People claim that coconut oil in your diet is damaging and causes heart disease.
But more often than not, the people making these claims have a vested interest in ruining coconut oil’s rep.
For example, the pharmaceutical industry has billions invested in the idea that cholesterol causes cardiovascular disease.
And they need everyone to believe that saturated fats raise serum cholesterol.
Now, one they’re partly right — one of these ideas is true.
But they other isn’t, and they don’t work together.
Is coconut oil good for me? I don’t know. But it’s not dangerous.
The inhabitants of the South Pacific eat a LOT of coconut and coconut oil.
And as far back as 1968, Western scientists realized that these people disprove the heart disease from coconut oil idea.
They knew then that coconut oil does not cause heart disease.
The scientist Ian Prior made the long trip to the isolated islands of Tokelau and Pukapuka in the South Pacific.
These natives were virtually cut-off from modern society.
So Dr. Prior spent weeks meticulously studying their diet.
He found that they ate mostly coconuts, fruit, taro root, and fish.
On Pukapuka Island, coconut accounted for 34% of their total energy and 63% on Tokelau.
Coconut is their main beverage too, and they use it in cooking.
The Islanders also ate pork and chicken that had higher saturated fat that normal (62 and 78%).
The animals also ate a LOT of coconuts since it’s so abundant there.
Pigs and chickens on these atolls also eat large amounts of coconut.
So, if you add the coconut oil to the fattier meats– you have a diet that is very high saturated fat intake.
And it’s higher than nearly anywhere else on this planet.
But, despite these massive intakes of cholesterol and saturated fat, the inhabitants didn’t have any heart disease.
In fact, Mr. Prior was unable to detect ANY signs of cardiovascular disease.
None at all.
Other researchers noticed the same thing among South Pacific Islanders on different islands.
Sinnett visited the coconut-eating Islanders of New Guinea in 1973.
And Page visited the Soloman Islands in 1974.
Both found zero signs of cardiovascular disease.
Stroke and ischaemic heart disease appear to be absent in this population.
And in 1993, yet another scientist conducted research on heart disease in the Pacific.
Lindeberg visited the Melanesian island of Kitava and found low (almost zero) incidence of abnormal ECG readings.
Over and over again, research proves that coconut oil and cholesterol have absolutely no connection to heart disease.
If it did, these populations would have much higher risk for it than the rest of the world.
Instead, they have practically ZERO heart disease risk!
What’s more, this research also showed that the classic formula for predicting total blood cholesterol is wrong.
A Mr. Ancel Keys created a formula to predict total serum cholesterol based on fat intake.
He was the founder of the Lipid Hypothesis we discussed before.
But the tropical island studies prove that it is fundamentally flawed and unable to predict cholesterol levels.
Here’s his equation: Δchol=1.35(2ΔS−ΔP).
Don’t ask me how to read it, but the research proves the equation is far too simplistic.
And it’s pretty much worthless when it comes to coconut oil.
The difference between predicted and measured values would probably embarrass Keys.
But according to these studies, it’s nowhere near accurate.
And the idea that coconut oil (and other saturated fat) causes heart disease is also a complete myth.
Even mildly elevated levels of serum cholesterol are unlikely to have any effect on cardiovascular disease.
So if cholesterol isn’t to blame, what is?
Well, we may have that answer.
Besides cholesterol, our blood has lipoproteins running through it.
And it’s much more predictive to measure lipoproteins to predict heart disease.
If you ask your doctor for the test, they will order the “serum concentration of Lp(a).”
Lipoprotein(a) is a specific type of lipoprotein.
It’s two different apoproteins linked together, Apo-A and Apo-B.
‘Apo’ just means without, and people use it when talking about the bare protein itself.
In this study, researchers studied the arteries removed from patients after bypass surgery.
They also took the patients’ blood days before the operation.
After that, they made comparisons to figure out which blood parameters correlated with which artery measurements.
They wanted to know if something in the blood stayed with the artery or flowed free.
Looking at this chart, the higher the number, the more closely linked the measurements are.
They found that serum Lp(a) levels, and its attached Apo-B protein, were far more related than cholesterol.
This means that blood cholesterol levels hardly determine the arterial cholesterol levels.
In other words, the cholesterol levels the blood didn’t mean that the arteries had higher cholesterol levels, too.
Cholesterol didn’t stick to the walls of the arteries because it’s not adhesive.
But something else is — apoprotein(a).
So Dr. Rath took things a step further.
He raised antibodies for Apo(a).
And he used them to demonstrate the Apo(a) clinging to the arterial walls of heart disease patients.
And Apo(a) wasn’t detected at all in many controls.
Lipoprotein(a) is low density, and LDL cholesterol measurements catch it.
But when many experimenters measure LDL, they usually don’t determine the Lp(a) concentration specifically.
However, the people who take the extra effort to measure Lp(a) directly always find that this is the most significant risk factor for heart disease.
Other scientists agree with Dr. Rath.
Here is a study conducted by Gerald Zenker in 1986, and he reports the same results.
He compared a group of his patients with cardiovascular disease against a group of controls.
Then he matched the blood parameters to the degree of artery hardening (atherosclerosis).
He found that Lp(a) had the most significant relationship to hardened arteries.
…and CVD, showed Lp(a) to be the most serious single risk factor, concerning serum lipids and lipoproteins for CVD.
The serum Lp(a) is the only lipid parameter that varies greatly in the blood.
It can range from over 100 mg/dL to undetectable.
All of the other lipoproteins have a relatively stable concentration.
So, what does this mean for you?
Well, to start, the focus needs to move from cholesterol levels to lipoprotein(a).
All of the attention should focus on lowering Lp(a) levels and strengthening the arterial wall.
If you look at most animals, you won’t find Lp(a).
Only primates, guinea pigs, and European hedgehogs have it.
These animals and humans have something else in common though.
We’ve all lost our ability to synthesize vitamin C.
We need vitamin C create collagen, and the arterial wall is roughly 50% collagen.
So the prevailing alternative theory is that vitamin C deficiency tells the body to increase Lp(a) production.
Then the lipoprotein helps stop internal bleeding when collagen production fails.
This could explain the findings on the South Pacific Islanders.
They had no atherosclerosis despite a massive intake of saturated fatty acids.
But they get plenty of vitamin C, so their bodies don’t substitute the lipoprotein.
Don’t think this means that everyone will stop blaming cholesterol though.
We won’t hear that vitamin C deficiency causes these issues.
Big Pharma is too invested in the status quo and Lipid Hypothesis.
So they’ll either suppress or just ignore the unprofitable idea of simple vitamin C.
They certainly won’t push for testing the idea, and they won’t encourage anyone else to see if this theory is correct.
But regardless of the precise nature of cardiovascular disease, it’s apparent that coconuts are not a risk factor.
Lipoprotein(a) as a Strong Indicator for Cerebrovascular Disease
Detection and Quantification of Lipoprotein(a) in the Arterial Wall of 107 Coronary Bypass Patients
Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies