Sunday, July 24, 2011

Is Insulin Resistance What Makes Me Fat?

According to Gary Taubes, the author of “Why We Get Fat and What To Do About It”, the answer is yes. But understanding why insulin resistance makes me fat requires some deep thinking, at least for a lay person such as myself. In previous posts, I shared Taubes’ insight that most of us have the cause and effect of obesity reversed. We don’t get fat because we consume more calories than we burn, but rather we consume more calories than we burn because we get fat. Said another way, calories that are stored in fat are unavailable for burning for fuel, so we need to eat more calories and/or move less to offset those lost calories in the fat.

Ok, what is insulin resistance and how does it make me fat? Here’s my interpretation of Taubes’ hypothesis.

When I eat a meal, the carbohydrates are broken down into glucose and enter my bloodstream. Glucose, a form of sugar, causes my blood sugar to increase. Since high blood sugar is toxic, my body instantly responds. First, any fat in my meal isn't immediately used for energy. Rather, it is shuffled to fat storage, at least temporarily, until the high blood sugar is reduced. I temporarily get a little fatter. Second, my pancreas secretes the hormone insulin. The secretion of insulin is in direct response to the increase in blood sugar. Insulin's job is to tell my body's cells to take in this glucose from the blood stream to reduce my high blood sugar.

Muscle cells will take in this glucose and burn it for energy and store some for future fuel as glycogen. Liver cells store some as glycogen and convert some to fat. Fat cells convert the glucose to fat for storage. As the cells in my body use up the glucose in my blood, the blood sugar will drop, and so the insulin will also drop. As the process occurs, fat is released from my fat cells so that they can be burned for fuel in place of the reduced glucose levels. I temporarily get a little leaner. My fat cells are acting as a temporary buffer for energy until my body deals with the toxic sugars.

Understanding the mechanism for how insulin communicates with my body's different cells is the key to understanding how I get fat. Insulin works through two enzymes on the cell: lipoprotein lipase (LPL) and hormone sensitive lipase (HSL).

LPL is on the outside of cell membranes and pulls fat from the bloodstream through the cell membrane. In muscle cells, this fat is used for fuel. In fat cells, it is simple stored and makes the cell fatter. LPL does its job by breaking up the fat from a triglyceride form (glycerol + 3x fatty acids) into individual fatty acids. When insulin is secreted due to high blood sugar levels, it activates LPL on fat cells resulting in fat being diverted from the bloodstream to the fat cells. Conversely, insulin suppresses LPL on muscle cell, so these muscle cells cant burn fat for fuel, but rather the muscle cells will burn the gluclose from the bloodstream to lower my blood sugar level.

HSL breaks down triglyceride fat in the fat cells into their individual fatty acids. Unlike the large triglyceride fat, the fatty acids are small enough to go through the fat cell membranes to be liberated into the bloodstream and eventually used for fuel in muscles. Insulin suppresses HSL. When insulin is secreted due to high blood sugar, it doesn't allow the HSL to liberate fatty acids so muscle cells need glucose for energy. When the blood sugar levels drop and insulin drops, then HSL activates the release of fatty acids into the bloodstream to be used for fuel by the muscles.

The reason why some of us seem to fatten more easily is that our body's muscle cells are less sensitive to insulin. Said another way, some of us are insulin resistant. And the reason why some of us fatten as we grow older is that our muscle cells become less sensitive to insulin. When our muscle cells are less sensitive to insulin they do not adsorb glucose as readily from the bloodstream. This makes our blood sugar levels higher which makes us secrete more insulin. More insulin secretion activates more LPL on fat cells so that they accumulate more fat. More insulin secretion suppresses more LPL on muscle cells so that they will not burn more fat. More insulin secretion suppresses HSL in fat cells so that fatty acids are not released for fuel. With more insulin secretion more calories will be stored as fat, fewer calories will be available to fuel the rest of the body, the more we will eat to replace those lost calories in the fat (or become more sedentary) and the fatter we will get.

Insulin resistance leads to metabolic syndrome, which is a condition with several signs besides fattening, including high blood pressure, high triglycerides, low HDL levels, glucose intolerance (trouble controlling blood sugar) and becoming sedentary (from caloric drain into fat tissues).

Taubes argues that there is a way to break this cycle. Reduce the quantity of carbohydrates and improve the quality of the carbohydrates in a meal. These two factors drive insulin secretion and the accumulation of body fat. Not all foods that contain carbohydrates are equally fattening. The most fattening carbohydrates are the ones that have greatest effect on blood sugar and insulin levels. The glycemic index is a measure of how our blood sugar responds to certain foods. If the glycemic index of food is minimized, then the secretion of insulin and fat stores is minimized. Foods with high glycemic index include refined flour (bread, cereals, pasta), liquid carbohydrates (beer, fruit juices, sodas) and starches (potato, rice, corn). Leafy green vegetables are an example of low glycemic index foods. They have more water and digestable fibers that make up their weight. They have low concentrations of carbohydrates.

My only criticism of Taubes' book is that it is easy to get lost in his argument against "calories in, calories out". He argues consistently that a positive caloric balance (eating more, moving less) is not the reason why we get fat. This seems illogical, and it is at face value. Taubes' argument is merely that a positive caloric balance is a side effect of getting fat, not a cause. The real cause for fattening is the loss of calories to fat cells caused by high insulin levels from too many carbohydrates in our food. An appreciation of this book requires an open mind and patience to follow a unique point of view.


  1. I have a lot of respect for Taubes, even thinking he deserves a Nobel prize in Medicine for GCBC. One of the old, pre-political Nobels that meant something.

    You mention that pasta is high glycemic index. I wrote the same thing once at one of my blogs and an alert reader corrected me: it's not. Here's a reference at See the table containing "spaghetti." Many spaghettis have a glycemic index under 50. If it's over-cooked, the GI is probably higher.

    Correct me if I'm wrong.


  2. Regarding foods with high glycemic index, I was summarizing Taubes from his new book. Perhaps I misunderstood. Actually, I still have a hard time grasping the concepts. In theory, it makes sense that carbs elevate insulin which causes us to store fat, but in practice, why aren't all these low-carbers as skinny as a rail after eating this way for years?

  3. ...and I still easily get confused by Taubes' arguments against calories in/out not causing obesity. Whether it's the cause or the effect, I still have to limit total calories to lose weight. Perhaps its easier to limit calories on a low carb diet, maybe due to even energy levels and not getting too hungry, but I believe calories in/out still matter.