Remember you were a kid?
Think about how many sins you got away with regarding your food intake.
A bag of potato chips, a handful of cookies (okay, maybe two), and a few glasses of Coca Cola on top of that.
Maybe you even consumed those foods several times a week.
And what happened?
Absolutely nothing at all...
You didn't gain a pound of weight.
Instead, you looked great, just as you always did. Compare that image to when you got older...
Going on a holiday for a week?
Congratulations, you're now 10 pounds heavier.
The holiday season?
Don't me started.
Sorry, I just made you gain weight...
So why is there such a massive discrepancy between how your body responds to food today compared to when you were young?
Sitting on the couch? Your resting metabolic rate is still active.
Working a desk job? Again, the resting metabolic rate remains active.
Chilling in the evening? Same story...
Men: multiply your weight in pounds by 6.23, add 12.7 times your height in inches, and subtract 6.8 times your age in years. Then add 66 calories to the total.
Women: multiply your body weight in pounds by 4.35, add 4.7 times your height in inches to that outcome, and subtract 4.7 times your age in years. Finally, add 655 to the total.
With that equation, anyone can calculate their expected basal metabolic rate.
Fat loss then becomes harder...
Aging is one reason why your resting metabolic rate slows down--previously being obese or extreme dieting are other important reasons.
You'll burn fewer calories all day every day. You've probably heard about the term "calorie". Calories - at the basic level - are simply measurements of energy.
The term "calorie" is often interchangeably used for the term "kilocalories". I'm using the term "calories" because you're probably acquainted with that term.
So how do calories work?
Food supplies you with calories, and higher calorie content food thus supplies your body with more energy. Meat from grass-fed cows are an example of healthy high-calorie foods--cookies an example of unhealthy high-calorie food.
As a kid, you could thus eat many higher calorie foods without gaining body fat.
Today that's different...
But what's the problem?
Most people use (extreme) diets to lose fat quickly. Dieting, however, does not work for most people.
In fact, dieting has a horrible track record. Exercise is somewhat similar...
That poor track record exists because your body tries extremely hard to hold onto the fat it has once you start eating very little. And even if you do successfully lose weight, your metabolic rate slows down - an evolutionary mechanism to prevent starvation.
The more weight you'll lose, the colder you'll feel, the less you move, and the more hunger you'll experience.
Your libido shuts down, your thinking ability goes down the drain, all until you re-feed yourself. Your body even has a "body fat setpoint" - a weight it is comfortable with and doesn't want to give up.
You'll then burn fewer calories each day, every day.
You may have weighed 200 pounds and burned daily 1,500 calories from your basal metabolic rate. After dieting down to 140 pounds, that basal metabolic rate may be as low as 900 calories per day.
So what's the solution?
If one your daily meals look like this your metabolism
may have slowed down
(I've included four other strategies in the full blog post):
A sun-filled holiday with evenings in candlelight and tons of
healthy food: the perfect way nudge yourself towards
long-term fat loss.
Another quick tip:
Simply making better food choices, preparing your own foods while only buying single ingredients in the supermarket already makes a world of difference for your long-term fat loss prospects.
In other words, processed and pre-packaged foods go out the window...
Giving a simple (oversimplified) example:
Let's say you were burning 1,500 calories a day through your resting metabolic rate (I'm excluding variables such as exercise here). That rate was subsequently brought down to 1,200 calories a day.
Sure, you may be 50 pounds lighter but you're also hungry all the time.
The solution is to slowly add 100 calories a week (mostly from fat or carbohydrates) to increase your caloric intake again.
You should be able to increase your calories with 10-20% again after a strict diet without gaining much fat. If you achieve that feat, you've just built a much stronger foundation to actually retain the fat loss.
You'll be included in the 5% of people who lose fat and keep it off after a year...
If you reverse diet slowly and steadily you'll mostly gain muscle mass. While many reasons for the obesity epidemic exist, poor resting metabolic rates is one important reasons. Other reasons will be treated in following installments of this series on fat loss.
Do read this full blog because many strategies, tips, and nuances are lost in this short summary.
There's no opt-out for hard work...
Last updated: March 25 2019
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*Post can contain affiliate links. Read my affiliate, medical, and privacy disclosure for more information.
Author: Bart Wolbers. Bart finished degrees in Physical Therapy (B), Philosophy (BA and MA), Philosophy of Science and Technology (MSc - Cum Laude), and Clinical Health Science (MSc).
Resting Metabolic Rate Basics:
How Basal Metabolic Rate (BMR) aka Resting Metabolic Rate works:
Improving Resting Metabolic Rate:
The Big(ger) Picture:
Ever felt you've gotten fatter on the same amount of food that did not budge the scale previously?
Yes, that really happens...
Say you were doing well on three meals a day for many years. Sure your body weight fluctuated, but on average your weight stayed similar.
You then successfully lost 40 pounds after a 4-month diet. You were on top of the world...
After a week or two of eating around the holidays, however, you regained most of the weight.
All that hard work down the drain...
To make matters worse: the three meals you were eating every day previously are now making you fatter.
How can that be?
You're back at the same weight as before, and yet, the same quantity of food that kept you at a stable body weight for so long now makes you fat?
That scenario every dieter's nightmare, and yet, it happens.
Just looking at this food makes you fat?
In that case, your basal metabolic rate may be low.
So even if you were mostly bed and couch-ridden because you broke a leg, that resting metabolic rate still exists, and you'd still need to eat to support that basal metabolic rate.
Your cells still need oxygen even if you're doing nothing, and the lining of your gut needs to be rebuilt every few days, your heart needs to pump, and your brain needs energy.
Many bodily processes cannot function without a basal metabolic rate. Let me also give a definition of metabolism to further clarify my position:
Metabolism is thus essential for living.
If your basic metabolic rate is lowered, then you may burn only 80% or 90% of the energy would ordinarily burn while sitting on that couch.
You may think: "big deal"
Well, your resting metabolic rate matters.
In this blog post I'll tell why that basal metabolic rate matters and lay out how to recover your metabolism.
On the bright side: the loss in basal metabolic rate is not permanent. You can thus regain that lost 10% of calories burned each day...
But why worry about being overweight or obesity in the first place?
Well, both matter as well.
There's no such thing as being healthy and obese. Being obese automatically carries health risks.
And many other conditions...
70% of people in the US are overweight.
30-40% of adults were obese in 2014. Even in children and adolescents, obesity rates are located at a whopping 17%.
What's even crazier is that this data was sourced 5 years ago - the problem is even bigger now.
Obesity rates have been increasing in the last decades, with no end in sight. And the problem is still expected to gets worse over the coming decade(s)...
Where does that trend end?
50% of US adults being obese?
On a worldwide scale, In 2010, 1 billion people were overweight while 300 million people are obese . Many other countries are starting to follow the US' example...
Whether you look at aboriginals in Australia, the Hadza or Maasai tribes in Africa, the Tukisenta and Kitvans in Papua New Guinea, or the Tarahumara in Mexico, all of these people have healthy body fat percentages.
The Maasai in Tanzania, Africa: no overweight or obese people to spot.
People in these societies do become obese, however, after transitioning to a Western diet - or better yet: a Western lifestyle. In fact, if you live in a traditional culture and transition to a Western diet you'll have greater risk for obesity than your Western counterparts within a short period of time.[74-77]
Insane but true...
I'll tell you soon...
Back to developed nations:
Even in developed nations, obesity rates were not as high 100 years ago. So changes in the environment (including food intake) must explain why obesity has skyrocketed.
Genetics do not change in a few generations to be able to explain the obesity problem. Genetics can thus not exclusively explain the obesity problem.
Sure, genetics can load the bullet, but it won't pull the trigger - it's the environment that opens fire...
Let's consider in more detail why "resting metabolic rate" or "basal metabolic rate" matters so much...
The best way to visualize that concept is with a savings account. When you've got more savings in the financial domain, you're more resilient against setbacks.
Car broke down?
No problem if you've got a couple of grand of savings. But if you're living from paycheck to paycheck, car problems can cause serious issues...
Smart persons save (some) cash...
With a higher resting metabolic rate, analogously, you're more resilient against setbacks in the health domain. The resting metabolic rate is thus a type of "savings account" for your health, allowing you to burn more calories at rest.
If you burn more calories while doing nothing, overeating on cake or junk food won't set you back (as much). I.e., eating some cheesecake or ice cream will not immediately pack on the pounds.
Sounds great, right?
But the logical follow-up question is: "why do many people have an empty savings account - the metaphor for basal metabolic rate?"
Simple: during starvation, extreme dieting, or if you lose a lot of body fat, your basal metabolic rate can become slower than before. That problem is almost never corrected for in medicine.
So let me tell you about my next steps:
Later sections then explore the concept of basal metabolic rate.
It turns out, "calories in, calories" out is not what many people think it is - and it's specifically the concept of basal metabolic rate that undercuts most people's understanding of calories in, calories out.
I'll look at both the flaws and benefits of that model to understand obesity.
Let's first consider what "calories" are.
A calorie is an energy metric. Although I'm oversimplifying, one calorie denotes the amount of energy required to raise one kilogram of water with one degree Celsius in temperature (1.8 degrees Fahrenheit).
In the same way that the energy of foods can be measured, coal or oil also have a caloric value. Simply put, different compounds in your environment can be measured for their ability to raise the temperature of water.
Of course, I'm considering food in this blog post--not fossil fuels. Foods thus also contain energy, which your body may be able to use.
When considering food, the term "Calorie" is often interchangeably used with the term "kilocalories". I'm going to use the term "calories" for "kilocalories", simply because more people use the term that way.
By stating that so and so food contains "100 calories", I thus mean that the food contains 100 kilo-calories.
So let's look at how this model is applied:
The "calories in" part of the equation signifies the calories from food that you take in. "Calories out" indicates the amount of energy that you burn every day, through your basal metabolic rate, exercise, movement, and the cost to process food.
If the "calories in" part of the equation is greater than the "calories out" part of the equation, you'll gain weight--and if calories in is smaller than calories out, you'll lose weight.
Caveat: I'm agnostic towards whether the "calories in, calories out" model is correct or incorrect - I think the model has upsides as well as downsides.
The upside of the model is that the model allows you to get a great grasp of your daily energy intake. One downside is that estimating your true energy needs is almost never correct.
Additionally, you may also have heard from the "eat less and exercise more" principle. That principle is often associated with the "calories in, calories out model". That "eat less and exercise more" principle is also called the "Gluttony and Sloth" theory of obesity.
Eat less and exercise more, implies at a very basic level that many people are overweight simply because they eat too much and exercise too little.
Well, you can adhere to the "calories in, calories out" model without thereby recommending adherence to the "eat less and exercise more" principle.
The reason for that difference is simple:
Through a changing basal metabolic rate, your daily calorie expenditure can change from 1,500 to 1,000 calories per day over time (without you gaining weight or muscle, or moving more).
"Eat less and exercise more" does no justice the occurrence of slowing or increase basal metabolic rate, and is thus faulty in principle.
The result of not understanding "calories in, calories out?"
So let's further further explore that "calories in, calories out" equation:
The more calorie-rich food you consume, the higher your calorie intake becomes.
So from a calorie perspective, if you eat lots of calorie-rich foods such as pizza and hamburgers, you're more prone to become overweight (and finally obese) than if you're relying on loads of vegetables in your diet.
Only in that specific sense is the "Guttony and Sloth" theory is correct.
Let's break the concept of "calories in" down further:
One gram of carbohydrates supplies you with 4 calories, one gram of fat with 9, and one gram of protein 4 calories. The more protein, carbohydrates, and fat you consume, the higher your daily caloric intake thus becomes.
Don't worry about remembering caloric values.
Taking the bigger picture: vegetables thus contain fewer calories than a steak, simply because vegetables contain very little protein, fat, and carbohydrates.
No controversy there...
Everybody knows you'll burn more calories if you run a marathon compared to if you're sitting on the couch all day.
The "calories out" part of the equation can change in many more ways than you may think, such eating more protein and increases in small movement even while you're sitting on the couch.[190-193] Fidgeting or moving your legs more can already influence the "calories out" part of the equation.
Of course, your basal metabolic rate also influences the calories out part...
But if calories out can change on the basis of many variables, then the "Gluttony and Sloth" theory cannot possibly be correct - and "eat less, exercise more" neither.
"Gluttony and Sloth" interprets human beings as machines:
energy is fuel, and excess energy spills over into fat tissues.
Quick remark: "calories in, calories out" is not accepted by all modern scientists for explaining obesity:
According to the carbohydrate-insulin model of obesity, carbohydrates specifically make you fat.
While I'm oversimplifying, the gist of the argument is that consuming carbohydrates (through wheat, rice, or coca cola) raises insulin levels. Proponents of this model then claim that insulin is necessary for energy to be stored as body fat, and that insulin-spiking foods therefore make you fat.
Lowering carbohydrate intake purportedly automatically leads to fat loss, because there's no insulin to shutter energy into fat cells. In other words, replace all carbohydrates by healthy fats, and you'll lose weight automatically.
Although the insulin model of obesity is still heavily being defended today, I'm not using that model in this blog post.[4-6] To me the "carbohydrate-insulin" model is mostly incorrect, as diets that are high in fat or high in carbohydrates have roughly the same outcome when daily caloric intake is kept equal.
The bread and sweets are displayed here are inherently
fattening according to the "carbohydrate-insulin model of obesity".
Basic metabolic rate generally consists of 70% of the daily calories that you expend. A slowdown of that metabolic rate thus matters.
If your metabolic rate slows down with 10%, you'd burn about 6.67% fewer calories every single day. With a 20% slowdown you'll burn 13.33% fewer daily calories.
Also, notice that a high resting metabolic rate is the easiest way to burn calories: you don't have to exercise to burn that energy off.
During a diet you can have "metabolic slowdown", in which you'll end up with a lower resting basal metabolic rate. In that case, you've lost many pounds, but you may now have a basal metabolic rate that's 10% lower than before.
Say you weigh 110 kilograms (242 pounds), are 30 years old, 6 foot tall, and male. With the data points of 1) your weight; 2) age; 3) length; and 4) gender it's possible to calculate your estimated basal metabolic rate.
(Note the word "estimated")
To calculate your basal metabolic rate:
The outcome you get should still be multiplied to correct for your daily activity level:
That multiplier is the same for both genders...
Again, you can only use the Harris-Benedict Formula as an approximation of your daily caloric expenditure. Hopefully you now know why the formula is not fully valid your metabolism can slow down or speed up, making the formula imprecise.
Sorry. Couldn't resist posting this...
