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When people find out I’m into this crazy diet stuff, they often ask: so what?
Is this whole blog just a valentine to the Atkins diet?
Don’t get me wrong. I love me my low carb. I credit the diet for helping me lose 20 pounds of fat and dramatically improving my HDL and triglyceride levels (as it often does for people).
But the concept I’ve been obsessed with — the Black Box — is a fundamentally distinct idea from low carb. I believe it has new lessons to teach us; and it offers us a chance to resolve paradoxes that have stymied obesity research for decades and that threaten to destroy our health care system and broader economy if unchecked.
Call me a zealot, but I believe the Black Box, or something like it, may be our only hope. :]
First some background…
A Brief Overview of the “Diet Wars”
99.99% of people think about obesity from the “Calories Count” perspective. When we eat too much and/or fail to exercise, we store excess calories as fat. The solution is to do the opposite: eat less, move more.
A ragtag group of rebels rejects this concept. These folks don’t blame overall calories per se as much as they blame carbohydrate calories. Famous advocates of this “Carbs Count” camp have included Alfred Pennington, Herman Taller, Robert Atkins, and Gary Taubes. Their basic thesis (I’m oversimplifying) is that excess carbs, not excess calories, make us fat. Low carb diets, therefore, may be the key to fat loss.
The often-ugly battle between the “Calories Count” and “Carbs Count” factions has raged for decades. Taubes and Dr. Peter Attia recently amassed an exhaustive catalogue of the research that’s been done on the topic here. Their non-profit, the Nutrition Science Initiative (NuSI), seeks to answer, definitively, which side is right.
Developed by pre-World War II European clinicians and resurrected by Taubes in his books Good Calories, Bad Calories and Why We Get Fat, Lipophilia tells us that what really matters is the balance of biochemical forces acting on the fat cells in our fat tissue.
Here’s the money quote, from a Vienna geneticist named Julius Bauer, who wrote these words way back in 1929:
“Like a malignant tumor or like the fetus, the uterus or the breasts of a pregnant women, the abnormal lipophilic [fat loving] tissue seizes on foodstuffs, and even in the case of under nutrition… It maintains its stock, and may increase it independent of the requirements of the organism. A sort of anarchy exists: the adipose [fat] tissue lives for itself and does not fit into the precisely regulated management of the whole organism.” [Taubes, Gary. "Good Calories, Bad Calories." New York: Knopf (2007), p.362.]
I have come to believe that Lipophilia is less a theory than it is a simple change in reference point.
It says, in effect: our focus on calories-into-and-out-of the body is misplaced; it is more accurate to focus on calories-into-and-out-of the fat tissue itself.
That shift may sound like semantic games. But I believe it’s really important!
When you shift your focus on a problem, you ask new questions and see new things.
Albert Einstein, as with many things, said it best:
The mere formulation of a problem is far more essential than its solution, which may be merely a matter of mathematical or experimental skills. To raise new questions, new possibilities, to regard old problems from a new angle requires creative imagination and marks real advances in science.
Unfortunately, almost every modern advocate for Lipophilia has also been a low carb advocate. Hence, these two ideas — “The Black Box Counts” and “Carbs Count” — have co-mingled. This is a huge problem. I believe this blurring of distinctions may be the source of our collective headache.
Because both the “Calories Count” and the “Carbs Count” ideas oversimplify.
Neither is 100% true. Both are diet-focused. But obesity is a condition that clearly transcends the amount and type of food we put into our bodies. As obesity researcher Steven O’Rahilly put it in the journal Nature [November 19, 2009]: “obesity is most simply defined as a state in which the total amount of triglycerides stored in adipose tissue is abnormally increased.”
Obesity is a biochemical problem, in other words, by definition. If changing the quality or quantity of food causes/fixes this problem, it only does so indirectly.
Okay, fine. But who cares? How is this semantic nit picking useful?
Good questions! :] Let’s dive in and find out…
#1. A New Perspective on Medication-Related Weight Gain
Here’s a quote from a WebMD article that hints at the dimension of the problem:
Experts say that for up to 25% of people, most antidepressant medications — including the popular SSRI (selective serotonin reuptake inhibitor) drugs like Lexapro, Paxil, Prozac, and Zoloft — can cause a weight gain of 10 pounds or more…. SSRIs aren’t the only class of antidepressants that may have weight gain as a side effect. Other antidepressant medications, including tricylics (like Elavil and Tofranil) and MAO inhibitors (drugs like Parnate and Nardil), may also cause patients to gain weight with both long-term and short-term use. [source]
Diabetes drugs also can make us fat:
Diabetes medications that help control blood glucose levels are essential for people with type 2 diabetes. Unfortunately, insulin, sulfonylureas and thiazolidinediones can cause weight gain — a special concern for many people with type 2 diabetes who are already overweight or obese. [source]
So what’s going on here? Why do certain drugs make certain people fat, and what can be done about it?
