daily foods

Daily Foods: The Usual Suspects

Four Criminals. One Line Up. No Coincidence.

Salt and Cholesterol #1 & #2

Salt and Cholesterol have stood the brunt of criticism over the years. The culmination of much vilification resulted in what now passes as a commonsensical recommandation. Namely: when it comes to cardiovascular health, we are better of consuming a low salt, low fat diet.

Both stories underlying the inception of these guidelines bear many similarities.

low salt diet, low cholesterol diet

The Founding Myths

The Salt-Blood Pressure Hypothesis

Two French scientists named Ambard and Beauchard theorized that salt elevated blood pressure in 1904. Basing their hypothesis on, mind you 6 of their patients. [1] Pretty shaky ground for science. Nonetheless they paved the way to establish the deep seated belief that salt consumption links to heart disease.

The Fat-Cholesterol Hypothesis

Ancel Key’s first hypothesized in the 1950s that high cholesterol was causing heart disease and that lowering it would logically provide a cure for what people were beginning to describe as a pandemic affliction. [2]

The Root of the Problem: Oversimplification

The seductive nature of both the Fat-Cholesterol and Salt-Blood Pressure hypotheses lies in their simplicity. Einstein warned us. “Everything should be made as simple as possible, but not simpler.”

As Dc DiNicolantonio explains in his excellent book The Salt Fix, we can sum-up the Salt-Blood pressure rationale as follows:

We eat salt => We get thirsty => We drink more water to “dilute the blood saltiness” => blood volume increases => high blood pressure results.

Voilà !

The tempting conclusion being that lowering salt consumption would prove invaluable in heart disease prevention.

The prevailing layman explanation for cholesterol artery clogging properties is compelling and appeals to common sense.

[…] the accumulation of cholesterol in lesions on the artery walls as a “biological rust” that can spread to choke off the flow [of blood], or slow it just like rust inside a water pipe so that only a dribble comes from the faucet. This imagery is so compelling that we still talk and read about artery-clogging fats and cholesterol, as though the fat of a greasy hamburger were transported directly from stomach to artery lining. Gary Taubes. Good Calories, Bad Calories

Additionally, two founding myths provide the scaffolding of the Fat-Cholesterol hypothesis.

One was Paul Dudley White’s declaration that a “great epidemic” of heart disease had ravaged the country since World War II. The other could be called the story of the changing American diet. Together they told of how a nation turned away from cereals and grains to fat and red meat and paid the price in heart disease. The facts did not support these claims, but the myths served a purpose, and so they remained unquestioned. Gary Taubes. Good Calories, Bad Calories [Emphasis mine]

Causation vs. Correlation

Despite their simplicity and how well they pleased mainstream thinking, neither higher blood pressure nor higher dietary cholesterol equals cardiovascular events.

“Just because one thing (salt) may sometimes lead to another thing (higher blood pressure), which happens to correlate with another thing (cardiovascular events), that does not necessarily prove that the first thing caused the third thing.” [1]

Correlation doesn't equal causation. Or how dietary myths come into existence.Click To Tweet

Likewise a diet high in cholesterol doesn’t necessarily entail cardiovascular diseases. Cholesterol is the main component of atherosclerotic plaque, true. But diet is not as relevant a factor in the development of plaque as it appears. This is a scientific fact.

Why do the myths persist then?

Cognitive Dissonance

People have a tendency to strive for individual consistency between what their do and experience and their set of beliefs. The uneasy feeling that ensues when a discrepancy arises has been dubbed “cognitive dissonance” [3]. The existence of cognitive dissonance will motivate the person to actively seek ways of reducing said discomfort. Either by rationalizing, or avoiding the source of discomfort. Usually scientists keep such emotional highjacking in a tight check. This has not been the case with salt and cholesterol. And apparently, proves to be a difficult endeavour for all things diet. Indeed, with the blood-pressure salt and fat cholesterol theories scientist have gone as far as designing experiments for the sole purpose of enshrining their views.

