LDL Studies and the Association Between LDL-C and Heart Disease, pt. 1
Previous - Part 1 - The Development of the Lipid-Heart and Diet-Heart Hypotheses
With a background understanding of how and why the lipid-heart and diet-heart hypotheses began to develop, we’ll now look at the research of the time, followed by more recent examples, that both do and do not support the general thesis of the LDL-disease paradigm. As mentioned in the previous installment, one significant study to be published during the rise of Keys, the AHA, and the general cholesterol paradigm was the Framingham study. An ongoing effort that persists to this day, the initial results were reported in 1957 and detailed a general relationship between cholesterol levels and future cardiac events. We’ll start with Framingham before examining several other lines of research concerned with the relationships between saturated fat, cholesterol levels, and heart disease.
Framingham
The Framingham Heart Study is an ongoing cardiovascular disease
project that has been tracking, and continues to track, heart disease for the
last several decades. The first published results, a 4-year follow up of
middle-age Americans, were made available in 1957. Among the published results was
a comparison of total cholesterol levels and atherosclerotic heart disease in men
over the age of 45. A couple relevant notes – Frist, science in the 1950s tended
to use “people” as a synonym for “middle-age white men who smoked a lot.” That’s
not meant to discredit the results, just a note of interest. Second, this study
predated the technique and practice to specifically measure LDL cholesterol,
and instead used the slightly less meaningful total cholesterol. We’ll define
and describe all the relevant terms in a coming section, but for now total cholesterol
can be thought of as LDL-C plus HDL-C plus a small contribution from triglycerides.
What these results showed was simply that the men with total
cholesterol over 260 mg/dl suffered more frequent heart disease during the 4-year
follow up than those with lower cholesterol (for reference, standard guidelines
today typically recommend a total cholesterol below 200mg/dl). Similar patterns
were noted for elevated blood pressure and obesity. While not a specific measure
of LDL cholesterol and not as “scientific” as modern research (this was simply
a measuring and counting exercise), the pattern was nonetheless unmistakable –
those men with elevated total cholesterol were more likely to suffer future heart
disease. At a time when the lipid-heart hypothesis was still gaining credence,
these results were instrumental in cementing its place in medical and public consciousness.1,2
Minnesota Coronary Experiment
While the Framingham study was only observational, the
Minnesota Coronary Experiment was a well-designed randomized controlled trial,
or RCT. This means that subjects were “controlled” for a long period of time in
their dietary habits, with results being tracked over time. In this case, the
study was conducted on some 10,000 Minnesota mental health patients, whose diet
and life were easily controlled, measured, and tracked. Half of the subjects ate
food cooked and served with highly saturated fats like butter, while the other
half consumed the same food cooked and served with generally unsaturated fats
like corn oil and margarine.
What also made the MCE experiment notable was that it the
brainchild of Ancel Keys, who designed the study in an effort to validate his
beliefs that saturated fat consumption drove cholesterol levels and heart
disease. In 1973, after five years of intervention and tracking, data was
published demonstrating that the intervention (unsaturated fat) group did indeed
have lower LDL-cholesterol levels (LDL-C measures were now common, unlike
during the initial Framingham results). While LDL-C levels had fallen only 4
mg/dl in the saturated fat group, they had fallen 32 mg/dl on average in the
intervention group. Perhaps Keys was right! This did in fact seem to validate,
to at least some degree, the notion that saturated fat consumption influenced cholesterol
levels.
You may be already asking the next relevant question – what about
disease and death? After all, lower cholesterol is supposed to portend
protection from heart disease. Well, that data was simply not published at the
time. In fact, it remained unpublished for decades. Only in the last decade,
with the death of Keys and his primary co-researcher, were these results made
public by his collaborator’s son, who “rescued” the raw data from his father’s
personal computer.
