Fat-loss, Water Retention and Whooshes - Hint: It's not caused by Cortisol

EDIT: I recently briefly discussed this topic during a Live stream Q/A. If reading isn't your thing or you just enjoy listening to my dulcet tones, you can view the excerpt from the live stream below.


Alternatively, read on!

Fat-loss, Water Retention and Whooshes - Hint: It's not caused by Cortisol


Easily one of the most common stumbling blocks people encounter is dealing with the stop-start nature of fat loss. One week they might drop two pounds, then nothing for weeks, then suddenly another four pounds, practically overnight.


Sound familiar?


A daily graph of your body confusing the shit out of you.

Unfortunately, human nature means that when we are presented with evidence that says we gained a pound since yesterday, we often forget the five pounds we lost over the last four weeks. This is actually one of the major problems with only using your weight as a metric for progress, but that is an article for another day.


Today I want to help you understand what is going on to cause these supposed plateaus: water weight.


Water Weight and "Whooshes"

For context (and due credit!) one of the first thought leaders to discuss the phenomenon of water retention during dieting was Lyle McDonald in "The Stubborn Fatloss Solution" and later in his blog article from 2009 "Of Whooshes and Squishy Fat".

Nope - Sorry guys, no mention of cortisol here.

Since then, several other fitness "gurus" (a term I use with great disdain) have written about weight loss plateaus and in particular water retention and "whooshes" claiming one of two phenomena are occurring, "fat cells filling with water" and "cortisol levels" rising with dieting.


Again, in the interest of fair representation, Lyle does mention the possibility of fat cells filling with water during fat loss, but doesn't claim that to be the cause as he could not find any supporting evidence, and makes zero mention of cortisol being the cause at all.


Since I cannot find any evidence (i.e. actual research) to suggest that the fat cells are increasing their intra-cellular water volume after releasing a triglyceride either, I am not going to address that claim until I can see some actual data on the subject.


The other major explanation often given for why we retain water during dieting is cortisol.


Cortisol


Cortisol rising during dieting is one of those claims that have existed in fitness literature for so long that it's not even questioned anymore.


The original research into cortisol rising during dieting comes from the work conducted by Ancel Keys in Experimental Starvation in Man often called the "Minnesota Starvation Experiment. During this research, Keys et al, noticed that research participants began to develop massive edema, or water retention, in the face and lower extremities usually within the second month of the experiment.


Whilst Keys did not explicitly state this was due to rises in cortisol, the fluid retention pattern was so similar to what was observed in patients who were administered exogenous cortisol that this eventually became the status quo explanation for why water was retained during dieting.


In the interest of completeness the logic that lead to people believing water weight fluctuations were the result of changing cortisol levels is:

  1. High doses of exogenous cortisol causes edema.

  2. People who are starved for long periods of time also develop edema in a similar pattern to that caused by cortisol.

  3. Re-feeding by increasing calories, but particularly carbohydrates, tends to reduce edema, there for the edema is caused by the caloric deficit.

  4. Therefor a caloric deficit causes rises in cortisol which in turn causes edema.

When you spell it out, there is some pretty big logic leaps there.....


However, pointing out that the above logic is fairly poor is not the same as disproving the argument so lets put this one to bed for good.


The Evidence against Cortisol


In 2017, Hulmi et al, released a paper which looked at the body composition and serum hormone changes in female fitness competitors, before starting the diet, after 20 weeks of dieting then again after another 20 weeks of recovery. There are a number of strengths to this study, but in particular they implemented a robust blinding method to the results, they used resistance trained athletes, and the total N value was quite high at 50 participants finishing the study and a very long study profile of over 40 weeks. On average, exercise participants experienced a 35-50% reduction in total body fat during the dieting intervention, they were all female and were conducting a physique competition prep, supposedly THE demographic most susceptible to stress/cortisol.


Yet, the data actually demonstrated the opposite! The dieting group had LOWER cortisol after 20 weeks of dieting and a 35-50% reduction in body fat than the control group.

Oddly - The dieting group had LOWER cortisol than the control group after 16 weeks of highly restricted dieting, in contrast to the "dieting causes Cortisol" hypothesis.

In a much more rigorous meta-analysis, Nakamura et al analysed the serum cortisol levels of energy restricted dieters over 13 studies with a total N value of 292 exercise participants. In order to organise the data, studies were grouped into either a Fasting (Complete abstinence from food), a Very Low Calorie Diet (VLCD) (consuming less than 800 kCal per day) or a Low Calorie Diet (LCD) (consuming greater than 800 calories per day).


Fasting Cortisol

A Hedges G score of 6 means that on average, the fasting group differed from the control group by 6 standards of deviation. This is statistically very relevant.

