Today’s Guest Post comes from my friend and colleague David Macklin, MD, Toronto
Not long ago I received a message from a colleague looking for help with a patient who was regaining weight. As I thought about my response, it occurred to me that there should be a comprehensive list of why this happens, yet I could not remember coming across one. The following is a more detailed reproduction of the list I sent back to my colleague that day. I’d like to thank Arya for suggesting that I share this list with his readership.
An important note regarding this list: Reason number one is the most important and most common reason for weight regain. The other reasons can make the primary reason more complicated.
The primary reason for weight regain is biology. The brain defends against weight loss because of an old biological play book. If our ancestors lost weight, it was not to look good for a wedding or because of bathing suit season. Back then, weight loss was either because of illness or an interrupted food supply. Simply put, defending against weight loss was defending against death.
In the last 30 years we have learned how the brain does this. The brain is expert at 1) recognizing fat loss, 2) defending against fat loss, and 3) promoting weight regain. The brain does this by:
a) increasing appetite – the motivation for calorie intake
b) decreasing metabolic rate
Increased appetite seems to be more complicit than slower metabolism in weight regain. Increased appetite, in the form of an increased motivation to eat, leads to increased overall calorie intake, which in turn leads to weight regain.
A reminder, the remaining reasons for weight regain operate through the main mechanism, biology.
The next common reason for weight regain relates to dieting. Note that dieting is not an effective method of preventing weight regain. Instead, the three pillars to preventing weight regain are behavioural therapy, medication, and surgery. Simply put, the risk of weight gain is greater the more “diet-like” the weight-loss method. Specifically:
a) if the weight-loss effort involved a commitment to a reduced calorie intake that was unsustainable.
b) if the weight-loss effort involved a commitment to a level and type of effort that was unsustainable.
c) if the weight-loss effort did not accept and involve a conscious commitment to the value of fun, food, drink, friends, socialization, and travel.
The greatest predictor of thwarting weight regain is sustained adherence to the method used to lose weight. The above methods predict poor adherence. They also predict that for someone losing too much weight, going to a weight lower than what is sustainable, weight loss will be overwhelmed by biology.
Thus, we have the definition of best weight. One’s best weight is arrived at by committing to the opposite of dieting. Best weight is discovered by committing to 1) a sustainable calorie level, 2) at a sustainable effort, 3) while accepting a conscious commitment to the value of fun, food, drink, friends, socialization, and travel. Best weight is the weight you softly land at when committing to a lifestyle that is, by definition, sustainable.
3. A CHANGE IN EXTERNAL CUES, TIMES AND SETTINGS
The next and rather poorly understood reason for weight regain is a sustained change in one’s overall environment. A common current example of this would be someone who was working in an office and is now working in their home, or the opposite: someone who was working at home and now is working at an office. Another example is someone who, during weight loss, avoided high-risk settings for the purpose of weight loss and now inevitably is re-engaging in these setting. For example someone who avoided social setting or restaurants temporarily just for the purpose of weight loss. The cues in our physical and social environments trigger the biological response of appetite – wanting – the subconscious motivation to eat. If the cues experienced during weight loss change, weight regain can follow.
4. DISCONTINUATION OR POOR COMPLIANCE WITH ANTI-OBESITY MEDICATIONS
Anti-obesity medications (AOMs) work by defending against an individual’s biology. AOMs defend against increased appetite and dampen the subconscious motivation for calorie intake (wanting). If AOMs are discontinued or poorly complied with, the defence against weight regain is lost and the biology does the rest.
5. DEMOTIVATING SELF-CRITICAL THINKING THAT FOLLOWS SETBACKS
A highly underestimated reason for weight regain is in an individual’s response to “weight loss setbacks.” Common weight loss setbacks include 1) the aftermath of off-track eating and/or drinking episodes, and 2) the moments after seeing a number on a scale not in one’s favour. Unless effective behavioural therapy has been provided, these setbacks may often be followed by negative self-critical thoughts and negative emotions including demotivation. Yet it is precisely when one is at a lower weight that they are most subject to their biological drivers of weight regain and most likely to experience over-consuming and unfavourable scale results. Screening for and treating these unhelpful cognitive responses is an important part of understanding and addressing weight regain. To reiterate, this is probably the most underestimated non-biological complication of weight loss.
6. WEIGHT-PROMOTING MEDICATION(S)
Weight gain can be a possible serious side effect of many commonly used medications. Some medications more commonly cause weight gain than others, and significant inter-individual differences exist. Weight regain may be caused by the addition of a weight-promoting medication and if possible, a substitution can be made for an alternative medication that is more weight neutral.