The findings may explain why data on death and disease was
never published by Keys. That extra 30 mg/dl drop in LDL-C had not in fact
saved lives, but was actually associated with a 22% increase in
all-cause mortality. Had these results seen the light of day in the early 70s,
they may have helped influence a different nutritional landscape in the years
that followed. Instead, the data only on LDL lowering, on top of the Framingham
results and multifaced efforts to demonize saturated fat, helped end any and
all reasonable debate on the nature of heart disease. The fraudulent efforts of
Keys, beginning years earlier with a fabricated relationship between fat
consumption and disease, continued, as did the now-entrenched notion that
saturated fat must be avoided to prevent heart disease.3,4
Other Early Studies
The MCE was not the only large trial of the time designed to
prove the diet-heart and lipid-heart hypotheses and, believe it or not, was not
the only one to hide its undesirable results.
The Sydney Diet-Heart Study was another large RCT designed
to explore the effects of replacing saturated fats with unsaturated vegetable
oils. The results of the SDHS were also slated to be published in 1973.
Instead, all that was published was the following:
“It is concluded that because of multiple changes in lifestyle men who
have had myocardial infarction are not a good choice for testing the lipid
hypothesis” 5
After
seven years (and who knows how much effort and money) of designing and tracking
dietary intervention in a population chosen by the researches, all they decided
to publish was an excuse that their chosen population was inappropriate for studying
the topic at hand.
Again, the
full results eventually became public and, again, they likely betray the reason
the researchers chose to hide them in the first place. The SDHS, like the MCE,
was not designed to seek objective truth, but to validate a subjective truth that
had already been pre-ordained. So when the data showed that the interventional
vegetable oil group was 70% more likely to suffer cardiovascular disease and
62% more likely to die, the researches chose to blame their methodology instead.6
This is
not to say that every study found an increased rate of death and disease in
subjects replacing saturated fat. The Oslo Diet Heart Study was perhaps the
most prominent study that did not confirm the (hidden) results of the MCE and
the SDHS. Instead, 206 heart attack patients consuming a self-selected diet
were compared to 206 similar patients consuming a controlled diet rich in
unsaturated vegetable oil. The results? In 11 years, the self-selected diet
group saw 102 cardiovascular disease deaths and 5 from other disease, while the
vegetable oil group saw 88 cardiovascular disease deaths and 12 from other disease,
for an approximately 14 percent decrease in cardiovascular mortality and a 7 percent
decrease in all disease-related mortality.7
With Framingham
and Oslo published and promoted and the MCE and SDHS covered up, the inescapable
scientific conclusion of the time confirmed what Keys, the AHA, the government,
and many doctors of the time already believed – saturated fat must be minimized
in order to lower cholesterol levels and prevent death and disease.
** This part
is purely my opinion: The Oslo study is absolutely horrible. Why? Because there
is no real control group. The MCE and SDHS, for example, controlled the diet of
both groups. This means that total calorie consumption, total sugar and
carbohydrate consumption, nutrient density, etc. were all roughly equal between
the two groups, and the difference in fat could be better assessed as the
reason for any differences. Oslo didn’t do that. They simply let the control
group eat whatever they wanted and made no effort to track it, while tracking every
aspect of the intervention diet. So while the interventional high-vegetable oil
group suffered slightly less disease, there isn’t really anything relevant to
compare it to. This is a common problem even in modern science, where a
population will go from a self-selected diet to one that’s fully controlled.
Low-fat, low-carb, vegan, keto, whatever…but the researchers don’t control for
calories. So any difference they find after the intervention could, in theory,
be attributable to a decrease in calories rather than the dietary pattern the
researchers are trying to assess. Because those in the Oslo study went from a
self-selected “heart attack diet” to one entirely controlled by the researchers,
it is entirely possible that the reduction in disease mortality was due to the intended
intervention itself, but… it could also be due a reduction in calories or sugar
or something else, and we have no possible way to know that. The increased
mortality of the vegetable oil groups in the better-designed MCE and SDHS lend
credence to the theory that vegetable oil is not the reason for the decreased
mortality in the Oslo study. In fact, it may be the case that the vegetable oil
is still causing excess disease, but that this effect is more than counterbalanced
by the reduction in disease caused by a decrease in calories, sugar, or any
change the researchers aren’t measuring or reporting.
Part 3 -
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