So let's return to the example I gave:
In that case you'll have to calculate the basal metabolic rate as a 242 pound 6 foot tall 30-year-old male. The outcome of that formula is:
(242*6.23) + (12.7 * 72) - (30 *6.8) + 66 = (1,507) + (914) - 204 + 66 = 2,283 = ~2,300 calories burned through your resting metabolism per day.
After dieting down to 90 kilograms (200 pounds) your resting metabolic rate becomes:
(200*6.23) + (12.7 * 72) - (31 *6.8) + 66 = (1246) + (914) - (204) + 66 = 2,022 calories.
You're now burning almost 300 calories less each day, which equals 4 eggs per day, or 28 eggs per week. Alternatively, you could eat 8 medium pacific oysters to consume those 300 calories, which equals 56 medium oysters per week...
And what if you lost 80 pounds? In that case you'd be able to eat even less.
And these numbers would have to be multiplied with 1.5 if you're engaged in physical labor with light exercise, you'd still expend fewer calories on a daily basis.
In a sense that metabolic slowdown is logical right? You're smaller, carry less weight, and thus burn fewer calories.
The problem, however, is that some people have very low basal metabolic diets after years of dieting. Another problem is that they're still fat - more on that later...
One reason for that decline is that teenagers have more "brown" and "beige" fat - fat is metabolically active.[69; 230] Women also have higher levels of brown fat than men.
By exposing yourself habitually to cold, you're able to build up those brown and beige fat deposits. Muscle mass losses are another reason why older people have lower metabolic rates.
Bottom line: your metabolism does slow down with aging, which partially occurs due to having less brown and beige fat and muscle mass.
Fat-free mass basically included any tissue in your body that is not fat. During dieting, you'll generally lose fat-free mass.[194-196]
Contrary to popular belief, it you can gain fat-free mass during your diet, doing so requires lots of resistance exercise.[197-200] In many cases, however, fat-free mass declines during dieting, thereby lowering your basal metabolic rate.
(Your body fat percentage is the total amount of fat in your body, divided by your weight.)
If you decide to diet down, you'll thus want to lose mostly body fat while maximizing the amount of fat-free mass you retain.
That's it: you now understand the complexity of the calories in, calories out model.
How you'll look after extreme dieting,
and losing most of your fat-free mass.
I've laid the groundwork...
In the following section, you'll learn about metabolic slowdown after near starvation (extreme dieting). The fourth section described metabolic slowdowns after reversing obesity.
In this section, I'll explore what happens if you deprive your body of calories for longer periods of time. In the most extreme case, you'll move your body towards (semi)-starvation because you simply need energy to function.
Before you decide on cutting down calories dramatically though, let me tell you a secret:
Dieting has a horrific track record.
Let me explain.
Even if you manage to lose 20 pounds in 4 months, you've still not lost these pounds permanently.
Short-term success means nothing.
What's even crazier is that dieting - especially losing weight and then gaining weight again - can set you up for more obesity in the long-run.
Now, don't get me wrong, overeating does cause you to gain weight over time - in the sense that you're consuming more calories than you expend. That excess of calories is stored as body fat.
(You'll later learn that overeating alone does not explain the obesity epidemic...)
These factors include:
While you might consider some of these strategies burdensome, you'll ave to implement a significant few of them to be successful in long-term weight loss.
A lowered resting metabolic rate is the main type of caloric output that changes after a diet: sure you're burning fewer calories by moving less, but metabolic slowdowns explained by the basal metabolic rate pack the biggest punch.
One instance in which metabolic slowdown occurs is lowering your body fat percentage to extreme levels, which elite athletes often do.[31-35] Such low body fat levels essentially mimic starvation.
As a result, you'll:[36; 37; 43-51]
If you experience (extreme) hunger, depression, a loss of your period,
or poor sleep, a very low body fat percentage is not healthy for you
All of these consequences occur because your body senses it's underfed and compensates by turning down many processes in your body.
Even your thinking ability, well-being, and libido will be negatively affected under extreme caloric restriction.
Yes, your body literally shuts down many processes because it thinks it's starving...
But why is there a metabolic slowdown in the first place?
If you do engage in caloric restriction you'll almost automatically move less than you'd otherwise do.[114-116] That decrease in movement occurs on an almost subconscious level, and demonstrates how hard it is to "trick" the body into burning more calories.
So if you use a diet that's really low in calories you can reasonably expect to fidget less, take fewer small walks, and even move your feet less frequently when seated.
In the mitochondria, the energy-producing factories of your cells, energy is lost as heat as a byproduct of energy production if you're on a higher calorie diet--a process which is now reversed.
Even your body temperature thus becomes lower under caloric restriction.[117-121]
A bag of cookies or tub of ice cream can be gone faster than the speed of light - and you'll still be hungry...
You'll in fact experience that hunger until your fat-free mass is recovered. But by the time you've recovered your fat-free mass by overeating, you've also added body fat tissue beyond your previous level if you start consuming many calories after a diet.
That's bad news...
In that case, you're worse off than before because you've now gained a few pounds. Another problem is that your basal metabolic rate is now down compared to your pre-weight loss levels, making you gain pounds much more quickly in the future.
And yet, hunger almost literally overtakes you during extreme diets and thus sabotages the results you've worked so hard for. The consequence of that hunger is that many people overeat - even binge eat.
Simple: by depriving yourself of food for weeks if not months your body ingests all the calories it can. And after gaining these new pounds of fat, your body determines that level as the "new normal" - even though you're heavier than before now.
Sorry for the bleak message...
Fat overshooting is dangerous precisely because an excess of fat is necessarily gained in order for your body to fully restore fat-free mass. The principle of fat overshooting also explains why so many people re-gain their pounds after a period of "successful dieting".
In other words, the hugner only stops after extreme dieting after you've replenished all your fat free mass (and extra body fat).
Keep in mind that metabolic slowdown or damage is not just restricted to one population group. The principle also applies if you've got an eating disorder, for example, which can cause extreme leanness - and backfire in the basal metabolic rate department.
I often introduce evolutionary arguments in my blog posts. I think there's convincing evidence showing an evolutionary perspective yields new insight into health that would be missed by regular medical studies (for nerds: e.g. randomized controlled trials).
In this case, metabolic adaptations occur as a defense mechanism against future starvation. if your ancestors had very little food 2 million years ago, their bodies increased its ability to store body fat once food stores became plenty again.
That increase in body fat stores boosted your chances for survival.
Remember that during starvation, or living at extremely low body fat percentages (which athletes sometimes do), your body becomes literally more efficient with any calorie that you ingest. Every single calorie you consume generates less heat as a byproduct of energy production, for example.
You'll literally end up with lower body temperatures.
When less heat is generated, your body can allocate more energy to your muscles to hunt. Any process that does not directly help your survival gets shut down, such as libido and spontaneous movement.
Based on the principle of natural section it can be concluded that the mechanism of metabolic adaptations confers a survival advantage--if it did not, ancestors with a strong propensity for metabolic adaptations (as opposed to weak or non-existent) would not have procreated, and you would not be here today.
In plain English: if the possibility of metabolic adaptations did not confer a survival advantage to your ancestors you'd probably not have that ability either...
Survival experts: lowering your body temperature to survive cold weather
(As humans, you cannot get such good insulation, unfortunately...)
Epigenetics studies the expression of certain genes.
If you were pregnant and survived the "Hunger Winter" on very little calories in the Netherlands during the German occupation in World War 2, for example, your children have metabolic adaptations that predispose them to greater body fat gains. The obesity-associated health risks would also be higher for your kids.[78; 79]
(I live in the Netherlands)
The weight of your mother may also influences your future susceptibility to weight gain.[80; 81] Evidence for metabolic adaptations to (near) starvation can thus be found everywhere...
That experiment was carried out by Ancel Keys, the same physician who later develop the (faulty) theory that saturated fat causes heart disease.
In the Minnesota Starvation Experiment, near starvation conditions were simulated on 36 participants.
The year was 1944.
The experiment lasted one full year.
After a 12 week control period where participants ingested a normal quantity of calories, they were placed on a 24-week starvation (mimicking) period.
Participants were prescribed 1,560 calories per day and physical labor was mandatory as well.
During the starvation period, their food intake simulated that of the concentration camps in Europe. Participants lost 25% of their body weight on average - some even had to quit.
After some time participants began to fantasize about food all day long, and used several strategies to make their food appear more voluminous. Controlling oneself became exponentially harder - many participants sank into depressions.
Even self-mutilation occurred: one participant chopped off three fingers with an ax, but due to an impaired thinking ability could no longer remember whether he had done so intentionally...
Heart rate, sex drive, and strength all declined.
Men had been very healthy no longer were. Still think extreme caloric restriction is the way to go for weight loss?
Fortunately, a 12-week re-feed period followed after the controlled semi-starvation. Participant's response to higher caloric intakes was then investigated.
Some participants had to slowly increase their caloric intake again as part of the controlled experiment--others started to binge eat, expressing nearly insatiable hunger. On average, participants needed about 4,000 calories per day to recover.
When left free, participants ate over 10,000 calories in one day.
The recovery period took years in some cases...
In other words, the loss of muscle mass during starvation cannot fully explain the extent to which your metabolism slows down. Fat-free mass does therefore not exclusively predict resting metabolic rate.
The moral of this section? Think twice about fixing your issues with "eat less and exercise more" - athletes who do so, or people who almost starve due to circumstances need lots of time to recover...
In the end, biology always wins out and you will binge eat on foods to compensate...
Give yourself some credit as well.
Just because you're investing in your health
by reading this blog post!
In the next section, we'll look at metabolic adaptation in people who previously were obese. I turns out obesity and starvation have commonalities...
You already know that once you lose lots of weight, it becomes exponentially harder to have a normal weight again. So if you've ever weighted 300 or 400 pounds, your body "remembers" that weight as "normal".[59; 212]
Building a lean 180 pounds physique will thus be harder if you've ever weighed 400 pounds compared to having had a maximum 200-pound weight in your lifetime - all other variables being equal.
And that's problematic:
You probably know yo-yo dieting.
Yo-yo dieters usually lose a ton of body fat, but then re-gain that bodyfat over time (plus more).
The term "yo-yo dieting" does not just refer to a person who loses and regains the weight once--the yo-yo principle is repeated over the course of many years.
The end result is that they're worse off than before because of metabolic adaptations. Every time you're engaging in caloric restriction, your basal metabolic rate slows down. If you regain the weight quickly, you've got a slower metabolic rate and more body fat.
Each time the cycle repeats the problems get worse and worse...
If you've previously been obese it can thus be difficult to retain the results you've worked so hard for. As a formerly obese person, any calorie you ingest is thus much more prone to be stored as body fat.
Let's explain that finding:
(Contradicting studies do exist.[e.g. 209])
Do you know the "Biggest Loser" TV show? On that TV show participants are put on a diet that contains very few calories. That low caloric diet is combined with several hours of exercise per day.
Participants of the "Biggest Loser"ended up with basal metabolic rates that was 700 calories lower than before losing the weight.
You may think: "they just have to recover from the impact of the extreme dieting"
Not at all...
The damage was still present 6 years after the participants finished with the TV program. 700 calories is a lot: 1 big steak contains 670 calories...
Bright side again: with the correct strategies metabolic adaptations are probably reversible. Metabolic damage is thus not permanent.
I do nonetheless feel for people who have lost lots of weight, as they've been guided into a hole due to improper guidance...
You'll help my metabolism back on track after I lose weight?
But what about if you're healthy and overeat?
Well, some of the excess calories are thus burned off as heat. For that reason, if you just return to a normal eating style after the holidays you'll often lose all the weight again over time.
A hormone called "leptin" is partially responsible for that effect.
(I'll treat leptin in full detail in another blog post).
The more body fat you have, the higher your leptin levels generally are. Body fat exerts leptin into the rest of your body. Leptin signals energy availability. Your brain senses that leptin (if you're healthy), and downregulates hunger once leptin levels are high.[61-63]
You may thus automatically eat less food after the holidays due to overfeeding the previous days. Combined with an increased basal metabolic rate, the body fat you accumulated after the holidays is thus slowly burned off over time.
In overweight and obese people, however, leptin signaling is off:
Although I'm oversimplifying, you'll have high leptin levels but the brain will not down-regulate hunger levels.[64; 65]
The reason for that mismatch is your brain has an inability to sense leptin. That condition is called "leptin resistance". The "hypothalamus" brain area is specifically affected by the leptin.[94-98]
As a response to dieting your leptin hormone levels can also change for the negative.[43; 107-109] Due to low body fat, low leptin levels tell your brain that energy is scarce and that you need to find food.
In both obesity and weight loss leptin levels can thus be off.
When your brain correctly senses leptin levels, however, that will help you keep the weight off.[214; 215] I'll return to leptin in the following section. For now, just ask yourself "why is leptin signaling off in the first place?"
I'll let you ponder about that...
So let's return to the previous subject:
To become obese, you'll not only need to eat more than you expend, but you need to increase calorie intake to adjust for the increase in caloric expenditure of an enhanced metabolic rate.
Remember the earlier case in which someone weighed 242 pounds with a basal metabolic rate of 2,300 calories? If they were to increase their weight to 270 pounds, their basal metabolic rate may increase to 2,500 calories.
In that case even more calories are needed to promote future weight gain (or to maintain that body weight). Normally, a negative feedback loop thus prevents you from achieving a 300 or 400 pound body weight.
(Assuming that their other calorie expenditures such as exercise stay the same).
Returning to the Holidays example: if you gain a few pounds around Christmas, your resting metabolic rate may increase with 100 calories per day, allowing you to lose excess body fat over the next couple of weeks.
If you consume just a few percent of calories more than you expend each year, and continue that pattern over long periods time, you'll end up morbidly obese.
As humans have not been underweight or obese for millions of years, body weight is thus tightly regulated under normal circumstances.
I've now ended up with a paradox: over-eating causes you to be obese, but eating less causes metabolic slowdown. The solution to that paradox is found in the next sections.
On another note:
One counterargument against increasing basal metabolic rate is that it's sometimes associated with an increase in mortality. That greater mortality can (partially) be explained because most people with higher metabolic rates are also obese in modern society. Higher metabolic rates are thus not problematic in isolation...
Just think about that...
How many times have you heard a personal trainer say: "it's great you've lost those 50 pounds, but now the real struggle begins"
The answer is probably never, and that's a shame...
Metabolic slowdowns should thus be avoided for long-term fat loss. I'll help you with that problem...
The subsequent two sections explore: 1) strategies to increase your basal metabolic rate; 2) how to increase your caloric diet after a diet without gaining lots of fat (to build your basal metabolic rate).