Calories Count Frame:
CAUSE: Obesogenic drugs somehow make people eat more and/or burn less.
SOLUTION: Eat less and boost metabolism to compensate.
Here’s typical Calorie-Centered thinking on this topic:
According to [George] Blackburn [associate director of the division of nutrition at Harvard Medical School], eating 100 to 200 fewer calories each day is enough to counteract the kind of weight gain you’d experience on most drugs, especially if you increase your exercise. [source]
Carbs Count Frame:
CAUSE: Many of these drugs stimulate carb-cravings, so maybe the people who gain weight do so because they unconsciously eat too many carbs.
SOLUTION: Clamp down harder on dietary carbohydrate.
Black Box Frame:
CAUSE: The drugs somehow directly impact the hormonal/metabolic environment of the fat tissue, causing more fat to be stored in the fat cells.
Astonishingly, researchers readily admit that this happens. Here’s a quote from Johns Hopkins Medicine’s site:
“Thiazolidinediones… cause fat cells to store more fatty acids from the blood, causing the fat cells to enlarge.” [source]
SOLUTION: Switch to a medication that doesn’t cause fat overstorage.
Startling Evidence That Supports the Black Box Perspective and Showcases the Limitations of the “Count Calories” Perspective
A bit of intrepid internet research reveals that thousands of people who’ve gained fat on medications have tried the “Count Calories” approach and failed epically. Here’s a sample of quotes from just one thread on one forum about one obesogenic drug:
- Since I’ve been on the lex[apro] I’ve gained about ten pounds. I’m very weight conscious and have been a daily exerciser for years. Weight training and cardio… Like so many other people that I read about, as hard as they try, no weight comes off. I eat healthy. Veggies, oatmeal, protein. No fast food and junk most of the time. Took my calories down to 800 hundred a day, exercised every day, did so well but the scale never moved. So so so discouraging. I have anxiety and panic attacks cuz I can’t take off the weight no matter how hard I try.
- A year ago I started taking Lexapro and Lorazepam… I went from 130 to almost 200 pounds in a year and I even got stretch marks from gaining so fast. I didn’t think much of it at first because my family is bigger but I can’t even lose any of it. I barely get 800 calories a day, I run a daycare with 6 kids every day of the week (no kids myself) and I’m constantly running or getting up to help or something. I eat small portions and only a few times a day. I don’t drink caffeine or any kind of pop.
- Lexapro definitely causes weight gain. I have exercised 30 minutes a day and lift weights and keep my calories below 2000 a day. I can’t lose weight on this drug no matter what I do. [source]
Are these three people (and the hundreds of thousands like them) all lying?
That’s the only way to explain their stories within the context of the “Calories Count” or “Carbs Count” paradigms: that they’re secretly eating way more calories (or carbs) than they say they are.
On the other hand, if you look at their experience through the “Black Box” lens, it suddenly makes sense.
They’re not all liars or delusional. The meds must be causing biochemical changes to their fat tissue — I’m guessing related to insulin sensitivity — causing it to “grow on its own” in much the same way that tumors and fetuses “grow on their own,” independent of whole body energy balance.
If that’s the case, then all of the advice dished out by people like Dr. Blackburn — advice to the effect of “just starve yourself to reverse the positive calorie balance caused by the meds” — is nonsensical and bound to fail.
When lipophilia is at work – when the fat tissue wants to suck up and hold onto fat, independent of the needs of the organism — you simply cannot “starve the problem away.” For a graphic, extreme lesson about this phenomenon, see here.
Think about how many millions of people struggle with medication related weight gain. They cannot win. They will not EVER win. Because their focus — and the focus of everyone who treats them — is embedded in the wrong paradigm.
Counting calories won’t fix things. Neither will counting carbs. Only an appreciation for the fundamental lipophilic effect of the drugs will help:
“CALORIES COUNT” PARADIGM
PATIENT: Doctor, I’ve gained 30 pounds in two months on my anti-depressant.
DOCTOR: Hmm. Dr. George Blackburn at Harvard says eat 200 calories less a day and go to the gym more.
PATIENT: But I’ve been doing that — starving myself — and it isn’t working.
DOCTOR: You must be secretly binge eating. Track your food and double down on your willpower.
PATIENT: But doc, I have been…!
DOCTOR: You sound really anxious. The meds must not be strong enough. I’m going to double your dose.
