Why We Get Fat And What To Do About It Part II

Hello again, so last time we took a break from How We Get Fat And What To Do About It, to learn a little about our inflammatory friend, Gout. If you haven’t checked it out yet, give it a read. It is really interesting, but then again I wrote it so I would think that. Nevertheless, let’s get into Part II of the review, and coincidentally, book II of the book. Much like with the last review we won’t be hitting on every chapter, but we will hit the high notes. The specific chapter we will be discussing will be chapters:

9.The Laws of Adiposity
11. A Primer on the Regulation of Fat
12. Why I Get Fat and You Don’t (or Vice Versa)
18. The Nature of a Healthy Diet

9. The Laws of Adiposity

Before we get into the chapter, let’s discuss what the heck adiposity even is. It is the start of being fat. The main point Gary Taubes hits home with this chapter is, that our bodies control the amount of adiposity we do or don’t carry based on our hormones. He illustrates his point by looking at a study that looks at rats, and how they gain or lose weight, “for his rats, that those who get fat do so because of the way their fat happens to be regulated and that a conspicuous consequence of this regulation is to cause the eating behavior (gluttony) and the physical inactivity (sloth) that we so readily assume are the actual causes.” In other words, they become lazy or gorge on food because they are already overweight. That may seem counterintuitive but it will make sense by the end of the review. Before we go into that, let’s look at Taubes, Laws of Adiposity. He has three of them, and they are as follows:

  • The First Law: Body fat is carefully regulated, if not exquisitely so.
  • The Second Law: Obesity can be caused by a regulatory defect so small that it would be undetectable by any technique yet invented.
  • The Third Law: Whatever makes us both fatter and heavier will also make us overeat.

Let’s briefly drill into each of these laws. His first law has to do with body fat regulation and the hormones that cause us to either store or burn fat. He explains that with wild animals will maintain a healthy weight for them. Some animals gain tons of weight (sometimes literally, in the case of whales) and others only gain weight as needed. Their fat tissues work for them, instead of against them. He specifically looks at the ground squirrel:

Ground squirrels, for example, which double their weight and body fat in just a few weeks of late summer. Dissecting these squirrels at their peak weight, as one researcher described it to me, is like “opening a can of Crisco oil—enormous gobs of fat, all over the place.” But these squirrels will accumulate this fat regardless of how much they eat, just like Wade’s ovary-less rats. They can be housed in a laboratory and kept to a strict diet from springtime, when they awake from hibernation, through late summer, and they’ll get just as fat as squirrels allowed to eat to their hearts’ content. They’ll burn the fat through the winter and lose it at the same rate, whether they remain awake in a warm laboratory with food available or go into full hibernation, eating not a bite, and surviving solely off their fat supplies. The fact is, there’s very little that researchers can do to keep these animals from gaining and losing fat on schedule. Manipulating the food available, short of virtually starving them to death, is not effective. The amount of fat on these rodents at any particular time of the year is regulated entirely by biological factors, not by the food supply itself or the amount of energy required to get that food.

How crazy is that? No matter if these ground squirrels are given excess food or not, they will still gain the needed weight to survive winter hibernation. So if an animal’s body can be so well regulated, what is keeping us from being so well regulated? Afterall, “when regulation breaks down, as it does in cancer and heart disease, the result is often fatally obvious. When people accumulate excess fat, this tells us that something has gone awry in the careful regulation of their fat tissue.”

This thought leads us right into the second law, which deals with the dysregulation that triggers obesity. This idea takes a whole chapter to understand (Chapter 4 to be exact,) however he sums up the chapter quite nicely when he states, “If we overeat by just twenty calories each day—adding just 1 percent or less to our typical daily caloric quota, without a compensatory increase in expenditure—that’s enough to transform us from lean in our twenties to obese in our fifties.” So, 20 calories are all that is needed to become obese, this can be the difference between finishing that last bite of food, or throwing it away. If your body fudges the numbers a bit more, then you can go from lean to obese in even less time. The main takeaway is that if we can keep our bodies running the way they are meant to, it becomes less about the quantity you eat, and more about the quality of your food.

Again, it’s like he planned this or something because the last law ties this idea up nicely. I will just quote it again, “Whatever makes us both fatter and heavier will also make us overeat.” Fully understanding this idea means that most of us have to deal with the cognitive dissonance that the calories-in/calories-out model has left us with. Which is, that we can gain weight without going into a calorie surplus. This can be done with changing where the calories are coming from. Said another way, “We don’t get fat because we overeat; we overeat because we’re getting fat.”

If we cannot understand that point, then you cannot fully get this book. Also once we understand that point, we can stop feeling like crap when we are unable to lose the weight we want, instead we can change our approach from calories to the hormonal impact of foods.

