LARP1 is the largest of a 7-member family of LARP proteins (others are: LARP1B, LARP3 (aka genuine La or SSB), LARP4A, LARP4B, LARP6 and LARP7). [9] All LARP proteins, including human LARPs, contain 2 conserved regions. The first conserved region shares homology with La proteins (called the La motif, see SSB) whereas the second conserved region (called the LA- motif) is restricted to LARP proteins. LARP1 and 1B also contain a conserved “DM15 region” within their C-terminus. [10] This region is unique and has been shown to be required for RNA-binding.Mouse Larp1 is expressed in dorsal root ganglia and spinal cord, as well as in developing organs characterized by epithelial– mesenchymal interactions . [6] Human LARP1 is present at low levels in normal, non-embryonic cells but is highly expressed in epithelial cancers (such as ovarian, colorectal, prostate, non-small cell lung, hepatocellular and cervical cancers). [11] [12] [13] [14] Some studies have shown that high levels of LARP1 protein correlate with worse prognosis in cancer patients. [15] [16] Prevailing evolutionary theory cannot explain the conundrum of homosexuality. Current theory requires defining homosexuality as an evolutionary accident as homosexual offspring would not be expected to reproduce. Is evolution so sloppy that the sexual preferences of 10% to 20% of the human population (78) is simply a random mistake of nature? And why does it also occur throughout the animal kingdom from sheep (79) on down to rats (80)? If one accepts group selection as a reality, the purpose of homosexuality has a simple explanation. Update #12 Turns out lamin A is missing in undifferentiated embryonic stem cells and is defective in the rapid aging disease of progeria : Yellow fungus infected toenails (under the nail)- I tried everything over 20 years and nothing worked-10 months of high dose Vitamin D3 and they are clear as a bell! 100% cured.

I had designated Werner’s syndrome as the dominant aging system that coopted and controlled all the other aging systems-you will see why when you study the table- but basically because WS shows all the symptoms of normal human aging while other rapid aging diseases just show a segment.. Because the large set of genes shut down by methylation during the aging process (as well as the upregulated LARP1 gene( a true aging gene) ) are primarily the same across all mammalian species it very, very, strongly suggests that aging evolved and is highly conserved. This is in complete contradiction to modern mainstream evolutionary theory which proclaims that aging could never have evolved because it is bad for the individual and reduces the spread of the individual’s genes. For most modern aging theorists, they think an evolved aging program is something akin to a perpetual motion machine, completely impossible. In fact, this was once the quote by Aubrey De Grey in his sophomoric paper about how programmed aging was impossible. Similarly, given that the LH and FSH subunits are found to be the #1 and #2 proteins that increase inside a cell during aging, it is not too far a leap to suggest that these proteins might have a central role in the methylation of the 36 genes that become hypermethylated with aging. LH and FSH not only increase dramatically during aging after the age of female menopause (in both men and women-up to 1,000%+!), they also have a primary role in initiating pre-pubertal/pubertal development in children as well when they increase. 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.Biologists in general tend to also discuss the evolutionary puzzle of homosexuality as mainly a human condition. Applying it to just humans makes the fact conveniently unique and a special category that can be ignored. They do it all the time. Menopause and suicide are also promoted by most biologists as being exceptions that apply to just humans. One other thing I have seemed to notice is that when you look at large groups of either homosexual males, or homosexual females, the males still tend to maintain their evolved desire to stand out and draw attention to themselves while groups of lesbians seem to act more like the camouflaged females of other species, who desire and have evolved to avoid attention. You can also do a crude test of this idea by searching google-images for group of gay men and then for group of lesbians and you will see the difference. Most of the pictures are along the lines that follow: (see pictures in the book). The first 2 sentences in the abstract of my paper claimed that aging evolved and aging and development were intimately linked. This new study proves it to be 100% true. “ The evolution of aging: a new approach to an old problem of biology” Werner’s Syndrome is caused by the WRN protein being improperly truncated so that it is too short to do its job properly of preserving the differentiation status of human stem cells. How is having homosexual offspring a defense to predation? Having homosexual offspring is a form of birth control for mothers who are considered by evolution to be unfit in the presence of predation. The stress from predator encounters if extreme enough can kill the mothers and their unborn babies. If the stress is less extreme it can lead to homosexual offspring that need to be nursed for a relatively significant period of time. Nursing prevents the mother from becoming fertile for mating. So, in a sense having homosexual offspring is just nature’s form of birth control for mothers perceived as temporarily “unfit” due to stress.

