I wanted to repost this article, in full, as there are some points in it I really like.

Take special note of:

• How people can gain fat whilst not eating more (due to prescription drugs).
• How people who exercise all day can still be overweight (exercise is not the solution to a bad diet, as one of my friends says, ‘you can’t out train a bad diet’!).
• How the advice given to us by nutritionists for the last 40 years has mostly been wrong and dangerous (because if it really worked, we’d be healthier and thinner, and we’re not).

Over to Dr. Jonny….

Documentary “The Weight Of The Nation”

by Dr. Jonny Bowden, Nutritionist, author on The Natural Health Sherpa

This week, a new documentary about the obesity crisis premieres on HBO. It’s called “Weight of the Nation”. And it’s take-home message is wrong, wrong, wrong.

You’ll be hearing a lot about this documentary, if you haven’t already. And with good reason. It’s the result of an unprecedented collaboration between the three major public-health institutions in America:

1.   the nonprofit Institute of Medicine (IOM)
2.   the CDC (Centers of Disease Control and Prevention)
3.   the NIH (National Institutes of Health)

“Weight of the Nation” is a sincere attempt to confront an epidemic (obesity) that costs the US alone 147 billion (in 2008, up from 78.5 billion in 1998).

“Obesity, and with it, diabetes are the only major health problems that are getting worse in this country, and they’re getting worse rapidly”, said CDC Director Thomas Frieden, MD, MPH, in a July 27 media briefing during the Weight of the Nation Conference. “Beyond the economic costs are the disability, the suffering and the early deaths caused by obesity”, he added.

Yet the documentary—made by sincere and well-meaning people, mind you- draws the wrong conclusion and sends the wrong message. And it’s unlikely to make the slightest bit of difference in the obesity crisis because its focus is on the wrong enemy.

Here’s why. For decades we’ve been being told that the reason we’re so fat is that we eat too much and we exercise too little. This diagnosis is so widely accepted that to question it makes you a heretic. We’ve variously blamed high-fat foods, saturated fat, too much protein and sedentary lifestyles for this situation, but what we haven’t blamed is the real cause of the problem:

Carbohydrate intolerance and a toxic diet.

The conventional wisdom is that we were never fatter, but the truth is we were fat during the depression, when bread lines and soup kitchens dotted the nation. As Gary Taubes asks in his superb Newsweek cover article The New Obesity Campaigns Have it All Wrong, “How can we blame the obesity epidemic on gluttony and sloth if we easily find epidemics of obesity throughout the past century in populations that barely had food to survive and had to work hard to earn it?”

When you get real close to it, even the common idea that we’re fat because we don’t exercise doesn’t pass the smell test. “Why is the world full of obese individuals who exercise regularly?” asks Taubes. Indeed. The Weight of the Nation shows construction workers in Arkansas laboring at back-breaking jobs that involve running up ladders with the equivalent of a 50 pound backpack, and lifting very heavy stuff all day long. If it were all about exercise, guys like this should be svelte.

They’re not.

And if it were all about eating too many calories, how do you explain the fact that some medications have as a “side effect” weight gain of anywhere from 20-140 pounds? Did the folks who gained that weight on the meds all of a sudden start eating twice as much?

No.

The fact is that weight gain is driven by hormones, and the most important hormone for weight gain—insulin- is driven by the engine of carbohydrates. It’s not that we’re eating too many calories (though that may be a part of the problem). And it’s not that we’re not exercising— (that is a huge problem, but not just from the point of view of weight).

The problem is that we’re eating too many carbohydrates. And the ones we’re eating are all the wrong ones.

We’ve been blaming fat (especially saturated fat) for years. Our health “authorities” have been promoting for decades what one writer called “the greatest nutritional experiment in history”—a high carbohydrate low fat diet. This grain- and carb-heavy diet—very similar to what’s used to fatten cattle—was best illustrated by the god-awful, thankfully discredited USDA food pyramid of 1992. (Your tax dollars subsidize the production of the very foods that are making us fat and sick, in the form of a corporate giveaway known as the Farm Bill.)

And of course, all these wonderful foods, made from corn, sugar and wheat, are virtually “fat-free”, so surely they’re healthy, right?

But fat was never the enemy, though acting as if it were made a lot of companies a lot of money.

The real enemy was- and is—sugar.

In the 1980’s, the FDA decided- in its infinite wisdom—that sugar was perfectly OK since the evidence against it “wasn’t conclusive”. (If you think this decision wasn’t influenced by the sugar lobby, I’d like to talk to you about a lovely bridge I have for sale in beautiful Brooklyn.)

“While the government spent hundreds of millions trying to prove that salt and saturated fat are bad for our health, it spent virtually nothing on sugar”, writes Taubes. “Had it targeted sugar then…our entire food culture….might have changed”.

And maybe we might have been told that the real culprits in our diet are not  meat* and saturated fat, but the overwhelming amount of sugar and processed carbs that we consume on a daily basis, and that are increasingly being linked to diabetes, cancer, Alzheimer’s and virtually every other disease of aging.**(Note that when I say “meat” isn’t to blame, I’m talking about pasture-raised meat, not the crap we get in supermarkets and restaurants.)

Meanwhile, we have a lot of very overweight people who not only suffer with their weight, but have the added indignity of being blamed for not having any “willpower”.

“Lack of will isn’t their problem”, says Taubes. “It’s the absence of advice that might actually work.”

Thanks Jonny,

So what’s the take home message here?

It’s that the diet industry is largely broken, and is promoting information that seems not to work (for most people).

What can you do if you want to get fit, lose weight and feel great?

Well you could do far worse than start by reading this post about how to set up a diet that works for YOU

And you could always get in contact and work directly with me to sort you out. Either way, do something different!

Yours in health,

George

The link to the podcast can be found here: http://chriskresser.com/the-healthy-skeptic-podcast-episode-11 

Chris Masterjohn on Cholesterol & Heart Disease (Part 1)

Danny Roddy: This turned out to be a longer show than we anticipated. To make it easier for those of you that are time challenged, the first hour is an extensive review of the theory that cholesterol causes heart disease. If you read Chris Masterjohn’s work regularly and you’re already familiar with his material, you might wish to skip forward to the 60 minute mark where we begin to discuss the role of oxidized LDL in heart disease, living with familial hypercholesterolemia and other advanced topics.

[Music Playing]

Danny Roddy: Hello everyone and welcome to the Healthy Skeptic Podcast. My name is Danny Roddy and with me is Chris Kresser, health detective and creator of thehealthyskeptic.org, a blog challenging mainstream myths about nutrition and health. Chris, how are you doing buddy?

Chris Masterjohn: I am doing great. Yeah. There’s two Chris’s down here.

Chris Kresser: We got Chris MasterJohn on the line too. Chris why don’t you tell us how are you doing first Chris?

Chris Masterjohn: I am doing pretty well Chris. How are you doing?

Chris Kresser: Good. Good. I am eagerly awaiting, the baby at this point is I think like something like 8 weeks left, you should, my wife, looks like she swallowed a basketball in the most flattering complementary possible way. She’s radiant and beautiful and it’s pretty exciting. As the time gets closer and closer it’s, I am just getting more and more excited. We haven’t even had an ultrasound so we have no idea whether it’s going to be boy or a girl or what little being is going to come into the world and change our lives forever pretty soon.

Chris Masterjohn: You are kicking it old school.

Chris Kresser: We are kicking it old school. Evolutionary, it’s the paleo style pregnancy. So, how about you Danny?

Danny Roddy: Honestly, I just got out of school. So I am lacing it up really hard and I am not doing anything. So, nothing with me, I know.

Chris Kresser: You do some tanning on the sidewalk?

Danny Roddy: Always. Always.

Chris Kresser: We are really excited to have Chris Masterjohn here. For those of you who don’t already – for the two or three people out there who don’t know who he is. Chris is the creator and maintainer of cholesterol-and-health.com, which is a website dedicated to stowing the benefits of traditional nutrient dense cholesterol rich foods and to elucidating the many fascinating roles that cholesterol plays within the body. Cholesterol-and-health.com is also home to his excellent blog, The Daily Lipid which is a must read if you’re not already subscribed to it. Chris is a frequent contributor to Wise Traditions which is a quarterly journal of the Weston A. Price Foundation which we have talked about of course a lot on the show and he’s a regular speaker at the Annual Wise Traditions Conference and writes his second blog on the Weston A. Price Foundations website called Mother Nature Obeyed. Chris is a doctoral candidate in Nutritional Sciences at the University of Connecticut which means he’s very smart. He has authored three peer-reviewed publications including a Hypothesis on the Molecular Mechanism of Vitamin D Toxicity, published in Medical Hypotheses, a letter to the editor published and in the Journal of American College of Cardiology challenging the conclusions of a study claiming to show adverse effects of eating coconut oil which we know as a very healthy food and a letter to the editor published in the American Heart Journal arguing that drugs used to raise HDL cholesterol should not be considered safe until their potential adverse effects on Vitamin E metabolism have been studied. He’s also recently authored human study on effects of Vitamin E on sugar metabolism that’s been accepted for publication in the Journal of Nutritional Biochemistry as well as a review on non-alcoholic fatty liver disease accepted for publication in nutrition reviews. So, Chris plans on graduating with his doctorate in the summer. Congratulations Chris! It must be exciting.

Chris Masterjohn: Thank you so much. Congratulations to you. You got a lot going on to.

Chris Kresser: Yeah. Everybody’s busy with some stuff. Yeah. So today, we’re going to talk about cholesterol and this is something I’ve wanted to revisit for a long time now. Actually, it started my blog 3 or 4 years ago now with some articles about cholesterol. It’s kind of how I got in to this whole thing. I’d have to say my understanding has evolved quite a bit since I wrote those original articles and even since I recorded the videos “I have high cholesterol and I don’t care” which you can find on my site. Chris, among the other people that I would say, especially Chris, has been instrumental in the evolution of my understanding of cholesterol and so on to have him on the show so we could talk about it. The idea here is to get sort of a 21^st century view of what we know about cholesterol and especially its relationship to heart disease. There is so much misinformation out there on both sides really and we’re going to talk a little bit about that. You’ve got one group that still out there saying that high cholesterol itself is the cause of heart disease and you’ve got another group, the Cholesterol Skeptics who say that it doesn’t, cholesterol makes no difference at all, it doesn’t matter, it’s not reflective of anything in the body, and you don’t have to worry about cholesterol. Chris is going to tell us why both of those arguments are not correct. So, Chris, again, we’re excited to have you here. Thanks for coming on the show.

Chris Masterjohn: Thank you so much for having me. I am excited to be here as well.

Chris Kresser: Great! So, let’s start with a kind of 101 elementary topic but it’s one that I think still a lot of people especially in the mainstream don’t really understand which is the screwed up nomenclature that’s used to talk about cholesterol. You know, if someone goes to the doctor and they come back and they tell their wife, “I’ve got high cholesterol.” But what they’re referring to is cholesterol is not actually cholesterol is it Chris?

Chris Masterjohn: Chris, that’s a great question. So, the only way to really describe this nomenclature is screwed up or at least very confusing. So, a lot of people when they go to get their cholesterol test the day their doctor tells them your LDL is such and such, your HDL is such and such. And what they’re actually referring to by the LDL and HDL are lipoproteins, low density lipoprotein and high density lipoprotein. But, the numbers that you’re getting are not your LDL and your HDL. They’re your LDL cholesterol and your HDL cholesterol. So if the numbers that you are getting are the amount of cholesterol that’s contained within each lipoprotein. But the lipoprotein itself is not a cholesterol. It’s basically a carrier or a transporter. So, in order to understand these few things, we should really look at, what are the roles that cholesterol plays in the body and what are the roles that these lipoprotein plays. What are the roles that these lipoproteins play, excuse me. And, what we see is we get two very different answers. So, 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 the basic life and growth of a human being. But 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 behaviour. So, you can start to see that cholesterol is basically affecting everything in the body. 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 they’re born 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 at consistency of olive oil not too fluid not too stiff. It’s very important to the brain. Out brain is 2% of our body weight but it contains 25% of our cholesterol. When we go to sleep at night, our brain makes more cholesterol that’s part of why sleep is good for us. And cholesterol is the limiting factor for the formation of connections between neurons so we can learn things and remember things. Cholesterol is necessary for the production of all the steroid hormones. So those regulate our blood sugar, our mineral metabolism and all our sex hormones and it’s necessary for the production of bile acids which is necessary for digestion. And it’s, a closely related compound, 7-Dehydrocholesterol is needed for Vitamin D synthesis.

Chris Kresser: Right.

Chris Masterjohn: So, this is cholesterol. In the blood – go ahead.

Chris Kresser: Yeah. I was just going to say. It’s a shame how a few people are aware of this because the common mentality, not in the paleo world but in the mainstream world, is that the lower your cholesterol is the better. If you could just get it down to zero, you’d be in great shape.

Chris Masterjohn: Yeah. 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 am 65 than have to go through this one on a little child. 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. But, when you get your lipoproteins tested, you’re really looking at something very different. People say there’s good cholesterol and bad cholesterol. But that one cholesterol compound is the one I was just talking about that does all of those things in the body. There are different types of lipoproteins that lipoproteins carry cholesterol. They aren’t a type of cholesterol. So, in your lipoproteins, you basically make a few different kinds but they can roughly be divided into LDL and LDL-like lipoproteins and HDL. And basically, the intestines and the liver are secreting these lipoproteins in order to transport cholesterol, fats and fat soluble vitamins such as Vitamin A, D, E and K, Coenzyme Q10 and so on to the many other cells in the body and to make sure that these nutrients are reaching those cells. And in some cases, for example HDL seems to be able to have a very specific role in delivering vitamin E to the blood vessels or cholesterol to the brain in some cases. So, these are transporters and their roles are primarily in the blood. And they’re primarily playing positive roles as well by delivering these nutrients to our cells if our cells don’t get these nutrients to get all kinds of other deficiency symptoms. And it’s also possible that lipoproteins play some role in the immune system as well.

Chris Kresser: Right. So, just broadly condemning LDL is bad, is just the silliest thing, cholesterol itself is bad.

Chris 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.

Chris Kresser: Right. So as long as we’re talking about nomenclature here, let’s talk about another common misunderstanding which is conflating the diet heart and the lipid hypothesis. So, why don’t you tell us what each of those is and then we can get in to whether either both of them are true.

Chris Masterjohn: Okay. Well, most of these terminologies are unfortunate because in either case you can say, “Well, what diet? Or what lipid?” The diet heart hypothesis sounds like it’s saying, “Well, diet plays a role in heart disease.” Of course, diet plays a role in heart disease. Diet plays a role in basically every condition that’s health and disease. So, there must be some sense in which some diet heart hypothesis is true. But, to understand how these are used in science, we should at least acknowledge the use of this terminology and its historical context. And in its historical context, the diet heart hypothesis refers to the idea that saturated fat and maybe cholesterol in the diet or in some cases total fat leads to an increased level of cholesterol in the blood and that causes heart disease. This is dependent on but nevertheless distinct from the lipid hypothesis. The lipid hypothesis says that cholesterol levels in the blood regardless of what causes them to go up or down are what determines our risk for heart disease. Now, it’s incredibly important to distinguish between these two hypotheses because we really aren’t going to be able to understand the truth of their heart disease unless we are able to make the finer distinctions. And in fact, conflating these two hypotheses is what led to the condemnation of bacon, butter and eggs in 1984 when the bright Coronary Primary Prevention Trial showed that a cholesterol lowering drug reduced the risk for heart disease. And then Time Magazine came along and said, “Now, it’s proven that bacon, butter, and eggs cause heart disease.” But of course there were no bacon, butter or eggs in that trial. And if we were thinking more scientifically and able to shoot that, “No, you were testing a drug” we wouldn’t have gotten into this mess in the first place with all this ridiculous mythology about diet.

Chris Kresser: That’s the famous Time Magazine cover with the two fried eggs and the bacon frowny face, right?

Chris Masterjohn: Right.

Chris Kresser: So let’s go back to the diet heart hypothesis. The idea that eating saturated fat raises cholesterol levels in the blood –A, and B that eating saturated fat causes heart disease. So, are either of those true?

Chris Masterjohn: It depends what data set you want to look at in terms of whether saturated fat increases cholesterol level in the blood, whether saturated fat causes heart disease. There’s been several randomized controlled trials that has refuted that. So, we can say for certain that the diet heart hypothesis in that sense is not true. But whether saturated fat raises cholesterol levels, is a more nuance question to answer. So, to deal with the easy portion of the question first, we can just go back to when these hypotheses, the diet heart hypothesis first began. And that basically traces back to the 1950’s. Ancel Keys was probably, should be known as the premiere sort of founder of the diet heart hypothesis, and as I am sure most of your listeners know he had come out with this comparison between 6 countries, later expanded it into a study of 7 countries. And he plotted the dietary fat intake of these 6 countries against their incidence of heart disease and he showed that there was these very clean straight line showing this linear relationship where the more fat people in a country ate, the more heart disease they got. And of course, there were a number of problems with this initial presentation. One of them was, this is an ecological comparison which is the least reliable of any kind of observation because heart disease occurs in individuals and food intake data for a country occurs in a country. You have population that don’t get heart disease, governments don’t get them people get them. That’s the first problem. The second problem is, as most of your listeners probably already know there was data available for 22 countries and when all those countries are included, the line doesn’t look pretty clean at all in the fact that you could draw the opposite line if you wanted to cheery pick 6 different countries. But in 1967, the state of the evidence says it is, there were studies showing that if you fed the people milkshakes where the fat was taking out of the milkshake and instead filled with corn oil or something like that, you would lower their cholesterol. And if you fed them milkshakes with butter fat or coconut oil or something in them, then you would raise cholesterol. And so, some people such as Ancel Keys were arguing “Ah-ha! Here we have the evidence that people who are at risk for heart disease and they just start decreasing their saturated fat intake so they can decrease their cholesterol.”

Chris Kresser: Chris, can I ask you a question? Do you know how long those studies lasted?

Chris Masterjohn: They were in general a couple of weeks.

Chris Kresser: Right.

Chris Masterjohn: So, the majority of studies are, addressing this, are based on the idea that plasma with its – reached their plateau from the effective diet after about a couple weeks. There’s different ways of trying to splice the data on exactly how long we should be looking at and how we should look at the long-term and they can get to those in a couple of minutes.

Chris Kresser: Yeah.

Chris Masterjohn: But the American Heart Association just came back and said, “Look, you have a statistical correlation here between cholesterol and heart disease you’re claiming. That doesn’t show that anything that changes cholesterol level is going to change heart disease risk. You need to do a clinical study and show that your treatment is affecting the disease outcome.” In 1961, the American Heart Association took a totally different tune and it wasn’t because the state of the evidence has changed. It was because Ancel Keys and a few other people gone on to that committee writing the report and there’s this few other people left, they knew the political change and all of a sudden the report looked totally different and said, “Now, everyone should start decreasing their saturated fat, animal fat intake, and increasing their vegetable oil intake if they’re at risk for heart disease.” So this is basically the beginning of the diet heart hypothesis and it haven’t been even tested yet in a clinical trial until several years after the American Heart Association started making its recommendations. Well, what did those trials show when it was actually tested? Well, the first one was published in 1965 and in this study, they fed people either corn oil or olive oil supplements and told each of these groups to reduce their intake of other fats, trim their meats more, reduce their butter intake and so on. So basically what you had was a replacement of traditional animal fats that’s olive oil and corn oil. In this study, the results were not statistically significant by the end of the trial. But, they were pretty close and what they found was that corn oil treated groups had the highest incidence of cardiovascular events and the olive oil thus intermediate between the corn oil and the control group, the control group being the people who are eating their traditional animal fat, and these authors made a very sensible conclusion which was that under the circumstances of this trial and I am quoting now, “Corn oil cannot be recommended as a treatment of ischemic heart disease. It is most unlikely to be beneficial and it is probably harmful.” So, that’s a pretty good conclusion, right?

Chris Kresser: Makes sense to me. (laughs)

Chris Masterjohn: Makes sense to me too. Now, there is another group who published a trial, Woodhill and colleagues in 1978 and they had a bit a different reasoning. They basically got the same result. The more vegetable oil diet had lower survival over the course of 5 years the last trial was 2 years. And so, you and I would probably say the same thing, maybe this high vegetable oil diet is possibly harmful and certainly not beneficial. But, you want to guess what they concluded? Here’s a quote. “It is concluded that men who has had myocardial infarction are not a good choice for testing the lipid hypothesis.” So here, it’s the study that’s the problem and not the hypothesis.

Chris Kresser: Right. If the shoe doesn’t fit -

Chris Masterjohn: Right. Right. So, this is the paradigm that one beautiful hypothesis can prove an ugly fact wrong. That’s the way that they look at it. So there were a couple of other trials that were done that didn’t show any significant results. In one particular case, they planned to do a 10 year trial and they just did the trial for 5 years. They found that there were 5 deaths in a group eating corn or safflower oil and 4 deaths in the group eating peanut and coconut oil. Of course, such a small number of deaths, it’s not significant could be doing a random chance. But at that point, they decided that instead of continuing for the next five years and seeing what the difference between these two groups were, they were going to pull these groups together and compare the combined groups, the general population, so at 10 years, they never told us what the difference between the two groups was. And they just said that the people who are in their study were healthier than the people who weren’t. So, they gave themselves credit for having a study that was good for you to be enrolled in. Then the last few studies that looked at this were the two studies that were double-blind. And in once case, they only followed people for an average of a year and in the other case, they followed people for 8 years. Now, in the case where they followed people for a year, they found no difference between the group that was eating low vegetable oil and the groups that’s eating high vegetable oil. That’s surprising since it’s such a short study. But the study that is the most interesting as a test of the diet heart hypothesis is the LA Veterans Administration Hospital Study. And, this study was slightly over 8 years long and it was double-blind. And what they had were Veterans who were in-patients in a hospital and they were randomized to eat every day, every meal for over 8 years in one of two different dining halls. And of course, the people are preparing the food, collecting the data, didn’t know which dining hall was serving which, neither did the people eating there. But in one dining hall, they put the exact same food, day in day out, meal in meal out but used a mix of vegetable oils. And in the other dining hall, they cook the exact same food that used butter. So, here we have a great example of a long-term study, double-blind, highly controlled testing a single variable. Now, superficially, if our first impression from the results will be there is support for the diet heart hypothesis because in fact the group that was fed vegetable oil had statistically, significantly lower heart endpoint atherosclerotic deaths at the end of the trial. Now there are several catches to this and several reasons why this trial, if we look a little close, more closely at it, suggest that vegetable oil is probably the last thing we want to be eating long-term. The first thing is that non-cardiovascular deaths were increased statistically significantly, so that total survival was not different between the groups and if anything may have been a little bit better in the butter group.