PATIENT: Won’t that just make me fatter still?
DOCTOR: Okay, headcase. I’ll triple it.
“BLACK BOX COUNTS” PARADIGM
PATIENT: Doctor, I’ve gained 30 pounds in two months on my anti-depressant.
DOCTOR: Hmm. The medication must be having a lipophilic effect on your fat tissue — it’s causing hormonal changes that are making your body store excess fat.
PATIENT: What do I do?
DOCTOR: Not sure. Are you having cravings for carbohydrate foods?
PATIENT: Yes! I’m so hungry for carbs. It’s weird.
DOCTOR: My guess, then, is that the meds may be screwing with your insulin system, somehow, but the science is so dodgy that I can’t say for sure. How about we try a different medication to see whether that works without the weight gain side effect?
PATIENT: Terrific idea, doc! I’m less depressed already knowing that I have such an awesome, knowledgeable doctor.
DOCTOR: Oh stop. You’re making me blush.
#2. A New Perspective on Couvade’s-Syndome Weight Gain
Klein H of the University of Texas Medical Branch, Galveston defines the problem:
Couvade is the common but poorly understood phenomenon whereby the expectant father experiences somatic symptoms during the pregnancy for which there is no recognized physiological basis. Symptoms commonly include indigestion, increased or decreased appetite, weight gain, diarrhea or constipation, headache, and toothache. Onset is usually during the third gestational month with a secondary rise in the late third trimester. Symptoms generally resolve with childbirth. [source]
Couvade’s leads to weight gain in many dads-to-be.
In fact, it happened to me… twice! I gained approximately 30 pounds of fat during both my wife’s pregnancies — all while on a low carb diet, mind you — and effortlessly lost all the weight after she delivered.
Other research suggests this daddy-weight-gain happens in other species, too:
Common marmoset and cotton-top tamarin fathers spend as much or more time caring for infants than mothers. Expectant males of both species showed significant increases in weight across the pregnancy whereas control males did not (five consecutive months for marmoset males and six months for cotton-top tamarin males). [source]
So what’s going on here? Again, let’s look through our three lenses:
Calories Count Frame:
CAUSE: Being around a pregnant woman somehow makes dads eat more and/or burn less energy.
SOLUTION: Eat less and boost metabolism to compensate.
Here’s typical Calorie-Centered thinking on this topic:
Expectant dads, worried about the massive impending life change, eat to comfort themselves, or simply eat more because Mom is eating. [source]
Carbs Count Frame:
CAUSE: Being around a pregnant woman somehow makes dads crave more carbs.
SOLUTION: Clamp down harder on dietary carbohydrate.
Black Box Frame:
CAUSE: Being around a pregnant woman somehow impacts the hormonal/metabolic environment of dad’s fat tissue, causing more fat to be stored in his fat cells.
SOLUTION: Wait it out or run away! :] Seriously, though, you probably can’t solve the weight gain with a pill or special diet, since the stimulus is fundamentally hormonal.
Startling Evidence That Supports the Black Box Perspective and Showcases the Limitations of the “Calories Count” Perspective
Emily Anthes wrote about the Couvade’s phenomenon in a 2007 article in Slate. She found:
Dads-to-be have elevated levels of cortisol and prolactin, hormones that are also present in high levels among mothers who are attached and responsive to their children. A father’s testosterone level also drops by about a third, on average, in the first three weeks after his child is born. These hormonal shifts, which are likely sparked by exposure to the pregnant woman’s hormones (there is correlational evidence that dads who spend time with moms experience the changes), mirror those experienced by mothers and may similarly prepare men for parenthood. [source]
I’m no doctor or obesity expert. But I feel safe in assuming that major changes to prolactin, cortisol and testosterone levels would majorly change the hormonal/metabolic environment of the fat tissue and lead (potentially) to the storage of excess fat.
Again, the shift in perspective is key.
Once I understood that the weight gain I experienced during both pregnancies was likely related to hormonal changes, I enjoyed tremendous peace of mind. I didn’t panic and starve myself or go nuts trying to reduce my carb levels even more. Because I knew that calories and carbs weren’t the problem.
Imagine if all the dad-to-be’s who experienced this weight gain (and other attendant symptoms) understood Couvades like I understood it. They might not be able to do anything to stop the weight gain, but at least they’d freak out about it less. And that’s certainly worth something!
#3. A New Perspective on the Relationship Between Anorexia and Obesity
Time to REALLY cook your noodle.
