Galantamine Beats Prescription Drugs for Combating Mental Decline
The natural way to keep your grip on memory and cognitive function
    by Will Block

United States Army recruiting posters used to proclaim, "Be all that you can be." That's good advice for all of us, although it gets harder and harder as we get older. Advances in medicine and nutrition have helped us live years longer than our parents and grandparents did, but very little has proved to be effective in fighting, let alone reversing, the gradual mental decline - especially in its severest form, dementia - that often accompanies aging.

The onset of dementia is marked by a continuing loss of memory and other cognitive functions, and a declining ability to perform such simple tasks as bathing, getting dressed, and climbing stairs.  While Alzheimer's disease looms as the most ominous of such brain robbers, we have all but cast aside our concern about the other forms of dementia.  After Alzheimer's disease, the most common form is vascular dementia (VaD), for which stroke is the most common cause; other causes include arteriosclerosis (hardening of the arteries), atherosclerosis (a type of arteriosclerosis caused by high cholesterol), hypertension, diabetes, abnormal heart rhythms, and autoimmune inflammatory diseases (such as lupus erythematosus).

Vascular dementia is traditionally viewed as a permanent, irreversible condition unrelated to Alzheimer's disease. However, a recent announcement by Dr. Timo Erkinjuntti at the World Congress of Neurology in London suggests that the same mechanism that undermines memory and cognitive abilities in Alzheimer's disease patients may also play a role in the development of VaD.1 This mechanism is a dysfunction in the cholinergic system, which is that part of the nervous system in which signals are carried from one neuron (nerve cell) to the next by the neurotransmitter acetylcholine (ACh). Through the cholinergic system, we relay signals to and from the brain, allowing us to learn, form and retrieve memories, and think clearly.

Unfortunately, cholinergic function does not remain constant throughout our lives. As we age, the system becomes less and less efficient, and our memory and cognitive functions slowly decline. Our brain's ability to use the ACh it makes is impaired, in part because the neuronal receptors that respond to ACh molecules tend to deteriorate and decrease in number.2 Small or modest decreases are evident in all of us as we get older, but some people experience more significant decreases, leading to more serious cognitive impairments. These are characterized as severe forgetfulness, an inability to learn new things, or failure to perform daily tasks competently.

Throughout our lives, the ACh levels in our nervous system are regulated by acetylcholinesterase (AChE), an enzyme that removes unused ACh by chemically degrading it. Ordinarily, this represents nothing more than a harmless molecular housekeeping process. If an imbalance results from too much AChE activity, however, our ACh levels can be reduced to the point that our ability to think clearly and function competently is compromised.

To short-circuit the removal of unused ACh, pharmaceutical companies have developed a class of drugs called acetylcholinesterase inhibitors. As the name implies, these compounds inhibit the action of AChE, thus maintaining higher levels of ACh. Tacrine was the first such drug, receiving FDA approval in 1993. Donepezil and rivastigmine soon followed, with approvals in 1996 and 2000, respectively. Although tacrine is rarely prescribed today, owing to its spectrum of severe side effects (notably liver damage), the other two drugs have become mainstays in the protocol for treating Alzheimer's disease.

Until now, pharmaceutical firms have had the upper hand when it comes to treating cognitive disorders, although their drugs come with a laundry list of deleterious side effects. The common ones include nausea, vomiting, diarrhea, headache, dizziness, drowsiness, fatigue, insomnia, flushing, hot flashes, skin rash, and tremor. Add to these factors the drugs' excessive cost and sometimes questionable benefits, and you have a situation that cries out for improvement. Recent discoveries - or, should we say, rediscoveries - have offered evidence that there is something better.

An AChE inhibitor backed by several thousand years of safe use has recently been found by scientists to be beneficial in treating dementia.  Called galantamine, it is extracted from flowering bulbs such as those of the common snowdrop (Galanthus nivalis), daffodil (Narcissus pseudonarcissus L.), and spider lily (Lycoris radiata).  Its recorded use dates back to the time of Homer, when it was administered to restore memory.  Both traditional and modern uses also indicate that galantamine has value for the relief of muscle soreness3 and for anesthesia.4

Galantamine is different from donepezil and rivastigmine in one very important way. In addition to boosting acetylcholine levels by inhibiting the action of acetylcholinesterase, galantamine has the unique ability to increase the receptiveness of nicotinic receptors to acetylcholine. (Nicotinic receptors are one of the two major classes of neuronal acetylcholine receptors; the other class is called muscarinic receptors.) This gives galantamine a major advantage in combating the impairments caused by a decline in cholinergic function.

Research has shown that galantamine's unique "one-two punch" has a profound effect on cholinergic function. In a new study of 592 patients who had vascular dementia or vascular dementia and Alzheimer's disease, scientists in the United Kingdom found that, after taking 24 mg per day of galantamine for 12 months, the 396 patients in the treatment group had better cognitive abilities than when they started the trial.1 The cognitive functions measured were memory, orientation, reasoning, and language skills.

The 196 patients in the control group were given a placebo for the first six months and were then switched to galantamine for the last six months. By the end of the first six months, their cognitive abilities had deteriorated. After receiving galantamine for the last six months, however, they rebounded and performed better on the cognitive tests than they had at the beginning of the study.

Research has shown that galantamine’s unique "one-two punch" has a profound effect on cholinergic function, which is governed by the vital neurotransmitter acetylcholine.

These results indicate that we may have underestimated the brain's regenerative capabilities. If we give our brains the right nutrients, it appears that we may be able to slow or even reverse the course of cognitive decline due to dementia.

