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Nutrition Past and Future

22 Cholesterol Confusion 5 Cholesterol Is Necessary for Life 

Take a listen to Chris Masterjohn as he talks to Chris Kresser on his podcast.

MASTERJOHN: If you want to understand what cholesterol does in the body, the best way to look at that is to look at cholesterol deficiency. And cholesterol deficiency can be seen in what’s referred to as Smith-Lemli-Opitz Syndrome, SLOS, and this is a genetic deficiency in cholesterol production. So if we look at the type of symptoms of this genetic deficiency in cholesterol, we can start to understand the types of things that cholesterol does. So in most cases someone who’s born with Smith-Lemli-Opitz – someone who’s conceived – most conceptions of Smith-Lemli-Opitz Syndrome are spontaneously aborted. So the first thing that we can see is that cholesterol is essential to fertility, to carrying on a normal pregnancy, and to basic life and growth of a human being.

Now bear in mind that this is Masterjohn’s opening material in this interview. The first thing he wants to tell us about is a rare genetic disorder that normally doesn’t even permit someone to be born. This is a subject he thinks he is going to use to enlighten us about cholesterol in nutrition.

MASTERJOHN: In the rare cases where someone’s actually born with this disorder, they have all kinds of facial and skeletal abnormalities. They can have mental retardation, autism, hyperactivity disorders, attention-deficit disorders, visual dysfunctions, endocrine dysfunctions, serious digestive problems, and self-injurious and aggressive behavior. So you can start to see that cholesterol is basically affecting everything in the body.

Notice that he had that list of horrors memorized and at the ready. He has obviously done at least a little research about this disorder. He apparently knows enough about it to feel comfortable bringing it up in an interview. At this point, an intelligent and skeptical listener should be wondering if there has ever been any case of someone developing autism or facial deformities from consuming a cholesterol-lowering diet. If that happened, I’m pretty sure the deniers would have told us about it by now. You might rightly be wondering why he is talking about SLOS and what his point is.

He goes on.

MASTERJOHN: And in fact the usual treatment for this syndrome has been a diet rich in cream and egg yolks, which are rich in naturally occurring cholesterol. But somewhat recently the FDA approved a pharmaceutical-grade cholesterol supplement to treat the disorder because these people’s digestive system is so bad that they can’t absorb cholesterol from food very well because cholesterol is necessary to digestion. So basically, what does cholesterol do in the body? Well, it’s an essential component of our cell membranes, where it helps maintain them the consistency of olive oil – not too fluid, not too stiff ...

Notice that Masterjohn has just stated a position that perhaps Thomas Dayspring might dispute. We do absorb dietary cholesterol after all, according to Masterjohn. I wonder why these guys disagree about that. Now the discussion is about to get really dumb. Chris Kresser is about to speak.

KRESSER: I was just going to say, it’s a shame how few people are aware of this because the common mentality, you know, not in the Paleo world but in the mainstream world is, the lower your cholesterol is, the better. You know, almost like if you could just get it down to zero you’d be in great shape.


MASTERJOHN: Yeah,and you can see exactly what happens when you get your cholesterol down to practically zero by looking at these rare genetic cases and you can see it’s actually a disastrous thing. I’d rather grow up and get heart disease when I’m 55 than have to go through this when I’m, you know, a little child, you know, no one would want to wish that upon another child. So we certainly want to prevent heart disease but the last thing we want to do is attempt to prevent it by getting cholesterol down to zero.

So let’s review the analysis we just heard. Kresser thinks more people should know about his exceedingly rare genetic disorder, a disorder that he thinks is relevant to diet even though most carriers of it have never lived long enough to eat anything at all. They weren’t born. He thinks it is possible to get your cholesterol all the way down to zero through diet somehow. He imagines there are people out there who think a thought this stupid and he and his buddy have a laugh at their expense. Who, exactly, are they laughing at? Masterjohn agrees with these comments and says that the choice we have is between suffering a rare genetic disorder in childhood and suffering heart disease in adulthood. The implication is that the children affected by this made a bad choice by not eating the way the cranks at the Weston Price Foundation want us to. Beside that, didn’t Masterjohn just admit that high cholesterol levels will put you at risk of heart disease at the age of 55? That is the one thing he said that I find reasonable. Are you keeping track of the layers of idiocy? Are you finding it ironic that these guys are concerned about avoiding mental retardation? They go on.

