On this page an attempt will be made to resolve the mystery of blood types. and eating for your blood type (blood type eating- i made a video on already, it has to do with the way we digest lectin differently)
notes: "Never worry.. for bloodlines cannot be maintained. because it is spirits which move."~shaman dr couwenberg , so even if there was a jesus descendant the body bloodlines may have had the spirits or the higher intelligable light leave that line because really earth is the super intelligence in energy control concresing the STAR's (super torriodal axiom reverberators) way. "~ben shaman dr couwenberg www.consciousazine.com universal flow of light vectorization, the higher morphs the lower forms so the forms are only carriers
https://www.youtube.com/watch?v=qi36RWK3LpY Virus Evolution Amazing Documentary Full HD - National Geographic Documentary 2015
Diet Debunked: Blood Type Diet- mic the vegan you seem to choose studies that suit you that is called cherry picking. for instance this time you say something in vitro isnt viable or the same in the body. but i bet if it was pro vegan related, as some of your other videos, you will happily quote in vitro ?- ben RE mic. Also saying we all are the same with same intestinal tract.. is a weak argument against blood type eating mic, because we know people are different hence some only have gluten intolerance to the point they just can not eat wheat. Ofcourse though there will always be a scale or spectrum; from 100% effected to 0% effected.
There intuitively must be something like a blood type diet, or foods to help and or avoid. Because hence differentiation, and if it is just that blood types differ due to viruses or something. these are all the questions i hope to uncover and conclude on here.
blood types: Elizabeth Greenway Neg mother if she has a pos baby her body will treat it like she would if it was a virus ..... builds up her immune system ..... next pregnancy if the fluids max at all the mothers body will literally kill the baby starving it of oxygen! If the fluid mixes in first pos pregnancy the baby could die too I think this is when the baby can be a blue baby Elizabeth Greenway We have more copper in our blood too. With this it's just neg and poss An O- mother could carry any neg child fine Elizabeth Greenway I know about blood Ben ask your question don't send a link about neg blood Some say AB started only about 2000 years ago. Some say jesus was AB but didn't say if it was + or - Some say AB is the oldest lol It seems to me from all I have read and listened to that I is the oldest. Then A. A is connected to O. B seems to be. It related. .. some say this is a different alien races front Hibiru. B is mainly in Asia. AB seems to be just an evolution thing with A and B. ABs parents can have any letter ! But unlikely to have another AB!. They can have A's or B's or O's! Lily is AB and her kids are B My best friend here Sunni is B- here mother AB- O and A are the most common by far.
ben: i suspect that the blood types differences has something to do with viruses. and possibly more so than allll the crazy talk about annunaki and that o's are blood of the gods , allll stemming from one mans interpretations of hyroglyphs of sumarian texts long ago, saccariah sitchins, which many scholars disagree with.
