Based on the number of comments I get and the number of questions that come through the email on our website, it seems that there is much confusion about the interplay of calories, the caloric deficit, weight loss, and weight gain. I’ll use this space to expand on my views of these complex and confusing issues.First, let’s look at a concept that will help explain a lot. It’s a concept that Gary Taubes explores in great detail in his book Good Calories, Bad Calories, which, by the way, is available now. (Grab a copy and spend a fascinating couple of days poring over it. The rewards will be immense.) The concept in question is interpretation of the energy balance equation, which looks like this:

ΔWeight = Calories in – Calories out

What this equation basically says is that the change in weight (ΔWeight) equals the number of calories consumed minus the number of calories burned off in the process of daily living.

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Since posting the piece on ketone bodies and their causing breathalyzer problems I’ve had enough comments and emails to make me realize that there are probably many people unsure of what ketones really are, where they come from and why. Let’s take a look at the goals and priorities of our metabolic system to see what happens. Fear not, I’m going to try to keep the biochemistry to a minimum.

The primary goal of our metabolic system is to provide fuels in the amounts needed at the times needed to keep us alive and functioning. As long as we’ve got plenty of food, the metabolic systems busies itself with allocating it to the right places and storing what’s left over. In a society such as ours, there is usually too much food so the metabolic system has to deal with it in amounts and configurations that it wasn’t really designed to handle, leading to all kinds of problems. But that’s a story for another day.

If you read any medical school biochemistry textbook, you’ll find a section devoted to what happens metabolically during starvation. If you read these sections with a knowing eye, you’ll realize that everything discussed as happening during starvation happens during carbohydrate restriction as well. There have been a few papers published recently showing the same thing: the metabolism of carb restriction = the metabolism of starvation. I would maintain, however, based on my study of the Paleolithic diet, that starvation and carb restriction are simply the polar ends of a continuum, and that carb restriction was the norm for most of our existence as upright walking beings on this planet, making the metabolism of what biochemistry textbook authors call starvation the ‘normal’ metabolism.

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We’ve all had the experience. We go off our low-carb diet for a while, then decide to get serious and get back on the straight and narrow. We start counting every carb and being good as gold, and suddenly we’re fatigued. We find ourselves puffing and panting just walking out to the mailbox. Old time low-carbers know this will pass, but newbies aren’t so sure. No one told them about this, and all they can think of are all the horror stories they’ve been told about low-carb diets.

I’ve had countless people tell me of how they tried a low-carb diet once and got so tired they had to give it up. They then usually tell me that a low-carb diet just doesn’t work for their bodies. I tell them that if they’ll just hang in there a while, it will all get better, and, in fact, they will have more energy and less fatigue than before they started the diet.

There is an adaptation period that takes place when starting a low-carb diet. Someone who has been on a high-carb diet–the standard American diet, for example–has to metabolize a lot of sugar. All metabolic processes require enzymes to carry them out. Our DNA codes for these enzymes, but we don’t make them unless we need them. And when we do need them it takes a while for them to get brought up to the necessary levels. So, when we’re on a high-carb diet, we’ve got a lot of sugar-metabolizing enzymes kicking around, ready to metabolize sugar. All the sugar-metabolizing pathways are working efficiently.

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There’s a hold up in the Bronx,
Brooklyn’s broken out in fights.
There’s a traffic jam in Harlem
that’s backed up to Jackson Heights.
There’s a scout troop short a child,
Kruschev’s due at Idlewild!
Car 54 where are you?

Anyone who watched TV in the early sixties no doubt remembers the hilarious show Car 54 Where Are You? starring Fred Gwynne and Joe E. Ross as New York uniformed police officers Francis Muldoon and Gunther Toody. Muldoon and Toody were well meaning but hopelessly inept, always screwing things up in outrageous fashion, causing no end of grief and embarrassment to their precinct commander Captain Block, who had to sort out the idiocy and try to make things right.

Now comes the medical equivalent of Muldoon and Toody in the persons of in-training physicians Tsuh-Yin Chen, M.D. and William T. Smith, M.D. The role of precinct commander in this production is played by one Klaus-Dieter Lessnau, M.D., who, unlike Captain Block, only adds to the problem with another layer of ignorance and stupidity. And whereas Car 54 Where Are You? left its viewers with their sides hurting from laughter, the repercussions of our medical drama will be felt painfully in the world of nutrition for years to come. A well-respected medical journal will have a blot on its record in much the same way CBS did after rushing to air the discredited George Bush Air National Guard story before it was authenticated, and, lastly, the whole episode will serve as a cautionary tale to anyone considering going to the emergency room of a teaching hospital.

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In going through and catching up on all the online issues of Science, I finally reached the most current issue, which contains an article of interest. Originally published in 1970 in the journal Nature, this article was featured in the current issue of Sage KE, an anti-aging supplement to Science, as a blast from the past in their Classic Papers section. The paper was the first to show that the accumulation of non-functional, or junk, proteins play a role in the aging process. This article caught my eye because of another I had read recently and had touched upon in a previous post.

Anti-aging scientists are now pretty sure that one of the forces behind the aging and senescence process is the junk protein matter that accumulates in the cells, hampering cellular function. If the junk builds up enough, it basically crowds out the working part of the cell, killing the cell off in the process. As this inexorable process proceeds, more and more cells function less and less well until we, as a being, cease to function. There are other processes driving the aging function besides this accumulation of cellular debris, but if we can make some headway with cleaning out the junk, then we should be able to make the cells, and by extension us, function better for longer.

We have little chemically-operated waste disposal systems in our cells called lysosomes. Cellular debris that gets hauled to the lysosomes and dumped in gets degraded into individual amino acids, which are released into the circulation and used to re-synthesize other, functional, proteins. The process of transporting the junk proteins to the lysosomes is handled by enzymes designed for that purpose found within the cells. As long as the enzymes are working up to snuff, the junk doesn’t accumulate. But as the Nature paper shows, the aging process takes its toll. Random errors in protein synthesis of these enzymes due to the aging process means that some end up being functional while others aren’t. The non-functional enzymes then not only don’t help haul the junk to the lysosomes, they themselves become junk. It’s easy to see what’s going to happen as time marches on.

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