I received a really interesting series of questions from a good friend of mine today. A common friend of ours had adopted a low-carb diet with apparently great results, and now my friend has a bunch of questions, largely concerning how insulin relates to our bodies' metabolism. I nearly started hyperventilating from the prospect of a captive audience interested in biochemistry ;)
Specifically, my friend had been directed to an author, whose main thesis is...well I can't seem to find a coherent thesis to summarize his post, but I want to make a few observations about it.
I will confess that he articulates a lot of potentially difficult information in a way that any reader can understand. He's good at providing real world analogies, and he uses descriptive terms and simple ideas that summarize his points well. The world can definitely use more people who are good at making these things easier to understand. Also, the basic physiological and biochemical ideas he's describing are pretty sound.
He rambles, a lot (I admit, I'm just as bad), and took a billion words to state the same concept a million different ways. He also has an odd habit of standing up for fat people who are undeservedly maligned, while in the same post accusing people who don't agree with his views of being fat and ignorant. wtf?
Most importantly, this guy is basically saying that he's solved the problem of overweight/obesity. Trust me, people, if someone ever tells you that they know the answer to a question that has been plaguing science for decades, feel free to pat them on the head and go find an adult to talk to. This is probably not a problem that's going to have a simple solution. Even if it does, you're not going to find it on some guy's blog--even if he's an MD. After all, I'll be an MD in two weeks, and sometimes I wear my shirt inside out without realizing it. LAWL
SO! What were those questions my friend (let's call him Tim) was asking? They are thusly:
1. How does fat get stored in our cells? Is it indeed insulin which triggers it?
2. Given 1, Is it true that even if there is fat available in the bloodstream, it won't be stored in our body without insulin? (ie without insulin, the body will flush out the excess fat without storing it)
3. What is insulin resistance?
4. Does insulin resistance actually affect liver cells before other cells? And does our liver actually secrete sugar into the bloodstream?
5. Does consumption of sugar and carbohydrates trigger an increased production of insulin?
6. Do obese people tend to have elevated insulin levels? (even when not eating)
7. Does glucagon actually counteract the effect of insulin?
8. Given 7, and given the rest of the low carb theory, why can't an injection (or pill) be created for glucagon to be administered after eating? That way as I understand (in my limited reading), wouldn't insulin levels reduce, allowing the body to consume the stored fat, providing energy between meals?
Amazing. Delicious. The thought of answering these questions makes me salivate. Let's dig in.
We need to start with a very cursory overview of basic nutrition. Our energy comes from 3 different macronutrients: carbohydrates, fat, and protein. Carbohydrates are sugars of varying complexity. You can make complex carbohydrates from combinations of the basic sugars. The fundamental basic carbohydrate in the human body is glucose. Fructose is another basic carb. A glucose molecule attached to a fructose molecule makes sucrose. Glycogen (which is almost the same thing as starch) is a huge molecule of hundreds of glucose molecules attached together. Glucose is stored as glycogen in the liver. Fats consist of different types of fatty acid chains and are stored in adipose (fat) tissue. Protein is made up from amino acids, and is the major structural component of all our cells, including muscle. The body can bascially turn any macronutrient into either of the other two (except certain amino acids, which we can't make on our own).
Questions 1, 2, 4, 5, and 7 can all be answered this way: yes. lol. To be more specific, refer to the image with all the blobby stuff. Basically, in fasting states, when you're hungry and your blood sugar is low, the pancreas releases a hormone called glucagon. This acts on the liver to release stored sugar and to create new sugar from scratch. That way, you don't die in between meals. Evolution win!
In "fed" states, after you've consumed a meal, your blood gets flooded with all the sugars from the food you ate. Blood glucose levels rise, which tones down glucagon and turns up insulin. Insulin promotes sugar uptake into the liver (and all cells, really) for storage, and promotes fat intake and storage in fat cells. Your body is always producing both insulin and glucagon, but their levels are balanced so as to keep your blood glucose levels at a constant level. (NB question 2 will be discussed in more detail with question 8 at the end of the post.)
Questions 3 and 6 get a little more complicated. It is based on a cellular molecular process called down-regulation. It's a negative-feedback process. The best example would be topical nasal decongestants. When someone is suffering from allergies, the blood vessels in the membranes of their nose get "leaky". Fluid seeps out and drains out the nose, producing some of the symptoms of allergy. Nasal decongestants work by spraying a drug into your nose that constricts the nasal blood vessels and stops the leaking. BUT! If you continue to use the spray regularly for a few days, the cells in the blood vessels get tired of being bombarded with drug. They then start to get rid of the receptors on their cell surface that bind the drug. So you end up needing more of the drug to get the same effect!
Insulin works the same way, but the response is much slower--it takes years, rather than just days. People who run their blood sugars high all the time (presumably by eating too much unhealthy food) have constitutively high levels of insulin in their blood. Eventually, the cells in their body get sick of listening to insulin's constant nagging, and they stop listening--by decreasing the expression of insulin receptors, so the insulin has less effect. So the body has to produce more insulin to keep glucose levels under control. Which leads to more down-regulation of insulin receptors. Eventually, the body can no longer produce enough insulin to keep up, and glucose levels go through the roof, leading to increased risk of cardiovascular disease, kidney failure, and blindness. This process is referred to as Type II Diabetes Mellitus, and it's one of the biggest medical problems facing our society today.
Questions 2 and 8 are sort of plausible/true in theory, but impractical for a number of reasons. Low insulin levels lead to high glucose levels, which is a trigger for insulin release. The only way to avoid a compensatory surge in insulin is by having a defective pancreas that can't produce insulin. Unfortunately, that's the pathological basis for Type I Diabetes Mellitus. People who can't make insulin get impossibly high blood levels of glucose, but the glucose can't get into their cells, so they actually think they're starving. This causes the body to synthesize ketones from stored fat, which eventually turns the blood to acid and causes death. :(
Conversely, giving a person an injection of glucagon might indeed lower their insulin levels, but it will still cause an increase in blood glucose levels. That's the stuff that leads to the cardiovascular disease and kidney failure and blindness :(
Now, the whole point of all these questions, I think, is probably related to the very common question: will the Atkins diet make me look like Megan Fox? I've done a little research into it, and I'd like to write about it, but I did promise my fiancé I'd clean the bathroom today. So let me get to that, and I'll see if I can extrapolate some of this sciencey stuff into practical stuff later.
58 minutes ago