It's not your thyroid.

I discussed my success with:
 Invokana (canagliflozin)  link


Halls article link 

Highlights edited by me to facilitate reading:

In summary, our results provide the first quantification of the energy intake feedback control system in free‐living humans. 

We found that appetite increased by ∼100 kcal/day above baseline per kilogram of lost weight
—an effect several‐fold larger than the corresponding energy expenditure adaptations. 

The few individuals who successfully maintain weight loss over the long term do so by heroic and vigilant efforts to maintain behavior changes in the face of increased appetite along with persistent suppression of energy expenditure  
in an omnipresent obesogenic environment. 
Permanently subverting or countering this feedback control system poses a major challenge for the development of effective obesity therapies.

Introduction

Body weight is believed to be regulated by feedback control of both energy intake and energy expenditure. 

Several experiments in humans have quantified how energy expenditure adapts in response to alterations of energy intake and body weight. 

For example, Leibel et al. found energy expenditure adaptations of several hundreds of kilocalories per day acting to resist weight loss  

In contrast, energy intake adaptations have yet to be accurately quantified in humans despite the widespread belief that feedback control of energy intake is critical for body weight regulation and acts as part of a complex neurobiological system to determine overall human food intake behavior 2.

First, we lacked the ability to accurately measure changes in free‐living energy intake in large numbers of people over extended time periods. ... Therefore, observations over long time scales are required, thereby making laboratory‐based studies impractical....To address this important problem, we recently validated an inexpensive mathematical method for calculating energy intake changes 

The second impediment to quantifying energy intake control in humans is that we lacked an intervention that increases energy output by a known amount without participants consciously knowing that this is occurring. 

Rather, most interventions that alter body weight or energy expenditure also evoke cognitive responses that may mask the effect of weight changes per se on the feedback control of energy intake. 

For example, engaging in an exercise program might increase energy expenditure and lead to weight loss, but exercise is a conscious behavior that does not have an effective placebo control. 

Furthermore, exercise has a complex role in modulating appetite and may induce compensatory changes in other components of total energy expenditure that are difficult to quantify. 

Therefore, changes in energy intake during an exercise program may not solely be due to feedback mechanisms controlling body weight but are likely to also involve conscious changes in behavior.

Here, we used data from a placebo‐controlled trial in patients with type 2 diabetes who were treated for 1 year with canagliflozin(Invokana), an inhibitor of sodium glucose transporter 2 (SGLT2), thereby increasing energy output in the form of urinary glucose excretion (UGE) 

In patients with type 2 diabetes, treatment with canagliflozin at a dose of 300 mg/day increases mean daily UGE(urinary glucose excretion) by approximately 90 g/day which is sustained at the same level throughout the duration of treatment without directly altering energy expenditure  or central pathways controlling energy intake and without the patients being directly aware of the energy deficit. 

In other words, SGLT2 inhibition provides a novel way to covertly perturb human energy balance that largely bypasses the volition and conscious awareness of the subjects. Any observed increased energy intake countering the weight loss induced by SGLT2 inhibition therefore likely reflects the activity of the feedback control system.

 We found that the feedback control of energy intake in humans was proportional to the amount of weight lost and was substantially stronger than the control of energy expenditure.

Results

 In response to the sustained increase in UGE (urine glucose excretion) with canagliflozin (Invokana) treatment, mean body weight declined and reached a new equilibrium several kilograms lower and significantly more than the placebo group whose mean body weight loss was less than 1 kg 

To explain the measured body weight changes in the treatment group given the estimated increases in UGE, energy intake was calculated to have increased by ∼350 kcal/day at steady state.

 In the placebo group, mean energy intake was calculated to transiently decrease by ∼100 kcal/day over the first several weeks and return to near baseline after 15 weeks.

Discussion

In the absence of ongoing efforts to restrain food intake (this means staying on a low calorie around 1500 cal for the rest of your life) following weight loss, feedback control of energy intake will result in eating above baseline levels with an accompanying acceleration of weight regain. 

This phenomenon has been also observed in lean men following experimental semi-starvation or short‐term underfeeding.

 Hyperphagia in these studies was believed to result from homeostatic signals arising from loss of both body fat and lean tissues  but a conscious desire to regain lost weight cannot be ruled out and may have contributed to increased food intake attributed to increased food intake.

Long‐term inhibition of SGLT2 (by Invokana) provides a unique probe for assessment of human energy homeostasis since :

1-the mechanism of action is clear, 

2-its effect on energy output is consistent, and 

3-the intervention is unlikely to directly affect central pathways involved in regulation of food intake. 

In contrast, other interventions aimed at increasing energy expenditure, such as exercise  or exogenous delivery of thyroid hormone 33, have pleiotropic effects and their impact on energy expenditure can be highly variable.

The suggestion that the signals controlling energy intake act as a proportional feedback system without integral feedback is consistent with 

the roughly proportional changes in appetite‐regulating hormones that occur rapidly in response to weight loss and do not further increase as weight loss is sustained (as would occur with integral feedback) 

 We do not yet know whether the simple proportional controller represented by Equation is valid for a range of weight losses. 

For example, it may be possible that small weight changes are uncompensated by changes in energy intake such that the control system engages only after sufficient weight loss to cross some threshold (usually 8-10% weight loss)

 Furthermore, larger weight losses may result in energy intake adaptations corresponding to a nonlinear function of body weight change.

Proportional feedback control of energy intake may help explain why the calculated exponential decay of diet adherence during weight loss interventions markedly contrasts with self‐reported measurements that indicate persistence of diet adherence and no significant differences in caloric consumption between the period of early weight loss compared with the later time when weight has plateaued  

This has led to speculation that the 6‐ to 8‐month weight plateau may be entirely due to slowing of metabolic rate rather than loss of diet adherence.

 Our results suggest otherwise and further illustrate that self‐reported energy intake measurements are quantitatively unreliable. (I think what they are saying here is the tremendous hunger from low leptin plays a big role)

Nevertheless, the relative constancy self‐reported energy intake over the first 6 months corresponds well with the calculated persistent effort to resist the increased appetite and the drive to overeat at above baseline levels.

 Therefore, self‐reported measurements of energy intake may more accurately reflect the perceived effort of the dieter to adhere to the intervention rather than their actual energy intake.