KRESSER: … I mean, LDL is bad is just as silly as saying cholesterol itself is bad.

MASTERJOHN: Right, if you don’t have the LDL particle, you’re not going to get those nutrients to where they need to be. That’s what LDL is all about.

Are you buying into this premise? You have control over whether or not you will have any LDLs at all in you. You should eat fatty animal foods to make sure you aren’t missing out on any LDLs.

As ludicrous as this conversation was, I think it will be illuminating for us to take Masterjohn’s premise seriously. Is SLOS, the genetic disorder he mentions, something that you can acquire or mimic through diet? And what will happen to you if you have extremely low LDL? When we explore these questions, we will see that a low carber has once again chosen to withhold important information in order to scare you and control you.

Let’s talk about SLOS. Before we get into it, I want to point out that a common argument I’ve seen from the confusionists is that familial hypercholesterolemia, or inherited high cholesterol, is a genetic disorder that should not be used as a model for heart disease in normal people. Those people who say that, in order to be consistent, should fault Masterjohn for attempting this argument. He is using a genetic disorder to argue this from the other side. Now, let’s look into SLOS a bit. One of the men after whom SLOS is named is John Opitz. You can see here that in a journal article he referenced Gary Taubes as he suggested that something called “lipophobia” may be abating with a return of some sanity in the discussion of health and dietary fat. He thinks that there had been a fear of fat that was something other than sane. This is a very unusual tone for a journal article and Taubes is a very unusual person to reference in a journal article.

Dr Opitz is the only person named under the “medical specialists” section at the SLOS Foundation website. The site has an egg yolk in a shell as a part of its logo. The website states that the abnormalities associated with SLOS are a result of a lack of cholesterol. We are told that a person who cannot make enough cholesterol will have an array of serious problems like poor growth and mental retardation. One would think that the only characteristic of SLOS is a highly damaging lack of cholesterol, which is due to a mutation which prevents the production of a key enzyme. The missing enzyme is called 7-dehydrocholesterol reductase.

As we look back at Dr Opitz’s journal article, we see that he says that the absence of this enzyme not only results in a deficiency of cholesterol, it causes the sterol that should be broken down by that enzyme to build up to levels sometimes a thousand times higher than normal. This sterol consequently becomes concentrated in blood and tissues. For some reason, Dr Opitz on his website and Chris Masterjohn in this interview forgot to mention that other part. Maybe if you build up some substance to a level a thousand times greater than it should be, that might just affect something in a bad way, perhaps?

These two animal fat lovers failed to mention that SLOS is diagnosed using a test to measure levels of this sterol. Read this slide and you will also see that one may have a normal cholesterol level and still have SLOS. Quoting here, “Although frequently low, plasma cholesterol levels can be within normal limits in SLOS patients.” Reading on, you can see that it is just as likely that the problems SLOS patients experience are caused by the buildup of that sterol, called 7DHC here, which probably becomes toxic at high concentrations.

Here you can see that it has been unclear what exactly causes the problems of SLOS patients. Yes, a deficiency of cholesterol may be the issue, but that is just one possibility.  This paper notes that those patients with the best response to dietary cholesterol treatment also have the lowest level of 7-DHC. In other words, they happen to have the least exposure to any potential toxic effects of excess 7-DHC.

Research on mice that have been given a mutation that emulates SLOS does argue for the a toxic effect of 7-DHC on brain structures.