Chris Kresser: The good old disease substitution.

Chris Masterjohn: Well, that’s what it appears to be at first. It appears to be disease substitution. But there are several more catches. The first one is that the randomization was unsuccessful in making the number of proportionate smokers the same in each group. So that the group consuming butter had 60% more moderate smokers and 20, I mean, excuse me, twice as many heavy smokers who are smoking more than two packs of cigarettes per day.

Chris Kresser: Not so good for your heart. (laughs)

Chris Masterjohn: Right. Smoking is bad for your heart. So right away, we’re not sure whether it was the butter leading to the increased cardiovascular death or the smoking. But we can perhaps say that maybe butter’s protecting against the effects of smoking on non-cardiovascular deaths. Now, the other point was, if you look at another paper they published about how they did this diet, it appears that they took special precautions not to refry the vegetable oils because they consider them delicate. But it appears that they did not take this precaution with the butter. As a result, the amount of Vitamin E, in the butter was about one third or even less actually, than you expect it to be. So ordinarily, you’d expect butter to have about three quarters of a milligram of Vitamin E for every gram of polyunsaturated fatty acid. And in this case, you had less than a fifth of a milligram. So, you have less than a third of what you would expect to be there. Now, good butter can range in fact between .5 if it’s not grass fed to 1.3 if its grass fed on good grass. So basically what we have is a diet where they cook the heck out of the butter and maybe it was really bad butter to begin with and we’re feeding them a Vitamin E deficient diet. So, now what we see is maybe butter is protecting against the effect of Vitamin E deficiency and smoking on non-cardiovascular deaths. And at best about cardiovascular deaths we can say, we’re not really sure if it’s the butter, the smoking or the Vitamin E deficiency that increases risks.

Chris Kresser: And it even did that, even recycled butter did it.

Chris Masterjohn: Right.

Chris Kresser: Three times.

Chris Masterjohn: Now, here’s the final catch that makes this study really scary. If you look at the survival curve for non-cardiovascular deaths, it looks roughly equal for the first seven years of the study. So this decrease that you get begins occurring at seven years and non-cardiovascular survival starts basically falling off a cliff between years 7 and 8, and continues falling off a cliff in those, the last at points greater than 8 years, that was really about 3 or 4 months. So in the last 3 or 4 months you get even greater fallen survival compared to what you had in the preceding year before that. You can imagine that survival would be abysmal if this study were carried on for 9 or 10 years if you look at this graph. So, what these authors were scared about was, it’s possible that when you consume vegetable oils for 7 or 8 or 9 years, it’s only then that you start to see increases in cancer and other deaths. So, what they suggested was, in the future, we have a very difficult question to address, maybe when we do these trials, we should consider anything less than 5 years completely inadequate and consider that these trials have to put at least 8 years. But instead of making longer trials, they sweep the issue under the rug, stopped doing these types of trials. And that’s the last one of its kind. So what we’re left with is the diet heart hypothesis is on the hole completely fails to in diet saturated fat in handling heart disease and seems to hint that over the course of 7, 8, 9 years consuming vegetable oils increases the risk of cancer and may increase the risk of all kinds of adverse effects that we didn’t anticipate.

Chris Kresser: Well, I am sure Dean Harris will be very upset to hear that.

Chris Masterjohn: I am sure he will after he takes a look at these studies.

Chris Kresser: Well, this brings up a few points. Number one, you can’t just read the abstract because obviously when you do that, you’re depending on the author’s interpretation of the study which as we’ve seen is not reliable. And you missed seeing all of the juicy tidbits that you just elucidated for us that you get by reading the full text.

Chris Masterjohn: Right. In this case, you have to read figure 14 if you want to see that the depths were increasing after several years. This is a really big paper. You need to read the whole thing and look at all the graphs if you want to make some sense out of it.

Chris Kresser: Right. So this is why we need folks like you and Stephan and others out there doing that hard work. This is one this like don’t try this at home type of a thing. (laughs)

Chris Masterjohn: Absolutely.

Chris Kresser: So I want to mention an article, I am not sure you saw it back in January that Stephan published it’s called “Does dietary saturated fat increase blood cholesterol? An informal review of observational studies.” Basically, what he argued in that article by reviewing the studies was that “Yes, dietary saturated fat does increase cholesterol in the blood but only short-term. And then if you look at longer term studies, there isn’t really a significant effect.” What do you think about that?

Chris Masterjohn: Well, first, I just want to say that I love Stephan’s blog and out of all the research science based blogs that I’ve read, Stephan’s is definitely my favourite. I did read that blog post and I agree up to a certain extent, I think it’s slightly more nuance than that. So, in the epidemiological study, I should say, just to begin with, we have this sort of conundrum when, it’s kind of a philosophical conundrum when we’re looking at what types of studies do we look at and how do we interpret them. I like to compare this to the uncertainty principle in chemistry or physics where if you try to look at an electron’s location, you don’t really know anything about its velocity. And if you try to look at its velocity, you don’t know anything about its location. I might be screwing that up a little bit maybe its momentum. In any case, we have a similar thing when we’re trying to look at observational studies and trials. In the observational studies, you have a real world context. But you have no idea what the cause and effect pattern is. You can’t attribute anything to an effect to a specific cause when you’re just looking at statistical correlations and observational data. On the other hand, you can be absolutely certain that your results apply to the real world because you’re looking at them in the real world. On the other hand, if you’re looking at randomized controlled trials, you get to the point where you can come very close to certainty about cause and effect but then you have no idea that translates outside of the laboratory into the real world situation.  So, what we need to always do is try to splice the data as many ways as we can and try to fit the data together and look at the big picture. I think what Stephan did is a really important step in viewing that. So, what we can see from these epidemiological studies is a high saturated fat diet does not seem to be associated with increased cholesterol levels. So, one of the differences is that we’re looking at people eating this long-term. But the other difference is that, if you look at a high saturated fat diet, you have a mix of whole foods that have tons other things in them. So, you can be eating more saturated fat because you are eating more meat. You can be eating more saturated fats because you are eating more coconuts. You can be eating more saturated fats because you are eating more, some kind of cake from, some kind of junk food from Starbucks that was made with some saturated fat. So there’s lots of different foods that have saturated fat in them and the things that they are associated with such as the Vitamins and minerals and the proteins in meat or the specific types of fatty acids in coconut or the junk food in some of this junk food products, may have very different effects on cholesterol. In the randomized controlled trials, what we’re usually seeing is the effect of a specific fatty acid or a specific fat, take those milkshake studies, they took the fat out of the milkshake and they put the corn oil in. So, you’re seeing the effects of the fat but the food is staying the same.

Chris Kresser: Right.

Chris Masterjohn: So, I think what Stephan’s post is showing is that over the long term, diets of whole foods rich in saturated fatty acids, together with whatever other compounding variables that we might not be able to identify, don’t seem to have an association with cholesterol levels. But if we look at this trial that I was just talking about, The LA Veterans Administration Hospital Study, we see something a little bit different. What we see is over the course of 8 years, there is still an effect of cholesterol when the only thing that they were changing was the fat in the diet. These people weren’t eating more or less meat or protein they were only eating butter versus vegetable oils. And the saturated fat group didn’t have higher cholesterol levels. I will say one caveat which is that it’s there’s a hint that maybe at the end of the study when we start to see these differences in non-cardiovascular survival, we might be seeing a levelling off of the difference between the two groups. So what I am saying now is I think that saturated fat by itself, isolated from the rest of the dietary context, probably does increase cholesterol levels. But there is, I’ll leave it as an open question that it’s possible that it’s not the case over the very long term.

Chris Kresser: Okay. Well, that’s a perfect segway into the next phase of this which is, okay, let’s say saturated fat does raise cholesterol levels in the blood or let’s say we have high cholesterol levels in the blood for some other reason. This lipid hypothesis that high cholesterol levels in the blood cause heart disease, let’s get in to this.

Chris Masterjohn: Alright. So, the lipid hypothesis, in terms of its name, dates back to around the 1970’s or so and Daniel Steinberg who was the head of the Coronary Primary Prevention Trial and the NIH consensus conference that Time Magazine was citing when it came out with that article with the frowning bacon face, he was probably the first person to use it in print. But it was probably, it seems to be Pete Ahrens, a couple of years later, who was the first person to popularize the term lipid hypothesis. What they both meant was the same thing that increasing cholesterol levels in the blood or decreasing them could alter the risk of heart disease. Now, Pete Ahrens, if you read the article that he originally wrote, he seemed like a very open-minded scientist who was hopeful about the lipid hypothesis but wanted to see it tested. But, you’ll often see him cited as a cholesterol skeptic because he remained very sceptical about this connection between saturated fat in the diet and the heart disease risk. If you read his original article, you can see why. He said, “Look, we’re testing the lipid hypothesis but we need to test it in different populations and we need to test it in different ways.” So, we can test it with a drug but if the drug is effective it doesn’t mean that food will be or vice-versa. If food is effective it doesn’t mean the drug will be. So we need to, he was basically saying that, what I was just saying, that we always need to splice the data in as many ways as we can, look at it from as many angles as we can. But historically, the origin of the lipid hypothesis traces back to the cholesterol-fed rabbit. And this was back to the days of Nikolai Anichkov around the turn of the 20^th century in 1913. And, Anichkov’s cholesterol-fed rabbit is often dismissed by what we can call cholesterol skeptics as irrelevant to humans because it’s a rabbit. I think there’s another case of mistaking diet heart hypothesis for lipid hypothesis. If you read Anichkov’s work, he never, ever, ever said that here’s feeding cholesterol to rabbits and producing heart disease indicated it in any way that feeding human’s cholesterol would cause cholesterol in humans. Anichkov was looking at a metabolic model of hypercholesterolemia and what Anichkov found was that if you increase the level of cholesterol in the blood of the rabbit greatly in this case by feeding dietary cholesterol, you could induce atherosclerosis in the rabbit. Now, it’s true that the rabbit is probably not the best model for human disease. But the cholesterol-fed rabbit model is incredibly useful for several reasons. And one is that so many other hypotheses had been tested in the rabbit leading up to Anichkov’s experiment and they all failed miserably. So, in these experiments, they injected rabbits with bacteria, all kinds of bacterial toxins, heavy metals, chemical toxins, plant toxins, hormones. They increased blood pressure by hanging the rabbits upside down by their feet, constricting the aortas. They gave physical injuries to the arteries by cauterizing them with steel wire by damaging them with silver nitrate, all kinds of things that they did to these rabbits. And, some of these treatments, many of them in fact, induced some arterial injury. But none of them induced anything that looked like human atherosclerosis. When Anichkov fed cholesterol to the rabbits, what he produced was something that looked very much like human atherosclerosis. Yes, there are differences that you can point out in the model. But this was the first and only thing in rabbits that produced something that looks like human atherosclerosis.

Now, one of the reason that we can increase our confidence that this is a valuable model is because subsequently, it was shown that you could use, if you could induce hypercholesterolemia in an animal, now I am calling it hypercholesterolemia just for now because this is what Anichkov thought he was inducing, and this is what most people think, who are researching this field think they’re inducing but we’ll get to the nuances later. If you can induce hypercholesterolemia in the baboon, you can induce atherosclerosis. In fact, you can do it in a cat, you can do it in a chicken, you can do it in a chimpanzee, a dog, a goat, a guinea pig, a hamster, a monkey, a mouse, a parrot, a pig, a pigeon, a rabbit, a rat. You can do this in any of these animal models as long, not necessarily by feeding cholesterol, but as long as you find some way to induce hypercholesterolemia, you can induce atherosclerosis in these animal models. Now, the generalizability to all these different animals regardless of their metabolic types, their dietary types seems to suggest that there is something in this model that’s generalizable to humans. Now, one of the reasons why we should pay close attention to the rabbit though, I’ll admit right off the bat, if you want to test a hypothesis like this in an animal that, it should probably a guinea pig because guinea pigs has the closest similarity to human lipoprotein metabolism and Vitamin C metabolism and some other things. But the reason the rabbit is useful is because if so many things were tested in the rabbit that Anichkov was able to develop a very complex concept of the multi-sectorial nature of heart disease just based on research in the rabbit that prior to 1930 or so. And this is what he said. He said that, “If you want to induce atherosclerosis you need to have hypercholesterolemia.” But, there were many other factors that will alter how bad the atherosclerosis is and exactly how it progresses besides the hypercholesterolemia. So he said for example that blood pressure would aggravate it. Inflammation he said would aggravate it. In section in toxins he said would aggravate it. Thyroid hormones, he said, would protect against it. Sex hormones would protect against it. Iodine would protect against it. All these different factors and there are more. If you read what Anichkov wrote, he had a very complex view of heart disease, and he identified all these that we still talk about now even in the cholesterol sKeptics field. Anichkov was talking about them back in 1920’s and 30’s because of the cholesterol-fed rabbit model. So that’s the key thing why I think we really need to pay attention to this model. Now, here’s the other thing. Anichkov actually proved the idea false that cholesterol causes heart disease. Now you say, “Whoa, wait a minute, I thought we were just saying Anichkov proved cholesterol does cause heart disease.” Well, in fact, that in fact he proved something much more a nuance than that. So here was the deal. If he fed the rabbits cholesterol, they would get atherosclerosis. But if he injected them with cholesterol, they would not get atherosclerosis. So, I mean, what’s the first thing that occurs in, either of you guys want to answer this, “What’s the first thing that occurs in your mind there if injecting cholesterol doesn’t have the effect?”

Danny Roddy: Chris, I’ll let you handle that one.

Chris Masterjohn: Okay.

Chris Kresser: It must have something to do with the metabolism of cholesterol from food.

Chris Masterjohn: Yeah, exactly. There’s something about the metabolism and it’s not just about the cholesterol. So when you eat cholesterol, it gets packaged into lipoproteins and they get secreted into your blood. If you inject cholesterol into the bloodstream there’s no lipoproteins, it’s just cholesterol.  So, it’s not the cholesterol in the blood that’s causing the heart disease, Anichkov proved this in the cholesterol-fed rabbit model way back in the 1920’s and 30’s. So this is an amazing fact that the people who support the lipid hypothesis as it’s called tend to ignore. Now, if they took the blood from the cholesterol fed rabbit, isolated the lipoproteins and injected the lipoproteins into rabbits, then the rabbits would get atherosclerosis. So, here we see this goes back to the distinction you wanted to make at the very beginning of our interview. We need to distinguish between cholesterol and lipoproteins.

Danny Roddy: Right.

Chris Masterjohn: Now, what does the lipoprotein looks like? Well, it’s kind, I am going to simplify, it’s like a round ball. It’s carrying some fats and cholesterol and some nutrients, and it has a membrane that are made up of certain types of lipids called phospholipids that basically help it be transported in the water soluble environment of the blood. And those phospholipids are rich in all different kinds of fatty acids including polyunsaturated fatty acids. And of course there’s also an important set of proteins in the membrane that are responsible for directing that lipoprotein to go where it’s supposed to go. As it turns out from the molecular biology that we’ve developed over the course of the years, what happens in the lipoprotein particle, in order to cause atherosclerosis, is the polyunsaturated fatty acids in the membrane of the lipoprotein particle are oxidizing. And this is basically means molecular degeneration, the molecules are falling apart. And once they oxidize, they become toxic. And in order to protect the blood vessels from these toxic degenerated lipids, the immune system comes along and forms an atherosclerotic plaque, that’s basically a protective mechanism. But overtime, if you get accumulation of these toxic lipids, you get inflammation other sources of oxidative stress, this plaques falls apart causes a clot and this is what ultimately leads to a clot in the blood.

Chris Kresser: Okay. Chris, let me just stop you and recap a little bit for the folks out there that might be getting a little bit lost. So, we’ve known actually for quite a long time that cholesterol plays a role in heart disease. That’s the infiltration theory that Anichkov mention. But we also know that it’s not the sole player and that there are several other factors that determine whether an elevated level of cholesterol in the blood will cause heart disease and that’s the combination theory. And one of the things that determines that is whether the LDL particle or more specifically the polyunsaturated fat in the membrane of the LDL particle oxidizes.

Chris Masterjohn: This is exactly right. Let’s break it down this way. Anichkov thought what he was discovering was that atherosclerosis was not a disease of degeneration it was a disease of infiltration. That meant, it wasn’t that anything was going wrong and falling apart and breaking down, it was that there was too much cholesterol in the blood. However, the injection studies we talked about showed that it wasn’t too much cholesterol. It was, in Anichkov’s view, too much lipoprotein. What Anichkov got wrong was he didn’t realize that it wasn’t the abundance of lipoproteins in the blood, but in fact it was the degeneration of the lipoproteins in the blood. So, when it comes down to it, what we wind up with, if we want to have a proper understanding of what happens, is that, “Yes, lipids are involved.” So, we shouldn’t distinguish between a lipid hypothesis and a non-lipid hypothesis, lipids are involved. What we need to distinguish is between the infiltrative idea that it’s just too much lipid. And the degenerative idea that it’s about those lipids breaking down. So once we realize that it’s about the degeneration of these lipids, then we can start to understand what are the metabolic factors that affect the degeneration of lipids and how do we move beyond our understanding of the amount of cholesterol in the blood to how do we protect these lipoproteins from degeneration. That’s what we need

Chris Kresser: Exactly. And that is what I spend the rest of the show talking about and what’s going to surprise a lot of people I think are the things that protect against that oxidative damage or that breakdown of the lipoproteins are in some cases exactly the opposite of what we’ve been told to do to prevent heart disease. The interesting thing about this Chris and Danny is that we still often hear people say, “God, you’re eating all that bacon, you’re going to clog your artery.” Which is this sort of, it sounds like the infiltrative theory like if you eat cholesterol that that’s just going to, like your arteries are like pipes and the cholesterol is just going to accumulate in there like junk in a pipe and then the bud won’t be able to move through it

Chris Masterjohn: That’s exactly the problem with the conventional theory as we know it today. In fact, that’s another beautiful thing about Anichkov’s work was, he showed way back in the day that arteries were nothing like pipes and in fact this was an inflammatory process and everything we understand about inflammation today, Anichkov showed at the cholesterol-fed rabbit model way back in the day. But arteries are nothing like pipes. You don’t have anything clogging anything up. You have this active process of the immune system trying to protect the blood vessels. In any case, the serious problem with the idea that eating saturated fat is going to make your arteries clog up from too much lipid is, regardless of what the long-term effect of saturated fat is on cholesterol levels maybe it increase or maybe it doesn’t, I think it probably does long term. Regardless of that, saturated fat can actually help protect against oxidative stress because saturated fats are not vulnerable to oxidative degeneration. It’s the polyunsaturated fats that are very delicate. They are not dead and they are not toxic but they are very delicate. I like to think of them like glass. If you have, if you use glass for a lot of things because it would be useful, when you drink water you use a glass, right? But if all you had around your house was tons of glasses that you weren’t using and all kinds of things made out of glass and they were piling up on the counter and they were all over the floor. You are probably, at some point, going to break a lot of them just because you have an over abundance of really delicate things. That’s the thing with polyunsaturated fatty acids. When you have an over abundance of this very delicate fatty acids, they are very vulnerable to oxidation and that will promote oxidative stress. So, what we really want to understand about fats is that saturated and mono unsaturated fat are the ones that are thoroughly stable and therefore they’re protective. And polyunsaturated fats are the risky ones, they’re delicate.

Chris Kresser: Right, which of course were the ones that were being promoted as heart healthy for so many years by the American Heart Association.

Chris Masterjohn: Exactly! When Time Magazine came out in 1984 with that sad bacon and eggs face article, they said basically that the American Heart Association is finally proved right when it was telling people 23 years ago to get rid of the animal fat in their diet and start eating corn oil. So, it was that same year that it was shown that what’s causing atherosclerosis in the LDL particles is the oxidation of these delicate polyunsaturated fatty acids in the membranes. So, Time Magazine probably should have made a retraction and said, “Hey, wait the second, these vegetable oils might be making the LDL particle much more vulnerable to oxidative degeneration.” But they never made that retraction.

Chris Kresser: Ops! Sorry about that. Let’s talk about another risk factor for oxidized LDL which is the particle size of LDL because a lot of people are aware now in this Paleo, Primal, Weston A. Price world that not all LDL is created equal so to speak. And that you’ve got two, at the extremes, two different types of LDL, you have large buoyant or sometimes called large fluffy LDL and then you’ve got small dense LDL. And that small dense LDL is more likely to become oxidized and that’s one of the reason it’s problematic. So, can you tell us a little bit about that?

Chris Masterjohn: Yeah. Okay. I am going to give you my take on this and I think in this case I am probably going to ruffle a few feathers here.

Chris Kresser: Alright.

Chris Masterjohn: Before that, let me just give a very basic and simple primer on what I think are the main factors contributing to oxidation. So, we’re concerned with the oxidation of the LDL particles. There are basically 3 factors here or actually let’s say 4. One is the vulnerability, the basic vulnerability of the LDL particle and that’s how many delicate fatty acids at the cabinets that are vulnerable to oxidation. The second thing is antioxidants. So when the liver sends this lipoprotein out into the blood, it packages it with antioxidants that will protect against the LDL particle. The third thing is oxidants. Once the LDL particle’s in the blood, the LDL particle and so on, these lipoproteins are facing oxidants in the blood that are produced from poor metabolism, toxins, inflammation and so on. And, those oxidants will eventually deplete the antioxidants and then the oxidation fuse. But, what causes the, what causes the final outcome of this interaction between antioxidants and oxidants to lead to atherosclerosis. Well, that missing factor is time, okay? So, if you take out, say you have some high vitamin cod liver oil in your refrigerator, you take it our every so often, you take your half teaspoon or whatever and you put it back in. What would happen if you took out that high vitamin cod liver oil and left it on the counter with cap open for 3 weeks?

Chris Kresser: Oxidative damage.