Yes, you've read that right:
Seven strategies to actually support your resting metabolic rate, no matter where you are in life - overweight, underweight, obese, or at a normal body weight.
This variable is enormously important, and yet, hardly emphasized in most health advice today.
Observe that the recommendation to "eat less and exercise more" does not imply in any way that sleep is important--"eat less and exercise more" implies that burning more calories is sufficient for fat loss.
In other words, "eat less and exercise more" hints that your daily burned calories fully explains weight loss, while your other behaviors in life don't matter.
I wholeheartedly disagree with "eat less and exercise more".
For the following reason:
That 24-hour rhythm is called the "circadian rhythm".
Let's explore precisely how light affects sleep quality.
I'll first consider the different types of light that can be found on the earth:
As you can see, 1) ultraviolet; 2) visible and 3) infrared exist:
All three types of light influence the biology of your body, and thus health.
So what does that circadian rhythm have to do with fat loss?
Let's find out:
Observe that blue and green light can be found in the visible light spectrum.
Sunlight was the source of that blue and green light for millions of years (but also yields ultraviolet, infrared, and the other colors of the light spectrum.)
That light influences your circadian rhythm because it tells your body it's daytime. How well you maintain your circadian rhythm is closely tied to your your sleep quality.
While that basal metabolic rate is slightly increased after a night of sleep deprivation, that increase mainly occurs because of higher stress hormone levels.[130-138] Circulating stress hormones such as adrenaline or cortisol thus temporarily increase basal metabolic rate.
And although some conflicting evidence can be found, poor sleep quality lowers basal metabolic rate in the long run - a huge problem.
Let's explore why I start my list of strategies with sleep:
Losing a night of sleep due to partying, or sleeping poorly for two month straight because you've just become a parent?
Losing sleep for years or decades, because you're snoring, drinking alcohol, or partying until 4 AM?
What's even scarier is that a colossal 45% of Americans experience low sleep quality every single night.
Could poor sleep be a massive problem that drives the obesity epidemic?
So independent of the food you eat, poor sleep can lower your basal metabolic rate.
Thought you'd never ask:
And I'm not done yet:
Lesson: Steer clear from poor sleep...
Please keep in mind that fixing your circadian rhythm is not a short-term strategy. You'll have to stick to a good circadian rhythm for the rest of your life for the advantage to persist.
No quick fixes...
As soon as you'll transition back to staying up until 2 AM, sleeping in on weekend, and then going to bed early on Monday night, you'll set yourself up for more weight (read: fat) gain again.
And remember the hunger-gatherer societies I talked about earlier? These societies don't have huge disruptions in their circadian rhythm, even though they may stay up late once in a while.
Diet is thus not the only explanatory reason why hunter-gatherer societies do better.
You can stay up until 1 AM for once in a while as long as you tightly regulate the light cycle. Thus make sure to wear your blue blocking glasses if it's New Year's Eve, so that the circadian rhythm in your head keeps following the pattern of the sun.
No need for a Spartan lifestyle...
Too many concessions to your sleep quality, however, will certainly have negative consequences.
If every one of your nights is like New Year's Eve, your health and fat loss will suffer...
What's interesting is that the supreme importance of the circadian rhythm is hardly emphasized in fat loss books.
Recent books such as Fat Loss Forever: How to Lose Fat and KEEP it Off by Layne Norton and Peter Baker only mention melatonin supplementation as an afterthought, after discussing the importance of diet for 4/5th of the book.
Circadian rhythms themselves are not treated in great detail, unfortunately. Instead, melatonin supplements are suggested as a proper solution, rather than fixing the light you're expose yourself to.
(In most cases, using melatonin supplements is analogous to injecting steroids because you've got poor hormone levels for athletic performance - both do not fix the underlying problem.)
A great book on food palatability by Stephan Guyenet, The Hungry Brain: Outsmarting the Instincts That Make Us Overeat, does dedicate a chapter to circadian rhythms but fat loss is not centered around that topic--overconsumption of hyperpalatable foods takes main stage.
One of the only books that does justice to the relationship between fat loss and circadian rhythms is Ari Whitten's Forever Fat Loss: Escape the Low Calorie and Low Carb Diet Traps and Achieve Effortless and Permanent Fat Loss by Working with Your Biology Instead of Against It.
Want to know more about the circadian rhythm? I'll go into more detail in my Health Foundation Program, which brings your health, well-being, and energy levels to the next level (and beyond).
You'd better have blackout curtains if you're trying to sleep here
The thyroid organ is located at the front of your neck, and responsible for your daily energy production. If you've got thyroid issues, your basal metabolic rate will be lower.
On a very low-calorie diet, an important thyroid hormone called "T3" decreases. T3 is the active thyroid hormone that can be taken up by your cells and is central to your body's energy production. Your liver converts lots of T4 (the inactive form of thyroid hormone in your body) into T3.
The higher you can keep your thyroid levels (while dieting), the more weight you'll lose.
In general, thyroid hormone levels are higher on a diet that contains more carbohydrates. Thyroid levels often tank on a lower carbohydrate diet--although a counterargument is that this decline is mostly observed on low-calorie low carbohydrate diets.
Many people who follow a low carbohydrate diet automatically start eating (much) less, which then sets them up for thyroid issues down the road. I'm thus not convinced that a low carbohydrate diets are detrimental to thyroid health by themselves.
Eating sufficient calories should thus improve thyroid health all by itself, whether you're on a Paleo or a higher carbohydrate diet.
For optimal thyroid function, I therefore do recommend including carbohydrates at least seasonally if you don't have any food intolerance.
Even if you're following a carnivore diet for countering food intolerances, I recommend testing safer carbohydrate sources such as ripe fruit or honey during the summertime (which should be least problematic).
(Yes, I know you're no longer following a carnivore diet if you're adding in carbohydrates into the mix...)
(Nerd section: While the topic of thyroid health is complex, I do recommend lab testing your thyroid levels if you suspect "hypothyroidism" or another thyroid problem.
Hypothyroid problems are most common, and (proper) lab testing is the only way to found out whether you've got an issue. Depression or lower well-being, fatigue, insomnia, brain fog, weakness, cold intolerance, weight gain, inflammation, and poor skin quality are all symptoms of hypothyroidism. If you've followed diets of extreme caloric restriction you're more at risk for hypothyroidism.
Lab testing your thyroid levels should not only include the commonly used TSH test, but also at least T4 and T3 (in both bound and free form), and thyroid antibodies. To place the outcome of the thyroid lab test in context, you'd also need to know your cortisol levels throughout the day, DHEA, vitamin D (as a proxy for the amount of sunlight you get), etcetera.
While the topic of thyroid testing lies beyond the scope of my argument in this blog post, I do recommend consulting your physician if you suspect an issue.)
Analogy: energy is not only in physics of massive importance, but also
in you as a biological organism. Your thyroid is central to your body's energy production
I know, I know...
Easier said than done.
I do hope by now you're becoming convinced that preventing being overweight or obese is the best thing you can do for your health.
Being obese is a like becoming an alcohol addict: if you've been addicted to alcohol, you may have a disadvantage in dealing with alcohol for the rest of your life.
(You may also not have a disadvantage, but it's best not to test your luck)
In the area of dieting, being overweight or obese may confer a disadvantage for keeping the weight off.
Again, if lose a lot of weight you can end up with a lower resting metabolic rate. Fortunately, the analogy is incorrect in the sense that the lower resting metabolic rate has to stay permanently low if you have been obese.
The underlying problem can thus be fixed in case of obesity...
Let's explore that statement:
Remember: if you become obese your basal metabolic rate increases. After losing weight, however, you'll end up with a lower basal metabolic rate than people who didn't become overweight - all other variables being equal.
That the lower basal metabolic rate cannot be just explained by lower levels of fat-free mass. Phrased differently, if you were formerly obese, your resting metabolic rate may be lower despite fat-free mass recovery.[163; 171]
Lower resting metabolic rates are also a risk factor in weight regain.[169; 170]
Of course, the grass is not only greener on the other side. With higher resting metabolic rates, you do have stronger hunger sensations - but you can also eat more.[167; 168]
The best way of preventing basal metabolic rate problems is thus to avoid getting fat in the first place. The second best way it to keep reading this post to help solve the problem.
The effect of minerals on your health is deceptively simple: if you're either deficient in minerals or have an overload, your basal metabolic rate takes a hit.
Let's consider a couple of minerals, starting with zinc:
Not only is zinc necessary for thyroid functioning, but the mineral also directly boosts your basal metabolic rate.[174-176] Unfortunately, more research is needed to confirm the relationship between adequate zinc levels and basal metabolic rate.
Iron deficiency, secondly, can also lower thyroid function and thereby lower basal metabolic rate.[177-181] The same is true for magnesium deficiency.[182-185]
It's easy to see, moreover, why mineral status can be a big problem for people on the Standard American Diet: about 80% of Americans have sub-optimal magnesium levels. For zinc, that number approximates 60%. Both iron an deficiency or overload are also more common than you'd assume.
The Standard American Diet is hugely problematic because it doesn't contain many foods that have highly absorbable levels of minerals. Instead, vegetable oils, refined grains, and processed food make up the bulk of this devastating diet - eventually trickling down to resting metabolic rate problems.
Keep in mind that many other minerals matter as well, such as iodine (which is important for thyroid function), selenium, and calcium.
The widespread mineral deficiencies due to following a poor diet will certainly lower your basal metabolic rate.
Oysters: they keep coming back on this blog
As a side note, the "calories in, calories out" model is often attacked with a "strawman argument" regarding minerals.
(In a strawman argument, you incorrectly display the claim of your opponent, and then "successfully" attack that incorrectly attributed claim.)
The strawman argument entails that the quality of food doesn't matter - only the caloric input of foods do. This section on minerals demonstrates should demonstrate that this is not necessarily the case.
The influence of minerals on resting metabolic rate can still be explained from a "calories in, calories out" perspective: mineral deficiencies lower your metabolic rate and thus set you up for weight gain.
Diets such as "If It Fits Your Macros" (IIFYM) - where exclusively caloric intake and proteins, fats, and carbohydrates count - are thus very shortsighted, simply because the role of the circadian rhythm and minerals are not included into the equation.
The same is true for "eat less, exercise more".
Although no cause and effect relationship has been established (yet), vitamin D levels do, for example, predict your resting metabolic rate.[234; 235]
Another reason to get your sunlight...
And with higher quality evidence, I suspect many vitamin and mineral deficiencies will be proven to have an effect on basal metabolic rate.
You may know Bisphenol A (BPA), a material that's often contained in plastics. BPA is an endocrine disruptor. In plain English, that means your hormone functioning is negatively affected if BPA enters your body.
BPA may affect hormones such as "testosterone" and your thyroid hormones, although evidence is thin (right now).[82; 83] Looking at BPA studies in more susceptible populations - such as children, negative effects can reasonably be expected for adults as well.
So let's explore these hormones:
Testosterone is a sex hormone that can be found in much higher levels in males and stimulates your basal metabolic rate.[84; 85] Remember that thyroid hormone is not only responsible for overall energy production in your body, but also increases basal metabolic rate.[86; 87]
Endocrine disruptors such as BPA are thus double trouble. Testosterone may even directly influence how much body fat you carry.
Many other endocrine disruptors exist, such as phthalates that can be found in perfumes, flame retardants in furniture, and so forth. All of these substances affect hormonal function--the problem is that studies have not yet investigated the effects of these substances on basal metabolic rate.
How does endocrine disruption work?
Well, one theory is that if you do consume excess calories, these calories will be more prone to be stored as body fat instead of muscle tissue. Remember that muscle tissue is metabolically active, while the same is not true for (white) body fat.
(But because you can theoretically also gain fat while losing muscle on a caloric deficit, endocrine disruptor avoidance is always recommended.)
Over time, endocrine disruptions may thus have a negative effect on your body composition. Body composition is the relationship between the amount of muscle mass and body fat you've got.
When you carry less muscle mass, you'll also have a lower basal metabolic rate, simply because muscle mass massively increases your fat-free mass.
All plastic may be problematic, but BPA is especially so.
The endocrine disruptor problem is worse than you think though:
Overall, thousands of toxins probably have an effect on either your body composition or your basal metabolic rate...
Removing toxins from your life is thus always a smart choice.
Movement is extremely important, not for your basal metabolic rate but for caloric expenditure outside that domain.
I even consider movement more important than exercise. Unfortunately, I cannot give away all my information for free, so I'd recommend you check out my Health Foundations Program which includes the topic of movement, to bring your health and energy to the next level (and beyond).
Exercise alone has a very poor track record of combating obesity.[91-94] You thus need to implement many more strategies to overcome the problem than just going to the gym.
The issue with exercise is that it may increase hunger if you're overweight, which makes you consume more calories to compensate for the increase in energy expenditure. On the contrary, exercise may also help to keep the pounds off - especially if you adhere to it.[99; 100]
Another reason to opt for exercise is due to the greater fat-free mass levels you'll gain.[103-106] Due to fat-free mass increases, exercise thus indirectly improving your basal metabolic rate, which helps you keep the pounds off.
Movement: as important as exercise,
if not more so.
Surprise, surprise: getting exposed to cold independently builds your resting metabolic rate.[220-226]
Well, you've got several types of fat in your body: white, beige, and brown. Beige and brown fat are "metabolically active", meaning that it takes energy to support these structures in your body. White fat, on the contrary, does not seem to have the metabolic activity of its beige and brown counterparts.
The result of that distinction is that beige and brown fat can actually burn white fat, and thereby increase your daily caloric expenditure. Brown and beige fat actually contain lots of mitochondria, which helps them burn the white body fat.
Building your brown and beige fat through cold showers or ice baths can thus indirectly increase basal metabolic rate. Read my guide on that topic to get started, but be careful with cold if you're in poor general health.
Besides using energy, brown and beige fat also increase insulin sensitivity - a big plus. If you do consume carbohydrates, they will be more prone to be taken up in your muscles for energy creation, instead of being used to create body fat.
Seven strategies to build your basal metabolic rate.
No empirical evidence can yet be found for these claims (yet), however. For that reason, I have not included the strategy of toxin reduction as a means to boost basal metabolic rate.
Nevertheless, because toxins such as heavy metals or pesticides undermine the health of so many systems in the human body, an basal metabolic rate lowering effect can reasonably be expected.
While my claims are speculative, they are not irrational...
As other toxins such as BPA have already been demonstrated to have indirect effects on fat loss, so I'm recommending you to steer clear from as many toxins as possible - especially if you're in poor health.