Two dubious animal experiments

Animal experiments picked to give credence to the Fat-Cholesterol hypothesis used rabbits. The issue being that rabbits are herbivores and unlikely to ever consume a high-cholesterol diet. How they handle excessive cholesterol is largely irrelevant and misleading when trying to apply it to humans. “This dietary regimen caused metabolic disturbances and unable to store the overflow of dietary fat it was stored in unseemly places such as tendons, and connective tissues as well as creating the thought after atherosclerotic plaque in arteries.” [2]

Perhaps even more striking is the mutant rats experiment that Lewis K. Dahl conducted. Unabated by his failure to showcase the correlation between salt in the diet and high pressure, he instead proceeded to bred his “Dahl salt-sensitive rats” to prove his point. This scientist actually engineered a breed of rats that would over react to salt in order to “prove” that a high salt diet was adverse to optimal health.

The “Paradoxes”

The famous 7 country study analyzed heart and vascular diseases repartition among countries having varied traditional eating patterns and lifestyles. Ancel Keys cherrypicked the 7 countries out of 22 which supported his claims. He also conveniently discarded those that did not. This is how what we now know as “The French Paradox” came into existence. An invention which sole purpose is to preserve the thesis that a high fat diet causes heart disease.

In the same vein “The Korean Paradox” rationalizes how a nation that indulges in copious intake of salt can get away with it and strut at the bottom of the list for cases of “hypertension, coronary heart disease and death due to cardiovascular disease.” [1]

Any evidence contrary to the founding hypotheses dissolved when labelled as “Paradoxes”.

The Proverbial Exception to the Rule

In fact in both cases what scientist presented as the overarching rule was really no more than an exception.

Biological phenomenons manifest along a wide spectrum of variations that are highly individual. [4] A minority of people can experience unusual reactions to nutritional interventions. These people are your outliers. Nutritional guidelines takes into account individual variations – to an extend. But they are exactly what the name says “guidelines.” It is the same as with medications, we are always reminded that “some people might experience [insert scary symptoms]” in the side effects lists.

Now, imagine basing national nutritional guidelines on these outliers… chaos would ensue. Well, this is basically what happened with salt and cholesterol.

Few people are salt sensitive:

But evidence in the medical literature suggests that approximately 80 percent of people with normal blood pressure (less than 120/ 80 mmHg) are not sensitive to the blood-pressure-raising effects of salt at all. Among those with prehypertension (a precursor to high blood pressure), roughly 75 percent are not sensitive to salt. And even among those with full-blown hypertension, about 55 percent are totally immune to salt’s effects on blood pressure. That’s right: even among those with the highest blood pressure, about half are not at all affected by salt. DiNicolantonio, James. The Salt Fix: Why the Experts Got It All Wrong–and How Eating More Might Save Your Life

Likewise only a minority of people are cholesterol sensitive. Dietary cholesterol, for instance, has an insignificant effect on blood cholesterol. It might elevate cholesterol levels in a small percentage of highly sensitive individuals, but for most of us, it’s clinically meaningless. [2]

In Peter Attia’s words, “cholesterol is just another fancy organic molecule in our body, but with an interesting distinction: we eat it, we make it, we store it, and we excrete it all in different amounts.”

Use of Palaeolithic Diets as Evidence

The discussion on the salt and fat hypotheses drew upon ancestral diets for justification. Scientist pushed evolutionary evidence as proof that a diet low in sodium and fat was natural. What such “evidence” doesn’t compute in is that skin, organs, bone marrow, blood contain copious amount of fat and salt and represented a significant portion of our ancestors’ daily regimen. [1] Additionally researchers often failed to account for aquatic vegetation and animals which would have constituted a significant part of our diet as well a rich source of sodium and fats. [1]

While it is true that data on Paleolithic diets is scarce, and subject to controversy, the previous observations draw attention to the fat that both salt and fat make up a big part of our physiological make-up.

Ubiquitous Substances

When analyzing the human body, you can’t fail to notice that salt and fat are prevalent.

Fat makes up 70% of your brain! Myelin, another fatty substance, makes up nerves and runs throughout our bodies to relay nervous impulses. Plus membranes cells are mostly fat. Bruce Lipton coined the term “mem-brain” to illustrate how crucial cellular membranes are when it comes to cellular behavior – what comes in the cell, what goes out, how cells communicate together how they move etc. [5]

Likewise, sodium chloride makes up as much as 90% of blood mineral content. No less!

