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| The whole point of science is to explain a phenomenon in a clear, verifiable way that does not possess any non-essential elements (such as personal attacks, obviously, or questioning the motives of those who are asking basic, straightforward, relevant, scientific questions). However, with "HIV/AIDS," I have found it nearly impossible to obtain useful answers to the most basic of questions. When there is a response, it is often something like, "didn't you read the title of the study - what more do you need?" The problem is that the title of the study is not necessarily consistent with the actual experimental findings - something that an undergraduate student of a scientific discipline should know. When I explain that the findings actually contradict the "HIV/AIDS" claim, a personal attack or obscenities have often followed. I have asked many "HIV/AIDS" advocates to participate in formal, moderated debates on very specific scientific issues, such as exactly what evidence exists for the claim that "retroviruses" can do harm to any mammal in any natural context, but no "HIV/AIDS" advocate has demonstrated the least interest in participating. Therefore, I decided to create this thread, which will be for specific scientific questions people have posed or would like to pose to the "HIV/AIDS experts." |
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I will begin with the following:
If the claim is based on correlations, where is the demonstration of the underlying mechanism? You do realize that statistical correlations are meaningless if the underlying assumptions are not correct, do you not?
In the early 1980s, "HIV" was to take about a year to 18 months at most to "progress to AIDS." Now, even among those who are "infected" but take no "medications," it is said to take about 8 or more years to progress to AIDS. So the obvious question is, where did all the gay men, who came to New York or San Francisco from Nebraska, or Iowa, or Missouri, or Alask, etc. get infected? Many were in their early to mid twenties, meaning that they would have to have been infected back in Nebraska (or wherever they came from) when they were teenagers. Who infected them? Where are all the "HIV/AIDS" cases in their home towns?
Considering the technology now available, exactly why has it been so difficult to determine the mechanism by which "HIV" causes low CD4 helper T cell levels? Since you can't ever find "HIV" viremia in anyone, ever, after over twenty years of looking, what could possibly cause a drastic fall in the T cell levels without "HIV" viremia?
Would you be willing to put up your own money to do an experiment to find "HIV" viremia, if you would get a full refund if it was found to be present? You would able to choose the person to be tested, assuming he or she was willing to provide blood and/or the tissue biopsy you would like to examine. This experiment would follow these guidelines:
"1. Only plasma centrifuged from fresh whole blood may be used in the experiment. No material derived from cultured cells will be considered, to rule out 'viral particles' which may be merely cultural artefacts.
2. The donor blood/plasma must be taken from a person/persons with a recent 'high-viral load' test result, and evidence for the date and result of the test (the number of 'HIV'- RNA's alleged) must be submitted, obviously with the name of the person/persons deleted to preserve donor confidentiality.
3. The donor must not be in receipt of protease inhibitors, AZT or any 'antiviral drugs'.
4. Only cold heparinised Ringer's solution may be used to dilute the plasma 1/1 ( i.e. 50%).
5. The diluted plasma shall be first filtered by aspiration-filtration, through a 0.6 millipore membrane. The resulting filtrate #1 will then be filtered again, this time using a 0.22 millipore membrane and filtrate #2 will be submitted to ultracentrifugation.
6. Centrifugation at 30,000 g for two hours will be used to prepare a pellet, likely to be extremely small. This pellet will be fixed with glutaraldehyde and osmium, then carefully detached and embedded in epoxy resins following routine EM procedures.
7. The electronmicrograph shall be at least 19,500 x magnification, and must resemble that published in Fig.1 of this article for particle size and shape, but with one notable and important variation. 'HIV' has been deemed to be a lentivirus, possessing a dense core of truncated conical shape. An ultrathin slice of randomly packed lentiviruses must inevitably show a number of particles bisected to show this core lengthwise, as well as end-on, with a resultant apparent mixture of round and 'rod-shaped' dense cores. Any micrograph which does not clearly show this feature will be deemed not to represent the lentivirus 'HIV'. "
Are you among those who argue that "HIV/AIDS" is a "closed book," even though science does not work this way - theories are constantly being subjected to validation or refutation experiments?
Would you argue that a "germ" is the sole cause of a "disease" if experiments were conducted that showed that only when certain conditions (not necessary to the survival or even health of the organism infected) were present, along with the "germ" that the disease occurred?
Assuming you understand that experiments need proper controls in science, can you explain exactly how "HIV" was isolated using such controls? In order to determine that some people are infected with a germ that is causing disease, you would need to obtain blood and/or tissue samples from those who appear to have this disease, as well as from those who appear healthy, and those who are afflicted with other diseases, correct? You would then have to do exactly the same thing (s) to all of the samples, correct?
