Elevated levels of plasma homocysteine are
associated with coronary heart disease and may be caused by genetic and
lifestyle influences, including low intake of folate and vitamin-B-6. JAMA 1998. 279: 359-364. The
results of this 14 year follow up study suggest that intake of folate and
vitamin-B-6 above the current Daily Value may be important in the primary
prevention of CHD among women. The primary nutrients associated with
inhibition of Homocysteine are Vitamin B-6, folic acid, vitamin-B-12 and trimethylglycine.
Elevated homocysteine levels and venous thrombosis is more prevalent
among women then men and increases with age.
High plasma homocysteine levels are considered a risk factor for
deep-vein thrombosis in the general population.
N Engl J Med. 1996; 334 (12): 759-762
Brain cell regeneration and improved brain function associated with methylcobalamin, phosphatidylserine
Japanese scientists have identified a form
of B-12 that protects against neurological disease and aging. Some of these disorders may be preventable or
treatable with oral methylcobalamin including
Parkinson's disease, peripheral neuropathies, Alzheimer's disease, muscular
dystrophy and neurological aging.
Published studies indicate that high doses of methylcobalamin
are needed to regenerate neurons, as well as the myelin sheath that protects
axons and peripheral nerves. In a group
treated with methylcobalamin or steroid therapy for
Bell's Palsy, it took the steroid group an average of
7.79 weeks to recover completely, in contrast the methycobalamin
treated group recovered in just 1.23 weeks.
The dosage was 30 to 40 mg daily.
Methods and Findings of Experimental
Clinical Pharmacology Oct. 1996 (17) 8: 539-544. It has been shown that methylcobalamin
protects against glutamate, aspartate, and nitroprusside induced neurotoxicity in rat cortical
neurons. Europ. J Pharm.
Sept. 1993; 241(1):1-6. Researchers
concluded that methylcobalamin protects against
neurotoxicity by enhancing brain cell methylation. Other synergistic methylation enhancing
nutrients would include vitamin B-6, trimethylglycine,
and folic acid. It is well known that
dopamine producing brain cells become toxic with the excessive release of
glutamate from neurons. Brain
Research Oct 1997; 771  159-162. Therefore, methlycobalamin
5 to 20 mg daily may enhance the therapeutic benefit of Sinemet
in Parkinson's patients over a longer duration of time. In a clinical study in which methylcobalamin was administered in large doses, I.V.,
Alzheimer's patients improved intellectual functions such as memory, emotions
and communication with other people. The
researchers concluded that methylcobalamin is a safe
and effective treatment for psychiatric disorders in subjects with Alzheimer's
type dementia. Clinical Therapeutics May 1992: 14 [31 426-437. Researchers provided methylcobalamin,
60 mg daily to subject suffering from multiple sclerosis, although motor disability
did not improve, clinical improvements were seen in visual and auditory MS
related disabilities. Feb. 1994
Internal Med. 33 . 82-86 It has been postulated
that methylcobalamin could increase protein synthesis
and consequently help regenerate nerves.
Researchers have shown that high doses of methylcobalamin
can produce nerve regeneration in laboratory animals. In addition the researchers assert that methylcobalamin might be of clinical benefit for subjects
with peripheral neuropathies. Apr.
1994 Journal of Clinical Neurological Science 122 .
140-143. In a study reported in the Journal
of Clinical Immunology April 1982 101-109, methylcobalamin
showed marked T- cell enhancing effects when these cells were exposed to
certain antigens. The scientists also
showed that methylcobalamin improved the activity of
helper T-cells. The scientists concluded
that methylcobalamin could modulate lymphocyte
function by increasing regulatory T-cell activity.
A double blind randomized controlled study
was conducted on 42 hospitalized demented patients to evaluate the therapeutic
effects of phosphatidylserine. To appraise patients, two distinct rating
scales were used: the Crichton Scale and Peri
Scale. A circle crossing test was
added. The results of these various
tests on the phosphatidylserine treated group
indicated a statistically significant improvement as compared to the placebo
group. The behavioral improvement shown
in this study is in agreement with experimental studies on aged animals. Acta. Neurol. Scand. 1986; 73: 136-140.
It was well documented in an open trial of elderly patients that phosphatidylserine is a useful tool in the treatment of
mild to moderate deterioration of cognitive functions. Clinical Trials Journal
1987. Vol. 24 No 1. A clinical trial was conducted at the University of Milano, Italy to determine the effects of phosphatidylserine, 300 mg daily on geriatric patients with
depressive disorders. Consistent
improvement of depressive symptoms, memory and behavior was observed by the
researchers in the phosphatidylserine treated
group. Acta. Psychiatr. Scand 1990, 81:
265-270. Over 14 controlled studies
reported in referred medical journals have without question documented the
efficacy of oral phosphatidylserine, 100 to 300 mg daily
in the treatment of various types of cognitive dysfunction and dementia. Most of these studies were done in Italy where phosphatidylserine is manufactured. In the USA most pharmaceutical
companies and the Universities that they endow consider phosphatidylserine
a nutrient, thus the lack of interest.
Vinpocetine found in the lesser periwinkle minor, is
an excellent vasodilator and cerebral metabolic enhancer. Alter Med Rev,
June 1999, 4(3):144-61 Early studies pertaining to vinpocetine
indicate five main mechanism of action: l. selective enhancement of brain
circulation and oxygen utilization, 2. increased tolerance of the brain towards
hypoxia and ischemia, 3. anticonvulsant activity, 4. inhibitory effects of phosphodiesterase (PDE) enzyme
and 5. improvement of rheological properties of the
blood and inhibition of aggregation of thrombocytes. The increased cerebral blood flow associated
with vinpocetine therapy is thought to contribute to
its neuroprotective properties. It has been clearly demonstrated that vinpocetine offers significant and direct neuroprotection both under vitro and in vivo
Pharm Hung, 66(5):213-24 1996 Sept.