Showing posts with label Germ Cell Replant Effect. Show all posts
Showing posts with label Germ Cell Replant Effect. Show all posts

Thursday, 18 February 2021

Relation between Cancer and Germ Cells | Chapter 7 | Highlights on Medicine and Medical Research Vol. 2

Background: Age of contraceptives, abortions,[20th, 21st centuries] initiated as observed by family welfare programs, increased global cancer, tumor, neoplasm and mortality incidence.

Objectives: Tumor altruistic association of contraception [if any] with growing cancer has been tried.

Methods: in 2012, retrospective study of cancer prevalence, tumor in 350 patients 20-35 years of age, 35-50 years of age, >50 years of age, from data collected by convenient stratified random sampling from different geographical locations between 2002-2012 and its association with presence, absence of contraception, abortion was performed; simultaneously, serum oestrogen levels were obtained from different geographical locations between 2002-2012 and its association with presence, absence of contraception, abortion; 212 patients treated for various forms of neoplasm, namely breast cancer, prostate cancer, cervix cancer and benign prostatic hyperplasia, were randomly allocated to the above 3 age groups from 1983-2012 clinical practice, and the data were analyzed for association with contraceptive status and potential significance.

Results: There was a 6-fold rise in the incidence of cancer among contraceptive users over >50 years with a p-value of <0.0005. Contraception was associated with a 4 to 7 fold increase in tumor prevalence with a p value of <0.0005 between >35 and >50 years. In 61 percent of contraceptive users with a p value of <0.0005, endogenous estrogen decreased to ~5-8 pg; endogenous estrogen values of up to ~0.4 pg were seen after hysterectomy. Due to reduced production of endogenous estrogen, diet deprived of cholesterol: androgen was also correlated with a 50 percent rise in tumor, cancer in youth without contraceptives. In well-differentiated breast cancers, associated with decreased levels of endogenous estrogen among contraceptive users, estrogen receptors were positive, indicating that estrogen receptor positivity may be a compensatory phenomenon; estrogen receptor positivity was not shown in anaplastic tumors. There was a 10-20 fold increase in breast cancer between 20->50 years, in contraceptive patients with a p-value of <0.0005; a 20-30 fold increase in prostate cancer between 35->50 years, in contraceptive patients with a p-value of <0.0005; in contraceptive patients with a p-value of <0.0005; in cervical patients with a 20-40 fold increase between 20-70 years; in contraceptive patients with a p-value of <0.0005.

Conclusion: Contraception of any sort results in shattered germ cell breakdown to centric fragments, ring chromosomes, chromatid breaks, auto immunity generation, substantial decrease in endogenous, reproductive hormones, without which genomic repertoire: embryo-like healing mechanism defaults, leading to a 275% rise in disease incidence, including cancers. Definition is acquired contraception preventing traversal of normal path by germ cells with consequent shattered destruction of germ cells, resulting in decreased endogenous estrogen: androgen surveillance, resulting in agonizing cellular genomic repertoire defects, unregulated multiplication followed by no cell cycle differentiation, metabolism, resulting in high cancer incidence, including. Increased estrogen receptors: androgen receptors in breast and well-differentiated prostate cancers are likely to be a compensatory spike, secondary to sudden artificially obtained contraception, resulting in a substantial reduction in contraceptive consumers of endogenous germ cell hormones. Reversal of contraception with chemotherapy, radiation therapy, surgery achieves preventing cancer development, decreases incidence, prevalence of neoplasm, as a phenomenon of cause and effect and not castration or anti-estrogen: antiandrogens that perpetuate, encourage neoplastic diseases by decreasing endogenous estrogen: androgen.

Author (s) Details

Elizabeth Jeya Vardhini Samuel
Department of General Medicine, Karpagam Faculty of Medical Sciences and Research, Coimbatore-32, Tamil Nadu, India.

View Book :- https://stm.bookpi.org/HMMR-V2/issue/view/20