Three Obesity Types - POSTED ON: Mar 12, 2018
The medical profession has no cure for obesity. While many people will diet, exercise, and thus, lose weight - keeping that weight off is where the real struggle lies.
Below is an article and a video in which Dr. Sharma, who-is-one-of-the-medical-obesity-experts-that-I-admire-and-respect, explores the complex biology behind weight loss and regain, and gives his medical opinion as to why obesity should be managed as a chronic disease rather than as a personal failure.
The Three Clinical Faces of Obesity
by Dr. Arya Sharma M.D.
In my experience, patients presenting with obesity tend to fall into three categories, each of which requires a distinct management approach. They are:
1) Active Gainers
2) Weight Stable
3) Post-Weight Loss
Active Gainers are patients currently at their lifetime maximum and continuing to gain significant amounts of weight – i.e. more than the usual 0.5 to 1 lb/year. Patients in this category require immediate attention – if nothing happens, their weight will most likely just continue to increase.
The good news is that in almost every patient in this category, there is an identifiable reason for the ongoing weight gain – this can be psychosocial (e.g. depression, binge-eating disorder, etc.), due to a medical comorbidity (arthritis, chronic pain, etc.) or medications (e.g. atypical antipsychotics, hypoglycemic agents, etc.).
From a management perspective, the sooner we identify and address the underlying problem, the sooner we can slow or even halt the rate of weight gain – in this patient – gaining less weight than before is the first sign of success. There is really no point trying to embark on losing weight as long as the underlying problem driving the weight gain has not been addressed, as this is likely to make sustained weight loss even more unlikely that it already is..
Weight Stable patients are those that present with excess weight but are relatively weight stable. Even though they may be at their lifetime maximum, they have been pretty much the same weight (perhaps a few lbs up or down but nothing drastic) for several years (sometimes even decades). By definition, a patient who is weight stable is in caloric balance, and thus, by definition is not eating too much. In fact, these patients are eating the exact number of calories needed to sustain their bodies, which is why they are weight stable. (Remember, even if you are weight-stable eating 4000 Cal a day, you are technically not “overeating”.)
These patients of course have experienced significant weight gain in the past (historical weight gain), but whatever it was that caused them to gain weight is no longer an active problem (e.g. pregnancy, past depression, etc) – and therefore, probably doesn’t need to addressed (although, I always find it of interest to find out what caused the weight gain in the first place). With these patients, we can determine whether or not their weight is affecting their health, and if it is, we can jump right into discussing treatment options (behavioural, medical and/or surgical).
The third group of patients, Post-Weight Loss, are those who are not at their lifetime maximum, or in other words, have already lost weight (by whatever means).
These patients generally present either because they want to lose even more weight (Doctor, my diet has stopped working! = “weight-loss plateau“), or are experiencing weight regain (Active Regainers).
In case of the patients experiencing a “weight-loss plateau”, one needs to determine if there is in fact any medical indication for further weight loss – many of these patients may already be at their “Best Weight”.
If there is indeed a medical indication for further weight loss, it generally means adding therapeutic options that may include anti-obesity medications and/or surgery. (In my experience, patients who have been maintaining a significant amount of weight loss on their own, generally leave little room for further behavioural intervention).
On the other hand, there are the post-weight loss patients who are actively regaining weight. These tend to fall into two groups:
1) The first group of Active Regainers are those, who have lost a significant amount of weight with a strategy that is in fact unsustainable (e.g. a very low-calorie diet, an excessive exercise program, or whatever else desperate patients will try just to drop their weight).
As the strategy they were on is not one that they can sustain (for good reasons), some weight gain is inevitable and the best we can do is to offer a weight management strategy that is sustainable in the long run (and may include medication or surgery) .
2) The other group of Active Regainers, are those that were on a more-or-less sustainable management plan (behavioural, medical or surgical) and have for some reason “fallen off”.
Here one needs to determine what exactly they have stopped doing (e.g. no longer keeping their food journal, stopped their anti-obesity medications, etc.) or what additional weight-gain promoting change has occurred that has thrown them off (again, reasons can be psychosocial or medical).
