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Misconceptions on Calories In and Calories Out

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JP Rushton

Richard Lynn

L:inda Gottfredson

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2550 words

(To those from “myproana.com”, DO NOT misconstrue what I wrote here. What I wrote here is perfectly understandable. I am NOT saying that “you have no metabolism”. My point is, low kcal dieting CAN and WILL destroy your metabolism. The literature is vast on this subject and it’s waiting for you to read it. Any further confusions, please comment and I will answer your questions.)

“Eat Less and move more!!! That’s how you lose weight!” What people who don’t understand about human metabolism and homeostasis is that when caloric reduction occurs, the body drops the metabolism to match the amount of kilocalories (kcal) it is receiving. Thus, weight will plateau and you will need to further decrease caloric consumption to lose more weight. In this article, I will go through what a calorie is, common misconceptions of Calories In and Calories Out, the reasons for metabolic slow down,  the process of thermodynamics that people who don’t understand this research cry out whenever it’s said, and finally starvation experiments that prove metabolic slow down occurs during a decrease in caloric intake and how this metabolic slow down persists after the diet is over.

A kilocalorie is the heat required to raise 1 kilogram of water 1 degree celsius. This definition is used whenever people say ‘Calorie’.

Misconceptions on kcal in/kcal out

  1. One of the biggest misconceptions people have on Calories In/Calories out is that these variables are independent of each other. However, they are extremely dependent variables.  When you decrease Calories In, your body decreases Calories Out. Basically, a 20 percent reduction in kcal will result in a 20 percent reduction in metabolism which the end result ends up being minimal weight loss.
  2. The next big assumption people have about Calories In and Calories Out is the assumption that the Basal Metabolic Rate (BMR) remains stable. Of course, measuring the caloric intake is simple. However, measuring caloric outtake is a much more complicated process. When ever the Total Daily Energy Expidenture (TDEE) is spoken of, that involves the BMR, thermic effect of food, nonexercise activity thermogenesis (the energy expidenture of all activities sans sports), excess post-exercise consumption (EPOC, a measurably increased rate of oxygen intake following increased oxygen depletion), as well as exercise. the TDEE can increase or decrease by as much as 50 percent depending on caloric intake as well as the aforementioned variables.
  3. The third misconception people have is that we have conscious control over what we eat. We decide to eat when we are hungry (obviously). But numerous hormonal factors dictate the decision on when to eat or when to stop. We stop eating when we are full, which is hormonally mediated. Like breathing, the regulation of body fat is under automatic control. Just like we don’t have to remind ourselves to breath or remind our heart to beat, we don’t need to remind ourselves to eat. Thus, since hormones control both Calories In and Calories Out, obesity is a hormonal, not caloric disorder.
  4. The fourth misconception is that fat stores are essentially unregulated. However, every single system in the body is regulated. Height increases come from growth hormones; blood sugar is regulated by insulin, glucagon, and numerous other hormones; sexual maturation is regulated by testosterone and estrogen (as well as the hormone leptin which I will return to later); body temperature is mediated by a thyroid-stimulating hormone, among numerous other biologic factors. Though, we are told that the production of fat cells is unregulated. This is false. The best researched hormone on the storage of fat cells that we know of is the hormone leptin which was discovered in 1994. So if hormones dictate fat gain, obesity is a hormonal, not caloric disorder.
  5. And the final misconception is that a calorie is a calorie. This implies that the only important variable on weight gain is caloric intake and thus all foods can be reduced to how much caloric energy they have. But a calorie of potatoes doesn’t have the same effect on the body as a calorie of olive oil. The potatoes will increase the blood glucose level, provoking a response from the pancreas, which olive oil will not. Olive oil is immediately transported to the liver and has no chance to induce an insulin response and so there is no increase in insulin or glucose.

All five of these assumptions have been proven false.

