A doctor from Mexico emailed today to tell me he enjoyed the previous two posts on calories. He apologized for his English (which a lot better than my Spanish), so I cleaned up the spelling and punctuation a bit, but here’s how he views the explanation that people get fat because they consume more calories than they burn:
It’s like saying it rains because water falls from the sky.
Somebody replies, “No, really, WHY did it rain?”
And you shout, “BECAUSE WATER FELL FROM THE SKY! ARE YOU DUMB?”
Yes, it’s true that when it rains, water drops fall from the sky, but that is not WHY it rains. You are simply saying it’s raining because it’s raining. What is the meteorological explanation? What conditions get together to cause the rain?
And later in the email:
In weight gain, the cause in the majority of the cases is the alteration of the hormonal pathway that normally controls that area of the physiology. The human body has multiple mechanisms of regulation. For everything else, scientists have very complex biochemical explanations. But for obesity, all they have is a religious explanation of gluttony and sloth, expressed in a mathematical form.
The hormone that controls the storage of energy is insulin. There are other factors in obesity, but all of them are affecting the hormonal, physiological mechanisms of control.
Well said, Doctor – in any language.
As for those other factors, I thought I’d mention a couple that I left out of the previous posts because the posts were already lengthy.
How many fat cells do you have?
This is an area I hope gets a lot more attention in future research. Apparently scientists have only known since 2008 that the number of fat cells we carry as adults is constant. Here are some quotes from a New York Times article:
Every year, whether you are fat or thin, whether you lose weight or gain, 10 percent of your fat cells die. And every year, those cells that die are replaced with new fat cells, researchers in Sweden reported Sunday.
The result is that the total number of fat cells in the body remains the same, year after year throughout adulthood. Losing or gaining weight affects only the amount of fat stored in the cells, not the number of cells.
“There is a system waiting to be discovered,” said Dr. Jeffrey S. Flier, an obesity researcher and dean of Harvard Medical School.
Dr. Flier and other obesity researchers cautioned, though, that even if scientists knew how the fat cell system worked, it was not clear that it would be safe or effective to treat obesity by intervening. One of the hard lessons of the past couple of decades has been that the body has redundant controls to maintain weight.
Redundant controls to maintain weight? Nawww, this stuff’s simple. If you consume fewer calories, your body goes and retrieves calories from your fat cells to make up the difference, and you lose weight. Works that way for everyone … although I seem to recall writing this in the Fat Head Kids book, in the chapter where we explained that Marty Metabolism, the ship’s chief engineer, is like a super-complicated software application:
Like all important apps, Marty’s code includes something called redundancy. That’s a programmer’s term that means if one block of code doesn’t work, the program switches to another … and another, and another, until the command is obeyed.
Anyway, back to the New York Times article:
“This is a new way of looking at obesity,” said Dr. Lester Salans, an obesity researcher and emeritus professor at Mount Sinai School of Medicine in New York.
“I suspect that the body’s regulation of weight is so complex that if you intervene at this site, something else is going to happen to neutralize this intervention,” Dr. Salans said.
Complex regulation? If you intervene, the body may respond by neutralizing the intervention somewhere else?
Geez, these obesity researchers just don’t seem to get it. It’s a simple matter of calories in vs. calories out, so just cut the calories. No other intervention needed.
There was a time a few decades ago, before the current interest in how the brain regulates how much is eaten, when obesity researchers spent all their time studying and discussing fat cells. Investigators discovered that fat people had more fat cells than thin people and that fat cells shrank with weight loss and bulged with weight gain.
The result was the fat cell hypothesis, a notion that obsessed researchers. Fat cells, the hypothesis said, are laid down early in life and after that, they can change only in size, not in number. When people lose weight and their fat cells shrink, that creates a signal to fill the cells again, making people regain.
There’s more to the article, but here’s the important point: Yes, it appears that when we get fatter as kids, we do so mostly by creating new fat cells. But when we get fatter as adults, we do mostly by enlarging our existing fat cells.
I poked around online for more information and found that some researchers believe (but haven’t proved) the number of fat cells we’re born with is largely genetic. In other words, people with a tendency to get fat easily — a trait that clearly runs in families — may have been carrying more fat cells from birth.
I also found that lean people typically have between 25 billion and 35 billion fat cells, while fat and obese people may have anywhere from 75 billion to 150 billion fat cells. (Another study, by the way, demonstrated that adults can grow new fat cells if they gorge themselves to gain weight quickly, but it’s a few billion, not an extra 100 billion.)
So … let’s suppose I make it to adulthood at a lean 15% body fat and have 30 billion fat cells. Let’s also suppose I’m six feet tall and weigh 200 pounds. That means I’m carrying 30 pounds of fat – one pound for each billion fat cells. Let’s suppose that’s the normal size for fat cells.
Now suppose my best friend is also six feet tall and has about the same lean body mass, but is cursed with 150 billion fat cells, perhaps because of genetics, or perhaps because he became very fat as a kid. Or perhaps a bit of both.