Chris Masterjohn: Right. And what’s the key factor there? It’s time, the time that it’s exposed to the oxidants. So, we know from genetic studies and from metabolism that the amount of time that the LDL particles spends in the blood is a major determinant of atherosclerosis risk and that the amount of time its spends in the blood is primarily dependant on LDL receptor activity which is LDL receptor is what takes the LDL particle into the cell, delivers those nutrients to where they want to go. Okay. We know that people who have genetic defects in the LDL receptor have dramatically increased risk of heart disease, people with genetic defects that increase the activity of this receptor have dramatically reduced risk for heart disease. So we have all this evidence that the amount of time that the LDL particle hangs out in the blood is going to be a main determinant of heart disease risk. Now, it is in this context that I try to interpret what do the markers that are associated with the risk of dying of heart disease mean, okay? So, two of those markers are the total to HDL cholesterol ratio and the LDL particle size.

Chris Kresser: Right.

Chris Masterjohn: Okay. What happens to these two markers when the LDL particle spends too long of a time in the blood because of poor LDL receptor activity. Well, one of the things that happens is that LDL particle is exposed to a number of enzymes that take out the triglycerides or fats from the particle and takes those fats up into the cell. What does this do to the LDL particle?

Chris Kresser: Makes it smaller I imagine.

Chris Masterjohn: What’s that?

Chris Kresser: I imagine it makes it smaller.

Chris Masterjohn: Yeah. It makes it smaller and it makes it denser because cholesterol is smaller and denser than triglycerides. So if you take out the triglycerides and leave the cholesterol behind, the LDL particle gets smaller and denser. Okay. The second thing that happens is, as we already talked about, the LDL particle starts to oxidize. When the polyunsaturated fatty acids in the LDL membrane oxidize, they get cleave off from the membrane and they get transferred on to lipoprotein A or LP little a. And when that happens, the LDL particle gets smaller and denser. Now, what’s the other thing that happens? The other thing that happens is LDL and HDL interact with one another so that triglycerides are transferred from LDL to HDL and cholesterol is transferred from HDL to LDL. This makes the LDL particle smaller and denser. What else does it do? It increases the amount of cholesterol in the LDL particle and it decreases the amount of cholesterol in the HDL particle. So as far as I am concerned, all of these markers such as the total to HDL cholesterol ratio or the LDL particle size can simply be seen as markers for poor LDL receptor activity and the LDL particle spending too long of a time in the blood. But they are not, in my view, the cause of atherosclerosis. It’s the oxidative degeneration that also takes place when LDL receptor activity is poor and the LDL particle spends too long of a time in the blood. So, I think it’s a great mistake to try to say whatever changes the total to HDL cholesterol ratio into a more favourable ratio is a good thing. And I think it’s likewise a mistake to say whatever changes LDL particle size to make it larger and fluffier is a good thing. Now, this does not exclude the possibility that the total to HDL cholesterol ratio or the lipoprotein particle size play a causal role in atherosclerosis. There are theories for both of these. For example in the case of the ratio people say, “It’s about reverse cholesterol transport. You want the HDL to carry the cholesterol out of the plaque and back to the liver.”

Chris Kresser: Right.

Chris Masterjohn: My problem with this type of reasoning is the one test of this hypothesis in humans is with the cholesterylester transfer protein inhibitor, a CETP inhibitor torcetrapib and it kills people left and right.

Chris Kresser: Huge failure.

Chris Masterjohn: That is what is known in the research world as an epic fail. There’s an old aphorism that can describe that trial which is the experiment was a success but the patient died, maybe because it was a success. The drug effectively increases the amount of cholesterol in HDL and effectively decreases the amount of cholesterol in LDL.

Chris Kresser: Right.

Chris Masterjohn: It was a success but the patient died, okay? Now, my question is, “Why should we apply the exact same logic to LDL particle size and assume that everything that affects LDL particle size and the so-called favourable fashion is going to have a positive outcome?” I don’t think we should. Nevertheless, there’s a hypothesis that LDL, small dense LDL is more likely to fit through the imbecillum to get through the lining of the blood vessel and to get into the area where you produce atherosclerotic plaque chemicals and where it’s oxidize. I am very sceptical about this oxidation thing simply because when you take out small dense LDL from someone’s blood, the evidence shows that it already is partially oxidized. Well jeeh! Why would that be? Because when LDL spends too long of a time in the blood, it oxidizes and gets small and dense. So, I don’t see any good reason to move beyond trying to increase LDL receptor activity and protect LDL from oxidation.

Chris Kresser: Right.

Chris Masterjohn: I will say this just to get it out there for fairness’s sake. Eating cholesterol improves LDL particle size and decreasing carbohydrate intake improves LDL particle size. And this is because, apparently, when VLDL is secreted with more cholesterol and less triglycerides, it’s ultimately metabolized to large, fluffy pattern A LDL instead of small dense pattern B LDL. So, eating cholesterol and reducing carbohydrate does improve that. I just don’t think it’s a good idea to make assumptions based on these surrogate markers for health outcomes.

Chris Kresser: Right. So, the name of the game, according to our current understanding, is to support healthy LDL receptor site function and lessen the amount of time that LDL’s floating around in the blood. And to reduce the chance that LDL will oxidize which is related to that first goal.

Chris Masterjohn: Right.

Chris Kresser: So, you mentioned in one of your articles, LDL doesn’t, there are no specific antioxidants that we can take to specifically prevent that. So, two questions, and the second question will kind of lead us in to the next topic that I want to talk about. But, is there a way for people to improve their LDL receptor function? And what are some of the main things outside of diet and what we’ve been talking about so far that regulate LDL receptor function.

Chris Masterjohn: Okay. So, here’s the basic big picture. The LDL receptor is expressed on many cells and plays a role in taking up LDL particles into many tissues. This includes the adrenals and the sex organs to produce the adrenal steroid hormones and sex hormones. So, LDL receptor activity’s a good thing. But, quantitatively, meaning, the sheer amount of cholesterol that’s converting into bile acids is much greater than the amount of cholesterol that’s converted into these other hormones. Consequently, the liver which is responsible for making those bile acids is the main site where the LDL receptor is expressed. This is how the liver contributes to blood cholesterol levels. It’s not by the amount of cholesterol it makes. All of your cells are making cholesterol. The liver doesn’t make, the liver mostly makes cholesterol for itself not for the whole body for the most part. But the main way the liver regulates blood cholesterol levels is by expressing the LDL receptor, making bile acids and excreting those bile acids into the intestines. Now, if you think of this, pretend you are a liver cell and to think to yourself, “How much LDL receptor am I going to make? How much LDL am I going to take into the blood at any given moment?” Your two concerns are basically how much cholesterol you have on hand, it’s kind of like managing your finances, you want to have a stable amount of money for your basic expenses before you determine how much you save or how much you spend. So, it’s concerned for itself that it has its basic needs met for cholesterol and then it’s concerned for the rest of the body, okay? This is true also of the sex organs and the adrenal glands too. The LDL receptor is going to respond to the needs of the body as well as to the needs of that cell. Now, the needs of the body are primarily communicated by thyroid hormone. And above thyroid hormone, you seem to have Leptin. So, basically what’s going on is Leptin is communicating the master governing signal about whether we are in a state of abundance or not. So, what are you going to do when you have plenty of nutritious and satisfying and calorically dense food available? Well, you are going to eat until you are stuffed. You are going to do what your new wife has been doing and make some babies, right? So, Leptin is basically communicating to the body that it’s time to get your groove on, to do what humans are biologically designed to do, to reproduce. That’s the signal that we are in abundance. It is time for virility and for fertility, okay? Now, one of, so, in this scenario, Leptin is kind of like the Chief Executive Officer. Now, I know there’s things that control Leptin. But in terms of communicating this abundant signal, Leptin is like the CEO of a company or the commander in chief of the armed forces here. Thyroid hormone is like a general, okay? So, thyroid hormone is under the hierarchy of Leptin but it is the main signal that’s communicating this back to that times are abundant, it is time to ramp up our energy, our virility, our fertility, time to reproduce and do all of these great things. Now, you can see this pattern of communication if you just look at the LDL receptor gene, it has two regulatory elements in it, two pieces of DNA that are made, not for producing the receptor but for communicating the needs of the cell in the body. One of those is communicate the level of cholesterol in the cell. The other is down by thyroid hormone and its receptor. So you can see right there. When the cell needs more cholesterol or when the body is telling the liver and telling the sex cells and telling the adrenal cells that life is abundant, things are abundant. This is when we get LDL receptor activity ramped up. So, what does this say about the primary problems of LDL receptor activity in our society? Well, it’s not genetics. You can have genetic defects in this. That’s where you get familial hypercholesterolemia.

Chris Kresser: Right.

Chris Masterjohn: But, we know that we have an epidemic of Leptin resistance because it appears that obesity is very intimately tied to Leptin resistance. And we can presume that this Leptin resistance is basically a failure of the body to communicate this signal that there is abundance. So all we have is this epidemic where we have abundance but that signal is not getting where it needs to go. There’s fund of miscommunication in the body. I think that’s a major role in LDL receptor activity.

Chris Kresser: Right. That sheds a really different way of looking at this whole high cholesterol problem, I mean, Leptin resistance or problems with Leptin signalling and thyroid issues are probably one of the last things that people think about and some people don’t think about them at all including a lot of health care practitioners. So, speaking of the LDL receptor, let’s talk a little bit about familial hypercholesterolemia because you wrote a great article about that awhile back that I think is a really useful way of looking at some of these problems. I think we have a question from a reader Danny. Maybe we could use that as a springboard to talk about it.

Danny Roddy: Yeah, definitely. This one’s from Hooray for Butter which is a fantastic single. What are Chris Masterjohn’s thoughts in living and thriving with familial hypercholesterolemia? Is there an alternative treatment besides statins? Is treatment necessary if you maintain a strict diet, fitness and reduce stress? Is the VLDL number and percentages more important? I currently have a 4/15 LDL, 85 HDL, feel great and getting stronger every month. I am in my late 40’s, my VAP test show a very low count on VLDL with 95% large and fluffy LDL. As per our conversation over the past couple of months, there doesn’t seem to be any easy answers. Thank you. What do you guys think?

Chris Masterjohn: Alright. So, first of all, is this person’s name is Hooray for Butter? I think I might be related to that person, we should probably get in touch. He might be a third cousin or something. In any case, so here is the question, so how do you deal with familial hypercholesterolemia? And I’ll be the first person to say that I don’t have the answers. I have some ideas. I love to share them. But most of these ideas are things that need to be worked out in the field under supervision in order to keep an eye on the person’s health and ultimately what we need is studies on this because in the mainstream medical profession, they’re still hung up on the idea that it is the amount of cholesterol in the blood. So, all of the therapy is based on reducing it and the therapy does seem to have some benefit, especially in the extreme cases of people who have to copies of this defective gene, they need to get a liver transplants or in some cases they just take their blood out, take the LDL particles and put the blood back. And this can extend their life somewhat.

Chris Kresser: Right.

Chris Masterjohn: But of course what they’re doing is taking out all the oxidized LDL because the LDL is oxidizing. So here’s the deal. You can reduce a person’s expression of this clinical phenomenon in a couple of ways. One of them is by giving them statins. I am telling you right now, I am not a big fan of statins. But the statins will increase the LDL receptor activity in the liver by inducing a local cholesterol deficiency in the liver cell and that can have a positive benefit in this particular disease but it can also have some very nasty side effects that I am sure you are well aware. The other thing that really needs some attention and I want to emphasize that this needs very close supervision if it’s to be experimented with. Thyroid hormone will increase LDL receptor activity in someone with heterozygous familial hypercholesterolemia, meaning someone with one copy of the defective gene, regardless of whether they are hypothyroid or not, because they have one copy of the defective gene, that means they have one copy of the good gene. And that good gene is responsive to thyroid hormone. Now, there were some experiments back in the beginning of the 20^th century where they showed that you could normalize someone’s cholesterol level regardless of, whether they are hypothyroid, in fact, that’s the diagnosis back then, they’re so imprecise because they weren’t able to measure thyroid hormone and antibodies and so on. So, they showed that you could use small doses of thyroid hormones titrating up from a very small dose, beginning I think with a quarter grain and working up to a maximum of two grains of hormone thyroid if I remember correctly. I’ll put the exact numbers on my blog at some point. You could give these very small doses and you could normalize cholesterol levels with no side effects. Then some overzealous people went off giving out huge doses of thyroid hormone and killed some people and this was completely abandoned. The only hint of it coming back was in the lipid hypothesis era back in the 60’s and 70’s. In that time period, they tried using this synthetic, fake form of thyroid hormone, not the one that you treat hypothyroidism but this isomer that was very different that lowered cholesterol but it didn’t have some of the other effects and that had negative effects too. So, I think that what we need, one thing that we need, some very cautious experimentation with at the clinical level, is people using very low doses of thyroid hormone to see if this is a safe and effective way to treat it.

Chris Kresser: What about the idea of using iodine to up-regulate thyroid function instead of thyroid hormone?

Chris Masterjohn: That’s another thing that you could do. And in fact, they did that back in the cholesterol-fed rabbit they did that. They used iodine and then had the same effect of thyroid which was just to prevent the atherosclerosis and there’s some anecdotal evidence for that like David Brownstein uses high dose iodine and he says that it’s greatly reduced the number of people he has to put on thyroid hormones. There are other people, as I know you know, who say iodine can have negative effects on the thyroid. So again, this is something that needs close and supervised study. It’s not something, I don’t want to tell people to go out by themselves and get thyroid hormones from Mexico under the counter or 100 milligrams of iodine and start eating bottles of it. I do not want to advocate that.

Chris Kresser: Yes. Please don’t.

Chris Masterjohn: Right.

Chris Kresser: I just want to throw in one more thing Chris. For people who are listening to this at regarding iodine and its relationship to autoimmune thyroid disease and it’s potential for causing flare-ups. There is a great series going on at Paul Jaminet’s blog right on Perfect Health Diet by a guy named Mario, I can’t remember his last name. But he’s arguing that, actually, iodine is only harmful in or only provokes a flare-up or damages the thyroid in the absence of sufficient selenium. And he’s written a couple articles about it and there’s some interesting studies there that link to. So if anyone’s interested they should head over there and check that out.

Chris Masterjohn: Yeah. That’s a pretty logical thing and in general I think that’s true with a lot of different nutrients. They’re harmful and you take one, when you have adequate, when you reinforce with the diet adequately and the whole balance of factors that promote health.

Chris Kresser: Right. I just wanted to mention that because I know that no matter how many times we say don’t do this at home, for sure, people are going to try to do it at home.

Danny Roddy: If they do it, at least do it right.

Chris Masterjohn: Yeah. Yeah. Exactly. But here’s the thing. Here’s what I think people can do at home. Now, you have a great point that you should focus on your weakest link. But you can make a counter point to that. In certain cases like this one, where your weakest link is the thing that you can do the least about, there is no totally safe, totally effective way to normalize LDL receptor activity in these folks. So, what we can do is try to improve the things that we can most impact. And that’s the oxidation of the LDL particle to some degree but to an even larger degree, it’s preventing the inflammation and pro-quadding environment that comes downstream from the formation of the atherosclerotic lesion. Anichkov’s rabbits didn’t get heart attacks. Why not? Because these plaques were stable, they never fell apart, caused clots that blocked coronary arteries. You see this across most animal models and one of the main factors might be that these animals can synthesize, most of them can synthesize their own vitamin C. And that not only prevents LDL oxidation but it stimulates collagen synthesis and it allows for this stability of these plaques. So, here’s the thing. Low LDL receptor activity is going to promote LDL oxidation no matter how little polyunsaturated fat you eat or how many antioxidants you take in. However, although it will contribute to inflammation to some degree, there are so many other factors that contribute to inflammation that it is not the specific cause of inflammation. So in this people, I suggest, first priority should be optimize the inflammation. Optimize the quadding cascade. You want to look at all the clotting factors and the inflammatory markers and you want to solve that piece of the puzzle. That’s what you can impact the most. What you can impact the next most is providing adequate antioxidants in the diet and avoiding the stimulation of oxidative stress. When I say antioxidants, I do not mean something specific like blueberries, okay? I mean the wide spectrum of antioxidants that are found in fresh whole animal and plant fruits.

Chris Kresser: Amen.

Chris Masterjohn: The Coenzyme Q10 is important in the LDL particle. You get this from beef and buffalo heart is probably the best source and to lesser extent in red meats other meats and then on down the line in plant fruits. Liver is a great source of B vitamins and Lipoic acid and all sorts of things that contribute to good energy metabolism that prevent oxidative stress. Plants and fruits and vegetables are good sources of polyphenols which through hormesis protect against oxidative stress. Raw fruits and vegetables especially are good sources of vitamin C which although the LDL particle is, the fats in it are fat soluble, the blood is mostly water. And in order to minimize oxidation of LDL in the blood you need vitamin C and all the water soluble antioxidants. You need to minimize inflammation because inflammation is a source of oxidative stress. You need to normalize energy metabolism and because taking in more energy than you can handle is a source of oxidative stress. And by this, I don’t mean caloric restriction. I mean normalize your calorie intake to what’s normal but increase energy capacity. Get the B vitamins, the Coenzyme Q10, all these different cofactors that you need for energy metabolism. In other words, eat a nutrient dense diet, lacking refined food, lacking vegetable oils, full of whole foods from both animal and plant products including animal organs. That’s the next thing you can do. And then after that try to mess with cholesterol levels because cholesterol level is and LDL time and a puzzle, those are the things that you can affect the least in familial hypercholesterolemia.

Chris Kresser: It’s a shame we don’t have more data on people doing these things with familial hypercholesterolemia because I suspect there are very small number ultimately and people that are following these guidelines that have it, it would be very interesting to see what the outcome would be over a period of time.

Chris Masterjohn: Right. That’s the thing. I just want to really emphasize this. Anyone who has familial hypercholesterolemia should in my opinion be under medical supervision. If you go to conventional medical supervision, you know what they’re going to do they’re going to give you a statin and so on and so forth. I will not tell people that they should therefore not be under medical supervision. If you don’t want to take a statin which I think is, I don’t like statins at all. If you don’t want to take a statin, you need to find someone who is going to work with you, monitor all your clinical values and optimize in a supervised way. Familial hypercholesterolemia is not something to play around with. It’s not a ticket to inevitable early death. But if you don’t treat it, it’s almost is.

Chris Kresser: Yeah. Don’t self-treat on this one folks. Well Chris, thank you so much for getting to the end of our time here and I know there’s some questions we didn’t get a chance to get to. But it just means we’re going to have to get you back on the show for part 2 I think.

Chris Masterjohn: Yeah. Thank you so much Chris.

Chris Kresser: We can look at this in sort of like the basics and the primer and the advanced course all put together and then the questions, when we have you back, the questions are going to make a lot more sense because we won’t have to do so much the background explanation. We can just get more into answering the questions specifically.

Chris Masterjohn: Yeah, definitely. I love to be back Chris. Thank you so much.

Chris Kresser: Great. Yeah. Thanks again. Yeah. We’ll hopefully talk to you soon Chris.

Chris Masterjohn: Alright. Great!

Chris Kresser: Alright. Bye-bye.

Chris Masterjohn: Bye.

Danny Roddy: That’s going to bring us to the end of this week’s episode. You can find all of Chris’s work at the HealthySkeptic.org. You can find me at DannyRoddy.com. Keep sending us your questions at thehealthyskeptic.org using the podcast permission link. If you enjoy listening to this podcast, head over to iTunes and leave as a review. Thank you for listening and thank you for your support.

For many of you reading this, this will be obvious, and elicit a ‘well, duh, of course’ type reaction.

This is fine, but bear with me.

One of the things I learned as a part of my NLP training was to look a little more deeply into language patterns.

This is useful here.

Less of what? 

That’s what we should really be asking.

You see, if you just eat less total calories you’ll join the millions of others who’ve tried this method and failed, they’ve lost weight, and then gained it all back again. That’s because your brain and body are much more clever than you and will always bring you back to where you were.

That would be fine it that was all that happened, but there are side effects from this type of fat rebound that you need to be aware of.

When you yo-yo diet, you don’t just go up and down around a range of weights, you gradually get heavier. Each time you regain weight, you gain it a little more. Eventually working your way up to fully obese. You don’t want to do this. You want to lose fat PERMANENTLY (there is also increasing evidence that this type of diet causes semi-permanent metabolic damage, which makes it harder to lose the fat each time you get too heavy again).

So we come back to the question, ‘less of what?’ again.

And the answer is quite simple. Less processed food.

Two recent experiences with clients will help this story.

Fat Loss Case 1

I have been working with a couple who I have recently lost a load of weight each (the male has lost over 3 stone so far). The male in the partnership had quite a lot to lose, but most people would say the female had no need for weight loss.

I could sum it up like this: “How to make weight loss inevitable by eating whatever you want from a wide range of limited foods!”

How did they do it?

I have been saying to them for a while now to make a few changes, but it was an outside influence that finally tipped the scales. They read an article by Art De Vany in a newspaper and bought into his ideas about how to create a diet, and the potential effects it could have (I’ve posted a copy of this article on my blog, here).

The Details

Art’s approach is pretty much a paleo diet with a few alterations. He emphasises eating as much green and leafy veg as possible, using this to help fill you up. He also encourages you to eat this food raw, as much as possible (as this makes it harder to chew and increases satiety). He then bases the rest around lots of protein foods, and minimises nuts, cuts out diary completely and cautions against lots of fruit (due to the potentially negative effects of the downstream metabolising of fructose, which your body doesn’t use very easily). Just as importantly he also advocates intense exercise, intermittent fasting and getting plenty of high quality rest.

I suspect the biggest thing that helped these two people implement this diet was that they did it together. I think that people will struggle to implement a new and (for many people) radical diet like this. There’s just so much to change from the Standard American Diet (SAD) or contemporary western diet. But the benefits are worth it, in my not so humble opinion.

One of the things that Art mentions in his book is that weight loss is practically automatic with this diet, because when you’re eating a diet that is very nutrient dense, yet low in calories, your body feels both satisfied and nourished and yet you also create a pretty decent calorie deficit, which if you remember from my first ‘fat loss tips’ post, is crucial when implementing a diet and exercise regime to create sustained fat loss. The other reason fat loss is to be expected with this diet is that you are doing the type of exercise that helps potentiate your food. I don’t want to talk too much about it in this post, as this little nugget is being saved for its own special post, but suffice to say, that when you do very intense exercise you also prime the body to use its nutrients more effectively.

Take Home Message?

Eat food, base it around meats, fish and lots of veg that grows above ground, add a little fruit, fast every so often and do some high intensity exercise.

http://artdevanyeatsvegans.tumblr.com/ find more like this, and laugh!