[9/21/16 edit:]


Calories in/out implies that during extended caloric restriction no matter the type of kcal (fat, CHO, protein, alcohol, except when alcohol is ingested your body puts fat storage on hold until all alcohol is metabolized from the body. You can see how wiith chronic drinkers as they are obese a lot of the time, with there being a strong link between alcoholism and obesity as there are nunmerous pathways related with each other that lead to excessive eating as well as dependance on alcohol and other drugs) ingested, as long as caloric restriction is continued that weight (fat) loss will be achieved. CICO adherents say that “a calorie is a calorie”, but what’s funny with that statement is that is violates the Second Law of Thermodynamics. Naturally, to CICO adherents since “a calorie is a calorie”, kcal would be restricted from fat since it’s the most calorie dense macro (alcohol coming in second at 7 kcal per gram). By doing this, CHO will be increased, as is recommended by all of the ‘experts’. “Increase CHO, fat leads to CD!!!” This isn’t true, that’s another reason for cutting fat, the supposed ‘increased risk of heart disease”. However, when this occurs, insulin is spiked and when insulin is spiked the body doesn’t use the fat stores for energy it uses the glucose from the carbs.

Putting this all together, let’s say someone’s TDEE is 2000 kcal per day (for a 14k kcal per week average) and they reduce it to 1200 kcal and go on a LFHC diet like is commonly recommended. Insulin remains high and therefore fat cannot be tapped into. This is due to the CICO mantra (which violates the 2nd LoT) “a calorie is a calorie” that leads people to believe that all calories are ‘equal’ in terms of hormonal responses in the body. Let’s take a piece of bread and a teaspoon of olive oil. When you eat the piece of bread, insulin is spiked in response to the glucose from the carbohydrate. When you drink the olive oil, it’s immediately absorbed by the liver eliciting no insulin spike. Clearly, with a long term LFHC diet, this will consistently occur and the body will be continuously using CHO for energy and not the fat stores as insulin is continuously spiked in the body. Insulin either tells the body to store fat or not burn it for energy. Eventually, over time, this leads to insulin resistance (however, insulin resistance may precede obesity and diabetes) and more metabolic problems amongst a myriad of other variables.

As kcal is reduced to 1200 per day, the body is forced to match its metabolism to what your intaking as it can’t get energy from anywhere else since “a calorie is a calorie”. This happens during any calorie restricted diet and is why diets are doomed to fail. This same thing happened with The Biggest Loser contestants. Notice how The First Law of Thermodynamics isn’t broken? It’s irrelevant.

See how the mantra “a calorie is a calorie” violates the Second law of thermodynamics and fails because the CICO model doesn’t take insulin into the equation, which is a causal factor with obesity?


[End edit]

The correlation between weight gain and caloric consumption has recently been discovered. Ladabaum, et al (2014) examined trends in obesity from 1988 to 2010. The trends they observed were: obesity, abdominal obesity, physical activity and caloric consumption in US adults. They discovered that the obesity rate increased at .37 percent per year while caloric intake remained virtually the same.

The Law of Thermodynamics

The first law of thermodynamics states that energy can not be created nor destroyed in an isolated system (this is important). People often invoke the LoT to support the Calories In and Calories Out model. Dr. Jules Hirsch says in this NYT article:

There is an inflexible law of physics – energy taken in must exactly equal the number of calories leaving the system when fat storage is unchanged. Calories leave the system when food is used to fuel the body. To lower fat content – reduce obesity – one must reduce calories taken in, or increase output by increasing activity, or both. This is true whether the calories come from pumpkins or peanuts or pâtés de foie gras.

To quote MD Jason Fung, author of The Obesity Code:

But thermodynamics, a law of physics, has minimal relevance to human biology for the simple reason that the human body is not an isolated system. Energy is constantly entering and leaving. In fact, the very act we are most concerned about-eating-puts energy into the system. Food energy is also excreted from the system in the form of stool Having studied a full year of thermodynamics in university, I can assure you that neither calories nor weight gain were mentioned even a single time. (Fung, 2016: 33)

We assume with the model of the calorie-balancing scale that fat gain or fat loss is unregulated, however, no system in the body is unregulated like that. Hormones tightly regulate all bodily functions. Body fat is no exception. The body actually has numerous ways in which to control body fat. Distribution of energy is the problem with fat accumulation. Too much energy is diverted to fat creation as opposed to body-heat production. Most of this is under automatic control, except exercise (which even then, there is a genetic basis for motivated exercise). We can’t decide whether or not to allocate calories to nail production or increase stroke volume. These metabolic processes are almost impossible to measure, and thus most assume that it’s relatively constant. Particularly, Calories In is not assumed to change in response to Calories Out. We assume these are independent variables. Reducing calories in only works if calories out remains constant. However what we find is that a sudden reduction of Calories In leads to a similar reduction of Calories Out and no weight is lost as the body balances its energy budget.

