Treatment of Dysmenorrhea with Physiological Modulators (A28): A Registry Study| Stephy Publishers

 


Pregnancy and Women’s Health Care International Journal - (PWHCIJ)| Stephy Publishers


Abstract

Background: Dysmenorrhea is a diseases affecting about 45% of menstruating women (approximately between 45 to 95 % of females) during the time of menses and causing a reduction of the quality of life.

Objectives: To reduce the symptoms of dysmenorrhea using a natural Physiological Mosdulator (A 28) consisting of low dosages of calcium salts, Vitamin D, bioflavonoids, lycopene, and astaxanthin.

Material and methods: Forty patients with severe dysmenorrhea were analyzed during two menstrual cycles: the first as baseline following a run-inn period, and the second during the treatment with A28. A simple VAS scale scoring the daily discomfort (from 0 =no discomfort to 6 =maximum discomfort) was used to measure the severity of the symptoms.The total score of first 3 days following the start of menses was calculated.The use of pain rescue cps during the two period was compared.

Results: Thirty-eight cases completed the experience. Before treatment, the mean of total scores was 8.1±2.40, while after A28 it was reduced to 1.7± 1.39 (U Mann Whitney p< 0.01) . The mean of pain rescue cps used was respectively 6.1±1.21 and 0.5±1.15 before and after the A28 treatment (p <0.01). No side effects were reported.

Conclusion: The use ofa combination of Physiological Modulators effectively decreased the daily discomfort due to dysmenorrhea.

Keywords

dysmenorrhea, physiological modulators, daily discomfort

Introduction

Dysmenorrhea is a diseases affecting about 45 % of menstruating women (approximately between 45 to 95 % of females) during the time of menses,1 causing an extensive personal and public health problem consisting of a high degree of absenteeism and severe economic loss. Recently some author has focused the attention on GABA and CaSRs (calcium sensing receptors): the GABA receptors are spread into the CNS and GI tract with inhibitory activity,2,3 while CaSRS are more expressed into the GI.4 The GABA receptors have an inhibitory activity which is modulated by estrogens and progestins, and their reduction allows the start of menses. At the same time, the hormonal shortage give rise to pain and GI hypermotility, the last being controlled by the CaSRs inhibitory activity. It may be interesting consider that receptors of any type (e.g. for serotonin, norepinephrine, GABA) are located primarily on the cellular membranes. The membrane functions in general belong to the oxidative condition of the membrane itself, and the receptor is maintained in place with the normal function depending upon the membrane structure around and within the receptor. The membrane around and within the receptor (rafts) can have a differential sensitivity to the oxidative stress (OS) depending upon the quantity of double bonds in the lipids constituting the phospholipids (PL) and the antioxidant reserve available in the cellular system.5 Lipids rafts, consisting of cholesterol/sfingolipids microdomains are involved in protein traffic, formation of signaling complexes and are abundantly represented in several postsynaptic dendrites.6 This means that a neuroamine receptor (e.g. for serotonin, dopamine) may be more sensible to the oxidation than an estrogenic receptor or vice versa. The consequence of this is that even a mild oxidation in absence of an adequate antioxidant capacity can trigger the dysfunction of some receptors only, whereas a massive oxidation generate a complete dysregulation of all the receptors. In any case, the oxidative stress tends to be an explosive process, and even a mild oxidation starting in one point/area of the cellular membrane may be spread out rapidly involving all the proximal areas. This means that is possible to stop the explosive process just limiting the membrane oxidation, and the relative clinical symptoms will not emerge. These last aspects make clear that OS may compromise directly (receptor per se) or indirectly (rafts oxidation) the neuronal firing, and inhibitory neurons can be more sensible than stimulating neurons, due the higher number of cysteine loops. The aim of this investigation was to analyze the activity of a Physiological Modulators Formula (A28) to control the daily discomfort due to dysmenorrhea symptoms. A28 is a combination of citrus flavonoids to control oxidative stress (OS), calcium salts to modulate pain an motility in the gut, Vitamin D to increase intestinal the calcium availability7, astaxanthin to reduce the OS in the brain,8 and lycopene to quench the oxidation in lymphocytes.


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