

IMO, what we learn from this is to get TC down to 150.  First by CR.  And if that doesn't get it low enough then by progressively reducing fat intake, first by eliminating obvious sources of saturated fat and, if TC remains above 150, other fat types also.  As previously discussed, long ago, I would include monounsaturated fats in the same category as saturated.  But that is not conclusively proven.

 

All good advice. But I would be careful not to read too much into the TC -> heart attack association. For example you say:

 

 

 

 ... the occurrence of some heart attacks at TC levels above 150 indicates that arterial deposits accumulate at any level above 150: only very slowly at 160,

 

Remember, people who have a TC of 150 or 160 today and have a heart attack may have built up a lot of plaque over the years during which they may have had a much higher TC, and only recently have cleaned up their diet and/or started taking statins when they (or their doctor) got concerned enough about their heart attack risk to motivate them to take action. Plus remember that serum cholesterol naturally drops as people get older, but (obviously) their risk of a heart attack doesn't go down correspondingly.

 

Cardiovascular disease develops over many years, and looking at their cholesterol at one point snapshot in time provides only very limited insight, and so shouldn't be overgeneralized or overinterpreted.

 

--Dean