One of the many tricks of the pharma industry concerns the massive dosage reduction of the putative antiretroviral medication and the switch to far less toxic substances over the last decades. One had started with 1500 mg AZT in the Burroughs-Wellcome trial in 1986/87,
• Richman et al., “The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A double-blind, placebo-controlled trial”, N Engl J Med, 1987 Jul 23;317(4):192-7, https://pubmed.ncbi.nlm.nih.gov/3299090/
“Twenty-one percent of AZT recipients and 4 percent of placebo recipients required multiple red-cell transfusions (P less than 0.001). Neutropenia (less than 500 cells per cubic millimeter) occurred in 16 percent of AZT recipients, as compared with 2 percent of placebo recipients (P less than 0.001).”
“Although a subset of patients tolerated AZT for an extended period with few toxic effects, the drug should be administered with caution because of its toxicity and the limited experience with it to date.”
Nobody can survive 1,5 g AZT per day(!) over months. The patients received blood transfusions to survive the treatment, because AZT damages the bone marrow where the blood cells are formed. That is all well documented but it was never mentioned by the press.
Over the next decades one reduced the dosages drastically and switched to far less toxic medications like Tenofovir. Many highly toxic substances have been taken from the market. Lo and behold, people treated that way live longer.
This dosage reduction over the last 37 years (counted from 1986) is not monitored and it is never mentioned in studies on the life expectancy of HIV+ measured persons under treatment. But the claim is that due to the "improved" substances HIV+ measures people live longer. The opposite is true. Because of the less toxic substances in much lower concentration they die less fast.
The latest putative HIV (not AIDS!) medication is Descovy. One of the active substances is Tenofovir. It is also used for PrEP, i.e. a supposed prophylaxis in HIV-neg. measured persons. Descovy contains by a factor of 9 less Tenofovir as the predecessor Truvada with respect to the molecular weight of the Tenofovir formulations. And people taking Descovy show much less kidney damages and reduction of the bone density than persons taking Truvada.
There was a real AID Syndrome in the 1980s and 1990 in homosexuals in the USA, who suffered from multiple infections with sexually transmitted diseases (due to frequent anal intercourse), after years of drug abuse (especially amyl nitrites, poppers) and years of antibiotics abuse (to protect against sexually transmitted diseases, like gonorrhoea, syphilis, herpes, hepatitis A and B, CMV and so on).
But it never had anything to do with a virus, that infects 1 in 5000 CD4 cells and thus in a far to low concentration to explain the decline of CD4 cells in the real AID Syndrome. In the real AID Syndrome, in severely drug addicted and multiple infected homosexuals, the not-infected CD4 cells died. That is called the "bystander cell enigma". This problem of the virus hypothesis of the AID Syndrome can be traced back to the 1980s and even publications by Robert Gallo on this point.
In a publication from 2013 John Coffin and Ronald Swanstrom point that problem out very clearly, "we still cannot answer the one big question: How does HIV-1 cause AIDS?”
“HOW DOES HIV-1 CAUSE AIDS? As is apparent from this article and the rest of the collection, in the 25+ years since its discovery, we have learned an enormous amount about HIV, but we still cannot answer the one big question: How does HIV-1 cause AIDS?”
“Even if we knew the mechanism of HIV-mediated cell killing, we would not know how HIV-1 causes CD4+ T-cell decline and AIDS in humans. The observation that virus and cell turnover rates in various SIVs in their natural hosts (such as SIVsm in sooty mangabeys), which do not progress to AIDS, are essentially identical to those in humans, who do progress, implies that cell killing alone cannot account for AIDS pathogenesis. Indeed, this result is consistent with the high natural turnover rate of activated effector memory helper T cells, the primary target for HIV-1 infection, on the order of 10^10 cells per day, of which only a small fraction are infected after the initial primary infection phase.”
We know from the co-discoverer of the HI Virus and Nobel Prize winner Françoise Barré-Sinoussi, that every HIV+ measured person carries his own variants of the HI virus.
• Barré-Sinoussi et al., “Expert consensus statement on the science of HIV in the context of criminal law.”, J Int AIDS Soc. 2018 Jul;21(7):e25161, https://www.ncbi.nlm.nih.gov/pubmed/30044059
“Mutations of the virus occur repeatedly so that every person living with HIV has more than one virus variant [154]. During transmission, a limited number of virus variants (one to a few) are transmitted, but these will also mutate to form new variants so that no two persons’ HIV is identical [155].”