i will attempt to discredit my own work, specifically my statement that we need meat for full optimal full length life, in my blood type eating video in consciousazine playlist
The Rh blood group system (including the Rh factor) is one of thirty-five current human blood group systems. It is the most important blood group system after ABO. At present, the Rh blood group system consists of 50 defined blood-group antigens, among which the five antigens D, C, c, E, and e are the most important. The commonly used terms Rh factor, Rh positive and Rh negative refer to the D antigen only. Besides its role in blood transfusion, the Rh blood group system—specifically, the D antigen—is used to determine the risk of hemolytic disease of the newborn (or erythroblastosis fetalis) as prevention is the best approach to the management of this condition. As part of prenatal care, a blood test may be used to find out the blood type of a fetus. If the Rh antigen is lacking, the blood is called Rh-negative. If the antigen is present, it is called Rh-positive. When the mother is Rh-negative and the father is Rh-positive, the fetus can inherit the Rh factor from the father. This makes the fetus Rh-positive too. Problems can arise when the fetus’s blood has the Rh factor and the mother’s blood does not. A mother who is Rh-negative may develop antibodies to an Rh-positive baby. If a small amount of the baby’s blood mixes with the mother’s blood, which often happens in such situations, the mother’s body may respond as if it were allergic to the baby. The mother’s body may make antibodies to the Rh antigens in the baby’s blood. This means the mother has become sensitized and her antibodies may cross the placenta and attack the baby’s blood. Such an attack breaks down the fetus’s red blood cells, creating anemia (a low number of red blood cells). This condition is called hemolytic disease or hemolytic anemia. It can become severe enough to cause serious illness, brain damage, or even death in the fetus or newborn. Sensitization can occur any time the fetus’s blood mixes with the mother’s blood. It can occur if an Rh-negative woman has had a spontaneous or undetected miscarriage of a Rh positive fetus. https://en.wikipedia.org/wiki/Rh_blood_group_system
Blood types were once thought to be with people for life. And, in almost every case, they're still thought to be with a person for life. But there is one patient whose blood type actually changed. A liver transplant, apparently, has a shot of changing a person's blood type. There was once a simple time in human history when everyone had just one blood type, and that blood type was O negative. It wasn't called O at the time, of course, because even if anyone was looking at it, it would just have been blood to them. But life kept up its usual trick of evolving, and suddenly, on the surface of the lovely, smooth, red blood cells were little agglutinations of protein. There was what's now known as the Rh factor, the thing that turns O negative blood into O positive blood. Then there were other little clumps of protein, which separated Rh positive blood and Rh negative blood into A and B types. For the vast majority of history, only the Rh factor caused any bother. The system of an Rh negative woman who became pregnant with an Rh positive baby could see the infant's blood type as an outside body, and attack it. This was such a selector that today eighty-five percent of people are Rh positive. Meanwhile, A and B types only began troubling humankind by the time blood transfusions and organ transplants were happening. (Before that, any human blood or organs entering the body generally came via the stomach, which isn't that fussy about blood types.) Again, the immune system would attack the strangely bedecked blood cells and cause medical problems. Type O patients, roughly forty-five percent of the population, could give out their blood and organs, but couldn't receive anyone else's. The Rh factor of the blood depended on what type of medical procedure was being done. And so the world became concerned with these little blobs on blood, and with the genes that caused them. Since it was genetic, blood type was for life, and there was no way around the variations (Two more of which were found just recently. The Junior and Langereis, which affect about 50,000 people in Japan.) so there wasn't anything to be done except finding universal O negative donors and draining them like Capri Sun juice bags. So imagine people's surprise when they found out that blood type can change. Technically, it depends on what people mean by blood type. The genes don't change. However, people noticed that after bone marrow transplants, recovered patients sometimes slowly developed their donor's blood types. The marrow was used making one kind of blood, and it would continue, slowly filling people with cells that didn't match their genotype. That made sense. Scientists had put a new manufacturing center in their patient. It would make what it had always made. It also made a certain, if surprising, sense that cancers that affected blood and bone marrow could change a person's expressed blood type as well.
