SERIPHOS, a Phosphorylated Serine chelate of Calcium and Magnesium, can help optimize the stress response. Like all macro minerals and amino acid derivatives, SERIPHOS is best absorbed when taken before meals.

Basic Chemistry
Phosphatidyl Serine (various brand names) when consumed in food, example, egg yolk, or in a capsule provides about 20% of active phosphorylated serine. Each 100 mg of phosphatidyl serine yield about 20 m of activated serine following consumption . The bulk of the weight is derived from 2 fatty acids, RI & R2. In the intestinal tract, the various enzymes (Brush border and pancreatic) clip off the fatty acids, predominantly unsaturated Rl & R2. These fatty acids are not reassembled in the body to the stump molecule. Rather different fatty acids are attached by the body to replace Rl and R2. The glycerol molecule is very abundant in the body because it is found in all body fat and in dietary fats/oils in great abundance.

In brief, the Phosphatidyl serine acts as a precursor molecule and is not the active form of this nutrient. In our tissues, the rate limiting step is the phosphorylation of the serine molecule.

Phosphorylated Serine (brand name, SERIPHOS) provides the activated or phosphorylated serine in a chelate form of magnesium and calcium. In the local tissue, the Phosphorylated Serine is linked to glyceroland, the appropriate fatty acids specific to each tissue, and is not linked to the fatty acids provided in the precursor Phosphatidyl Serine.

Phosphorylated Serine (brand name SERIPHOS) is a pure product not derived from animal tissue. The serine is from vegetable sources and the phosphate is from a pure phosphate compound.

Each capsule contains:

Calcium Magnesium Phosphorus

45 mg 45 mg 190 mg

Special Dietary Ingredients: Phosphorus, Calcium and Magnesium. Derived from a phosphorylated mixture of L-Serine and Ethanolamine. Each capsule provides 90 mg of active phosphorylated serine. Store in cool dry place.

Suggested use: One capsule 15 minutes before a meal or as directed by a health care professional.

1. Early Cortisol Escape Phenomenon Reversed by Phosphatidylserine In Elderly Normal Subjects. Nerozzi, Dina et al, Clinical Trials Journal, 1 89, vol 26 (1).

Summary
The early cortisol escape phenomenon observed after administration of I mg of dexamethasone in 50% of the elderly subjects in the study was reversed by two-months therapy with phosphatidylserine (PS), 3 x 100 mg tablets daily.

An action of the compound at the neurotransmitter level is hypothesized.

A number of alterations of the HPAA (Hypothalmic Pituitary Adrenal Axis) was detectable in our study in normal elderly subjects; abnormal elevation of basal morning cortisol values (3 subjects); disruption of the circadian cortisol pattern (4 subjects); early cortisol escape phenomenon observed in seven of our subjects. A true non-suppression was visible only in two individuals. Therefore, the early cortisol escape phenomenon appears to be the most consistent abnormality found in our subjects.

The question of contribution of non-specific stress factors to cortisol hypersecretion obviously cannot be ruled out. However, in our opinion, an intrinsic neuro-endocrine disturbance, which may be part of a central dysfunction associated with aging, could be at the root of a substantial part of the hypersecretion.

According to the membrane hypothesis of aging, age-dependent changes of the membranes can negatively interfere with tropism of the neurons, with cell to cell communication and ultimately with neurotransmission and thus with most functions linked to neurotransmission, including hormonal secretion.

According to Massarotti, PS seems to stimulate some sort of morphogenetic neuronal plasticity, which acts as a compensatory adaptive mechanism to cell deterioration, and is capable of preventing or delaying the age dependent decline of neurotransmitter function. On the basis of our findings we can speculate that existence of an analogous mechanism which acts on neurotransmission similar to that observed in animals treated with PS.

However, when we consider the impairment of HPAA as a marker of a more central neurotransmitter imbalance, we can suppose that the re-adjustment of such an altered parameter7 although partial, may be brought about by some action at the neurotransmitter level .

1. Sund & Sun. Top. Geront., 1979; 15:34-53. 2. Massarotti. M. In: Bes A, ed. Senile Dementias.

2. Effects of Phosphatidylserine in Age Associated Memory Impairment H. Crook. Ph.D.; J. Tinklenberg, MD; J Yesavage, MD; W Petrie, Ml; M.G. Nunzi, Ph.D; and D.C. Massari, Ph.D.;Neurologv, 1991, 41:611-649

Article Abstract
We treated 149 patients meeting criteria of age associated memory impairment (AAMI) for 12 weeks with a formulation of phosphatidylserine (100-150 mg PS bid) or placebo. Patients treated with the drug improved, relative to those untreated, with learning and memory tasks of daily life.

Analysis of clinical subgroup suggested that persons within the sample who performed at a relatively low level prior to treatment were most likely to respond to PS. Within this sub group, there was improvement on both computerized and standard neuropsychological performance tests, and also on clinical global ratings of improvement.

The results suggest that the compound may be a promising candidate for treating memory loss in later life.