Here one needs to determine if the patient can in fact go back to doing what was “working”, which may require addressing the new problem that has arisen or add additional therapeutic options (e.g. medications or surgery).
Thus, as each type of patient needs a somewhat different assessment and management strategy, I find this approach to thinking about each patient most helpful.
About Dr. Sharma:
Dr. Arya M. Sharma, MD/PhD, FRCPC is Professor of Medicine & Chair in Obesity Research and Management at the University of Alberta, Edmonton, Canada. He is also the Clinical Co-Chair of the Alberta Health Services Obesity Program.
Dr. Sharma is founder and Scientific Director of the Canadian Obesity Network, a network of over 10,000 obesity researchers, health professionals and other stakeholders.
He is also the Past-President of the Canadian Association of Bariatric Physicians and Surgeons.
His past appointments include positions as Professor of Medicine and Canada Research Chair (Tier 1) at McMaster University (2002-2007), Professor of Medicine at the Franz-Volhard Klinik – Charité, Humboldt University Berlin (2000-2002) and the Free University of Berlin (1994-2000). His research focuses on the evidence-based prevention and management of obesity and its complications.
He has authored and co-authored more than 350 scientific articles and has lectured widely on the etiology and management of obesity and related cardiovascular disorders. Dr. Sharma is regularly featured as a medical expert in national and international TV and print media and maintains a widely read obesity blog at www.drsharma.ca.
Video Below: How to Lose 50 Pounds and Keep Them Off
Fat Cells are Forever - POSTED ON: Oct 04, 2017
Once fat cells reach a certain size -- that is, they become filled to capacity with fat content -- then new fat cells will begin to form. The fat cell number and size increases and shrinks based on deposits from food intake.
“We have a seemingly infinite capacity to recruit new fat cells, but we cannot get rid of them once they have been recruited" said Michael Rosenbaum, associate professor of clinical pediatrics and medicine at Columbia University. "in most cases, weight gain initially reflects ... enlargement of existing fat cells followed by an increased growth of new fat cells.”
Research has shown that obese people who have weight loss surgery have just as many fat cells two years after the surgery as before it, even though they have become much thinner.
Scientist, Dr. Rudy Leibel, says that "the body controls the number of its fat cells as carefully as it controls the amount of its fat". Fat cells die and new ones are born throughout life. Scientists have found that fat cells live for only about seven years and that every time a fat cell dies, another is formed to take its place.
Below see a 2017 New York Times article about this matter.
Are Fat Cells Forever?
By Alice Callahan
February 17, 2017 - New York Times
Once fat cells are formed, can you ever get rid of them?
The number of fat cells in a person’s body seems to be able to change in only one direction: up. Fat cell number increases through childhood and adolescence and generally stabilizes in adulthood.
But this doesn’t mean that fat cells, or adipocytes, are stagnant. The size of individual fat cells is remarkably variable, expanding and contracting with weight gain or weight loss. And as with most cell types in the body, adipocytes die eventually.
“when old ones die, they are replaced by new fat cells,” said Dr. Michael Jensen, an endocrinologist and obesity researcher at the Mayo Clinic. Cell death and production appear to be tightly coupled, so although about 10 percent of adipocytes die each year, they’re replaced at the same rate.
Even among bariatric surgery patients, who can lose massive amounts of weight, the number of fat cells tends to remain the same, although the cells shrink in size, studies show.
Liposuction reduces the number of fat cells in a person’s body, but studies show the weight lost is typically regained within a year. It isn’t known whether this regain occurs through the production of new fat cells or expansion of existing ones.
People who are obese tend to have more fat cells than those who are not, and several studies have found an increase in fat cell number with weight regain following weight loss.
"The fact that fat cell number can be increased but not decreased most likely contributes to the body’s drive to regain weight after weight loss", said Dr. Kirsty L. Spalding, a cell biologist at the Karolinska Institute in Sweden and the lead author of a 2008 study showing that fat cells die and are replaced. Beyond their role in storing fat, adipocytes secrete proteins and hormones that affect energy metabolism.
