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Month: December 2016

Excerpt from an Article

Excerpt from an Article

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Is there a “metabolic advantage” to being in ketosis?

Few topics in the nutrition blogosphere generate so much vitriolic rhetoric as this one, and for reasons I can’t understand. I do suspect part of the issue is that folks don’t understand the actual question. I’ve used the term “metabolic advantage” because that’s so often what folks write, but I’m not sure it has a uniform meaning, which may be part of the debate. I think what folks mean when they argue about this topic is fat partitioning, but that’s my guess. To clarify the macro question, I’ve broken the question down into more well-defined chunks.

Does ketosis increase energy expenditure?

I am pretty sure when the average person argues for or against ketosis having a “metabolic advantage” what they are really arguing is whether or not, calorie-for-calorie, a person in ketosis has a higher resting energy expenditure. In other words, does a person in ketosis expend more energy than a person not in ketosis because of the caloric composition of what they consume/ingest?

Let me save you a lot of time and concern by offering you the answer: The question has not been addressed sufficiently in a properly controlled trial and, at best, we can look to lesser controlled trials and clinical observations to a make a best guess. Believe me, I’ve read every one of the studies on both sides of the argument, especially on the ‘no’ side, including this one by Barry Sears from which everyone in the ‘no’ camp likes to quote. This particular study sought to compare a non-ketogenic low carb (NLC) diet to a ketogenic low carb (KLC) diet (yes, saying ‘ketogenic’ and ‘low carb’ is a tautology in this context). Table 3 in this paper tells you all you need to know. Despite the study participants having food provided, the KLC group was not actually in ketosis as evidenced by their B-OHB levels. At 2-weeks (of a 6-week study) they were flirting with ketosis (B-OHB levels were 0.722 mM), but by the end of the study they were at 0.333 mM. While the difference between the two groups along this metric was statistically significant, it was clinically insignificant. That said, both groups did experience an increase in REE: about 86 kcal/day in the NLC group and about139 kcal/day in the KCL group (this is calculated using the data in Table 3 and Table 2). These changes represented a significant increase from baseline but not from each other. In other words, this study only showed the reducing carbohydrate intake increased TEE but did not settle the ‘dose-response’ question.

This study by Sears et al. is a representative study and underscores the biggest problems with addressing this question:

  1. Dietary prescription (or adherence), and
  2. Ability to accurately measure differences in REE (or TEE).

Recall from a previous post, where I discuss the recent JAMA paper by David Ludwig and colleagues, I explain in detail that TEE = REE + TEF + AEE

Measuring TEE is ideally done using doubly-labeled water or using a metabolic chamber, and the metabolic chamber is by far the more accurate way.  A metabolic chamber is a room, typically about 30,000 liters in volume, with very sensitive devices to measure VO2 and VCO2 (oxygen consumed and carbon dioxide produced) to allow for what is known as indirect calorimetry.  The reason this method is indirect is that it calculates energy expenditure indirectly from oxygen consumption and carbon dioxide production rather than directly via heat production.  By comparison, when scientists need to calculate the energy content of food (which they do for such studies), the food is combusted in a bomb calorimeter and heat production is measured.  This is referred to asdirect calorimetry.

Subjects being evaluated in such studies will typically be housed in a metabolic ward (don’t confuse a metabolic ward with a metabolic chamber; the ward is simply a fancy hospital unit; the chamber is where the measurements are made) under strict supervision and every few days will spend an entire 24 hour period in one such chamber in complete isolation (so no other consumption of oxygen or production of carbon dioxide will interfere with the measurement).  This is the ‘gold standard’ for measuring TEE, and shy of doing this it’s very difficult to measure differences within about 300 kcal/day.

Not surprisingly, virtually no studies use metabolic chambers and instead rely on short-term measurement of REE as a proxy.  In fact, there are only about 14 metabolic chambers in the United States (and I will be spending a day inside one next week, but that’s another story).

A broader question, which overlays this one, is whether any change in macronutrients impacts TEE.  If you’re interested in the entire review of the literature on this topic, refer to this appendix from the exhaustive review we did at NuSI, along with this summary and narrative.  This review spans over 80 years of research and 1.2 million subject-days. 

Despite the limitations we allude to in the summary of this review, there is a growing body of recent literature (for example this study, this study, and this study) that do suggest a thermogenic effect, specifically, of a ketogenic diet, possibly through fibroblast growth factor-21 (FGF21) which increases with B-OHB production by the liver. 

These mice studies (of course, what is true in mice isn’t necessarily true in humans, but it’s much easier to measure in mice) show that FGF21 expression in the liver is under the control of the transcription factor peroxisome proliferator-activated receptor a (PPARa), which is activated during starvation. Increased FGF21 promotes lipolysis in adipose tissue and the release of fatty acids into the circulation. Fatty acids are then taken up by the liver and converted into ketone bodies. FGF21 expression in liver and adipose tissue is increased not only by fasting but also by a high fat diet as well as in genetic obesity which, according to these studies, may indicate that increased FGF21 expression may be protective. Hence, ketosis may increase TEE either by increasing REE (thermogenic) or AEE (the ketogenic mice move more).  Of course, this does not say why. Is the ketogenic diet, by maximally reducing insulin levels, maximally increasing lipolysis (which dissipates energy via thermogenic and/or activity ‘sinks’) or is the ketogenic diet via some other mechanism increasing thermogenesis and activity, and the increased lipolysis is simply the result?  We don’t actually know yet.