As Gary Taubes compellingly phrases it: “Any tinkering of any of the aforesaid substances can have potentially wide ranging effects on the organism.”

Ubiquitous doesn’t mean essential though. It is necessary to operate the distinction.

Essential Nutrients

What distinguishes essential from non essential nutrients? Essential nutrients are, quite unsurprisingly, “essential” to bodily functions in the sense that the body cannot synthesize them on its own. Basically if you don’t get these from your diet you will die – conditions and duration of demise may vary.

What are the essentials nutrients for humans? There are few.

We have essential amino acids, essential fatty acids, minerals, vitamins.

Of course, they are not the same for every species, this is why experimenting on animals has its limitations.

You need to get these essentials from your diet. But the necessary doses vary hugely. This is why we speak about micro vs macronutrients.

Another consideration is storage.

The body is clever and able to store nutrients. Depending on fat solubility some nutrients can be kept in copious amounts. Due to their hydrophobic nature vitamin Bs can’t be stored in significant amounts – baring the case of vitamin B12 which is stored in the liver. In fact some nutrients are stored in organs. Salt can be stored in the skin and bones.

Now some nutrients are conditionally essential. This means the body is usually able to manufacture these. But taxing conditions such as stress and illness can impede said production and require a dietary output. [8]

When talking about nutrients it is important to distinguish between minimal amounts necessary for life and prevention of disease and optimal amounts. Similarly, there exists an upper limit. The upper limit is determined by issues of toxicity. For instance despite being essential manganese is still toxic in doses above 7mg. Toxicity depends amongst other things on how efficiently the body can excrete said substance. And the metabolic cost of said excretion.

Can the substance be stored? Is it excreted freely? How does the body cope with too much of a substance? How can outside factors (genetics, polution, environmental parameters influence use, excretion and storage ?

Cholesterol is not essential. Sodium is. Carbohydrates are non essentials – with a tweak, but more of that later.

Ultimately whether a substance is essential or not will be reflected in how the body excrete it.

Adding or Relieving Stress

Kidneys are a sturdy organ. Healthy kidneys can excrete 10 time the recommended sodium daily allowance no problem. [1] We got it wrong as DiNicolantonio underlines. Stress in the kidneys stems from having to reabsorb the sodium, not from excreting it. Up to 70% basal energy is used by the kidneys for salt reabsorption.

Plus a host of hormonal reactions are necessary to maintain sodium levels high enough for optimal function. This will ultimately put a heavy toll on adrenal function.

Low salt diets force the body to tap into its sodium stores. The precious sodium can be found the skin reserves or in a more hazardous endeavour, within bones. Bones will give away calcium, potassium and sodium altogether. Therefore low sodium becomes a risk factor in osteoporosis.

Contrary to common beliefs, most dietary cholesterol is not absorbed. More than 50% of the exogenous cholesterol (i.e., cholesterol from food) is excreted. Endogenous production varies in accordance to dietary input and is a tightly regulated process.

In the case of salt, over consumption is not as much of a stress as underconsumption.

The body regulatory processes are better equipped to deal with excess than scarcity. Negative feedbacks are stronger. Think for instance of your taste buds and satiety controls. If you were to eat salt and cholesterol ad libitum you’d likely stops pretty quick. Can you eat a whole bar of salted butter in one sitting? A whole bag of cookies….?

Multifactorial issue

In both cases one nutrient was singled out when the etiology was multi factorial.

Salt/potassium balance

Ultimately, it is “a combination of a high-salt and low-potassium intake that leads to hypertension, and still only in those who were genetically susceptible.” [1]


Atherosclerosis is an accumulation of sterols which oxidize and elicit a maladaptive inflammatory state – read an immune response running wild.

Contrary to common thoughts LDL and HDL are not good or bad because they transport cholesterol back or forth. Respectively from gut and liver to periphery for cellular maintenance and steroid production. And from periphery back to liver.

