Selected excerpts (turned into a lot of excerpts as the book was rather well-spoken)...
It (insulin) prompts cells in your lean tissues and organs to take up carbohydrates and use them for fuel; it inhibits them from burning fat and lets that fat escape back into the circulation, where it can be returned to storage. Insulin simultaneously causes the fat tissue to hold on to fat and the muscle cells to do the same with protein. Protein consumption also stimulates secretion of two other hormones, glucagon and growth hormone, the former of which will work to limit fat storage, while the latter will help promote growth and repair.
With insulin decreasing, the fat tissue will eventually experience that negative stimulus of insulin deficiency, and the fat cells will release the fat from storage—they will mobilize it—and we will burn that fat for fuel. This is what happens or should happen between meals; it happens overnight while we’re sleeping, and it will happen for days, weeks, or even longer if we have to survive a lengthy famine or self-imposed period of fasting.
Since we have such limited storage space, our bodies have three options: Use the carbohydrates for energy, which at least puts them to use; turn them into fat, which the liver will do if necessary; or dispose of them in our urine...
Without that negative stimulus of insulin deficiency—if insulin remains elevated above some unknown baseline threshold—we will store fat.
Excess fat, specifically above the waist, is an exceedingly good sign of insulin resistance, in which case insulin is indeed elevated higher than it should be and elevated for longer than it should be.
High blood sugar, which you can have when you either are diabetic or have eaten a carb-rich meal, will prompt your pancreas to secrete insulin, which in turn will prompt you to burn the carbohydrates for fuel, store glucose as glycogen and fat, and prompt your fat cells to store the fat you’ve eaten and the fat made from glucose and hold on to the fat it already has.
Insulin is the signal that the body has been fed carbohydrates. The fat we eat won’t stimulate insulin secretion.
(“The first principle” of science, as the Nobel laureate physicist Richard Feynman put it so aptly, “is that you must not fool yourself and you’re the easiest person to fool.”)
(The reality is that virtually all hormones, with the notable exception of insulin, are technically fat-mobilizing hormones, although they won’t mobilize fat when insulin is elevated. The insulin signal overrides that of these other hormones.)
Ketones are measured in units of millimoles per liter, abbreviated as mmol/l. On a typical carbohydrate-rich diet, your ketone level is likely to be about 0.1 mmol/l, which is the product of the liver’s ketone body synthesis machinery idling in the background state. If you go twelve hours without eating, which you’ll often do in your life—from finishing dinner at seven p.m., say, to having breakfast at a reasonable hour the next morning—your pre-breakfast ketone body levels will have tripled, up to 0.3 mmol/l, as your insulin is low and your liver is synthesizing ketones to help feed your brain, if nothing else. Continue to fast for more than several days, and you’ll be at 5 to 10 mmol/l. † On an Atkins diet—aka nutritional ketosis—your ketones might be as high as 2 or 3 mmol/l. After exercise on the same diet, when insulin is very low, you might even hit 5 mmol/l, all relatively low numbers compared to those in diabetic ketoacidosis, the state that so justifiably worries physicians and diabetes specialists.
In diabetic ketoacidosis, fat cells dump their stored fat into the circulation, the liver wildly synthesizes ketones, and carbohydrates are not being taken up and used for fuel at anything like the rate that’s necessary. Meanwhile the liver is also generating glucose to use for more fuel. All these fuels are accumulating in the bloodstream, and pathological, metabolic hell is clearly breaking out: Ketone body levels in diabetic ketoacidosis are typically well over 20 mmol/l. This is a condition to be rightly feared, but it is an entirely different physiological state than nutritional ketosis.
In other words, as Yalow and Berson pointed out, if you’re actually getting fatter, your fat cells must be responding to insulin regardless of what is happening elsewhere in your body. Your fat cells must still be insulin sensitive. It seems to be a precondition of the fattening process.
It means that fat cells sense and respond to the presence of insulin in the circulation at levels so low that other cells and tissues don’t even know it’s there, and fat cells continue to respond to insulin long after those other cells and tissues become resistant.
Worth noting is that ketones themselves stimulate some insulin secretion, and the insulin secretion in turn inhibits ketone synthesis. This is a naturally occurring negative feedback loop that prevents ketone levels from getting pathologically high merely from changing our diets.
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.
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.
Willpower, however, had little or nothing to do with it. Those who are lean and insulin sensitive cannot imagine the hunger for carbohydrates that will be induced in those predisposed to fatten, in those who are insulin resistant, when confronted by this aroma and the thought of the bun. It is a subjective experience that lies outside their ability to understand because they never experience it.
One reason all diet authorities now agree more or less that we should cut back on our consumption of highly processed grains (white flour) and sugars (sucrose and high-fructose syrups) is that these refined grains and sweet refined sugars are relatively new to human diets.
Recall what the hundred-plus Canadian physicians wrote in HuffPost about their observations, their experiences, when their patients embraced LCHF/ketogenic eating: “What we see in our clinics: blood sugar values go down, blood pressure drops, chronic pain decreases or disappears, lipid profiles improve, inflammatory markers improve, energy increases, weight decreases, sleep is improved, IBS [irritable bowel syndrome] symptoms are lessened, etc. Medication is adjusted downward, or even eliminated, which reduces the side-effects for patients and the costs to society. The results we achieve with our patients are impressive and durable.” Physicians who now prescribe these diets commonly say that they rarely if ever prescribe drugs to their patients for blood sugar control or hypertension; rather, they de-prescribe, they get patients off medications. That’s compelling testimony.