Indeed, the severity of the defects associated with SLOS are correlated with the ratio between 7-DHC and cholesterol. This does not say the defects correlate best with cholesterol only. 7-DHC is clearly a major player in SLOS. For some reason, Masterjohn didn’t think that was worth mentioning. He had that list of symptoms well memorized. Clearly he has paid attention to the literature for this condition. He just decided that a thousand-fold elevation of a potentially toxic compound wasn’t important enough to tell you about. He wanted to scare you into eating artery-clogging fats and to do that, he had to withhold this information.

One more thing. It appears that the feeding of dietary cholesterol actually reduces cholesterol synthesis in SLOS. You heard that right.
Dietary cholesterol may cause the SLOS patient’s body to produce less cholesterol. Moreover, SLOS patients are commonly treated with both dietary cholesterol and a statin, a cholesterol-lowering drug.

Let’s remember that the lesson of all this in Chris Masterjohn’s mind is that we should eat a lot of cholesterol to avoid developing SLOS-like problems. It is better to die of heart disease than to experience all that. Let’s now examine what happens when someone has very low cholesterol levels and see if he has a point.

This is an amazing paper authored by the great Daniel Steinberg along with Scott Grundy and others in 1979. Here they report on a 67-year old man with a genetic condition called familial hypobetalipoproteinemia.  This man had LDL of only 4 to 8 milligrams per deciliter. You, dear viewer, will never get your LDL that low no matter what diet you choose, and it is probably impossible to get your LDL that low even with drugs. This man did have mild fat malabsorption and a disrupted fat metabolism. However, he did not exhibit any of the serious features of Smith-Lemli-Opitz Syndrome.

His total cholesterol was only 47, yet this man served an entire career as a Navy chaplain. Apparently he wasn’t mentally retarded.

The cholesterol levels of his family members were tested. As you can see, two compound heterozygotes scored a 1 for their LDL. His relatives had no symptoms related to neurological disorders, retinal disease, or fat malabsorption. Once again, if you have normal metabolism of your beta lipoproteins, you cannot achieve these numbers no matter what you do…

Short of contracting the wrong strain of hepatitis. I don’t care if you become a fruitarian or if you do McDougall or Pritikin, you cannot get LDL this low through diet.

These people in this study didn’t have any of the scary symptoms of SLOS and their numbers were astonishingly low. Please note that the chaplain had elevated triglycerides.

These folks had no heart disease. One of the compound heterozygotes was called extremely healthy at the age of 75. His mother, who would have carried this mutation as well, lived to be 95. A sibling of that mother lived to 105. And yet Chris Masterjohn seems to think low cholesterol will not allow someone to be born. He’s only off by 105 years or so. And doesn’t living to 105 sound a lot better to you than dying of heart disease at 55?

Here is one more slide from that paper to show you their very low cholesterol levels and their lack of developmental and neurological problems.

Doesn’t Uffe Ravnskov think that an alleged cause of disease must perfectly track with disease occurrence, or else that factor isn’t really a cause? Does Masterjohn think Ravnskov is wrong here? Or will he admit that if people with extraordinarily low cholesterol can live into old age, then low cholesterol doesn’t cause all the problems he claims? Once again, the apologists for saturated fat can’t seem to think through a consistent story.

Here is another paper looking at people with hypobetalipoproteinemia. In contrast to our previous paper, in this one children are described as having neurological and developmental problems, among others. However, they had a combination which we did not see in the chaplain. They had extraordinarily low cholesterol levels and in addition, they had extraordinarily low triglycerides. We are no longer looking at a cholesterol deficiency only. We are seeing a more generalized inability to transport fats in the blood here. Notice that the authors here use a quote saying that “no clinical abnormalities have been consistently found in all patients with hypobetalipoproteinemia.”

This paper references the Steinberg paper which you just saw.

This paper states that as of 1993, only twelve people had been identified with the homozygous form of this mutation. Their LDL ranged from 0 to 21. Of the homozygotes with normal triglycerides, most had been asymptomatic.

Heterozygotes, on the other hand, were said to be free of symptoms. The authors thought that their lack of LDL was compensated for by their HDL. These authors noted that these people had a much lower rate of coronary disease.