Starvation experiments

In 1919, a landmark study was carried out by Francis Benedict. The volunteers in the study agreed to a semi-starvation diet ranging from 1400 to 2100 kcal, approximately 30 percent of the subject’s bodyweight. The question was whether or not decreased caloric intake lead to a decrease in metabolism. The results were shocking.

The subjects experienced a 30 percent reduction in metabolism, with their initial caloric expidenture being 3000 kcal dropping to 1950 kcal. A 30 percent reduction in kcal resulted in a 30 percent decrease in metabolism. The First Law of Thermodynamics is not broken. 

Towards the end of WWII, Dr. Ancel Keys wanted to improve understanding of starvation and better help Europe after the War. With an average height of 5 feet 10 inches and an average weight of 153 pounds, these were normal men, which Dr. Keys wanted to see the effects of a semi-starvation diet on those with a normal weight. For the first three months of the study, they were given slightly over 3000 kcal. Though over the next six months, they were given 1570 kcal. Eventually, some men were decreased to less than 1000 kcal a day. They were given a diet of foods high in carbs and low to no animal meat as that was the condition in Europe at the time. Moreover, they also had to walk 22 miles a week as exercise. Again, the results were shocking.

Dr. Keys showed that they had a 40 percent decrease in metabolic rate. The body decreased its metabolism to match the amount of calories consumed. They showed a 20 percent decrease in strength, a significant decrease in heart rate (55 to 35 beats per minute), stroke volume decreased by 20 percent, body temperature dropped to 95.8 degrees Fahrenheit (which makes sense since less caloric consumption means less energy for the body to convert into heat), physical endurance dropped by half, blood pressure dropped, they became tired and dizzy and finally their hair and nails grew extremely brittle. They couldn’t stop thinking about food. Some of them wrote cookbooks, others dreamed about food. They became obsessed with eating. All of these causes go directly back to decreased caloric consumption as the amount of heat produced by the body decreased due to an increase in caloric consumption. In sum, the body responds to a decrease in caloric intake by dropping metabolism.

Metabolic slow down

Recent data has come out on decreased energy expidenture due to dieting from contestants on the show The Biggest Loser. The contestants were followed for six years after the show ended. Fothergill, et al (2016) showed that after six years, most contestants gained back the original weight they lost, but their metabolism was still decreased by 600 kcal.

The mean metabolic adaptation had increased to 500 kcal per day, which explains why RMR remained 700 kcal per day below the baseline level despite a 90 lb body weight regain. The researchers even said that this large metabolic difference couldn’t be explained by the different calirometer used at the end of the six year period. 

Substantial weight loss induces biological changes that promote weight gain.

Moreover, after a period of dieting, your brain panics and thinks it’s starving. During this time, the the production of the hunger hormone ghrelin increases. Levels of this hormone increase right before a meal and steadily decrease after. This is one of the many hormones that control when we’re hungry and this is one of the many reasons why diets fail and do not work long term.

Our bodies have homeostatic mechanisms that cause us to gain back or lose weight whenever caloric consumption is increased or decreased. The main cause is the body weight set-point which I will cover in a future article.

