The Problem With Eating Less

Most people, when they start to contemplate that big weight change in their life, fall back on the calories in versus calories out method, often called CICO. But there’s a problem with this. It does not work.

That’s right. It has a 95% fail rate over a five-year period.

The big question is why. It’s logical, it makes sense, but...

In short, CICO is a misapplication of physics. Yes, energy cannot be created or destroyed. But CICO assumes the body is a simple furnace with a fixed metabolic system, a closed system, rather than a complex biological system that alters as a survival mechanism and is completely influenced by hormones. Hormones you cannot override. Hormones you cannot ignore. Hormones that tell you what to do, not the other way around.

In short, the CICO method is an oversimplification of a much more complex model.

The calorie assumption

Let’s begin with the idea of a calorie and the assumption that it equals a fixed energy unit. That assumption says a pound of fat is equal to 3,500 calories, and that reducing 3,500 calories results in a pound of loss. Thus, CICO.

It’s a neat thought. It’s tidy. It’s easy to follow. Only it’s wrong. Yep, a pound of fat is not actually 3,500. A guy called Wishnofsky proved that much. What he found turned the industry on its tail. He said a pound of fat was closer to 4,000 calories, but that it also varies from individual to individual and from food to food.

That’s right, an efficient athletic body utilizes fat differently than a sedentary person. Shocking, right? The athlete also burns a greater percentage of fat per calorie (80%) while an obese person burns less (50%). In other words, while we assume fat is approximately 9 Kcals per gram, it’s actually closer to 9.5, and for the obese, maybe as much as 11 calories per gram metabolically.

The second law of thermodynamics assumes that a calorie is a calorie, no matter the source, and this ignores the actual second law, which relates to energy efficiency and entropy. OK, so, in English, entropy is a measure of molecular disorder, randomness, or unavailable energy in a closed thermodynamic system. It represents the natural tendency of systems to evolve from order to chaos, with high entropy indicating high disorder. What does that mean to us?

Well, macronutrients can have different efficiencies in how they are used. In other words, they can be used to supply energy, store fat, or become heat energy. This is determined by total calories consumed, whether those calories are stored as fat, and the effect of insulin production. It’s also determined by whether the body they enter is fit or unfit, active or inactive. You see, not a simple system.

Plus, some foods spike insulin and increase fat storage. Other foods have little to no effect on insulin, regardless of their caloric value.

That means all calories are not created equally. They never were. Sure, a bomb calorimeter says they are, but we are not built like that. We have adjusting metabolisms and hormones, and we treat calories from different sources differently. I see some of you shaking your heads. So, let’s lay that concept out.

A calorie of sugar is not metabolically equal to a calorie of fat or protein, especially since each triggers different hormonal responses. That is what drives obesity. Saying otherwise would be like saying a Twinkie has the same outcome as the caloric equivalent of steak. They may be similar calorically, but then there are those pesky hormones and metabolic responses that make food act differently once it is inside a human than when it was sitting on a table.

Put like that, CICO doesn’t even begin to make sense, does it? Would you lose weight if all you ate were Twinkies? But what if you ate the equivalent in steak? It’s not even logical that these two substances would have similar effects on the body if consumed in equal caloric proportions. But let’s humor ourselves more.

Sugar, insulin, and fat storage

Those Twinkies are full of sugar. The sugar spikes in the blood, and the pancreas releases insulin. The insulin forces cells to absorb that sugar, including the fat cells. If you ate only 500 to 600 calories of Twinkies a day, the body would stimulate enzymes such as hormone-sensitive lipase (HSL) to absorb more calories as fat in order to survive. The metabolism would also go down in order to preserve calories.

In case I’ve lost you here, you do not want to absorb more fat while burning fewer calories on a lower metabolism, right?

That was a simple explanation, of course, and it leaves out some critical information. Not everything we eat behaves the same once it enters digestion. Some substances do more than provide energy. They send specific instructions to the cells of the body. Fructose is one such “food.” Yep, while we think of all calories being a unit of the same energy, fructose is different. Fructose leans heavily toward fat production.

We’re no longer talking about calories as a unit of energy. Now we are talking about the effect certain calories have on the body. Instead of calories being used to sustain life by being broken down into adenosine triphosphate (ATP), we are talking about fructose and how it signals fat storage, even in small amounts.

That means the calories-in part (CI) is unpredictable as far as whether you use calories as energy or store them as fat. The less active you are, the more you tend to store. Just for fun, here’s a little more information: the less muscle you have, the less energy you burn.

But fructose doesn’t care about that. It’s not broken down in the cells. It’s broken down in the liver. Too much can cause liver stress, and that triggers lipogenesis, the making of fat, which also promotes nonalcoholic fatty liver, inflammation, insulin resistance, and even fibrosis and liver cirrhosis.

