Calorie Partitioning: Part 2

In Calorie Partitioning Part 1, I looked at some of the factors which determine where calories ‘go’ or ‘come from’ when you overeat or under-eat respectively. In this article, I want to discuss the specifics of what happen when someone either diets or overfeeds.


So you start your diet, reducing carbs, calories or both. Blood glucose and insulin levels are going to be reduced. This is good, it releases the ‘block’ on fat mobilization. Additionally, catecholamine release typically goes up, further increasing fat utilization. Blood levels of fatty acids will start to increase. This is good, as it tends to promote fat burning in tissues such as liver and muscle. This effect is facilitated if you deplete liver and muscle glycogen as glycogen depletion tends to increase the use of fatty acids for fuel. The increas in blood fatty acid levels also has the short-term effect of causing insulin resistance which, as I mentioned, is a good thing on a diet since it spares glucose and helps promote fat oxidation. So far, so good, right?

Unfortunately, those are the good effects. Along with this, a lot of bad things start to happen. Although the drop in insulin causes better fat mobilization, it causes other problems. One is that testosterone will bind to sex-hormone binding globulin (SHBG) better, lowering free testosterone levels. As well, insulin is anti-catabolic to muscle, inhibiting muscle breakdown. The increase in cortisol that occurs with dieting enhances protein breakdown as well as stimulating the conversion of protein to glucose in the liver. Cortisol also prevents the amino acid leucine from stimulating protein synthesis. Additionally, a fall in energy state of the muscle impairs protein synthesis (although it increases fatty acid oxidation). The mechanism behind this is more detail than I want to get into here.

On top of that, high blood fatty acid levels tend to impair the uptake of T4 (inactive thyroid) into the liver. There are also changes in liver metabolism that impair the conversion of T4 to T3 (active thyroid). There is some evidence that high blood fatty acid levels causes tissues to become resistant to thyroid hormone itself (this is part of why just taking extra thyroid on a diet doesn’t fix all of the problems). There is also a drop in nervous system output (that can occur in as little as 3-4 days after you start a diet). Along with the drop in thyroid, insulin and leptin, this explains a majority of the metabolic slowdown that occurs. The change in liver metabolism (and the reduction in insulin) also impairs the production of IGF-1 from GH.

With caloric restriction comes a drop in leptin which causes various effects on tissues such as muscle, liver and fat cells. Additonally, a hormone called ghrelin (released from the stomach and responsive to food intake) will go up. The interaction of these three hormones (and probably others) send a signal to your brain (lateral hypothalamus) that you’re not eating enough (do note that the response is not immediate, there is a lag time between the changes in all of these hormones and the body’s response).

This causes changes in the various neurochemicals such as NPY, POMC and the rest to occur, signalling further changes downstream. Levels of testosterone fall (along with the increased binding to SHBG) along with an increase in cortisol, these both tend to have a negative effect on muscle mass. In addition to the problems with conversion mentioned above, thyroid output tends to decrease over time; I already mentioned the drop in nervous system output.

All of these adaptations serve two main purposes. The first is to slow the rate of fat loss, as this will ensure your survival as long as possible. Related to that, the body tends to shut down calorically costly activities. This includes protein synthesis, reproduction and immune function; there’s little point keeping any of these functioning when you’re starving to death. The drop in leptin, and the changes in hormones that occur are a huge part of why men tend to lose their sex drive (and ability) and women lose their period when they get lean/diet hard.

The second is to prime your body to put fat back on at an accelerate rate when calories become available again. As I mentioned earlier, this makes perfect evolutionary sense, even if it presents a huge pain in the ass to us. Ok, enough about dieting, what about overfeeding.


To a great degree, most of the adaptations that occur with dieting reverse when overfeeding. Actually, that depends a lot on the situation. As I mentioned above, the body as a whole tends to defend against underfeeding better than it does against overfeeding; which is why it’s generally easier to gain weight than to lose it. Studies where leptin has been increased above normal (i.e. to try and cause weight in overweight individuals) have generally borne this out: except at massive doses, raising leptin above normal does very little.

There are a few reasons for this. One theory is that normal leptin levels send essentially a 100% signal, that is they tell the body that all systems are normal. It should seem clear that raising leptin above 100% isn’t going to do much. Another problem is something I alluded to above: leptin resistance. It’s thought that people have varying degrees of leptin resistance which means, in essence, that they don’t response as well to leptin as they should. On top of this, when leptin levels go up, it appears to stimulate resistance to itself. That is, when leptin gets and stays high, it causes you to become resistant to its effects.

