By now it's not exactly news that choline is good for your brain. It's been known for a long while that choline is probably the most basic nutrient necessary for optimal cognitive function. That's because choline is a precursor for acetylcholine, a key neurotransmitter (signaling molecule) without which we couldn't move, think, remember, or sleep. The body also uses choline for synthesizing phosphatidylcholine (PC), a component of the fatty membrane of every cell, brain cells included. In addition to its role as a structural element in cell membranes, PC can act as a choline reservoir for synthesizing more acetylcholine when needed.


Aging humans and animals tend to suffer from impaired short-term memory. This loss of working memory is largely the result of deficient functioning of the cholinergic neurons in a part of the brain known as the basal forebrain. (Cholinergic neurons are the brain cells involved in acetylcholine synthesis, signaling, and metabolism.) The age-related deficits in this part of the brain include decreased synthesis and release of acetylcholine, as well as decreases in the number of cholinergic brain cells and in the number and function of acetylcholine receptors on such cells.

The same neurons that are vulnerable in aging are especially vulnerable in Alzheimer's disease (AD). In AD the cholinergic cells of the basal forebrain shrivel and die in manner resembling normal aging but at an accelerated pace. This abnormal behavior is partly the result of defective cell membranes caused by decreased availability of choline and increased breakdown of phosphatidylcholine. When choline is in short supply and cholinergic cells are active, any available choline goes to make more acetylcholine at the expense of building membranes. Eventually enough choline is withdrawn from the membrane so that the amount of PC in a cell actually decreases, a process known as autocannibalism . In other words, the cell takes itself apart in an attempt to maintain normal acetylcholine signaling.

You might reasonably conclude from this that all we need to do to slow down brain aging or Alzheimer's disease is supply more choline to the brain, but you'd be only partly right. The problem is that choline transport into the brain is not especially efficient and tends to decline with age. Attempts have been made to treat dementia and cognitive impairment with choline supplements such as lecithin (dietary PC, typically derived from eggs or soy), but a review of all unconfounded, randomized trials comparing lecithin with placebo revealed no particular benefit. Alternatives to choline or lecithin are clearly needed in order to reverse age-related cognitive decline.

CDP-choline is an essential intermediate in the biosynthesis of phosphatidylcholine. Cells make CDP-choline out of choline and some other precursors before further processing it into PC. CDP-choline has been shown to improve performance on behavioral and psychological tests among patients with mild to moderate Alzheimer's disease. It can also counteract the amnesia induced by scopolamine, a compound which blocks acetylcholine receptors, thus confirming the role of the cholinergic system in the cognitive enhancing effects of CDP-choline. And it can promote cognitive recovery from a recent stroke.

More generally, a review of all relevant, controlled clinical trials concluded that CDP-choline is beneficial for treating cognitive and behavioral deficits caused by chronic brain disease in the elderly. This is in striking contrast to a similar review cited earlier that found no benefit for treating cognitive decline with choline in the form of lecithin. The superiority of CDP-choline over lecithin as a choline source should be evident.

L-DOPA is an amino acid precursor to dopamine that is widely used in treating Parkinson's. Animal studies have shown that oral CDP-choline treatment enhances the effects of L-DOPA by increasing the release of dopamine newly synthesized from it . In human trials, a combination of CDP-choline with L-DOPA was able to improve neurological symptoms with a smaller effective dose of L-DOPA than patients had previously received without CDP-choline. This result is important because chronic use of L-DOPA eventually results in neurotoxicity and loss of clinical effectiveness. The hope is that by combining CDP-choline with smaller doses of L-DOPA, it may be possible to prolong the period during which L-DOPA remains effective.

Since chronic cocaine abuse is likewise associated with dopamine depletion and increased turnover of cell membranes, the choline-dopamine connection predicts that CDP-choline should be effective for treating cocaine addiction. CDP-choline should be helpful in treating attention deficit hyperactivity disorder (ADHD), either as an adjunct to stimulants like Ritalin or as stand-alone supplements. This is based on the conclusion of the known involvement of dopamine metabolism in ADHD as well as on the dopamine-releasing and cognitive enhancing effects of CDP-choline discussed in previous paragraphs.

$29.00size/dose: 60 -250mg cps