August 2, 1893
Elliott P. Joslin
Dr. Joslin Makes First Entry in Diabetic Ledger
Dr Joslin begins a ledger on diabetes after meeting a frail young Irish girl named Mary Higgins who was suffering from Type 1 Diabetes. He prescribed a low carb diet and recorded all of his cases over his entire career in his ledger.
On this day in 1893, a student at Harvard Medical School made the first entry in a ledger he would keep for the rest of his long career. Elliott Joslin examined a frail young Irish girl, who was suffering from diabetes. Long before he became one of the world's leading authorities on diabetes, he understood the importance of careful documentation. Keen observation of his patients helped him develop a novel approach to the treatment of diabetes. He prescribed a strict diet that regulated blood sugar levels and helped patients manage their own care. The introduction of insulin in 1921 confirmed the effectiveness of Joslin's approach. Elliott Joslin saw 15 patients a day until a week before his death in 1962, at age 93.
Unlike many other men who made Boston a center of medical innovation, Elliott Joslin was born in Massachusetts — in the town of Oxford, 40 miles west of Boston. The son of a wealthy shoe manufacturer, Elliott was an unusually focused, driven young man. He attended Yale College, graduated at the top of his Harvard Medical School class, and served an internship at Massachusetts General Hospital. After additional study in Europe, he returned to Boston in 1898 and opened a private office in the house his father had bought in the Back Bay.
Although Joslin had been interested in diabetes since medical school, he began his career as a general practitioner. Physicians who specialized in one particular disease were still rare in American medicine, and it would be almost 20 years before Elliott Joslin emerged as one of the most influential people in the study and treatment of diabetes.
Mary Higgins's case sparked his interest and convinced him of the need to chart in detail the course of a patient's illness. Joslin began keeping a diabetic ledger in 1893; Mary Higgins was the first entry in the first volume. He documented every patient he treated for the next 70 years. Eventually, his ledgers filled 80 volumes and became the central registry for diabetes in the United States, the first system for recording patient diabetes data outside of Europe.
January 1, 1963
Human Nutrition and Dietetics
Nutrition textbook writes “the intake of foods rich in carbohydrate should be drastically reduced since over-indulgence in such foods is the most common cause of obesity.”
In 1963, Sir Stanley Davidson and Dr. Reginald Passmore wrote in the textbook Human Nutrition and Dietetics, the definitive source of nutritional wisdom for a generation of British medical practitioners, that “the intake of foods rich in carbohydrate should be drastically reduced since over-indulgence in such foods is the most common cause of obesity.” They didn’t understand yet why physiologically this was the case—it was just then being worked out in laboratories—but the fact seemed undeniable. That same year Passmore coauthored an article in the British Journal of Nutrition that began with the declaration: “Every woman knows that carbohydrate is fattening: this is a piece of common knowledge, which few nutritionists would dispute.”
Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 479-484). Knopf. Kindle Edition.
January 1, 1975
A program of weight reduction in children
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."
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.
January 1, 1985
George Blackburn and Bruce Bistrian of Harvard Medical School create the protein-sparing modified fast to treat patients with obesity: 650-800 calories a day of nothing but lean fish, meat, and fowl. It had effectively no carbohydrates. In 700 patients over 4 months, they lost 50 pounds on average while feeling little hunger. However, Blackburn and Bistrian thought this diet was lethal due to being high in saturated fat.
Another example of this thinking also dates to the 1970s and comes from George Blackburn and Bruce Bistrian at Harvard Medical School. Bistrian and Blackburn developed what they called a “protein-sparing modified fast” to treat patients with obesity: 650 to 800 calories a day of nothing but lean fish, meat, and fowl. It had effectively no carbohydrates, making it a ketogenic diet, albeit a very low-calorie version. Bistrian and Blackburn prescribed the diet to thousands of patients, as Bistrian told me when I interviewed him in January 2003, and half of them lost at least forty pounds. In one 1985 publication reporting on almost seven hundred patients, the average weight loss was nearly fifty pounds in four months. The patients felt little hunger while on the diet. “They loved it,” Bistrian said. “It was an extraordinarily safe way to get large amounts of weight loss.”
But one point that Bistrian made in our interview was critically important: If he and Blackburn had tried to balance these diets by adding, say, vegetables, whole grains, and legumes, meaning the patients would obviously be eating more calories and more carbohydrates, the diets would have failed. You’d think more calories would mean less hunger, but it would cause more. Bistrian was the first one who pointed out to me the different responses between Ancel Keys’s starvation experiment subjects—eating 1,600 calories a day and, well, starving—and the experiences of the patients he and Blackburn were working with, or Sidbury was treating, who were perfectly content consuming far fewer than 1,000 calories a day. “The proof of the pudding,” he said to me, “was in the eating.”
Alas, Bistrian and Blackburn’s thinking, and Sidbury’s, was flawed. They were telling their patients—Sidbury’s were kids; Bistrian’s and Blackburn’s were adults—to severely restrict calories because that was what they still thought was necessary. Despite everything they knew about insulin and fat metabolism, they too couldn’t escape the trap of energy balance thinking. Because Bistrian and Blackburn were feeding their patients so few calories, this created a problem that appeared to the two researchers to be insurmountable. It had to do with maintaining the weight loss.
For a diet to work for a lifetime, it has to be maintained for a lifetime, and for a diet to work—to get us lean, or relatively so—it has to remove or limit the cause of why we get fat. If the cause is too many calories, then a lifetime of calorie restriction at some level is necessary. If the cause is elevated insulin levels and too many carbs, then a diet that maintains insulin at a low threshold for a lifetime—carb-restricted, high in fat—is necessary. There seems no getting around it. Bistrian and Blackburn were perfectly aware of this problem. They knew that if their patients went back to eating the way they did, they’d gain the weight back. If they ate more calories but still worked to keep insulin low, they’d be restricting carbohydrates and replacing them with fat. They’d be eating what Bistrian and Blackburn thought of as an Atkins diet. And unless you believed that eating all that fat was benign—as many physicians finally do today—that was unacceptable. Bistrian said this was a primary reason he and Blackburn left the field. They had two choices, they thought: Tell their formerly fat patients to take appetite-suppressing drugs so they could spend a lifetime battling hunger on a calorie-restricted but balanced diet, or tell them to eat the Atkins/ketogenic way, to satiety of fat and protein. They considered neither to be a safe option. “All that saturated fat,” Bistrian said to me. He and Blackburn turned their attention to other things. We don’t have that luxury.
Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 1733-1734). Knopf. Kindle Edition.
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