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Psychiatric Times. Vol. 19 No. 11
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Using Complementary Treatments

By Wadie Najm, M.D.
| November 1, 2002
Dr. Najm is a family physician with certificate added qualification in geriatrics. He has completed several training courses in complementary and alternative medicine and is conducting research in the field.

Huperzine A

An alkaloid extracted from a moss, huperzine A (Huperzia serrata) is used in Chinese medicine for a variety of conditions including memory problems. It is currently being sold in the United States as an over-the-counter dietary supplement to enhance cognition for people with memory loss.

Research has shown huperzine A to be a selective and reversible inhibitor of acetylcholinesterase. It also has been shown to lessen neuronal toxicity caused by glutamate. Initial small investigations reported improvement in cognitive functions of subjects with AD (Xu et al., 1999; Xu et al.,1995). Further evaluations are warranted.

The proposed dose of huperzine A is 30 mcg to 200 mcg bid. Possible adverse reactions include blurred vision, GI effects, hyperactivity, anorexia and bradycardia. Use of huperzine A might worsen overflow incontinence.

Theoretically, huperzine A could have an additive effect on cholinergic and acetylcholinesterase inhibitors and interact adversely with anticholinergic drugs.

DHEA/DHEA-S

Dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEA-S) are secreted by the adrenal glands and are the precursors of androgens. Their exact effect on cognition is unclear, but some authors attribute it to neurotransmission. Levels of DHEA peak at puberty and fall slowly as people get older (Schneider et al., 1992). Restoring low levels of DHEA has been reported to improve the overall well-being of older adults (Huppert et al., 2000).

Two prospective studies of 833 community-dwelling men and a middle-class cohort of 270 men, respectively, found no association between levels of DHEA-S and cognitive decline (Barrett-Connor and Edelstein, 1994; Moffat et al., 2000). Other studies reported similar findings among men and women. A clinical observational study of patients with AD found no association between cognition and DHEA-S level. Huppert et al. (2000) concluded that the data offered no support for an improvement in memory or other aspects of cognitive function in normal older people.

Commercial products are manufactured from a wild yam extract. The proposed dose of DHEA or DHEA-S is 25 mg/day to 250 mg/day qid. Determination is based on measured blood levels. Possible adverse reactions include acne, hair loss, hirsutism, decreased high-density lipoproteins, insulin resistance, mania, hypertension, abdominal pain, liver dysfunction and menstrual irregularity.

Since DHEA inhibits cytochrome P450 3A, it can potentially affect all drugs metabolized through this mechanism. Caution is required for people with diabetes as DHEA may increase insulin resistance. Individuals with hormone sensitive neoplasm, liver disease and bipolar disorder should avoid DHEA. Theoretically, soy may decrease the effect of DHEA.

D-Cycloserine

A broad-spectrum antibiotic previously used for the treatment of tuberculosis, D-cycloserine is a structural analogue of the amino acids glycine(Drug information on glycine) and D-alanine.

There is accumulating evidence that supports an important role for N-methyl-D-aspartate (NMDA) receptors in learning and memory through long-term potentiation. The activity of NMDA receptors can be modulated by the activity of glycine. These glycine receptors are also stimulated by the antibiotic D-cycloserine. Hence, it has been suggested that D-cycloserine might improve memory and other cognitive processes. An initial study using low doses of D-cycloserine reported a reversal of scopolamine-induced memory impairment in healthy young subjects (Laake and Oeksengaard, 2002).

In a review of four studies (two large and two small) using varied doses in subjects with different levels of memory impairment, Laake and Oeksengaard (2002) found no evidence of differences with placebo in the measurement of Clinical Global Improvement Scale (CGI), mini-mental state exam (MMSE), and other cognitive and functional scales. The number of dropouts was much higher in the treatment group than in the placebo group.

The proposed D-cycloserine dose is 10 mg to 200 mg divided into two doses per day. Adverse reactions are dose-related and include ankle clonus, confusion, dysarthria, headache, hyper-reflexia, irritability, nervousness, paranoid reactions, psychotic states with suicidal tendencies, vertigo, paresis, seizures and tremor. No adverse interactions have been reported.

Theanine

An amino acid found in green tea, theanine is a glutamate analog. Theoretically it can provide neuroprotection by antagonizing the effect of glutamate and NMDA receptors.

Animal studies indicate a possible protective effect of ischemic neuronal death (Kakuda et al., 2000). No human studies were located for this review.

No typical dose in humans has been proposed and the possible adverse reactions are unknown. Theanine can interact adversely with catecholamine and cause vasoconstriction, so it should be used with caution in people with hypertension.

