By Sten van Aken | Reading Time: 9 minutes |

In the first part of the ad libitum series we learned how ad libitum dieting is a natural attitude towards dieting, rather than a specific set of rules that makes up a diet. We also learned that we’ve relied on this attitude for thousands of years and we share this attitude across and between biological species that habit this planet.

We then went on to explore how we as a species, although sharing many similarities with other species, is complicated and negatively affected by a variety of factors to use this attitude in our modern-day environment on the basis of our emotions and behaviors.

Finally, we learned that dietary adherence to a diet in the long run has far less to do with calories and far more with our ability to rely on our emotions our feelings.

The article was concluded on the note that this did leave a number of unanswered questions.

• What is the exact dietary basis for ad libitum dieting and how do we determine whether we or our clients are sufficiently equipped with strategies to (largely) let go of numbers and instead rely more on our systems ability to give sensory feedback and its ability to self-regulate?
• What are scientifically validated strategies and ways of reliably resonating with sensory feedback that we can employ in an ad libitum fashion of dieting that further builds on the principles of maximizing the satiating effectiveness of the approach, as well as helping adhering to our diets?

Before we can adequately tackle those questions, we first must make a case against the common perception that our appetite is governed by our energy intake.

Ad Libitum Dieting II:  The Paradox of Short- and Long Term Feedback

Homeostasis revisited

One can’t help but not ignore how there can be large energy discrepancies between diets, yet on a per-Calorie basis, some can be more satiating than others. Thus, contrary to popular belief, the fact that body weight appears to be relatively stable is not scientific proof that body weight is actively regulated.

To help us understand the implications of what it means if our daily appetite is not governed by our daily energy intake as much as we’d like to think, we’re starting with an analogy put forth by Rogers and Brunstrom (2016) by the use of a bathtub and a saucepan to illustrate the regulation of our energy stores.^[1]Rogers, PJ. / Brunstrom, JM. (2016): Appetite and energy balancing. In: Physiol Behav. URL: https://www.ncbi.nlm.nih.gov/pubmed/27059321.

Model of energy balance and appetite: The thick arrow represents the acute but relatively strong appetite inhibition, which increases and decreases by filling successive meals, which are then emptied from the upper intestine (cooking pot). The thinner arrow represents a much weaker but chronic appetite inhibition proportional to the body fat content (represented by the water in the bathtub), which makes up the majority of the body’s energy stores. Note that the cooking pot and bathtub are not to scale: For a lean adult, the bathtub contains about 180 times the energy content of an average meal. (Graphic Source: Rogers & Brunstrom, 2016)

The saucepan is analogous to the digestive tract, more specifically the short-term acute feedback from the gut to the brain. The bathtub is analogous to the bodily energy stores. The purpose of the ad libitum series is to highlight the impact of the saucepan. However, in order to fully grasp the significance of the saucepan we have to fully understand the impact of the bathtub and in what ways this system is fighting change. why the majority of diets is more likely to fail around the 4- to 6 month mark.

Since the bathtub represents our energy stores, its quite useful to know what it roughly represents to get an idea of the significance of the saucepan. In the image below is an adapted and adjusted scenario of the typical capacity of an 65-kg adult male.^[2]Frayn, K. (2010): Metabolic Regulation: A Human Perspective. Wiley-Blackwell. Available at Amazon.com.

Table 1: Energy storage in a 65 kg adult male. (Source: Adapted from 9.1, Frayn, 2010)

The typical male has about a 55 days’ worth of fat storage, if that was the only thing he could rely on. Add to this the capacity of the human body to give away its bodily protein and we further increase the means by which the body can give away energy. Now, as you might bring up correctly, the body will fight change in any direction. Thus, for the purposes of this analogy, we’re going to add an additional component: a sink.

What merely could be viewed as a sink would, upon closer inspection, more accurately resemble something like a highly advanced combination dial for the safe holding all the energy. And as you know, the body is far better equipped against starvation, than it is against overeating.^[3]Agu, J. (2020): A Scientific Overview of the Concept of ‘Starvation Mode’. In: Metal Health Rx: URL: https://metalhealth-en.aesirsports.de/free-articles/biology/a-scientific-overview-of-the-concept-of-starvation-mode/. Thus, given the body can already thrive well up to 75 days for an average male weighing 65 kg, this excludes any adaptation.

In order to get an impression of the specificity of the sink, we can look at a plethora of studies – but in this article the purpose is to get a better understanding of ad libitum dieting. There is a good reason most diets tend to fail around the 4 to 8 month time-mark. This starts with the distinction between both short- and long term (energy) homeostasis, and how short-term homeostasis is more familiar to us science enthusiasts and practitioners because it is predictable. But zooming in too much on this system causes you not to see the forest for the trees. The sink is ultimately what we’re trying to outsmart.

What happens if the pot miscalculates?

One of the first studies that deserves our attention is one by Pollidon et al (2016) that treated participants with canagliflozin  for 52 weeks.^[4]Polidori, D., et al. (2016): How Strongly Does Appetite Counter Weight Loss? Quantification of the Feedback Control of Human Energy Intake. In: Obesity (Silver Spring). URL: https://www.ncbi.nlm.nih.gov/pubmed/27804272. Canagliflozin is an antidiabetic and selective SGLT-2 inhibitor.

A way to understand what canagliflozin does is by comparing it to a ringworm. After all, the reason someone can’t gain weight must truly be due to this friendly magic purple-like parasitic worm that surfs your inner intestines like a unicorn running over a colored rainbow eating all your food before it gets to be absorbed. Since the ringworm in the system is just like the finger you put through the hole in a donut, it isn’t technically inside the donut – just like food moving through your digestive system isn’t either.