And there's more:
Almost everything you do can thus build your basal metabolic rate or break it down over time...
I suspect many other variables to have an effect on building your basal metabolic rate over time, such as your overall stress levels or your social life. Hopefully scientists will research these domains in more detail in the coming decade(s).
That's it... 7 strategies for long-term fat loss. In the next section I'll explore how to make your dieting efforts sustainable in the long-run.
In this section I've got two goals:
Firstly, I'll mainly explore the concepts of "reverse dieting". Reverse dieting means increasing caloric intake to boost your basal metabolic rate. Reverse diets are often used after an intense weight loss period.
Secondly, I'll also explore the concept of a "body fat setpoint". The body fat set point is an equilibrium at which your body feels comfortable holding fat.
A body fat set point at a fat percentage of 20% thus entails that your body will defend that equilibrium, preventing fat gain or loss from that 20%. Depending on your circumstances, that set point can be good or bad.
First of all, even though it's not fully known what causes metabolic adaptations during obesity and subsequent fat loss (i.e., the metabolic slowdown), you can avoid strategies proven to do damage.
Hence: yo-yo dieting and quick weight loss solutions are thrown out the window.
Slow weight loss generally gives you the best results because you'll retain most of your muscle mass.[122; 123]
An argument for quicker weight loss can nonetheless be made in case you're really stressed out by dieting. In that instance, make sure to lose the weight quickly and double down on your efforts to maintain that weight loss afterward.
For the long-term solutions, nutritional habits always enter the picture. You'll thus want to develop sustainable eating habits that are sustainable for years. Food quality matters enormously.
One swallow does not make a summer:
Habits are king.
If the answer is "no", then the diet is unsustainable.
Assume you're going to lose weight by only eating rice and beans - for every one of your three daily meals. You'll then ask: "can I keep eating that way for a couple of years?"
The answer is a resounding "no".
Not only will you get sick and tired of eating beans and rice every day, but you'll also severely limit your social life and nutritional profile.
On a social level, it becomes almost impossible to go out with friends because you might end up at a steak or sushi restaurant. That diet is also horrendous because you'll miss out on important nutrients such as vitamin K2, B12, minerals such as zinc, and healthy fatty acids.
A fruit and vegetable juice diet?
Unsustainable in 1 year time, let alone 5 years.
Back to the drawing board to devise a long-term plan.
Diets should additionally support your basal metabolic rate in the long run - living off very few food types or calories rarely achieves that goal. I say rarely because thousands of people live on a carnivore diet nowadays, having done so successfully for years.
Reverse dieting slowly is the key to preventing body fat re-gain. I cannot emphasize the point of slowly increasing calories enough...
So let's say you've lost 60 pounds. In that case, you can slowly add 100 calories of high-quality foods every week until you're somewhat closer to your previous caloric intake.
If you stay at the very low caloric intake that helped you lose the weight, you'll feel very much off.
If you used lots of exercise during to lose your weight, you can also slowly decrease the amount of exercise you do instead of adding in more calories.
Removing part of your (intense) exercise routine combined with the addition of calories frequently leads to more fat gains. That scenario simulates why people re-gain lots of weight after a diet: they make one mistake, think "d*** it", eat tons of food again and gain weight faster than the speed of light.
You're thus actively trying to prevent yourself from rebounding, as you'll recall that high fat percentage levels and obesity are causing lots of health problems.
Again: slower is better in this case.
Foods that have an extremely high "palatability" - i.e., are extremely rewarding - will make you much more prone to over-consume. Highly palatable foods often combine fatty acid with carbohydrates and different kinds of (artificial) flavors.
Examples are fast food or candy that you can buy in the supermarket - it's very hard for most people to eat just a few of these pieces.
Very rarely can people consume one donut...
That highly palatable food is additionally low in vitamins and minerals--and I've mentioned before that these micronutrients may be a very important prerequisite for high basal metabolic rate.
That's double trouble...
Then there's another question: what diet should you follow?
Paleo, carnivore, high-carb low-fat, keto, the Bulletproof diet, or something else?
If a carnivore diet prevents you from over-consuming on food, that's great. If a low carb diet with lots of seafood, meat, and vegetables does the trick, that's amazing too. If you do better on a higher carbohydrate diet with lots of fruit, more power to you.
Pick whatever habit works to keep the weight off while you're eating mostly whole foods at the same time.
It's thus essential to develop habits that you can maintain for years (not 8 or 16 weeks) in which you will not chronically over-consume food.
A quick detour:
The dopamine system in your brain - which is centrally occupied with reward and motivation - is tied to how your brain values food. Highly palatable foods are much more rewarding and drive you to eat an excess of poorly nutritional calories.
The more different foods you combine into a meal or day, the more prone you're to overeat as well. So if you've had two Big Macs you may not be able to eat the third one, but consuming a dessert with the same number of calories will still be possible.
That's easier said than done for most people.
The problem is that the brain may be sensitized by that food, which leads to an ever-expanding increase in caloric intake over time - and thus obesity. You'll end up consuming lots of calories while consuming food that's essentially deprived of vitamins and minerals.
Exposing yourself to this table while following a diet?
Run Forest, run!
Oysters? That's one ingredient. Ground beef? Single ingredient. Spinach? Again, one ingredient.
Pizza? A multi-ingredient food. Same for hot dogs, frozen paella, or other processed food.
Yes, even paella can contain crap if it's store bought. If you want to make that dish, build it from scratch with single ingredients. Stay on such a diet for half a year, and you'll probably lose fat automatically.
Pizza: refined grains which spike blood sugar, salt,
oils, and food additives - sensitizing your brain.
Of course, many other variables play a role for successful fat loss, such as impulse control, but let's assume for now that there is good scientific evidence that processed foods - even meals with refined grains with lots of fat and salt - will alter brain structure in negative fashion over time.
Winding off processed food thus becomes like winding off cigarettes: your brain will protest, and yet, by doing so, you may habituate yourself to consuming primarily whole foods (and even enjoy them).
Rome was not built in a day, so winding of crappy foods will take you a few months.
From that day onward, you will have more control over the food you consume. If you consume a diet with high-quality foods, you'll be far less likely to experience cravings.
Relying on processed food can negatively affect your basal metabolic rate because overeating contributes to obesity, and through that mechanism, metabolic slowdown after you've lost the weight through dieting.
Assume that you're eating 1,400 calories per day after successful weight loss, and you weigh 150 pounds now.
Also assume that you're eating about 1 gram of protein per pound of body weight per day. In that case, you'll be eating 100 grams of protein per day, equaling 400 calories.
(Higher levels of protein are almost always recommended due to protein giving you higher satiety levels.[187-190])
You'll now have 1,000 calories left. Lastly, assume that you're following a high-fat diet, and eating 100 grams of fat (900 calories), which leaves you with 25 grams of carbohydrates (100 calories).
Before dieting, you may have been able to eat 1,800 calories per day as your baseline, while not gaining or losing weight. But now you can only eat 1,400 calories without the scale budging.
If you'd eat 2,500 calories for a few days, due to extreme hunger levels that are present now, your weight would re-bound like crazy - while your resting metabolic rate would still be slower on a relative basis.
Quickly bumping calories is thus dangerous...
Women with very low body fat percentages
often experience metabolic adaptations.
100 calories equal about 1.5 egg, or 2 ounces (66 grams) of steak eaten every day. As a result, you may gain a bit of fat, but it will not be too much.
Yes, you'll need to learn to calculate calories to accomplish this feat. While I may seem crazy for being so detailed with these numbers, they do matter.
Depending on the context, losing (lots) of weight can be a precision science and you're much more prone to succeed if you control all that can be controlled - that's my main argument in favor of the "calories in, calories out" model.
Let me explain:
Losing fat long-term is harder than many people assume - you'll want all the advantages you can get to increase your chances. The reason for calorie counting is that most people are simply not aware of the amount (or even type) of food they're taking in.
Hence using an online calorie tracker gives you additional data - Chronometer is a great place to start. When you become aware of your intake, calorie counting can be discarded.
The best method to reverse diet is to increase both your carbohydrate and fat intake by a few percents per week.
How do I know this approach works?
Studies have demonstrated that while resting metabolic rate may be lower a 6 months after weight loss, but after a period of 2 years that resting metabolic rate can recover.
Feeling and performing better.
Remember that many people simply don't feel like themselves when eating very little.
Your mood may be lower, your libido non-existent, sleep quality suffers, and you're not performing so well anymore.
How you'll feel after successfully restoring
your basal metabolic rate AND keeping the weight off.
Slow the process down if you're gaining weight too quickly or at the wrong places.
If your weight goes up, and the weight gain cannot be traced back to your waist or buttocks, then you're gaining some muscle - a very good sign.
After dieting for 12 or 16 weeks, many people gorge on tremendous amounts of fast foods because they've "deserved it".
Again, that method inevitably leads to fat gain and may set you back even further. If you do increase your fat stores a lot after dieting, you may end up with the same amount of fat as before while having a slow metabolic rate simultaneously.
You'll also end up depressed and really disappointed in your body.
After losing that 60 pounds your body now thinks its starving.
To protect itself against future starvation, your body puts on fat at a quicker pace than you normally would - in part because your basal metabolic rate is slow after fat loss.
Any junk food you consume thus makes you gain fat much faster than when you were still overweight. Reverse dieting is absolutely essential for that reason.
Don't be the person who undoes months of dieting by one or two weeks of eating lots of food - even though your body's hunger impulse says you should eat that way.
Following the hunger impulse is dangerous in this case...
It's difficult to reverse diet purely based on gut instinct or intuition - most people have big trouble estimating their daily calorie needs, and tend to overeat without being consciously aware of doing so.[204-207]
With lean, I mean that you're neither overweight or obese--no need to venture into the other direction of having extremely low levels of body fat.
If you've lost your weight with exercise, especially interval-like sports such as sprinting, Crossfit, weightlifting, football, etcetera, then I do not recommend cutting out exercise. Exercise will help you maintain muscle mass during a reverse diet.
Hedonism and a healthy body can get together
if you learn to cook properly...
Lots of anecdotal evidence of hundreds if not of thousands of individuals exists that eating a healthy diet at (or just above) your daily caloric expenditure heals your metabolism over time.
(I do have to say this option is more speculative.)
And because you're eating healthy foods your hunger levels automatically regulate themselves.
An example of a book that takes such an approach are How to Heal Your Metabolism: Learn How the Right Foods, Sleep, the Right Amount of Exercise and Happiness Can Increase Your Metabolic Rate and Help Heal Your Broken Metabolism.
That method includes making better food choices, managing stress, and increasing calories at or slightly above your daily expenditure. The goal is to train your body to increase basal metabolic rate over time.
Caveat: only ever experiment with increasing your food intake if you're already eating high-quality foods. Never increase your intake of junk or processed food as an excuse to boost metabolic rate.
The slight caloric increase method seems to work best in people who have a pattern of too much dieting and exercising - because they need calories to recover their metabolism.
Too much exercise and dieting closely mimic starvation conditions--which is something many people are unaware of.
The problem with an extreme approach is that you'll not only increase your basal metabolic rate but also gain tons of fat. Fat gain above a certain amount, again, has many negative health consequences.
The gradual approach works much better as there are only so many calories your metabolism can generally handle before body fat is gained. Gaining lots of fat in the process thus entails that you're going too quick.
Your resting metabolic rate only moves up very slowly - consuming many more calories above your daily need does not speed up that progress.
Some studies suggest that increasing carbohydrate periodically can increase resting metabolic rate more so than reverse dieting with proteins or fats. Fortunately, you'll probably increasing your caloric intake through carbohydrates in the case you're starting to eat more anyway.[216-219]
With "chronic dieters" I refer to people who've tried many different diets in their lifetimes, such as Atkins, Paleo, the South Beach diet, a juice fast diet, heavy exercise, intermittent fasting, but never kept the weight off for good.
Chronic dieters tend to experiment with a new diet every season - chronic dieting is thus similar to yo-yo dieting.
Don't think for a second that increasing caloric intake is easy to do though: most yo-yo dieters have cycles of extreme caloric restriction followed by periods of binge eating to make up for the restriction.
Again: managing your caloric intake after heavy dieting takes tons of discipline.
50 or 100 years ago, people didn't have such an extreme relationship with food.
You didn't consume extreme amounts of calories from processed food back then, but you didn't diet either.
That last statement is, to me, is just as important puzzle piece to understanding the obesity epidemic as is overeating. Of course, our circadian rhythms have also changed for the worse, and are horribly underestimated as an explanatory factor for why obesity exists.
Both factors are under-emphasized in the obesity epidemic discourse ...
So let's conclude:
I've called basal metabolic rate the "holy grail" of fat loss, simply because disruptions in that metabolic rate are so central in both obesity and starvation.
Once you reverse such a condition, your basal metabolic rate has already taken a hit. The solution to that problem is to avoid extremes as much as possible: yes, lose your body fat but also make sure to regain your health afterward.
Use strategies such as boosting your mineral intake, optimizing your circadian rhythm, and reverse dieting for restoring your basal metabolic rate.
People who are engaging in heavy exercise 5 times a week combined with a weekly 2-day fast will almost certainly slow their metabolism down over time.
The same is true if you massively overeat: you're adding so much energy to your body that your body cannot burn that energy off quickly - leading to increased fat stores.
Your circadian rhythm, the minerals you ingest, and the toxins you're exposed to, all influence that "calories in, calories out" equation very indirectly.
Those influences are commonly not accounted for by "calories in, calories out" proponents. If you see food just as energy while not seeing the bigger picture, you're thus going to misunderstand the calories in, calories out equation.
Extreme dieting, exercise, or weight gain can all beget structural changes to the body which lower your overall health, set you up with new health problems, and make you worse off than before.
The current "calories in, calories out" formula looks a lot like the Aristotelian worldview in during the Scientific Revolution - more and more ad hoc adjustments to the theory need to be added to keep the model consistent with current data.
A last surprise?
Even I have been part of that tradition, exercising 1.5-2 hours a day, 6 days a week, to develop a maximally muscular physique:
At least I ate enough during that process, as otherwise I'd had done gotten into big problems with metabolic slowdown.
So I know all about exercising more and using stress to develop "the perfect physique". You don't have to make mistakes.
Let me explain:
Coming back to the topic of evolution: it's time to question the message of glorifying athletes with extremely low body fat (which I did not yet achieve, fortunately).
Semi-starvation should not be exalted.
Instead of honoring models who achieve very low levels of body fat, celebrate the person with an average weight who thinks and sleeps perfectly instead.