“Following weight loss, adipocytes become smaller, generally smaller than those from people with a similar B.M.I.,” Dr. Spalding said. One hypothesis is that those smaller cells might send signals to increase appetite and fat storage, which could help to explain why weight loss is so difficult to maintain, though much more research is needed.
Our Weight is Regulated by Our Biological System - POSTED ON: Oct 01, 2017
I continually read a great many books, articles, blogs, and forum posts on the subject of obesity.
No one,…. not even the most qualified medical doctor or scientist, … knows everything or holds only beliefs that are absolutely correct.
However, I am often amazed by the vast amount of existing misconceptions, myths, and wishful-thinking that gets spread and promoted by people who present themselves as obesity “experts” or “gurus”.
One thing that Scientists know for sure about obesity management, is the sad fact, that no diet, exercise, medication, not even bariatric surgery, will permanently reset the body’s tendency to defend and regain its body weight to its set point .... this generally being the highest weight that has been achieved and maintained for a notable length of time.
Thus, any effective long-term treatment MUST OFFSET the complex neurobiology which is designed to eventually doom every weight-loss attempt to ultimately "fail".
A comprehensive review recently published in Endocrine Reviews describes the complexity of the biological system that regulates our body weight.
The 30+ page research paper, backed by about 350 scientific citations, was written by the undisputed leaders in the medical field of Endocrinology (Michael Schwartz, Randy Seeley, Eric Ravussin, Rudolph Leibel and colleagues) and is actually a “Scientific Statement” from the Endocrine Society.
In other words, these Scientists know that they are talking about when they speak about the Science of Energy Balance, and in this paper they outline in excruciating scientific detail just how complex the biological system that regulates, defends, and restores body weight actually is.
From the Abstract of this research paper:
We included evidence from basic science, clinical, and epidemiological literature to assess current knowledge regarding mechanisms underlying excess body-fat accumulation, the biological defense of excess fat mass, and the tendency for lost weight to be regained.
A major area of emphasis is the science of energy homeostasis, the biological process that maintains weight stability by actively matching energy intake to energy expenditure over time.
Growing evidence suggests that obesity is a disorder of the energy homeostasis system, rather than simply arising from the passive accumulation of excess weight.
Their position is that, despite all we have learned about this system, we are still far from fully understanding it.
Science knows about one of the pathways, but there are many pathways in a complex network of multiple interacting pathways that involve virtually every part of the brain.
They say that the medical field currently needs a great deal more information about the specifics of this issue:
The identification of neuromolecular mechanisms that integrate short-term and long-term control of feeding behavior, such that calorie intake precisely matches energy expenditure over long time intervals, will almost certainly enable better preventive and therapeutic approaches to obesity.”
To be viable, theories of obesity pathogenesis must account not only for how excess body fat is acquired, but also for how excess body fat comes to be biologically defended.
Answering this question requires an improved understanding of the neuro-molecular elements that underlie a “defended” level of body fat. What are the molecular/neuroanatomic predicates that help establish and defend a “set point” for adiposity? How do these elements regulate feeding behavior and/or energy expenditure, so as to achieve long-term energy balance? By what mechanisms is an apparently higher set point established and defended in individuals who are obese?”
They conclude that:
Given that recovery of lost weight ... (the normal, physiological response to weight loss irrespective of one’s starting weight) ... is the largest single obstacle to effective long-term weight loss, we cannot overstate the importance of a coherent understanding of obesity-associated alterations of the energy homeostasis system.”
So, in essence, this scientific paper shows why no simple solution to obesity is in sight; details the existence of an enormous Problem; and raises Questions for which Science still needs to find answers.
To get a simple explanation of the basic concept, see: Set Point.
Any “health & wellness” professional, medical doctor, or guru who claims that any particular Diet, Behavior, or LifeStyle can fundamentally change the part of the body’s biology which acts to protect and restore body fat in the long term is Simply Wrong.
They are either spreading a Lie, sharing a Myth, or offering a hypothesis for which no proof or reasonable evidence exists… which means that they are simply sharing their own Wishful-Thinking.
At this point, all credible Scientific Research indicates the following:
No matter how much weight gets lost, or is maintained for the short-term, …
No matter whether that weight loss was slow or fast, ...
