Day 74 - "Why We Get Fat" Pt. 3

Today is a continuation of Gary Taubes' "Why We Get Fat". I will be focusing my discussion on chapters 10 through 15.
A Historical Digression on "Lipophilia"
The term lipophilia (or the love of fat) dates to 1908 when the German Gustav von Bergmann created it to explain why parts of the body differ in their affinity for stockpiling fat (Taubes, 106). According to Taubes, "Von Bergman's approach to obesity was straightforward: he considered it a disorder of excess fat accumulation and then set out to learn what he could about the regulation of our fat tissue." (106) Von Bergmann's observations led him to believe that some tissue is lipophilic and accumulates fat easily, while other tissue is not. He also noted that there were differences from person to person in which tissues were lipophilic. Taubes said his observations of fat compared to that of hair on the body: some areas of the body grow hair while others don’t, and some people are hairier than others (106).
According to Taubes, "those who are predisposed to grow obese, fat tissue is driven to grow, to expand with fat, and it will accomplish this goal, just as the tumor does, with little concern about what the rest of the body might be doing." (107) While the theories of lipophilic tissue continued to be accepted into the 1930s, it vanished by the end of WW2. This was because some of these physicians/researchers were killed, some fled and had more pressing issues to worry about, and because of the anti-German sentiment after the war (Taubes, 108). Then, in the 1960s, psychologists took over the research on obesity and officially made it an eating disorder and causing any more research on the regulation of fat tissue to dwindle (Taubes, 108). One postwar expert who had the most perceptive take on why we get fat happened to be the one who had the most expertise in hormones and hormone-regulated disorders - Edwin Astwood of Tufts University," Taubes tells us (109). Astwood not only believed that people's predisposition to fat was something largely determined by our genes - a heritage, but also that "the amount of fat that would be stored in any single person or at any single location on the human body would be determined by the balance of these competing regulatory forces." (Taubes, 110)
A Primer on the Regulation of Fat
This section may get a little lengthily because there is so much to understand in order to fully comprehend how the body accumulates and regulates fat. However, I don't want to leave anything out and I promise that if you read all of this, you will have a much more complete understanding of fat regulation and what to do to about it.
The biggest question to ask is why do we get fat in the first place? Some of it is for insulation, some is for a protective padding for our fragile insides, but what about the rest? Taubes tells us that many experts typically see fat storage as a long-term savings account (113). The main idea behind this is that your body takes the excess calories and stashes them away for later use as fat, then they remain in the cells until you find yourself underfed one day and then the fat is moved and used for fuel (Taubes, 113). This view, however, is not correct! "As it happens," Taubes says, "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." (113)
Nutritionists will carbohydrates are somehow preferred fuel for the body, but this is also wrong. Rather, your cells will burn carbohydrates before they'll burn fat, simply because they need to keep the body's blood sugar levels in check after a meal (Taubes, 114). So when eating a meal with carbohydrates and fat, the fat will be digested and shipped off directly to the fat cells for storage. In the meantime, the body will deal with the carbohydrates first and then go back to the fat (Taubes, 114). When carbohydrates enter the body, they go into the bloodstream in the form of glucose (the sugar in "blood sugar"). The body will burn this glucose for fuel and use it to replenish their back up fuel supplies, but they need help in regulating the high amounts of glucose that go into the body (Taubes, 114). That's where the hormone insulin comes in.
Insulin's critical role in the body is to keep blood sugar under control. When a flood of glucose goes into the bloodstream, insulin "signals cells throughout the body to increase the rate at which they're pumping in glucose from the bloodstream. Muscle cells store the glucose in the form of a molecule called "glycogen". Liver cells store some as glycogen and convert some to fat. And fat cells store it as fat." (Taubes, 115) When the level of sugar in the blood goes down, insulin levels will decrease as well and more of the fat stored during the meal will be released from the fat tissue. So as you eat a meal you will get a tiny bit fatter (more fat goes into cells), but then you will get leaner after the meal is digested (more fat comes out of the cells), and even leaner still when you sleep (Taubes, 115). Taubes tells us that it is "only when the reserves of fat are reduced to some minimum amount that you start to get hungry again and are motivated to eat." (116)