Yes, I know that's a shocking change in philosophy - and in fact, it may take society 50 or 100 years to adapt to that change.
By 2100, hopefully, you're glorifying people with perfect sleep and brain power...
Getting back on topic:
You've been led to believe that restriction on food will work in the long term--in reality, that process leads to dangerous metabolic adaptations, which set you up for further fat gains.
But now you can do it, with a more balanced approach.
If you ever start a diet, please use a strategy to build yourself up again afterward. By understanding your resting metabolic rate you can control that obesity now.
Your body will thank you.
Your health will thank you.
And you will thank you...
 Howell S, Kones R. "Calories in, calories out" and macronutrient intake: the hope, hype, and science of calories. Am J Physiol Endocrinol Metab. 2017 Nov 1;313(5):E608-E612. doi: 10.1152/ajpendo.00156.2017. Epub 2017 Aug 1.
 Hall KD, Guyenet SJ, Leibel RL. The Carbohydrate-Insulin Model of Obesity Is Difficult to Reconcile With Current Evidence. JAMA Intern Med. 2018 Aug 1;178(8):1103-1105. doi: 10.1001/jamainternmed.2018.2920.
 Hall KD. A review of the carbohydrate-insulin model of obesity. Eur J Clin Nutr. 2017 Mar;71(3):323-326. doi: 10.1038/ejcn.2016.260. Epub 2017 Jan 11.
 Astley CM, Todd JN ... Florez JC. Genetic Evidence That Carbohydrate-Stimulated Insulin Secretion Leads to Obesity. Clin Chem. 2018 Jan;64(1):192-200. doi: 10.1373/clinchem.2017.280727.
 Ludwig DS, Ebbeling CB. Raising the bar on the low-carbohydrate diet. Am J Clin Nutr. 2016 Nov;104(5):1487-1488.
 Ludwig DS, Ebbeling CB. The Carbohydrate-Insulin Model of Obesity: Beyond "Calories In, Calories Out". JAMA Intern Med. 2018 Aug 1;178(8):1098-1103. doi: 10.1001/jamainternmed.2018.2933.
 Flegal KM, Kruszon-Moran D, ... Ogden CL. Trends in Obesity Among Adults in the United States, 2005 to 2014. JAMA. 2016 Jun 7;315(21):2284-91. doi: 10.1001/jama.2016.6458.
 Flegal KM, Kruszon-Moran D, Carroll MD, Fryar CD, Ogden CL. Trends in Obesity Among Adults in the United States, 2005 to 2014. JAMA. 2016 Jun 7;315(21):2284-91. doi: 10.1001/jama.2016.6458.
 Ogden CL, Carroll MD, ... Flegal KM. Trends in Obesity Prevalence Among Children and Adolescents in the United States, 1988-1994 Through 2013-2014. JAMA. 2016 Jun 7;315(21):2292-9. doi: 10.1001/jama.2016.6361.
 National Institute Of Diabetes And Kidney Diseases. Overweight & Obesity Statistics. August 2017.
 Al-Goblan AS, Al-Alfi MA, Khan MZ. Mechanism linking diabetes mellitus and obesity. Diabetes Metab Syndr Obes. 2014 Dec 4;7:587-91. doi: 10.2147/DMSO.S67400. eCollection 2014.
 Leitner DR, Frühbeck G, ... Toplak H. Obesity and Type 2 Diabetes: Two Diseases with a Need for Combined Treatment Strategies - EASO Can Lead the Way. Obes Facts. 2017;10(5):483-492. doi: 10.1159/000480525. Epub 2017 Oct 12.
 Malone JI, Hansen BC. Does obesity cause type 2 diabetes mellitus (T2DM)? Or is it the opposite? Pediatr Diabetes. 2019 Feb;20(1):5-9. doi: 10.1111/pedi.12787. Epub 2018 Nov 5.
 Han SJ, Boyko EJ. The Evidence for an Obesity Paradox in Type 2 Diabetes Mellitus. Diabetes Metab J. 2018 Jun;42(3):179-187. doi: 10.4093/dmj.2018.0055. Epub 2018 May 31.
 Garg SK, Maurer H, Reed K, Selagamsetty R. Diabetes and cancer: two diseases with obesity as a common risk factor. Diabetes Obes Metab. 2014 Feb;16(2):97-110. doi: 10.1111/dom.12124. Epub 2013 Jun 12.
 De Pergola G, Silvestris F. Obesity as a major risk factor for cancer. J Obes. 2013;2013:291546. doi: 10.1155/2013/291546. Epub 2013 Aug 29.
 Stone TW, McPherson M, Gail Darlington L. Obesity and Cancer: Existing and New Hypotheses for a Causal Connection. EBioMedicine. 2018 Apr;30:14-28. doi: 10.1016/j.ebiom.2018.02.022. Epub 2018 Feb 27.
 Jiang SZ, Lu W, Zong XF, Ruan HY, Liu Y. Obesity and hypertension. Exp Ther Med. 2016 Oct;12(4):2395-2399. Epub 2016 Sep 6.
 Re RN. Obesity-related hypertension. Ochsner J. 2009 Fall;9(3):133-6.
 Aronow WS. Association of obesity with hypertension. Ann Transl Med. 2017 Sep;5(17):350. doi: 10.21037/atm.2017.06.69.
 Son WM, Kim DY, Kim YS, Ha MS. Effect of Obesity on Blood Pressure and Arterial Stiffness in Middle-Aged Korean Women. Osong Public Health Res Perspect. 2017 Dec;8(6):369-372. doi: 10.24171/j.phrp.2017.8.6.02. Epub 2017 Dec 31.
 Scherer PE, Hill JA. Obesity, Diabetes, and Cardiovascular Diseases: A Compendium. Circ Res. 2016 May 27;118(11):1703-5. doi: 10.1161/CIRCRESAHA.116.308999.
 Kachur S, Lavie CJ, ... Ventura HO. Obesity and cardiovascular diseases. Minerva Med. 2017 Jun;108(3):212-228. doi: 10.23736/S0026-4806.17.05022-4. Epub 2017 Feb 1.
 Mandviwala T, Khalid U, Deswal A. Obesity and Cardiovascular Disease: a Risk Factor or a Risk Marker? Curr Atheroscler Rep. 2016 May;18(5):21. doi: 10.1007/s11883-016-0575-4.
 Harms S, Larson R, Sahmoun AE, Beal JR. Obesity increases the likelihood of total joint replacement surgery among younger adults. Int Orthop. 2007 Feb;31(1):23-6. Epub 2006 May 11.
 Sowers MR, Karvonen-Gutierrez CA. The evolving role of obesity in knee osteoarthritis. Curr Opin Rheumatol. 2010 Sep;22(5):533-7. doi: 10.1097/BOR.0b013e32833b4682.
 King LK, March L, Anandacoomarasamy A. Obesity & osteoarthritis. Indian J Med Res. 2013;138:185-93.
 Douglas CC, Lawrence JC, ... Darnell BE. Ability of the Harris Benedict formula to predict energy requirements differs with weight history and ethnicity. Nutr Res. 2007 Apr;27(4):194-199.
 Sabounchi NS, Rahmandad H, Ammerman A. Best-fitting prediction equations for basal metabolic rate: informing obesity interventions in diverse populations. Int J Obes (Lond). 2013 Oct;37(10):1364-70. doi: 10.1038/ijo.2012.218. Epub 2013 Jan 15.
 Kruizenga HM, Hofsteenge GH, Weijs PJ. Predicting resting energy expenditure in underweight, normal weight, overweight, and obese adult hospital patients. Nutr Metab (Lond). 2016 Nov 24;13:85. eCollection 2016.
 Dulloo AG, Jacquet J. Adaptive reduction in basal metabolic rate in response to food deprivation in humans: a role for feedback signals from fat stores. Am J Clin Nutr. 1998 Sep;68(3):599-606.
 Dulloo AG, Jacquet J, Montani JP. How dieting makes some fatter: from a perspective of human body composition autoregulation. Proc Nutr Soc. 2012 Aug;71(3):379-89. doi: 10.1017/S0029665112000225. Epub 2012 Apr 5.
 Maclean PS, Bergouignan A, Cornier MA, Jackman MR. Biology's response to dieting: the impetus for weight regain. Am J Physiol Regul Integr Comp Physiol. 2011 Sep;301(3):R581-600. doi: 10.1152/ajpregu.00755.2010. Epub 2011 Jun 15.
 Dulloo AG, Jacquet J, Montani JP, Schutz Y. How dieting makes the lean fatter: from a perspective of body composition autoregulation through adipostats and proteinstats awaiting discovery. Obes Rev. 2015 Feb;16 Suppl 1:25-35. doi: 10.1111/obr.12253.
 MacLean PS, Higgins JA,... Hill JO. Peripheral metabolic responses to prolonged weight reduction that promote rapid, efficient regain in obesity-prone rats. Am J Physiol Regul Integr Comp Physiol. 2006 Jun;290(6):R1577-88. Epub 2006 Feb 2.
 Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002.
 Korbonits M, Blaine D, Elia M, Powell-Tuck J. Metabolic and hormonal changes during the refeeding period of prolonged fasting. Eur J Endocrinol. 2007 Aug;157(2):157-66.
 Knuth ND, Johannsen DL, ... Hall KD. Metabolic adaptation following massive weight loss is related to the degree of energy imbalance and changes in circulating leptin. Obesity (Silver Spring). 2014 Dec;22(12):2563-9. doi: 10.1002/oby.20900. Epub 2014 Sep 19.
 Fothergill E, Guo J, ... Hall KD. Persistent metabolic adaptation 6 years after "The Biggest Loser" competition. Obesity (Silver Spring). 2016 Aug;24(8):1612-9. doi: 10.1002/oby.21538. Epub 2016 May 2.
 Knuth ND1, Johannsen DL, Tamboli ... Hall KD. Metabolic adaptation following massive weight loss is related to the degree of energy imbalance and changes in circulating leptin. Obesity (Silver Spring). 2014 Dec;22(12):2563-9. doi: 10.1002/oby.20900. Epub 2014 Sep 19.
 Johannsen DL, Knuth ND, ... Hall KD. Metabolic slowing with massive weight loss despite preservation of fat-free mass. J Clin Endocrinol Metab. 2012 Jul;97(7):2489-96. doi: 10.1210/jc.2012-1444. Epub 2012 Apr 24.
 Zinchenko A, Henselmans M. Metabolic Damage: do Negative Metabolic Adaptations During Underfeeding Persist After Refeeding in Non-Obese Populations?
 Lecoultre V, Ravussin E, Redman LM. The fall in leptin concentration is a major determinant of the metabolic adaptation induced by caloric restriction independently of the changes in leptin circadian rhythms. J Clin Endocrinol Metab. 2011 Sep;96(9):E1512-6. doi: 10.1210/jc.2011-1286. Epub 2011 Jul 21.
 Yang H, Youm YH, Nakata C, Dixit VD. Chronic caloric restriction induces forestomach hypertrophy with enhanced ghrelin levels during aging. Peptides. 2007 Oct;28(10):1931-6. Epub 2007 Aug 19.
 Yang H, Youm YH, Nakata C, Dixit VD. Chronic caloric restriction induces forestomach hypertrophy with enhanced ghrelin levels during aging. Peptides. 2007 Oct;28(10):1931-6. Epub 2007 Aug 19.
 Cangemi R, Friedmann AJ, Holloszy JO, Fontana L. Long-term effects of calorie restriction on serum sex-hormone concentrations in men. Aging Cell. 2010 Apr;9(2):236-42. doi: 10.1111/j.1474-9726.2010.00553.x. Epub 2010 Jan 20.
 De Andrade PB, Neff LA, ... Dorchies OM. Caloric restriction induces energy-sparing alterations in skeletal muscle contraction, fiber composition and local thyroid hormone metabolism that persist during catch-up fat upon refeeding. Front Physiol. 2015 Sep 16;6:254. doi: 10.3389/fphys.2015.00254. eCollection 2015.
 Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes (Lond). 2010 Oct;34 Suppl 1:S47-55. doi: 10.1038/ijo.2010.184.
 Agnihothri RV, Courville AB,... Celi FS. Moderate weight loss is sufficient to affect thyroid hormone homeostasis and inhibit its peripheral conversion. Thyroid. 2014 Jan;24(1):19-26. doi: 10.1089/thy.2013.0055.
 Douyon L, Schteingart DE. Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. Endocrinol Metab Clin North Am. 2002 Mar;31(1):173-89.
 Rosenbaum M, Hirsch J, Gallagher DA, Leibel RL. Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight. Am J Clin Nutr. 2008 Oct;88(4):906-12.
 Wing RR, Phelan S. Long-term weight loss maintenance. Am J Clin Nutr. 2005 Jul;82(1 Suppl):222S-225S. doi: 10.1093/ajcn/82.1.222S.
 Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8.
 Montesi L, El Ghoch M, ... Dalle Grave R. Long-term weight loss maintenance for obesity: a multidisciplinary approach. Diabetes Metab Syndr Obes. 2016 Feb 26;9:37-46. doi: 10.2147/DMSO.S89836. eCollection 2016.
 Hays NP, Roberts SB. Aspects of eating behaviors "disinhibition" and "restraint" are related to weight gain and BMI in women. Obesity (Silver Spring). 2008 Jan;16(1):52-8. doi: 10.1038/oby.2007.12.
 Kruseman M, Schmutz N, Carrard I. Long-Term Weight Maintenance Strategies Are Experienced as a Burden by Persons Who Have Lost Weight Compared to Persons with a lifetime Normal, Stable Weight. Obes Facts. 2017;10(4):373-385. doi: 10.1159/000478096. Epub 2017 Aug 16.
 Pasquet P1, Apfelbaum M. Recovery of initial body weight and composition after long-term massive overfeeding in men. Am J Clin Nutr. 1994 Dec;60(6):861-3.
 Keys, A., Brozek, J., Henschel, A., Mickelsen, O., & Taylor, H. L., The Biology of Human Starvation (2 volumes), University of Minnesota Press, 1950.
 Müller MJ, Bosy-Westphal A, Heymsfield SB. Is there evidence for a set point that regulates human body weight? F1000 Med Rep. 2010 Aug 9;2:59. doi: 10.3410/M2-59.
 Chhabra KH, Adams JM, ... Low MJ. Reprogramming the body weight set point by a reciprocal interaction of hypothalamic leptin sensitivity and Pomc gene expression reverts extreme obesity. Mol Metab. 2016 Aug 5;5(10):869-881. doi: 10.1016/j.molmet.2016.07.012. eCollection 2016 Oct.