The lack of coronary disease does seem to be a nice side benefit to this condition. Here is a paper published in JAMA in 1978 reporting that an autopsy of a 76-year-old woman found absolutely no atherosclerosis. She had familial hypobetalipoproteinemia. No disease could even be found under the microscope. Wouldn’t it be nice if you could have arteries free of disease?

The authors called her condition remarkable.

Now all this is not to say that hypobetalipoproteinemia has no downsides. Homozygotes often have clinical problems and heterozygotes sometimes do. I must also note that there is a condition called abetalipoproteinemia, which means the patient has no beta lipoproteins. This is a much more severe condition and it definitely results in serious problems. Once again, this is not something you can acquire.

If you are a normal person and you really try to get your cholesterol as low as possible through diet, you may well be able to have arteries as clean as those of Nathan Pritikin. Upon autopsy, he was found to have only fatty streaks. He had no manifestation of heart disease.

Meanwhile, the typical overweight and obese individuals who fall prey to the fat pushers are carrying around an excess of cholesterol all through their bodies. They don’t need to imagine themselves with a cholesterol deficiency because they are storing a lot of cholesterol inside their fat stores that their bodies cannot use. If you were stick thin and were 100% low-fat vegan, you could never give yourself anything resembling SLOS. Instead, I’ll speculate that the typical Masterjohn fan is overweight and eating a lot of animal fat. They may have a lot of health issues to be concerned about but a cholesterol deficiency is not one of them. If they are feeding their fat bellies fatty foods because they are afraid of winding up with an SLOS-like condition, then they are being played as fools.

The whole subject of cholesterol deficiency is entirely irrelevant to discussions about diet. However, we have very good reason to be concerned about the possibility of having too much cholesterol. To show you why, I’ll skip the obvious stats and studies about heart disease and show you instead how excess cholesterol can destroy your cells. When it comes to cholesterol, too much is too much.

The team of Brown and Goldstein famously elucidated the activity of the LDL receptor, and later, they explained the regulatory mechanisms of cholesterol used by the cell. When your cells want cholesterol to be brought inside them, they make LDL receptors which fix themselves on their outer surface. There, LDLs dock with them and deliver their cargo of cholesterol into the cell. As a cell becomes filled with all the cholesterol it can take, it dials back on its production of LDL receptors. Cells can also make their own cholesterol, and they cut back on this activity when no more cholesterol is needed. In this way, they prevent themselves from becoming overly loaded with cholesterol.

Cholesterol delivered by the LDL literally blocks the process the cell uses to make new receptors. That term you see here, SREBP, means sterol regulatory element binding  protein. This molecule motivates the genetic transcription of new receptors. When there is enough cholesterol in the cell, the SREBPs can’t get the receptor synthesis process going. That’s all well and good for the cell but what if there is a high amount LDL cholesterol floating around outside the cell? What are the LDLs supposed to do with their cargo if they aren’t finding takers among their usual customers? You might say that they are hung out to dry, and consequently they just hang out getting into trouble. The LDLs attach to artery walls. They attract immune cells. They cause inflammation. Over time they cause the buildup of plaque. Is all this the fault of the cells, who stopped doing business with them? Of course not. The cell does its job fine. Whatever caused all the excess cholesterol to get into the blood, that’s what messed up. What messed up? Usually, it’s the brain, the brain of the gluttonous meat and fat eater. It’s the brain that decided on the wrong things to feed its body that should be blamed.

In this paragraph Brown and Goldstein give you a litany of ways that the cell regulates how much cholesterol it makes and receives. You should read through this. But first, skip to the last line. “Through these regulatory mechanisms, cells keep the level of unesterified cholesterol in membranes remarkably constant despite wide fluctuations in cholesterol requirements and exogenous supply.” Think about that. You can have high cholesterol or you can have low cholesterol. Either way the cells can deal with it. So what are you worried about, saturated fat eaters? Your cells don’t share your concerns.

