Of course Gardasil works in Australia. At least, it might when they’ve used it for long enough. But we won’t see that for many years down the line, because most the girls who have received the vaccine, were probably already having sex, and therefore will have picked up HPV types. By the way, you’re not supposed to know that HPV 16 and 18 can be got by a baby from it’s mother, and child to child, … and that it’s regularly found in tonsils removed from children, etc, etc, etc…. Merck needs to at least exceed the 7 year patent limit time before anyone admits to any “mere anomalies”. The Gardasil golden goose must continue to lay, you know.
Did your doctor tell you that there were two grades of smears? Low grade smears which require no action and high grade smears which do? Did you doctor tell you that out of every 8 HPV positive smears, 7 will be low grade? On top of that ,for every two high grade high grade lesions, one will not be HPV 16 or 18 positive. The other 50% are lots of other types.
So, 1 per 8 is 12.5%, and half of that is 6.25% Remember when we were told that 70% of all HPV positive smears would be 16 and 18 and that Gardasil would nuke that possibility? As to the 7 out of 8 low grade lesions… well, 30% of them contain the four strains of interesting 6, and 11 – which don’t “cause” cancer, and 16 and 18 which do. How much of that 30% is 16 and 18? Why don’t they say? Isn’t that important?
Looking at a bigger picture, some of the article’s main points are exactly what we’ve been saying for years:
Most pap test abnormalities are caused by HPV types not preventable with current vaccines.
Well hello? Weren’t you told that this vaccine would reduce your chances of getting an abnormal smear by 70 – 80%?
Not the same message, huh?
Have we been sold Gardasil on flawed arguments? But more interestingly, they seem to be shifting the goal posts. Why? Because what they are seeing, isn’t what they thought they would see?
But here’s another bit that gets me furious. The article says “the two HPV vaccines do not contain live virus nor any oncogenic viral proteins of infectious material. Therefore the vaccine is not responsible for any smear detected abnormalities that may be found after it was given.”
Funny that. Merck’s trials found that in women already exposed to HPV before vaccination – just like these women she’s talking about… that there was a 46% excess of other HPV types. And they don’t know why. The FDA licenser specifically mentioned that fact in a press conference just after it was approved. Merck dismissed that, as perhaps an insignificant artifact, or something peculiar in that cohort. Which must mean they didn’t work out the confounders very well huh?!!! What else didn’t they work out very well? 46% is insignificant? Merck has blinkers on.
There are some other perfectly good explanations. The first explanation can be gleaned from an article written by the vaccine maker himself, insultingly called "God's gift to women: The Human Papillomavirus Vaccine."
In this article he details how the natural immunity of HPV simply isn’t known. The majority of women who have natural immunity to HPV don’t have antibodies and those who do, only have low levels. Simplistically, his answer is that MORE will therefore be better. More must be better, because less is no good, right?
Did you know that there’s a long history in vaccinology of giving a person a specific vaccine, and that vaccine backfiring? The latest version of that, is the Canadian studies which showed that people given the regular flu vaccine were more likely to get swine flu. This backs up an earlier article which showed that giving specific flu vaccines, reduces a person’s immunity to much broader range of influenza protection they would have got naturally.
Just recently, a medical study came out showing that the acellular whooping cough vaccine increased your chances of getting another whooping cough like disease called para-pertussis by a neat little 40%.
In the 60’s an adenovirus vaccine resulted in the recipients getting adenovirus infection, far more seriously than those who weren’t vaccinated, and the killed measles vaccine, resulted in recipients getting a harder to diagnose, and more serious form of measles called “atypical measles” which those vaccine recipients can get again and again. And for those who have forgotten, remember the recent trial Merck HIV vaccine, which also had no infectious particles in it, which increased the rate of HIV in the vaccinated?
And then there’s Lewis Thomas’s little gem in his book called "The Youngest Science: notes of a medicine-watcher" (1984) pages 75 – 78 where he found that vaccinating rabbits against a specific meningitis resulted in those rabbits becoming susceptible to all the other types not in the vaccine. Those rabbits lost broad spectrum natural immunity. Here’s the details for the naysayers:
“So we packed again, and flew to Halifax, where I went to work on the treatment of meningococcal meningitis with a new sulphonamide called sulfadiazine, of which I had never heard, and Beryl was recruited as a laboratory assistant to keep the records and carry cultures from one place to another.
We were in Halifax for about a month, culturing the spinal fluid of several hundred patients with meningitis, collecting samples of serum from these patients and other people who did not develop meningitis but were in close contact, in order to study the possible role of antibodies in protection against the disease, and recording with care the clinical course of the illness under treatment with sulfadiazine, which was administered to all patients with an established diagnosis. Sulfadiazine was wonderfully effective. The only patients who filed to recover were those with a rapidly developing and overwhelming infection – some of them became comatose within a few hours and were brought to the hospital in deep shock, their skin surfaces covered everywhere by areas of hemorrhagic necrosis (looking very much like the Shwartzman phenomenon which I was to study several years later), and these patients were dead before we could start treatment. All the rest, the majority, recovered promptly when given sulfadiazine, and we saw none of the late complications – blindness, deafness, mental confusion – which had occurred in earlier epidemics of untreated meningococcal meningitis.