And a quote from Sandra Aamodt’s book “Why Diets Make Us Fat“:

“Leibel finds that metabolic suppression persists in dieters who have kept weight off for one to six years, so he scoffs at claims that the successful weight loss story disproves his ideas. “If you talk to people who’ve done it – not the studies, but people who actually manage to lose weight and keep it off – they’ll tell you what I’m telling you,” he says: that the only way to achieve this goal was to allow themselves to be hungry all the time while increasing their physical activity substantially. Indeed, his point is supported by data on the eating and exercise habits of people listed in the National Weight Control Registry, who have lost at least thirty pounds and kept it off for one year. A calorie calculator says that Dennis Asbury should have needed 2,100 calories to maintain his weight at 150 pounds, but instead he found that he needed to eat 400 to 500 calories less than that. Such metabolic suppression is the difference between being within the defended range and being below it. Many people blame others for eating too much or exercising too little, assuming incorrectly that both are under voluntary control, but it’s much harder to justify holding people responsible for diet-induced changes in the way the body burns energy.” (Aamodt, 2016, pg. 68)

Conclusion

The fact of the matter is, kcal in and out is completely misunderstood due to a non-understanding of human metabolism. As we decrease our caloric intake, our body adjusts its metabolism down to match the amount of kcal we are currently consuming. This is why Calories In and Calories Out does not tell the whole story. Our body constantly fights to maintain what is normal, its set-point. When thrown out of what the brain considers ‘normal’ the brain through the hypothalamus does whatever it can to get us back to its set-point. Thus, obesity is a hormonal, not a caloric disorder.

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4 Comments

  1. ni67 says:

    My biggest problem with this is that…

    Mass is proportionable to food eaten/drinks dranked

    Obviously metabolism/ATP/oxidative phosphorylation/glycolysis/respiration is involved.

    Obviously horomones are released to bring you back to a homeostatic balance, by either making you more hungry or be more efficient with cellular respiration or by limiting growth rate/etc.

    However, no matter how many cravings of food and no matter how much efficiency gains can be made, when you walk or do any work (force proportional to distance), your body has to break down chemical bonds to create heat/let you move. I didn’t eat for a week or more before (somehow) and nearly lost 10lb-15lb (most was water). This is obviously a caloric deficit/mass deficit.

    Nearly all mass lost has to be through respiration or excretion or evaporation.

    Your body can’t just simply say, oh I’ll eat 50% calories less and therefore your body will utilize 50% less “energy”, especially if you are doing tons of non-exercise activity thermogenesis (although it might make you do it less often).

    The problem I have with the conclusion that obesity is a hormonal disorder is that if you put any individual from Canada/US to Japan who were/was previously obese, these individuals will be forced to adapt to smaller portion sizes as a result of high economic cost/a million other factors/social ostrachization (propensity for self-control), and will ultimately lose weight by caloric reduction.

    Various studies have been done on alternate fasting, caloric restriction, diet modification, caloric restriction with excerise and they all lead to the same conclusion of a drop in some % of BMI. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516560/

    So while yes, it’s not as simple as energy in and energy out, I fail to see how your body can systematically lower heat thermogenesis to zero or how change in adiposity distribution or glyclolytic/ketogenesis/biomolecule break-down changes affect the macro level process of creating “thin air mass” into your body to counteract the effects of pure caloric reduction.

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    • RaceRealist says:

      Mass is proportionable to food eaten/drinks dranked

      Yes it is.

      Obviously horomones are released to bring you back to a homeostatic balance, by either making you more hungry or be more efficient with cellular respiration or by limiting growth rate/etc.

      More the first. When in a caloric deficit for an extended amount of time, the hunger hormones Neuropeptide Y (PPY) and ghrelin to name two, increase in the body. Conversely, satiety hormones such as leptin decrease. So due to these physiologic effects, you want to eat more and it’s hard to feel full because of the blunted satiety hormones. This, obviously, is an evolutionary mechanism.

      I didn’t eat for a week or more before (somehow) and nearly lost 10lb-15lb (most was water). This is obviously a caloric deficit/mass deficit.

      Of course it was mostly diuresis. The longest I’ve ever fasted was for 48 hours. It’s great I love it. Some studies show that 4 days of fasting increase metabolic rate 17 percent.

      Nearly all mass lost has to be through respiration or excretion or evaporation.

      Of course. On the other hand, energy can be stored as fat as well. The point of this piece was to show that ‘a calorie is not a calorie’. Saying that is fallacious and violates the 2nd Law of Thermodynamics. To say that calories only can and should be broken down to how much caloric energy they contain clearly is not working. Because all calories are not equal once in the body. Yea you can burn food in a bunsen beaker and see 4 grams for protein, 4 for carbs and 9 for fat, but when you eat it different things happen in your body (some spike insulin more, some less, which is the driver of obesity).