We may have underestimated the brain's regenerative capabilities.
With the right nutrients, we may be able to slow or even reverse
the course of cognitive decline due to dementia.

Also measured in this study were the patients' ability to perform routine daily tasks, such as bathing, dressing, and housework. Over the 12-month period, patients in both the treatment group and the control group experienced deterioration in these functions. The decline in the control group, however, was more than twice as great as that in the treatment group. It is reasonable to suppose that the control group's decline would have been greater still, had they not been taking galantamine for the last six months of the study.

Besides the broad spectrum of side effects of donepezil and rivastigmine, one of the major drawbacks of these drugs is the relatively short duration of their effectiveness. Although they do boost acetylcholine levels, they become less effective the longer they're used. After about one year, the nicotinic receptors have become desensitized to ACh and no longer respond well to it. When that happens, the patient is almost back to square one, and dementia tends to accelerate.

Unlike the prescription drugs, galantamine appears to have no limit on its ability to maintain the sensitivity of nicotinic receptors to ACh. Since the receptors continue to respond to ACh indefinitely, galantamine may help slow the progression of the dementia - with important financial as well as health consequences. According to a study conducted by the independent consulting firm Caro Research, galantamine treatment could save $3000 annually per patient compared to those receiving no treatment, owing to the diminished need for paid help.5 As a bonus, the patient's improved condition (relatively speaking) would surely lighten the emotional burden on caregivers.

Since galantamine is a plant-based nutrient, it does not bring with it the usual baggage of unpleasant side effects that accompany donepezil and rivastigmine. Actually, galantamine's adverse effects are almost nonexistent, the worst being mild gastrointestinal problems.6 Research indicates that starting with 8 mg/day of galantamine and building up to 16 mg/day after four weeks will minimize these problems.


Summary of Galantamine's Advantages
Over Prescription Drugs

It is increasingly apparent from the scientific literature on the treatment of dementias with acetylcholinesterase inhibitors that galantamine is the safest and most effective of these agents. Because galantamine is so beneficial in both vascular dementia and Alzheimer's disease, it stands to reason that it should also help alleviate the far less severe symptoms of age-related cognitive decline (ARCD), the gradual dulling of our mental faculties as we grow older. The main advantages of galantamine over prescription drugs are:

  • Galantamine stimulates the nicotinic receptors in the brain's cholinergic system, thereby enhancing cholinergic function. Donepezil and rivastigmine do not.
  • Galantamine has no known limit on the duration of its effective use, as it does not appear to cause desensitization of nicotinic receptors. Donepezil and rivastigmine are effective for about one year.
  • Galantamine has few and mild side effects, whereas the common side effects of donepezil and rivastigmine include nausea, vomiting, diarrhea, headache, dizziness, drowsiness, fatigue, insomnia, flushing, hot flashes, skin rash, and tremor.
  • Galantamine is available without prescription as a dietary supplement, whereas donepezil and rivastigmine are available only by prescription.

The advantages of galantamine over the prescription drugs can be augmented by adding two other nutrients that help boost cholinergic function: choline and vitamin B5. Choline is a chemical precursor to acetylcholine, and vitamin B5, better known as pantothenic acid, is an essential cofactor for choline.

The Belgian drug company Janssen Pharmaceutica received FDA approval in February 2001 for its drug Reminyl®, which contains galantamine but not choline or vitamin B5.  Because Reminyl lacks these two ingredients, it may not be able to achieve the full potential of galantamine.  Janssen has opted to market Reminyl as a prescription drug, which has shot the price into orbit and made it inaccessible except to patients who are under a doctor's care.

Galantamine as a dietary supplement is available without prescription to those who feel they might benefit from cholinergic stimulation.  The cost is much lower - about one-third that of Reminyl, in fact.

The effective serving size of Galantamine is not the same for everyone. Some people may find that two capsules (16 mg) per day are sufficient to regain lost cognitive abilities, whereas others may need three capsules (24 mg) per day. If you encounter any gastric disturbance, reducing the amount taken for a few days will usually clear it up.

Galantamine can do everything for you that the prescription drugs can do - and more - and you won't have to suffer with side effects. Galantamine offers the best of both worlds: long-term effects at about one-third the cost.

Galantamine  food for mind and body
Galantamine  rescues brain cells  
Galantamine  and memory enhancement
  Galantamine  fights Alzheimer's
  Galantamine  the old become young


  1. Woodman R, Kmietowicz Z. Galantamine shows further promise in treating vascular dementia. Reuters Health, June 19, 2001.
  2. Ji D, Lape R, Dani JA. Timing and location of nicotinic activity enhances or depresses hippocampal synaptic plasticity. Neuron 2001;31(1):131-41.
  3. Venturi VM, Piccinin GL, Taddei I. Pharmacognostic study of self-sown Galanthus nivalis (var. gracilis) in Italy. Boll Soc Ital Biol Sper 1965 Jun 15;41(11):593-7.
  4. Paskov DS, Stoyanov KA, Saev SK, Tenev KA, Mincheva ML. Clinical experience with Nivalin as anticholinesterase drug in anaesthesiological practice. Proc First Eur Congr Anesthesiol, Vienna, Sep 3-9, 1962.
  5. Woodman R. Shire's Reminyl shows further promise in vascular dementia. Reuters Health, June 19, 2001.
  6. Farlow MR. Pharmacokinetic profiles of current therapies for Alzheimer's disease: implications for switching to galantamine. Clin Ther 2001; 23 Suppl A:A13-24.


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