Fat flows in an out of the cells in the form of fatty acids. This kind of fat is also the form that we burn for fuel. Then we store fat in the form of Triglycerides, which are made up of three fatty acids bound together by the molecule glycerol (Taubes, 116). While fatty acids are small enough to fit through the cell membrane of fat cells, allowing them to flow back and forth; triglycerides are too big to flow through the membrane. Therefore, triglycerides must be constructed within the fat cell from their component fatty acids, this construction from components is called esterified (Taubes, 116). So, when a fatty acid flows into a fat cell, it will be bound to two other fatty acids with the molecule glycerol and then will be too big to exit the cell again. Therefore, anything that works to increase the number of fatty acids flowing into the fat cells will work to increase the production of triglycerides, and thus will make you fatter (Taubes, 117).
Taubes tells us that "insulin also works simultaneously to orchestrate the storage and use of fat and protein. It makes sure, for instance, that your muscle cells get enough protein to do whatever rebuilding and repair is necessary, and it makes sure that you store enough fuel to function effectively between meals." (118) Thus, insulin is termed the "principle regulator of fat metabolism", and it accomplishes this job primarily through two enzymes (Taubes, 118).
The first enzyme insulin uses is lipoprotein lipase (LPL). LPL is the enzyme that sticks out from the membranes of different cells and then pulls fat out of the bloodstream and into the cell (Taubes, 119). LPL works to break down triglycerides in the bloodstream so the component fatty acids can then flow into the cells and thus increase fat storage (Taubes, 119). As he discussed in an earlier chapter, Taubes also tells us that the female sex hormone estrogen works to inhibit LPL, which will decrease fat accumulation (119). The activity locations of LPL depends based on gender too. In men, LPL activity is higher in the gut and lower below the waist, causing men to gain weight above the waist and especially in the stomach area. Testosterone also suppresses LPL in the abdominal area for men, so less testosterone will mean more fat accumulation. In women, the LPL activity is higher in the fat cells below the waist, causing women to gain fat in their hips and butt area (Taubes, 119).
LPL also helps to explain why exercise doesn't work so well for decreasing fat accumulation. While we are exercising, LPL activity decreases on our fat cells in order to increase on our muscle cells. This helps to encourage the release of fat from our fat tissues in order to burn it in our muscle cells (Taubes, 119). However, when we are done working out, the opposite happens. LPL activity on the muscles shuts down while the LPL activity goes up on fat cells in order to replenish all that was lost (Taubes, 120). Insulin, then, is the primary regulator of LPL. Insulin activates the LPL activity on fat cells. The more insulin we secrete, the more active the LPL on the fat cells, and the more fat is diverted from the bloodstream into the fat cells to be stored. Insulin also happens to suppress LPL activity on the muscle cells, assuring they won't have as many fatty acids to burn." (Taubes, 120).
The second enzyme insulin influences is hormone-sensitive lipase (or HSL). HSL works to make fat cells, and us, leaner by working inside the fat cells to break down triglycerides into their component fatty acids. This allows the fatty acids to exit the cell and escape into circulation (Taubes, 120). Therefore, the more active the HSL, the more fat we liberate and burn for fuel, and the less fat we store (Taubes, 120). Insulin works to suppress this enzyme and prevents the breakdown of triglycerides, thus reducing the flow of fatty acids out of the fat cells (Taubes, 121).
Insulin also turns on a mechanism in the fat cells to pump in glucose - just as it does in muscle cells - and this increases the amount of glucose the fat cells metabolize (Taubes, 121). This increases the amount of glycerol molecules (byproduct of glucose metabolism) which can then be bound to fatty acids to create triglycerides (Taubes, 121). To make sure we have the room to store all these molecules of fat, insulin also works to create new fat cells in case the ones we have are full (Taubes, 121). The bottom line is: insulin works to make us fatter (Taubes, 121).

Furthermore, it is the carbohydrates that break down into glucose and increase the secretion of insulin that ultimately determines how much fat we accumulate (Taubes, 122). Taubes even goes so far as to tell us the process our body goes through as we eat: (Taubes, 123)
1. You think about eating a meal containing carbohydrates.
2. You begin secreting insulin.
3. The insulin signals the fat cells to shut down the release of fatty acids (by inhibiting HSL) and take up more fatty acids (via LPL) from the circulation.
4. You start to get hungry, or hungrier.
5. You begin eating.
6. You secrete more insulin.
7. The carbohydrates are digested and enter the circulation as glucose, causing blood sugar levels to rise.
8. You secrete still more insulin.
9. Fat from the diet is stored as triglycerides in the fat cells, as some of the carbohydrates that are converted into fat in the liver.
10. The fat cells get fatter, and so do you.
11. The fat stays in the fat cells until the insulin level drops.
While most other hormones have a hard time getting fat out of the cells if the insulin levels are elevated, cortisol provides an exception. Cortisol is a hormone we secrete in response to stress or anxiety. "Cortisol," according to Taubes, "actually works to put fat into our fat tissue and to get it out." (124) It puts it into the cell by activating LPL as well as by exacerbating a condition known as insulin resistance, causing you to secrete more insulin and store more fat (Taubes, 124). This helps to explain why people put on more weight when they get stressed anxious, or depressed and eat more, and why others don't.