Thus every HIV+ measured persons has his own individual infection. But it is supposed to be always the same molecular mechanism.
There is absolutely no proof, that at least 13 zoonoses occurred in Africa around 1930 from SIV in apes and monkey to HIV in humans, as science claims,
“How the AIDS epidemic actually began, what the contributing factors were, and why it appeared in the mid- to late 20th century (and not before) are not known. Whatever the final answers are, they must account for
(i) at least seven separate introductions of SIVcpz and SIVsm viruses into humans;
(ii) the fact that the HIV-1 group M, N, and O viruses are significantly more closely related to SIVcpz viruses from P. t. troglodytes than to the single SIVcpz isolate from P. t. schweinfurthii; and
(iii) the estimation of 1930 (range 1910 to 1950) as the timing of the last common ancestor of the HIV-1 group M viruses.”
“More in detailed studies showed that SIVs from chimpanzees and gorillas have crossed the species barrier on at least four occasions leading to HIV-1 group M, N, O and P in humans [6,23]. The different HIV-2 groups are the result from at least nine independant transmissions of SIVs from sooty mangabeys in west Africa [6,23,24].”
That would have been a very bizarre coincidence in Africa around 1930 which 50 years later lead to an epidemic among homosexuals in the USA.
Until today there is no animals model for HIV. Apes don't get AIDS.
I have someone sitting beside me who has full blown AIDS with less than 50 CD4 cells. He tried following a natural path as you suggest and that has taken him to place from which he might have permanent damage. He started meds last week and has already seen significant improvement. I have seen this happen literately hundreds of times. I worry that more people will follow what you say and may occur permanent damage like may have happened to my friend.
“ Mysterious White Blood Cell Disorder Not Just 'AIDS Without HIV.”
It’s an interesting article. I wanted to share here. I would very much like to be in contact with you to share my story. I don’t know how to facilitate that. I know Celia for many years. I’ve been involved with the issues you write about here for many years. And I am desperately looking to share my story. If there is a way to reach out and communicate with you I would very much appreciate it.
With regards chemical imbalance and MH there is one but it is not serotonin nor dopamine you are correct - researchers looked at the metabolites in the cerebrospinal fluid and found the levels all over the place - it's between glutamate and gamma- Aminobutyric Acid being as GABA is synthesized from glutamate decarboxylase and the active form of B6 pyridoxal 5′-phosphate. Tip - if anyone suffers from anxiety you'll find the active form of B6 helpful, It can also stop akathisia at high dose.
For those who do not know the condition which causes suicide ideation, suicide, violence upto homicide is called Akathisia there are over 100 drugs that can cause it including almost all psych drugs. It's a massive scandal that has been going on for decades. It's going on because the doctors and coroners can hide it under the guise of serious mental illness. There are thousands of people who die from akathisia every year.
One of the many tricks of the pharma industry concerns the massive dosage reduction of the putative antiretroviral medication and the switch to far less toxic substances over the last decades. One had started with 1500 mg AZT in the Burroughs-Wellcome trial in 1986/87,
• Richman et al., “The toxicity of azidothymidine (AZT) in the treatment of patients with AIDS and AIDS-related complex. A double-blind, placebo-controlled trial”, N Engl J Med, 1987 Jul 23;317(4):192-7, https://pubmed.ncbi.nlm.nih.gov/3299090/
“Twenty-one percent of AZT recipients and 4 percent of placebo recipients required multiple red-cell transfusions (P less than 0.001). Neutropenia (less than 500 cells per cubic millimeter) occurred in 16 percent of AZT recipients, as compared with 2 percent of placebo recipients (P less than 0.001).”
“Although a subset of patients tolerated AZT for an extended period with few toxic effects, the drug should be administered with caution because of its toxicity and the limited experience with it to date.”
Nobody can survive 1,5 g AZT per day(!) over months. The patients received blood transfusions to survive the treatment, because AZT damages the bone marrow where the blood cells are formed. That is all well documented but it was never mentioned by the press.
Over the next decades one reduced the dosages drastically and switched to far less toxic medications like Tenofovir. Many highly toxic substances have been taken from the market. Lo and behold, people treated that way live longer.
This dosage reduction over the last 37 years (counted from 1986) is not monitored and it is never mentioned in studies on the life expectancy of HIV+ measured persons under treatment. But the claim is that due to the "improved" substances HIV+ measures people live longer. The opposite is true. Because of the less toxic substances in much lower concentration they die less fast.