The calories-out problem

Are you still with me here? If you are, you might begin to understand that the calories-out part of the equation (CO) is also not fixed. That’s right. In order for the CICO formula to work, the calories-out part must be fixed. Otherwise, any reduction in overall calories would defy the very formula it was hyped up to be.

But metabolism is known to reduce when not enough food calories are consumed. In fact, there is a sensitivity of only a 500-calorie difference between what you need and when the metabolism jumps into survival mode. Not only that, there’s something called thermoregulation, where eating too much increases heat energy and eating too little reduces it.

The CICO formula requires the CI part to work against a metabolism that remains unchanged in order to work.

But it doesn’t.

As you can now see, metabolism is not fixed. It changes to meet the demands of a body’s caloric requirement. It can burn more energy during exercise and less during sleep. It can increase heat energy if we eat too much and decrease itself if we eat too little. It is anything but fixed.

So, your metabolism is known to reduce on a low-calorie diet, and not just through thermoregulation, but also metabolically. However, food also invokes hormonal responses such as ghrelin, leptin, insulin, and a host of others that influence fat storage and use.

For instance, in the obese, the hormone adiponectin is reduced. That means a reduction in calories does not always result in linear, predictable weight loss, which is what CICO suggests.

To be clear, adiponectin is a protein hormone secreted by fat tissue that regulates glucose levels, fatty acid oxidation, and insulin sensitivity. It acts as an anti-inflammatory, anti-fibrotic, and antioxidant agent, often improving metabolic health and reducing risk factors for obesity-related diseases, cardiovascular issues, and diabetes. But the fatter you get, the less adiponectin you make. Thus, the less protection.

That also means that although the timing of metabolic adaptations with low-calorie dieting is not exactly clear during the early phase of weight loss (which is mostly water), over time, hormonal and neural regulatory mechanisms develop that trigger reductions in resting energy expenditure, protein turnover, and other metabolic processes. So, again, NOT FIXED.

The muscle problem

Now let’s consider a caloric deficit of greater than 500 Kcals a day, which has been proven to cause lean mass loss. Dieting typically causes a loss of 20% to 30% of total weight as lean tissue (muscle, bone, organs, water), often increasing to 25% to 40% with rapid weight loss or glucagon-like peptide-1 (GLP-1) medications.

This is going to affect your metabolism, or resting metabolic rate (RMR), which is slightly higher than basal metabolic rate (BMR). RMR is generally used to represent 60% to 70% of total daily energy expenditure (TDEE), thus the lion’s share of metabolic function.

Since fat is burned in muscle (or by the derivatives produced by muscle), the ability to lose weight in subsequent diet cycles becomes more difficult with each cycle and less muscle.

That means, in English, calorie-deficit diets usually cause a reduction of 20% to 40% in lean mass. That reduction comes mostly from muscle, particularly when the deficit exceeds 500 calories per day or when there is no resistance training. Then the ability to burn fat is radically affected.

While rapid, severe deficits maximize muscle loss, moderate deficits (e.g., 300 to 500 kcal/day) combined with high protein intake and resistance training can minimize, though not entirely eliminate, the loss of lean tissue. Keep in mind that non-exercising people also experience sarcopenia (natural muscle loss with age), compounding the difficulty of fat reduction.

Plus, rapid weight loss significantly reduces leptin levels https://pmc.ncbi.nlm.nih.gov/articles/PMC2430504/, which I will cover in a moment.

The body learns

So, let’s summarize. While caloric-deficit diets may appear effective for short-term weight loss, they are often criticized for being unsustainable, causing metabolic slowdown and nutrient deficiencies, promoting unhealthy relationships with food, and releasing a hormonal cascade while upregulating ApoC3. I know, right, another thing to learn.

ApoC3 is a protein primarily produced in the liver and intestine that inhibits lipoprotein lipase (LPL, which is how fat gets out of the fat cell) and hepatic (liver) uptake of triglyceride-rich lipoproteins. Elevated levels lead to high blood triglycerides (hypertriglyceridemia), weight gain, and atherosclerosis. Exercise reduces ApoC3 while dieting increases it. In short, the body learns how to store more fat on less food, but adapts into a body that releases less fat.

That makes long-term weight loss impossible. It also makes each cycle of weight loss more difficult.

Critics of CICO diets rightly argue that they ignore hormonal impacts on hunger, lead to muscle loss, and often trigger rebound eating, making them ineffective for long-term health or weight loss. CICO diets can also promote cycles of weight gain and loss, which are well associated with cardiovascular disease.

Instead of restricting, experts suggest focusing on lifestyle (increasing activity while eating enough whole foods to support it), eating nutrient-dense, high-fiber, and high-protein foods for satiety, and focusing on long-term habit changes rather than quick fixes. In other words, if you cannot sustain the diet you are on, don’t do it.

Hormones decide more than calories do

So let’s make it easier to understand. Our entire body works on energy from food. Good food produces healthy energy. Bad food upsets the delicate hormonal balances necessary to run a healthy body and triggers hunger and fat absorption.