No matter when food intake occurs ...
No matter whether “unprocessed” or “healthy” food is eaten, ...
Ultimately NO diet or behavior
manages to “reset” the body-weight set point to a lower level,
in order to biologically “stabilize” weight loss for the long-term.
NOTE: Originally posted on 7/23/2017. Bumped up for new viewers.
Set Point - POSTED ON: Sep 30, 2017
We do not understand how the body resists weight change and why, after weight loss, so many people regain it. The concept of a set point for weight is widely accepted.
The set point is like the thermostat in our central heating system. It is switched on when the temperature falls below a critical (set point) temperature and is switched off when that is exceeded.
Using the word “rachet” might help one conceptualize the set point concept.
To rachet is to cause to increase or decrease by increments. A rachet is a mechanical device consisting of a toothed wheel or rack engaged with a pawl that permits it to move in only one direction.
A person has an existing set point. That person gains weight, and then gains and sustains even more weight gain. This causes the set point to be racheted up, and once it passes each rachet, there is no going back. The rachet is the biological set point and it can be easily driven upwards, but is very difficult to drive back down.
Using the fat cell theory is helpful to further explain how this works.
For an example, let’s assume an average fat cell contains 0.4 micrograms of fat each. A person gaining weight might see that fat cell load expand to 0.6 micrograms. This is an acceptable load increase, and when the person loses weight, the fat cell level drops back to 0.4 micrograms.
This seesaw can go on forever, but when the weight gain loads the fat cell up to 0.8 micrograms, a tipping point is reached, and the fat cell divides. Now we have two fat cells, each containing 0.4 micrograms. Click! That was the ratchet turning irreversibly.
When we want to return to the previous weight, we must lose half the fat we gained. The problem with this is that each fat cell now has the standard fat load of 0.4 micrograms each, and to halve this to just 0.2 micrograms per cell requires us to get the cells to live a life they do not like. If we let our mind tell us what to eat, we can overcome the disgruntled fat cells which are below their fat quota. But all the time the basic animal biology of our body will be waiting to return to 0.4 micrograms per cell.
Then, along comes an event like a vacation, a holiday, or other eating occasion, and we take our eye off the ball .. lose our mental concentration, but the fat cells in our body didn’t rest, and we’ve regained our weight. The body is now back to the new set point it made when we went past the older set point and hit a new rachet.
In a 2007 research study, a team of Swedish researchers examined fat biopsies from about 680 lean and obese Swedish people. They found obese people can have as much as twice the number of fat cells as do lean people. The researchers also followed 20 gastric bypass patients who lost weight after their operations. Over the course of two years, their fat cells shrunk in size, but the total number stayed constant.
Fat cells can shrink, but once created, they never disappear. The body’s job is to work hard to get all of its cells (including fat cells) to survive and even to thrive. It is easy to continually rachet the biological set point up, but it is almost impossible to rachet it down.
A fat cell is not merely a passive container that stores fat. Leptin is one of the hormones produced by fat cells. Among other things, leptin tells the brain how much fat is in the body, and provides a direct communication link between the brain and fat cells.
Fat cells are the hub of a complex communication system that regulates many metabolic functions, continuously telling the brain how much energy the body has left, signaling muscles when they can burn fat, instructing the liver and other organs when to replenish fat stores, and controlling the flow of energy in and out of cells.
Because fat is so vital to survival, nature has created a complex system of overlapping feedback loops that make it very difficult to override the body's imperative to store energy. People with extra fat cells tend to regain lost weight rapidly.
This biological truth is the basic problem that exists with all of those “Non-Diet”, “Intuitive Eating” theories. A reduced obese person cannot rely on one’s BODY to make or to keep him/her lean. In fact… it is just the OPPOSITE. A reduced obese person’s BODY has the specific biological imperative of refilling EACH fat cell to its basic quota, which will return that person back to his/her former obesity set point.
The DietHobby ARCHIVES contain many other articles which also discuss this issue.
NOTE: This article was bumped up for new viewers. Originally posted on 12/9/2012.
