The Development of the Lipid-Heart and Diet-Heart Hypotheses
The lipid-heart and diet-heart hypotheses. The average
person may not know them by their name, but certainly everybody knows them in
some capacity or another. Quite simply, their combined assertion is this: consuming
dietary fat and cholesterol causes cholesterol levels in the blood to rise, and
these rising levels of cholesterol are the primary factor in the development of
heart disease. Put even more simply – eat too much fat, risk a heart attack.
This singular basic message has formed the backbone of nutrition
and dietary advice for decades, for as long as most who will read this have
been alive. One would be forgiven if, somewhere along a road lined with high-school
health classes, heart-healthy checkmarks, and ubiquitous advertisements for
low-fat yogurt and statins, that these ideas were settled science existing in a
space far beyond any credible doubt. But what makes the longevity of these twin
concepts so notable is both the absence of strong evidence to support the
assertions, and the incredible simplicity of the model that allows them to
persist unabated nonetheless.
The simplicity is apparent and approachable – eating fat and
cholesterol causes cholesterol to accumulate in the bloodstream, where it…. gets
stuck, basically. The mechanics of WHY cholesterol behaves this way are less
apparent and rarely explained, but it seems the basic idea presented to the
public is simply that cholesterol is a sticky substance that, in large amounts,
inevitably attaches itself to the walls of the arteries and blocks the normal flow
of blood. Obviously, things are not this simple. Likely surprising to many, cholesterol
does not exist “in” the bloodstream at all, but in carrier “boats” called
lipoproteins, and so the basic construct by which it sticks to the blood
vessels needs at least some greater level of detail. In fact, it requires a
much greater level of detail, which will be explored over the course of this
series of posts.
But before exploring the realities of cholesterol and the
failures of the lipid-heart and diet-heart hypotheses, one needs to understand
where these parallel concepts came from and the factors that allowed them to thrive.
Some 70 years ago, as it is today, heart disease was a
common killer in western society. Autopsies of young soldiers killed in action found significant
atherosclerosis, artery-clogging deposits that contained, among other things, a
waxy substance known as cholesterol. In an era that still saw doctors recommending
their preferred brand of cigarette, the heavy rates of smoking among these young
soldiers and the population at large didn’t jump off the page as an obvious
candidate in the search for the heart-stopping culprit.
Around the same time, a University of Minnesota physiologist
named Ancel Keys presented to the World Health Organization his theory that the
consumption of fat (saturated fat from animal products in particular) was the
primary factor in the development of cardiovascular disease. To support this
claim, Keys hand-selected six countries, from a complete dataset of about two dozen,
that allowed him to draw the most pronounced connection between increasing fat
consumption and increasing heart disease. This extremely biased methodological
error, in which Keys dismissed all available data contradicting his beliefs,
led him to be publicly refuted in his original attempt at promoting his idea.1
2However, other factors were also developing that would eventually
assist Keys in his effort to demonize the consumption of saturated fat. In
1911, while attempting to use vegetable oil as a base for soapmaking, the
company Proctor and Gamble inadvertently discovered that they could create a
partially solid product that reasonably resembled butter at room temperature. Vegetable
oils, previously used primarily as industrial lubricants, were suddenly an appealing
option for the creation of a cheap, shelf-stable, butter-like compound that
could be marketed as a cooking product. Thus was born Crisco, an industrially-produced
product with little saturated fat.3
For the next couple of decades, sales grew steadily as P&G
marketed their butter-replacement product as a cheaper, easier cooking
alternative. However, their big moment came in 1948 with their large donation
to a fledgling non-profit known as the American Heart Association. On the back
of this cash influx, the AHA, presided over at this time by Dr. Paul Dudley White,
would go from an organization with little influence or notoriety to the largest
non-profit in the nation in just more than a decade.4,5
In 1955, during the AHA’s rise to prominence, President Dwight
D. Eisenhower, himself a heavy smoker, suffered a heart attack that would be
instrumental in shaping the American dietary paradigm. His personal doctor, the
same Dr. White who presided over the AHA during the Crisco partnership and who
was himself unsurprisingly opposed to saturated fat consumption, entrusted the
role of the President’s personal nutrition advisor to the like-minded Ancel Keys.
Eisenhower bought in to the “prudent diet” approach being offered by Keys, whose
relationship with the popular president helped push him and his ideas forward
in the American consciousness.6,7
Now in lockstep with the President, Keys and the ever-growing
AHA led a national charge to erase the menace of heart disease from American society.