Then an infant with rubella, who has been typed as A many times in the first eight weeks of her life, suddenly lost her A agglutinations. At four months old, her blood type had actually changed. This may sound eerie to us, but it was good news to those who wanted to turn blood into a fluid that can be donated from anyone to anyone, including to and from one of those 50,000 people in Japan. Anything that could shear off agglutinations could make every bag of blood into a universal donor bag. It just, preferably, shouldn't be rubella. After years of searching, the best candidate for an agglutination-snipper came from a special mushroom. (No, not that one.) An enzyme isolated from fungi was found to turn any blood, any blood at all, to type O, and it did it while the blood was in the bag, not in the patient. This can change blood into a fluid that can be given to anyone, and given the shortages at blood banks, anything that made blood more available to all patients is a good thing. The method is still being tested, but hopefully blood will become a lot more common soon. But there is still one extraordinary blood type change mystery still out there, in the form of what today is a nineteen-year-old girl. As a nine-year-old, the girl's liver failed. A transplant liver was found, and the surgery was successful. Unfortunately, the girl began to get sick on the drugs that she had to take to force her body not to reject the new liver. Rejection is a huge concern for all donors. People have to take anti-rejection drugs their whole lives. Sickening immediately when taking them was a very bad sign. And then scientists typed her blood. The girl had spontaneously changed her blood, or rather her liver had spontaneously changed her blood. Stem cells from the liver got to her bone marrow, and then to her entire immune system. Slowly her blood type change from O negative to O positive, and her body accepted the liver. She was taken off the drugs, since she didn't actually need them anymore. Doctors called it an one-in-six-billion event. It would be great, for many transplant patients, if someday we could make the odds a little better than that. https://io9.gizmodo.com/5887569/how-to-change-your-blood-type-without-even-trying
Genetics:
http://blogs.plos.org/dnascience/2016/04/21/no-pain-and-extreme-pain-from-one-gene/ Posted April 21, 2016 by Ricki Lewis, PhD in Uncategorized: The family from northern Pakistan is one of the strangest to appear in the scientific literature. At its center is a 10-year-old, a street performer who walked on hot coals and inserted daggers through his arms before astonished crowds – feeling absolutely no pain. He died at age 13 from jumping off of a roof, considering himself impervious to all injury. I’ve included this story in my textbooks for so long that I recently began to wonder if I’d been perpetuating an urban legend. Then a study in this week’s Science Translational Medicine led me back to the Pakistani boy. He was real. And it turns out that different mutations in the same gene can cause complete absence of pain, or attacks of pain so severe that sufferers compare the sensation to dipping one’s feet into hot lava. In these extremes lie clues to developing new painkillers. In 2006, James Cox at University College London and Frank Reimann of the University of Cambridge and their colleagues pinpointed a mutation in the gene SCN9A, which encodes a sodium channel, as the likely cause of the Pakistani boy’s inability to feel pain.
Life without pain is dangerous. Babies chew off their tongues and lips, become scalded from hot food and drink, and without the feedback of pain toddlers bruise and even break bones. Older children learn from observation and context when to grimace so as to appear normal. Results of the study from a decade ago were intriguing. The 6 youngsters could feel touch, warmth and cold, pressure and tickles, and had a sense of where their body parts were in space, called proprioception. Many signs of nervous system function were just fine: the kids could move body parts when requested, and gagged, sweat, cried, and didn’t pee unless the urge and facilities were present. Nerve biopsies were normal. But pain was different. Strong prodding, poking, and even withdrawing blood elicited no response. Only a handful of similar cases had ever been reported, and the nomenclature was confusing and overlapping. So the researchers named the condition from Pakistan ‘channelopathy-associated insensitivity to pain’ and identified the mutation in the sodium channel gene. But this was in the olden days of 2006. Instead of sequencing the children’s genomes in under a day, as the researchers might today, they used painstaking positional cloning and linkage to narrow down chromosome sections that the families shared, leading them to the same part of chromosome 2. Each family had its own nonsense mutation, turning a DNA triplet that encodes an amino acid into one that encodes “stop.” The result: a stunted protein. The SCN9A gene encodes a subunit of a sodium channel, called Nav1.7, that festoons the tips of dorsal root ganglion neurons that function as nociceptors – sensing pain from the body’s periphery. The sodium channel is one of ten types, distinguished by its binding tetrodotoxin. That’s the stuff in pufferfish, a delicacy that makes one’s lips tingle when one eats it, and which I wrote about in 2002 when its genome was sequenced.
Burning People Syndrome: The mutations in the children who couldn’t feel pain are “loss-of-function” – their nociceptors can’t generate the action potentials that provoke the sensation. Mutations in the same gene that introduce a “gain-of-function” cause something quite different — inherited erythromelalgia (IEM), aka “burning man syndrome.” These people suffer episodes of acute pain upon warmth or mild exercise. Yet another variation is “paroxysmal extreme pain disorder,” which causes intense pain in the face and around the rectum.
