The conventional wisdom of our health professionals is that a calorie is a calorie. "From a purely thermodynamic point of view, this is clear because the human body or, indeed, any living organism cannot create or destroy energy but can only convert energy from one form to another."
That’s what Andrea C. Buchholz and Dale A. Schoeller from the Department of Nutritional Sciences, University of Wisconsin-Madison wrote and the prestigious American Journal of Clinical Nutrition published three years ago.
But it’s not true. It depends on what you eat.
Most of us with type 2 diabetes want to lose weight. On a typical high-carbohydrate diet the establishment tells us that we should eat even less fat. That seemed to make sense because each gram of fat has 9 calories, more than twice as much as the four calories that each gram of carbohydrate or protein has.
As we all know, that’s a tough path to descend.
On the other hand, our body’s chemistry is radically different on a low-carb diet. A calorie from one source doesn’t act like one from another source.
Dr. Richard K. Bernstein learned this experimentally. The leading exponent of a low-carb diet for people with diabetes and the author of Dr. Bernstein’s Diabetes Solution (third edition, 2007), Dr. Bernstein answered 50 questions in his telecast last week.
This was the question and answer that interested me the most:
Q. What’s the best way to prevent weight loss without increasing the carbo, increasing the fat or protein or both?
A. This reminds me of an experiment that I did many years ago when I had patients on a low carbo diet, all of whom were taking insulin and they all wanted to gain weight. So I gave them extra fat in the form of olive oil to the tune of a shot glass in the morning and a shot glass in the afternoon. This was 3 ounces of extra calories, which boiled down to 900 extra calories a day. Over the course of 6 months not one of four patients gained a pound. So giving fat on a low carbo diet will not make you fat. You will metabolize it. It’s been proven subsequently. On a low carbo diet you metabolize your fat, rather than store it.
Unlike Dr. Bernstein’s questioner and the four patients in his experiment, I would like to lose a few more pounds, not prevent weight loss or gain weight. But I am now following a low-carb diet. Since I don’t have all those carbs in my diet like I used to have, can I really eat a lot more fat and still lose weight?
So far, it looks like I can. I have liberalized my fat intake with no weight gain and possibly some weight loss.
Then I wrote Dr. Bernstein. The way it works, he suggested, was through "insulin sensitive lipase." Googling that term, I found his explanation online:
The beta oxidation (or "burning") of fat by the body requires the action of an enzyme called insulin-sensitive lipase. This enzyme is turned off by insulin. Eating carbohydrate obliges the body of a nondiabetic to make insulin in proportion to the amount consumed and obliges many diabetics to inject insulin to prevent blood sugar elevation. When insulin levels go up, fat oxidation therefore goes down, and since insulin is also the fat-storage hormone, dietary fat is stored. Furthermore, insulin signals the liver to convert the carbon backbone of carbohydrates (glucose) to saturated fat, which then appears in the blood as triglycerides, which are subsequently stored. So calories of fat are handled much differently on a low-carbohydrate diet than on a high-carbohydrate diet. Recent studies on humans eating equivalent amounts of fat show that those eating more carbs store more fat.
But that raised another question. What recent study was Dr. Bernstein referring to that showed that people eating more carbs store more fat?
First, he provided some background on his experiment with the four people he gave 900 extra calories of olive oil a day.
"When I was treating them with olive oil there was a problem of taste," Dr. Bernstein told me. "What I ended up with that everyone liked was Myers’s dark rum. Why did I pick that? Because I knew alcohol was miscible with oil and was more likely to disguise the flavor. Everyone liked it.
"So we had these people doing this for six months. I couldn’t understand how we got that miraculous result. 900 extra calories a day. No effect on weight.
"I called the head of biochemistry at my medical school who was a friend of mine and who specailized in carbohydrate and fat metabolism. He had no idea, which sort of surprised me, and he asked arround all his buddies in that field. No one had any idea."
Then, Dr. Bernstein saw an article in a professional journal. "And when he read that, he said to himself, "‘Ah, of course’ It’s lipoprotein-lipase, also called insulin-sensitive lipase. These enzymes gets turned off by insulin. So if you have high insulin levels you cannot break down fat. Furthermore, we know that insulin is the major fat-building hormone. You can only build it and you can’t break it down if you are on a high carbo diet."
Unfortunately, Dr. Bernstein didn’t remember just where or when he read that study. So he asked me to search a few years’ worth of Diabetes and Diabetes Care. "I need that article so badly for so many arguments," he told me.
Being able to help someone who has done so much for people with diabetes as well as to learn something for this article was enough to activate my research gene. Working together, we found the article today.
The April 2000 issue of Diabetes contained the article, "Increase in Fat Oxidation on a High-Fat Diet Is Accompanied by an Increase in Triglyceride-Derived Fatty Acid Oxidation" by Patrick Schrauwen and four of his colleagues.
The Diabetes study investigated the mechanism behind the oxidation - rather than the storage - of fat on a high-fat diet. It suggested that insulin might play a role. But, they concluded, "The mechanism behind the increase in fat oxidation on a high-fat diet is unknown."
Now, seven years later, thanks to the work of Dr. Bernstein and of Gary Taubes we know that the mechanism is lipoprotein-lipase, which works to oxidize our dietary fat, except when our insulin levels are high.
In his important new book, Good Calories, Bad Calories, Taubes explains how lipoprotein-lipase works. Any cell that uses fatty acids for fuel or stores fatty acids uses it. When a triglyceride-rich lipoprotein passes by in the circulation, the lipoprotein-lipase will grab on, and then break down the triglycerides inside into their component fatty acids. This increases the local concentration of free fatty acids, which flow into the cells, either to be fixed as triglycerides if these cells are fat cells, or oxidized for fuel if they’re not.
What’s the primary regulator of lipoprotein-lipase activity? It’s insulin. In fat tissue, insulin increases lipoprotein-lipase activity, while in muscle tissue, it decreases activity. As a result, when insulin is secreted, fat is deposited in the fat tissue, and the muscles have to burn glucose for energy. When insulin levels drop, the lipoprotein-lipase activity on the fat cells decreases and the lipoprotein-lipase activity on the muscle cells increases. The fat cells release fatty acids, and the muscle cells take them up and burn them.
There’s still another way of looking at the carb problem, which seems to me to be an especially damning conclusion. "As long as we respond to the carbohydrates by secreting more insulin," Taubes writes, "we continue to remove nutrients from our bloodstream in expectation of the arrival of more, so we remain hungry, or at least absent any feeling of satiation. It’s not so much that fat fills us up as that carbohydrates prevent satiety, and so we remain hungry."
Now that I understand both the theory and practice of eating a low-carb diet, I relish the freedom that it gives me to eat the fats I love. Will the last 10 pounds that I want to lose just melt away? I will let you know here.
David Mendosa was a journalist who learned in 1994 that he had type 2 diabetes, which he wrote about exclusively. He died in May 2017 after a short illness unrelated to diabetes. He wrote thousands of diabetes articles, two books about it, created one of the first diabetes websites, and published a monthly newsletter, “Diabetes Update.” His very low-carbohydrate diet, A1C level of 5.3, and BMI of 19.8 kept his diabetes in remission without any drugs until his death.