Bottom line: There is sufficient clinical evidence to suggest that carbohydrate restriction may increase TEE in subjects, though there is great variability across studies (likely due the morass of poorly designed and executed studies which dilute the pool of studies coupled with the technical difficulties in measuring such changes) andwithin subjects (look at the energy expenditure charts in this post).  The bigger question is if ketosis does so to a greater extent than would be expected/predicted based on just the further reduction in carbohydrate content. In other words, is there something “special” about ketosis that increases TEE beyond the dose effect of carbohydrate removal?  That study has not been done properly, yet.  However, I have it on very good authority that such a study is in the works, and we should have an answer in a few years (yes, it takes that long to do these studies properly).  

Does ketosis offer a physical performance advantage?

Like the previous question this one needs to be defined correctly if we’re going to have any chance at addressing it. Many frameworks exist to define physical performance which center around speed, strength, agility, and endurance.  For clarity, let’s consider the following metrics which are easy to define and measure

  1. Aerobic capacity
  2. Anaerobic power
  3. Muscular strength
  4. Muscular endurance

There are certainly other metrics against which to evaluate physical performance (e.g., flexibility, coordination, speed), but I haven’t seen much debate around these metrics.

To cut to the chase, the answers to these questions are probably as follows:

  1. Does ketosis enhance aerobic capacity? Likely
  2. Does ketosis enhance anaerobic power? No
  3. Does ketosis enhance muscular strength? Unlikely
  4. Does ketosis enhance muscular endurance? Likely

Why? Like the previous question about energy expenditure, addressing this question requires defining it correctly.  The cleanest way to define this question, in my mind, is through the lens of substrate use, oxygen consumption, and mechanical work.

But this is tough to do! In fact, to do so cleanly requires a model where the relationship between these variables is clearly defined.  Fortunately, one such model does exist: animal hearts.  (Human hearts would work too, but we’re not about to subject humans to these experiments.)  Several studies, such as this, this, and this, have described these techniques in all of their glorious complexities.  To fully explain the mathematics is beyond the scope of this post, and not really necessary to understand the point.  To illustrate this body of literature, I’ll use this article by Yashihiro Kashiwaya et al.

The heart is studied because the work action is (relatively) simple to measure: cardiac output, which is the product of stroke volume (how much blood the heart pumps out per beat) and heart rate (how many times the heart beats per minute).  One can also measure oxygen consumption, all intermediate metabolites, and then calculate cardiac efficiency.  Efficiency increases as work increases relative to oxygen consumption.

Before we jump into the data, you’ll need to recall two important pieces of physiology to “get” this concept: theacute (vs. chronic) metabolic effect of insulin, and the way ketone bodies enter the Krebs Cycle. 


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Post #4

Post #4

Well, I’m on my 2nd full day of the low-carb/Adkins/ketogenic diet. The last time I got on the scale (I think it was Friday night) I was at 268. That was my getting started, foot-in-the-ground, I’m Not Living This Way Anymore moment. I’ll weigh in again tomorrow and see where we are.

I’ll tell you what . . . once you get going on the no-carb deal it’s not terrible. Don’t misunderstand me, it’s not fun. It’s just not terrible. Who and I kidding??? I LOVE nearly every type of bread. This diet sucks.

Here’s what’s crazy about me and food. I’m am completely allergic to onions. I’ve developed a couple of allergies as an adult. That’s one. So any type of food with onions is a no-go for me. But I’ve got some other hang-ups as well. Fruits like bananas, grapes, what else? Well, anything with a soft or mushy texture . . . I can’t eat them. I mean, I literally can’t eat them. I’ve got some kind of a mental block that causes me to gag and vomit them up. Sorry for the mental image

That’s a lot of healthy fruits and vegetables that I just can stomach. It’s not that I don’t want to. I wish I could eat really healthy. As you can imagine, that makes finding good food choices pretty difficult. It’s a good thing I’m a naturally boring person who doesn’t mind eating the same things over and over and over.

Here’s what I can remember eating today.

Breakfast – nothing.

Lunch (around 1p) – Chinese Restaurant – all different types of chicken.

First Dinner (around 6:30p) – A couple of cheeseburgers (no bread) and an Adkins meal bar.

Second Dinner (around 11p) – A piece of boneless, skinless, baked chicken and green beans. That was about an hour ago. And I’m already hungry again. So that’s a very good sign.

I remember a few years back when I did this the first time, I was so hungry ALL THE TIME. It drove me nuts. But I remember that I always felt really good about being hungry. It’s how I knew my metabolism was working.

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Post #3

Post #3

So a little more about my health journey . . .

Back in 2014 my family moved to Memphis, TN to plant a church. That was a challenging experience. Side note: If you’ve ever thought or are thinking about church planting hit me up. I’d love to be a resource for you.

So, obviously, your health is directly affected by everything going on in your life. And this season for us was no exception. It was a stressful and difficult season for me (and my family). And unfortunately this spilled over into my eating habits. Over the course of the year that we were in Memphis I started gaining back a lot of the weight that I worked so hard to lose. But it wasn’t terrible. So I was able to brush it off and ignore it. I think I probably gained about 20 lbs.

A little over a year ago we closed the Memphis chapter of our lives and moved back to Florida. Unfortunately, though, my bad eating habits followed me. In this past year and a half I’ve gained another 20 lbs. As you can see, I can’t hardly drive by a McDonalds without gaining a couple of pounds. Forget about actually walking in (or hitting the drive thru) and ordering something.

I’m that “unlucky” person who can’t eat whatever I want. I’ve just never had that type of body with a naturally high metabolism. Nor am I able to increase my muscles easily. That’s just part of my life.

I’m really pissed at myself for screwing up all the hard work that I put in. I think it especially bothers me that I’ve gotten to the point that I don’t like what I see in the mirror again. The “breaking point” for me was when my favorite pair of jeans were tight. I think it was last Sunday morning and my pants were too tight. Unacceptable. That was it.

So here I am.


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