HDL – the good cholesterol doesn’t bear the whole brunt of the journey back a.k.a Reverse Cholesterol Transfer as the original theory has it. LDL do its part as well, actually these molecules do most of the job. [10] Hence LDL is usually as good as HDL but sometimes it gets in places it should not.

How atherosclerotic lesions develop

Called the Response-to-Retention model of atherogenesis, it emphasizes what we concluded was the root cause and necessary initiating event of atherogenesis: the subendothelial retention of apolipoprotein (apo) B containing lipoproteins in susceptible but still prelesional areas of the arterial wall. Biological responses to retained and subsequently modified lipoproteins, notably a chronic and maladaptive macrophage- and T-cell dominated inflammatory response and changes in smooth muscle cell localization and phenotype, could explain virtually all of the features known to exist during the initiation and progression of atherosclerosis [6]

In plain English LDL molecules end up somewhere they should not be and inflammatory mayhem ensues.

Direct evidence exists that remnant lipoproteins are retained in lesion-prone areas of the arterial wall and that patients with high plasma levels of remnant lipoproteins are at markedly increased risk for atherosclerotic heart disease [6] Lipoprotein remnants are “products of the lipolytic degradation of triglyceride-rich lipoproteins produced by the liver and intestine” [9] the returning HDL which deflate to become smaller. Interesting side note, insulin resistance plays a role as a risk factor in the accumulation of plaque. [9]

Indeed chronic elevation of blood glucose tampers with lipoproteins structure on the cellular membrane. Then it causes cells to become resistant to insulin message.

Cost Benefit Analysis 

When we consider treating a disease with a new therapy, we always have to consider potential side effects such as these. If a drug prevents heart disease but can cause cancer, the benefits may not be worth the risk. If the drug prevents heart disease but can cause cancer in only a tiny percentage of individuals, and only causes rashes in a greater number, then the tradeoff might be worth it. No drug can be approved for treatment without such consideration. Why should diet be treated differently? Taubes, Gary. Good Calories, Bad Calories

In hindsight, the governmental guidelines proved harmful. And tradeoffs, bitter-sweet.

Walter Willett, chair of the department of nutrition at the Harvard School of Public Health uttered this media shocking statement: “It now increasingly recognized that the low fat campaign has been based on little scientific evidence and may have caused unintended health consequences.” Duh! People of my generation have been brainwashed into thinking that fat is evil. Unfortunately, it created huge damages to at least 3 generations of Western World humans.

As early as 1980, several studies were drawing parallels between cancer and low cholesterol. “The most consistent association was between colon cancer and low cholesterol in men.” [2]

Low fat diet are also conductive to the development of fat soluble vitamin deficiencies. As well as antioxydant depletion.

Fats are crucial to brain health.Thanks to Dc Perlmutter, the lay public is know privy to the fact that low fat diets and the subsequent increase in carbs consumption, paves the way to neurological degenerative diseases [11.] Inflammation is the big killer, not fat, which is protective.

The heart, ironically, loves fat as energy – as its tissues are very dense in mitochondria to allow beta oxydation. Large scale efforts to preserve heart health were in fact quite detrimental to this organ.

Salt caused heart disease or so we thought. When low salt diets cause in reality the heart to pump harder and therefore put undue stress on the organ. The depletion of blood volume due to low sodium causes a phenomenon known as “total peripheral resistance” meaning the arteries become more constricted and the heart needs to pump harder. [1] And this is real health concern.

#3 Carbs

One of the most nefarious effect of low salt, low cholesterol, low fat diets is the development of insulin resistance.

Salt deficiency displays an alarming link to insulin resistance. “With over 50 percent of adults in the United States now considered diabetic or prediabetic, low-salt diets may be causing harm to over half the adult population” [1.] In 2010, a study published in the Annals of Internal Medicine proposed that it’s the palmitoleic acid, which occurs naturally in full-fat dairy products, that protects against insulin resistance and diabetes. [12]

Glucocorticoids and mineralocorticoids determined the effects that dietary salt had on blood pressure and not salt intake per se. [1] And it turns out sugar increases glucocorticoids not salt. Insulin resistance causes high tension not salt, and low sodium causes insulin resistance.

Plaque gets out of control because of inflammation…

So many evidences point toward carbs as being evil that it would make sense to suppress completely carbs, right?