Both theories make good evolutionary sense. Your body doesn’t want to be lean but it doesn’t really mind getting fat. If calories are available all the time, it would make little sense for you to get full and/or start burning them off. This is what would happen if you were extremely sensitive to leptin. So high levels of leptin induce resistance to itself; keeping you hungry and eating while the food is available.

But we’re not really talking about raising leptin above normal here, we’re talking about reversing or preventing the drop that occurs with dieting. In that situation, many of the above adaptations will reverse to one degree or another (depending on how lean you are, how long you diet, and how long you overeat).

So now you increase your calories and carbs. This raises blood glucose and insulin, reversing the binding of testosterone to SHBG; cortisol also goes down. With increased carbohydrates, you increase both liver and muscle glycogen. In the muscle, while this decreases fat oxidation, this improves protein synthesis (along with the increase in insulin and testosterone and the decrease in cortisol).

Of course, with increasing insulin, there is a decrease in blood fatty acid concentrations which improves insulin sensitivity. Skeletal muscle insulin sensitivity is enhanced even more by exercise.

The decrease in blood fatty acids, along with changes in liver metabolism will improve both the uptake and conversion of T4 to T3; along with improvements in nervous system output, this will help to increase metabolism.

And, of course, there are all of the central adaptations that occured during dieting, that will reverse to some degree while overfeeding. Leptin will go up (noting that it goes up more quickly than bodyfat comes on) along with insulin, ghrelin goes down. This signals the hypothalamus that you’re eating again, and many of those changes will reverse. So NPY, CRH, POMC and the rest go back towards normal, helping to renormalize all of the hormones that were screwed up in the first place.

To a very limited degree, some of these adaptations would be expected to try and limit fat gain and, to a very limited degree, this is what happens. But, as above, the body is better at preventing weight loss than weight gain.

Summing Up for Now

Ok, let’s put the above two sections together in chart form so that it’s easier to see. A + means an increase while a – means a decrease.

  Overfeeding Underfeeding
Calories Increased Decreased
Protein Increased or No Change No Change or Increased
Carb/Fat Intake Increased Decreased
Insulin Increased Decreased
Total Testosterone Increased or No Change Decreased
Free Testosterone Increased Decreased
Growth Hormone Increased Increased
IGF-1 Increased Decreased
Thyroid (T3) Increased Decreased
Catecholamine Decreased Increased
Cortisol Decreased Increased
Leptin Increased Decreased
Ghrelin Decreased Increased
Cellular Energy State Increased Decreased
Protein Synthesis Increased Decreased
Body Fat Levels Increased Decreased
Muscle Mass Increased Decreased
Net Effect Overall Anabolic Overall Catabolic

So now, in greater detail, you’re starting to understand the problems involved, especially for the genetically normal. Underfeeding is necessary for fat loss but will always have a negative impact on muscle mass. It also induces any number of adaptations that tend to prevent further fat loss. Overfeeding is necessary to gain but will always have a negative impact on fat mass. However, it can reverse many (if not all) of the adaptations that occur with dieting.

A Final Note on Leptin

Hopefully the above sections have made you realize that there is far more to the adaptations to either dieting or overfeeding than just leptin. Rather, it’s an integrated response involving leptin, insulin, ghrelin, fatty acids, liver, fat cell and skeletal msucle adaptations, and probably factors that haven’t been discovered yet. This probably explains why injecting leptin into dieting humans only reverses some but not all of the adaptations.

For example, just injecting leptin would be expected to fix a defect in TSH (and thyroid output) but it won’t fix the problems with conversion that occur at the liver. Similarly, while injecting leptin would normalize LH and FSH output, it won’t correct the problem with increased binding of testosterone caused by lowered insulin. Hopefully you get the picture. So, you ask, what’s the solution?

The Solution: Cyclical Dieting

Ok, great, I’ve just spent nearly 10 pages making a case for cycling dieting, periods where you alternate a low-calorie intake with a higher calorie intake. in this fashion, you alternate between periods of low calories/carbs with high calories/carbs to alternate between periods of anabolism (tissue building) and catabolism (tissue breakdown). Fundamentally, of course, this is nothing new.

Several years ago, when I first started making some of the connections with leptin and everything else, this really pointed out the need to do periodic refeeds (or cheat days or whatever you want to call them) on a diet. If nothing else, it pointed to another reason why the Bodyopus diet worked as well as it did: by forcefeeding carbs and calories for 2 days, not only did you refill muscle glycogen and hopefully generate an anabolic response, you probably reversed some of the adapatations inhernet to dieting.