Here’s the process you set off with your poor dietary choices. Dietary saturated fat and cholesterol downregulate your LDL receptor synthesis. Your cells fill with cholesterol. They shut down the mechanism that brings new cholesterol into them. LDL cholesterol builds up outside your cells in your blood. A dysfunctional new normal sets in for you as you are stuck with high cholesterol. That new normal has nothing to do with the needs of your cells. So why would you want that situation?

Why would you eat the foods that interfere with the normal balance and cause your LDL concentration to increase?

Why would you want more cholesterol floating around than you need, more than your cells even want? In the center of this paragraph, Brown and Goldstein mentioned that excess cholesterol inside the cell can be turned into cholesterol esters for storage.

The cells have a limited ability to store excess cholesterol in the form of cholesterol esters. The cells can’t break down and rid themselves of their excess cholesterol. They need to send their excess cholesterol to the liver through  your HDL.

The small amount of cholesterol stored in the cell as esters is tightly regulated. Too much would cause cell death.

Ira Tabas of Columbia has focused his research on lipotoxicity. He has written papers that enumerate all the many ways excess cholesterol disrupts the cell and risks its survival. All those ways Brown and Goldstein described for regulating cholesterol in the cell should be interpreted as evolved redundant systems to prevent the buildup of excess cholesterol, and these redundant systems exists because this is a very important job. Cell lipotoxicity probably accounts for what happens when the macrophages of your immune system turn into the foam cells of your plaque.

I encourage you to seek out this article and contemplate what it means for our diet choices. These are all the ways that free cholesterol may harm the normal workings of the cell. Notice the first one, “loss of membrane fluidity.” I’ll come back to that at length in my Brown and Goldstein video.

A cholesterol confusionist may tell you about an obscure disease that causes retardation in an effort to scare you away from a diet that will protect your heart. When you hear this pitch, you should ask yourself why the confusionist has not also told you that the cholesterol in your blood cannot even get into your brain due to the blood-brain barrier. The turnover of cholesterol in your brain is very slow and your brain makes almost all the cholesterol it needs. So is a confusionist like Masterjohn trying to protect you from deformities and mental impairment? Or is he using his education to scare you, exploit your ignorance, and cause you to risk your health just to further his fringe beliefs which he adopted before he ever got his education?

Why doesn’t he tell you that excess cholesterol accumulation in fat tissue is associated with obesity and insulin resistance, and that that cholesterol in the fat gets there from the blood?

Aren’t obesity and insulin resistance very common problems caused by poor nutrition? Why not focus on those rather than something like SLOS, which you cannot possibly acquire or simulate through any kind of dietary restriction?

I think you should resist the efforts of the cholesterol confusionists to trick you into believing in false dichotomies. Yes, you need cholesterol. You have plenty of it, though, so there is no reason for you to give a second thought to whether you need to ingest more. Look at the writings of real scientists who are not trying to prop up Sally Fallon and Barry Groves at the Weston Price Foundation. Real scientists are smart. They can hold two ideas in their heads at the same time. They may say that cholesterol is necessary for life and that it shouldn’t be seen as a bad thing.

They also can say that cholesterol must be precisely regulated or else it can kill cells and cause heart disease. All this can be true at the same time. There is no reason for confusion. There is no need to spit hairs about the vitamin E content in butter or to go on and on about thyroid hormone. That is all a distraction. It’s an attempt to get you to stop thinking and stop listening to the people in cardiology and vascular biology who really know what they are talking about. The scientists I reference don’t do blogs for the Weston Price Foundation. They may not even know that the Weston Price Foundation exists. What should that tell you?

You can probably tell that I am pretty serious about getting the word out that plant-based diets offer real solutions to some of our common degenerative diseases. I am so serious about pursuing my goal of clearing away all the confusion around cholesterol, I am even willing to publicly challenge people who I really like. They say you have to crack some eggs to make an omelet. I’ll have to crack at least a couple for my discussion of dietary cholesterol and eggs, just ahead in the next video.