Most people know that low carb diets, like Atkins, can be used to treat obesity. The following picture says it all:
But did you know that low carb has been able to treat anorexia, too? No kidding:
In their book, Life Without Bread, German doctors Allan and Lutz describe how they successfully treated anorexics with a low carbohydrate diet:
The low carbohydrate program augments the anabolic processes that contribute to increased body mass… over a long period of time, they [i.e. anorexics] will eventually reach a larger body mass compared to when they began the low-carbohydrate program. **The new weight, however, will be in all the right places. [P. 144 Life Without Bread]
**bold is mine
Assuming the good doctors Lutz and Allen observed correctly, we must come to one of two conclusions:
Conclusion #1. Low carb diets are magical.
These diets somehow make anorexics eat more/exercise less, so they gain weight, but somehow this “positive energy balance” winds up fattening them in a good way. They store excess calories in “just the right places.” So you don’t get a beer belly or fat thighs, in other words — your face fills out so you look less emaciated.
These diets magically have the converse effect on obese/overweight people. They somehow cause them to eat less/exercise more, so they lose weight, but somehow this “negative energy balance” winds up making them leaner in a good way. The energy gets burned off from “just the right places.” You burn off the beer belly or fat thighs, in other words — but your face doesn’t become gaunt.
Conclusion #2. Low carb diets do something to normalize how the fat tissue is regulated — to fix the Black Box.
These diets add in “good stuff” or subtract “bad stuff” or both.
As a result of these good changes, the fat tissue reaches a healthier equilibrium. In this model — the only model that makes sense, IMHO — anorexia and obesity should be seen as different instantiations of the same basic problem. They’re both problems of fat tissue dysregulation, possibly induced by/worsened by diet. The damaging dietary element – possibly the carbohydrate load – does different bad things to different people, depending on stuff like their metabolic history, their hormones, their genetics, their muscle tissue’s sensitivity to insulin, etc.
So a bad diet makes some people anorexic and others obese, because of how these foods impact the body and the fat tissue’s homeostatic mechanisms. And when the carbs are removed, the body starts to partition its fuels properly — the Black Box is fixed! — and the anorexia or obesity resolves.
Magic not required.
#4. A New Perspective on the Dozens of Other Hugely Important Phenomena
I hope you’re getting the gist. Any time we find obesity (or anorexia), our very first thought should be “what biochemical factors are causing the abnormal fat storage?” NOT “why are these people overeating (or undereating)?”
Here are 8 more whole categories of phenomena — situations in which fat gain occurs — that can best be explained (and dealt with) by the Black Box frame.
- Fat gain from quitting smoking
- Fat gain from genetic diseases (e.g. Cohen Syndrome; Leprechaun Syndrome; Bardet-Biedl, etc)
- Fat gain from brain injury (e.g. lesions to the ventromedial hypothalamus)
- Fat gain from epigenetic influences
- Fat gain from menopause
- Fat gain from influences of other stuff in the food supply (transfats, omega-3/omega-6 fat ratio, etc)
- Fat gain from changes in other hormones/enzymes (leptin; cortisol; dopamine; testosterone, progesterone, etc)
- Fat gain from weird types of obesity (e.g. progressive lipodystrophy)
Let’s take a closer look at one phenomenon: smokers who quit almost always gain fat. Why?
Well, you can guess by now what the “Calories Count” folks will say. They’ll tell you that quitting stimulates appetite/slows metabolism; and that, if you want to “fight” the weight gain, then you should starve yourself and exercise more to reverse the calorie balance.
As they say, when all you have is a hammer, the whole world looks like a nail.
But this calories-centric POV once again ignores some underlying (and very important!) biochemistry.
Nicotine, for instance, directly suppresses the action of an enzyme called lipoprotein lipase (LPL), which normally acts to stuff the fat cells with fat. When you quit smoking, this suppression stops, so LPL revs up and causes more fat to be stored.
Hence, your body will store serious extra amounts of fat, irrespective of how much (or what) you eat or how much you exercise! In this case, it’s not about the calories. It’s not about the carbs. This time, it’s about the LPL.
So What the Heck Do We Do Now? (7 Mental Shifts We All Need to Make)
Shift #1. Stop focusing on calories-into-and-out-of the whole body; Start focusing on calories-into-and-out-of the fat cells of the fat tissue.
Whenever you read or think about obesity — yours or other people’s — start by framing the problem in terms of biochemistry and work backwards.
Not: “Ugh, I look so fat in these jeans. I need to crash diet.”
But rather: “Ugh, I’m storing excess triglycerides in the fat cells of my thighs and buttocks. I wonder what factor, dietary or otherwise, has changed how that fat tissue is being regulated and what I might be able to do, if anything, to normalize that regulation.”
Okay, the second phrase is a tad clunky! But I hope you appreciate the gist — think of obesity as primarily an “overstoring” problem, rather than an “overeating” one.