Fat Loss Case 2

I’ve just started working with a new client who has lost a bucket load of fat, and now wants to make sure his workouts are hitting the spot. He started using weight watcher a few months ago, has stuck with it like glue, and benefitted a whole lot.

When I talked to him about his diet it was obvious that two things were going on:

1/ He was eating less!

2/ He was eating much higher quality foods.

He went from a diet of highly processed food, to one of very little processed food. Interestingly, he also has found that he now enjoys the odd treat, whereas before, when he was eating a whole of treats, he didn’t enjoy them that much at all. I guess you can have too much of the things you like!

In going from processed to real foods he’s also found that he’s got much more energy, doesn’t get afternoon slumps, is sleeping better and feels happier, more of the time. Sounds like a good set of benefits to me.

As you can see, the commonality from these two case studies is simple; eat real food.

Another thing these two cases prove to me is that you don’t have to follow the same route to get the same set of results. You just need to find a way that works for you, and stick with it.

In another post I made the statement, ‘if you can’t pick it or kill it, you probably shouldn’t eat it’ and I stand by that.

If you aim to get 90% or more of your food from items that fulfil that criteria, you’ll lose weight. It’s really hard to overeat on carrots, or beef, or grapes. Sure, you can do it, but it’s a lot more work than doing it with cakes, pasta or store bought curries (I do love my curry, but I mostly eat it when I’ve made it, that way I’ve got control over my ingredients).

Because sometimes laughing is good medicine!

Connecting Fat Loss Tip 1 and Tip 2

Remember how I said that you should aim to fulfil three criteria when creating diet that helps you lose weight in the long term?

For all our benefits, here they are again:

• 1: Create a calorie deficit.
• 2: Eat real food.
• 3: Eat the types of foods that are right for you.

What you may make out from the list above, when combined with the information presented in this article, is that all we have missed talking about is point 3, Eat a diet that’s right for you.

One thing I have noticed, with myself and with clients, over the years is that when you eat real food you are also more likely to be able to select the types of foods that help you and your metabolism work effectively. The foods that help you speed up your weight loss, feel more satiated and have much more daily energy. I suspect (and I also know that there is research to back this up with highly processed foods) that one of the many negative effects of eating processed food is that your body is tricked by the food, and then feels a sense of lack, or insufficiency. This lack needs to be filled, and it seems that the body, having been tricked once, will take a more shotgun approach, rather than an accurate sniper shot, and just try and get more and more foods in. Setting up a whole, horrible negative feedback loop that just keeps making you fatter and fatter, despite your best attentions at getting it going the other way.

So, to sum up, when you eat real food you make it easier to eat the right type of foods for you, you seemingly automatically create a calorie deficit (the thing that can throw this out is eating too many nuts and using too much fat in your cooking) and then you also end up eating less of the wrong foods.

I like the sound of that.

Till Fat Loss Tip No 3…

George

Body Rx Show Transcripts: #1

Introduction To The BodyRx Show :: Guest: Vince Andrich

{The original mp3 file can be found on this page Body Rx Radio Archives. Direct mp3 link Body Rx Radio Epidsode #1. iTunes Link.

You’re listening to the BODYRX SHOW with Dr. Scott Connelly!

Carl: Hey. Hey. Welcome to the BODYRX SHOW. My name is Carl Lanore. I’ll be helping out here with Dr. Scott Connelly. How are you doing Dr. Connelly?
Dr. Connelly: Great! How are you doing Carl?

Carl: Very good! Very good! So this is a monumentous moment huh? We’re launching a brand new radio show and we need to explain to people today what this show is going to be about, what they can expect and so on. We also have another guest on the line. I’m going to bring him in now and that is Vince Andrich. How are you doing Vince?
Vince: I’m very good Carl. How are you today?

Carl: Very good! Very good! This is very exciting moment in time, isn’t it?
Vince: Absolutely!

Carl: I’m going to turn it over to you Dr. Connelly because I think we really, most people don’t know what to expect from this show. We said we were going to be doing this show but we really didn’t tell people too much what they should expect. So why don’t you give a lay of the land on how you see this show being instrumental and changing health and nutrition.
Dr. Connelly: Well, Carl, as the title of this show implies, BODYRX is intended to deliver pragmatic, scientifically authenticated information relative to self intervention strategies that can be accessed through the application of either a nutritional platform or an exercise regimen or more importantly a combination of the two to essentially deliver extremely powerful mitigating influences on all the factors that really underscore the root of cardio metabolic disease and its associated degenerative properties. One of the opportunities that people have is related to the science of this field and that is, is that a lot of this has to do with the dislocation of energy homeostasis which is quite different than saying people in this country simply eat too much and exercise too little. That’s part of the naivety that has fuelled a fusillade of impotent gestures and solutions that really only compound the problem. In fact, one of the notions that we will develop is that if your primary interest with respect to self-intervention strategy is maintenance of an ideal body composition and hence controlling body fat mass then actually adopting a calorie strategy that circumvents the actual physiology and metabolic regulation of the adipose tissue mass by simply stopping eating or truncating the number of calories you intake per day actually is self-defeating. It sets up an iterated sequence of regulatory loops that in the long run make it much easier for the person who has managed their way through a period of severe caloric restriction to regain all their weight and a disproportion of that weight regain will be more adipose tissue. That reflects the underlying mechanism of energy homeostasis and that is a dysregulation of the hormone insulin. So, we’re going to be doing a lot of talking over the course of the coming weeks and months about insulin and how it can integrate with just about every self-imposed intervention strategy that you care to take whether it’d be exercise primarily or exercise and diet in combination. You’re going to learn the facets of the molecular regulatory loops that basically explain why a person who goes on a low calorie diet has a 90 plus percent chance of experiencing weight regain within a 6 to 12 month period of time. One of the reasons that this show is going to be distinguished from others is that it is going to present opposing points of view from recognized experts in these areas. Basically, I’m going to serve as a referee because one of the issues that this show will attempt to address and counteract is what has been referred to in a recent book called Unscientific America by Chris Monney and Sheril Kirshenbaum about the basic level of understanding of the average American citizen relative to any field of science. In fact, there’s been a sharp sort of turn away from science and scientist with respect to the general population’s appreciation of the value of a baseline understanding of scientific principles. Basically, an appreciation for what scientists who are actually working very hard on a day to day basis to uncover secrets of the life organism systems that people can actually access and control, one of the issues is that a lot of people have either a distain for science or a very simplistic view of science and we’re going to hope to look at that in depth and make people understand the limitations of scientific experimentation and hopefully allow them to fend off unreasonable and outrageous claims about products, about protocols.

Carl: Before we go there, I want to ask you a couple of questions, okay? It could be said that in the 1800’s, the big problem was infectious disease, correct?
Dr. Connelly: Correct.

Carl: Okay. And then, and now, today the mantra is chronic disease but they used this term chronic disease like it’s a variety of diseases out there each of them is independent of each other. But isn’t it true that probably 80% of all the diseases that are common today are somehow linked back to the management of glucose and insulin production?
Dr. Connelly: Well, that’s a perspective that certainly has gained a lot of credibility over the pass 10 to 15 years. One of the more nuance aspects of molecular biology that has focused very, very rigorously on these chronic degenerative disease states like cardiovascular disease and the attendant sub domains of heart and neurological insult peripheral vascular disease, the associated metabolic dislocations of diabetes etc. etc. All of which have been clustered in the medical literature under a rather amorphous heading called metabolic syndrome or syndrome X.

Carl: Right. Right.
Dr. Connelly: One of the issues is what is the common denominator to all of these entities? And there’s been quite a lot of work that basically has placed an emphasis on looking at the mechanisms of inflammation at the cellular level. It’s hard for an average person who has no grounding in this particular area of science to understand really what that term means when you think of inflammation you think of a sun burn or the inflammation that attends a superficial cut or something like that.

Carl: Yeah. Edema, right? Which is a response to inflammation, right.
Dr. Connelly: So there are many manifestations of overt inflammation that people are aware of. Cellular inflammation is a very different animal and it revolves around essentially again the dislocation of nutrients in storage and oxidation and excess storage of lipid especially in depots or areas of the body where lipid is not meant to be stored like in the walls of your artery etc. etc. can produce very, very, very serious untoward effects on tissue function.

Carl: So like visceral fat. They talk about that all the time. That actually visceral fat is the most dangerous fat because it actually simulates the production of hormones and so on. This is where we should not be storing fat, correct?
Dr. Connelly: Well, fat is meant to be stored in adipose tissue. The design of adipose tissue is very clear if you look at it from a standpoint of compared physiology across different mammalian species. Fat functions very much like a high capacity battery that you find in a car, an airplane or something else that relies very strongly on battery power under certain circumstances. A high capacity battery implies that you have a battery that’s able to put out a great deal of energy. Now, human batteries are limited by what is called an amp load or an amperage limitation whereas the human fat stores as long as there is resonant triglycerides stored in human adipose tissue the fat store the body can deliver energy regardless of demand. So it actually is like a high storage capacity battery but it’s very different in that it is not restricted by loads. So, whatever the system cries out for in terms of energy as long as there’s a stored fat, that energy can be delivered. Unfortunately, most of the storage of lipid now comes from not fat but glucose. Obviously, glucose at high levels in the blood is a toxic event to the system and the glycogen storage pool of the human body is very small. And so, tidal waves of glucose appearing in the blood and so forth have to be dealt with either oxidatively have to be used up or they have to be put somewhere. And so basically, the largest storage depot for excess glucose is actually fat tissues through its chemical conversion to fatty acid and then stored triglyceride. So in essence, one of the themes that will be recurrent throughout this is that the proper perspective to look at all areas of metabolic regulation is a perspective that recognizes that cells and tissues are very much like a business. A business has essentially input and output variables and has to run according to certain management schemes. One of the issues that we’ll talk about in depth is the preeminent role that glucose plays in this management scheme because glucose is a very unusual substrate or component of our food stuff that is available for energy provision. What we’re going to focus on Carl is basically the theme that, aside from the absolute energy content of the three major food stuffs and that would be amino acids from protein, glucose from carbohydrate and fatty acids from fat source. On the relative energy densities as determined in static systems like bomb calorimeters and things like that, we’re going to look at the signalling power of these nutrients in the context of this system as a whole. The system as a whole is basically a system where there’s an absolute requirement for energy at a very, very basic level. But because of the special position and prominence that glucose plays in this three ring circus, there is also an allocation requirement and we’ll develop this fully over the course of many sessions. But in essence, the listener will be treated to a very different explanation of how the storage and utilization of nutrients is regulated in the body. We are not going to be telling you stories about counting 500 calories a day, deficit in that other good diet, counting times seven which is a week, and there you lose magically one pound of fat. That thing’s never happened. It has never been recorded in all of scientific history.

Carl: We’re going to take a quick commercial break. When we come back, we’re going to talk about a couple of things that are going to make this show unique beyond any radio show that you’ve ever heard before. It’s really important to denote this sort of stuff. So, we’re going to take a quick commercial break. You’re going to notice that there are no commercials. You’re just going to listen to some music because that’s the way Dr. Connelly wants it. We’ll be right back.

[Music Playing]

This is the BODYRX SHOW with Dr. Scott Connelly.

Carl: Welcome back to BODYRX. I’m on with Dr. Scott Connelly and Vince Andrich. Vince, you’re still there, right brother?
Vince: Yes I am.

Carl: Okay, good. We’re going to get to you here in just a second. One of the things that I wanted to mention as we were going into the break that you’ll notice, you won’t hear any commercial breaks. We’re going to have a little musical interlude to kind of allow people to clear the mental palate because we are going to be delivering a lot of concentrated information. A lot of these messages will be rung over and over again to make sure people get it. Dr. Connelly wanted it this way. There would be no commercials per say at this point in time. This show is strictly informational. Now Dr. Connelly, that makes this show unique in a couple of different ways because number one not having sponsors means that we can be as truthful as we want without upsetting anybody, right?
Dr. Connelly: Well, that’s actually one of the preeminent reasons for my interest in the show is that, as I said, one of the goals of the show is to clearly articulate to a person who is not scientifically trained what the limitations of science are with respect to messaging. Obviously, unscrupulous manufacturers take advantage of glib statements made by online Google University experts and turn those into front of package messaging that basically relates to either no benefit or a benefit that is so deminimous that an individual really who’s well informed wouldn’t even pay attention to a large number of the products that are being marketed aggressively.

Carl: Give the example that you gave to me on the phone recently about, for instance, over the counter orange juice containers.
Dr. Connelly: Well again, front of package labelling is a very big deal in nutrition marketing obviously. One of the nuances of recent time is the discussion of Omega 3 supplementation. Obviously, everyone who’s attuned to any kind of nutritional marketing has been bombarded by messages about Omega 3s. Omega 3s are obviously a very important component of the analysis of the fatty acids signalling mechanism in the body. But along with the importance has to be an understanding of what the actual details of that are. This show is all about the details. The devil is in the details. What is not consistent from the standpoint of manufacturers marketing is any attention to the details. For example with respect to orange juice, if you look conservatively, I know Vince can chime in on this because he has a much more broader perspective on it than I do from the standpoint of the actual data. But if you look at the recent marketing explosion for, say for example, Minute Maid orange juice which I believe is a Coca-Cola product. You’d come to believe very quickly after reading their material that the solution to all of mankind’s metabolic problems is simply to drink Minute Maid orange juice and all of its various and sundry forms with all of its various and a sundry supplementation schedules and everybody would be fine. You could basically exist off Minute Maid orange juice several times a day. And with all the goodies that are in it, you basically were home free.

Carl: Right.
Dr. Connelly: Well, for example with respect to the Omega 3, I mean, how many milligrams do you think you could place in a serving of orange juice of a bile-tasting, basically fish based oily product, not many right?

Carl: Yeah. Without changing in to a disgusting taste, right?
Dr. Connelly: So obviously, that would not make the Minute Maid marketing people happy that people were drinking orange juice that tastes like DW40 and probably taking one sip and spitting that out and then throwing the carton in the waste basket. So, the objective obviously is to convince people by front of package labelling that the fortification with DHA or EPA or combination or any of the, all of the above is basically substantive. It’s significant. If you drink this orange juice as opposed to an orange juice that does not have this kind of supplementation, you’ll receive a discernable and discreet benefit. And the fact of the matter is with the low levels that would be contained in a single serving, it is impossible to discern any benefit. You could drink that glass of orange juice every morning for the rest of your life and I would defy anyone in the Minute Maid marketing department to show me data that that mere fact of drinking their orange juice everyday for the rest of their lives would have any impact on any of the known metabolic end points that Omega 3 fatty acid metabolism plays into.

Carl: Well, what about this Dr. Connelly, do you think that the ingredient that they’re putting in to enhance the Omega 3 content of that orange juice has a higher cost to them than the change of the front of that carton or vice-versa?
Dr. Connelly: Well, that would be an interesting question. I think probably that the front of package marketing message and the change in artwork would probably, in a long run, cost just as much if not more than the dusting as it’s called in the industry of the actual active.

Carl: Do they really call it dusting Vince?
Vince: Yes, they do. It’s a salt and pepper, dusting, sprinkling, label flap, all of the same.

Carl: So, what is, can you expand on what Dr. Connelly was just talking about as far as, do you have special interest and knowledge in this particular subject, the orange juice or are there other things that you feel also fall into this category where these manufacturers are putting in a dusting of something and changing the label so that people automatically think, “Oh, I’m getting this now.”
Vince: Well, the Minute Maid orange juice is just a glaring example but throughout my career it’s been a sore subject for me. I mean, I’ve been at some of the best or most respected sport nutrition companies whose main priority, once they reach a certain level of sales, was to reduce the cost of goods for all their most popular products at the detriment of the and user’s benefits.

Carl: For those people…
Vince: For example…

Carl: Okay. I’m sorry.
Vince: Well, I mean, for example, Scott mentioned the DHA, EPA/DHA for the orange juice. You’ve got a product here by Minutes Maid which is their, it’s basically a brain, help nourish your brain, okay?

Carl: Right.
Vince: And, you get 50 milligrams of DHA, EPA/DHA per 8 ounces which is basically one sixth of just the basic clinical trial level that someone would go out and use, actually I’m looking at a Penn State list of clinical trials that they’re going to do and that’s the lowest level they wanted to give their subjects was 300 milligrams a day.

Carl: Right.
Vince: For that, if you drink the 6 glasses of Minute Maid, you would get 258 grams of sugar, 45 grams per serving.

Carl: Right.
Vince: So there you have it. I mean, it’s kind of like a Trojan horse for these companies to infiltrate these healthy living markets which they know there’s money there, I mean, it’s in our DNA. We all want to live longer and look better. So now, they’re trying to figure out how to pick our pocket and they realized that the cost can’t be too high nor the taste profile can’t be too far in a way out of sync with what the mainstream populous will handle and so they have a problem on their hands. They have to create a product that basically is ineffective because otherwise the price point is too high or it doesn’t deliver enough margin to fuel massive marketing campaigns that basically shed out to mislead or propagate a sacred cow out there or some kind of myth that DHA just on its own in feather dusted amounts is going to nourish your brain. They’re not stupid.

Carl: For the people out there who don’t know who you are Vince, because I want to do this, I should have really done this at the beginning of the show, I missed to do this. For the people who don’t know who you are, give a brief verbal CV of your background in the health fitness and nutrition industry.
Vince: Well, I started in this industry as, I was a sports enthusiast and then turned into a body builder, want to be body builder in the 80’s. And I believe like a lot of people I think still should believe that nutrition is the cornerstone of that whole deal. I got involved as a distributor for many brands including some that people will know as Twinlab, Weider, PowerBar, Nature’s Best, and others. And that turned in to a job that as vice-president of sports nutrition for all of Weider. We were making other people’s products, I’m sure people, the audience, many are familiar with Weider brands. And then from there, I went to work for Dr. Connelly at Met-Rx and great experience there by the way obviously. Then I went to EAS after Met-Rx are sold, I went to EAS after the founders sold two thirds of that company and I was there to keep the health and fitness part of the business going and why that might be important to our listener is this. I was always fighting with management because, like I said before, their goal was to mainstream the brand. However, it’s very difficult to take products that have efficacious dosages of proven ingredients in a product and then try to take them, as they would say upstream to the masses because of course the fitness community is too small for them. So, all you get from them in every meeting is how can you make this thing cheaper?

Carl: Right.
Vince: At some point, I’ll tell you some very really, really funny stories about management there and their ideas on how to take a product that’s effective in these dosages of ingredients and then try to talk to say Wal-Mart, the thing becomes Frankenstein. But from there I went to PROLAB nutrition which was a division of NATROL. I handled chosen marketing in product development and really that’s where I was placed in most of these companies and then became a consultant and some of the brands I worked with are: Nutrex, Biotest, in Special Salons, Instone, several bar companies.

Carl: That didn’t last too long, did it?
Vince: No, it did not.

Carl: It’s unfortunate. But isn’t that typical, Dr. Connelly, isn’t that typical of the supplement industry. Somebody finds a study. They find a couple sentences in the study that coincide with their mission which is to sell this supplement. They attach a celebrity name or a celebrity persona to it or athletic professional athlete’s persona to it, they go to the market and people just stop buying it.
Dr. Connelly: Yeah. Obviously Carl, that’s another feature of the dislocation of real science from the public and the public is now bombarded with messaging from inappropriate sources, from illegitimate sources like for example the media, the entertainment industry, I mean, Al Gore is probably named as one of the top scientists by the average American if you take a poll. In fact, I think there’s actually data from a couple of years ago where they asked a sample of American adults, name a science role model. If I remember the data correctly, I think over 40, maybe in 50% could name anybody. The other 50% named either people who are dead like Albert Einstein or people who are in sciences like Al Gore.

Carl: But you better now piss him off Dr. Connelly because he invented the internet and we are using the internet to spread the word. We don’t want him to take it away from us.
Dr. Connelly: I know. He lives across the bridge for me now so he could lob a 20 millimetre rocket over to me. But anyway, the point is, is that the messaging that’s out there now is from all of the wrong places. And that’s one of the purposes of this show, is to bring real scientists who have opposing views on critical issues. What are those going to be? Well obviously, they’re the big ones. I mean, in American health scene today, the big issues are obviously obesity and its attendant disorder, satellite disorders, cardiovascular disease and its satellite disorders. To me, from the standpoint of risk assessment, the most perilous plague in America if not the free world is the emerging rise in type 2 diabetes. So, from the standpoint of what we’re going to try to do, we’re going to bring experts who have opposing views on some of these topics together on the program to discuss essentially very, very important practical issues. For example, there’s been a lot of talk on television in the last few several years about cholesterol drugs.

Carl: Okay. Wait a minute, that’s a subject we have to cover in some detail. Let’s do this. We’re right on a break here. Let’s take a quick commercial break and when we come back we’re going to be talking more about cholesterol. We’re also going to tell you some secrets about this show that are going to astound you. You’re going to want to listen to this show because Dr. Connelly and Vince Andrich are going to be busting myths about supplements out there that are built on Shoty-Science. You’re listening to the BODYRX SHOW with Dr. Scott Connelly. Stay tuned. We’re going to have a little musical interlude to clear the mental palate. We’ll be right back.

[Music Playing]

Bullshit is not a supplement. This is the BODYRX SHOW with Dr. Scott Connelly.

Carl: Welcome back to BODYRX. Dr. Connelly, you were just about to start talking about a subject that is near and dear to my heart and I think a lot of people out there are under some grave misconceptions because of propaganda promoted by the medical orthodox about cholesterol. Why don’t you talk about cholesterol a little bit? Sorry about that Dr. Connelly. That’s my fault. I didn’t un-mute. Sorry. Go ahead sir.
Dr. Connelly: Hello.