Hormones tell your body whether to burn fat and lose weight or to store fat and gain weight. Hormones also find metabolic balance and assist in weight maintenance. It’s not the amount of calories eaten (CICO). It’s the type of calories eaten.

When it comes to your body “deciding” what state to be in, there are two key hormones that regulate food intake and energy balance: the adipocyte hormone called leptin and the pancreatic hormone called insulin. While there are many other hormone players with complex interactions between them, understanding these two hormones (which you could think of as the hormones of fat gain or loss) will give you important insight into how the diet and lifestyle choices you make can help you achieve and maintain a healthy weight.

Insulin

The hormone insulin, which is released by the pancreas in response to increased blood sugar, assists in the transport of glucose into the cells of your body and signals to the liver to convert glucose into glycogen for storage.

But there’s a problem. You don’t have an infinite ability to do this. When the glycogen stores are maxed out, increased insulin levels stimulate the production of more triglycerides, and that triggers more fat storage. (By the way, the less muscle you have, the less glycogen you can store, and your “max out” time comes sooner.)

It gets more complicated, though. Insulin does more than control blood sugar levels. It also tells the fat cells to tell the brain to stop eating.

So eat more carbs to lose weight, right? Nope, that’s not how it works, sorry. When circulating insulin enters the brain, it binds to receptors in the hypothalamus region to tell the brain to shut off hunger. This makes sense on a low-information level. You eat, blood sugars go up, insulin is released, and your brain gets the signal that you’ve had enough.

But the amount of glucose-stimulated insulin secretion is a function of body fat. The more fat you have, the more insulin you make. So far so good, right? But there’s a maximum amount of insulin that can actually cross the blood-brain barrier to stimulate satiety. As the blood concentration of insulin increases, there comes a point where no further signaling to the brain can occur.

Yep, you might have guessed it. Insulin resistance occurs when more insulin is required to maintain a normal level of blood sugar, and perhaps there are fewer insulin receptors in the brain, meaning those high levels of circulating insulin cannot depress appetite like they can in a normal body.

But here’s the problem. Eating sugar supplies the body with its need for energy. If you keep giving the body sugar, it never needs to burn fat.

Leptin

Now, fat storage cells, called adipocytes, produce a hormone called leptin. Leptin acts as a sort of negative feedback control for fatness. Leptin is secreted by the fat cells in direct proportion to the amount of fat you have.

Similar to insulin, leptin enters the brain and binds to its own receptors to trigger a reduction in hunger, and it also increases energy expenditure. Again, this makes sense. You need to be able to turn off your hunger with more than one hormone. So, now both insulin and leptin can tell you to stop.

But we can become less sensitive to leptin too, just like insulin. This can occur from being overweight, overconsuming calories, fasting, or low-calorie dieting. Did you catch that last one? Still think CICO is the way to go?

It gets more interesting too. Early researchers believed that leptin’s role was to tell the brain to stop eating, but new studies find something different. Leptin may also mediate the adaptation to fasting. Yep. And that means fasting or consuming too few calories on a regular basis can lower sensitivity to leptin, which then leads to increased hunger, cravings, and more energy conservation (burning fewer calories). Yeah, that means you gain more weight in the long term.

So, when it comes to CICO, this has important implications. Especially during weight loss regimens that lower calories more than 500 calories below normal intakes. This is augmented when those lower-calorie diets cause a loss of lean mass, which causes a lower metabolism (you burn fewer calories), and a fat cell that uptakes more fat along with an increased hunger stimulus.

See the problem? This is the main problem with CICO. It causes cycle weight gain and makes it harder to lose weight in subsequent attempts. It has a 95% failure rate, remember?

There also may be a link between leptin and cortisol release, which may explain the cortisol spikes that many experience in response to intermittent fasting. Like almost all hormones, leptin has more than one function. I believe we will find out more as we study it, but leptin has been associated with the regulation of reproductive, thyroid, human growth hormone, and adrenal axes independent of its role in energy balance.

True, as of the publication of this blog, only the hormones leptin and insulin are known to act as adiposity signals, but their interaction suggests much more.

So what do you do?

For now, it is true that leptin and insulin in the blood correlate with obesity. Thus, a reduction of obesity should begin with controlling these hormones. To be clear, they are not controlled by CICO. They are, in fact, allowed to proliferate. So your first steps in losing weight are to cycle back to the known factors:

1. Reduce or eliminate sugar and processed carbohydrates.

2. Eliminate junk foods and eat only whole foods.

3. Up your protein intake.

4. Avoid any food that spikes insulin, which also means keeping your fasting sugar levels below 100. Continuous glucose monitors are good for this.

5. Exercise programs should be focused on increasing lean mass.

6. Focus on losing about one half-pound a week. Faster weight loss forces the body into protective modes.

So, there you have it. Now you can do it the right way, right?