 Kelesidis T, Kelesidis I, Chou S, Mantzoros CS. Narrative review: the role of leptin in human physiology: emerging clinical applications. Ann Intern Med. 2010 Jan 19;152(2):93-100. doi: 10.7326/0003-4819-152-2-201001190-00008.
 Flier JS . Clinical review 94: What’s in a name? In search of leptin’s physiologic role. J Clin Endocrinol Metab . 1998;83:1407–1413.
 Zhou Y1, Rui L. Leptin signaling and leptin resistance. Front Med. 2013 Jun;7(2):207-22. doi: 10.1007/s11684-013-0263-5. Epub 2013 Apr 12.
 Sáinz N, Barrenetxe J, Moreno-Aliaga MJ, Martínez JA. Leptin resistance and diet-induced obesity: central and peripheral actions of leptin. Metabolism. 2015 Jan;64(1):35-46. doi: 10.1016/j.metabol.2014.10.015. Epub 2014 Oct 23.
 Crujeiras AB, Carreira MC, ... Casanueva FF. Leptin resistance in obesity: An epigenetic landscape. Life Sci. 2015 Nov 1;140:57-63. doi: 10.1016/j.lfs.2015.05.003. Epub 2015 May 18.
 Hall KD, Chen KY, ... Ravussin E. Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men. Am J Clin Nutr. 2016 Aug;104(2):324-33. doi: 10.3945/ajcn.116.133561. Epub 2016 Jul 6.
 Cypess AM, Kahn CR. The role and importance of brown adipose tissue in energy homeostasis. Curr Opin Pediatr. 2010 Aug;22(4):478-84. doi: 10.1097/MOP.0b013e32833a8d6e.
 Zurlo F, Larson K, Bogardus C, Ravussin E. Skeletal muscle metabolism is a major determinant of resting energy expenditure. J Clin Invest. 1990 Nov;86(5):1423-7.
 Gilsanz V, Smith ML, ... Hu HH. Changes in brown adipose tissue in boys and girls during childhood and puberty. J Pediatr. 2012 Apr;160(4):604-609.e1. doi: 10.1016/j.jpeds.2011.09.035. Epub 2011 Nov 1.
 Gilsanz V, Hu HH, Kajimura S. Relevance of brown adipose tissue in infancy and adolescence. Pediatr Res. 2013 Jan;73(1):3-9. doi: 10.1038/pr.2012.141. Epub 2012 Oct 22.
 Wang Z, Heymsfield SB, ... Gidwani S. A cellular level approach to predicting resting energy expenditure: Evaluation of applicability in adolescents. Am J Hum Biol. 2010 Jul-Aug;22(4):476-83. doi: 10.1002/ajhb.21020.
 Lecoultre V, Ravussin E. Brown adipose tissue and aging. Curr Opin Clin Nutr Metab Care. 2011 Jan;14(1):1-6. doi: 10.1097/MCO.0b013e328341221e.
 Siparsky PN, Kirkendall DT, Garrett WE Jr. Muscle changes in aging: understanding sarcopenia. Sports Health. 2014 Jan;6(1):36-40. doi: 10.1177/1941738113502296.
 O'Dea K, Patel M, Kubisch D, Hopper J, Traianedes K. Obesity, diabetes, and hyperlipidemia in a central Australian aboriginal community with a long history of acculturation. Diabetes Care. 1993 Jul;16(7):1004-10.
 McLennan AK, Ulijaszek SJ. Obesity emergence in the Pacific islands: why understanding colonial history and social change is important. Public Health Nutr. 2015 Jun;18(8):1499-505. doi: 10.1017/S136898001400175X. Epub 2014 Aug 29.
 Young TK. Are the circumpolar Inuit becoming obese? Am J Hum Biol. 2007 Mar-Apr;19(2):181-9.
 Styne DM. Childhood obesity in American Indians. J Public Health Manag Pract. 2010 Sep-Oct;16(5):381-7. doi: 10.1097/PHH.0b013e3181e887ae.
 Ravelli GP, Stein ZA, Susser MW. Obesity in young men after famine exposure in utero and early infancy. N Engl J Med. 1976 Aug 12;295(7):349-53.
 Schulz LC. The Dutch Hunger Winter and the developmental origins of health and disease. Proc Natl Acad Sci U S A. 2010 Sep 28;107(39):16757-8. doi: 10.1073/pnas.1012911107. Epub 2010 Sep 20.
 Dabelea D, Hanson RL, ... Knowler WC. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships. Diabetes. 2000 Dec;49(12):2208-11.
 Catalano PM, Farrell K, ... Amini SB. Perinatal risk factors for childhood obesity and metabolic dysregulation. Am J Clin Nutr. 2009 Nov;90(5):1303-13. doi: 10.3945/ajcn.2008.27416. Epub 2009 Sep 16.
 Nakamura D, Yanagiba Y, ... Nakajima T. Bisphenol A may cause testosterone reduction by adversely affecting both testis and pituitary systems similar to estradiol. Toxicol Lett. 2010 Apr 15;194(1-2):16-25. doi: 10.1016/j.toxlet.2010.02.002. Epub 2010 Feb 6.
 Mínguez-Alarcón L, Hauser R, Gaskins AJ. Effects of bisphenol A on male and couple reproductive health: a review. Fertil Steril. 2016 Sep 15;106(4):864-70. doi: 10.1016/j.fertnstert.2016.07.1118. Epub 2016 Aug 4.
 Welle S, Jozefowicz R, Forbes G, Griggs RC. Effect of testosterone on metabolic rate and body composition in normal men and men with muscular dystrophy. J Clin Endocrinol Metab. 1992 Feb;74(2):332-5.
 Traish AM. Testosterone and weight loss: the evidence. Curr Opin Endocrinol Diabetes Obes. 2014 Oct;21(5):313-22. doi: 10.1097/MED.0000000000000086.
 Mullur R, Liu YY, Brent GA. Thyroid hormone regulation of metabolism. Physiol Rev. 2014 Apr;94(2):355-82. doi: 10.1152/physrev.00030.2013.
 Kim B. Thyroid hormone as a determinant of energy expenditure and the basal metabolic rate. Thyroid. 2008 Feb;18(2):141-4. doi: 10.1089/thy.2007.0266.
 Casals-Casas C, Desvergne B. Endocrine disruptors: from endocrine to metabolic disruption. Annu Rev Physiol. 2011;73:135-62. doi: 10.1146/annurev-physiol-012110-142200.
 Diamanti-Kandarakis E, Bourguignon JP,... Gore AC. Endocrine-disrupting chemicals: an Endocrine Society scientific statement. Endocr Rev. 2009 Jun;30(4):293-342. doi: 10.1210/er.2009-0002.
 Le Magueresse-Battistoni B, Labaronne E, Vidal H, Naville D. Endocrine disrupting chemicals in mixture and obesity, diabetes and related metabolic disorders. World J Biol Chem. 2017 May 26;8(2):108-119. doi: 10.4331/wjbc.v8.i2.108.
 Ross R, Janssen I. Physical activity, total and regional obesity: dose-response considerations. Med Sci Sports Exerc. 2001 Jun;33(6 Suppl):S521-7; discussion S528-9.
 Pronk NP, Wing RR. Physical activity and long-term maintenance of weight loss. Obes Res. 1994 Nov;2(6):587-99.
 de Roon M, van Gemert WA, ... Monninkhof EM. Long-term effects of a weight loss intervention with or without exercise component in postmenopausal women: A randomized trial. Prev Med Rep. 2016 Dec 9;5:118-123. eCollection 2017 Mar.
 Thaler JP , Yi CX , ... Schwartz MW . Obesity is associated with hypothalamic injury in rodents and humans. J Clin Invest . 2012;122:153–162.
 García-Cáceres C, Fuente-Martín E, Argente J, Chowen JA. Emerging role of glial cells in the control of body weight. Mol Metab. 2012 Aug 9;1(1-2):37-46. doi: 10.1016/j.molmet.2012.07.001. eCollection 2012.
 Dorfman MD, Thaler JP. Hypothalamic inflammation and gliosis in obesity. Curr Opin Endocrinol Diabetes Obes. 2015 Oct;22(5):325-30. doi: 10.1097/MED.0000000000000182.
 Berkseth KE, Guyenet SJ, ... Schwartz MW. Hypothalamic gliosis associated with high-fat diet feeding is reversible in mice: a combined immunohistochemical and magnetic resonance imaging study. Endocrinology. 2014 Aug;155(8):2858-67. doi: 10.1210/en.2014-1121. Epub 2014 Jun 10.
 Douglass JD, Dorfman MD, ... Thaler JP. Astrocyte IKKβ/NF-κB signaling is required for diet-induced obesity and hypothalamic inflammation. Mol Metab. 2017 Jan 28;6(4):366-373. doi: 10.1016/j.molmet.2017.01.010. eCollection 2017 Apr.
 Foright RM, Presby DM, ... MacLean PS. Is regular exercise an effective strategy for weight loss maintenance? Physiol Behav. 2018 May 1;188:86-93. doi: 10.1016/j.physbeh.2018.01.025. Epub 2018 Jan 31.
 Turk MW, Yang K, ... Burke LE. Randomized clinical trials of weight loss maintenance: a review. J Cardiovasc Nurs. 2009 Jan-Feb;24(1):58-80. doi: 10.1097/01.JCN.0000317471.58048.32.
 De Maddalena C, Vodo S, Petroni A, Aloisi AM. Impact of testosterone on body fat composition. J Cell Physiol. 2012 Dec;227(12):3744-8. doi: 10.1002/jcp.24096.
 Allan CA, McLachlan RI. Androgens and obesity. Curr Opin Endocrinol Diabetes Obes. 2010 Jun;17(3):224-32. doi: 10.1097/MED.0b013e3283398ee2.
 Stiegler P, Cunliffe A. The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss. Sports Med. 2006;36(3):239-62.
 Hopkins M, Finlayson G,... Stubbs RJ. Modelling the associations between fat-free mass, resting metabolic rate and energy intake in the context of total energy balance. Int J Obes (Lond). 2016 Feb;40(2):312-8. doi: 10.1038/ijo.2015.155. Epub 2015 Aug 17.
 Alberga AS, Prud'homme D, ... Kenny GP. Does exercise training affect resting metabolic rate in adolescents with obesity? Appl Physiol Nutr Metab. 2017 Jan;42(1):15-22. doi: 10.1139/apnm-2016-0244. Epub 2016 Aug 22.
 Cullinen K, Caldwell M. Weight training increases fat-free mass and strength in untrained young women. J Am Diet Assoc. 1998 Apr;98(4):414-8.
 Rosenbaum M, Goldsmith R, ... Leibel RL. Low-dose leptin reverses skeletal muscle, autonomic, and neuroendocrine adaptations to maintenance of reduced weight. J Clin Invest. 2005 Dec;115(12):3579-86.
 Greenway FL. Physiological adaptations to weight loss and factors favouring weight regain. Int J Obes (Lond). 2015 Aug;39(8):1188-96. doi: 10.1038/ijo.2015.59. Epub 2015 Apr 21.
 Sumithran P, Prendergast LA, ... Proietto J. Long-term persistence of hormonal adaptations to weight loss. N Engl J Med. 2011 Oct 27;365(17):1597-604. doi: 10.1056/NEJMoa1105816.
 Ravussin E, Burnand B, Schutz Y, Jéquier E. Energy expenditure before and during energy restriction in obese patients. Am J Clin Nutr. 1985 Apr;41(4):753-9.
 Doucet E, St-Pierre S, ... Tremblay A. Evidence for the existence of adaptive thermogenesis during weight loss. Br J Nutr. 2001 Jun;85(6):715-23.
 Leibel RL, Hirsch J. Diminished energy requirements in reduced-obese patients. Metabolism. 1984 Feb;33(2):164-70.
 Weigle DS, Sande KJ, Iverius PH, Monsen ER, Brunzell JD. Weight loss leads to a marked decrease in nonresting energy expenditure in ambulatory human subjects. Metabolism. 1988 Oct;37(10):930-6.
 Hunter GR, Fisher G, Neumeier WH, Carter SJ, Plaisance EP. Exercise Training and Energy Expenditure following Weight Loss. Med Sci Sports Exerc. 2015 Sep;47(9):1950-7. doi: 10.1249/MSS.0000000000000622.
 Müller MJ, Enderle J, Bosy-Westphal A. Changes in Energy Expenditure with Weight Gain and Weight Loss in Humans. Curr Obes Rep. 2016 Dec;5(4):413-423.
 Chung N, Park MY,... Lim K. Non-exercise activity thermogenesis (NEAT): a component of total daily energy expenditure. J Exerc Nutrition Biochem. 2018 Jun 30;22(2):23-30. doi: 10.20463/jenb.2018.0013.
 Ricquier D. Uncoupling protein 1 of brown adipocytes, the only uncoupler: a historical perspective. Front Endocrinol (Lausanne). 2011 Dec 28;2:85. doi: 10.3389/fendo.2011.00085. eCollection 2011.
 Berger A, Brand M, O'Rahilly S. Uncoupling proteins: the unravelling of obesity? Increased understanding of mechanisms may lead, in time, to better drugs. BMJ. 1998 Dec 12;317(7173):1607-8.
 Busiello RA, Savarese S, Lombardi A. Mitochondrial uncoupling proteins and energy metabolism. Front Physiol. 2015 Feb 10;6:36. doi: 10.3389/fphys.2015.00036. eCollection 2015.
 Soare A, Cangemi R, Omodei D, Holloszy JO, Fontana L. Long-term calorie restriction, but not endurance exercise, lowers core body temperature in humans. Aging (Albany NY). 2011 Apr;3(4):374-9.
 Bevilacqua L, Ramsey JJ, ... Harper ME. Effects of short- and medium-term calorie restriction on muscle mitochondrial proton leak and reactive oxygen species production. Am J Physiol Endocrinol Metab. 2004 May;286(5):E852-61. Epub 2004 Jan 21.
 Garthe I, Raastad T, ... Sundgot-Borgen J. Effect of two different weight-loss rates on body composition and strength and power-related performance in elite athletes. Int J Sport Nutr Exerc Metab. 2011 Apr;21(2):97-104.
 Cava E, Yeat NC, Mittendorfer B. Preserving Healthy Muscle during Weight Loss. Adv Nutr. 2017 May 15;8(3):511-519. doi: 10.3945/an.116.014506. Print 2017 May.
 Weyer C, Walford RL, ... Ravussin E. Energy metabolism after 2 y of energy restriction: the biosphere 2 experiment. Am J Clin Nutr. 2000 Oct;72(4):946-53.
