More on fat.

February 2, 2009

I’m in a mood now, so you get to read a rant, this time on fat.

As I said in my previous posts, I am fat.  This has had certain negative impacts on my life, mostly psychological, but is not an aspect of me that I find particularly controlling (except on a dietary level).  I will also volunteer that I am not perfectly peachy being as heavy as I am, BUT since I am not cripplingly overweight I do not consider it a pressing OMGISSUE!!!

Anyway, let me talk about fat.  Specifically, fat, obesity, the “Obesity Epidemic”, and type II diabetes.  And scientists.  Especially scientists.

Seriously.  Scientists have this nasty habit of saying things that make me want to hit my head on the desk.  You’d think for people who’ve been studying this as long as they have they would GET IT ALREADY, but apparently not.  I refer to the correlation between obesity and Type II diabetes.

According to (some) scientists, obesity raises your risk for getting Type II diabetes.  They’ve come to this conclusion because they have noticed a correlation between the people who are obese and the people who are diabetic.  Well, I give them props for figuring out the connection, but I’m afraid they’re still a bit far from the truth.

I would now like to take a moment to put in a good word for my (sadly deceased) “personal dietary instructor”, Dr. Robert Atkins.  The guy is well known for, of all things, suggesting a low-carbohydrate diet.  In the face of the low-fat, high-carb dogma most dietitians were pushing, this was both shocking and met (perhaps rightly) with great skepticism.

His diet proposed that it was not the consumption of fat that was causing weight gain, but the consumption of excessive carbohydrates.  And his reasoning was quite solidly based on the diabetes-obesity connection, believe it or not.  Yep, back in the 1970’s, he’d caught on to it.  Let me explain how it works – at least, for fat-retaining, diabetes-developing people.

Firstly, a look at the human digestive system.  Humans run on four different sources of energy: carbohydrates, protein, fat, and alcohol.  We get these all from the food we eat, and process them through digestion before we can use them to run our bodies.  Since each of these sources is made from different material, we process them in different ways, and some are easier to process than others.

You probably already know that carbohydrates are the quickest and easiest of our usual diet to digest, followed by protein and fat.  What you may not have learned is that carbohydrates, being made of significantly different material from the other two sources, are processed in rather a different manner.

Broken down into their simplest form, carbohydrates are known as glucose, or blood sugar.  This is extremely basic sugar that occupies your body until such time as you get around to metabolizing it (burning it for energy).  It’s a very nice energy source, but it’s dangerous to have too much in your body at once.  Enter the pancreas.

The pancreas has multiple functions, but the best-known is its ability to release insulin.  Insulin is the hormone that forces your body to take care of excess sugar.  Basically, it instructs your cells to take the excess glucose, change it into glycogen, and store it in your liver until it can be used later (something else that the pancreas causes).

For people like me, though, it’s not so easy.  I have a condition known as hypoglycemia – or, in layman’s terms, a hyperactive pancreas.  If I ingest too high a number of carbohydrates – or too simple of carbohydrates, which break down more rapidly – the resultant overload of sugar causes my pancreas to overreact.  It will produce much more insulin than usual, causing my cells to lock away nearly all of the glucose in my system, resulting in low blood sugar.

As if it wasn’t bad enough already, there’s another problem that results from this.  Your liver can only hold so much glycogen, and with my pancreas constantly locking away all the glucose in my system, it gets full in a huge hurry.  Once my liver is loaded, my cells have no choice but to move the glycogen to a secondary storage area: my fat cells.

Fat cells are a bit weird.  They don’t reproduce to expand, like other cells.  Instead, they feed on the glycogen and grow larger.  This is a useful system for animals such as bears, who must go for long periods without food and will metabolize the fat while they sleep.  Not so much for people like me, who have a ready supply of food.

This isn’t a problem for people with a normally-functioning pancreas.  Since most of the glucose they consume remains in their systems, they are able to digest it without a problem.  For the hypoglycemic, however, the sudden crash in glucose requires them to put a new energy source in their body immediately.  If I’m constantly adding new carbohydrates to my system, the resultant raise in insulin will prevent the deglycification process (glycogenolysis, in medical terminology), and my body will never get the chance to use the glucose stored in my liver – or to metabolize the fat reserves built up in my body.

Obesity isn’t the only result, though.  Repeated spazz attacks take their toll on the pancreas.  Eventually, it wears out and loses its ability to effectively produce insulin.  Without insulin to tell the body’s cells when to store glucose, blood sugar levels can raise dangerously.  This condition is normally referred to as Type II diabetes.

Not that every case of Type II diabetes – or even obesity – is caused solely by poor genetics.  Starvation early in life can lead to metabolic problems, as can other factors.  And now I’m going to annoy probably everyone, because I would like to shine some light on the real star of this story (at least here in America): processed flour and sugar.

They’ve become a staple in our diets.  They’re so light and fluffy or sweet and sticky.  We love the taste, the texture, everything about them.  And we’ve allowed them to become a regular part of our diets.

But all the processing they’ve gone through has done two things: broken them down, so that they digest faster, and removed extra material (such as fiber) that may have provided backup nutrition.  Even a healthy pancreas, when exposed to a shot of high-impact sugar, is forced to go into overdrive.  It may not produce enough insulin for a full-out hypoglycemic attack, but it will certainly end up locking away large quantities of glucose.  And once the liver gets full, you know what has to happen.

So why doesn’t a low-fat diet work?  After all, without fat particles to digest after the glucose runs out, your body should just switch to your internal sources and you should be good.  Well, it does, but since the only time this works is when you’re not busy digesting carbohydrates, your food is going to have worn out by the time you get around to raiding your fat cells.  Ever felt hungry all the time on a low-fat diet?  That’s why.


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