Conagliflozin works in a similar fashion, but doesn’t wear the purple color of the ringworm. It causes you to lose glucose by inhibition of the SGLT2-receptor (“sodium dependent glucose transporter”). It is registered and thus is subjective to feedback, unlike the purple ringworm.

However, it does so initially by bypassing feedback from the bathtub and saucepan. It is the combination dial of the safe holding all the energy that subtly tells the stomach and saucepan that they’ve miscalculated. This is clearly shown in the below image, where without the knowledge of the participants, they started eating increasingly more to match the loss. At this point leptin might come to mind, but hold my beer. There is one more study that further builds on this complex dynamic.

Body weight and energy intake change during placebo and SGLT2 inhibition. (A): Average body weight measurements in the placebo group (□) and the SGLT2 inhibition group (■) together with mathematical model simulations presented as dashed and fixed curves, respectively. (B): Calculated changes in energy intake in the placebo group (◊) and the SGLT2 inhibitor group (◆) together with mathematical model simulations (curves). Mean value ± 95% CI. (Graphic Source: Pollidon et al., 2016)

The second example is one of recent investigation by Jansson et al (2018) that led to an interesting discovery by which fat mass and bodyweight were regulated independently of leptin.^[5]Jansson, JO., et al. (2018): Body weight homeostat that regulates fat mass independently of leptin in rats and mice. In: Proc Natl Acad Sci U S A. URL: https://www.ncbi.nlm.nih.gov/pubmed/29279372.

The body weight sensor (gravitostat)

In this fascinating study, weighted capsules were inserted in the abdomen of healthy rats, and mice with diet-induced obesity, that represented 15% of their bodyweight. The capsule weighed 3% of their bodyweight respectively, which the control rodents had too.

The researchers found that increased loading led to a decrease in biological weight. There was no difference in relative biological weight loss between rodents. And it observed that this decrease was not due to an increased energy expenditure – rather – it was due to decreased food intake.

To investigate if this could have to do with the position of the insertion, rodents were also inserted with the same capsule in the back area. No differences were found. The increased loading did come with the accompanied improvements in biomarkers such as HOMA-IR, simultaneously reducing serum insulin before, during and after oral glucose exposure.

The researchers then, after the initial loading, de-loaded both rodents in the experimental group. They found that the rodents increased their biological weight and fat mass, but skeletal muscle was not affected, suggesting this body weight sensor was functional in both directions without affecting muscle mass. They then went on to show that increased loading led to loss of biological weight in both lab and wild mice, and even in those that were leptin deficient, thus revealing two independent negative feedback systems.

It was also found that two obesity-promoting neuropetitdes (AGRP and NPY) were expressed due to a failed compensatory mechanism that is normally suppressed by leptin.

Short Vs. Long term

These findings, together with the findings of increased caloric intake – or as we now get to understand it – food intake – perfectly fits the narrative of the compensatory feedback mechanisms that have to do with a lot more than just fat cells screaming for help because they’re starving.

We’re now getting to a point where things should start feeling familiar. But there’s a catch as you know by now. No matter what holds true in the short run, doesn’t necessarily translate to the long run. And what doesn’t hold true in the long run, doesn’t hold true in the short run. Vice versa.

What if we could use this to our advantage? Well, that requires us to understand both forces, like good and evil. Ideally, we’d want to give our system the feedback that it isn’t losing any weight at all. But over time, this also causes the body to adapt. Thus, nothing is really permanent, because we’re continuously subject to change. Resisting change only works for a limited amount of time. Thus, the question isn’t really how, but rather when. This is where the saucepan comes in.

Not only our first subject of interest, but also where we get to exert the most power.

For lasting results you should know how to manipulate hunger and satiety in your favour. The key lies in the optimal operation of the “cooking pot”. (Image Source: depositphotos / undrey)

Connecting the dots

By now you learned the various ways by which the body is able to regulate itself and that the game we’re actually playing is between cat (saucepan) and mouse (bathtub). Since we started with the analogy with of the bathtub, saucepan and sink, we’re now stuck with a cat and mouse game. For sake of simplicity, we’re sticking with original analogy. Now on to the saucepan.

The ability of the saucepan to add anything at all to the bathtub requires the saucepan to pour in more than 2400 kcal a day. Since a typical lunch would represent around 800 kcal, the bathtub in retrospect is 180 times larger than the bathtub.

But not only would we have to pour in more in terms of energy, we’d also be faced with the limitations of the saucepan. Here’s some characteristics to put this in perspective.

• First, the saucepan resists significant overfilling and thus is limited by its total capacity. This is feedback exerted by weight, volume and mass.
• Second, it can only process and (pre)digest so much at a time, because it can take hours before a bolus is fully processed. No wonder there is such a thing called a food coma.
• Third, there is quite literally a load (see what I did there, hehe) of other factors that affect the aforementioned factors, such as the duration at which content is held (e.g. rate of gastric emptying), the type of macronutrient and its characteristics (e.g. fat floats on water) and finally the mastication (finer food equals higher surface area equals better enzymatic coverage).

So how do we trick our bodies into believing it’s not losing weight? How do we turn the very systems that keep us alive today, working in our favor?

It is upon manipulating the shortcomings of our own bodies that we are capable of beating the system. In order to answer those questions together with the questions that came up in the introduction, the next article will go into depth about the science of energy density and how, by mastering our appetite and thus optimizing the ad libitum dieting approach.

Title Image Source: depositphotos / AndrewLozovyi