Within years of President Eisenhower’s heart attack, Keys was featured on the
cover of TIME magazine as an expert on diet and heart health, while the AHA
formalized guidance that saturated fat consumption should be strictly limited for
the prevention of heart disease. These guidelines, based on effectively no clinical evidence, did not yet push for the elimination of all fat from the
diet, arguing that the replacement of saturated fat with polyunsaturated fats
such as Crisco would do the trick. As we will see in the next section, clinical
trials launched after the fact were meant to validate the guidelines already put
in place, but failed notably in this endeavor.
Unfortunately for President Eisenhower, the prudent diet approach
assigned by Keys was ineffective, as he would go on to suffer multiple
additional heart attacks, a stroke, and develop diabetes before his death from
obstructive coronary disease. Now, much of this declining health is again
likely attributable to smoking, but it is without question that the public face
of America’s new low-fat diet experiment fell well short of resounding success.
Meanwhile, scientists such as John Yudkin advocated not for
a low-fat, but instead a low-sugar approach to dietary intervention. In the mid-1960s,
a series of studies pointing towards sugar as the primary driver of cardiovascular
disease helped, briefly at least, keep alive the fat vs sugar debate. In an
effort to combat the impact of these studies the research director of the Sugar
Research Foundation, John Hickson, paid two Harvard scientists to author editorials
in the New England Journal of Medicine that would discredit the research and
exonerate sugar as a disease-causing agent. One of these scientists would
become an administrator for the USDA, while the other would lead the Kellogg’s-funded
nutrition foundation at Harvard.8,9
Efforts such as these, combined with the growing prominence
of Keys and his like-minded followers, the influence of the AHA, and the full resolve
of the US government, helped cement the lipid-heart and diet-heart hypotheses
as the standard dietary paradigm. While evidence was still extremely limited,
one major observational study had now confirmed a general association between cholesterol and heart disease (the Framingham study, which we’ll examine in
detail in the next section), with the promise of more and better research to
come being promoted by Keys and others. While some of these research efforts
would ultimately do more to discredit than to confirm the attack on saturated
fat and LDL cholesterol levels, they would not do so until such notions were
firmly entrenched in the minds of scientists, health care professionals, and
the general public.
The lipid-heart and diet-heart hypotheses, weak and unsupported
as they may be, were here to stay.
Part 2 – LDL Studies and the Association Between LDL-C and Heart Disease, pt.1
1. 1957_Yerushalmy_Hilleboe_Fat_Diet_Mortality_Heart_Disease.pdf.
Accessed December 12, 2022.
http://library.crossfit.com/free/pdf/1957_Yerushalmy_Hilleboe_Fat_Diet_Mortality_Heart_Disease.pdf
2. Deep
Nutrition: Why Your Genes Need Traditional Food - Catherine Shanahan, M.D. -
Google Books. Accessed December 12, 2022.
https://books.google.com/books?hl=en&lr=&id=1fs3DAAAQBAJ&oi=fnd&pg=PP1&dq=deep+nutrition+cate+shanahan&ots=YNQWfUTs9a&sig=tVMLoLV8CQ34Lhsq4Rduo__tQdg#v=onepage&q=deep%20nutrition%20cate%20shanahan&f=false
3. MSEd
LWB. This Is How Crisco Is Really Made. Mashed. Published July 9, 2020.
Accessed December 12, 2022.
https://www.mashed.com/224919/this-is-how-crisco-is-really-made/
4. History-of-the-American-Heart-Association.pdf.
Accessed December 12, 2022.
https://www.heart.org/-/media/Files/About-Us/History/History-of-the-American-Heart-Association.pdf
5. Teicholz
N. The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy
Diet. Simon and Schuster; 2014.
6. Dwight
Eisenhower: Treating his Heart Attack. Accessed December 12, 2022.
https://doctorzebra.com/prez/z_x34mirx_g.htm
7. Paul
Dudley White. In: Wikipedia. ; 2022. Accessed December 12, 2022.
https://en.wikipedia.org/w/index.php?title=Paul_Dudley_White&oldid=1125479668
8. Taubes
G. The Case against Sugar. First edition. Alfred A. Knopf; 2016.
9. Fredrick
J. Stare. In: Wikipedia. ; 2022. Accessed December 12, 2022.
https://en.wikipedia.org/w/index.php?title=Fredrick_J._Stare&oldid=1079782061
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