Therefore, the one thing we know that we absolutely must do in order to get leaner is to lower our insulin levels and to secrete less insulin to begin with (Taubes, 124). If we continue to keep our insulin levels high, the fat will not be available, nor will protein, which our cells need for fuel. Since we can't use the carbohydrates we've stored in the liver and muscle tissue either, because insulin keeps that locked up too, the cells find themselves starved for fuel, and we can literally feel their hunger (Taubes, 126).
Why I Get Fat and You Don't (or Vice Versa)
Taubes reminds us that "the effect of a hormone on any particular tissue or cell depends on a host of factors, both inside and out side the cell - on enzymes, for instance, such as LPL and HSL. This allows hormones to differ in their effect from cell to cell, tissue to tissue, and even at different stages of our development and our lives." (127) He tells us, "one way to think about insulin in this context is as a hormone that determines how fuels are "partitioned" around the body." (127)
Many things determine how insulin partitions energy. One major factor is how sensitive to insulin our cells happen to be and how quickly they become insensitive in response to the insulin you secrete, called insulin resistance (Taubes, 129). According to Taubes, "the more insulin you secrete, the more likely it is that your cells and tissues will become resistant to that insulin. It will take more insulin to do the same glucose-disposal job, keeping blood sugar under control." (129) This resistance occurs when a lot of insulin is secreted in response to foods like easily digestible carbohydrates and your cells are likely to resist the effects of that insulin, because they are getting enough glucose already. "If these cells become resistant to insulin, more insulin is required to keep blood sugar levels in check, so now you secrete more insulin, which prompts more insulin resistance. And all the while, that insulin is working to make you fatter, unless your fat cells are also resistant to it." (Taubes, 129)

Another factor is that your cells respond differently to insulin. Different types of cells (fat, muscle, liver, etc) do not all become resistant at the same time, to the same extent, or in the same way (Taubes, 130). If, for example, your muscle cells are relatively insensitive to insulin compared with your fat cells, then your fat tissue will accumulate more of the fat, causing you to become fatter and more sedentary (Taubes, 130).
A final factor in how tissues respond to insulin depends on age. As we get older, we get more insulin-resistant. "This," Taubes tells us, "almost invariable happens to your muscle tissue first and only later, if at all, to your fat tissue." (130) As you enter into middle age, it becomes very difficult to remain lean. You will also begin to gain a lot of metabolic issues because of the insulin resistance and high levels of insulin in the body; such as high blood pressure, HDL cholesterol goes down, you become glucose intolerant, etc (Taubes, 131). Also, as we age, "our muscles will become increasingly resistant to insulin, and this partitions more of the energy we consume into fat, leaving less available for the cells of muscles and organs to use for fuel. These cells now generate less energy, and this is what we mean when we say that our metabolism slows down." (Taubes, 131)
Finally, children today are tending more and more to be born predisposed to accumulating fat easily. This may be because of genetics, and even more so based on the mother's diet. Since children in the womb are supplied nutrients from the mother, if the mother's blood sugar is higher, then her child will get more glucose. The pancreas in the child will respond to this higher level of glucose by creating more insulin-secreting cells; causing the child to have a tendency to over secrete insulin and become insulin-resistant as it gets older (Taubes, 132)
What We Can Do
Taubes tells us that "whether you're born predisposed to get fat is beyond your control. What Adiposity 101 teaches us, though, is that this predisposition is set off by the carbohydrates we eat - by their quantity and their quality." (134) Not all carbohydrates are created the same though - and this depends based on the types of foods they are contained in. The most fattening foods are the ones that have the greatest effect on raising blood sugar and insulin secretion, the concentrated sources of carbohydrates that can be digested quickly; such as anything made with refined flower, liquid carbohydrates, and starches (Taubes, 134). Interestingly, these foods are also the cheapest, explaining why the poorer we are, the fatter we tend to be.