Stephen Waxman from Yale and co-author of the new paper wrote an editorial that accompanied the 2006 paper on the Pakistani families who couldn’t feel pain. In a paper from 2007, he described a 15-year-old who’d suffered the burning episodes to his hands, feet, and ears since early childhood. Each attack lasted minutes to hours, he had several a day, and it was induced by exercise as well as alcohol, caffeine, or “sometimes melon.” He wore open-toed shoes and fought the urge to plunge his searing feet into buckets of ice, for doctors told him this would kill the tissue. An extensive pedigree revealed 36 burning people over 6 generations of his family – classic autosomal dominant inheritance consistent with a gain-of-function mutation. The paper published yesterday in Science Translational Medicine also addresses the inappropriate pain of IEM in five people with different mutations in SCN9A, but with an intriguing side experiment: recapitulating the disease in sensory neurons derived from induced pluripotent stem (iPS) cells. The group is from the Pfizer Neuroscience and Pain Research Unit, and includes Lishuang Cao, Anja Nitzsche, Edward Stevens, and James Bilsland.
Enter Stem Cells: The researchers were assessing efficacy of a drug candidate that blocks the sodium channels by inducing attacks in the participants with hot probes, and results were promising. But at the same time, they derived induced pluripotent stem (iPS) cells from the blood of four of the patients. The iPS route was necessary because neurons don’t divide and therefore are not sustainable in cell culture. But the researchers could watch what happens as iPS cells from patients divide and spawn daughter cells that differentiate as sensory neurons. Painkillers and Precision Pain Scales? Other aspects of the SCN9A sodium channels suggest they’re a good painkiller target. The channels are not on neurons in the heart or of the central nervous system, and the children in whom the channels don’t work do not have any symptoms other than their painlessness. The possibility of adverse effects seems low.
Commentators have long looked forward to the “thousand-dollar human genome” — the ability to sequence accurately all 3bn letters of an individual’s DNA for less than $1,000. In 2016 it seems likely to happen, 15 years after the completion of the first whole human genome in a decade-long $3bn research programme. The consequences for personalised healthcare could be profound. Veritas Genetics, a Boston start-up company, announced in March the availability of whole genome sequencing together with interpretation and genetic counselling for $999 — the first time the price of a consumer genomics product has fallen below the thousand dollar barrier.
While a host of companies such as Veritas and Human Longevity offer genomic services, backed by deep scientific and clinical knowledge about the relationship between genes and health, the instruments they use to read DNA come almost entirely from one source: Illumina. This Californian company’s machines are generating an estimated 90 per cent of the world’s DNA sequence data — thanks to technology acquired in 2007 when Illumina bought Solexa, a spinout from Cambridge university in the UK, for $650m.
Although the cost of DNA sequencing per genome has fallen sharply, the machines are still big and expensive. This year Illumina launches its smallest and cheapest sequencer so far, the $49,500 MiniSeq, and it has promised a new machine called Firefly for late next year at a price below $30,000. For a radically smaller, cheaper and more portable DNA reader, researchers can turn to the recently introduced MinIon from Oxford Nanopore, a start-up from Oxford university that focuses on a quite different technology: nanopore sequencing. MinIon is no larger than a mobile phone, fits into the USB port of a laptop computer and costs no more than $1,000 (though consumable reagents add to the running expenses). The technology employs a microscopic hole within bacterial proteins — the nanopore — to act as a biosensor. A voltage is applied across the pore and, as DNA moves through it, the electric current changes in a way that distinguishes between the four biochemical “letters” of the genetic code: G, A, T and C. This direct electronic reading is quite different from the “sequencing by synthesis” technology developed by Illumina, which attaches fluorescent molecular tags to the DNA and uses a computerised camera to read the results. http://www.ft.com/cms/s/2/f97395c8-e620-11e5-a09b-1f8b0d268c39.html?utm_source=taboola&utm_medium=referral#axzz44y0gZ2bQ