Protect your brain against Alzheimer’s disease with this common spice

Yesterday, I reported on the Alzheimer Association’s (AA) reluctant endorsement of three “non-drug” therapies. They anticipated the happy day when we can give yet-be-discovered Alzheimer’s disease (AD) drugs in combination with these three real, available, proven, and natural therapies.

But why wait?Homemade Decorated Gingerbread Men Cookies

The proven, natural therapies exist now. Plus, now we can add another natural remedy to the list of potential, non-drug therapies overlooked and ignored by the misguided Alzheimer’s Association–ginger.

In fact, new cutting-edge science–published in the Indian Journal of Experimental Biology–suggests that ginger may be the ideal natural AD treatment.

I pay careful attention to this kind of news. Especially when I compare it to the evidence for the current AD drugs on the market, well known for their harmful side effects and lack of effectiveness.

Indeed, today’s AD drugs rely on patented derivatives of petrochemicals that are inherently toxic to the brain. The neuroscientists who conducted the new study said using these toxic drugs is the equivalent of declaring chemical warfare on the human brain. In fact, brain seizures are one of the most common side effects of these drugs.

By comparison, ginger is a safe, non-toxic remedy. Plus, for this new study, researchers found that it protects the brain against AD in three specific ways.

First, it targets inflammation and oxidation. Previous research shows these two actions cause premature degeneration of neural brain tissues, as we see in AD patients.

Second, ginger protects against the development of A-beta, a molecular abnormality in the brain. More specifically, A-beta is a type of improper folding of a key protein that causes neurotoxicity. Plus, we know the presence of A-beta is one of the adverse brain changes that occur in AD patients. A 2013 study in lab animals found that ginger actually reversed dysfunctional behaviors caused by this brain abnormality.

Third, ginger seems to work as a natural acetylcholinesterase inhibitor. (Many popular AD drugs work in this way, but they cause terrible side effects.)

These inhibitors prevent the enzyme acetylcholinesterase from breaking down acetylcholine, a key neurotransmitter your brain needs for learning and memory.

Interestingly, the researchers in the new study found that ginger increases the level of this key neurotransmitter in the brain. Plus, it increases how long the neurotransmitter stays active in the brain. As a result, it stimulates normal brain functions.

So–how much ginger should you take to help boost your brain function?

You can probably tolerate ginger at doses up to 2 g (2,000 mg) daily. You can add this amount to your foods as a spice. You can also get this amount as a dietary supplement. At this dose, there was no known acute toxicity.

I suggest keeping some fresh ginger root in your kitchen year-round. And with the holidays coming up, I’m sure you can find more than one good recipe calling for ginger.

You can sprinkle it on baked goods and include it in beverages. You can slice it into healthy salads. And use it as a garnish for fish, meat and vegetables. Of course, you can also use it when you make your favorite Asian dishes. And shredded ginger makes a great topping for (moderate) servings of ice cream or chocolate dishes.

At this time of year, I like to remember the folk tale of the Gingerbread Man. As you may recall, Gingerbread Man taunts his many pursuers with the famous line:

Run, run as fast as you can!

You can’t catch me. I’m the Gingerbread Man!

Of course, the tale ends with a fox catching and eating the Gingerbread Man who cries as he’s devoured, “I’m quarter gone…I’m half gone…I’m three-quarters gone…I’m all gone!”

According to this new research, if you make ginger a part of your daily regimen, perhaps your brain won’t go the way of the Gingerbread Man…a quarter gone…half gone…all gone


1. “In Vitro Evaluation of Anti-Alzheimer’s effects of dry ginger extract,” Indian Journal of Experimental Biology, June 2014; vol 52: 606-612