      Kcal out also does not stay constant. Exercise is also not the only equation in kcal out as well. It’s way more complicated. Exercise isn’t even good for weight loss.

      Your body can’t just simply say, oh I’ll eat 50% calories less and therefore your body will utilize 50% less “energy”, especially if you are doing tons of non-exercise activity thermogenesis (although it might make you do it less often).

      That’s pretty much what happens. Your metabolic rate increases or decreases depending on how much you eat. When in a caloric deficit for an extended amount of time, your body stops doing so many involuntary movements as your getting less energy. Then weight loss will plateau, you need to further decrease kcal and then the diet gets broken due to hormones and the brain.

      The problem I have with the conclusion that obesity is a hormonal disorder is that if you put any individual from Canada/US to Japan who were/was previously obese, these individuals will be forced to adapt to smaller portion sizes as a result of high economic cost/a million other factors/social ostrachization (propensity for self-control), and will ultimately lose weight by caloric reduction.

      Japan is coming over to our Standard American Diet (65 percent CHO, 20 percent protein, 15 percent fat). But without refined carbohydrates and other sugary foods, serum insulin won’t be spiked as much and weight loss can occur.

      Also, you can’t willpower your way to weight loss and obesity is not about a lack of willpower.

      Various studies have been done on alternate fasting, caloric restriction, diet modification, caloric restriction with excerise and they all lead to the same conclusion of a drop in some % of BMI.

      I love IF. Been doing it almost 7 years. With a low-fat diet, weight loss can be achieved. Because you solved the insulin problem. But, diets don’t usually work.

      Dieting is a stressor on the body. Cortisol increases. This is the physiologic response to either fight or flight. When this occurs, insulin increases with it. Body fat is stored and fat burning is put on hold until the glucose is metabolized. Then and only then when the glucose is metabolized and serum insulin levels are low can fat burning occur.

      Since the conventional wisdom from the “experts”, ADA, AMA, NIH and other health organizations get funding from Big Food. Coca-Cola funded a study showing that sugar is OK. Basically saying “a calorie is a calorie”, even though saying that violates the Second Law of Thermodynamics. They spend billions to “show” that soda and the like don’t cause obesity. These drinks are loaded with sugar and sugar spikes insulin. Big Food pays a lot of these people and they fund a lot of studies in an attempt to show that their processed garbage is ‘healthy’ and ‘not fattening’.

      With the carbohydrate-insulin hypothesis, we see why weight loss doesn’t occur. Sugar and other refined carbohydrates are the cause for the obesity epidemic, as insulin drives weight gain and obesity.

      So while yes, it’s not as simple as energy in and energy out, I fail to see how your body can systematically lower heat thermogenesis to zero or how change in adiposity distribution or glyclolytic/ketogenesis/biomolecule break-down changes affect the macro level process of creating “thin air mass” into your body to counteract the effects of pure caloric reduction.

      It’s not about thermogenesis getting to 0, it’s about the body matching its metabolic rate with how much you’re eating (adaptive thermogenesis). The more people eat, their metabolism increases. A study done on Vermont prisoners shows that metabolism increased when people overfed. It was tightly controlled and the researchers eventually upped their caloric intake and they gained 30 percent of their weight. When put back on their regular diets they effortlessly lost weight. This is evidence for the body weight set point (BWSP).

      The point is, a calorie is not a calorie. Eating carbs in place of fat spikes your insulin more. Insulin raises the BWSP causing secretion of ghrelin, PPY and other hunger hormones blunting the satiation hormones. This makes you eat more to get to the set weight. Decreases in expenditure come about due to getting fat.

      We don’t get fat because we eat more, we eat more because we get fat. When the set point is raised higher due to the intake of processed carbs and excessive insulin, this causes one to eat more and decrease expenditure. Insulin tells the body to either store fat or not burn it for energy. Glucose is burned for energy, and fat cannot be tapped into due to the insulin increased in the body due to the glucose, thus the glucose gets used for energy and not fat.