Finally, there is a finite list of internal states that may promote weight regain. It is intuitive to most that stress, fatigue, lack of sleep, depressed mood, and lower levels of activity may promote weight regain. For many individuals, especially in a state of reduced body weight, each of these factors can increase wanting, the motivation to eat, and decrease self-regulation skills (restraint). If someone is regaining weight, it is imperative to screen for each of these modulators and to recognize how a change in any of these may be leading to higher calorie intake and weight regain.
For clinicians, and for those who struggle with weight, I hope this list is helpful.
David Macklin, MD
About the author: David A. Macklin, MD, is a lecturer at the University of Toronto and a University of Toronto trained family physician. He has practiced obesity medicine since 2004. He is the Medical Director of the Weight Management Program at the Toronto Medcan Clinic and co-author of the Canadian ACTION Study and the Psychology and Behavioural Treatment Chapter of the 2020 Canadian Clinical Practice Guidelines for the treatment of Obesity in adults.
The last few weeks have been abuzz about the remarkable weight loss seen with the dual GIP/GLP-1 agonist tirzepatide in the SURMOUNT-1 study. While this degree of weight loss surpasses that of the GLP-1 analogue semaglutide by several percentage points, this is not the most important implication of these findings.
Rather, the real implication of the SURMOUNT-1 data is, that we will soon see another major global pharmaceutical player, namely Eli Lilly, enter the obesity space.
Over the past decade or so, the only major international player in this field has been Novo Nordisk. With the introduction of liraglutide, recently followed by the approval of semaglutide for the obesity indication, Novo Nordisk has not only played a flagship role in developing the field of obesity medicine, it has also had to bear the considerable costs associated with raising obesity awareness, medical education, engaging payers, supporting obesity NGOs, and generally promoting the notion of obesity needing to be managed as a chronic disease.
While Novo Nordisk must be commended for their remarkable efforts in promoting a better understanding of obesity as a chronic disease, much more remains to be done in this regard. Thus, having another major company enter the field of obesity medicine should considerably increase the resources that can be put towards professional and public education and supporting the work of the various NGOs working on this issue.
For those, who are are perhaps sceptical about industry involvement in physician education or support for NGOs, it is important to remind ourselves of the fact that industry actually provides much of the evidence from large randomised controlled trials on which we base our guidelines and treatment algorithms.
Moreover – like it or not – industry also supports substantial academic research, investigator-initiated trials, training of new professionals, and a host of other activities that ultimately benefit our patients. In fact, I cannot think of a single disease area in which most significant therapeutic advances are not largely attributable to industry efforts.
We perhaps also need to remind ourselves that the pharmaceutical industry, in contrast to the free-for-all-anything-goes predatory billion-dollar “weight-loss industry”, underlies strict regulatory oversight and is held to ethical codes and standards that provides a transparent and effective framework for their promotional activities.
Thus, my expectation is that with the entrance of another major global player like Eli Lilly into the obesity area, we will not only see much-needed competition but also a major expansion of funding and support for activities that will ultimately benefit those living with obesity.
Finally, I can only hope that with the successful development of novel medications like semaglutide and tirzepatide, other major pharmaceutical companies will now take heart at the success of Novo Nordisk and Eli Lilly and finally venture into this space.
Despite the fact that these companies have clearly raised the bar for what is now possible with effective anti-obesity medication, hopefully, more major companies will make the necessary investments into this area of medicine – which has been underfunded and largely ignored to the detriment of the vast number of people living with obesity who have had to wait far too long for advances in this important therapeutic area.
Today’s guest post comes from Emilia Huvinen, MD, PhD, Gynecologist, Helsinki, Finland
My first step into the world of obesity research and care began with my PhD studies on gestational diabetes.
For a young gynecologist, it was all new in the beginning but soon I found myself immersed in the world of behavioural medicine, adiposity and glucose metabolism. As years went by, and I learned more and more about different aspects of healthy behaviours and the complex biology of weight regulation, I finally got involved in actually treating women with obesity for their obesity.
As a gynecologist, it is not difficult to see how obesity can play a crucial role in several periods of a woman’s life; starting from having early puberty and continuing to heavy menstrual bleeding, infertility, pregnancy complications, and stronger menopausal symptoms. Treating obesity can also be beneficial when treating women with polycystic ovaries syndrome (PCOS), infertility and endometrial hyperplasia, a pre-stage of uterine cancer. As obesity is associated with several pregnancy complications, helping our patients better manage their weight preconceptionally can improve pregnancy outcomes and hopefully even influence the health of the next generation.
As a gynecologist, being the trusted long-term doctor for women, we have the privilege of being really close to our patients’ lives. We are also very used to discussing intimate and even very delicate issues in our everyday practice. However, it is apparently still a million-dollar-question how to get more gynecologists involved in obesity care.
Unfortunately, the general advice currently given to women living with obesity is still to just “eat less and exercise more”. Many of us are still unaware that obesity is a chronic disease, and that people need care and treatment, not guilt and accusations.
