Here’s another pearl of wisdom from Four Hour Body by Tim Ferris.
Men acutely exposed to cold for two hours (in a liquid-conditioned suit perfused with 10°C [50°F] water) have been observed to increase heat production by 2.6-fold and increase the oxidation rate of plasma glucose by 138%, of muscle glycogen by 109%, and of lipids by 376%. Raising the body’s heat in response to cold exposure is done mostly by burning lipids (50%), then glycogen from muscles (30%), then blood glucose and proteins (10% each).
I will argue in this book that the fault lies entirely with the medical orthodoxy—both the belief that excess fat is caused by consuming excess calories, and the advice that stems from it. I’m going to argue that this calories-in/calories-out paradigm of adiposity is nonsensical: that we don’t get fat because we eat too much and move too little, and that we can’t solve the problem or prevent it by consciously doing the opposite.
This is the original sin, so to speak, and we’re never going to solve our own weight problems, let alone the societal problems of obesity and diabetes and the diseases that accompany them, until we understand this and correct it.
The observation that monounsaturated fats both lower LDL cholesterol and raise HDL also came with an ironic twist: the principal fat in red meat, eggs, and bacon is not saturated fat, but the very same monounsaturated fat as in olive oil.
I love eating bacon. I’m not joking when I tell people I eat a pound of bacon in one sitting.
All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.
I believe this, so does my doctor and my blood work.
The results of his seven trials have been consistent: the lower the fat in the diet and the higher the carbohydrates, the smaller and denser the LDL and the more likely the atherogenic pattern B appears; that is, the more carbohydrates and the less fat, the greater the risk of heart disease.
In the case of diet and heart disease, Ancel Keys’s hypothesis that cholesterol is the agent of atherosclerosis was considered the simplest possible hypothesis, because cholesterol is found in atherosclerotic plaques and because cholesterol was relatively easy to measure. But as the measurement technology became increasingly more sophisticated, every one of the complications that arose has implicated carbohydrates rather than fat as the dietary agent of heart
I am reading this awesome new book on my Kindle. Get it if you want to lose fat or go from “Geek to Freak” by gaining huge amounts of muscle.
It’s both fun to read and informative.
RULE #4. DON’T USE SKEPTICISM AS AN EXCUSE FOR INACTION.
As the good Dr. Noakes also said to me about one Olympic training regimen: “This [approach] could be totally wrong, but it’s a hypothesis worth disproving.” It’s important to look for hypotheses worth disproving. Science starts with educated (read: wild-ass) guesses. Then it’s all trial and error. Sometimes you predict correctly from the outset. More often, you make mistakes and stumble across unexpected findings, which lead to new questions. If you want to sit on the sidelines and play full-time skeptic, suspending action until a scientific consensus is reached, that’s your choice. Just realize that science is, alas, often as political as a dinner party with die- hard Democrats and Republicans. Consensus comes late at best. Don’t use skepticism as a thinly veiled excuse for inaction or remaining in your comfort zone. Be skeptical, but for the right reason: because you’re looking for the most promising option to test in real life. Be proactively skeptical, not defensively skeptical. Let me know if you make a cool discovery or prove me wrong. This book will evolve through your feedback and help…
Gary Taubes has a new book coming out…Here’s an article he wrote on his blog to tide you over until it’s available.
Simply put, anyone who tries to diet by any of the more accepted methods (i.e., Weight Watchers), and anyone who decides to “eat healthy” as its currently defined, will remove the carbohydrates from the diet that may be — if the carbohydrate/insulin hypothesis is correct — the most fattening. And if they’re trying to cut calories, they’ll be removing some number of total carbohydrates as well. And if these people lose fat on these diets, this is a very likely reason why.
Accepting that high-calorie diets can lead to greater weight loss than semi-starvation diets requires overturning certain common assumptions.
It does seem like quite a stretch but I’m living proof. I am down 65 pounds in since April of 2010.
Insulin is the fatness culprit:
By the mid-1960s, four facts had been established beyond reasonable doubt: (1) carbohydrates are singularly responsible for prompting insulin secretion; (2) insulin is singularly responsible for inducing fat accumulation; (3) dietary carbohydrates are required for excess fat accumulation; and (4) both Type 2 diabetics and the obese have abnormally elevated levels of circulating insulin and a “greatly exaggerated” insulin response to carbohydrates in the diet.
Here’s a little bit on how it works:
This remarkably dynamic process, however, is regulated by a remarkably simple system. The flow of fatty acids out of the fat cells and into the circulation depends on the level of blood sugar available. The burning of this blood sugar by the cells—the oxidation of glucose—depends on the availability of fatty acids to be burned as fuel instead. A single molecule plays the pivotal role in the system. It goes by a number of names, the simplest being glycerol phosphate. This glycerol-phosphate molecule is produced from glucose when it is used for fuel in the fat cells and the liver, and it, too, can be burned as fuel in the cells. But glycerol phosphate is also an essential component of the process that binds three fatty acids into a triglyceride. It provides the glycerol molecule that links the fatty acids together.†116 In other words, a product of carbohydrate metabolism—i.e., burning glucose for fuel—is an essential component in the regulation of fat metabolism: storing fat in the fat tissue. In fact, the rate at which fatty acids are assembled into triglycerides, and so the rate at which fat accumulates in the fat tissue, depend primarily on the availability of glycerol phosphate. The more glucose that is transported into the fat cells and used to generate energy, the more glycerol phosphate will be produced. And the more glycerol phosphate produced, the more fatty acids will be assembled into triglycerides
This link show’s passages that others have quoted using their Kindles…Pretty cool stuff from both the book and the Kindle.
In Good Calories, Bad Calories Gary Taubes reviews the medical research that established connections between fat and cholesterol in our diets and heart disease. Traubs shows how this well accepted dogma has never been proven and makes a clear case that carbohydrates are responsible for obesity. The “diseases of civilization” are exacerbated by following the advice of these studies and subscribing to a fat is bad hypothesis.
I’m currently reading the first section and the reviews of the research that lead us to believe in low-fat diets is startling.
Here are a few truths that most Americans, including doctors, would consider blasphemous.
Dietary fat does not make us fat
The link to dietary cholesterol and blood cholesterol levels is very weak or non-existant
Lowering total cholesterol does not improve mortality rates
Wild and crazy I know. Read the book…it will make more sense.