Certain food combos and situations dramatically impact whether or not fat is stored or burned. It goes beyond calories in, calories out. Info here.
We all know that eating too many calories and burning too few make you gain weight. But if that’s all there is to getting fat, why do sleep deprivation and chronic stress have such an impact on fat gain?
These things don’t have calories, and you can’t eat them, yet they impact whether we store fat or burn it. They also dramatically affect our hunger, motivation to work out, and cravings.
So while it’s true that calorie excess is required to gain weight, just as calorie deficits are required to lose it, this is shortsighted. The body is a highly complex biochemical machine, not a simple math equation. When you really begin to look into the question, “What makes us gain weight?” you find it’s a bit more complex than the “eat less, exercise more” model leads us to believe.
Fat gain and fat loss is multi-factorial and specific. It involves understanding individual genetics, unique metabolic expression, and psychological sensitivities. However, there does appear to be some overarching themes.
Here it is:
(F + S) x St = Fat Gain
And here’s what that means:
High fat (F) along with high sugar (S) combined with stress (St) is the recipe for fat gain.
I can hear the calorie zealots now scoffing at the ridiculousness of this assertion. Sure, you can get fat overeating anything, including broccoli and chicken breasts… except that it’s virtually impossible for any living human to do.
A high-fat/sugar combination has been shown in mammals to completely disrupt the normal metabolic regulation that occurs with either high-fat or high-sugar diets. So, this combo is not only a higher calorie diet, but it seems to assure we continue to crave high fat, high sugar foods in the future as well. The combo alters brain chemistry in a way that disrupts the natural ability to self-regulate calorie intake.
Here’s how it works: You have a control center for appetite in your brain that resides in the hypothalamus. There are chemicals that stimulate eating: Neuropeptide Y (NPY) and Agouti-related peptide (AGRP). And there’s a chemical that suppresses food intake: Proopiomelanocortin (POMC).
Think of NPY and AGRP as feeding gas pedals. They make us hungry and make us eat. Think of POMC as the brakes on food intake. If you’re wondering how hunger hormones like ghrelin and leptin figure into this, they work by impacting these chemicals.
Two diets containing the same number of calories can impact these hunger regulation chemicals differently. Fat and sugar, in combination, short-circuit the hunger centers, resulting in a constant desire for food.
A study published in the International Journal of Obesity examined this issue in rats. The animals were fed a base diet of healthy rat chow. They were then given free access to either extra fat, extra sugar, or both extra fat and sugar.
Imagine you were part of a study where the researchers gave you a normal healthy diet but then put you in a group with free access to bacon, cream cheese, and other high-fat items. That’s the high-fat group.
Or perhaps you end up in the group that got the healthy diet with additional access to cotton candy, Coca-Cola, and other high-sugar, no-fat items. That’s the high-sugar group.
Or maybe you got to be in the high fat and high sugar group, receiving a normal healthy diet plus cupboards stacked with cookies, cakes, pastries, ice cream, and other foods loaded with BOTH fat and sugar, which you could eat freely. That’s obviously the high-fat, high-sugar combo group.
Well, the rats exposed to all-you-can-eat palatable foods did what we humans do: they ate the normal rat chow and then chowed down on the fat and sugar items.
All three groups consumed extra calories and gained weight. But within a week or so, two groups, the high fat and high sugar groups, were able to self-regulate their food intake, lower their calories, and adapt by shutting off hunger.
This natural adaptation did NOT occur with the high fat and high sugar combination group. In other words, eating a high-fat, high-sugar diet caused a loss in 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 the exact same hormone response from the diets (i.e., leptin, a hunger hormone, had the same response). This caused the researchers to look for other hormones or nerve signals that may have caused this. What they discovered is that something about the high-fat, high-sugar diet was being communicated to the brain via the gut and liver.
Studies show humans, who are isolated in a metabolic chamber and given free access to highly palatable foods, do what the rats do: they overeat by huge margins.
The participants in these studies end up eating close to a 1,000-calorie surplus and gain, on average, 6 pounds in only 7 days. While the metabolism does ramp up its calorie burn as well, you can see something very detrimental happens when these types of junk foods are chosen. Several other studies show a similar effect.
There’s one more very interesting piece to this formula. Remember, we talked about the fat-storing formula as being (F+S) X St or fat combined with sugar magnified by stress. Stress is like the cherry on top of the fat-storing, hot fudge sundae.
When you think stress, you probably think cortisol. If you’re really savvy, you’ll also think catecholamines. If you’re really, really savvy, there’s one more hormone you think about: NPY.
NPY is involved with hunger in the brain, and it’s also released from the sympathetic nervous system during times of stress. When under acute stress, we release more of the catecholamines and cortisol. When we’re under chronic stress, we release more NPY.
And, unlike the catecholamines and cortisol, which are mainly catabolic hormones (i.e., they burn fat), NPY makes you gain fat, especially when it’s around cortisol. When NPY is released in large amounts, it causes fat cells to go from immature baby fat cells to full-grown, mature fat cells. And cortisol makes the body more responsive to NPY. In other words, NPY makes us grow more fat cells, and cortisol enhances its efficiency to do so.
Confused? Let me restate it:
- Chronic, continuous stress releases a unique mix of NPY and cortisol.
- Cortisol combined with catecholamines, like it is in short-term stress, helps us burn fat.
- Cortisol combined with NPY, as it is in chronic stress, equals increased fat cells.
Another interesting aside: Even when you feed mice high amounts of fat and sugar, obesity is not guaranteed. But add stress on top, and BOOM, you can induce obesity very easily.
One final note on the stress weight gain response: Low-calorie diets increase cortisol levels and perceived psychological stress. Some researchers believe this is one of the key reasons low-calorie diets fail.
If you read all this carefully, you’ll notice a couple of interesting things. A high-fat diet with the same number of calories as a high-fat/high-sugar diet has a very different impact on metabolism.
The metabolism adapts to the extra calories in a high-fat diet by decreasing appetite so that, after a few weeks, the calories are no longer high. This explains why studies on the high-fat Atkin’s diet usually show a low-calorie, not high-calorie, intake over time. The metabolism adapts.
The high fat and sugar combination creates the exact opposite changes in the hunger-signaling molecules in the brain and results in insatiable hunger that continues. Ironically, this change is almost exactly the pattern seen in starvation.
We can see that high-fat, high-sugar foods aren’t just simply high-calorie, but they also cause us to lose our ability to regulate and suppress hunger. They cause hyperphagia (the fancy medical term for continuous eating). And, when we add chronic stress on top of this, we create the perfect fat-storing atomic bomb.
The solution? Well, obviously, don’t follow the fat gain formula.
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