Certain food combinations and situations can greatly affect whether fat is stored or burned. It goes beyond calories in, calories out. Information here.
We all know eating too many calories and consuming too few can make you gain weight. But if that’s all about getting fat, why do sleep deprivation and chronic stress have such a big impact on fat gain?
These things have no calories and you can’t eat them, but they affect how we store or burn fat. They also greatly affect our hunger, motivation and desire to exercise.
So while it is true that gaining weight requires an excess of calories, just as losing weight requires a calorie deficit, this is short-sighted. The body is a highly complex biochemical machine, not a simple mathematical equation. When you actually start looking at the question, “What’s making us fat?” you’ll see that it’s a bit more complicated than the “eat less, exercise more” model we’d lead us to believe.
Fat gain and fat loss are multifactorial and specific. It involves understanding individual genetics, unique metabolic expressions, and psychological sensitivities. However, there do seem to be some overarching themes.
here it is:
(F + S) x St = fat gain
What does it mean:
High fat (F) and high sugar (S) combined with stress (St) is the recipe for fat gain.
I can hear calorie fanatic Now laugh at the absurdity of that statement. Of course, you can binge eat anything, including broccoli and chicken breasts… except that’s pretty much impossible for anyone alive.
The high fat/sugar combination has been shown in mammals to completely disrupt the normal metabolic regulation that occurs on a high fat or high sugar diet. So this combination is not just a high-calorie diet, but seems to ensure that we will continue to crave high-fat, high-sugar foods in the future. The combination alters brain chemistry in a way that disrupts the natural ability to self-regulate calorie intake.
Here’s how it works: Your brain has an appetite control center located in the hypothalamus. There are chemicals that stimulate feeding: neuropeptide Y (NPY) and agouti-related peptide (AGRP). There is also a chemical that inhibits food intake: proopiomelanocortin (POMC).
Think of NPY and AGRP as feeding the gas pedal. They make us hungry and make us eat. Think of POMCs as a brake on food intake. If you’re wondering how hunger hormones like ghrelin and leptin work, they work by affecting these chemicals.
Two diets containing the same number of calories had different effects on these hunger-regulating chemicals. The combination of fat and sugar short-circuits the hunger centers, resulting in constant cravings for food.
A study published in the International Journal of Obesity looked at this question in mice. The animals were fed a basal diet of healthy rat chow. Then they’re free to get extra fat, extra sugar, or extra fat and sugar.
Imagine you’re part of a study where researchers give you a normal healthy diet, but then put you in a group where you’re free to eat bacon, cream cheese, and other high-fat foods. That is the high fat group.
Or maybe you end up in the healthy-eating group with extras for marshmallows, Coca-Cola, and other high-sugar, fat-free treats. That is the high sugar group.
Or maybe you have to be in the high fat and sugar group and eat a normal healthy diet, plus a cupboard full of cookies, cakes, pastries, ice cream and other foods high in fat and sugar that you can eat as you please. That’s clearly the high-fat, high-sugar combo group.
Well, mice exposed to unlimited amounts of palatable food did what we humans do: they ate normal mouse chow, then gorged on fatty and sugary treats.
All three groups burned extra calories and gained weight. But over a week or so, the two groups, the high-fat group and the high-sugar group, were able to self-regulate their food intake, lower their calories, and adapt by eliminating hunger.
This natural adaptation did not occur in the high-fat and high-sugar combination group. In other words, eating a high-fat, high-sugar diet can lead to a loss of the ability to properly regulate appetite, almost like an appetite-stimulating drug.
The researchers noticed that the high-fat group and the fat/sugar combo group had exactly the same hormonal response to the diet (ie, leptin, a hunger hormone, had the same response). This led researchers to look for other hormones or neural signals that might be causing this. They found that something about the high-fat, high-sugar diet was being communicated to the brain through the gut and liver.
Studies have shown that humans sequestered in metabolic chambers and given free access to very tasty food do what mice do: they overeat.
Participants in these studies ended up eating close to 1,000 extra calories and gained an average of 6 pounds in just 7 days. While it’s true that your metabolism increases your calorie burn as well, you’ll find that something very harmful happens when you choose these types of junk food. Several other studies have shown similar effects.
There is also a very interesting part to this formula. Remember, the fat storage formula we’re talking about is (F+S) X St or the combination of fat and sugar amplified by stress. Stress is like the cherry on top of a hot fudge sundae that stores fat.
When you think of stress, you probably think of cortisol. If you’re really savvy, you’ll also think of catecholamines. If you’re really, really savvy, there’s another hormone that comes to mind: NPY.
NPY is associated with hunger in the brain, and it is also released from the sympathetic nervous system during times of stress. During acute stress, we release more catecholamines and cortisol. When we are under chronic stress, we release more NPY.
And, unlike catecholamines and cortisol, which are primarily catabolic hormones (i.e., they burn fat), NPY will make you gain fat, especially when it’s in the vicinity of cortisol. When NPY is released in large quantities, it causes fat cells to transform from immature baby fat cells to fully mature fat cells. Cortisol makes the body more responsive to NPY. In other words, NPY makes us grow more fat cells, while cortisol makes it more efficient.
Confused? Let me reiterate:
- Chronic, ongoing stress releases a unique blend of NPY and cortisol.
- Cortisol binds to catecholamines, just like during short-term stress, to help us burn fat.
- Cortisol binds to NPY as it is under chronic stress, equating to increased fat cells.
Another interesting side note: Even when mice are fed lots of fat and sugar, they don’t necessarily become obese. But add stress to it, BOOM, and you can easily induce obesity.
A final note on the stress weight gain response: A low-calorie diet increases cortisol levels and perceived psychological stress. Some researchers believe this is one of the key reasons low-calorie diets fail.
If you read through all of them, you’ll find some interesting things. A high-fat diet with the same number of calories as a high-fat/high-sugar diet has very different effects on metabolism.
this metabolism Adapt to the extra calories in a high-fat diet by reducing your appetite, so after a few weeks, the calories are no longer high. This explains why studies of high-fat Atkin diets typically show low rather than high caloric intake over time. Metabolic adaptation.
The combination of high fat and high sugar produces the exact opposite changes in hunger signaling molecules in the brain and leads to a constant feeling of insatiable hunger. Ironically, this change is almost exactly the pattern seen in starvation.
We can see that high-fat, high-sugar foods are not only high in calories, but also make us lose our ability to regulate and suppress hunger. They can cause hyperphagia (the medical term for persistent eating). And, when we add chronic stress on top of that, we create the perfect fat storage atom bomb.
solution? Well, obviously, don’t follow a fat gain formula.
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