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By Tom Dennen, the paranoid historian (Reporter)
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Why is Junk Food “Bad” REALLY? It Prompts The Collapse Of Ancient And Mutually Beneficial Gut Bacteria Symbioses.

Monday, February 10, 2014 7:42

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(Before It's News)

“We’re already familiar with a version of this ‘inflammation’ dynamic: this “Metabolic Syndrome”, tooth decay, which is as old as teeth, but it intensified with increased consumption of refined carbohydrates, like sugar, just before and during the industrial revolution.

Before cheap sugar became widely available, plaque microbes probably occupied the warm and inviting ecological niche of your mouth more peaceably. But dump a load of sugar on them and certain species expand exponentially. Their by-product acid, which in normal amounts, protects you from foreign bacteria—now corrodes your teeth. A once cooperative relationship becomes antagonistic.

Something similar may occur with our gut microbes when they’re exposed to the highly refined, sweet, and greasy junk-food diet. They may turn against us.

Children born to obese mothers have hardened arteries at birth, a risk factor for cardiovascular disease. They have a greater risk of asthma. Some studies suggest they’re

more likely to suffer from attention deficit disorders and autism.

Why Are We Increasingly Prone To Obesity?

The long-dominant explanation is simply that too little exercise and too many calories equals too much stored fat. The solution: more exercise and a lot more willpower. But there’s a problem with this theory: In the developed world, most of us consume more calories than we really need, but we don’t gain weight proportionally.

A pound of body fat contains roughly 3,500 calories. If you run a daily surplus of just 500 calories—the amount in a bagel with a generous serving of cream cheese—you should, judging by the strict calorie-in-must-equal-calorie-out model, gain a pound of fat per week. Most of us do run a surplus in that range, or even higher, but we either gain weight much more slowly, or don’t gain weight at all.

Here’s the traditional understanding of metabolic syndrome:

You ate too much refined food sopped in grease.

Calories flooded your body.

Usually, a hormone called insulin would help your cells absorb these calories for use.

But the sheer overabundance of energy in this case overwhelms your cells. They stop responding to insulin. To compensate, your pancreas begins cranking out more insulin. When the pancreas finally collapses from exhaustion, you have diabetes. In addition, you develop resistance to another hormone called leptin, which signals satiety, or fullness. So you tend to overeat. Meanwhile, fat cells, which have become bloated and stressed as they try to store the excess calories, begin emitting a danger signal—low-grade inflammation.

But new research suggest another scenario: Inflammation might not be a symptom, it could be a cause. According to this theory, it is the immune activation caused by lousy food that prompts insulin and leptin resistance.

Sugar builds up in your blood.

Insulin increases.

Your liver and pancreas strain to keep up.

All because the loudly blaring danger signal—the inflammation—hampers your cells’ ability to respond to hormonal signals.

Maybe the most dramatic evidence in support of this idea comes from experiments where scientists quash inflammation in animals. If you simply increase the number of white blood cells that alleviate inflammation—called regulatory T-cells—in obese mice with metabolic syndrome, the whole syndrome fades away. Deal with the inflammation, it seems, and you halt the dysfunction.

Now, on the face of it, it seems odd that a little inflammation should have such a great impact on energy regulation. But consider: This is about apportioning a limited resource exactly where it’s needed, when it’s needed.

When not under threat, the body uses energy for housekeeping and maintenance—and, if you’re lucky, procreation, an optimistic, future-oriented activity. But when a threat arrives—a measles virus, say—you reprioritize. All that hormone-regulated activity declines to a bare minimum. Your body institutes a version of World War II rationing: troops (white blood cells) and resources (calories) are redirected toward the threat. Nonessential tasks, including the production of testosterone, shut down. Forget tomorrow. The priority is to preserve the self today.

Now, on the face of it, it seems odd that a little inflammation should have such a great impact on energy regulation. But consider: This is about apportioning a limited resource exactly where it’s needed, when it’s needed. When not under threat, the body uses energy for housekeeping and maintenance—and, if you’re lucky, procreation, an optimistic, future-oriented activity.

But when a threat arrives—a measles virus, say—you reprioritize. All that hormone-regulated activity declines to a bare minimum. Your body institutes a version of World War II rationing: troops (white blood cells) and resources (calories) are redirected toward the threat. Nonessential tasks, including the production of testosterone, shut down. Forget tomorrow. The priority is to preserve the self today.

This, some think, is the evolutionary reason for insulin resistance. Cells in the body stop absorbing sugar because the fuel is required—requisitioned, really—by armies of white blood cells. The problems arise when that emergency response, crucial to repelling pillagers in the short term, drags on indefinitely.

Imagine it this way. Your dinner is cooking on the stove. You’re paying bills. You smell smoke. You jump up, leaving those tasks half-done, and search for the fire before it burns down your house. Normally, once you put the fire out, you’d return to your tasks and then eat dinner.

But now imagine that you never find the fire, and you never stop smelling the smoke. You remain in a perpetual state of alarm. Your bills never get paid. You never eat your dinner. Your house smoulders. Your life falls into disarray.