If his fat cells are the same size as mine, he’ll be carrying 150 pounds of fat. I weigh 200 pounds (170 lbs. lean, 30 lbs. fat), but he weighs 320 pounds (170 lbs. lean, 150 lbs. fat). I’m at 15% body fat, he’s at 47% body fat … but our fat cells are the same size.
If I live on pizza and beer during my 20s and balloon up to 250 pounds, I’m not saying it would easy to lose the weight. But to return to 200 pounds, I’d only have to shrink my overly-large fat cells back to their normal size.
But for my obese buddy to get down to 200 pounds, he’d have to shrink all his fat cells to one-fifth their normal size and keep them shrunk. I’d be very, very surprised if those redundant controls to maintain weight don’t fight against that.
So if change my diet and get back down to a lean 200 pounds, and my buddy changes his diet but only manages to get down to 245 pounds, it still means he shrunk his fat cells to half their normal size, while I merely shrunk mine back to normal. I’d be a bit of a jackass if I judged him a failure because he’s still 45 pounds overweight. His weight loss was almost certainly more difficult than mine, and will be more difficult to maintain.
In my review of the 2017 low-carb cruise, I wrote this:
Another lecture I enjoyed was delivered by Erynn Kay, a physician’s assistant who works with Dr. Jeffrey Gerber. She spoke about the importance of feeding our good gut bacteria – a topic I don’t believe gets enough attention in low-carb circles. Our hunter-gatherer ancestors weren’t gathering bacon, after all. They were gathering plants with fibers that feed the gut microbiome.
If you’re trying to lose weight by living on cheeseburgers, bacon, eggs, butter, heavy cream and a bit of broccoli now and then, you’re not feeding your gut bugs. Bad idea. That’s why there’s a chapter in the Fat Head Kids book titled To stay healthy, you need to feed trillions of your closest friends.
One of the low-carb doctors who does write extensively about the importance of feeding the gut microbiome is Dr. William Davis, author of Wheat Belly and, more recently, Undoctored.
Speaking of Undoctored, pardon me while I go on a bit of sidebar rant …
In Undoctored, Dr. Davis stresses again and again that we can’t simply trust the health-care system (which he points out is a sick-care system that has little to do with health) to take care of us. We have to pay attention and be our own advocates.
We saw another example of that recently. Chareva’s father was hobbled by a stroke many months ago. He’s also an insulin-dependent type 2 diabetic. He recently fell and broke his hip while trying to limp to the bathroom in the middle of the night.
After surgery to repair the hip, he was placed in a rehab center. Someone forgot to tell someone else he’s a diabetic, even though it was written on the admission form. He wasn’t given insulin for four days, and only then because Chareva’s mom asked someone on the staff how his blood sugar was doing. Then, and only then, did a nurse finally check his blood sugar. It was over 600, and had probably been that high since he was admitted.
In an age when one-fourth of all senior citizens are type 2 diabetics, how in the @#$% do you not check a 75-year-old man’s blood sugar?
Don’t just trust the medical staff to pay attention and do their jobs. Ask. Demand.
End of rant.
Anyway, here’s a video by Dr. Davis I think everyone on a low-carb or keto diet should watch and consider carefully:
In a post back in 2015, I explained why I went back to a high-protein diet. It’s still low-carb, but not VLC, and not ketogenic. I gave the same explanation, albeit more briefly, during a Q&A session aboard the low-carb cruise later that year.
(Jimmy Moore was so upset with me for explaining why I dropped the keto diet, he bought me drinks in the bar later, encouraged me to give another presentation on the next cruise, and made plans to visit over Thanksgiving. You know how these with me or against me types think.)
Going with a low-carb approach (75 to 100 grams per day, sometimes a bit more) certainly gives me more flexibility. I like that. But more importantly, it means I can eat more of the foods that feed the gut microbiome.
Since I knew I’d be writing this post tonight, I measured and counted the ingredients in two of my meals today instead of just eyeballing them. I looked up the calorie and macro counts. I also checked my blood sugar reactions.
Breakfast was three eggs, two tablespoons of butter, a cup of shredded cheese, and a medium potato — cooked and cooled and then rewarmed. Add plenty of salt, mash it all together, and it’s delicious. It comes out to 770 calories, 37 grams of protein, 32 carbs. An hour later, my glucose peaked at 121. It was at 85 an hour after that.
Dinner was 4 ounces of chicken breast meat, one cup of refried black beans, one cup of shredded Mexican cheese, two tablespoons of sour cream, some hot sauce, and a big scoop of salsa. It comes out to 640 calories, 55 grams of protein, 41 carbs, and – the important part – 13 grams of fiber from the black beans. That’s the feed-the-gut-bugs part of the meal. My glucose peaked at 110.
In a podcast interview with Tim Ferriss, Dr. Peter Attia said most of the patients he put on ketogenic diets did very well. They lost weight and their lab markers moved in the right direction. But he said a dozen or so patients didn’t do well at all. Their markers moved in the wrong direction, and some of them gained weight quickly. So he did the smart thing and took them off the diet.
When asked, he said he doesn’t know why some people don’t get good results. Based on what Dr. Davis explained in the video, I’d say failure to feed the good gut bacteria might be part of the problem.
So don’t do that. Feed your little friends.
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