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January 1, 1975

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Dr James Sidbury instructed parents to feed only fat and protein up to 700 calories to their obese children - when carbohydrates are omitted, the kids with obesity are satisifed with less food. "The satiety value of such diets is superior to diets high in carbohydrate and low in fat."





A program of weight reduction in children


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We have to live with two realities: that fat cells are exquisitely sensitive to insulin, and that this is a threshold effect. The two together have profound consequences for how different foods will affect not just weight but appetites—our hunger and the foods we crave. Those consequences, in turn, speak directly to the question of whether a drastic, supposedly “unbalanced” diet that removes an entire food category may be necessary. 

As I suggested earlier, think of this fat-cell, insulin-sensitivity threshold as a switch that’s either on or off. When it’s on, above the threshold, your fat cells are storing fat; the rest of your body is fueling itself on carbohydrates. When the switch is off, when insulin is below the threshold, your fat cells are mobilizing fat; you’re burning fat for fuel; you’re getting leaner or at least not getting fatter. 

If you’re insulin resistant, these dynamics still hold true. But now you have more insulin circulating through your body than is ideal, and the amount of insulin will remain high for longer than ideal. This means you’ll spend that much more time above the threshold, with the switch on, storing fat. It’s likely this will be the case even long after you’ve eaten, after blood sugar levels have returned to normal and you might not have carbohydrates (glucose) readily available to burn. Your cells will be primed to burn carbohydrates—that’s what the insulin is telling them to do—but blood sugar will already be in the low range of healthy. And while the insulin is pushing the mitochondria in your cells to burn carbs, it’s actually pushing those same cells, through the same signaling pathway (as it’s technically known), not to burn fat and not to burn protein. Elsewhere, the insulin is causing the fat cells to hold on to fat and the lean cells to hold on to their protein. 

In short, when insulin is above the threshold, when the switch is on, your body is running on carbohydrates. They are your fuel. So it makes sense that you’ll hunger for carbohydrate-rich foods. This is likely why you may not be able to imagine life worth living without your morning bagel, or your sweets, or your pasta. (For me, it was fresh-squeezed orange juice at breakfast.) Ultimately, as we’ll discuss, these carbohydrate-rich foods become your favorites. A likely reason is that your brain has learned to respond to these foods by rewarding you with pleasure when you eat them. 

When insulin is below the threshold, when the switch is in the off position, your body is burning the fat you’ve stored. It will continue to burn fat as long as you remain below the threshold. Now your body has access to plenty of fuel. Twenty pounds of body fat provides fuel for well over two months. Even a lean marathoner like Olympic gold medalist Eliud Kipchoge, who in October 2019 ran the first sub-2-hour marathon ever, at 123 pounds, has enough fat stored to fuel his body on his fat stores alone for a week. Your body is being constantly fed on this supply of stored fat, so it’s satisfied. Your appetite will be blunted. The brain has no reason to think more food is necessary. Your body has no need to ingest more food, hence there’s little or no urge to do so. You experience weight loss—the burning of your stored body fat—without hunger.

Above the insulin threshold, you have to replenish frequently. You have a limited supply of carbohydrates, and insulin works to keep the carbohydrates you’ve stored (a maximum of about two thousand calories of glycogen) locked away as well. As your blood sugar drops, you’ll get hungry. And because carbohydrates are your fuel above the threshold, you’ll hunger for carbohydrate-rich foods. 

These dynamics almost assuredly explain the urge to eat between meals, despite how many days’ or months’ worth of calories we may have stashed away in our fat tissue. It’s why we feel hungry when we should, ideally, be happily living off our own fat. It’s why we don’t feel hungry when insulin is low and we can burn that fat. Another way to think of this is that when you’re restricting carbohydrates and insulin is below the threshold, you’re not starving your body to get fat out of your fat tissue; you’re not at war with your body to lose weight and burn fat, you’re working with it, you’re allowing your body to do what it will now do naturally. 

The relative absence of hunger on these LCHF/ketogenic diets is as consistent an observation as can be found in nutrition science. Remove the carbohydrates and replace the calories with fat, and the stimulus for hunger (and for the obsessive thinking about food that goes with calorie-restricted diets) is lessened significantly. Even those physicians and researchers in the 1960s who were convinced that eating less and semistarvation were the only way to lose weight would often comment in their papers that this didn’t mean it wasn’t easier to do so on an LCHF/ketogenic diet. As one researcher said in the most famous of the papers from this era, “The satiety value of such diets is superior to diets high in carbohydrate and low in fat.” If diets without carbohydrates are more satiating than diets with them, that’s just another way of saying that diets with carbohydrates make us hungrier than diets without. The reason they should is clear. 

My favorite example of a physician researcher designing a diet based on this awareness of insulin’s role in fat accumulation and the implications for our appetites is James Sidbury, Jr. In the mid-1970s, Sidbury was a pediatrician at Duke University and one of the world’s leading authorities on diseases of carbohydrate metabolism—in particular, rare disorders of carbohydrate (glycogen) storage, one of which is named after him. For this reason, it may have been natural for him to think of obesity as a fat-storage disease. Because he was a pediatrician who studied metabolism, the physicians in the Duke medical system would send him their (then) rare cases of children with obesity, hoping he could help them. 

Sidbury knew that carbohydrates stimulate insulin and insulin facilitates fat formation and traps fat in fat tissues. He also knew, as he noted in a 1975 book chapter on this work, that kids with obesity crave carbohydrate-rich foods—“crackers, potato chips, french fries, cookies, soft drinks, and the like.” Restrict the carbohydrates and feed these kids only fat and protein, he reasoned, and their insulin would come down, and their fat metabolism would work as it does in lean kids. These children would burn their stored fat and lose weight without obsessive hunger and without constantly grazing on carbohydrates. He instructed parents to feed their children with obesity only 300 to 700 calories a day, made up of virtually all protein and fat. The kids lost weight as if by magic. “Many parents do not believe their child can be satisfied with so little food,” Sidbury wrote. “Their attitude changes completely,” however, when they see the results and, eventually, the “obvious change in the amount of food which satisfies the children.”

Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 1709-1710). Knopf. Kindle Edition.

Topics: (click image to open)

The harm of eating carbohydrates.
Insulin is a hormone produced by the pancreas that plays a vital role in regulating blood sugar levels in the body. It allows cells to take in glucose from the bloodstream and use it as a source of energy. Insulin also helps store excess glucose in the liver for later use. In individuals with diabetes, either the pancreas does not produce enough insulin (Type 1 diabetes) or the body's cells become resistant to the effects of insulin (Type 2 diabetes). As a result, blood sugar and insulin levels can become elevated, leading to various health complications.
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