Carl: Yeah. There you go. I’m sorry about that. Go ahead Dr. Connelly. Go ahead and talk about cholesterol a little bit.
Dr. Connelly: Well, cholesterol is a very good example of the intersection of the issues that we’re going to be constantly referring back to with respect to a lack of understanding of the basic principles of science and that is. There’s been a lot of talk recently amongst mainstream cardiologist about the utility of literally prescribing to essentially asymptomatic people who have no essentially overt symptomatology referable to cardiac disease. These drugs, particularly statin drugs that have been shown in various in a sundry trials, epidemiologic trials, for example, the most renowned is probably the Jupiter trial to have an impact on say for example the marker or the biomarker known as CRP. CRP has long been contested to be either an instigator of inflammation, a promoter, an aggravator, a marker, etc. etc. One of the inappropriate conclusions that the Jupiter study authors came to after stopping the trial prematurely which several people, myself included, would argue very strongly shouldn’t have been done, is that the data is so convincing with reference to mitigation of CRP levels that this drug should be prescribed to asymptomatic people. From the standpoint of just a basic understanding of how that ties-in with a physician’s sort of mandate to first do no harm, I find that to be a totally indefensible position. The fact of the matter is, is that from 2008 forward, the result of a lot of these both unilateral and combined Statin trials is been extremely disappointing. What it speaks to in general with respect to the science perspective that’s developed is basically something that Karl Popper and his thesis that was called Conjectures and Reputations in 1963, elegantly describes the dilemma of people who don’t understand the true nature of science. Those people routinely mistake a scientific experiment as being proof of something. In reality, all of the design and all of the biometrical mathematical analysis that goes behind the study is specifically designed to disprove something. Basically, Popper’s thesis as science as falsification essentially states that it is not inherent in any theory of science to focus relentlessly on accumulating positive data to back up your theory, one of the problems with that from the standpoint of just pure biomathematics or biometrics statistical analysis is if you have one set of data that relates to a given heuristic hypothesis about relating variables A and B, you do this and B changes predictably by XYZ mechanism.

Carl: Right.
Dr. Connelly: Well, there’s criteria about what actually constitutes proof in that scenario and that’s called Necessary and Sufficient. So, if you applied that and you would never get B unless A was around. That’s the necessary part.

Carl: Right.
Dr. Connelly: Basically, if A is existing by itself, it would be sufficient to produce B without any help from any other intervening variables. You’re never going to find that kind of proof statement in any data relative to biology for one simple reason. And that is all the manifestations of living organisms are dictated by their gene products. The gene products are represented as a myriad of functional sort of variance of one another that are called Polymorphisms. These things essentially make it virtually impossible absent perhaps in the case of a monozygotic twin study to really separate what the influence of the various gene products is. A good example is the cholesterol thing. In essence, there never has been a convincing demonstration to my knowledge that oblation of cholesterol has the expected end point of mitigating reasonably defined markers of overt cardiovascular disease. So, if I could point to a single observation where the theory that XYZ causes cholesterol to go down or up in the consequences with the X and Y for the cardiac disease events, all I have to do is show you one example where the cholesterol manipulation had no effect on those variables and I’ve disproved your theory and that’s quite easy to do.

Carl: Isn’t it true that the pharmaceutical companies that promote statin drugs don’t have to prove to the FDA that their statin drugs are cardio protective but just that their statin drugs reduce the production of cholesterol. Isn’t that the case with a lot of those studies?
Dr. Connelly: Yeah. But again Carl, the point is and this was adequately demonstrated with various significance statistical power in the European Enhanced Study that reductions in cholesterol of B that they were achieved by the drug didn’t have any influence over the marker that they chose which is essentially the thickness of the arterial wall of the carotid artery.

Carl: Right.
Dr. Connelly: So, there you have this case where, well, the drug did lower the cholesterol. It’s an HMG-CoA Reductase Inhibitor and it was combined with a binder. So it’s a two drug protocol and in fact the serum cholesterol levels did drop. What didn’t drop was the end point marker that they chose to say this is a manifestation of cardiac risk, the thickness of the arterial lining of the carotid artery. That’s called the Intima. And that variable didn’t change. The cholesterol did but that didn’t.

Carl: Are you familiar with the study that was produced by the University of Hawaii that actually showed elderly individuals with the highest cholesterol levels were the most robust and lived the longest?
Dr. Connelly: Well, it’s interesting because I know that study. But it’s one of many. I mean, one of the interesting things is that, is that at the end of calendar 2008 and after all the big three meetings in America and Europe for all the various cardiology associations had been concluded and the data, the epidemiology studies have been presented, there was a resounding disappointment from all fronts as to the validity of this theory about the necessity of driving everybody’s cholesterol down, even the data from the original Framingham Heart failed to show that any more than half of the identified cases, identified cases mean I can show you angiographically coronary lesions, I can show a demonstrated coronary event with a documented myocardial infarction, less than half of those identifiable events were associated with abnormalities in cholesterol. So, is cholesterol irrelevant? No, it’s not. Obviously, in the context of a wide range of different convening variables, cholesterol is an important one. If you have a family history of heart disease that’s strong and significant, it be-who’s you to pay attention to your LDL cholesterol and specifically sub fractions of that some are more iatrogenic than others. And again, devils in the details. So, the whole scale announcement to the world that everybody should be on a statin drug whether they have symptoms or not, it is preposterous and indefensible from the standpoint of what Popper’s definition of true science is.

Carl: Okay. I don’t want to get too far off of the purpose for this show also is to give people a taste of what they can expect in the future. I want to ask you a question about your opinion of the current Surgeon General because I know that we would like to have the Surgeon General on this show at some point of time, correct?
Dr. Connelly: Well, I’d love to have her on the show.

Carl: Explain to the audience what your desire to have her on the show is for, you want to debate her, correct?
Dr. Connelly: I find it personally and professionally offensive that there are so many barking dogs out there about the tragedy and the devastation that has been heaped on the country by these degenerative chronic diseases, the metabolic syndrome diseases, and how terrible it is that our obesity problems and incidence is what it is and rising, blah, blah, blah. And yet, the mechanisms and the proposals to combat this has put an effective mitigating series of interventions in place, has been completely absent. And that’s symbolized by the appointment of somebody who obviously has a problem with body fat themselves and obviously hasn’t been able to deal with that successfully to put that person in the position of pre-eminence and then have that person join forces with the First Lady and say, “We’re going to take care of this. We’re going to plant vegetables in the White House garden and that’s going to fix everything.” Well, it’s not going to fix anything and it’s really actually, to me, a disgrace that this level of essentially nonsense is hoisted on the American people over the airwaves of mainstream media as being plausible or credible. I mean, it’s basically insulting and laughable. I would like to see anyone document that there is any evidence that calorie restriction and exercise, when applied over the long term, is an effective strategy for combating obesity. I’d like to point out one of the sort of “Oh gee, this is another one of those inconvenient truce that Al Gore made really famous.”

Carl: Right.
Dr. Connelly: One of the most revealing studies about obesity is the Quebec Family Study. We’re going to have a guess on the show named Gary Tubbs who’s written a book called “Good Calories, Bad Calories” which I consider over the years one of the most important contributions in the field in either lay or scientific literature in publications. And his basic approach to this is spot on. He says correctly that it is useless to try and ascertain why obesity results by studying people who are already obese you really have to start with people who are not obese and watch them over a period of time and see what factors or variables influence people becoming obese.

Carl: Right.
Dr. Connelly: In essence, that’s kind of what the Quebec Family Study has done. It’s a prospective trial of long duration and one of the interesting things to come out of that study is the demonstration quite clearly that some of the most important predictors of obesity not “Oh, you’re an obese person. Let me categorize what things you have on board.” No! We take people, we watch them over time, we predict variables that will say this person has a greater chance of becoming obese and when you do that, two of the most important variables that they identify, quite separate and distinct from high density calorie diets or high fat diets and sedentary activity were low intakes of dietary calcium and short sleep duration. So in essence, you look at that and you go, “This is nonsense” and I would fire back, “Well, of course, it’s not nonsense. The duration of daylight cycles plays an important if not vital role in the coordination of energy homeostasis.” And all you have to do again is look back to our partner in crime here, insulin, and notice that in all mammals who secrete insulin or an ortholog of it, the insulin secretion peaks shortly before the animal’s dormant cycle. Hence, in a rodent who’s a nocturnal animal is in insulin surge immediately before morning when the animal’s becoming dormant.

Carl: Right.
Dr. Connelly: In humans who sleep when the sun is down, there is an insulin surge right before sundown and obviously from studies in shift workers and various other human populations that have experienced a significant dislocation in their day night cycle, there are all sorts of observations about the central nervous system aberrations in energy homeostasis and insulin control and glycemia control that obtain from that. It circles all the way back to the staggering effects of having 90% of the population vitamin D deficient. And yet, you look at the data on supplementation, you see that in some studies upwards of 50-55% of the adult human population takes a vitamin mineral supplement thinking that’s the cure. But they have no notion of what the difference between the different vitamins is. They focus on vitamin C, thinking it’s going to keep them from getting a cold and basically ignore vitamin D. Well, my perspective and hopefully what we’ll show people or teach people on the show is that there are some vitamins, D being one of them, A, E, K too and perhaps E and C as well are more hormone like than they are vitamin like. So in essence, the constellation of all the factors that have impacted modern life from the shift, from a non-carbohydrate intake to almost a hundred percent carbohydrate intake, the dilution of the protein intake fraction, the shift in day-night light cycles, the sleep duration issues, all of these things feed back into the circadian regulatory loops that manage distribution utilization of energy. This show will not talk about calorie counting ever.

Carl: Right.
Dr. Connelly: We will basically show why that is, in essence, in most cases, a complete waste of time and perhaps very, very counterproductive.

Carl: Okay. We’re going to take our last commercial break and when we come back we’re going to wrap up the show and talk more with Vince Andrich because Vince is going to have a special segment on this show that we’re very excited about. You’re listening to the BODYRX SHOW. Enjoy the music for a couple… We’ll be right back.

[Music Playing]

Powered by the strength of his abs alone, this is the BODYRX SHOW with Dr. Scott Connelly.

Carl: Welcome back to BODYRX. Dr. Connelly, one of the things that I’m kind of excited about with this show is the segment that Vince Andrich is going to be doing. Vince, you want to talk a little bit about the, what we’re actually going to be exploring label claims, correct?
Vince: That’s correct.

Carl: You have a lot of background in this as well I know. Something that you told me about the manufacturing of some of the protein bars out there that a lot of manufacturers will manufacture protein bars very loosely adhering to the label claims until the bar is very successful or they get called on the carpet and then they tighten things up, is that a true assessment of how things work sometimes?
Vince: Yes it is. Unfortunately, it’s very prevalent in bars but it’s, it can also be found in even other product categories where a company or brand per say wants to get a jump on the marketplace, they come out with something with either ridiculous claims that can’t be substantiated, they do a money grab which helps them fuel a future company let’s say that is less aggressive with their claims and is trying to play it, essentially trying to go straight, when you see it in the bar category, you see companies that will mislabel the amount of protein, carbs and fats once they gain a tremendous amount of marketing share, they have enough sales and call with retailers and consumers alike whether they can slowly change the label or the contents of the bar to meet the label claim. But by then, the crime’s already been committed.

Carl: Right. So they basically, isn’t that the American way? Didn’t Joseph Kennedy make bootlegging his living and then cleaned his act up by getting his son into the white house? Isn’t that the way we do it in the United States? We do a little dirt in the beginning and then we, with always the intention of we’ll go straight later on once we make our first million.
Vince: I think so. I think that there’s a little larceny in almost every industry and when you get to, like for example, I’ve been in this industry a long time, so as Dr. Connelly, you start to see and hear the types of tricks that are being used. I’m sure there’s all sorts of tricks being used in other industries. We’re just tribute to the ones that are ours.

Carl: Right. Right.
Vince: But it does go to the American way. When you’re immersed in a business, because you are supposed to know the rules and regulations, you also know where possible loopholes are where the government really isn’t watching and they’re not enforcing. And so, those are the places that get exploited. And another thing with the case of bars, in any protein products that gets manufactured because a lot of brands if not more often than not the brand itself, XYZ brand doesn’t make their own food bar, they have somebody co-pack it for them. Well, a co-packer that’s manufacturing a bar has a duty through the good manufacturing practices regulations to make sure that the brand doesn’t send a bar label or a wrapper so to speak into the manufacturing plant that is not correct.

Carl: So, what do the manufacturers, do they turn their back not to lose a client?
Vince: That happens a lot. I was at a fairly large manufacturer on Long Island and we actually had companies send products in and we’d quote on them and they’d say, “Yeah. You know, you’re high on your quote” and we’d say, “Well, just a little tidbit for you. Your label says you have 750 milligrams of BTAs per cap. We weigh the caps and the powdering caps doesn’t even come out to 750 milligrams.” So therefore it’s impossible with the excipients and the flow agents and stuff to make these kinds of thing run. We’re telling you you’re short and they don’t want to hear it. A lot of them do not want to hear that. Why? They’ve already…

Carl: Committed.
Vince: Basically, they’d committed to their retailers and their consumers that they have a price on XYZ product and they’re not going to bite the bullet.

Carl: Right.
Vince: A true manufacturer, some of the things that we did at Phoenix were this, if you want to send your, you’re going to send your label in then I need to see your label and I need to approve it and have it on file. And when I run that product, that label better be, the supplement facts better be the same as the…

Carl: The mixture. Right.
Vince: Basically, yeah, the recipe. If not, I reject it.

Carl: Right.
Vince: There’s all kinds of tricks that go on and that’s some of the stuff that we’re going to be talking about, I mean, there’s GNPs in place, every manufacturers over 10 employees is supposed to be following these good manufacturing principles or practices. But a lot of times it takes, it’s not all times, it takes two companies to be complicit with each other to pull the karma.

Carl: Right. The wall over the consumer’s eyes. Dr. Connelly, without giving too much away, I know that, for those people who don’t know who you are, you’re one of the founders of Met-Rx, correct?
Dr. Connelly: I was the founder of Met-Rx.

Carl: Okay. You were the Met-Rx. Okay. I know that this particular subject about the bars has a special place in your heart and, I don’t want to give anything away, but you’ve already started testing bars, isn’t that correct?
Dr. Connelly: Yeah. That’s correct. I mean one of the instances where I was kind of shocked and it takes a lot to shock me with respect to nutritional products. But I was out in about, it happened into a store actually to pick up something else and noticed cash registrar display of some bars that were labelled 2 to 1 and I kind of

Carl: Meaning what? 2 to 1 ratio of protein to carbohydrates?
Dr. Connelly: Well, that was the affirmation because that there was twice as much protein as there was carbohydrate then I was holding in my hand obviously an extruded bar product. Well I, through Met-Rx, was probably the first company to produce a very high protein bar and that was an extruded product and I produced several extruded bar products in subsequent 6 year, 7 year period that I own the company. And I can tell you or at least I knew intuitively that it’s impossible to make an extruded bar that has twice as much protein as it does carbohydrates. It’s impossible.

Carl: Right.
Dr. Connelly: It can’t be done. The sort of food science technology to have put that over on people is not there. So, it became sort of a source of interest because I realized that this thing had quite an impressive trajectory in the marketplace. And so, I had it analyzed and other people have had it analyzed, several people have had it analyzed, we all came to the same conclusions when we view the reports from reputable labs and in most cases it is 2 to 1 but in the opposite directions, there’s twice as much carbohydrates as there is protein. In essence, the premise that this is a bar that has a great taste, it has twice as much protein as it does carbohydrate anything, let alone carbohydrate as monosaccharide sugar is a pretty impressive and seductive claim to someone in this sector. That’s a pretty powerful front of package claim to have out there. It’s just not true when you analyse the product it doesn’t measure up. So this is a kind of thing that we are going to talk about. We’re going to talk about major issues of misrepresentation and fraud. And the fact of the matter is we’re going to take shots at all the companies in this industry, big and small alike. Like for example we talked about Minute Maid orange juice, I mean, where’s the line between misrepresentation, deception, etc, and fraud really start and stop. Is it okay to tell people that this is a great product because it has 50 milligrams of DHA per serving? Is it really true that if I wanted to get say 300 milligrams, which by the way will not produce any noticeable changes in human metabolism whatsoever I guarantee you that, that will not happen in that study, most of the study show the discernable effects begin at 3 grams per day and those are diminimous, if you want real effects that are robust and sustained, you’re talking 12 to 15 grams a day. So certainly 50 milligrams is not going to do it and if you wanted to get to 300, well that’s 6 eight ounce servings of orange juice and Vince mentioned the sugar load that you would get. So that’s like saying, “Well, I’m going to eat a salad with some fruit and that’s going to be a cover up for the 6 packages of Benson and Hedges that I smoke a day and a quart of all Veranda that I down in the last hour.”

Carl: Right.
Dr. Connelly: But at least I got my fruits and vegetables. Again, that brings up an important point that we’re going to talk about. And that is, most of the integration that occurs in response to meal ingestion is what we call “In the post absorptive state” that is immediately after ingestion. That’s when the big hits come. So in essence, it doesn’t matter that you have had a serving of orange juice with 50 milligrams of Omega 3 if the rest of your day is 55% to 60% carbohydrate.

Carl: Right.
Dr. Connelly: That’s not going to help. The notion that CRP can be reduced by statins, an alternative explanation or an alternative strategy would be, don’t have people walking around with high CRPs to begin with. And you can do that with carbohydrate restriction.

Carl: Right.
Dr. Connelly: You don’t need a statin drug to minimize CRP. So these are the things that we’re going to put out there. We’re going to challenge people who have opened their mouth in public forums and said, “You must do this. 8 servings of fruits and vegetables a day is a good idea.” Well, not only is it not a good idea, it’s not even pragmatic. The whole calorie restriction for longevity is a bust from the get go.

Carl: Right.
Dr. Connelly: In New York City, when they require that restaurants publish calorie values on all their menus, the result was that people ate more. So anyone in this country that thinks that calorie restriction and exercise enhancement are going to have any measurable impact on any of these issues is deluding themselves.

Carl: Yeah.
Dr. Connelly: Their history is uniform and consistent and it is a history of abject failure. Stop putting your hand on the hot stove. Listen to this program. We are going to teach you the BODYRX metabolic advantage plan and it can save this nation’s healthcare problems.

Carl: Bingo!
Dr. Connelly: We will show you clearly that when you look in the mirror every day, you’re staring at your personal healthcare reform plan.

Carl: I like that a lot. We won’t need healthcare reform if everybody gets on the boat. Listen, Dr. Connelly, I want to thank you for doing this today. This is a great service that you’re doing for the public. Vince thanks for being here. We’re going to have lots more of Vince. Listen to BODYRX every week on Tuesday at 4PM Pacific, 7PM Eastern. We’ve got a great line-up of shows for you coming up. We will see everybody next week with another episode of BODYRX.

You’re listening to the Super Human Channel. Don’t hate us because we feel good.

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Ask yourself ‘what’s the relationship between your current exercise routine and the last one?‘

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The sameness people

The sameness with exceptions group

Give me some change, I’m bored!

But what about the other filters?

Body Rx Show Transcripts: #26

Midnight Smacks

Metabolic Consequences of Short Sleep Duration

{The original mp3 file can be found on this page Body Rx Radio Archives. Direct mp3 link Body Rx Radio #26

The following paid program does not necessarily reflect the views or opinions of the staff and management of Triceptor Productions or the Super Human Channel. Triceptor Productions and the Super Human Channel are not responsible for any claims, warranties or guarantees made during this program. You’re listening to the Body RX Show with Dr. Scott Connelly.

Carl: Welcome back to Body RX. I’m Carl Lanore and we’re joined today by Vince Andrich and of course Dr. Connelly. Later in the show, we’ll have Dr. Layne Norton and of course the Paleolithic nutrition expert, Robb Wolf. How are you doing Dr. Connelly?

Dr. Connelly: I’m here Carl.

Carl: Okay. Sorry about that. Okay. That will be an edit point right there. Anyway, okay, so what are we talking about tonight Dr. Connelly?