Running DOWN the UP Escalator - Weight Loss & Maintenance - POSTED ON: Sep 30, 2017
This article "hits the nail on the head" in the way it accurately describes my own personal experience, as well as what I’ve witnessed for years while watching the experiences of others.
It contains one of most accurate analogies for Weight-loss and Maintenance that I’ve ever heard.
Some might find it depressing, but here in my 8th year (now starting my 12th year) of maintaining a very large weight-loss, I find it encouraging and positive to hear a medical professional, who is an expert in obesity, speak the unvarnished Truth.
Despite the fact that this Truth is rather unpleasant, and isn’t something we’re ever going to hear from Marketing Interests… (which includes most doctors and nutritionists) …. Facing it, Understanding it, and Accepting it, can be very helpful.
Running Down the Up Escalator
By Dr. Ayra Sharma, M.D. (a Canadian Obesity Specialist)
One of the games I used to play as a kid was to run Down the UP escalator.
To get to the bottom, I had to run faster than the escalator was moving up. If I ran any slower, the escalator would gradually but steadily take me back to the top.
In fact, even to just stay half-way down, I’d have to keep running at about the speed the escalator was moving up. If I stopped running even for a second, I’d be moving up again.
As you may guess, I am using this analogy, to illustrate the challenge of losing weight and keeping it off.
The escalator represents all the complex neuroendocrine responses to weight loss that will always want to take you back to the top – the only way to reach the bottom or to even maintain your place half-way down is to keep running.
Alas, in real life, the weight-loss escalator is even trickier. For one, there is no real bottom – i.e. no matter how fast you run, you will never reach the bottom and be able to simply get off. No matter how far down the escalator you manage to get, you are still running on the escalator and it will keep moving you back up to the top the minute you stop running.
But things get even more depressing, because, the further down the escalator you get, the faster it runs. This means that the further down the escalator you manage to get – the harder you have to keep running to just stay where you are.
Or, in other words, when you start from the top, the escalator is running relatively slowly and you may easily manage to get down the first 5 steps. But as you go down, the escalator picks up speed and so, if you just keep up running with the speed you started at, you may not even manage to hold your place 5 steps down.
And, to get to 10 steps down, you’ll definitely have to speed up – unfortunately, with every additional step you manage to make your way down, the escalator moves up even faster.
By the time you manage to get down 20 steps, the escalator is moving upward so fast that it is all you can do to just try and not be carried back up.
If we could only find a way to slow down the escalator. Or even better, if you could only get to the bottom and get off!
Alas – that is not how our bodies work.
Yes, for some people the escalator moves more slowly than for others – this is why they find it easier to run down and it takes them less effort to maintain their position half-way down. Others have to fight harder to get there and for others, the escalator simply gets too fast, eventually carrying them all the way back up – no matter how hard they try.
Bariatric surgery and obesity medication can help slow down the escalator or rather, prevent it from speeding up quite as fast as you try to run down. This is why you can maintain a lower spot on the escalator with the same effort as before – but go off your meds or reverse the surgery and the escalator speeds up again only to carry you back all the way to the top.
Why is the escalator analogy important to understand?
At this point I want to add a couple of important points to this analogy.
Firstly, it is important to remember that whatever took you to the top of the escalator, if not addressed, will make the descent even harder (if not impossible).
In the simplest case – to use an analogy that a reader sent in – imagine trying to run down the escalator on one leg – it’s going to be so much harder than with two legs. So if arthritis in one knee took you to the top of the elevator in the first place, trying to get back down while your knee is still killing you is going to be so much more difficult than if your knees were OK.
Similarly, if depression or binge eating took you up the escalator, trying to get down that escalator while still depressed or still not in control of your eating is going to to be so much harder than if these problems were resolved.
It may help to think of whatever took you to the top of that escalator as additional baggage that you have to lug along as you try to run down – the heavier the bags, the harder it is going to be.
As readers will realize, those excess bags could be anything – from a genetic predisposition, to medications that you might be on, to lack of sleep, to high stress levels, to intimate saboteurs, to relationship issues, to loneliness, to body image issues, to childhood trauma – the list goes on and on….