Perhaps unsurprisingly, completely abstaining from food (fasting lengths were between 2.5 and 6 days), resulted in a large increase in serum cortisol above baseline. This indicates that extended fasting of greater than about 48 hours results in large increases in serum cortisol and is another reason why they are likely to be less than optimal for sustained fat loss.


But what about in the VLCD and LCD groups?

The Hedges G spread of -1 to +2 shows a very weakly positive and statistically non-relevant increase in cortisol compared to the control.

In complete contrast to the cortisol hypothesis, there appears to be no statistically relevant increase in serum cortisol, provided you are not fasting for greater than 48 hours per day and are consuming on average greater than 800kCal per day (this should be almost everyone FYI).


The inquisitive among you may now be asking if there was a time vs effect component for cortisol increases, and that perhaps the cortisol increase is only observed after sustained dieting? Nakamura et al investigated that too (they did good science!).

The red circle and text is my own emphasis.

At first glance, it appears that cortisol is greatest during the early phase of dieting with it actually having a negative correlation with time. This is in contrast the hypothesis that protracted dieting causes increases in cortisol. But when we analyse the graph a little further we note that the graph is biased by the inclusion of the fasting data which only occurred over the (relative) short term.


When we remove the fasting data a very different story is told.

The line of best fit was added by me by visual approximation (read: BAD SCIENCE) and is only there to demonstrate the concept.

What we can now see is that there is a very weak correlation with increases in cortisol during the first few days of energy restriction, and no correlation at all if we exclude the outliers (E, K and N). Whilst this is certainly not a silver bullet, it does indicate that not only does dieting not increase cortisol, but there is no correlation at all with prolonged dieting and rises in cortisol (in fact the opposite is true).


Finally if cortisol were the cause of the edema during calorie restriction we would expect a "whoosh", or the sudden release of water retention, to be precipitated by the sudden decrease in serum cortisol beforehand. Yet I have been unable to find any evidence that this is observed. It therefore stands to reason that if a reduction in cortisol did not cause the whoosh, an increase in cortisol is unlikely to be the cause of the edema either.


Okay, we get it, it's not cortisol.


So what IS causing the water retention?


The Glycerol Hypothesis


Before I get into the nitty gritty, recall that every gram of intramuscular glycogen is stored with 4 grams of water and that every triglyceride (or fat molecule) is really three fatty acids bound together with a single glycerol molecule (hence triglyceride).



When fat is being burned due to being in a caloric deficit an enzyme first separates the fatty acids from the glycerol molecule and all four are then moved into the bloodstream to be made available for the production of ATP.


In the case of the fatty acids this is actually a very straight forward process. In short, the fatty acid is "cut up" by cleaving off two carbon molecules from the fatty acid chain at a time to form Acyl-CoA to be used in the Citric Acid Cycle via a process known as beta-oxidation.


In contrast, Glycerol cannot be directly metabolized into ATP and must first be converted to glyceraldehyde 3-phosphate via a seven step process, before it can then enter the liver to produce glucose via glycolysis or glycogen via gluconeogenesis. Each of these steps along the process are enzymatically rate limited, which essentially means that the amount of glycerol that can be converted into glucose or glycogen is limited by the availability of the required enzymes.


This means that during a steep caloric deficit, it is entirely possible to release glycerol into the bloodstream faster than the liver's ability to convert it into usable energy substrates.


Further, during a caloric deficit, and especially if in ketosis, it is likely that glycerol is preferentially converted into glucose to provide energy to cells which cannot use fat for energy such as red blood cells (due to the lack of mitochondria), AND it would compete with the much more available amino-acids to produce glycogen via gluconeogenesis, essentially closing off an entire method of disposing of serum glycerol.


The net effect is a steadily increasing concentration of serum and interstitial (more on this soon) Glycerol molecules waiting their turn to be converted into either glucose or glycogen.


Cool, what does this have to do with water retention?


It turns out, much like glycogen, glycerol also likes to hang out with several water molecules.


In fact, this phenomenon is actually used by endurance athletes to "hyper hydrate" prior to a race (1, 2, 3, 4, 5), by consuming large quantities of glycerol diluted in water and electrolytes.


Unfortunately, unlike muscle glycogen, glycerol doesn't hang out in muscle cells. Instead the glycerol molecules concentrate in the interstitial fluid area between cells (1), increasing the bodies interstitial fluid volume. In sufficient quantities, this results in a soft, rounded appearance and appears visually and on the scale as if fat gain has occurred.


Simultaneously hard training dieters (most trainee's are heavily over training, especially when in a deficit!) are constantly depleting muscle glycogen via training. This results in the reduction of intramuscular water retention which then gives the muscles a soft rounded look, a lack of muscularity and an inability to get a pump.

Not today Satan, not today.