In those years, various approaches have come and gone. In general, short refeeds, lasting from 5 to 24 hours were used every so often while dieting. I’ve tried them all. The Bodyopus diet was aimed at this goal, alternating 5 days of low-cal/ketogenic dieting with 2 days of high-carbohdyrate eating. Other approaches such as the Anabolic Diet or Rob Faigan’s Natural Hormonal Enhancement followed roughly the same scheme. There have been numerous other schemes over the years that alternated periods of low and high calories. The question is whether or not those programs were optimal. In my opinion, they aren’t for several reasons.

One of the factors I’ve been considering to a great degree has to do with the length of the overfeeding period. While it’s true that 5 (or 12 or 24) hours of concentrated overfeeding will raise leptin, the more important question is whether that’s sufficient to ‘tell’ the brain that you’re fed. While data (especially in humans) is nonexistent, my hunch is no.

There’s a lag time of several days between the drop in leptin and the drop in metabolic rate (nervous system output) for example; I’d be surprised if a mere 12 or 24 hours was sufficient to reverse this. Rather, I’d expect it to take a similar amount of time for the reversal to occur. The reasons I feel this way are sort of beyond the scope of this book, send me an email if you really must know.

Now, this isn’t to say that short carb-loads/refeeds aren’t of benefit. They refill glycogen, turn off catabolism and maybe induce an anabolic response to boot. They also let you eat some of the crap you’re really craving which helps psychologically. But I doubt they are sufficient to affect metabolism very much. Instead, a longer refeed is necessary. The drawback, of course, is that longer refeeds have a tendency to put too much bodyfat back on which goes agains the entire goal of dieting.

Another problem with many cyclical dieting approaches is that they don’t coordinate training with the diet. Bodyopus was an exception but, for various reasons, I think the Bodyopus workout plan was screwy. If anything it was backwards, putting tension workouts on low-calorie/low-carb days (where you aren’t very anabolic) and glycogen depletion workouts before you are eating a lot seemed wrong to me years ago and wronger to me now. This will make more sense as you read the next chapters.

Ultimately, all of this introductory stuff, brings us to the final question: how do we optimize the entire system to maximize fat loss and either muscle maintenance or muscle gain (or, if you’re a performance athlete, how do we generate fat loss while maintaining performance). To understand that, I need to get into a few more details regarding muscle gain and fat loss, which will help you to understand the overall system.



8 thoughts on “Calorie Partitioning: Part 2

  1. Hello. I love the amount of detail you’ve put into these Mini articles. That said: Please elaborate on the following- “There’s a lag time of several days between the drop in leptin and the drop in metabolic rate (nervous system output) for example; I’d be surprised if a mere 12 or 24 hours was sufficient to reverse this. Rather, I’d expect it to take a similar amount of time for the reversal to occur. The reasons I feel this way are sort of beyond the scope of this book, send me an email if you really must know.”

  2. A few times in the article you mention that lowering insulin will increase the binding of testosterone, and also that overfeeding will increase growth hormone and vice versa. I’ve seen studies (which I’m probably misinterpreting) that conclude that growth hormone tends to increase when your UNDERfed and will decrease with rising insulin. A recent study concluded that doses of glucose significantly lowered testosterone, up to 25%.

    I’m getting cognitive dissonance here.

  3. Jack,

    GH does go up when you underfeed as shown in the charge above (GH is listed as increased for both over and underfeeding)

    But the effect is not anabolic. Rather, GH goes up to mobilize fuels (fatty acids) and this occurs to spare lean body mass loss. But in a low insulin state, this is not anabolic in the least.

    And if I recall, the studies showing that carbs lowered testosterone were probably because it was increasing testosterone clearance into tissues.


  4. So then would it be more advantageous to select 7 days of 10% deficit for a static .5lb fat loss or choose 5 days of 15% and 2 days at maintenance/refeed for metabolism.

    Situation A seems like it would put less stress on the body and less metabolic slowdown would occur; however, situation B seems like the refeeds would counter any potential harm from the slightly larger deficit.

    I know both of these are small, but I think you understand the crux of my question. Does the concept of increasing calories one or two days cancel out any potential benefit, simply because a larger deficit must be created on other days to make up for it?


  5. With respect to questions raised by the last paragraph in this article, which next article or book would be the most logical follow on to learn more about this particular topic?

    Thank you ~

  6. Nice article..

    Do you have a version of “the solution” where the objective is to increase muscle mass. I.e. leverage calorie partitioning to improve the P-ratio so that more muscle mass is created vs fat tissue?

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