One must wonder about the seemingly high levels of human homosexuality. Were so many mothers severely stressed by predators or wars during pregnancy? Not likely. However, a source of artificial stress has been unleashed this century on humans in epidemic proportions: cigarette smoking. Nicotine from smoking induces a significant increase in cortisol levels. If a pregnant female has the genetic predisposition to bear homosexual children when stressed, and she smokes during early pregnancy, the nicotine-induced cortisol increase may be sufficient to induce homosexuality in her offspring. This speculation could easily be confirmed or refuted with a simple epidemiological study.

This book tells you detailed results of my experiment, dangers to avoid, and also discusses a simple and elegant new theory that suggests how High Dose Vitamin D3 therapy Should help PREVENT OR CURE all the epidemics of disease and health issues that have been plaguing us since the 1980’s when Doctors started warning us to stay out of the sun and always use sunscreen. This has created the huge epidemics we see today of Obesity, Autism, Asthma, and many others! NEW STUDY DISPROVES ALL MAINSTREAM THEORIES OF AGING-AND REVEALS THE NEW: PROGRAMMED LOSS OF CELLULAR DIFFERENTIATION THEORY OF AGING What kind of gene product would we be looking for that truncates differentiation proteins? The easiest way to truncate proteins would not be at the protein level, but rather at the mRNA level. The way proteins are produced is that the genes in our DNA are read and copied to a very similar molecule called mRNA which is almost identical to DNA with the exception of using the base pair Uracil in place of Thymine in the GCAT alphabet of your DNA. The only difference between Uracil and Thymine is a single methyl group (CH3) which is found attached to the 5’ carbon in thymine but only an H is attached to the 5’ carbon in uracil. High dose Vitamin D3 therapy over the last year-CURED ALL MY CHRONIC CONDITIONS-SOME THAT I’D HAD FOR 20+ YEARS!or >>>>>>>>> https://youtu.be/UsQ3D8BaYVk but make sure you look over this blog post afterwards has a lot more interesting explanations of additional very interesting things like progeria and Werner’s syndrome , rapidly aging salmon, etc. This update discussion has been deleted I am still working on it but I provide an interesting abstract to consider

Objectives: Similar characteristics of molecular pathways between cellular reprogramming events and tumorigenesis have been accentuated in recent years. Reprogramming-related transcription factors, also known as Yamanaka factors (OCT4, SOX2, KLF4, and c-MYC), are also well-known oncogenes promoting cancer initiation, progression, and cellular transformation into cancer stem cells. Long non-coding RNAs (lncRNAs) are a major class of RNA molecules with emerging roles in stem cell pluripotency, cellular reprogramming, cellular transformation, and tumorigenesis. The long intergenic non-coding RNA ROR (lincRNA-ROR, linc-ROR) acts as a regulator of cellular reprograming through sponging miR-145 that normally negatively regulates the expression of the stemness factors NANOG, OCT4, and SOX2. The main assumptions that this theory relies upon are that free radicals catalyze the demethylation of 5mC while antioxidants catalyze the methylation of 5mC by influencing DNA methyltransferase activity. This theory was constructed prior to the author’s knowledge that there existed any evidence that supported the above assumptions. After studies were located that confirmed the major assumptions of this theory, the likelihood of it being correct increased significantly.” Introduction: Liver cancer is a major cause of mortality and is characterized by the transformation of cells into an uncontrolled mass of tumor cells with many genetic and epigenetic changes, which lead to the development of tumors. A small subpopulation of cell population known as Cancer Stem Cells (CSCs) is responsible for cancer stemness and chemoresistance. Yamanaka factors [octamer-binding transcription factor 4 (OCT4), SRY (sex-determining region Y)-box 2 (SOX2), kruppel like factor 4 (KLF4), and Myelocytomatosis (MYC); OSKM] are responsible for cancer cell stemness, chemoresistance, and recurrence. At this point in evolution, reproduction likely occurred through parthenogenesis and possibly the complete dissociation of the multi-celled organism into a myriad of single cell, clonal spores; in an unrestricted environment, this would provide a great reproductive advantage.” Richard Dawkins, as courageous as he is, at least gives an explanation a try in a 2015 YouTube video. I share the link with you below. If you want a good laugh give it a watch. I am not laughing at Dawkins himself just at him trying to perform the impossible task of explaining homosexuality from the selfish gene point of view.LARP1 binds to and regulates the translation of terminal oligopyrimidine motif (TOP mRNAs ) and can directly interact with the 5′ cap of mRNAs. [17] [18] It has also been shown to interact with the 3′ end and coding regions (CDS) of other genes. [17] LARP1 protein colocalizes with stress granules and P-bodies , [19] which function in RNA storage and degradation . It has been suggested that LARP1 functions in P-bodies to attenuate the abundance of conserved Ras– MAPK mRNAs. The cluster of LARP1 homologs may function to control the expression of key developmental regulators. [19] Update 3- It appears this aging system is kind of a case of antagonistic pleiotropy (AP). How? It is a new kind of AP where something that was good for your distant ancestors (dissolution of the organism into millions of billions of single cell clones that can each grow into a new adult) from an evolutionary perspective, evolves into something that is bad for the more modern descendants of the ancestral species. The ancient, dramatically prolific system of reproduction has evolved into something that now kills an individual at a programmed time.