In case you weren't aware, looking soft round, pudgy, losing vascularity and not being able to get a pump is the bodybuilders equivalent to a circus clown trying to eat your liver whilst on the phone to your mother-in-law...The stuff of nightmares.





How does this explain "whooshes"?

There are a few things going on here.


Firstly we know caloric restriction is not linear. We naturally go through daily cycles of being in a caloric excess post feeding, and then a caloric deficit usually whilst sleeping or fasting (I mean intermittent fasting, not a multi-day abstinence from food (i.e eating disorder)).


Similarly, we are actually pretty bad at counting calories in general and statistically speaking our actual energy intakes vary as much as 20-40% from the amount we thought we ate on a daily basis, even when trying to count diligently.


The net result of this is that these variations in caloric intake (and thus fat metabolism) means that there will be periods where glycerol is accumulating faster than it can be metabolized into glucose, and periods where the liver is able to catch up. It is these periods where the liver is able to catch up that we observe a rapid reduction in water weight occurring and a "whoosh" is born.


This also explains why a refeed of any type, but in particular carbohydrates, causes a whoosh to occur.


By increasing calories, we effectively reduce the body's requirement to breakdown adipose tissue into fatty acids and glycerol, which in turn then also provides an opportunity for the liver to catch up with the glycerol production. Because of the increased availability of energy substrates and dietary glucose, amino-acid conversion to glycogen is reduced, which in turn reopens the secondary pathway for the liver to dispose of the serum glycerol into glycogen. The net effect is a rapid increase in muscle glycogen with a reduction in interstitial glycerol giving a visual appearance of being lean, hard and muscular and having dropped several pounds of water weight.


Now that we understand whats going on, how can you use this information?


A very common mistake by dieters is to take the evidence of water weight fluctuations as justification to alter their diet. This occurs in one of two flavors:

  1. A further reduction in calories to "encourage" fat loss (this is a mistake).

  2. A weekly refeed since it appears that refeeding results in renewed fat loss (potentially also a mistake).

I will address each of these individually.


Reduce calories further


Essentially, because it appears that their weight loss has stalled, many dieters become despondent that their diet is no longer working and reason that they need to lower calories further to compensate for Adaptive Thermogenesis. In the vast majority of cases, this is a big mistake.


In reality, a stall in weight loss coupled with appearing visually softer and less muscular in the mirror (the effect is easier to observe the leaner you are) is actually strong evidence that the diet is working. If the diet were not working (i.e you did not have a great enough caloric deficit) we would actually expect to see an apparent decrease in water weight and increase in muscularity.


If you are currently dieting, are experiencing a stall and think you look softer this week than you did previously, keep doing exactly what your doing. All is well.


Plan a refeed


The other common reaction to a stall is to conduct a refeed or occasionally a diet break. This is often employed by "advanced dieters" (a term I use VERY loosely) as a technique to either "reset their metabolism" or to bust through a plateau and restart weight loss.


On the surface at least, these appear to be very effective.


By conducting a weekly refeed, they are effectively periodically reducing their caloric deficit which in turn allows the liver to catch up with that weeks glycerol accumulation and a whoosh to occur as discussed above. This results in a weekly reduction of accumulated water weight and reveals the previously hidden fat loss that had occurred over the preceding 6 days.


Depending on the individual, this can either be a good thing or a bad thing.


For some people, particularly those that crave instant gratification, a weekly refeed can provide assurance to them that the caloric deficit is working by revealing that weeks fat loss. This, in turn, may improve dietary adherence over the long term by providing regular encouragement and assurance that the diet is working. I employ the same technique frequently with clients as it helps keep them sane (A REAL concern!).


For others though, the line between a refeed and a "cheat" can become very blurred. It is not uncommon to see someone conduct a very poorly executed refeed only to undo several days worth of dieting, overconsume sodium comparative to potassium (e.g. processed, carb and fat heavy, hyper palatable foods) and end up not only sabotaging their fat loss, but also looking worse the day after due to sodium induced water retention.


In some this can even be the trigger for multi-day or even week(s) long binge fest. Often, complete abstinence is mentally easier than moderation.


In these dieters they would have been much better served by simply being patient and waiting for the whoosh to occur in a week or so.


What does all this mean for you?


Water retention, looking soft and bloated, losing vascularity and scale weight appearing to stall are all signs that a diet is resulting in fat loss. Rather than become despondent and altering your plan, you should instead take this as encouragement to keep doing what you're doing, since the plan is working.


If however, your are the kind of person that struggles to diet without constant feedback and desiring instant gratification, conducting a weekly refeed is an effective way of reducing the water retention and periodically improving your physical aesthetics. The trade off for this is of coarse losing a day of effective dieting, or undoing several days worth of progress if the refeed is conducted poorly.


Hopefully you should now feel more empowered about what is going on in your body and what it means to you. <3 Ella

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