Knoitol™ (Huperzine-A) 200 mcg x 100 tablets

Overview

Knoitol makes prescription drugs for Alzheimer’s look like snake oil.

Huperzine-A (HupA), a substance found in the club moss Huperzia serrata, has been used in China for centuries.

The Chinese Academy of Sciences took a renewed interest in HupA in the 1980s and developed it as a treatment for dementia, particularly the dementia of Alzheimer’s Disease.

Medical research has so far provided support for the following applications of HupA:

• reduction of brain inflammation
• cognitive improvement and memory enhancement in Alzheimer’s patients
• cognitive improvement and memory enhancement in healthy people
• amelioration of dementia, including Alzheimer’s dementia
• repair of stroke damage in the brain.

In most respects HupA appears to be superior to all anti-Alzheimer’s drugs currently approved by the U.S. Food and Drug Administration — drugs such as tacrine, donepezil, and rivastigmine. Unlike these expensive prescription drugs, huperzine-A

• protects nerve cells from free radicals generated in the ‘beta-amyloid’ protein plaques found in Alzheimer’s brain tissue;
• interferes with the formation of these destructive beta-amyloid plaques;
• interferes with the ‘suicide’ programming that causes nerve cells to die when they receive spurious ‘time-to-die’ signals, as they do under Alzheimer’s conditions;
• increases the brain’s production of nerve growth factor (NGF) — a substance involved in replacing lost cells;
• increases the brain’s production of NGF receptors — cell-surface proteins that are required for NGF activity.

Most recent clinical studies of huperzine-A use 400–800 mcg/day.

Read Knoitol Monograph

Huperzine-A (HupA), a substance found in the club moss Huperzia serrata, has been used in China for centuries to treat swelling, fever, and blood disorders.¹ The Chinese Academy of Sciences took an interest in HupA in the 1980s and developed it as a treatment for dementia, particularly the dementia of Alzheimer’s Disease.

In most respects HupA appears to be superior to all anti-Alzheimer’s drugs currently approved by the U.S. Food and Drug Administration — drugs such as tacrine, donepezil, and rivastigmine. HupA has better penetration through the blood-brain barrier, higher oral bioavailability, fewer side effects, and a longer duration of action than these expensive prescription drugs.^2,3

The medical studies

Nearly all medical research on huperzine is the work of researchers in China who conducted animal studies and human clinical trials. During the 1980s, 1990s, and early 2000s, they reported that HupA enhances memory and protects nerve cells from the kinds of damage typically seen in Alzheimer’s Disease. Double-blind, placebo-controlled clinical trials in patients with and without Alzheimer’s resulted in significant improvements in cognitive function and in the quality of life.^1,4,5,6,7,8 But these results had little impact in the medical world outside China. Finally, in 2004 the U.S. National Institutes of Health (in collaboration with a company that hopes to turn HupA into a prescription drug) organized a clinical trial to study HupA in Alzheimer’s patients. The trial was completed in 2006, but the results have not yet been published.⁹

Animal studies have shown that HupA protects the nervous system from organophosphate nerve-gas agents.^2,10 This fact has no relevance to supplement buyers except insofar as it provides further evidence of huperzine’s powerful neuroprotective action.

How does huperzine work?

HupA appears to affect multiple biochemical pathways in the brain, several of which are involved in Alzheimer’s Disease. The best understood of these pathways is the one in which the neurotransmitter acetylcholine carries signals from one nerve cell to another in certain parts of the brain. In Alzheimer’s Disease, there is a shortage of acetylcholine, and consequently an impaired signalling ability. HupA is an inhibitor of the enzyme that breaks down acetylcholine. Thus, HupA causes this neurotransmitter to accumulate in the space between the cells, permitting higher levels of signalling to take place.

If this were huperzine’s only effect on Alzheimer’s, it would have no advantage (other than price) over the prescription drugs currently available — i.e., it would merely compensate temporarily for the impairment caused by damaged and dead nerve cells, but it would not slow the destruction of nerve cells or bring about the repair of damaged tissue. But as luck would have it, HupA has additional modes of action:^{11,12,13,14,2,6,15}

• It protects nerve cells from free radicals generated by the ‘beta-amyloid’ protein plaques found in Alzheimer’s brain tissue.
• It interferes with the formation of these destructive beta-amyloid plaques.
• It interferes with the ‘suicide’ programming that causes nerve cells to die when they receive spurious ‘time-to-die’ signals, as they do under Alzheimer’s conditions.
• It increases the brain’s production of nerve growth factor (NGF) — a substance involved in generating replacements for lost cells.
• It increases the brain’s production of NGF receptors — cell-surface proteins that are required for NGF activity.

Dosage used in Alzheimer’s studies

Until recently, supplement companies sold huperzine as a cognitive enhancer for people whose cognitive abilities fell into the normal range, and the dosages were small — 50 mcg/day, for example. But now that the Chinese studies on Alzheimer’s patients have become known outside of China, it is realized that larger doses are needed. The latest clinical studies use 400–800 mcg/day.⁹LifeLink has therefore increased the dosage in its hupA product Knoitol to 200 mcg.

Does huperzine repair stroke damage?

Although the final word has not been heard on this subject, preliminary experiments with gerbils and other animals indicate that HupA limits memory deficits and neuronal damage after stroke-like brain injuries. Gerbils were given HupA orally at 0.1 mg/kg twice per day for 14 days. (This is a much larger dose than is used in human Alzheimer’s studies.)^16,17