The results of those five studies were consistent. The participants eating the LCHF/ketogenic high-fat diet lost more weight, despite the advice to eat to satiety, than those who ate the American Heart Association and the British Heart Foundation recommended low-fat, low-saturated-fat diet. Moreover, their heart disease risk factors showed greater improvement.
Since then, as of the spring of 2019, close to one hundred, if not more, clinical trials have published results, and they confirm these observations with remarkable consistency. The trials are still incapable of telling us whether embracing LCHF/ketogenic eating will extend our lives (compared to other patterns of eating the authorities might recommend), but they continue to challenge, relentlessly, the conventional thinking on the dangers of high-fat diets, and they tell us that in the short term, this way of eating is safe and beneficial.
In June 2019 Hallberg and Virta Health published a paper on how two years of LCHF/ketogenic eating had influenced heart disease risk factors in its subjects. The bottom line was that twenty-two of twenty-six established risk factors improved (compared to what these physician researchers call “usual care”), three remained unchanged, and only one—LDL cholesterol—on average got worse. When the Virta Health researchers worked out the numbers for what’s called the “aggregate atherosclerotic cardiovascular disease risk score,” a measure of ten-year risk of having a heart attack developed by the American College of Cardiology and the American Heart Association, the Virta Health patients decreased their risk of having a heart attack by over 20 percent, compared to the usual treatment program for diabetes and all the drug therapies typically prescribed. Even with the rise in their LDL cholesterol, these patients got significantly healthier, as did their hearts.
Just as the evidence has inexorably accumulated over the years supporting the observation that LCHF/ketogenic diets make us healthier, the evidence supporting the idea that saturated fat is deadly and that we should all eat low-fat diets has been fading, despite the best efforts of the orthodoxy to prop it up.
Now, thirty years later, the most recent unbiased review of this evidence—from the Cochrane Collaboration, an international organization founded to do such impartial reviews—concluded that clinical trials have failed to demonstrate any meaningful benefit from eating low-fat diets
By the mid-1990s, though, the experts who assembled a seven-hundred-page report on this question for the World Cancer Research Fund and American Institute for Cancer Research— Food, Nutrition and the Prevention of Cancer —could find neither “convincing” nor even “probable” reason to believe that fat-rich diets were carcinogenic.
While LDL does seem to play a role in the atherosclerotic process, it’s not the cholesterol in the particle that’s the active player but rather the LDL particle itself and specifically the number and maybe the size of particles in circulation.
Finally, the medical community has known since 1977 (if not twenty years earlier) that low HDL cholesterol is a far better predictor of heart disease than high LDL cholesterol, many times more likely to be regrettably right, and that high triglycerides are at least as predictive as high LDL.
Both clinical trial data and clinical experience tell us that this body-wide disruption of metabolic syndrome—the disruption that appears to begin with insulin resistance and so elevated levels of insulin and poor blood sugar control—is normalized or corrected by removing the carbohydrates from the diet and replacing them with fat.
Researchers have known, at least since the 1970s, that carbohydrate consumption lowers the apparently beneficial HDL cholesterol compared to eating fats, and that it raises triglycerides as well.
As for blood pressure, insulin induces your kidneys to hold on to sodium. (Salt is sodium chloride, and the sodium is the player here.) This is one of the many things insulin does. When your insulin levels are high, your kidneys retain sodium rather than excreting it in urine.
By then, though, we were all being told that high blood pressure was caused by eating too much salt, another speculative hypothesis that continues to suffer from a dearth of experimental, clinical trial evidence. It was embraced nonetheless. It sounded right, and so the authorities believed it. We believed it because they did, and we never let it go.
Anyone who makes an ironclad guarantee for any way of eating—that one diet will assuredly make you live longer than others—as Gladwell suggested and I tend to agree, is probably selling something (although perhaps with the best of intentions).
A diet that restricts carbohydrates and replaces those calories with fat corrects your weight by lowering it. It corrects your blood pressure by lowering it. It corrects your inability to control your blood sugar. It’s not the equivalent of taking a pill that will make you healthy; rather, it removes what makes you unhealthy, replaces those calories with a benign macronutrient (fat), and in so doing, fixes what ails you.
The message should be straightforward: Carbohydrate-rich foods are fattening. Or to complicate it slightly such that naturally lean people might more likely understand: For those of us who fatten and particularly those who fatten easily, it’s the carbohydrates that we eat—the quantity and the quality—that are responsible. The relevant mechanism appears to be simple, as well: Carbohydrate-rich foods—grains, starchy vegetables, and sugars—work to keep insulin elevated in our circulation, and that traps the fat we eat in our fat cells and inhibits the use of that fat for fuel.
When we consume these sugars, the glucose enters the circulation, becomes blood sugar, and stimulates an insulin response, but the fructose mostly doesn’t. It’s metabolized first in the small intestine and then the liver. These organs, the liver particularly, are then tasked with the job of metabolizing an amount of fructose, day in and day out, which they are apparently ill-equipped to do.
Like any device tasked to do a job it isn’t designed to do, the liver does a poor job of metabolizing this daily flood of fructose. Liver cells use as much of the fructose as they can to generate energy, but they convert the rest, the excess, to fat. Reasonably reliable research suggests that this fat is trapped in liver cells, leading to a condition known as nonalcoholic fatty liver disease, which is associated with obesity and diabetes
Robert Cywes, a pediatric surgeon who now runs bariatric surgery and weight-control programs for adults and adolescents in Florida, said to me, “To cut to the chase, we are a carbohydrate substance abuse program, not a weight