I suspect that the most common obstacle preventing more gynecologists getting involved in obesity medicine, is simply lack of information. Starting a conversation on obesity feels uncomfortable and delicate, and there’s a general assumption that specific skills are needed that are best left to obesity specialists. Often it is also a question of time, and many feel that it might not be worth the effort. For gynecologists, medications for obesity treatment are also unfamiliar and different from the ones we typically use.
My wish is to develop a sustainable and practical protocol for treating and supporting my patients living with obesity. Developing multi-professional networks together with skilled dietitians and psychologists is crucial. I also believe that by using electronic technologies like video consultations, we can offer better access to obesity care even to women living in remote areas – which in Finland is not uncommon!
Even if most gynecologists currently may not feel comfortable treating obesity, I hope we can at least all talk to our patients in a sensitive way and support and guide our patients with obesity to places where care is offered. We should also acknowledge that as doctors we often play a major role in creating obesity stigma.
As new and highly effective treatments for obesity are now becoming available, I clearly see a golden opportunity for us as gynecologists to become more involved in obesity medicine as part of our practice. Our patients certainly deserve comprehensive care, which includes helping them better manage their obesity.
Dr Emilia Huvinen,
About the author: Dr Emilia Huvinen, MD PhD, is a specialist in Obstetrics and Gynecology and currently works as an OBGYN in Aava clinic and treats women with obesity in weightclinic.online. She’s also a postdoctoral researcher at University of Helsinki. Her PhD studies focused on heterogeneity of GDM and long-term health of GDM women, but in recent years her research has expanded from lifestyle and pregnancy to metabolomics and genetics and their interplay in the health of women and their children.
Starting patients on insulin is not easy. Patients have to be counseled, educated, introduced to self-monitoring, and need to be seen more frequently till they are comfortable and have achieved their treatment goals.
For this, in many countries, there are dedicated billing codes – some of which can be rather attractive. As a case in point, in Germany, billing codes for starting patients with type 2 diabetes on insulin, have resulted in Germany perhaps being the world leader in the use of insulin in patients with T2D.
As we now enter the era of increasingly effective anti-obesity medications, resulting in two-digit weight loss, there will be a growing number of T2D patients, who will eventually need to be taken off their insulin.
This again, is not as simple as it sounds. Many T2D patients are on rather high doses of various types of insulin and will need to be gradually tapered off. During the time of active weight loss, insulin doses will need to be adjusted, both to avoid hypoglycemic episodes but also to ensure that the HbA1c targets are maintained.
This is extra work for doctors (and their staff) and will need to be accounted for.
Thus, it may be reasonable to ask whether it is time to introduce billing codes for stopping insulin, given the large number of patients who are currently on it but will need to come off as they experience significant weight loss.
We have already seen such situations in patients undergoing bariatric surgery, but there, due to the rather rapid improvement in glycemic control, we can often simply hold the insulin following surgery.
With the more gradual weight loss seen with anti-obesity medications, this process will take longer and needs to be closely monitored.
In jurisdiction where there are no special billing codes for starting insulin, this may not be an issue.
However, in jurisdictions, where such billings provide an incentive to doctors to start patients on insulin, we may need to create new billing codes to incentivise docs to take their patients off insulin as effective anti-obesity medications become more widely available.
Today’s guest post comes from Sean Wharton, my friend and colleague from Toronto, well known to all of us working in obesity medicine.
Since the George Floyd incident in the United States, the entire world has taken greater account of instances of racism and discrimination in all walks of life. Medicine is no different and it is therefore no surprise that much of medicine is steeped in racism. Many people refer to this as the social determinants of health, but the structure and underlying reasons for those determinants, in many countries, is racism.
In America, the remnant of slavery also lives on in the social determinants that drive the obesity epidemics in African Americans. African American women have an incidence of obesity of 57%, compared to white women at 40%. This is 42% higher!
This is a staggering difference. What accounts for this?
We now have a greater understanding that most disparities in health, including hypertension, diabetes and obesity, are due to racial and ethnic inequities, many of which are a legacy of their past history.
For obesity in African Americans, we can start by looking at the nutrition during slavery. A slave’s diet was primarily made up of inexpensive foods that were high in sugar and fat, designed to provide fuel that would be burned off during the day.
As reported historically slave rations could include:
10 quarts rice or peas
1 bushel sweet potatoes
2-3 mullet or mackerel salt fish
1 pint mollasses
2 pounds pork
Thus, African Americans became accustomed to this diet and continue to have a palate for such as evidenced by the menu in many Southern African American restaurants and homes.
Today food choices for African American follow a similar pattern as in the times of slavery. Foods – high starch, fat, sodium, cholesterol, and caloric content, and are inexpensive and often low-quality nature of the ingredients such as salted pork and cornmeal.