Dr. Connelly: Well, we left off last time talking about the summary points that we’ve been trying to emphasize since we started this show several months ago and that is that of all of the variables that have been empathically reiterated over and over again about how to approach mitigating the worldwide increase in prevalence of obesity that the standard variables of increased caloric intake and decreased physical activity continue to dominate the conversation which basically means that once again the calorie theory of body composition modulation has remained preeminent in all of the mother goose discussions that dominate the mainstream media. We’ve been trying to essentially overturn that prejudice by demonstrating through legitimate science in both cross sectional and prospective studies in human beings that calorie issues have in fact very little to do with the persistence and increase in this problem worldwide. We had discussed some of the attributes of different dietary constituents that provide powerful metabolic signals that can skew the relative proportion of the oxidation and storage which is what we call partitioning. Partitioning is like, you can visualize it as a seesaw over the fulcrum being in the centre and oxidation and storage on either end of the seesaw. Obviously, the prevalence and incidence increases worldwide in obesity indicate that the partitioning of fat balance that is the difference between fat storage and fat oxidation has been grossly prejudice to the side of the storage. We’ve constantly reiterated this from the context of people talking about weight control. This has nothing to do with body weight control. This has to do with the amount of dietary or other energy stored as fat. Obesity is a disorder of fat balance which essentially speaks to the dynamic of fat storage versus fat oxidation. We’ve discussed the intersection of several metabolic loops that have to do with the monitoring and the disposal of ingested nutrients. We spent a lot of time talking about amino acids as primary drivers. We’ve spent some time in the last few weeks talking about fatty acids and their signalling power in this particular continuum. We ended last week with sort of emphasizing the paradox that one of the variables that has been identified as a very powerful predictor of weight gain in both cross sectional and prospective studies in humans that would predict essentially untoward gain of body fat overtime has nothing whatsoever to do with calories. So, these are variables that are, in one sense, have no a priority calorie value on or their face have no calorie value that can be assigned to them. One of the most dramatic demonstrations of this phenomenon is sleep duration. Obviously, sleep duration has received a lot of sort of airtime in the public media. In fact, just last week, there was an article in U.S. News and World Report, the title of which was six ways lack of sleep is costing you a fortune and this was an article out of their finance section. Essentially, the article was skewed towards the demonstration of the impact of shortened sleep duration on your financial health but it also included a mention of the topic we’re going to talk about today and that is sleep duration and obesity. But for kind of starting off this show with the evidence that sleep duration has been truncated pretty dramatically since the 1960’s to the present day with the 1960 numbers from the National Sleep Foundation being somewhere in the vicinity of average of 9 hours down to less than 7 hours. Now, in 2010, the most recent publication of their data, a lot of different groups have sort of written or studied aspects of this truncation in sleep duration on impact of human behaviour and quality of life. The article in U.S. News and World Report had this sort of six features of shortened sleep durations for purposes of our talk today will set a limit at truncated sleep duration as anything under 7 hours in duration for consistency purposes. So, with that in mind, they identified that you’re essentially more accident prone and they used some statistics that showed that 30 to 40% of all heavy truck accidents are indeed caused by fatigue and if you basically try to correlate the fatigue of a truck driver with their sleep duration, you get a pretty consistent positive relationship. They also noticed that they, people who don’t get enough sleep are more likely to have, overall all kinds of different health issues. So, one of their focused areas was if you don’t get enough sleep, you’re bound to incur a lot of increased medical expenses. From investor perspective, they also had an article, a bullet point that had to do with making bad financial decisions if you don’t sleep enough. Essentially, one of the things that they looked at was the cost of insomnia from a standpoint of employees who cost employers money because they don’t get enough sleep and they had an interesting statistic that, I think it was employees that were reported to suffer from insomnia cost their employers $3200 more than employers who do get enough sleep just because they essentially make bad decisions. Obviously, one of the points they had brought up in this article which wasn’t the focus, the article was more on sort of the economic impact of poor sleep habits but they did mention that you’re more likely to suffer from obesity. That’s a trend that has been picked up in the literature and discussed in ever increasingly detail and focus for the past decade really. This is not a topic that has just surfaced. This has been researched by a number of different groups across the world using as I said both cross sectional studies that is studying people as they exist and prospective studies, taking a group and then following them forward in time trying to ascertain how the correlates of different aspects of physiology and body composition change overtime and if they in fact are related in any mathematical consistent way with sleep duration. From the standpoint of looking at this from an aerial view, you would expect that a lot of impact would be felt throughout the body by disturbing a sleep pattern. Remember that a sleep cycle is regulated by the same what we call clock genes that regulate all sorts of physiologic phenomenon that are ultimately tied to the day, the light dark cycle of organism’s existence. These light dark cycles’ circadian rhythms can be extremely powerful in controlling metabolic regulation and skewing portioning influences for all of the macronutrients in a dramatic way. Sleep deprivation which is volitional in most cases in modern humans is essentially a powerful dysregulator of these circadian physiologic loops. It wouldn’t be unexpected to think that a chronic disturbance of sleep duration that exist because of the preponderance of artificial light sources and the tendency for modern humans to work longer hours, recreate longer hours and thus extend their activity pattern way beyond the natural dark period of the day that that would have a profound effect on a lot of different physiologic systems. In fact, when you look at a number of different physiologic variables that have been scrutinized with respect to this aspect that it’s very clear that reducing the total numbers of hours of sleep can lead to a lot of very bad problems for almost any body organ system that you want to take a look at and just sort of just a review of some of the things that have been studied and documented on average overall immunity as measured by several different biomarkers for example inflammatory markers such as the release profile circulating of the interleukins, interleukin 1, interleukins 6 and the tumour necrosis factor. Alpha compounds sleep deprivation is linked to increased daytime levels of all of those things and there’s a significant interaction between sleep duration and the overall functioning of the immune system with respect to its ability to respond through acute stressors which would activate an immune reaction. So, starting kind of at that gross level and proceeding on, you can have data that clearly shows that sleep for five subjects, again those people who have less than 7 hours per night of sleep are a higher risk for developing high blood pressure, Dyslipidemia from the standpoint of blood lipids, type 2 diabetes is now recognized as being very particularly related to short sleep duration. But also, other aspects of Neurocognitive function and disorders of Neurocognitive function including depression and more serious psychiatric disorders are all apparently impacted by shortened sleep duration overall mortality is impacted in a negative way. There’s a bunch of study which show that behavioural sleep deprivation leads to alterations in substrate metabolism including profound changes in glucose metabolism and regulation and some of the hormones that are known to affect peripheral peripherally mediated and secreted messengers that signal appetite and energy expenditure. We know that there are different components of sleep, slow-wave sleep, REM slate, etc. etc. There’s a bunch of more nuance studies which I’ve looked at specific and dislocations of different phases of sleep with respect to specific changes in hormones and other cytokines that have been released. Now, what’s interesting is that there is now literature in what I consider to be abundance that points to the fact that these particular aberrant consequences of shortened sleep duration are more profoundly felt in children. There’s been a number of studies and literature in the paediatric area of medicine which recently have come to the forefront that suggest that our kids in particular are very, very susceptible to these adverse effects including the more profound metabolic disturbances which lead to the elaboration of the metabolic syndrome, biomarker proliferation and also the change in body fat accumulation leading to childhood and adolescent obesity. So, this is an area of research that has received a lot of focus in the last decade and it continues to produce a plethora of interesting research which looks at not only the overall mathematical relationship on an epidemiologic scale with respect to all of these different problems and metabolic interleukin and immune sequelae of shortened sleep durations. But more recently, studies have begun to look at the more mechanistic aspects of why this might be the case. There was a recent study that was circulated through our band of merry men last week that came out in the American Journal of Clinical Nutrition, it was done by the group out of the Netherlands, couple of authors that are very, very prolific in that field of metabolic regulation and evaluation. They had looked at specifically the effects of disrupting sleep via procedure of frequently waking people up during the night with an alarm clock type methodology so that their sleep was really kind of disrupted on a fragmentation type basis. What they wanted to do is to look at the effects of this sort of staccato interruption of their sleep pattern on their energy expenditure, their substrate oxidation, physical activity and their perceived levels of exhaustion as measured in a metabolic chamber. This group in the Netherlands is renowned for publishing studies that have to do with observations accrued in their metabolic chambers which were essentially little apartments that have the requisite oxygen and CO2 sensors to essentially do indirect Calorimetry measurements on people who are extensively free living. Although living up until little tiny metabolic compartment is not exactly replicative of free living existence. It’s better than the older antiquated methods of the hood Calorimetry. So, these studies have, at their core, some inherent limitations because of the somewhat obvious departure from your life existence but they don’t suffer from the same limitations and restrictions that earlier studies that used this more antiquated hood methods of measuring metabolic rate are prone to and couple of the interesting observations that came out of that study was that in contrast to what you might intuitively expect by interrupting somebody’s sleep periodically throughout the night that they would be a train wreck the next day and be somewhat less active.

Dr. Connelly: In contrast to what you might intuitively expect by interrupting somebody’s sleep periodically throughout the night that they would be a train wreck the next day and be somewhat less active. They actually found that the activity associated energy expenditure in these truncated sleep subjects was actually higher. Again, we talked about this last week from the standpoint of a conceptual paroxysm that is why would short sleep duration which allows you to be more active during the day and essentially expend more energy and activity be associated with a higher chance of becoming obese over time. This group actually documented that their control subjects anyway, the activity energy expenditure portion of total 24 hour energy expenditure was actually slightly increased above their control subjects. But what they found which was pretty interesting and consistent with a study that we’ll talk about after our guest, Robb Wolf, comes on is the fact that when they looked at total energy expenditure that is on a 24 hour basis between the control subjects and the sleep disrupted subjects, they really didn’t find any significant difference. And other studies that have looked at this from the standpoint of the amount of “Kilocalorie” expenditure that would accrue when you reduce somebody’s sleep I say less than 7 hours a night amounts to less than 200 kilocalories on average of activity related energy expenditure. So, that would not be expected to have a monumental effect on someone’s average 24 hour energy expenditure under any circumstances. But it’s interesting in this case the total energy expenditure as measured by their equipment was not different between the two groups and yet the changes that were profound were that the fragmented sleep group experienced a marked increase in their respiratory quotient which is associated with an increase in carbohydrate oxidation at the expense of fat oxidation. And that was one of the most interesting aspects of the study was that in essence although total energy expenditure was not affected in a substantive way the percentage of fat oxidation was reduced quite considerably. And this is interesting from several respects because it speaks to the issue of the duality of the influence of some of the hormones that have been postulated to control appetite and energy expenditure and Greylan being a good example which we discussed on the previous show. Greylan obviously has discernable effects on appetite promotion but it also has effects independent of appetite stimulation that effect energy expenditure from the standpoint of the efficiency of fat oxidation which has nothing to do with the energy content of the food but the ease with which your body takes those ingested nutrients and partitions them into fat stores. So their demonstration in this study that there was little or no effect on total energy expenditure but a qualitative shift in the oxidation of substrate towards carbohydrate away from fat is demonstrative of the concept that we’ve been trying to drill down on for several weeks on this show that the absolute determination of a final body composition is a representation of a balance between what has been referred to as the respiratory quotient which is simply a mathematical representation of the relative contribution of carbohydrate, fat and protein to total energy consumption or oxidative phosphor relation and what’s called the food quotient which is the body’s ability to store or to oxidize each one of the macronutrients with relative ease or relative difficulty. People who are prone to become obese have a dislocation of the RQ/FQ continuum. They may in fact have an unfavourable RQ which favours carbohydrate over fat oxidation and coupled with that due to differences primarily in body fat mass, a dramatically different ability to oxidize fat. If you combine those two things overtime, you have human beings who will experience under the influence of a carbohydrate rich diet and increase propensity to gain fat irrespective of the fact that they really don’t eat in terms of number of calories per day a larger amount of dietary energy. So, with that in mind, I’m going to turn this over, well maybe we could take a quick break here, music break as usual and when we come back we’ll have one of our favourite guess, Robb Wolf has graciously agreed to join us again today to talk about this subject with respect to his perspective and his advice that he gives to his clients. And so, with that in mind, we’ll take a quick break and we’ll be right back.

[Music playing]

Carl: Welcome back to Body RX. Vince you want to intro our guest this hour.

Vince: Absolutely! He’s Robb Wolf and as Dr. Connelly mention, one of our favourite guests and he’s an expert in Palaeolithic nutrition, author of the Paleo Solution the original human diet, and he’s got a lot to talk about with respect to sleep and we’re glad to have him. Want to give his evolutionary perspective on the topic as we move forward. So, Robb are you there?

Robb: I’m here.

Vince: Good to have you again. Thanks.

Robb: Thanks for having me guys. Good to know that the last show didn’t completely ruin your listenership.

Vince: No way. I know that you have, you’ve written in your books on the topic of sleep and last, I think on our last show you mentioned something that’s stuck out of my mind is getting to sleep in a pitch black room. Why don’t you start with maybe how we got to where we are from an evolutionary perspective, what were our ancestors doing with regards to sleep before the invention of the light bulb.

Robb: Well, we can tackle this thing both from a little bit of anthropological perspective which is interesting but not super solid from a scientific perspective. We can look at this from the big picture macro level and get some insights from this kind of evolutionary biology caveman kind of gig but we can also, we are now with a level specification with this stuff where we can explain all this stuff from a mechanistic standpoint forward. So I’ll try to like weave both of those things together but in pretty simple terms we like every other creature on this planet are woven into some sort of a Circadian Rhythmicity some sort of wake-sleep patterning. It’s pretty interesting. We usually folks associate our perception of light just with our eyes but the forefront proteins in our red blood cells actually can absorb blue wavelengths of light and communicate that to the brain. Folks who are blind have a normal Circadian Rhythmicity just like the other folks around them because this information is communicated to the brain. So we have some fairly complex biophysical mechanisms could tell us when to go to bed, when to wake up. It’s very much tied in to food procurement, reproduction, you name it [indiscernible] DNA and a lot what we [indiscernible], this interface between the endo-bium, the creatures that our intestinal [indiscernible] are hopefully beneficial creatures and kind of a dynamic tension between those things and our immune system. And typically through the day we see an overgrowth of bacterial activity. At night, we actually see a proliferation of our immune cells and [indiscernible] it’s kind of a dynamic equilibrium there if everything is working well and we tend to maintain insulin sensitivity, we have restoration of neurological function. The process of sleep is still very, very black box. It’s kind of like opening the astrodome and hanging a microphone into the astrodome and trying to figure out what’s going on during a football game or a baseball game or something which we hear a bunch of noise but we really don’t know what exactly is going on and our understanding of what exactly sleep is, what it does, how it benefits us is still at that very impure goal kind of 30,000 foot level but we know for a fact that it’s very, very tightly tied into blood sugar regulation, androgen levels, its systemic inflammation and ultimately kind of our overall health and longevity and like I mentioned, we also understand a little bit of that interface on say like the musculoskeletal level, the neurological level of understanding that missed sleep can dramatically impact like their influence to this things like that. So from a big macro perspective, when we’re talking about sleep, we’re just talking about a normal biological function that’s kind of woven in to every creature that creeps and crawls [indiscernible] desire or [indiscernible].

Carl: Robb.

Vince: Are you there Robb?

Carl: Robb, could you hear us?

Robb: Yes!

Carl: Robb, your phone every now and then fades in and out. I don’t know if you’re in a good spot where you’re sitting or if you’re mobile and walking but we lost the last couple sentences there.

Robb: Okay.

Carl: But you were saying, you want to just pick it up?

Robb: Just basically, the big picture of sleep is just that it’s a inner goal feature of pretty much everything alive and similar to exercise levels, similar to different food intake we have kind of a genetic optimum woven in to us.

Carl: Okay.

Robb: And our diet, our lifestyle really is kind of add odds with what’s kind of woven into our genetic.

Carl: So what is our genetic optimum?

Robb: Really kind of racking out when the sun goes down and then getting up when the sun comes up and some folks have talked about like Polyphasic sleep and some things like that. It’s a really interesting point. The key feature was that, I think that this is why when we make a general recommendation for folks almost nobody racks out when the sun goes down. We play on the internet. We watch TV. And so what we do is we expose ourselves to a photoperiod that is significantly longer and of significantly greater intensity than what we would have normally experienced. And this has some interesting effects on insulin sensitivity and also more and more and more on linking more of this stuff back to problems with systemic inflammation that is actually born of kind of Dysbiosis of systemic problem of Lipopolysaccharide this part of the exoskeleton or the our cell membrane of bacteria when we are exposed to a photoperiod that’s too long our immune system doesn’t prune back the intestinal bacteria the way that they should and we actually get some Lipopolysaccharide that migrates via the M cells and the epithelium and it holds this Lipopolysaccharide into circulation. And if Dr. Connelly can point out, somebody who experiences acute severe sepsis they become very, very insulin resistant, they have a broad ranging systemic inflammation and they can die from this because of blood sugar dysregulation, because the inability for the liver, the pancreas and the brain to communicate effectively about how to manage blood sugar maintenance. And what’s happening in my opinion and it’s pretty probably kind of percolating up within the evolution of biology community, is the lack of sleep and extended photoperiod is actually leading to some systemic inflammation that’s probably born of kind of literally bacterial overgrowth.

Carl: Interesting.

Vince: Wow.

Carl: I want to just make a statement or actually a question for your consideration Robb, and that is that for the part of our audience that is athletic minded, performance minded, there is some evidence that disruption of the suprachiasmatic nuclei which is not just responsible for the hormonal milieu that occurs but also fine tuning the receptors that these hormones then interact with can actually, there’s a lot of guys out there who believe that, drug using or not, that they can burn the candle at both ends and still see the results that they want. And it’s been my experience that that interfering with proper sleep can actually push back your progress regardless of the presence of drugs or not.

Robb: Yeah, I mean, without a doubt. I do a fair amount of work with some of our special operations folks have done some work with naval special work errands from other groups. What we see is the selection process in professional athletics, in special operation groups in the military for people who typically can maintain normal hormonal functioning, a reasonable kind of nerve transmitter signalling even while pretty beat up, while sleep deprived etc. This similar to almost everything that we see whether it’s carbohydrate tolerance or maybe grain intolerance or something like that. We see a spectrum within the population at large. But that said, just because somebody can tolerate this stuff, say like one guy can “get by on 5 hours of sleep and still have what is for him pretty good performance” doesn’t mean that he’s not going to perform better both in the short run and in the long run, something that folks forget we’re talking about potentially performance health and longevity. So, how long can you maintain this work output and at what percentage of say like your genetic optimum, something that you’re 32 years old and all the systems are firing that’s usually when males kind of report their kind of best lifts, most explosiveness, all that sort of jive and then from there it’s just kind of a slow slide into the grave. Well, depending on how you manage lifestyle features you can maintain much more of that. Again, these guys in the special operations community, they have dudes that will barely sleep, they’ll go out and drink all night and they’ll smoke everybody on PT test but 5 years, 10 years down the road, the toll that it’s taken on this people is catastrophic. And so, it really is kind of burning the candle at both ends and not to get preachy about it like if folks want to live a particular way, by all means go for it but we’re not going to pharmaceutical our way out of that. Now, it may supplement things, it may augment things for a period of time you may manage it better than without but you’re not getting away and escape.

Carl: Very cool.

Vince: Robb, I’m making a few notes here. It would seem that when you’re younger and of course if you’re genetically predisposed to be able to handle some of these things better as you mentioned, wouldn’t that make sense and you could talk to this point that you’re pushing certain hormones and the hormones will obviously have to dock with receptors as Carl just mentioned over time is that clarity or sensitivity tune down is that what is going on over time, you can handle it for a while but all of a sudden it’s like faulty spark plugs.

Robb: Yeah. I think, again, it’s like almost anything, like one of my best friends Charles is half black half Filipino if you stick he and I out in the New Mexico sun, I’m going to get a sunburn quicker than Charles because he’s got genetic adaptation that presents him, he’s going to be able to withstand more solar radiation before he gets his skin gets damaged. If we move both of us to the Arctic Circle, Charles is going to develop rickets first because he’s not going to manufacture as much Vitamin D. And so, what we’ve got within an individual is their genes, so their genome, and then we’ve got the epigenome which is the environmental interaction with genes and we just have basically potentialities there. Some people are going to potentially get by better than other folks on abbreviated suite. Most people who end up going into medicine like just the kind of the selection process. They can navigate a functioning at least at a certain level getting by on less sleep but what we find is that the survivability of physicians is not too much better than NFL linemen which is horrible.

Vince: Wow.

Robb: And so you absolutely pay that back somewhere. And again, with the interest of that, I don’t really know because obviously we need like night shift yard auction stuff like that but I think having some eye towards that so that people can do the best of their ability instead of doing like 36 or 72 hours on or something like that. We need more punctuated elements to shift work it. Then there’s sort of this control recognized shift work which is effectively extended photoperiod. They recognize that there’s a known percentage on pro with ionizing radiation in asbestos. And so that, it definitely it causes an impact but again we have a spectrum of either susceptibility or resistance to that. When part of what’s happening with the sleep immediately is that we lose insulin sensitivity, immediately we start seeing disruption of liver functioning mainly related to glucose metabolism. So we may have high levels of blood glucose but the signalling between the brain, the pancreas and the liver kind of goes south in the sleep deprived state. So now we burn through glycogen, we breakdown glycogen first and then we start taking up gluconeogenesis to pump out blood sugar in that sleep deprived state. It looks almost identical because effectively it is. It’s almost identical to the type 2 diabetic individual which also looks almost identical to the subject individual. And when we start doing that stuff, when you talk about all kinds of different hormonal signalling, if we up regulate cortisol production then via the pregnenolone steal we’re suppressing both testosterone and oestrogen production. We have 3 or 4 different mechanisms where elevated cortisol production can curtail thyroid production ultimately directly cortisol inhibits the conversion of T4 to T3. So if we see normal levels of thyroid releasing hormones, thyroid stimulating hormones, good levels of T4 or T3, elevated cortisol, then we know that we’ve got a problem there in sleep, overtraining, all these things can drive right into that. And then as these progresses along we can start right into the hypothalamic dysregulation and block thyroid production right at that spot. So, on a big, kind of big picture level we immediately have mechanisms affecting insulin, leptin, growth hormone, cortisol, and testosterones. And I mean, if you mess that stuff up, what the hell can you do other than like cry yourself to sleep watching Hallmark commercials and stuff like that. Everything goes south.

Carl: Now Robb, I’ve got a question for you. Since, we understand that we’re hardwired to sleep when the sun goes down. In fact melatonin production generally occurs with the onset of dusk. And we’re designed to arise when the sun rises or the photoperiod occurs but that’s a pretty long period of time. It’s far longer than the requisite 8 hours that we’re told that we need to sleep. And, I remember doing a show a long time ago where this whole notion of Polyphasic sleep, was it necessarily sleep during daytime once and a while, which if your body needs it you’ll probably should. But this notion that as humans maybe before even Palaeolithic times, we would go to bed so to speak when it got dark. But we didn’t necessarily sleep all that time. We would sleep for a while, wake up, we really couldn’t do much because we didn’t want to go out and be eaten by something so we laid there and then when we fell back to sleep again and we had maybe several of these episodes of sleep. Can you shed any light on this notion that do we have to sleep a certain amount of time, concurrently hours or is it okay to sleep in little partials so to speak?

Robb: Well, I think the key feature of all of that is photoperiod and then that when we get the photoperiod kind of dialled in then we produce melatonin, we suppress cortisol levels and then we sleep to the degree that we need to sleep. I think the way that modern humans sleep is actually an attempted adaptation to try to pack in as much resorted sleep in the time that we typically allot ourselves.

Carl: Right.

Robb: If we take it so normally, we go into REM sleep and then like stage 1, stage 2, through stage 4, stage 4 is like the deep restore development where neurotransmitters status is re-established and what not. If we take somebody and sleep deprive that person significantly for weeks on end and then allow them to sleep or even a few days, that person will tend to pass through the stages of sleep very, very quickly and they will tend to sleep like the dead and they’ll sleep that whole 8-9 hours or whatever and they will have much more tight REM sleep cycles and it will transition from cycle to cycle much more quickly. And so, I think that that’s on the far end of the spectrum where we take even a modern living human being subject them to significant sleep stress and then we’re going to see their sleep patterning really, really tighten up like all the grizzle gets trimmed out of there whereas that we’re living a more in spectrally consistent lifestyle, they might think that we’re going to accrue probably the same amount of sleep, it’s going to be broken up and a bit Polyphasic but again the real key with that is that photoperiod is less. And so, the recommendations that I’ve given to our clients and I mention in our folks is just blackout your room as best you can into the degree that you’re sleeping in a dark room that will buy you a pretty good chunk towards re-establishing normal neurotransmitters, keeping you lean, keeping insulin functioning good. It’s shocking what just sleeping in a dark room will do for folks. It’s amazing what other things you can do from pharmaceutical to extremely monitoring your diet and other things. Those things will end up comparatively failing relative to what just a good toll of night sleep will do.

