Here is an attempt to perhaps hone in a bit further on some
of the points that have been made in this quite interesting discussion:


Mary Enig and Sally Fallon recently posted:

>If the consumption of saturated fat within the context of the "average
American >diet" is "deadly", why was heart desease so rare among Americans at
the turn of >the century, who consumed large amonts of saturated fat from
dairy products, >lard, tallows and coconut oil?

On Sat, 31 Jan 1998 Edward Campbell posted:

>I feel this is a good question.  During a recent lecture, Robert Atkins, MD
>also cited this evidence.  He mentioned that all the great anatomists of the
>19th Century rarely reported on seeing any atheroscerlosis in the many
>autopsies performed.  Atkins says that it was not until around 1912 that
>atheroscerlotic plaques began to be observed upon autopsy.  This was approx.
>20-30 years after "altered foodstuffs" (flour, cereals, refined sugars, trans
>fats, etc.) began to be common components of the American diet (this
>coorelates to Cleave's "Law of 20's").

It does seem that the jury is still out wrt to the relationship
between dietary sat. fat and CHD. However, it is important to recognize
that when we are dealing with a condition that is influenced by
many factors (such as CHD), single-variable correlations
within a given population (whether US in late 19th C or France today)
are weak evidence (at best) of a causative relationship (or lack thereof).
There are numerous factors that could explain the relative low rate
of CHD in a population despite its having a relatively high
per capita consumption of sat. fat. I think it would be difficult
to do a good multi-variate cross-country analysis to determine
the role of various factors due to lack of data for some of the variables.

One cautionary note wrt relying on the low rate of CHD
in the US up to early 20th C (actually, I haven't seen anyone
provide statistics on this) was made a few months ago:
that CHD is mainly a condition of the elderly, and since
the life expectancy was lower back in the good old days, the
rate of CHD across the whole adult population would have been
lower than today even if the rate among the elderly was the same
as today. Of course, anecdotal evidence regarding low rate of
etheroscerlosis back then has been presented, and in fact I am
very willing to believe that the CHD rate AMONG THE ELDERLY was lower
than today due to higher prevalence of cardio-protective factors such
as exercise and lower prevalence of factors contributing to CHD
such as smoking and others that have been mentioned on this list.

But logically that does not allow one to give sat. fat a "clean
bill of health" wrt CHD.

For example, Loren Cordain recently posted:

<Under isocalorically controlled conditions in which dietary saturated fat is
<increased at the expense of any other lipid or macronutrient, there will
<be a characteristic increase in LDL cholesterol as shown time and again
<with meta analyses (9) under metabolic ward conditions (10) and
<corroborated by in vitro and in vivo data showing that LDL receptors are
<down regulated by dietary saturated fat (11).

On the other hand, Mary and Sally raised concerns regarding the relevance
of short-term feeding studies under metabolic ward conditions --
do others share their concern?

Mary and Sally also question the linkage between LDL cholesterol level
and incidence of CHD from the Framingham study -- can anyone comment
on this point?

Mary and Sally also raised strong doubts regarding the relationship
between serum cholesterol and risk of death from CHD (perhaps it
would be better if the Grundy study had looked at incidence of CHD
rather than CHD death?) -- does Loren or anyone else have a rebuttal
to their points here?

Ed continued:

>Also, the 10/21/97 issue of Circulation contained an article called: "Fasting
>Triglycerides (TG) and HDL and Risk for Myocardial Infarction".  This Harvard
>study concluded that the ratio of TG:HDL was the most significant risk factor
>in developing CHD.  The TG:HDL ratio was a better predictor than total
>cholesterol (TC), better than TC:HDL ratio, and better than LDL:HDL ratio.

>Reducing carbohydrates, particularly refined ones and other "altered
>foodstuffs", is the best way to reduce TG levels.  Maybe this is one
>explaination for why 19th Century Americans and primitive cultures that
>consumed some dairy products and  whole grains were remarkably clear of
>atherscelosis and CHD.

Could be, but note that this study only considered the standard blood
lipid risk factors for CHD, not the whole range of risk factors.

Can anyone provide a reference for the higher effect on reduced TG of
reducing REFINED carbs?


Steve Meyers
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