11. A Primer on the Regulation of Fat

In this chapter, we take a look at what exactly goes into the regulation of fat storage. After all, if we cannot understand how we get fat, how will we know what to do about it? Punning on the name of the book aside, why the heck do we even store fat? Well, let’s look at what Taubes has to say about it:

Fat is continuously flowing out of our fat cells and circulating around the body to be used for fuel and, if it’s not used for fuel, returned to the fat cells. This goes on regardless of whether we’ve recently eaten or exercised….Over the course of any twenty-four-hour period, fat from your fat cells will provide a significant portion of the fuel that your cells will burn for energy. The reason nutritionists like to think (and like to tell us) that carbohydrates are somehow the preferred fuel for the body, which is simply wrong, is that your cells will burn carbohydrates before they’ll burn fat. They do so because that’s how the body keeps blood sugar levels in check after a meal.

This is also where insulin comes into the picture since it is vital to keeping your blood sugar under control. Insulin basically gets your body ready to eat, and it decreases or increases depending upon the type of food that is consumed. After you eat and as the insulin decreases, the more fat can be taken out of your fat stores to be used as energy. The longer you go between meals, the more fat that is used for energy, instead of sugar.

So the correct way to think about fat tissue is that it’s more like a wallet than a savings or retirement account. You’re always putting fat into it, and you’re always taking fat out. You get a tiny bit fatter (more fat goes into your fat cells then comes out) during and after every meal, and then you get a tiny bit leaner again (the opposite occurs) after the meal is digested. And you get leaner still while sleeping. In an ideal world, one in which you’re not getting any fatter, the calories you store as fat immediately after meals during the day are balanced out over time by the calories you burn as fat after digesting those meals and during the night.

Insulin may be to master fat regulator, but it is not a one-man powerhouse, it works in concert with a few other mechanisms to allow us to maintain, or fluctuate our weight. One such mechanism is an enzyme called LPL, Lipoprotein Lipase. LPL “is the enzyme that sticks out from the membranes of different cells and then pulls fat out of the bloodstream and into the cells. If the LPL is on the surface of a muscle cell, then it directs the fat into the muscle to be used for fuel. If it’s on a fat cell, then it makes that fat cell fatter.” LPL also allows men and women to fatten differently. It also allows us to release, use and burn fat from out tissues as fuel during a workout.

LPL is not the only enzyme that insulin regulates:

Insulin also influences an enzyme that we haven’t discussed, hormone-sensitive lipase, or HSL for short. And this may be even more critical to how insulin regulates the amount of fat we store. Just as LPL works to make fat cells (and us) fatter, HSL works to make fat cells (and us) leaner. It does so by working inside the fat cells to break down triglycerides into their component fatty acids so that those fatty acids can then escape into the circulation.

This can all be boiled down to, insulin is the driving factor in how we burn or store our fat. However, it is not the only hormone that regulates our fat sorts, in fact, all of them instruct the body to do something, “In this sense, every hormone but insulin works to release fat from our fat tissue. They make us leaner, at least temporarily.” However, the other hormones cannot do their job if insulin levels are elevated. Because insulin is like the Snorlax at the top of a waterfall keeping the water from flowing down. Once we wake Snorlax up, the water starts flowing and the other hormones can start doing their jobs.

Now it wouldn’t be a rule if there was not an exception. This exception is cortisol. “Cortisol actually works to put fat into our fat tissue and to get it out. It puts fat in by stimulating the enzyme LPL, just as insulin does, and by causing or exacerbating a condition known as ‘insulin resistance,’ Ever wonder why we are more likely to gain weight or eat more while stressed? Thank cortisol!

With that exception out of the way, it is important to remember that if insulin is high, we cannot use fat for energy. In other words: we can end up in a situation where our pantry is full, but we cannot get the door open to eat, which causes us to starve. Once the insulin goes down the pantry can be accessed.

12 Why I Get Fat and You Don’t (or Vice Versa)

This chapter goes into how our bodies regulate our fat. From the hormones to the food that seems to affect weight and so on. It really builds on the foundation that the rest of the book lays down. Taubes uses a wonderful example of how to think about fat regulation. Think of the fuel gauge in a car. The “E” stands for “Energy,” and the “F” stands for, “Fat.” If the needle points to “E” it means that you are burning the calories you consume, which in turn means less will be available to be stored as fat. This also that you will have the energy to be physically active, this, in turn, allows you to easily become and stay lean.

On the other hand, “F” means that your insulin is high which causes a larger amount of the calories you consume to be stored as fat rather than burned. This will cause you to gain weight, and less energy is available for physical activity, which causes you to become more sedentary. The closer to “F” the needle points, the fewer calories you can use for energy, and the more sedentary you will become.