 Guyenet SJ. The Hungry Brain: Outsmarting the Instincts That Make Us Overeat. Flatiron Books 2017
 Engin A. Circadian Rhythms in Diet-Induced Obesity. Adv Exp Med Biol. 2017;960:19-52. doi: 10.1007/978-3-319-48382-5_2.
 Potter GD, Skene DJ, ... Hardie LJ. Circadian Rhythm and Sleep Disruption: Causes, Metabolic Consequences, and Countermeasures. Endocr Rev. 2016 Dec;37(6):584-608. Epub 2016 Oct 20.
 Chong SYC, Xin L, Ptáček LJ, Fu YH. Disorders of sleep and circadian rhythms.Handb Clin Neurol. 2018;148:531-538. doi: 10.1016/B978-0-444-64076-5.00034-X.
 Sharma S, Kavuru M Sleep and metabolism: an overview. Int J Endocrinol. 2010;2010. pii: 270832. doi: 10.1155/2010/270832. Epub 2010 Aug 2.
 Spaeth AM, Dinges DF, Goel N. Resting metabolic rate varies by race and by sleep duration. Obesity (Silver Spring). 2015 Dec;23(12):2349-56. doi: 10.1002/oby.21198. Epub 2015 Nov 5.
 Knutson KL, Spiegel K, Penev P, Van Cauter E. The metabolic consequences of sleep deprivation. Sleep Med Rev. 2007 Jun;11(3):163-78. Epub 2007 Apr 17.
 Jung CM, Melanson EL, ... Wright KP. Energy expenditure during sleep, sleep deprivation and sleep following sleep deprivation in adult humans. J Physiol. 2011 Jan 1;589(Pt 1):235-44. doi: 10.1113/jphysiol.2010.197517. Epub 2010 Nov 8.
 Nedeltcheva AV, Kilkus JM, ... Penev PD. Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med. 2010 Oct 5;153(7):435-41. doi: 10.7326/0003-4819-153-7-201010050-00006.
 de Jonge L, Zhao X,... NIDDK Sleep Extension Study Group. Poor sleep quality and sleep apnea are associated with higher resting energy expenditure in obese individuals with short sleep duration. J Clin Endocrinol Metab. 2012 Aug;97(8):2881-9. Epub 2012 Jun 11.
 Buxton OM, Cain SW, ... Shea SA. Adverse metabolic consequences in humans of prolonged sleep restriction combined with circadian disruption. Sci Transl Med. 2012 Apr 11;4(129):129ra43. doi: 10.1126/scitranslmed.3003200.
 Jun JC, Polotsky VY. Sleep and sleep loss: an energy paradox? Sleep. 2012 Nov 1;35(11):1447-8. doi: 10.5665/sleep.2184.
 Benedict C, Hallschmid M, ... Lange T. Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr. 2011 Jun;93(6):1229-36. doi: 10.3945/ajcn.110.006460. Epub 2011 Apr 6.
 Penev PD. Update on energy homeostasis and insufficient sleep. J Clin Endocrinol Metab. 2012 Jun;97(6):1792-801. doi: 10.1210/jc.2012-1067. Epub 2012 Mar 22.
 Van Cauter E, Spiegel K, Tasali E, Leproult R. Metabolic consequences of sleep and sleep loss. Sleep Med. 2008 Sep;9 Suppl 1:S23-8. doi: 10.1016/S1389-9457(08)70013-3.
 Schmid SM, Hallschmid M, ... Schultes B. A single night of sleep deprivation increases ghrelin levels and feelings of hunger in normal-weight healthy men. J Sleep Res. 2008 Sep;17(3):331-4. doi: 10.1111/j.1365-2869.2008.00662.x. Epub 2008 Jun 28.
 Greer SM, Goldstein AN, Walker MP. The impact of sleep deprivation on food desire in the human brain. Nat Commun. 2013;4:2259. doi: 10.1038/ncomms3259.
 Leproult R, Van Cauter E. Role of sleep and sleep loss in hormonal release and metabolism. Endocr Dev. 2010;17:11-21. doi: 10.1159/000262524. Epub 2009 Nov 24.
 Donga E, van Dijk M, ... Romijn JA. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8. doi: 10.1210/jc.2009-2430. Epub 2010 Apr 6.
 Buxton OM, Pavlova M, ... Adler GK. Sleep restriction for 1 week reduces insulin sensitivity in healthy men. Diabetes. 2010 Sep;59(9):2126-33. doi: 10.2337/db09-0699. Epub 2010 Jun 28.
 Liu A, Kushida CA, Reaven GM. Habitual shortened sleep and insulin resistance: an independent relationship in obese individuals. Metabolism. 2013 Nov;62(11):1553-6. doi: 10.1016/j.metabol.2013.06.003. Epub 2013 Jul 10.
 Van Cauter E. Sleep disturbances and insulin resistance. Diabet Med. 2011 Dec;28(12):1455-62. doi: 10.1111/j.1464-5491.2011.03459.x.
 Briançon-Marjollet A, Weiszenstein M, ... Polak J. The impact of sleep disorders on glucose metabolism: endocrine and molecular mechanisms. Diabetol Metab Syndr. 2015 Mar 24;7:25. doi: 10.1186/s13098-015-0018-3. eCollection 2015.
 Leproult R, Van Cauter E. Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA. 2011 Jun 1;305(21):2173-4. doi: 10.1001/jama.2011.710.
 Barrett-Connor E, Dam TT, ... Osteoporotic Fractures in Men Study Group. The association of testosterone levels with overall sleep quality, sleep architecture, and sleep-disordered breathing. J Clin Endocrinol Metab. 2008 Jul;93(7):2602-9. doi: 10.1210/jc.2007-2622. Epub 2008 Apr 15.
 Andersen ML, Alvarenga TF, ... Tufik S. The association of testosterone, sleep, and sexual function in men and women. Brain Res. 2011 Oct 6;1416:80-104. doi: 10.1016/j.brainres.2011.07.060. Epub 2011 Aug 6.
 Patel P, Shiff B, Kohn TP, Ramasamy R. Impaired sleep is associated with low testosterone in US adult males: results from the National Health and Nutrition Examination Survey. World J Urol. 2018 Sep 17. doi: 10.1007/s00345-018-2485-2.
 Joo EY, Yoon CW, Koo DL, Kim D, Hong SB. Adverse effects of 24 hours of sleep deprivation on cognition and stress hormones. J Clin Neurol. 2012 Jun;8(2):146-50. doi: 10.3988/jcn.2012.8.2.146. Epub 2012 Jun 29.
 Irwin M, Thompson J, Miller C, Gillin JC, Ziegler M. Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications. J Clin Endocrinol Metab. 1999 Jun;84(6):1979-85.
 Song HT, Sun XY, ... Bai J. Effects of sleep deprivation on serum cortisol level and mental health in servicemen. Int J Psychophysiol. 2015 Jun;96(3):169-75. doi: 10.1016/j.ijpsycho.2015.04.008. Epub 2015 Apr 23.
 Leproult R, Copinschi G, Buxton O, Van Cauter E. Sleep loss results in an elevation of cortisol levels the next evening. Sleep. 1997 Oct;20(10):865-70.
 Wright KP, Drake AL, ... Czeisler CA. Influence of sleep deprivation and circadian misalignment on cortisol, inflammatory markers, and cytokine balance. Brain Behav Immun. 2015 Jul;47:24-34. doi: 10.1016/j.bbi.2015.01.004. Epub 2015 Jan 29.
 Voderholzer U1, Hohagen F, ... Riemann D. Impact of sleep deprivation and subsequent recovery sleep on cortisol in unmedicated depressed patients. Am J Psychiatry. 2004 Aug;161(8):1404-10.
 Kim B. Thyroid hormone as a determinant of energy expenditure and the basal metabolic rate. Thyroid. 2008 Feb;18(2):141-4. doi: 10.1089/thy.2007.0266.
 Cavallo E, Armellini F, ... Bosello O. Resting metabolic rate, body composition and thyroid hormones. Short term effects of very low calorie diet. Horm Metab Res. 1990 Dec;22(12):632-5.
 Celi FS, Zemskova M, ... Pucino F. Metabolic effects of liothyronine therapy in hypothyroidism: a randomized, double-blind, crossover trial of liothyronine versus levothyroxine. J Clin Endocrinol Metab. 2011 Nov;96(11):3466-74. doi: 10.1210/jc.2011-1329. Epub 2011 Aug 24.
 Liu G, Liang L, ... Sun Q. Thyroid hormones and changes in body weight and metabolic parameters in response to weight loss diets: the POUNDS LOST trial. Int J Obes (Lond). 2017 Jun;41(6):878-886. doi: 10.1038/ijo.2017.28. Epub 2017 Jan 31.
 Abreu IM, Lau E, ... Carvalho D. Subclinical hypothyroidism: to treat or not to treat, that is the question! A systematic review with meta-analysis on lipid profile. Endocr Connect. 2017 Apr;6(3):188-199. doi: 10.1530/EC-17-0028. Epub 2017 Mar 1.
 Astrup A, Gøtzsche PC, ... Buemann B. Meta-analysis of resting metabolic rate in formerly obese subjects. Am J Clin Nutr. 1999 Jun;69(6):1117-22.
 James WP, Davies HL, Bailes J, Dauncey MJ. Elevated metabolic rates in obesity. Lancet. 1978 May 27;1(8074):1122-5.
 Hoffmans M, Pfeifer WA, ... Hautvast JG. Resting metabolic rate in obese and normal weight women. Int J Obes. 1979;3(2):111-8.
 McMurray RG, Soares J, Caspersen CJ, McCurdy T. Examining variations of resting metabolic rate of adults: a public health perspective. Med Sci Sports Exerc. 2014 Jul;46(7):1352-8. doi: 10.1249/MSS.0000000000000232.
 Blundell JE, Finlayson G, ... Hopkins M. The biology of appetite control: Do resting metabolic rate and fat-free mass drive energy intake? Physiol Behav. 2015 Dec 1;152(Pt B):473-8. doi: 10.1016/j.physbeh.2015.05.031. Epub 2015 May 31.
 Caudwell P, Finlayson G, ... Blundell JE. Resting metabolic rate is associated with hunger, self-determined meal size, and daily energy intake and may represent a marker for appetite. Am J Clin Nutr. 2013 Jan;97(1):7-14. doi: 10.3945/ajcn.111.029975. Epub 2012 Nov 28.
 Astrup A, Buemann B, Toubro S, Ranneries C, Raben A. Low resting metabolic rate in subjects predisposed to obesity: a role for thyroid status. Am J Clin Nutr. 1996 Jun;63(6):879-83.
 Ravussin E. Low resting metabolic rate as a risk factor for weight gain: role of the sympathetic nervous system. Int J Obes Relat Metab Disord. 1995 Dec;19 Suppl 7:S8-S9.
 Johannsen DL, Knuth ND, ... Hall KD. Metabolic slowing with massive weight loss despite preservation of fat-free mass. J Clin Endocrinol Metab. 2012 Jul;97(7):2489-96. doi: 10.1210/jc.2012-1444. Epub 2012 Apr 24.
 Luke A, Schoeller DA. Basal metabolic rate, fat-free mass, and body cell mass during energy restriction. Metabolism. 1992 Apr;41(4):450-6.
 de Jonge L, Bray GA, ... Sacks FM. Effect of diet composition and weight loss on resting energy expenditure in the POUNDS LOST study. Obesity (Silver Spring). 2012 Dec;20(12):2384-9. doi: 10.1038/oby.2012.127. Epub 2012 May 7.
 Wada L, King JC. Effect of low zinc intakes on basal metabolic rate, thyroid hormones and protein utilization in adult men. J Nutr. 1986 Jun;116(6):1045-53.
 Evans SA, Overton JM, Alshingiti A, Levenson CW. Regulation of metabolic rate and substrate utilization by zinc deficiency. Metabolism. 2004 Jun;53(6):727-32.
 Nishiyama S, Futagoishi-Suginohara Y... Matsuda I. Zinc supplementation alters thyroid hormone metabolism in disabled patients with zinc deficiency. J Am Coll Nutr. 1994 Feb;13(1):62-7.
 Li S, Gao X, Wei Y, Zhu G, Yang C. The Relationship between Iron Deficiency and Thyroid Function in Chinese Women during Early Pregnancy. J Nutr Sci Vitaminol (Tokyo). 2016;62(6):397-401. doi: 10.3177/jnsv.62.397.
 Khatiwada S, Gelal B, Baral N, Lamsal M. Association between iron status and thyroid function in Nepalese children. Thyroid Res. 2016 Jan 27;9:2. doi: 10.1186/s13044-016-0031-0. eCollection 2016.
 Eftekhari MH , Keshavarz SA, ... Simondon KB. The relationship between iron status and thyroid hormone concentration in iron-deficient adolescent Iranian girls. Asia Pac J Clin Nutr. 2006;15(1):50-5.
 Ravanbod M, Asadipooya K, ... Omrani GR. Treatment of iron-deficiency anemia in patients with subclinical hypothyroidism.Am J Med. 2013 May;126(5):420-4. doi: 10.1016/j.amjmed.2012.12.009.
 Jones JE, Desper PC, Shane SR, Flink EB. Magnesium metabolism in hyperthyroidism and hypothyroidism. J Clin Invest. 1966 Jun;45(6):891-900.
 Hsu JM, Root AW, ... Kepford G. The effect of magnesium depletion on thyroid function in rats. J Nutr. 1984 Aug;114(8):1510-7.
 Wang K, Wei H,... Zhu M. Severely low serum magnesium is associated with increased risks of positive anti-thyroglobulin antibody and hypothyroidism: A cross-sectional study. Sci Rep. 2018 Jul 2;8(1):9904. doi: 10.1038/s41598-018-28362-5.
 Cinar V. The effects of magnesium supplementation on thyroid hormones of sedentars and Tae-Kwon-Do sportsperson at resting and exhaustion. Neuro Endocrinol Lett. 2007 Oct;28(5):708-12.
 Shibutani Y, Yokota T, ... Sakamoto K. Plasma and erythrocyte magnesium concentrations in thyroid disease: relation to thyroid function and the duration of illness. Jpn J Med. 1989 Jul-Aug;28(4):496-502.
 Johnstone AM, Murison SD, Duncan JS, Rance KA, Speakman JR. Factors influencing variation in basal metabolic rate include fat-free mass, fat mass, age, and circulating thyroxine but not sex, circulating leptin, or triiodothyronine. Am J Clin Nutr. 2005 Nov;82(5):941-8.
