Why the Inflammation is the new Menace for Brain

Scientists now suspect chronic low-level inflammation may underlie much diverse neurological damage, including Alzheimer’s disease. This discovery may help explain many odd facts: why people who take anti-inflammatory drugs, as for arthritis, have low rates of Alzheimer’s and slower mental decline (more than twenty studies show this to be true); why fish oil, an anti-inflammatory substance, protects against brain damage and can alleviate depression; why aspirin, which fights inflammation, may reduce the risk of cerebrovascular disease in general and ischemic (blood clot) strokes in particular; why certain antioxidants that have anti-inflammatory activity, such as vitamin E and C, appear to protect against brain cell death and deterioration; and even why cholesterol-lowering statin drugs help ward off strokes and heart attacks. New research finds they are a potent anti-inflammatory.

Inflammation is a newly recognized enemy underlying gradual brain destruction, contributing to strokes, mood disorders, schizophrenia, and neurodegenerative diseases such as Alzheimer’s, as well as “normal” mental decline. Knowing that inflammation is in a sense a slow-acting nerve toxin, why would anyone want to regularly flood brain cells with the fuel to ignite inflammatory agents?

They probably wouldn’t. But then most people don’t know that omega-6-type fat is such a fuel. It is scientifically well established that omega-6 fatty acids tend to be extremely pro-inflammatory.

It is a complex process, but essentially here’s how it happens: When fats are metabolized (broken down for use), they spew off byproducts, some benign, some harmful, depending on the type fat. The metabolism of omega-6s sets off ferocious fireworks of incendiary byproducts of hormonelike substances known as eicosanoids—including prostaglandins, leukotrienes, and cytokines—as well as free-radical chemicals, all of which can trigger inflammation.

For example, researchers consistently detect high levels of one type of pro-inflammatory prostaglandin—a hormone-like substance—in the brains of Alzheimer’s patients, but not in the brains of nondemented elderly people. Dr. K.N. Prasad and colleagues at the University of Colorado Health Sciences Center in Denver have branded specific prostaglandins as “neurotoxins” because they kill brain cells. Such discoveries cause researchers to believe that the activation of such inflammatory mechanisms causes the degeneration of brain cells.

Pouring omega-6 fats into brain cells lights a fire throughout the brain that may end in nerve cell destruction.

One of the most frightening pro-inflammatory agents produced by the conversion of omega-6-type fat in cells is a chemical called arachidonic acid. Under certain circumstances it is deeply involved in nerve cell death. Besides spawning inflammatory eicosanoids and superawful free-radical chemicals, arachidonic acid also can stimulate production of glutamate, a neurotransmitter, which is a natural-born cell killer.

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Recent research incriminates glutamate as the primary initiator of the execution of neurons, involved in brain damage from aging and strokes as well as degenerative brain diseases, including Alzheimer’s.

By unleashing the fury of glutamate in cells, arachidonic acid triggers a cascade of molecular events ending in cells’ actually being “excited” to death. Excessive glutamate provokes neurons to fire over and over, until they are exhausted. In so doing, a steady stream of free radicals is created and cellular calcium regulation gets so screwed up, levels build up inside neurons to toxic levels. At this point the nerve cell may become so dysfunctional, it issues an order to self-destruct.

The cellular obituary lists as cause of death a process called “excitotoxicity.” This “excitotoxicity” is thought to be one reason nerve cells die in Alzheimer’s disease. If at any point this process can be interrupted, the neuron may survive. There are many possibilities for rescue—taking antioxidant supplements and anti-inflammatory drugs, even aspirin, for example. Another one is to stop eating so many omega-6s, thereby preventing oversupplies of toxic arachidonic acid from flooding brain cells. (For foods with the most omega-6s, see a later post)

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Eating more omega-3 fish oil also helps defuse the “excitotoxic” brain damage, research shows. You could also save your brain from excessive production of arachidonic acid and other agents of destruction in the first place by turning down inflammatory processes.

Such inflammation was probably rare in ancient brains because of the proper balance of omega-6 fatty acids to omega-3 fatty acids. If you have enough omega-3s in brain cells, they can neutralize the ill effects of omega-6s. Thus, sending in forces of omega-3 molecules by eating fatty fish can help cool the fires kindled by omega-6s and curtail potential brain damage.

Omega-3 fats, in a word, help curtail the damage omega-6 fats can inflict on your brain cells, including the “excitotoxicity” process researchers believe is implicated in brain degeneration. Perhaps that’s why people with lower levels of omega-3 fatty acids, particularly the fraction called DHA which is most active in nerve cells, are more apt to develop Alzheimer’s disease.

So spectacular are the newly discovered brain benefits of eating omega-3 fish oil that the next chapter is devoted entirely to that amazing new research.

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