Shift #2. Stop focusing on short-term fixes and miracle diets; Start seeing obesity as a chronic disease that develops over long periods of time and that may take a while to resolve, if success is even possible.
Different diets may work for different folks at different times. Obesity, for instance, likely does not lend itself to one-size-fits-all solutions.
One blogger I respect asserts that:
Post-obese people are metabolically not the same as undieted people of the same weight, the biological drive to regain is and always will be there… “No diet book or paleo guru is going to tell you this but the truth is that obesity is a permanent endocrine disorder and it cannot be cured through diet alone or through any other currently clinically available means, not even stomach mutilation surgery. As shown in clinical trials, you can trick the brain into thinking that adipose stores are still adequate by administering leptin replacement therapy to weight-reduced people, but this is not a real cure in the real sense of the word because you still have hyperplastic fat tissue and that’s a permanent problem. [source]
Shift #3. Stop focusing on BMI or other absolute measures of fatness; start focusing instead on fat tissue HEALTH.
Here are a few cartoons I drew to illustrate this idea:
What’s the purpose of a diet? Is it merely to lose weight? To lose body mass? Because, if so, there are easy ways to do that:
Obviously this is not what anyone wants. (Right?) What people want is to lose FAT. A lot of it. So more like this…?
Hold it! Hold it! That’s TOO much fat.
Oh, right. People want to lose the RIGHT amount of fat. Say, 50 pounds’ worth…
No, no, no. Dammit! You know what I mean, Adam.
Oh, right. You want THIS:
That’s right! Finally, you get it!
Only in our last example does the woman look healthy. It’s not that she’s lost weight or even lost fat… her fat tissue itself has been re-regulated to be healthier.
What dieters fundamentally want — desperately crave — isn’t weight loss or even fat loss, per se; it’s healthy fat tissue.
Shift #4. Stop thinking about the fat tissue as a simple system that responds to inputs and outputs in a linear fashion; start thinking of it as a complex adaptive system that responds to inputs and outputs in a non-linear fashion.
We’ve all been taught to think about fat in cartoonish terms. For instance, you probably know that a pound of fat contains 3,500 kilo-calories worth of usable energy. Based on this fact, millions of people believe they can “burn off” a pound of unwanted fat just by starving themselves and/or going nuts on the treadmill to create a 3,500 calorie deficit.
We hear “logic” like this so often that we don’t stop to appreciate how fakakta it is.
Why do we always assume that it’s fat that we’ll burn — and unwanted fat, at that? How do we know that the “energy deficits” we create won’t come from our brains or muscles or other organs?
According to the Straight Dope message boards (and I don’t know how accurate this is), a small human brain contains 1,755 kilo-calories. So if you burn 250 calories in an hour on the treadmill, and you run for 8 hours straight, you could burn off your whole brain and then some!
Obviously, that wouldn’t happen. The brain would find a way to “protect itself” from being “burned off” — just like your kidneys and liver and heart would find ways to protect themselves from being burned off.
So why do we all assume that the fat tissue wouldn’t also strive to protect itself from being burned off in such a crude manner?
The answer is that all we’ve been trained — brainwashed is maybe a better term — to think about obesity in a way that’s inaccurate. The reality is that the adipose tissue (a.k.a. the fat tissue) is an active endocrine organ. It’s an organ, just like the liver and the kidneys. And organs are hella complex biological structures.
Shift #5. Stop seeing obesity as a moral failing; start seeing it for the medical/biological problem it is.
I’m lean and fit. I’ve never been obese. At my heaviest, I was maybe 15-20 pounds “overfat.” I think it’s very hard for people like me to understand what it’s like to struggle with obesity. But I’m convinced that obesity is no more a moral failing than being super tall is. There are plenty of lean people with no willpower who eat crap food (think teenage boys). Likewise, there are plenty of obese people with tremendous willpower who eat very healthy food.
The sooner we can break free from the moralistic view of obesity — that it’s caused by the twin sins of gluttony and sloth and purged by the twin virtues of restraint and productivity — the better.
Shift #6. Stop seeing the obesity epidemic as a peculiar, idiosyncratic event; start seeing it as a single instantiation of a larger, more diversely embedded pathology.
I wrote a whole essay on this point here.
Shift #7. Stop focusing solely on diet and exercise; Start focusing on other factors that could be important.
These could include:
- Managing sleep and stress;
- Supplementing appropriately;
- Getting enough sunlight;
- Dealing with other underlying endocrine issues;
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I deeply believe this frame can help us make progress on all sorts of problems in a more compassionate, accurate and successful way.
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To Better Counting,