 Krieger JW , Sitren HS, Daniels MJ, Langkamp-Henken B. Effects of variation in protein and carbohydrate intake on body mass and composition during energy restriction: a meta-regression 1. Am J Clin Nutr. 2006 Feb;83(2):260-74.
 Paddon-Jones D1, Westman E, ... Westerterp-Plantenga M. Protein, weight management, and satiety. Am J Clin Nutr. 2008 May;87(5):1558S-1561S.
 Halton TL, Hu FB. The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr. 2004 Oct;23(5):373-85.
 Westerterp-Plantenga MS, Lemmens SG, Westerterp KR. Dietary protein - its role in satiety, energetics, weight loss and health. Br J Nutr. 2012 Aug;108 Suppl 2:S105-12. doi: 10.1017/S0007114512002589.
 Reed GW, Hill JO. Measuring the thermic effect of food. Am J Clin Nutr. 1996 Feb;63(2):164-9.
 Sutton EF, Bray GA, ... Redman LM. No evidence for metabolic adaptation in thermic effect of food by dietary protein. Obesity (Silver Spring). 2016 Aug;24(8):1639-42. doi: 10.1002/oby.21541. Epub 2016 Jun 29.
 Westerterp KR. Diet induced thermogenesis. Nutr Metab (Lond). 2004 Aug 18;1(1):5.
 Heymsfield SB, Gonzalez MC, ... Thomas D. Weight loss composition is one-fourth fat-free mass: a critical review and critique of this widely cited rule. Obes Rev. 2014 Apr;15(4):310-21. doi: 10.1111/obr.12143. Epub 2014 Jan 22.
 Hall KD. Body fat and fat-free mass inter-relationships: Forbes's theory revisited. Br J Nutr. 2007 Jun;97(6):1059-63. Epub 2007 Mar 19.
 Blundell JE, Caudwell P, ... Finlayson G. Body composition and appetite: fat-free mass (but not fat mass or BMI) is positively associated with self-determined meal size and daily energy intake in humans. Br J Nutr. 2012 Feb;107(3):445-9. doi: 10.1017/S0007114511003138. Epub 2011 Jul 7.
 Demling RH, DeSanti L. Effect of a hypocaloric diet, increased protein intake and resistance training on lean mass gains and fat mass loss in overweight police officers. Ann Nutr Metab. 2000;44(1):21-9.
 Josse AR, Phillips SM. Impact of milk consumption and resistance training on body composition of female athletes. Med Sport Sci. 2012;59:94-103. doi: 10.1159/000341968. Epub 2012 Oct 15.
 Josse AR , Tang JE, Tarnopolsky MA, Phillips SM. Body composition and strength changes in women with milk and resistance exercise. Med Sci Sports Exerc. 2010 Jun;42(6):1122-30. doi: 10.1249/MSS.0b013e3181c854f6.
 Paoli A, Grimaldi K, ... Palma A. Ketogenic diet does not affect strength performance in elite artistic gymnasts. J Int Soc Sports Nutr. 2012 Jul 26;9(1):34. doi: 10.1186/1550-2783-9-34.
 Polidori D, Sanghvi A, Seeley RJ, Hall KD. How Strongly Does Appetite Counter Weight Loss? Quantification of the Feedback Control of Human Energy Intake. Obesity (Silver Spring). 2016 Nov;24(11):2289-2295. doi: 10.1002/oby.21653.
 Münzberg H, Qualls-Creekmore E, ... Berthoud HR. Hedonics Act in Unison with the Homeostatic System to Unconsciously Control Body Weight. Front Nutr. 2016 Feb 15;3:6. doi: 10.3389/fnut.2016.00006. eCollection 2016.
 Dulloo AG, Jacquet J, Girardier L. Autoregulation of body composition during weight recovery in human: the Minnesota Experiment revisited. Int J Obes Relat Metab Disord. 1996 May;20(5):393-405.
 Levitsky DA, Raea Limb JE, ... Hunter J. Lack of negative autocorrelations of daily food intake on successive days challenges the concept of the regulation of body weight in humans. Appetite. 2017 Sep 1;116:277-283. doi: 10.1016/j.appet.2017.04.038. Epub 2017 May 5.
 Almiron-Roig E, Solis-Trapala I, Dodd J, Jebb SA. Estimating food portions. Influence of unit number, meal type and energy density. Appetite. 2013 Dec;71:95-103. doi: 10.1016/j.appet.2013.07.012. Epub 2013 Aug 8.
 Abramovitch SL, Reddigan JI, ... Kuk JL. Underestimating a serving size may lead to increased food consumption when using Canada's Food Guide. Appl Physiol Nutr Metab. 2012 Oct;37(5):923-30. doi: 10.1139/h2012-071. Epub 2012 Jul 31.
 Forwood SE, Ahern A, ... Marteau TM. Underestimating calorie content when healthy foods are present: an averaging effect or a reference-dependent anchoring effect? PLoS One. 2013 Aug 14;8(8):e71475. doi: 10.1371/journal.pone.0071475. eCollection 2013.
 Kalm LM, Semba RD. They starved so that others be better fed: remembering Ancel Keys and the Minnesota experiment. J Nutr. 2005 Jun;135(6):1347-52.
 Weinsier RL, Nagy TR, ... Weiss HL. Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory. Am J Clin Nutr. 2000 Nov;72(5):1088-94.
 Paris HL, Foright RM, ... Melby CL. Increasing energy flux to decrease the biological drive toward weight regain after weight loss - A proof-of-concept pilot study. Clin Nutr ESPEN. 2016 Feb;11:e12-e20. doi: 10.1016/j.clnesp.2015.11.005. Epub 2015 Dec 29.
 Fehm HL, Kern W, Peters A. The selfish brain: competition for energy resources. Prog Brain Res. 2006;153:129-40.
 Melby CL, Paris HL, Foright RM, Peth J. Attenuating the Biologic Drive for Weight Regain Following Weight Loss: Must What Goes Down Always Go Back Up? Nutrients. 2017 May 6;9(5). pii: E468. doi: 10.3390/nu9050468.
 Byrne NM, Wood RE, Schutz Y, Hills AP. Does metabolic compensation explain the majority of less-than-expected weight loss in obese adults during a short-term severe diet and exercise intervention? Int J Obes (Lond). 2012 Nov;36(11):1472-8. doi: 10.1038/ijo.2012.109. Epub 2012 Jul 24.
 Strohacker K, McCaffery JM, MacLean PS, Wing RR. Adaptations of leptin, ghrelin or insulin during weight loss as predictors of weight regain: a review of current literature. Int J Obes (Lond). 2014 Mar;38(3):388-96. doi: 10.1038/ijo.2013.118. Epub 2013 Jun 26.
 Coll AP, Farooqi IS, O'Rahilly S. The hormonal control of food intake. Cell. 2007 Apr 20;129(2):251-62.
 Schwarz JM, Neese RA, ... Hellerstein MK. Short-term alterations in carbohydrate energy intake in humans. Striking effects on hepatic glucose production, de novo lipogenesis, lipolysis, and whole-body fuel selection. J Clin Invest. 1995 Dec;96(6):2735-43.
 Westerterp KR. Food quotient, respiratory quotient, and energy balance. Am J Clin Nutr. 1993 May;57(5 Suppl):759S-764S; discussion 764S-765S. doi: 10.1093/ajcn/57.5.759S.
 Shafrir E. Overnutrition in spiny mice (Acomys cahirinus): beta-cell expansion leading to rupture and overt diabetes on fat-rich diet and protective energy-wasting elevation in thyroid hormone on sucrose-rich diet. Diabetes Metab Res Rev. 2000 Mar-Apr;16(2):94-105.
 Horton TJ, Drougas H, ... Hill JO. Fat and carbohydrate overfeeding in humans: different effects on energy storage.Am J Clin Nutr. 1995 Jul;62(1):19-29.
 Saito M. Brown adipose tissue as a regulator of energy expenditure and body fat in humans. Diabetes Metab J. 2013 Feb;37(1):22-9. doi: 10.4093/dmj.2013.37.1.22. Epub 2013 Feb 15.
 Scheele C, Nielsen S. Metabolic regulation and the anti-obesity perspectives of human brown fat. Redox Biol. 2017 Aug;12:770-775. doi: 10.1016/j.redox.2017.04.011. Epub 2017 Apr 11.
 Wu J , Cohen P, Spiegelman BM. Adaptive thermogenesis in adipocytes: is beige the new brown? Genes Dev. 2013 Feb 1;27(3):234-50. doi: 10.1101/gad.211649.112.
 Kajimura S, Spiegelman BM, Seale P. Brown and Beige Fat: Physiological Roles beyond Heat Generation. Cell Metab. 2015 Oct 6;22(4):546-59. doi: 10.1016/j.cmet.2015.09.007.
 Kim SH, Plutzky J. Brown Fat and Browning for the Treatment of Obesity and Related Metabolic Disorders. Diabetes Metab J. 2016 Feb;40(1):12-21. doi: 10.4093/dmj.2016.40.1.12.
 Sidossis L, Kajimura S. Brown and beige fat in humans: thermogenic adipocytes that control energy and glucose homeostasis. J Clin Invest. 2015 Feb;125(2):478-86. doi: 10.1172/JCI78362. Epub 2015 Feb 2.
 Mulya A, Kirwan JP. Brown and Beige Adipose Tissue: Therapy for Obesity and Its Comorbidities? Endocrinol Metab Clin North Am. 2016 Sep;45(3):605-21. doi: 10.1016/j.ecl.2016.04.010.
 Ruggiero C, Metter EJ, .... Ferrucci L. High basal metabolic rate is a risk factor for mortality: the Baltimore Longitudinal Study of Aging. J Gerontol A Biol Sci Med Sci. 2008 Jul;63(7):698-706.
 Duarte LC, Speakman JR. Low resting metabolic rate is associated with greater lifespan because of a confounding effect of body fatness. Age (Dordr). 2014;36(6):9731. doi: 10.1007/s11357-014-9731-3. Epub 2014 Dec 11.
 Pfannenberg C, Werner MK, ... Stefan N. Impact of age on the relationships of brown adipose tissue with sex and adiposity in humans. Diabetes. 2010 Jul;59(7):1789-93. doi: 10.2337/db10-0004. Epub 2010 Mar 31.
 Field AE, Austin SB, ... Colditz GA. Relation between dieting and weight change among preadolescents and adolescents. Pediatrics. 2003 Oct;112(4):900-6.
 Stice E, Cameron RP, Killen JD, Hayward C, Taylor CB. Naturalistic weight-reduction efforts prospectively predict growth in relative weight and onset of obesity among female adolescents. J Consult Clin Psychol. 1999 Dec;67(6):967-74.
 Lowe MR. Dieting: proxy or cause of future weight gain? Obes Rev. 2015 Feb;16 Suppl 1:19-24. doi: 10.1111/obr.12252.
 National Sleep Foundation’s inaugural Sleep Health Index
 Calton EK, Pathak K, ... Hamidi A. Vitamin D status and insulin sensitivity are novel predictors of resting metabolic rate: a cross-sectional analysis in Australian adults. Eur J Nutr. 2016 Sep;55(6):2075-80. doi: 10.1007/s00394-015-1021-z. Epub 2015 Aug 26.
 Sajjadi SF, Mirzaei K, ... Keshavarz SA. Vitamin D Status and Resting Metabolic Rate May Modify through Expression of Vitamin D Receptor and Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1 Alpha Gene in Overweight and Obese Adults. Ann Nutr Metab. 2018;72(1):43-49. doi: 10.1159/000485662. Epub 2017 Dec 19.
 McConnell R, Gilliland FD, ... Mittelman S. Does near-roadway air pollution contribute to childhood obesity? Pediatr Obes. 2016 Feb;11(1):1-3. doi: 10.1111/ijpo.12016. Epub 2015 Mar 27.
 CERP Policy Portal. The evolution of BMI values of US adults: 1882-1986
 Pan DA, Storlien LH. Dietary lipid profile is a determinant of tissue phospholipid fatty acid composition and rate of weight gain in rats. J Nutr. 1993 Mar;123(3):512-9.
 Riedl RA, Atkinson SN, ... Kirby JR. The Gut Microbiome, Energy Homeostasis, and Implications for Hypertension. Curr Hypertens Rep. 2017 Apr;19(4):27. doi: 10.1007/s11906-017-0721-6.
 Kavanagh K, Jones KL, ... Rudel LL. Trans fat diet induces abdominal obesity and changes in insulin sensitivity in monkeys. Obesity (Silver Spring). 2007 Jul;15(7):1675-84.
 Woods AL, Rice AJ, ... Thompson KG. The effects of intensified training on resting metabolic rate (RMR), body composition and performance in trained cyclists. PLoS One. 2018 Feb 14;13(2):e0191644. doi: 10.1371/journal.pone.0191644. eCollection 2018.
 Cadegiani FA, Kater CE. Body composition, metabolism, sleep, psychological and eating patterns of overtraining syndrome: Results of the EROS study (EROS-PROFILE). J Sports Sci. 2018 Aug;36(16):1902-1910. doi: 10.1080/02640414.2018.1424498. Epub 2018 Jan 9.
 Yong MS, Lee YS, Lee HY. Effects of breathing exercises on resting metabolic rate and maximal oxygen uptake. J Phys Ther Sci. 2018 Sep;30(9):1173-1175. doi: 10.1589/jpts.30.1173. Epub 2018 Sep 4.
 Dibner C, Gachon F. Circadian Dysfunction and Obesity: Is Leptin the Missing Link? Cell Metab. 2015 Sep 1;22(3):359-60. doi: 10.1016/j.cmet.2015.08.008.
 Ando H, Kumazaki M, ... Fujimura A. Impairment of peripheral circadian clocks precedes metabolic abnormalities in ob/ob mice. Endocrinology. 2011 Apr;152(4):1347-54. doi: 10.1210/en.2010-1068. Epub 2011 Feb 1.
 Kettner NM, Mayo SA, ... Fu L. Circadian Dysfunction Induces Leptin Resistance in Mice. Cell Metab. 2015 Sep 1;22(3):448-59. doi: 10.1016/j.cmet.2015.06.005. Epub 2015 Jul 9.
 Nguyen J, Wright KP. Influence of weeks of circadian misalignment on leptin levels. Nat Sci Sleep. 2009 Dec 16;2:9-18. Print 2010.
 Buonfiglio D, Parthimos R, ... Cipolla-Neto J. Melatonin Absence Leads to Long-Term Leptin Resistance and Overweight in Rats. Front Endocrinol (Lausanne). 2018 Mar 27;9:122. doi: 10.3389/fendo.2018.00122. eCollection 2018.
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