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, and vinpocetine.
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 thatmethylcobalamin 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 ofmethylcobalamin 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 thephosphatidylserine 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 theUniversity 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 considerphosphatidylserine 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 ofphosphodiesterase (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 vinpocetineoffers significant and direct neuroprotection both under vitro and in vivo conditions. Acta Pharm Hung, 66(5):213-24 1996 Sept.