The longer you fuel gauge point to “F,” means that your sensitivity to insulin becomes dull. Think of it like the more often you drink coffee, alcohol or soda over time you will need more to get you feeling the same effect as before. You become desensitized to the caffeine, alcohol, or sugar. This also happened to insulin receptors in your body, and it is called “Insulin Resistance.” What this means to your body is that the more insulin your body makes (in response to the foods you eat,) the more your body will become resistant to it. Said another way, over time your body will need to make more insulin in order to nullify the same amount of blood sugar, or glucose, as before. Remember insulin is triggered because too much sugar, or glucose, in your blood can be toxic.

Another point regarding insulin is that each part of your body will not only respond differently to insulin but may also become resistant to insulin at different times and to different extents. For example, “if your muscle cells are very sensitive to insulin and your fat cells less so, then the needle of the fuel-partitioning gauge points toward fuel burning. Your muscles will take up a disproportionate share of the glucose from the carbohydrates you consume, and they’ll use it for energy. The result: you’ll be lean and physically active.” The converse, however, would be, “if your muscles are relatively insensitive to insulin compared with your fat cells, then your fat tissue will be the repository of a disproportionate share of the calories you consume. As a result, you’ll be fat and sedentary.”

Does insulin sensitivity only come into play, if we are spiking blood sugar which causes a rise in insulin? No, in fact, in utero the baby is affected by the mother’s’ blood sugar levels. If a pregnant mother has abnormally high blood sugar levels their child is more likely to develop a higher amount of insulin-secreting cells. Meaning the baby will be born fatter (this is why mothers with gestational diabetes have larger babies than those without.) This may cause the babies body to have a high tendency toward the oversecretion of insulin which means they are more likely to become insulin resistance as they age. Which causes them to gain fat easier than their peers.

18. The Nature of a Healthy Diet

This is our last and final chapter together. Before I dive into this topic; I want to take a long quote from a previous chapter that I did not include in my overview. I am including the quote here because it fits with this chapter perfectly, and it will serve as a good primer for this chapter:

Not that all foods that contain carbohydrates are equally fattening. This is a crucial point. The most fattening foods are the ones that have the greatest effect on our blood sugar and insulin levels. These are the concentrated sources of carbohydrates, and particularly those that we can digest quickly: anything made of refined flour (bread, cereals, and pasta), liquid carbohydrates (beers, fruit juices, and sodas), and starches (potatoes, rice, and corn).

I started this discussion talking about carbohydrates because I want to highlight that despite what common wisdom says it is an excess of these kinds of carbohydrates that trigger weight gain the most. I have personally tested this, the results were dumbfounding. I will post them at a later date. It all boiled down to a large fry added inches to my waist for a few days, and the same amount of calories of fatty steak added no inches to my waist.

My N=1 aside let’s look at what Gary Taubes has to say about the nature of a healthy diet. I think my favorite point he makes in this chapter is the unbalanced diet argument, considering nutritionists and the like argue that is it tantamount to treason if we exclude any food group. Yet they seem to forget that their prescribed diet almost completely eliminates a food group as well (meat cough, cough). But I digress. Tubes directly addresses this point by saying:

The unbalanced diet argument makes little sense if starches, refined carbohydrates, and sugars do indeed make us fat because it’s hard to argue rationally for anything other than avoiding these carbohydrates to fix the problem. When our doctors counsel us to quit smoking because cigarettes cause lung cancer, emphysema, and heart disease, they don’t care if we find life less fulfilling without them. They want us to be healthy, and they assume we’ll get over the absence, given time. Since these carbohydrates make us fat—and maybe cause a host of other chronic diseases, as I’ll discuss—the same logic holds here. If you cut back on all calories equally, or preferentially restrict fat calories, as we’re often counseled, you’ll be eating less fat and protein, which are not fattening, and more of the carbohydrates that are. Not only won’t this diet work as well, if it works at all, but hunger will be a constant companion. If you restrict only carbohydrates, you can always eat more protein and fat if you feel the urge, since they have no effect on fat accumulation.

Said another way: Why are we coached to eat all we want of the foods that make us fat while we limit the types of foods that make us feel full? It makes no sense. If you are trying to lose weight cut the carbs, not the fat. You might lose weight without being hangry. You’re not you when you’re hangry.