This is why it makes a lot of sense to first deal with what took you to the top before beginning your journey down that up-escalator.
Clearly, simply jumping on that escalator without first dealing with the underlying problem will make losing weight and keeping it off so much more difficult - remember, running down the escalator with no baggage is already hard enough
But, even if the underlying problem is dealt with – you will still be trying to run down the up-escalator – that unfortunately will never change – it will only get somewhat easier the less baggage you have to carry.
But why does the escalator move up in the first place and why does the escalator analogy have important implications for how we address obesity treatments?
Why use the escalator analogy at all? Why is the escalator moving up? Why does it get faster as you get further down? And why is there no bottom, where you can simply get off?
Let’s start with the upward moving escalator – most of us are on it to start with as most of us tend to gain weight with age – unfortunately, some people faster than others. Very few of us manage to keep our teenage weights into late adulthood. There are many reasons for this – for one, our metabolism “slows down” as we get older, so do our levels of physical activity. Then there are other drivers of weight gain that tend to accumulate as we get older – stress, lack of sleep, arthritis, medications, to name a few. This means that for most of us, to not be carried higher on that escalator, we already have to take the occasional step down – the faster our personal escalator is moving up, the more effort we will have to put into simply “marking time”.
But that’s the easy part (preventing initial weight gain is always easier than treating obesity). To lose weight, you have to actually start moving down the escalator faster than it is moving up. Depending on how fast your personal escalator is moving up, the more effort this will take. The tricky part comes when the escalator starts speeding up as you make your way down – this is what is often referred to as the “starvation response” – a complex series of metabolic and behavioral responses aimed at preventing further weight loss and promoting weight regain.
In previous posts I have discussed some of these factors – leptin, ghrelin, sympathetic nerve activity, body temperature – the net result is that as you get lower down on the escalator, the fewer calories you need and the greater your hunger and appetite gets. This is why, keeping weight off gets harder and harder rather than easier and easier the more weight you lose. (Many people think that if I can only lose the first 20 lbs, losing the next 20 will be easier – that is almost never true).
Finally, why is there no bottom where I can simply get off? This is because based on the “setpoint theory” (which is actually far more than just a “theory”), your body always wants to get back to its highest weight (or back to the top of the escalator). Unfortunately, from everything we know about weight management, there is no “cure” for obesity – meaning you will always have to continue doing whatever it is you did to lose the weight to keep it off.
As I noted in my previous post, anti-obesity medications or surgery may make keeping weight off somewhat easier, but they do not “cure” obesity – stop your medications or reverse your surgery and your weight comes right back. This appears to be a rule in weight management – when you stop the treatment, the weight comes back (the same goes for “diet and exercise” as a treatment).
Although depressing, I do hope the escalator analogy is helpful in understanding how weight management works, why keeping weight off is so difficult, why very few people can ever hope to reach and maintain their “dream weight”.
Anyone, who promises you anything else is simply not being honest.
No doubt we need more effective treatments for obesity and perhaps one day we may even find a “cure” – till then, we’ve got to work with what we have.
Dr. Sharma’s Obesity Notes – www. drsharma.ca
I’ve experienced a lifetime of dieting in order to avoid, and to end, my obesity. I always thought that: if, and when, I got to normal weight, and managed to stay there for 5 years, by then my body would adjust to being normal size, so that eating only what my body needed to maintain my weight-loss, would become more “natural”, and therefore be less difficult.
This has not been the case.
Here in my 8th year, (now working on my12th) I am still running Down the Up escalator, and the past several years, that escalator HAS been speeding up. Maintaining my body at a normal weight is harder now in my 8th year (now 12th year) than it was the first two years after arriving at my goal weight. … and it was NOT easy then.
Nevertheless, I am committed to continue.
NOTE: DietHobby originally posted this article on 7/7/2013, and I'm bumping it up for new members.
Feb 01, 2018 DietHobby: A Digital Scrapbook. 2000+ Blogs and 500+ Videos in DietHobby reflect my personal experience in weight-loss and maintenance. One-size-doesn't-fit-all, and I address many ways-of-eating whenever they become interesting or applicable to me.
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