Carl: We can’t ignore the fact that we live in an RF soup in this day and age whether that’s from routers and cordless phones to sailor transmitters that perhaps cast shadows on our homes but we live in this soup of electromagnetic field if you will in a very, very high frequency ranges one gigahertz and above and there is lots of evidence just study after study that shows that these frequencies create a neuro-excitability in the brain. Studies that, everything from close proximity like cell phones to just ambient RF and there is some evidence that these frequencies can actually impede the production of melatonin all the way up to stimulating the brain to a point where the brain cannot go through all of the different phases of sleep. I’m in total agreement with you about the prevalence of diseases, modern diseases if you will and it’s not one thing. We can look at diet absolutely plays a role but sleep plays a role as well. Is it possible in your humble opinion to even get good quality sleep, even if you blackout the room given the fact that we are in this RF soup.

Robb: Well, I think it’s going to be better whether or not it’s a good, when we vacation we tend to go off the grid, I mean, like mega off the grid so we’ll go to this little islands up the each coast of Nicaragua and I mean, there’s literally, not even like a generator on the island or if there is, it’s still [indiscernible] site.

Carl: Do you notice that you sleep differently?

Robb: I totally do. I sleep like a dead man in when your back pack you tend to.

Carl: See. There you go.

Robb: That’s very observational, it’s N equals one the study size and all that but it’s kind of a whacky thing too occasionally the power goes out, a power accident, lightning strikes, something like that. And all of a sudden you’re just not quite as frisky and you just kind of want to go to bed.

Carl: And there’s a noticeable vacuous feeling about when the electricity goes out in the whole town which has happened several times here in Louisville. It’s like this is, it’s almost like the same sensation when it snows where everything seems so quiet and serene and peaceful. And it’s not just an audible change. It’s actually a change in the way you feel.

Robb: Yes. Yes. It is almost like that goal hum from some place that you don’t know where it’s really coming from.

Carl: Yeah. Interesting. Very interesting.

Vince: I was going to say Robb, my wife and I, we visited her parent’s farm and it’s way, way out in the middle of nowhere. They just basically got, I think a cable connection that, it wasn’t a telephone line and I sleep like a dead man. You’re not kidding. I mean, it’s so quiet, so dark, obviously much less stuff going on. It’s unbelievable. It’s like when I go there I’m going to the sleep centre.

Carl: The sleep centre, that’s funny. There’s actually, I actually talked about this about a year and a half ago, there’s actually carbon based paints that are made as a primer that you can paint your bedroom with that act as an RF shield, take a Spectro analyzer in your bedroom. I always thought metallic but the person who thought me about this said, “No, metallic would actually attenuate, would attract RF” but there’s carbon based paints that you can paint your ceiling and walls with and then you can get carbon panels to put beneath your rug for instance and you can shield your bedroom by 90% of the RF that’s getting in there and kind of make a little cocoon for yourself. And I predict that in the upcoming years, this is going to be a regular thing that people are going to be talking about.

Robb: So, do I have to take down my ads for temple hats off my website.

Carl: They do work. I can attest for that because I do wear one.

Robb: I’ve been making a mint off those things so that’s going to suck.

Vince: Speaking of tin foil, Vegas has tons of shift workers, 24 hour town, I grew up there and the most common in the 60’s and 70’s way to block the sun out was renal draft tin foil on the windows.

Robb: Right.

Vince: What was that doing?

Robb: Increasing profits obviously. The gambling scene is funny. It’s dark but not super dark. You’ve got nicotine, alcohol and push up bras everywhere and it spends every dopaminergic neurotransmitter I can think of other than just directly snoring cocaine. So, that’s a good scene there.

Vince: My father was born and bred in the business and said it’s the only dope you don’t get to get by. There’s no product. It’s in the mist.

Robb: Right.

Vince: It’s in the mist.

Robb: Just along that line I’m actually supposed to do a gig for a mega dig casino chain and what their problem is that it’s a their employees are racking up staggering healthcare cost related around metabolic arrangements, crash in, all this other things and it’s the shift work, shift work and booze and a bunch of other stuff. But it is so shocking that these people are the higher ups are kind of like, “Okay we need to do something” or it’s like either one bankrupt us from the healthcare cost and two it’s kind of frightening because they’re literally looking at just like a whole blip or a whole generation of this people dying really, really prematurely due to the complications from their work.

Carl: Well, I wasn’t going to bring this up because I didn’t know if it’s appropriate to discuss in this show but now that you’ve said this it begs the question. You take an organization like that, when you point out to them, “Well, you’re killing people because you’re making them work the graveyard shift.” What are they going to do? Do you think they’re going to go, “Okay, we’re going to be a casino that closes at 10 o’clock at night or what does UPS or FedEx do? Clearly, this is something that needs to be examined.

Robb: Well, the thing is that, for me, I’m pretty libertarian in my politics so I don’t want to go in and try to regulate it or shut it down per say I would really like to educate both them and the folks who are working there. These folks that are being exposed to an extended photoperiod and eating a really poor diet a very pro-inflammatory diet, they’re not getting enough omega 3s, I mean, on and on and on. Can we at least figure out a way to say, “Hey guys, if you could choose like a stake and a salad for dinner before you go to bed after you get off shift versus a giant plate of nachos or a pizza then you might live long enough to see your kids graduate college”, but I mean, that’s also a big feature of this is that these folks working these jobs, they’re probably taking care of their kids during the day and then working the night shift at night and so it’s not necessarily just like the evil corporation but they’re providing legitimate work for people that need it but then you just have a remarkably unhealthy culture that grows out of the whole thing. How do you fix that? I mean, we could go to a different scenario in which it doesn’t look so unseemly which is that police, military and fireman.

Carl: Right.

Robb: Do we just have our police officers and fire-fighters just not responding? And that’s part of the reason that these people really are providing a service and they really in my opinion are providing a sacrifice because they take a significant impact on their health not just from the stress and the difficulty of the job but also because of the shift work. And that’s part of why I absolutely love those folks because they don’t even know in some ways how hard they’ve got it, how difficult that work is when you throw in the shift component.

Carl: But see, I can appreciate those jobs and I can understand why those jobs may require a more heroic effort or commitment. But the fact that, I mean, I can remember a day I’m dating myself. But I can remember a day when businesses were close on Sundays and where TV stations went off the air at midnight because people were asleep by then.

Robb: Right.

Carl: The ever raising competition for dollars has people working round the clock not just, I mean, let’s face it, workers are lining up to take that graveyard shift. I am not saying companies are being villains here but companies in order to be competitive, how are they going to cut back, how is FedEx going to say, “You know what? We’re going to deliver packages the following afternoon because we’re going to let our workers sleep at night because it’s healthier.” And people are going to go, “Wow. That’s a really noble idea. Hey, call UPS because this package has to be there by 9AM.”

Robb: Right.

Carl: How do you get people to understand that we’re killing ourselves in the pursuit of green bucks here?

Robb: I don’t know, I mean, for me, what I try to do is just try to educate folks as best I can, so like that UPS shift worker, when that woman or that guy comes home from work, then what I want them to do is eat a pretty low carb meal and generally they’re probably going to need to eat low carb in general and hopefully they lift some weights and then do a little bit of activity to keep their muscle mass and their insulin the best they can and they supplement with vitamin D and they supplement with fish oil and when they go to bed they sleep in the pitch black room and they protect that nugget of sleep that they do get with bayonets and barbwire.

Carl: Right.

Robb: And that will improve things. Does it make it optimum? Absolutely not but then, at least providing some education for these folks so that when they’re like, “God, I feel like I’m dying and I’m only like 35 years old and I feel like I’m just aging like crazy” and it’s like, “Well, you are.” And so, we’re going to provide a little bit of resources for you to think about your food, to think about your sleep, your sleep hygiene and everything. They’ll go to bed and they’ll have kind of a dark curtain and they’ll put on a sleep mask but they don’t understand the biophysics of the whole thing which is that any of that ambient light that’s trickling in is just adding to their total photoperiod exposure and it’s not doing them any favour so it’s very deleterious.

Carl: But Robb, is it, I mean, I had Dr. Russel Ritter on my show a couple of times. Is it simply darkness? Or isn’t the body also attuned to more than just darkness? Wouldn’t it benefit a shift worker to come home at 8AM in the morning, put the blinders on, get in that pitch black room, quiet room, but also take maybe 600 micrograms of melatonin just to kind of ensure that the body produces some?

Robb: Absolutely. Absolutely and I mean, how expensive of a fix is that? I mean, maybe 6 bucks for like the 6 months of life.

Carl: Right.

Robb: I mean, yeah, yeah. And then we’re talking about dramatically improving the quality of life in a lot of people, dramatically improving probably the services provided and let’s think about that was like police, military, fire and medical scenarios in which people’s lives are at stake and then let’s look at the health of these individuals and by providing them some education about sleep in a dark room, take a little melatonin, eat a lower carb diet, lift some weights and do a little bit of exercise everyday to re-establish your insulin sensitivity as best you can, that will save their lives. And that doesn’t hardly cost anything, I mean, now compliance with the whole other deal but I mean you can have people existing on a normal schedule and they can do all kinds of squirrely lifestyle stuff to kill themselves. So, you’re not going to save everybody with that. But the problem that I see is just that there is no education about this topic at all. And this is a lot of the thing that I end up doing for the special operation community is just making this dudes aware that, “Okay, you are going to be awake for two or three days at a time occasionally when, and that’s just your job, you’ve signed up for it, we’re not going to be pussies about this and we’re just going to deal with that.” But, when you get home or you get back from an operation, you need to sleep in a pitch black environment and it’s been pretty cool, the folks that we’ve worked with, they’re getting some really good support from the higher ups who not surprisingly are doing these things, sleeping in the dark room, keeping their carbohydrate intake matched to what their physical expenditure is and stuff like that. So, it’s improving their insulin sensitivity. We’re considering things like food intolerances because those things all feed into systemic inflammation and stuff. We’re making sure that the guys and girls get adequate vitamin D and these are dirt cheap interventions which provide just shocking return on investment.

Carl: Yeah.

Vince: Yeah. Well, I was just going to mention Carl I know we’re getting ready to take Layne Norton.

Carl: Right.

Vince: Robb, can you join us?

Robb: Sure.

Vince: After the break in a minute here with Layne Norton and Dr. Connelly?

Robb: Absolutely.

Carl: Okay.

Vince: I wanted to just bring one thing up which is, I have a 14 year old daughter and her, I mean, talk about pushing the envelope with the homework and the activities that they have, they’re really pushing it into the late hours and now with all the electronic devices that they communicate with. That’s probably going to come back to bite us for sure.

Carl: Yes.

Robb: We just might get sophisticated enough that we no longer able to reproduce at some point.

Carl: But you know what? Don’t laugh, I mean, reproduction, people think about reproduction the wrong way. If we can’t reproduce it’s because we’re not supposed to because this species is not supposed to go on any further. So, it is really scary and you’re right. And being on the cell phone for a half hour before going to sleep, for as little as 15 minutes can actually impair your ability to get into the deepest stages of sleep for the first 3 hours you spend with your eyes closed so because of that neuronal stimulation that excitatory effect of those higher frequencies on the brain. So, make sure that your kids shut the cell phones off at least a half hour before you intend for them to go to sleep.

Vince: And you can’t read any romance novels either Carl.

Carl: Because of the Kindle?

Vince: Well, no, you can’t get excited. So you can’t Tom Clancy novels and romance novels, you can’t do that either.

Carl: Why? They stimulate you too much before sleep, is that what it is?

Robb: I think the romance novels are fine for the ejaculation they always remind you of medical school point and shoot which is a parasympathetic sympathetic and so you’re actually trying to do in a full system reset.

Carl: I love that.

Robb: If danger goes enough, then it’s kind of like flipping the reset switch.

Vince: That’s a full reboot.

Carl: There you go. You know what? I have to confess. I’m a big proponent of watching one episode of Family Guy right before going to sleep because I believe that a good hard laugh before you go to sleep is very therapeutic.

Robb: Agreed.

Carl: There you go. There you go. Alright, Vince, you want to go ahead and take our musical interlude now?

Vince: Sure. We’re going to take a quick musical break and we’ll be back with Dr. Connelly, Dr. Layne Norton, and Robb Wolf.

Carl: There you go. We’ll be right back.

[Music Playing]

Vince: We’re back with Dr. Connelly, Dr. Layne Norton and Robb Wolf talking about sleep duration.

Carl: Welcome Dr. Layne Norton.

Dr. Norton: Hey guys, how’s it going?

Vince: Very good.

Dr. Norton: Good.

Carl: Dr. Connelly, you did a lot of listening this last segment.

Dr. Connelly: That’s because I was catching up on my sleep.

Carl: You stinker. What stage of sleep were you in Dr. Connelly before I interrupted you?

Dr. Connelly: 7.5

Carl: Very good. Very good. Good.

Robb: I have that effect on people, when I talk, usually they’re called illusioning of the bowels or they talk right up in a narcoleptic style.

Vince: I have to mention something to the listeners. Dr. Connelly sleeps like 1.5 hours per night.

Carl: Is that the truth Dr. C?

Dr. Connelly: No, I actually sleep 2.3 hours per night.

Carl: But truthfully, do you sleep very short periods of time?

Dr. Connelly: Yeah. I think it’s a function of, a mandatory adjustment to lifestyle, as active clinically between the OR and the ICU that I was directing, I would frequently spend most of my evening in continuously interrupted sleep patterns whether it’s in the hospital because I was the call attend, on the call attending or whether it was at home. I had unusual responsibilities because of my position on the cardiac transplant team that if we had a transplant patient regardless of whether it was on-call or not I still was on call. So, I spend several nights in the hospital just out of necessity because going home would have been ridiculous. And as a result of that lifestyle, I got very acclimated to extremely short sleep duration over a period of many, many years, decades actually.

Carl: Do you feel that, has that had an effect on you? Has that any effect on you, you think?

Dr. Connelly: Well, I think to, on point to what Robb had said, I think the impact on me was mitigated by the fact that regardless of my lifestyle from the standpoint of sleep duration, my waking hours were always structured around getting as much resistance exercises I could and obviously I practice nutritional surveillance for my entire adult life. So I think the impact on me would have been less mitigated as compared to maybe one of my colleagues who didn’t have the proclivity that I did for exercise and nutritional consistency. I can’t tell if it did or not. I know that from the standpoint of my energy levels and so forth that it appears to have had no impact. There were rare occasions where I would be forced by virtue of emergency case loads to just stay up for 3 nights straight with no sleep at all. One of the interesting things I found personally was that I learned very early on that if I was going to be challenged by an extended period of waking in an environment which required me to be extremely focused mentally. These emergency cases at night involving people who are best door were not cases that you could take a nap through. So, I found that if I did try to grab say like an hour or two hours of sleep in between the finishing case and the next case that it would put me in a state of complete dysfunction. Staying up and pushing through was always a better choice than trying to grab a couple of hours because after the couple of hours, I was pretty much non-functional. It was really dramatic demonstration that, you accrue some significant deficits physiologically and cognitively when you’re acute sleep deprivation which is different than truncated sleep duration over time. I had several instances when I was acutely sleep deprived and I found this personally that if I tried to grab a couple of hours, 2 or 3 hours sleep in between those periods, it was devastating on my performance capabilities. So I would just push through.  And interesting enough, the last time this happened to me was the last year that I had in the operating room environment. I agreed to take an extended on-call period during the Christmas holiday because I was not married and did not have children and my partners did. So I accepted the holiday call willingly. And I had a case come in about 7PM on Christmas Eve that was a dissection of the aorta that required the hypothermic circulatory arrest technique where in order to fix this guys aorta, we had to disconnect from his heart and replace it with a Dacron patch and re-implant his carotid artery. So, his cerebral circulation had to be interrupted for a protracted period of time which normally is pretty bad for you. That happens. So, we resorted to examining the patient into the cardiopulmonary bypass machine and cooling his body temperature down to 18 degrees centigrade and arresting his heart in the process of cooling. And we, since it drained all the blood out of his body, restored him with an electrolyte amino acid potassium insulin glucose solution to keep his anaerobic capability at its highest level of functionality so that the tissues would not devitalize and then operated on the guy for an hour and 16 minutes with no flow or no circulation to the head. And he had Morphine syndrome, a connective tissue disorder that creates very abnormal connective tissue in the root of the aorta. So we had to end up doing this on-off technique 4 times and it lasted, that case lasted 27 hours. So, starting at 7PM on Christmas Eve, I went all the way through 27 hours and had essentially a horrendous post operative nightmare with him that lasted into the next day and then subsequently two other very acute cases came in. So it ended up, this was starting on a Thursday evening essentially operated or work the ICU continuously from Thursday evening to Monday morning with zero sleep.

Carl: Wow.

Dr. Connelly: That was kind of the epitome of my experience in the standpoint of acute sleep deprivation and concomitant high velocity stress. And it was interesting that the night that I actually retired, I went to sleep that Monday night at my usual late hour and I woke up the next day at 4:30 like I always do. So, it’s kind of a curious demonstration that you can become quite adapted to this and get your normal 4 or 5 hours of sleep and even a protracted period of acute deprivation, I could still, I was functioning normally, I obviously didn’t have the opportunity to assess my acute insulin response to a glucose load or anything of that sort. But from the standpoint of functionality, a perceived level of fatigue and what not, I was fine if I got 4 hours after 3 full days of deprivation.

Carl: Wow. Dr. Connelly, earlier in the show and this discussion that we’re having right now with you makes me want to ask you for your professional opinion. When someone is in the hospital, it’s quite regular practice to wake them up throughout the night for this, for that, sometimes they’re waking them up because they have to check vital signs, sometimes they’re just waking them up because the nurse has to go in and do something in the room. And anybody who stayed in the hospital for a few days knows that you don’t get good sleep. What impact does that have on recovery of a patient?

Dr. Connelly: Well, I can’t give you a real objective answer to that Carl but obviously that practice is problematic from the patient’s perspective for sure. But as you said, a lot of the instances, this is really kind of a necessity especially with people who are somewhat unstable who are on vasoactive or metabolic medications they really can’t be left unmonitored asleep for extended periods of time. But I know in the situations where I was in practice, most of those patients who required that kind of interruption were always in high monitoring units, either ICU or step-down ICU and the regular patients would pretty much be left alone.

Carl: Wow. Okay. Okay. What, Dr. Connelly, you sat back and listened for quite a while, while Robb was discussing and answering our questions. Did you have any opinions or there was anything that you wanted to say about that portion of the show?

Dr. Connelly: Well, I think that in large measure I agree with everything Robb said. The perspective that wanting to make sure we check everybody out on with respect to the listening audience is that it’s important to realize that they’re in a relationship between what occurs normally as metabolic regulation as a function of circadian physiology is representative of really on a micro scale what happens when you have, in all mammals, an occasion where that mammal is confronted with an ongoing depletion of energy stores as would occur in a protracted period of fasting or low-calorie dieting. And since we’ve been pretty obsessive about counselling people against the methodology employed by most diet programs which is essentially calorie restriction of a pretty significant nature, one of the things that we need to remind our listeners who are on board with us with respect to how to modulate body composition appropriately are not relying on a pure calorie strategy. It’s interesting to note that in humans there is data that shows that there’s a sort of compounding effect on the adverse effects of truncating sleep duration and essentially low-calorie dieting in that a recent study about a year old that was done in University of Chicago looked specifically at that, was there a compounding effect between abrogating a person’s normal sleep duration significantly while having them on a typical low-calorie diet protocol. And, what’s interesting is that in that study there was a dramatic intersection between those two variables, both of which would tend to essentially reduce metabolic exchange rates as measured in this case by the RMR and also to impact non-resting energy expenditure in a way that would typically in an adaptive situation occurring naturally in the world with a mammal or human. For example, seasonality of food availability and things like that that essentially, in those circumstances, the response of the metabolic regulatory system is to reduce energy expenditure and conserve vital structures and the adjustments in all of the circulating hormones, cytokines, and their ancillary players are kind of adjusted in tune to that. This is different than a one dimensional response to a perturbation in a system that we call homeostatic response or in other words if your body temperature elevates because your working out hard in the gym and your body temperature starts to go up, there’s an immediate homeostatic response to that that essentially involves an objective response in the formation of sweat. And in essence, that’s a one dimensional homeostatic response to a single variable perturbation of body temperature. There are other things that occur that are invisible from the standpoint of that specific stress and response that are really not homeostatic but what are called allostatic and those changes are adaptive and they involve a highly orchestrated integration of responses that accrue and are incurring in parallel to a primary homeostatic adjustment. The observation from a lot of different parameters and studies in biology suggests that allostatic adaptations if protracted can be maladaptive in the long run. And one of the issues that has a very prominent degree of significance with respect to what is the consequences of having chronic sleep disruption or shortened sleep duration in terms of our primary focus which is always been how to optimize body composition is that we know from this recent Chicago study that if you are reducing energy deliberately via dietary strategy and have as an attendant complicating factor short sleep duration, you’re going to reduce your ability to oxidize fat which is your primary goal and you add the added maladaptive response of accelerating tissue os. So once again, under circumstances where these two things are occurring simultaneously, it’s important to remember Robb’s point that you have some tools to offset, not eliminate but to at least mitigate some of the adverse metabolic regulatory consequences that would accrue and those would be pay attention to the macronutrient distribution of the food that you’re eating especially surrounding your waking and sleep cycles and that I would agree very emphatically with Robb that you need to be more conscious of protein intake in a very conspicuous way and you need to be very, very conscious about restricting carbohydrates. As we have said over and over and over again, this particular solution set has a great deal of variability within the confines of the human race there is a huge range of responsiveness and susceptibility to the adverse effects of these kinds of perturbations in waking and sleeping cycles. And this is evident at the level of all aspects of glucose regulation and body fat oxidation and so forth and so on. But if you’re a person who historically knows that you are prone to gain fat, then this issue of short sleep duration and the dietary intersection of short sleep duration and your energy intake, your activity profile and the macronutrient distribution that you’re accustomed to can have a pretty significant effect. So, in essence, we know that a short sleep duration type of profile chronically over time will tend to reduce the proportion of energy expended as fat. That will deteriorate your body composition over time to more fat less lean tissue. Not good. If you compound that with a truncated calorie intake because you’ve listen to somebody on the news say that despite all the hoopla about this, that and the other thing, it still all boils down to calories in and calories out. And you simply can’t resist embracing that proclamation then short sleep duration will compound the adverse effects of that calorie restriction. So again, in keeping with the main sort of message here, is that there are a lot of variables that are fine-tuned to control higher body senses in response to energy deprivation and excess. Those are intimately related to circadian rhythms that primarily skew, as Robb said, off of light-dark cycles. And obviously, the manifestation of this in the extreme is, are rocky, are gray, North American gray, ground squirrel who hibernates. And all of these manifestations come to a zenith of precise regulations in those animals that hibernate successfully. So, I think we should probably take maybe our last music break at this point and then come back and have the gang kick around some ideas about how to practically address these issues and in and out of the gym.