Another argument that comes from the low-fat camp it that a diet the limits the above stated fattening carbohydrates will be deficient in essential nutrients (ie: vitamins, minerals, amino acids). That is a load of bollox, pardon my language but it is true. Let’s go back to Taubes for the reasoning:

First, the foods that you would be avoiding are the fattening ones, not leafy green vegetables and salads. This alone should take care of any superficial anxieties about vitamin or mineral deficiencies. Moreover, the fattening carbohydrates that are restricted—starches, refined carbohydrates, and sugars—are virtually absent essential nutrients in any case. Even if you believe that weight loss requires cutting calories, these fattening carbohydrates would be the ideal foods to cut for just this reason. If you follow the conventional wisdom and so cut all calories, say, by a third, you’re also cutting all essential nutrients by a third. A diet that prohibits sugars, flour, potatoes, and beer, but allows unlimited meat, eggs, and leafy green vegetables, leaves in all the essential nutrients.

Another thing I would like to bring up it that, “meat contains all the amino acids necessary for life, all the essential fats, and twelve of the thirteen essential vitamins in surprisingly large quantities.” For something that is supposed to clog our arteries, it is a little crazy, that it seems so healthy for us, in fact, “Meat is a particularly concentrated source of vitamins A and E, and the entire complex of B vitamins. Vitamins B12 and D are found only in animal products (although we can get sufficient vitamin D from regular exposure to sunlight).”

With all of this pro-meat talk, I am not saying that you should stop eating veggies in lieu of an all meat diet, although some have with no ill effect. I only say this to defend meat, after all, it has gotten a bad wrap over the past 60 or so years and wrongfully so. Which is why I went so in depth with these first two book reviews. I know for me there was so much relearning and conditioning I had to go through in order to not feel guilty about eating meat, specifically saturated fat.

A major bonus, in my opinion, to a diet that limits the amount of carbohydrates you get is that if your carbohydrates are low enough you can switch from burning carbohydrates for energy and instead use fat (internal or dietary), if your carbohydrates are low enough you will also make and burn a fuel called ketones. To find out more about that process check out the Healthy Lifestyle tab one my site that goes into the adaptation stages, or if you want to know more about the diet the get you into burning fat/ketones check out the LCHF (Low-carb, High-fat) or Ketosis parts of my site for more tips on implementing the diet.

The next argument he deconstructs is the heart disease argument. Since last month we reviewed The Big Fat Surprise, I will only give a brief summary of his points because their conclusions are virtually the same. Which is: Fat in the diet is not the cause of either heart disease nor high triglycerides. The former seems to be linked to chronic inflammation, and the later seems to be triggered by carbohydrates. Check out the book The Big Fat Surprise here if you want a copy of your own.

With that said, let’s talk about the final argument he brings up which is the cause of metabolic syndrome. He first gives a high-level look at what steps seem to lead to metabolic syndrome, which is: insulin-resistance, which causes us to gain weight (mostly around the waist), then a bunch of other metabolic problems occurs like :

blood pressure goes up; triglycerides go up; HDL cholesterol goes down. What I didn’t mention earlier is that LDL particles become small and dense. We become glucose-intolerant, which means we have trouble controlling our blood sugar. We might even develop type 2 diabetes, which happens when the pancreas can no longer secrete enough insulin to compensate for the insulin resistance. This combination of heart-disease risk factors is now known as “metabolic syndrome,” and it is, in effect, the intermediate step on the way to heart disease.

The main driver of this set of problems seems to be an overconsumption of fattening carbohydrates. Note I did not say fat. Remember the long quote from above, but it basically boils down to, limit grains, sugar and starch.

The finger is pointed at an abundance of carbohydrates because what drives insulin-resistance? Carbohydrates. If we take carbohydrates out of the equation the weight starts to come off. In fact, a bunch of clinical trials show that “low-carbohydrate, high-fat diets improve each and every one of the metabolic and hormonal abnormalities of metabolic syndrome—the low HDL, the high triglycerides, the small, dense LDL, the high blood pressure, and the insulin resistance and chronically elevated levels of insulin.”

Before I let you go there are a few more points I want to add about metabolic syndrome, which is the link to Alzheimer’s and most cancers. We already knew that metabolic syndrome, obesity, and diabetes were linked. However, as more is found out about the effects of elevated blood sugar inflammation in the body we can start to understand these interlinked diseases more and more. Specifically to Alzheimer’s, “Researchers have begun to work out mechanisms through which insulin and high blood sugar might cause the brain deterioration symptomatic of Alzheimer’s (some researchers have even taken to referring to Alzheimer’s as “type 3 diabetes”) and how high blood sugar, insulin, and the related hormone, insulin-like growth factor, spur tumor growth and cause tumors to metastasize.

I know this may seem like a lot to handle, especially since this is a condensed version of a very dense book. But if you take nothing else from this, at the very least remember this: It’s not about the calories; it’s about hormonal regulation by limiting carbohydrates.

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