This gives us some explanations regarding the disparity in the incidence of obesity between the races, and now we deal with the fact that there is are difference in success of obesity treatment between the races. Again this is likely due to the very same social determinants.
Our own research has documented that women of colour lost less weight at weight management clinic, but when adjusted for the number of visits, the weight loss was the same.
It was clear that the system was not built for women of colour to access the care. There was no biological difference, just a difference in access.
There is a lot of discussion regarding whether the reason for health disparities is biological or due to societal differences between races. There is now considerable research that points to the fact that race is a social construct and determinants of health are based on racism and discrimination and not biology.
Interestingly, as a recent example, the equation for adjustment in eGFR for renal failure, for Black people, has been removed by most labs as it has no scientific validity and does nothing apart from fueling racism. Remember also, the check box for the adjustment for renal function was Black or White, so what box would Barack Obama, or Beyonce check?
My hope is that the social determinants that define this dramatic differences in rates of obesity and success of obesity treatment will improve as we work to break down the walls of racism around the world.
About Sean Wharton:
Dr. Wharton has a doctorate in Pharmacy and Medicine from the University of Toronto and is the medical director of the Wharton Medical Clinic, a community based internal medicine weight management and diabetes clinic. He is an adjunct professor at McMaster University in Hamilton and York University in Toronto. He also academic staff at Women’s College Hospital, and clinical staff the Hamilton Health Sciences. Dr. Wharton’s research focuses on bariatric medicine and type 2 diabetes. He is the co-lead authour of the Canadian Obesity Guidelines. Apart from his interest in obesity medicine, Dr. Wharton is enthusiastically involved in activism to achieve health equity in Canada. In 2000, he founded the BMSA (Black Medical Students Association) at the University of Toronto, now recognized as a leading mentorship organization across Canada.
Over the past decade or so, alternative explanations for the rise in obesity rates, that de-emphasize the role of caloric intake vs. the role of specific nutrients, have had a field day.
Leading amongst these, no doubt, is the Carbohydrate-Insulin-Model (CIM) of obesity, whereby, carbs stimulate insulin release, which in turn stimulates expansion of adipose tissue, which in turn leads to insulin resistance, resulting in even higher insulin levels, ultimately resulting in a vicious cycle that can only be interrupted by religious adherence to a low-carb diet.
Although this model has had broad populistic appeal, spawning a whole industry of best-sellers, low-carb products, and even treatment programs built around this paradigm, as pointed out in rather comprehensive article by Kevin Hall and a host of notable obesity experts, published in the American Journal of Nutrition, CIM (which has undergone several modifications since its inception), does not quite concur with all of the pre-clinical and clinical evidence.
In this paper, the authors make a rather compelling argument in favor of the Energy-Balance-Model (EBM), which pretty much aligns with virtually everything we know about the science of body weight regulation.
According to the authors,
“The EBM proposes that the brain is the primary organ responsible for body weight regulation via integration of external signals from the food environment along with internal signals from peripheral organs to control food intake. Specific brain regions, such as the hypothalamus, basal ganglia, and the brainstem modulate food intake below our conscious awareness via complex endocrine, metabolic, and nervous system signals acting in response to the body’s dynamic energy needs as well as environmental influences…..whereas day-to-day energy intake and energy balance of an individual can be highly variable, neural regulation of energy balance is generally achieved over prolonged time scales.”
The key term in all of this is “positive energy balance”, without which there can be no accumulation of excess weight. Ergo, as calories are the currency of energy balance, there can be no excess energy balance without excess calories.
As the authors go on to explain, the physiological processes that determine caloric intake are subject to a host of biological and environmental perturbations, explaining both the differences in individual susceptibility as well as the wide variability in shape and size evident even in populations with similar environmental exposure. Furthermore, this model also explains the wide variation in response to dietary, pharmacological, or even surgical manipulations that modify the functioning of the system.
Importantly, while the EBM model of obesity fully accommodates a role for high-glycemic foods and a role for insulin, it also allows for a number of alternative mechanisms that ultimately drive positive energy balance.
Recognizing the central role of caloric intake, does not mean that we all need to go back to calorie counting or restrictive caloric dieting – rather, it is clear that such approaches tend not to be very effective in the long-term and may in fact be counterproductive in terms of obesity management.
However, turning to simplistic alternative notions that disregard the fundamental importance of caloric balance is neither helpful nor in line with the basic laws of physics that govern conservation of energy.
Or, as the authors highlight,
“…the CIM sets forth a single exposure as the primary determinant of common obesity and proposes a single “practical strategy” to treat obesity by prescribing low-glycemic-load diets despite evidence that such interventions are no more effective than prescribing higher-glycemic-load alternatives.“
As a general rule, when faced with simple explanations or solutions to a complex problem, a certain level of skepticism is generally in order.