A painful snapping hip syndrome which I had been suffering from for 23 years and no Dr could help me-It is now 100% gone. No pain and NO SNAPPING!!Another glaring fact that screams “aging is programmed” is the existence of semelparous aging. The most famous example consists of the rapid aging and death of the Pacific Salmon immediately after breeding around the age of three years old. When the Pacific Salmon is castrated , it can live 7 or more years. How was this explained using the other theories of aging of the past? Simply by saying semelparous aging is not a real form of aging and can be ignored! It had long been hypothesized that the rapid aging and death of the Pacific Salmon was caused by its huge exertion of energy and large amounts of resources spent in traveling the long journey from the ocean to its riparian birthplace to reproduce. Some suggested that the Salmon just died of exhaustion. Others made a slightly less simple case and suggested that the hormonal changes occurring during the great trip of the Salmon led to very high levels of the stress hormone cortisol. Supposedly that was what was killing them, although the cortisol increase comes long before they reproduce. And it turns out that there are still animals on earth that can reproduce this way..take the immortal jellyfish for example: Several studies have demonstrated that LARP1 deficiency selectively affects the recruitment of TOP mRNAs to polysomes In some cancer cells, LARP1 deficiency reduces proliferation and activates apoptotic cell death. [13] Even though a decrease abundance of proteins encoded by TOP mRNAs has been reported in LARP1 silenced cells, some researchers believe that this can be explained simply by the reduced number of TOP mRNA transcripts in LARP1-deficient cells. Swaab D. Gooren L. Hofman M. Gender and sexual orientation in relation to hypothalamic structures. Hormone Research. 38 Suppl 2:51-61, 1992. After about 4 months upped the dose to 50,000 IU a day or 150X the old recommended “safe” dose I then boosted it to 100,000 IU a day or 300 x TIMES the old maximum safe dose!

Transdifferentiation and reprogramming: Overview of the processes, their similarities and differences The Dramatic Hyaluronic Acid Decline (After Age 40) that Causes Wrinkles, Hair Graying/Thinning, Arthritis, Chronic Pain/Diminished Eyesight/Joint Replacement In 1998, I published a paper titled “The Evolution of Aging: A New Approach to an Old Problem of Biology” Well, what do you know?? LARP1 has a unique region that binds to RNA transcripts! My guess is that this is the protein that is involved in truncating the Lamin A protein in normally aging cells, and likely it is truncating the WRN protein in normally aging cells (truncated WRN protein being found in normally aging and senescent cells has yet to be shown true-but I predict someday this will be found to be occurring). Well as mentioned before, LARP1 seems to fit the description of this hypothetical protein! It has a very unique sequence that is specific for binding to RNA transcripts. It is found at high levels in cancers. Werner’s Syndrome victims suffer from normal cancers at a high rate as well- is LARP1 cleaving the WRN protein which leads to cancer?This updated edition has a fascinating new look at diabetes as an evolved defense to freezing damage in winter gone out of control

In summary, we have found that WRN protein, besides its role in DNA repair, functions to safeguard heterochromatin stability ( fig. S11). Our results unveil that the progressive heterochromatin disorganization observed in WRN deficient MSCs underlies cellular aging, but more extensive studies are needed to examine its role during physiological aging.” I theorized in my 1998 paper, that more primitive organisms , early in evolution, probably reproduced in this manner- a quote-

Based on Evidence, Case Studies, & Evolutionary Logic

Upon realizing that taking 4,000 IU of Vitamin D3 a day was not enough for me, I decided to embark on a “dangerous” experiment that directly contradicted everything MD’s had told me for years: A number of studies in rodents have shown that if you stress the pregnant mother at certain times during her pregnancy she will tend to give birth to homosexual males and promiscuous females and a smaller number of homosexual females. Finally, we asked whether heterochromatin disorganization could be a common hallmark for physiological human stem cell aging. For this purpose, we compared the levels of heterochromatin marks in primary dental pulp MSCs derived from six young (7–26 year old) and six old (58–72 year old) individuals ( fig. S10I, and Table S4) ( 20). A marked downregulation of WRN protein associated with a decrease in H3K9me3, HP1α, SUV39H1, and LAP2β levels in MSCs derived from old individuals ( Fig. 4E). Therefore, specific heterochromatin changes may underlie both pathological as well as physiological mesenchymal stem cell aging.