Phosphatidylserine

Most studies of the phospholipid phosphatidylserine used bovine brain sources, but, due to concerns about mad cow disease, soy or cabbage sources are now available. Phosphatidylserine is active at cell membranes, including synaptic membrane zones. Partial improvement of learning and recall capacity was noted in subjects with age-related cognitive decline (Crook et al., 1991).

The proposed dose is 100 mg/day to 300 mg/day. Possible adverse reactions include GI upset and insomnia at high doses. Phosphatidylserine may interact with uric acid and alanine aminotransferase (ALT/SGPT) lab tests. There have been no reported adverse interactions.

Conclusion

Among the many dietary supplements used for memory impairment, several have shown some evidence of effectiveness. Others are still awaiting proof through well-designed studies. Despite the great interest in and use of dietary supplements, the collection of scientific evidence on their efficacy is still in its infancy, and better-designed studies are needed to provide us with answers. For now, clinicians need to use caution in interpreting available information and in counseling their patients.

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References
1. Barrett-Connor E, Edelstein SL (1994), A prospective study of dehydroepiandrosterone sulfate and cognitive function in an older population: the Rancho Bernardo study. J Am Geriatr Soc 42(4):420-423.
2. Crook TH, Tinklenberg J, Yesavage J et al. (1991), Effects of phosphatidylserine in age-associated memory impairment. Neurology 41(5):644-649.
3. Ernst E, Pittler MH (1999), Ginkgo biloba for dementia: a systematic review of double-blind, placebo-controlled trials. Clinical Drug Investigation 17(4):301-308.
4. Higgins JP, Flicker L (2000), Lecithin for dementia and cognitive impairment. Cochrane Database Syst Rev (2):CD001015.
5. Huppert FA, Van Niekerk JK, Herbert J (2000), Dehydroepiandrosterone (DHEA) supplementation for cognition and well-being. Cochrane Database Syst Rev (2):CD000304.
6. Kakuda T, Yanase H, Utsunomiya K et al. (2000), Protective effect of gamma-glutamylethylamide (theanine) on ischemic delayed neuronal death in gerbils. Neurosci Lett 289(3):189-192.
7. Laake K, Oeksengaard AR (2002), D-cycloserine for Alzheimer's disease. Cochrane Database Syst Rev (2):CD003153.
8. Masaki KH, Losonczy KG, Izmirlian G et al. (2000), Association of vitamin E and C supplement use with cognitive function and dementia in elderly men. Neurology 54(6):1265-1272 [see comment].
9. Moffat SD, Zonderman AB, Harman SM et al. (2000), The relationship between longitudinal declines in dehydroepiandrosterone sulfate concentrations and cognitive performance in older men. Arch Intern Med 160(14):2193-2198.
10. Rodriguez-Martin JL, Qizilbash N, Lopez-Arrieta JM (2001), Thiamine for Alzheimer's disease. Cochrane Database Syst Rev (2):CD001498.
11. Sano M, Ernesto C, Thomas RG et al. (1997), A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study. N Engl J Med 336(17):1216-1222 [see comments].
12. Schneider LS, Hinsey M, Lyness S (1992), Plasma dehydroepiandrosterone sulfate in Alzheimer's disease. Biol Psychiatry 31(2):205-208.
13. Singh HK, Dhawan BN (1982), Effect of Bacopa monniera Linn. (brahmi) extract on avoidance responses in rat. J Ethnopharmacol 5(2):205-214.
14. Singh RH, Singh L (1980), Studies on the anti-anxiety effect of the medyha rasayana drug, Brahmi (Bacopa monniera Wettst.). J Res Ayur Siddha 1:133-148.
15. Thal LJ, Calvani M, Amato A, Carta A (2000), A 1-year controlled trial of acetyl-l-carnitine in early-onset AD. Neurology 55(6):805-810 [see comment].
16. van Dongen MC, van Rossum E, Kessels AG et al. (2000), The efficacy of gingko for elderly people with dementia and age-associated memory impairment: new results of a randomized clinical trial. J Am Geriatr Soc 48(10):1183-1194.
17. Vogler BK, Pittler MH, Ernst E (1999), The efficacy of ginseng. A systematic review of randomised clinical trials. Eur J Clin Pharmacol 55(8):567-575.
18. Wettstein A (2000), Cholinesterase inhibitors and Gingko extracts-are they comparable in the treatment of dementia? Comparison of published placebo-controlled efficacy studies of at least six months' duration. Phytomedicine 6(6):393-401.
19. Xu SS, Cai ZY, Qu ZW et al. (1999), Huperzine-A in capsules and tablets for treating patients with Alzheimer disease. Acta Pharmacologica Sinica 20(6):486-490.
20. Xu SS, Gao ZX, Weng Z et al. (1995), Efficacy of tablet huperzine-A on memory, cognition, and behavior in Alzheimer's disease. Acta Pharmacologica Sinica 16:391-395.


 
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