The problems with the paper were caused by my trying to put all the aging puzzle pieces together without enough information. For example, I imagined that the protein that is defective in Werner’s Syndrome (truncated) was generating excessive free radicals during the DNA unwinding process that catalyzed the demethylation of cytosines in the DNA. I thought this allowed pro-aging genes to be expressed, filling the body with destructive proteins. I received endless ridicule and derision from mainstream aging theorists who believed that the evolution of pro-aging genes was impossible. The new study shows that there are pro-aging genes, just not as many as I had imagined. It turns out that a lot of the programmed aging is caused by the suppression of genes that make transcription factors involved in maintaining cellular differentiation during and after development. Certainly, this must be harder for selfish gene promoters to explain than sex. At least with sex, the reproducer gets to pass on half of his or her genes. Here the selfish gene-ist has to explain how it evolved that someone passes on NO GENES WHATSOEVER! Given the very tough problem to solve here, the topic of homosexuality is just ignored for the most part, by evolutionary biologists. Connolly P. Choate J. Resko J. Effects of endogenous androgen on brain androgen receptors of the fetal rhesus monkey. Neuroendocrinology. 59(3):27 1994 Mar.Reprogramming, or generation of induced pluripotent stem (iPS) cells (functionally similar to embryonic stem cells or ES cells) by the use of transcription factors (typically: Oct3/4, Sox2, c-Myc, Klf4) called “Yamanaka factors” (OSKM), has revolutionized regenerative medicine. However, factors used to induce stemness are also overexpressed in cancer. Both, ES cells and iPS cells cause teratoma formation when injected to tissues. This raises a safety concern for therapies based on iPS derivates. Transdifferentiation (lineage reprogramming, or -conversion), is a process in which one mature, specialized cell type changes into another without entering a pluripotent state. This process involves an ectopic expression of transcription factors and/or other stimuli. Unlike in the case of reprogramming, tissues obtained by this method do not carry the risk of subsequent teratomagenesis. The study proves conclusively that aging is selected for by evolution and is programmed. A result that contradicts all major mainstream theories of aging that have been proposed since the early 1900’s. It turns out August Weisman got the right answer in 1882 but with the wrong reasoning.

So, that’s about it for homosexuality. If we have learned another fact about evolution, we can say that homosexuality fits in to the big picture as follows: If the process were to continue long enough the skin cell would be unrecognizable eventually. In some ways you could say the skin cell is returning to its undifferentiated, earlier (younger) state, but in an unhealthy way that ends up killing the bearer of these undifferentiated cells throughout the body. Counterintuitively, detrimental aging appears to actually be caused by cells becoming younger in a way, less differentitated, more like an embryonic stem cell! Ohkawa T. Sexual differentiation of social play and copulatory behavior in prenatally stressed male and female offspring of the rat: the influence of simultaneous treatment by tyrosine during exposure to prenatal stress. Nippon Naibunpi Gakkai Zasshi-Folia Endocrinolgica Japonica. 63(7):823-35, 1987 Jul.A HUGE NEW PROBLEM FOR EVOUTIONARY BIOLOGISTS (ACTUALLY THERE ALSO CO-EXISTS A SECOND SMALLER AGING SYSTEM THAT INVOLVES THE ACTIVATION OF PRO-AGING GENES BY AGE-RELATED CHANGES IN HORMONES-BUT THIS IS OLDER NEWS-AT LEAST TO ME & IT WILL ALSO BE DISCUSSED HEREIN) They looked at the DNA methylation changes with age in 59 different tissue types from 128 mammalian species to see what they all had in common.