The carbohydrates found in leafy green vegetables are a different story though. They are bound to indigestible fiber and take much longer to be digested and enter our bloodstream. They also contain more water and fewer digestible carbohydrates for their weight, causing us to have to eat more to get the same load of carbs. Since they take longer to digest, our blood sugar levels remain relatively low when we eat them, and they initiate a far more modest insulin response, making them less fattening (Taubes, 136).
Fruits provide a different story even still. While they are full of water and vitamins, they also contain a uniquely fattening type of sweetener: fructose. The fructose in many artificial sweeteners (like high-fructose corn syrup) that is combined with glucose might be particularly effective in making us fat. When we digest sugar or high-fructose corn syrup, much of the glucose ends up in the general circulation, raising our blood sugar levels. The fructose, however, is metabolized almost exclusively in the liver, which has the necessary enzymes to do it. So fructose has no immediate effect on our blood sugar insulin levels." (Taubes, 137) But the key word here is immediate - it does have lots of long-term effects. While fructose exists in small amounts in fruits (30 calories per serving), our sodas today contain amounts so high that our bodies are not evolved to handle (80 calories in one soda) (Taubes, 137). Our bodies respond to the high amounts of fructose by simply turning much of it into fat and shipping it to our fat tissue. Fructose is, after all, the most lipogenic carbohydrate - the one we convert most readily to fat (Taubes, 138). So even though fructose has no immediate effects, it may have long-term effects on insulin resistance, helping to store more calories as fat (Taubes, 138).

Injustice Collecting
Taubes message of Adiposity is a simple one, that to become leaner and lose more fat, we have to lower the number of insulin-raising carbohydrates in our diet. Unfortunately, the implications of this message are that we cannot do this without some kind of sacrifice. Unfortunately, the foods that we crave the most (pasta, bread, bagels, french fries, etc) rank highest on the list of foods responsible for making us fat.
In addition to this, insulin secretion also helps us to crave these types of food. Increases in insulin levels allows us to perceive the food tasting better - more insulin will create a tastier experience of eating. Sugar is a little bit different than most other carbohydrates. In addition to having some insulin increasing effects, sugar also triggers a "reward center" in the brain that causes addiction to it (Taubes, 142). So unfortunately," the foods that make us fat also make us crave precisely the foods that make us fat" (Taubes, 143).

Why Diets Succeed and Fail
The most likely explanation for why diets succeed is because the "dieter restricts fattening carbohydrates, whether by explicit instruction or not. To put it simply, those who lose fat on a diet do so because of what they are not eating - the fattening carbohydrates - not because of what they are eating." (Taubes, 144) We specifically rid the body of the worst carbohydrates because they are the easiest and most obvious to eliminate when trying to get healthy or in shape; such as beer, sodas, candy, desserts, donuts, potatoes, rice, refined carbohydrates - and we will replace with more green vegetables, salads, and whole grains (Taubes, 145). It is very rare for someone to continue eating these products when they are exercising five times a week to try to lose weight.
"When calorie restriction diets fail, as they often do," according to Taubes, "the reason is that they restrict something other than the foods that make us fat. They restrict fat and protein, which have no long-term effect on insulin and fat deposition but are required for energy and for the rebuilding of cells and tissues. They starve the entire body of nutrients and energy, or semi-starve it, rather than targeting the fat tissue specifically." (147) Taubes says that "what adiposity 101 ultimately teaches us is that weight-loss regimens succeed when they get rid of the fattening carbohydrates in the diet; they fail when they don't." (147)
Exercise: Continuing on my journey of getting better. I'm almost to Sunday or Monday when my workouts will finally resume and I'm looking forward to it. Today is a yoga/run day. I recommend getting a good 20 to 30 minute run in today and then participating in some yoga to strengthen and stretch your sore muscles.
Eat: How much fresh produce should we eat? The USDA guidelines suggest that we eat anywhere from 5 to 13 servings of fruits and vegetables per day depending on age, gender, physical activity, and overall health. In order to know how much a serving is, use the size of your fist for an approximate measurement for one serving, which is one cup.
Relax: Before bed tonight, I sat down and played one of my absolute favorite video games in the world… and it's a classic: Harvest Moon 64. Sometime's it's just so nice to sit down and relax while getting into a game/story line. I will probably have to play this more over the weekend… I forgot how much I love this game!