      Insulin inhibits breakdown of fat in adipose tissue by inhibiting the intracellular lipase that hydrolyzes triglycerides to release fatty acids.

      Insulin facilitates entry of glucose into adipocytes, and within those cells, glucose can be used to synthesize glycerol. This glycerol, along with the fatty acids delivered from the liver, are used to synthesize triglyceride within the adipocyte. By these mechanisms, insulin is involved in further accumulation of triglyceride in fat cells.

      From a whole body perspective, insulin has a fat-sparing effect. Not only does it drive most cells to preferentially oxidize carbohydrates instead of fatty acids for energy, insulin indirectly stimulates accumulation of fat in adipose tissue.

      Physiologic Effects of Insulin

      Lastly, we have gotten fat over the past 50 years since we were told that fat was bad and carbs were good. Moreover, we have went from 286 minutes between meals to 210 minutes, a 30 percent decrease. We have sent from 3 meals a day to 5. We continuously spike our insulin. We're constantly in a glucose burning state and not a fat burning state due to the increased insulin and glucose in the body.

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  2. ni67 says:

    Here is a personal example. I travelled to my “home country” and ate more and more. My weight gain was incredulous as I was offered food all the time.

    I came home and ate normally, my weight returned back to a ‘set point’ and I did not feel ‘hungrier’.

    So perhaps its more of the fact that we have a ‘set point’ that our body is adapted to being used to, and that it is in fact modifiable if we drop the weight down systematically to a level where we are at x pounds, then rebound back x+y pounds by slowly increasing food intake to stabilize our new ‘set point’ – thereby preventing the upregulation/sensitivity responses of hunger instead of chronic dieting everyday.

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    • RaceRealist says:

      So perhaps its more of the fact that we have a ‘set point’ that our body is adapted to being used to, and that it is in fact modifiable if we drop the weight down systematically to a level where we are at x pounds, then rebound back x+y pounds by slowly increasing food intake to stabilize our new ‘set point’ – thereby preventing the upregulation/sensitivity responses of hunger instead of chronic dieting everyday.

      That’s the point. Decrease insulin, decrease the set point. Though, lowering body weight indefinitely for many people is hard to impossible. This is due to the body set weight.

      Though when the body is at a high weight for a while, that’s what the brain becomes used to. The brain doesn’t know the difference between obese and nonobese, so when in a caloric deficit, your brain releases the aforementioned hormones.

      The hypothalamus regulates food intake through insulin and glucose (sugar).

      The researchers discovered that when the brain is low on glucose, a hypothalamic enzyme is triggered called AMPK, which changes the properties of the molecules called PPY that the brain uses to communicate. This occurs because of autophagy, which is the process alluded to when the title said “Consumption from within“. Autophagy is a natural destructive mechanism in which the body disassembles, through a regulated process (like all bodily processes, including body fat, are) unnecessary or dysfunctional cellular components. This allows our body to recycle and reuse cells.

      The hypothalamus activates AMPK which sets increased autophagy into motion. This cellular process then dictates how Neuropeptide Y (PPY) and POMC act on a cellular level showing us how increased food intake and weight gain occur.

      Basically, combining the results of all of their studies show that knocking down AMPK changed the PPY and POMC expression at a genetic level and decreased caloric intake and weight loss occurred.

      Then ithe article says:

      By demonstrating how AMPK-activated autophagy controls the expression of neurohormones in the brain’s hypothalamus, researchers are one step closer to understanding the dynamics of our eating behavior. The next step is to untangle how autophagy itself modulates (up or down) our brain’s neurohormones, such as NPY, to regulate our appetite.

      When the brain doesn’t get enough glucose, it activates AMPK which then has the brain release PPY and POMC to have you eat more to further the cellular regeneration. As described above, since autophagy is the cellular process to break down and recycle useless cells, what’s probably going on here is that when the autophagy process occurs, the brain tells you to eat more through the PPY and POMC hormones so cellular regeneration can occur due to the autophagy destroying useless cells.

      This study is huge. It shows that when AMPK is activated, that it changes how PPY and POMC work on a genetic level. Those two hormones control appetite.

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