Often, "hypotheticals" are used in science when direct experimentation can't be done (or is not allowed, due to "ethical" considerations). Because so many "HIV/AIDS" advocates like to cite studies, rather than explain exactly what they are claiming (and in many if not most cases, the findings of the studies contradict their arguments), the hypothetical may be a way of "teasing" basic information and crucial out of them.
Here is the hypothetical: let us assume that there is a new disease," and the scientific investigators believe that a virus is to blame. They insist that the disease must be caused by one virus and nothing else. What would they have to do, exactly, to demonstrate that they are right, in a way that adheres to the scientific method? |
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Note that the 7 conditions listed in the above post were put forth by Alexander Russell. Let us assume that this experiment was conducted as specified. What do you think the results would be, since you are so sure of the "HIV/AIDS" claim? If the experiment was conducted according to these guidelines and no "HIV" was found, what would you conclude, assuming it was conducted properly, of course?
Do you feel that it is impossible for you to be wrong about "HIV/AIDS," and if so, is this not entirely inconsistent with science at its most basic?
If not, the please explain what critics could do, experimentally, to refute the "HIV/AID" claim. |
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| If you claim that a person has a "high viral load" of "HIV," then surely it would make sense to take blood or tissue samples and just look at them with an electron microscope (using no "stimulants" on the samples), to show the "dissidents" that "HIV" is in fact present in amounts large enough to cause serious damage to the immune system, correct? If not, then can you explain, in a way that most people would understand, why it is not possible to find a lot of "HIV" in people who you claim have "high viral loads?" |
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Hans-
I decided to post this here since the other thread it rather long.
Do you mind helping me in my research on anti-HIV medications? I am trying to find out what benefits NRTIs and NNRTIs have in people who are not HIV+.
I have researched this quite a bit, but I can mostly only find research on what protease inhibitors do in HIV- persuns.
These drugs clearly have some benefits to HIV+ people, and since I don't believe HIV is the problem I want to know what other mechanisms they might be aiding these people other then lowering their "viral load". |
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| Well, the first place to look is in the "oxidative stress" context. You could search google or pubmed.com, for example,. for the name of the drug, both generic and brand names, along with the word oxidative. Also, other words like inflammatory, inflammation, arachidonic, nitrosative, reactive oxygen species, lipid peroxidation, and free radicals can be used in the search, along with the drug's name. Let me know if you find anything interesting. |
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Actually, what I am finding is that, with the original medications atleast, HAART increases oxidative stress in persuns who are "HIV+"
This particular study only looked at "markers", but it seemed pretty accurate. I would say this is not an accurate representation of today's medications though. I have done extensive research on the medicationd my boyfriend is taking and they are not associated with DNA mitochondrial toxicity like the older drugs are. They are not without side effect, but have a much better safety profile then the older drugs.
This study did not include any protease inhibitors, CCR5 receptor antagonists, integrase inhibitors, or newer NRTIs.
BTW- My boyfriend is still feeling really good. Him and his doctor have agreed that every 6 months they will evaluate his need for the medication or not. He has really felt a lot better though. His regimen is much "less toxic" then other regimens available, and hopefully we will figure out a way to get him off of them permanently eventually. I am just so scared that he is going to die in the next few years. He is eating the least amount of PUFAs as possible, and hopefully that will amorleiate (spelling) some of the damage of HAARt on his body. |
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| What study? I didn't see a citation. Oh, I went to a local Trader Joe's, and they have a lot of SFA rich stuff, such as wafers that are 10 g of fat per serving, 9 of which are saturated, with no cholesterol, so that's a place to visit if you get a little bored with your diet. |
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Sorry, here is the study:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1557529 |
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I like how they start off by explaining the basics:
"Free radicals are compounds possessing an unpaired electron, which renders them highly reactive and capable of causing oxidative damage to all the major macro-molecules in cells, including lipids, proteins and nucleic acids. A major family of free radicals is the reactive oxygen species, derived metabolically from molecular oxygen via super oxide anions. Oxidative attack on proteins results in the formation of protein carbonyls [2], often with the loss of functionality of the parent protein. Polyunsaturated fatty acids, which are major components of cell membranes, can also undergo free radical attack, producing lipid peroxidation products like malondialdehyde (MDA) and 4-hydroxynonenal."
And also their conclusion is something I would have guessed, though obviously, I would argue that "HIV" is effect, not cause (and is not a "traditional virus" at all):
"HIV infection increases the oxidative stress process, while anti retroviral combination therapy compounds this effect by increasing lipid oxidation. The decrease in antioxidants that accompanies HIV infection suggests a potentially important role of nutritional supplementation and good nutrition in general in the proper management of HIV/AIDS."
Notice how they talk specifically about lipid peroxidation. A diet rich in SFAs and low in UFAS and oxidized cholesterol should be helpful, if not a total "cure." |
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