We came back to Boston with crates of cultures and sera, and my laboratory was committed to the problem of the meningococcus and the mechanism of its peculiar affinity for the surfaces of the brain and spinal cord in human beings. None of the conventional laboratory animals were particularly vulnerable to this organism: rabbits, guinea pigs, rats and mice could tolerate the intravenous injection of huge numbers of live meningococci without turning a hair, and the bacteria disappeared from their bloodstreams within ten minutes or so. It was evident that the animals possessed a highly effective mechanism for their protection, and I settled down to find out more about this. The first and simplest possibility, that they were able to kill off the injected meningococci by means of an already existing “natural” antibody, was easiest to test in rabbits, so rabbits became the laboratory’s routine animal. We quickly learned that the serum of a normal adult rabbit was capable of destroying almost any number of meningococci; when up to a million organisms were added to a single millilitre of freshly obtained rabbit serum, and the mixture then incubated for a few hours at 17 degrees Centigrade, the specimens became sterile. If the serum samples were heated at 56 degrees Centigrade for an hour before adding the bacteria, the bactericidal action was complete lost, indicating that the killing power depended on the presence of complement (a sequence of proteins, still incompletely understood, which makes possible the action of antibodies against antigens on the surface of bacteria).
We though it useful, given so powerful an example of natural immunity already in existence in animals, to see whether we could obtain even stronger antibacterial sera by immunizing the rabbits. We injected animals with suspensions of heat-killed meningococci, and collected sera at weekly intervals. These samples were set up as in the initial experiments adding various numbers of live bacteria to the serum specimens and determining how many were killed and how quickly. Within the next few days we encountered our paradox: the sera from the immunized rabbits, which had been capable of killing a million meningococci in a few hours, had now lost this property. There were potent and specific antibodies in these sera, as we could show in other kinds of tests – agglutination, precipitation, and complement fixation tests. But with the appearance of a specific antibody, the bactericidal activity vanished.
Moreover, something of the same sort could be show in the whole rabbit in vivo. When we injected live bacteria into the bloodstream of our immunized animals, and then measured the survival of bacteria by serial blood cultures, we were surprised to learn that the blood cultures were still positive twenty-four hours later in the more intensively immunised rabbits, in contrast to the unimmunised animals, in which all of the meningococci had disappeared within ten to fifteen minutes.
By this time, it was late April of 1941 and I was in a hurry. The problem had turned into something fascinating, involving both paradox and surprise. I knew I was expected back in New York the next January to become a neurologist, so I worked as fast as I could. What I had run into was an antique immunologic phenomenon called the “prozone”, in which an excess of antibody turns off the immune reaction unless the serum is sufficiently diluted. However, the difference in my laboratory – what was new – was that it worked in vivo: an immunized animal could lose, as the result of being immunized, its own natural defense. This might I thought, have useful implications for susceptibility in certain human infections beyond meningitis – typhoid fever and brucellosis, for example – and I wanted to get on with it.
However, as it turned out, I never got to finish the problem or even answer the principal questions. Nor did I ever get back to the Neurological Institute. The Rockefeller Institute was put on notice in late 1941, then mobilized as a naval medical research unit; I was assigned to it as lieutenant, and received orders to turn up in New York, in uniform, by the end of March 1942. John Dingle and I reluctantly agreed to bring the still inconclusive problem of the in vivo prozone to a premature end and write the work up; to this day, I’ve never been able to return, full-time, to the problem. It still hangs there in my kind, and I don’t believe any other laboratory has ever settled it.”
Note about the author: Lewis Thomas was chancellor of the Memorial Sloan-Kettering Cancer Center in New York city, and a member of the National Academy of Sciences. He served as Professor of Pediatric Research at the University of Minnesota, as Chairman of the Departments of Pathology and Medicine, and also Dean at the New York University-Bellevue Medical Center, and as Chairman of Pathology and Dean at Yale Medical School.
So exactly what is going on with Gardasil? Are they too scared to look?
This is why we need the National Immunisation Register expanded to include crucial health data, because the way New Zealand vaccination programmes are run now, we are guaranteed to know absolutely nothing about the crucial determinants of side effects, "efficacy" or whether Gardasil, or any other vaccine, might turn around and bite girls in a way they and their parents never expected.
So here’s the deal for all the girls out their whose parents want them to have Gardasil.
If you want to have a vaccine made by someone who hasn’t the foggiest as to how natural immunity to HPV really happens: who assumes that in terms of antibodies "more is better", and who promises you that sometime down the line this will all work out just hunky dorey, then fine.
But believer beware. Trusting experts has a knack of coming back to bite you on the backside.