[Music Playing]

Vince: We’re back! Discussing sleep deprivation and want to turn the show over to practical solutions to fight either occupational hazards, environmental hazards or if you’re just battling the bulge and you suspect that sleep may be a problem. Dr. Layne Norton, we haven’t heard from you yet.

Dr. Norton: Thanks Vince. I’ll be the first to kind of say that this is definitely not my area of expertise but everything I can gather from the research I’ve seen on sleep, probably the organization has done more research on sleep than any other I’d say is the military. They have a very obviously vested interest in performance and how sleep intersects with that considering especially some of their commando type units or high level Special Forces units are going to be often operating on very limited sleep. What I’ve seem to see here is a lot of this problems you get with sleep deprivation isn’t necessarily the fact that you’re getting sleep deprivation, it’s the fact that it causes you to have a very pronounced stress response. Dr. Connelly mentioned earlier that once he was in his routine of what he was doing and got adjusted to that, that he didn’t really have that many problems with kind of the weird sleep schedule he was all in and this is kind of what some of the research has shown is that you’re going to have an odd sleep cycle but if you’re adjusted to it and if you know what’s happening, it makes a difference. Let me expand on that. The military did some research where they looked at if they woke people up from a truncated sleep without telling them. So, they wake them up after, let’s say, 3 hours and they administer some kind of test, some kind of tactical test in order to test their cognitive ability and their performance ability. They found that it was severely impaired. However, if they told them the night before, they said, “Look, we’re going to be waking you up in 3 hours and you’re going to be taking a test.” Just by telling them that, just by doing that, it improves their performance significantly. So, there seems to be some kind of this just cognitively knowing that you’re going to have truncated sleep seems to help in terms of how to get not be such a problem. So I guess, for those of us who are not in the military, the kind of the comparable thing was the, “Okay. Well, we know you have an early flight the next morning. You’re going to have to get up early.” For one day, you can push through that and you’re probably fine. The problem comes to be where you’re going to sleep and then your dog goes nuts in the middle of the night and wakes you up and now you take it back to sleep and now you’re stressed. It has that stress response and that stress response manifest in the way of hormonal, even proteolysis in terms of muscle protein breakdown and performance in resuming your everyday activities. And so, I think that, for example, we’ve kind of had this debate before in the show, is it worthwhile to wake up in the middle of the night and eat something or you don’t have a meal or stake or what have you. This is something I’ve always done because our lab has shown that most of the protein synthesis drops off after an overnight fast and Connelly stated many times that he prefers that, that he prefers to sleep all the way through. I don’t think there’s a right or wrong answer here but I am accustomed to getting up. I know that I’ll be getting up, cognitively I know this, I know it happens every night because I wake up to go to the bathroom, I drink a lot of water before bed and it’s never affected my performance at all. Even cognitively, sometimes I’ll wake up, I’ll go drink my shake and while I’m drinking my shake, I’m going through emails on my phone and just kind of answering emails. So, cognitively, it doesn’t seem to affect my performance because I know that I’m going to be doing that. Now, if I get woken up an hour in to sleep or two hours in a sleep, I haven’t had much sleep if it’s something more abnormal than what I’m accustomed to, then I’ll have problems. And that’s kind of what this research has shown that if you have, you can become accustomed to weird sleep cycles as long as you, one, it’s regular, it’s not kind of irregular and two, you know kind of ahead of time exactly what’s going to be happening. Whereas if you have a very irregular sleep cycle where you don’t really know when you’re going to be getting up, that seems to be the worst case scenario. Again, this is not my area of expertise but that’s kind of what I’ve gathered from the research and kind of the outcomes of this or as Scott said, increase muscle protein breakdown, decrease fat oxidation and that’s probably because when you go to sleep, when you sleep for long periods of time, your body responds by trying to spare carbohydrates, increase fat oxidation to spare that carbohydrate and that’s in a form of increase growth hormone which increases lipolysis and several other things. So when you get sleep deprivation and irregular sleep you have decrease growth hormone output, you have decrease testosterone, increase proteolytic activity and so it’s kind of a convergence of things you don’t want happening together. So, I think, again, most important thing is just to kind of try to make sure your sleep cycle is as regular as possible and kind of know when you’re going to have to have abnormal sleep. Those seem to be the two biggest things at least from what I can pick out from the research.

Vince: Thanks Layne. And so, Robb, in your opinion, awareness versus, let’s say, the shock factor of a car alarm going off or a dog barking, what’s your play or take on that?

Robb: That makes a ton of sense honestly, I mean, that definitely makes a lot of sense but the unknown always kind of trips this up worst than the known and that’s part of why in this selection committees whether it’s a meeting on a professional sport team or something like the fields or rangers or something like that. They try to figure out as many horrific ways to make these guys experience the unknown and discomfort in a comparatively controlled environment, one which they’re probably not going to get killed so that when they’re thrown in to a completely unknown, completely open ended uncontrolled environment, but to some degree they can match that stuff up intellectually and physically and stuff like that. My thing with that though is that it’s my opinion that that stuff still comes at a cost that I still think relative to and otherwise like ideal sleep scenario that you’re going to see some sort of negative side on that and so it would be interesting to check out some of the studies there like were these folks just within operational parameters, did it take them off of optimum, it would be interesting to see some of that. But I have no doubt that trying to stress inoculate people making them more aware getting them on a schedule such as they know what the stressors are going to be, is going to be if you’re but then that’s completely emphatitical frequently to the very nature of the way that these folks operate. It is interesting like fire houses they no longer have the blaring alarms that just jolt you out of bed. It’s actually, it starts off relatively quietly. It’s not a jolting up a noise. The guys don’t hit the deck quite as quickly and get going but they are finding that they also don’t die from the experience. So, kind of lose a little up front but you keep a lot on the back end.

Vince: Yeah. The anxiety factor is got to play huge in all of this, short and long term. And then it’s kind of like not really watching your diet but thinking you can over exercise to overcome it.

Robb: Right.

Vince: Well, I’d like to talk a little bit about nutritional interventions beyond higher protein, lower carbohydrate, things like that, like maybe magnesium, I know you’ve talked about that before Robb, we talked about melatonin. Robb do you want to start off and maybe talk about some things that folks can do to, I guess, stack the odds in their favour a little bit more?

Robb: Yeah. Yeah. The standard deal like magnesium citrate, I really like the natural calm stuff just because it taste kind of good you throat some of that and some water. Those on melatonin just seems to be huge as to the variance as to what will produce results in people, some people respond very favourably to as little as like a quarter of a milligram but I have a friend of mine who’s a fundee at the University and she will routinely prescribe people 30 to 40 milligrams of melatonin depending on their situation. So, that shit’s a shocking variability in the amount that folks take. When I travel, I will take 5 to 10 milligrams if I’m on a really, really tight sleep schedule, say like, I rise on an evening and then the following morning I have to speak and I’m going from west coast to east coast. So it’s going to be really hard for me to rack out and go to sleep and I’ll do 5 to 10 milligrams in that is so much better. I may be a little bit groggy the next day but it’s infinitely better than lying awake until 3 or 4 o’clock at night and then waking up 2 or 3 hours later and needing to get going. I’ve actually read some stuff in doing vitamin D in the evening because of some of the effects on calcium, some of the effects that the calcium would have on neurotransmitter status and what not, I’d historically recommended people take the vitamin D in the morning. And this first kind of got on my radar when I was at a naval special warfare speaking gig and they had a sleep expert at the event and he had some pretty interesting insights but I was kind of tickled that the rest to the protocols he was recommending, pitch black room on a little bit on the cold side so he had to like curl up under the blankets, magnesium, lower carb diet, etc. etc. etc. He was totally spot on with all, I would flip around and said he’s the sleep expert not me but I’d flip that around and say he was in pretty solid agreement on that. It played around with some things like valerian and what not. I just haven’t seen good juice out of that stuff. So, I would say one thing. Folks will frequently have a drink or two in the evening with the kind of misguided thought that it’s going to help them sleep but it just destroys melatonin production, curtails growth hormone production, it may kind of conk you out but the sleep quality is terrible and that this is some stuff that we see again out of the military where they have go pills and no go pills, the no go typically being something along the line of Ambien and they will put you out but the restored development that the sleep is just not all that good as compared to like melatonin or something like that. But sometimes you’re so fired up that you need something that’s a little bit more aggressive to actually get some movement.

Vince: And you mentioned, real quick, magnesium, what about the relationship with calcium? Is there a relationship that you suggest Robb?

Robb: Definitely and I tend and this is maybe being a Nervous Nellie and Dr. Connelly can probably comment on this and set this straight one way or another, I’m a little nervous about very much calcium supplementation because of some fears of cardiac events because calcium is the precipitator of most clotting cascades and there is some stuff in the literature that seems to indicate, aggressive calcium supplementation can be problematic. But again and again, the thing that I’m falling back on is that when looking at a lot of these studies in sick populations, if we’re dealing with another healthy population and this is going to be a problem. But if that’s, that’s why I historically kind of aired on the very conservative side on the calcium supplementation.

Vince: Interesting. Well then the other topic I wanted to just touch on with the whole crew is the neurotransmitter precursors. I know you mentioned herbal valerian but what about 5-HTP or tryptophan?

Robb: For me, again, I’ve seen more juice come out of melatonin although, I’ll throw in a copy out of that, depending on how different people are wired up, I’ve seen 3 to 4 grams of Gaba do amazing things for certain people. So I think depending on which access of the neurotransmitter scene you’re trying to address that help people to fall asleep then I have seen both Gaba and melatonin in my opinion have seem to work better than tryptophan or 5-HTP.

Vince: Well yeah, I agree, especially if you have a whole gutful of protein, those precursors and the amino acid precursors tend to not work much at all.

Robb: Right.

Vince: Layne, do you have anything else to add as far as on the nutritional, beyond the surveillance of your diet, maybe some tricks you have up your sleeve?

Dr. Norton: I think, since we will cover that, I definitely, if I have trouble falling asleep melatonin will usually put me out pretty good but it’s a nice, it’s hard to describe but I guess it’s kind of a nice, I’m in the 3 to 6 milligram range that was pretty low for me. And it’s kind of a nice relaxation. It’s not really, you just in a point where you just won’t, you’ve got to go to sleep. It’s kind of like a nice, makes you relax then you kind of gradually drift off and which I prefer as opposed to something just puts me right out. So that’s definitely one thing. As far as kind of mitigating the problem, I guess if you’re somebody who’s just really on the go and you, you can only get 4 or 5 hours of sleep at night and that’s all excusable for you and those sorts of things because I know some people though they told me like, I work a job, I commute, spend some hour with my family, for me to train, it all boils down to, yeah, I can get 6 to 7 hours of sleep but that also means I don’t train. Obviously, our little secret getting into, all I want to say it’s always better to train some than not get that sleep but if I was fit between, I was healthier, 5 hours of sleep versus 6 and have 8 hours of training in there I would say by 5 I will be out of training. So, you’ve got to kind of live life that way and you’re making sacrifices, I think you need to treat kind of the symptoms in terms of stress responses. And so, taking something that will help restore any kind of lost testosterone increases, something like ascorbic acid that will kind of moderately increase kind of make up for whatever decrements you might get from lack of sleep. I got to be careful. I don’t want to make that recommendation gladly you need to, VAA is still pretty new, they don’t seem to be any health effects associated with it but as always you need to kind of wait and see what happens. As far as stress, there are some decent herbal things that will reduce cortisol and I’ll be honest with you I can’t think of some of them off the top of my head but there are a few things out there that will reduce cortisol and the reason I don’t really know those things at hand is because most times I don’t think that reducing cortisol is that big of a deal. Everybody kind of gets all up in arms about the cortisol response to training and you want to limit cortisol response to training. I think that’s pretty stupid. I think that short term increases in cortisol really don’t mean that much to stress response, mobilization response to training, actually some of the research out there they’ve actually found that groups that get the dust hypertropin response to training also to the highest cortisol response. I’m not big on trying to mitigate short term lyses in cortisol in response to exercise. However, long term low level increases in cortisol as a stress response are definitely something that I don’t think are a good thing and I think trying to limit those to kind of a supplementation route may have benefits especially when you get sleep deprivation. I guess that would kind of be what I would throw in there as kind of a way to mitigate things. I’ll also say that training wise, I’d probably stay away from doing a whole bunch of cardio, I mean, if your goal is, if you have very limited time to where you’re trading sleep for training, weight training is going to have a bigger metabolic impact on your muscles than getting on treadmill for 30 minutes and just walking or whatever, you kind of got to pick your training in terms of what you’re going to be doing because you’re trading minutes. So I would definitely favour a quicker phase weight workout as opposed to cardiovascular work.

Vince: Interesting. Well, what about the 500 pound gorilla that was always in my life which is caffeine, they’re the most widely used drug on the planet.

Dr. Norton: I think that, caffeine’s one of those tricky things because those people who metabolizes slowly, those people who metabolizes quickly, those people who are very responsive to it, very sensitive to it, there’s people who aren’t very sensitive to it. So it’s tough to really make general recommendations for caffeine consumption but I would say it begins to be a problem when you can’t function without 3 cups of coffee but then you need a sleep aid to get to sleep. Like that’s the problem. I don’t know, it was Robb talking about, I mean, it’s not maybe on the pain scale of taking go pills and then Ambien. But I’d say if you got in a cycle where you’re taking a bunch of caffeine to get up and take a bunch of melatonin to go asleep, that’s probably a problem.

Robb: Herbal elements at that point I think are not good.

Dr. Norton: Yeah. Exactly. You kind of somebody switch it out for decaf and tell you its caffeine.

Vince: Well, it’s like most of our, all of our shows, we have the educational piece but then we also have the practical piece that comes from really awareness what are you doing on a day to day basis. And if you’re one of those people that has trouble sleeping but has to use 2 pots of coffee to get it up then maybe you need to make some adjustments.

Dr. Norton: Yeah. Exactly. I think that maybe a case where it’s time to start seeing a physician who specializes in sleep because obviously you are tired because you’re having trouble getting up but you’re having difficulty also falling asleep.

Carl: You know what the problem with that Layne, is that most physicians who “specialize in sleep” are just going to prescribe something like Ambien or some sort of sleep aid.

Dr. Norton: That’s a good point.

Carl: And you know what? Robb made an excellent point, I know physicians that recommend to their client that their patients who are having trouble sleeping have a glass of wine before bed and I’ve known for a long time the disruptive qualities of alcohol, people, just because you close your eyes for 8 hours, doesn’t mean you’re really sleeping for 8 hours, there are people who take antihistamines to help them go to sleep. That’s the frustrating part. Sleep is so important but it’s really hard to get good advice on how to correct sleep problems. What do you think about that Robb?

Robb: I definitely agree, I mean, histamine production is the precursor to growth hormone production. So you’ll do a little bit of Benadryl or something like that or some of the similar antihistamine products and it’ll kind of knock you out but you’re really not sleeping, really not recovering all that well. What I’ve just seen over the course of time is running a gym and kind of seeing people roll in and stressful jobs, high achieving people, all the rest of that but to get in this kind of zombie life stupor and they function and they go on like they may run very big, very successful companies and stuff like that or have a lot of important things that they do. I think they’re just way tougher than I am, the schedule that they keep would kill me and they’re far from optimum in doing some of these things like the sleep aids it doesn’t really do them any good, it’s a short term deal because you went through a time zone change or something like that you see that being solid. But there again, you quit running your business, I mean, what do you do, I think you do the best you can to manage the stress, try to go to bed earlier, cover the sleep hygiene. It goes back around again like lowest carb diet, resistance training, mitigate other stressors, vitamin D levels, taking Probiotics, there’s some other things that’s typically they are not on the radar of folks but if we try to make them aware of it and try to hand hold them through the process.

Carl: The vitamin D thing makes perfect sense because when is vitamin D produced in sunlight?

Dr. Norton: I think I’m messing this up. But I think it’s a little bit interesting like the light-dark cycle in the photosynthesis. I think we get some of the precursor stick of steroid manufacture during the day and then I think the actual vitamin D production happens at night. I could be wrong on that. I’ll double check that if I’m wrong a thousand pardons but I think we actually get a precursor stick of steroid production during the day and then actually it’s kind of a night cycle thing where the D is actually produced so that would make sense, I just thought of that.

Carl: Well, I mean, vitamin, maybe I misunderstood, Dr. Connelly, am I misunderstanding, isn’t vitamin D synthesize on the surface of the skin and works its way in to the skin after sunlight exposure?

Dr. Connelly: Yeah. There’s some pathway for alternate roots of synthesis but the sunlight aspect of it is pre-eminent and with respect to the issue of this supplement and stuff for sleep, the things that have always impressed me are the natural agents which act with, in the confines of the pre-eminent neural circuitry patterns that influence sleep wakefulness through impacts on Rexigen A and B and some of the other Gaba and NMDA pathways. Obviously, that leaves you with a couple of obvious choices. One is melatonin and there’s some recent data on a new form of protracted release melatonin that’s I think a 2 milligram dosage that has an altered release characteristic. The safety inefficacy studies on that have been continuing to come out and show especially in older adults that that’s a really a precocious supplement. The other thing that people have talked about that you guys have mentioned is the magnesium and I think people underestimate the power of magnesium because it’s not as well-known sort of in the public domain as the melatonin story is but magnesium has a powerful effect in the pathways that you would really want to target. It’s a pretty potent Gaba agonist and it works in doses like 30 millimoles so you don’t have to worry about any kind of gastrointestinal issue or anything like that. It’s a pretty effective supplement for sleep. I don’t think many people know that but for those of the audience who are looking for something, you’ve tried melatonin maybe not been satisfied with it, you may consider adding the magnesium as a solution to that.

Carl: Robb, do you have any opinions on transdermally delivered magnesium oils and creams and stuff like that?

Robb: I’m going to piss somebody off here but it doesn’t make any sense to me. We met Malone tonight, he’s an organic synthetic chemist at Harvard, he and I dug through the literature and I tried to figure out what the heck I would have to do to divalent metal ion to make it transdermally absorbed and/or if there have been any simple studies, just basic kinetic studies where we would apply this stuff dermally and then see an uptick in plasma magnesium concentration and I’m just not seeing it.

Carl: So, it’s not even getting through the skin, you’re saying.

Robb: It doesn’t make any sense to me that it would. Otherwise, when we jump in salt water we would eliminate and pop like a red blood cell. So, in Lester’s sub, this is getting out there and just getting wowo in trying to do a hat tip to a bunch of observational stuff. If there’s something to it, then maybe it’s modifying some sort of dermal electrical conductivity because of the divalent metal ion floating around on there. We know for a fact that Epsom salt baths are very therapeutic. They’re not absorbing into us. But we know that there’s something therapeutic there, that see, bath types up, salt water types up, things would be therapeutic for recovery but as far as the mechanism, if it is doing anything, I am daggered as to what the mechanism is.

Carl: Cool Dr. C, how much magnesium do you need to take you think for it to be effective to help sleep?

Dr. Connelly: The studies that humans that really look at very objective, empirical and markers such as for example EEG changes, and nocturnal neuro endocrine fluxes and some of the hormonal cascades that are relevant to the issue, the optimal dose of, if memory serves me correctly, is about 30 millimoles of divalent magnesium.

Carl: So, okay, 30 millimoles, does that translate to any type of oral dose? Are we talking about just plain old magnesium? What is it?

Dr. Connelly: It will again depend on the form that you took to salt form so you’d have to just pick a particular compound to determine what its aggregate composition is and then do a simple calculation, go to online and say convert this to millimoles of magnesium.

Carl: Okay.

Dr. Connelly: But 30 millimoles of magnesium is what I remember the efficacious dose in humans to be to as again absorb not only symptomatic benefits in other words efficacy for promoting sleep but also in terms of recording reversal of sleep EEG changes that occur with insomnia and also balancing the nightly release of neuro endocrine factors that that’s the dose that I recall as being effective for those two parameters.

Carl: Okay. Vince, we’re coming to the end of the show. Do you want to wrap it up? Do you want Dr. Connelly to go ahead and summarize what we’ve discussed here?

Vince: Well, I just would say that, what I grab from it was being aware, we’re in a situation right now of modern living, so to speak, that isn’t probably optimal. So, we have to do everything we can to optimize our sleep hygiene as Robb would say and I think this show touches on just about everything you can do with respect to this. I did have one question actually for the group, maybe Dr. Connelly. With the wide use of prescription, are there any that don’t disrupt your sleep as versus another?

Dr. Connelly: I don’t really pretend to know that literature. The problem with a lot of this commonly sold sleep preparations is that may be show and that is that sleep curtailment is really is endemic, I mean, let’s face it. Sleep curtailment is now part of modern existence and it’s important as incest to understand what some of the consequences of that might be and to try and mitigate those with activity profiles and nutrient surveillance protocols that would minimize the midnight smack, all that is going to be delivered to the metabolic regulatory system what are those issues they are downward regulation of total energy expenditure on a long term basis with a more adverse impact of skewing reduction in fat oxidation in favour of carbohydrate oxidation hence the deterioration of body composition. This is usually intended if protein intake is not absolutely optimized with a tendency to compound the loss of mean body mass which most humans suffer as a result of aging. So, this is another variable. Another non-calorie based variable that can sort of pile on with other non-calorie based variables that are also characteristic of our daily modern existence. And they are simply issues that again remind those who care about what’s going on with their body and how it functions and how it looks that sleep duration has an impact on these variable that’s substantive, it’s not trivial. So, if you are someone who by necessity because of your requirements for your daily life have less than 6 or 7 hours of sleep, that probably would, I would urge you to be more conspicuous and more aware of your exercise and dietary habits and the person who’s getting 8 hours or more a night. So I think from my perspective that’s the important message from the show, is that like many other variables that have no a priority caloric value, sleep deprivation can have a significant impact over the long term on your optimizing your body composition which extensively is what most people listen to this show care about.

Carl: Okay. So, we’re going to wrap it up then on that note. Thank you very much Dr. Norton. Thank you very much Robb Wolf. Of course Vince Andrich and to the listeners thank you for listening to the Body RX Show tonight. We’ll see you in two weeks.

Dr. Connelly: Okay. Thanks Robb.

Robb: Thanks guys!

Dr. Norton: Thanks Guys!

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