Could It Be “One of those” in the words of Ray Dalio

We should be wary of creating new dietary outcasts.Click To Tweet

Using principles is a way of both simplifying and improving your decision making. While it might seem obvious to you by now, it’s worth repeating that realizing that almost all cases at hand are just another one of those, identifying which one of those it is, and then applying well-thought-out principles for dealing with it. This will allow you to massively reduce the number of decisions you have to make. Identifying which “one of those” each thing is is like identifying which species an animal is. Doing that for each thing and then matching it up with the appropriate principles will become like playing a game, so it will be fun as well as helpful. Dalio, Ray. Principles: Life and Work

It is the same caveat and lest we fall into the very same trap and castigate sugar let’s have a look at an interesting piece of news.

#4 Coconut Oil

With the emergence of ketogenic diets and the hype surrounding coconut oil. Something was bound to come up in the press. The news never disappoint, meet the: “coconut oil controversy”

The AHA is back at it saying that coconut oil and saturated fats are evil and trying to push margarine down our throats.

The reasoning is as follow coconut oil promotes a phenomenon known as endotoxemia. It is basically sepsis’ little sister. It is not going to kill you but comes with all flavours of unwanted conditions such as obesity, diabetes, heart disease, cognitive dysfunction  etc

Coconut oil, it seems, allows endotoxins to take a ride into the blood stream. Normally they don’t escape the gut in any significant amount.

But let’s backpedal a little bit.

Beneficial bacteria, neutral and potentially harmful bacteria compose our micro biome. The microbiome is akin to an ecosystem. Normally the beneficial bugs keep the bothersome one in check. In reality, the troublesome bugs are not all bad, we need them, but we need them in check!

Each kind of species feeds on specific nutrients. Similarly some bacterial strains relish fat and sugar whereas other prefer fiber – thats something of an oversimplification, but an helpful one.

Gram negative bacteria the “bad bugs” have LPS in their membranes. LPS is a toxicant. We dont want any significant amount of these endotoxins in our blood stream as it leads to serious conditions as we’ve seen earlier.

How to keep these in check? First: Preserve gut lining integrity. In case of a leaky gut, endotoxemia can run out of control. Second: A diet rich in polyphenols offers protective effects against endotoxins.

A healthy diet relies on natural foods, a variety of foods. We’ve known it all along. Coconut oil is not evil. Neither is cholesterol. Neither are carbs…. you have to earn them and remember that the only essential carb is fiber.


1. DiNicolantonio, James. The Salt Fix: Why the Experts Got It All Wrong–and How Eating More Might Save Your Life

2. Gary Taubes. Good Calories, Bad Calories

3. A Theory of Cognitive Dissonance, Leon Festinger

4. Biochemical Individuality, Williams, Roger

5. The Biology of Belief, Bruce H. Lipton

6. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis, Update and Therapeutic Implications

Ira Tabas, MD, PhD; Kevin Jon Williams, MD; Jan BoreÌn, MD, PhD

7. The Canadian experience: why Canada decided against an upper limit for cholesterol, McDonald BE

8. Supplemental conditionally essential nutrients in cardiovascular disease therapyKendler BS

9. High Plasma Concentration of Remnant Lipoprotein Cholesterol in Obese Children and Adolescents, Yong Jun Choi, MD.

10. Cholesteryl ester transfer protein: At the heart of the action of lipid-modulating therapy with statins, fibrates, niacin, and cholesteryl ester transfer protein inhibitors, M. John Chapman, Wilfried Le Goff, Maryse Guerin, and Anatol Kontush

11. Grain Brain: The Surprising Truth about Wheat, David H. Perlmutter and Kristin Loberg

12. Saturated Fat Helps Avoid Diabetes, Dc Mercola

13. Low-salt diet increases insulin resistance in healthy subjects, Garg R, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK.

14. Coconut Oil & Endotoxin: The Missing Link to the AHA Controversy, Mike Mutzel. 

15. Metabolic Endotoxemia Initiates Obesity and Insulin Resistance. 

16. Metabolic endotoxaemia: is it more than just a gut feeling?