The latest putative HIV (not AIDS!) medication is Descovy. One of the active substances is Tenofovir. It is also used for PrEP, i.e. a supposed prophylaxis in HIV-neg. measured persons. Descovy contains by a factor of 9 less Tenofovir as the predecessor Truvada with respect to the molecular weight of the Tenofovir formulations. And people taking Descovy show much less kidney damages and reduction of the bone density than persons taking Truvada.
There was a real AID Syndrome in the 1980s and 1990 in homosexuals in the USA, who suffered from multiple infections with sexually transmitted diseases (due to frequent anal intercourse), after years of drug abuse (especially amyl nitrites, poppers) and years of antibiotics abuse (to protect against sexually transmitted diseases, like gonorrhoea, syphilis, herpes, hepatitis A and B, CMV and so on).
But it never had anything to do with a virus, that infects 1 in 5000 CD4 cells and thus in a far to low concentration to explain the decline of CD4 cells in the real AID Syndrome. In the real AID Syndrome, in severely drug addicted and multiple infected homosexuals, the not-infected CD4 cells died. That is called the "bystander cell enigma". This problem of the virus hypothesis of the AID Syndrome can be traced back to the 1980s and even publications by Robert Gallo on this point.
In a publication from 2013 John Coffin and Ronald Swanstrom point that problem out very clearly, "we still cannot answer the one big question: How does HIV-1 cause AIDS?”
• Coffin, Swanstrom, “HIV Pathogenesis: Dynamics and Genetics of Viral Populations and Infected Cells”, Cold Spring Harb Perspect Med. 2013 Jan; 3(1), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530041/
“HOW DOES HIV-1 CAUSE AIDS? As is apparent from this article and the rest of the collection, in the 25+ years since its discovery, we have learned an enormous amount about HIV, but we still cannot answer the one big question: How does HIV-1 cause AIDS?”
“Even if we knew the mechanism of HIV-mediated cell killing, we would not know how HIV-1 causes CD4+ T-cell decline and AIDS in humans. The observation that virus and cell turnover rates in various SIVs in their natural hosts (such as SIVsm in sooty mangabeys), which do not progress to AIDS, are essentially identical to those in humans, who do progress, implies that cell killing alone cannot account for AIDS pathogenesis. Indeed, this result is consistent with the high natural turnover rate of activated effector memory helper T cells, the primary target for HIV-1 infection, on the order of 10^10 cells per day, of which only a small fraction are infected after the initial primary infection phase.”
We know from the co-discoverer of the HI Virus and Nobel Prize winner Françoise Barré-Sinoussi, that every HIV+ measured person carries his own variants of the HI virus.
• Barré-Sinoussi et al., “Expert consensus statement on the science of HIV in the context of criminal law.”, J Int AIDS Soc. 2018 Jul;21(7):e25161, https://www.ncbi.nlm.nih.gov/pubmed/30044059
“Mutations of the virus occur repeatedly so that every person living with HIV has more than one virus variant [154]. During transmission, a limited number of virus variants (one to a few) are transmitted, but these will also mutate to form new variants so that no two persons’ HIV is identical [155].”
Thus every HIV+ measured persons has his own individual infection. But it is supposed to be always the same molecular mechanism.
There is absolutely no proof, that at least 13 zoonoses occurred in Africa around 1930 from SIV in apes and monkey to HIV in humans, as science claims,
• Hahn et al. “AIDS as a zoonosis: scientific and public health implications.”, Science. 2000 Jan 28; 287(5453):607-14, https://www.ncbi.nlm.nih.gov/pubmed/10649986
“How the AIDS epidemic actually began, what the contributing factors were, and why it appeared in the mid- to late 20th century (and not before) are not known. Whatever the final answers are, they must account for
(i) at least seven separate introductions of SIVcpz and SIVsm viruses into humans;
(ii) the fact that the HIV-1 group M, N, and O viruses are significantly more closely related to SIVcpz viruses from P. t. troglodytes than to the single SIVcpz isolate from P. t. schweinfurthii; and
(iii) the estimation of 1930 (range 1910 to 1950) as the timing of the last common ancestor of the HIV-1 group M viruses.”
• Peeters et al., „Origin and diversity of human retroviruses.”, AIDS Rev. 2014 Jan-Mar;16(1):23-34, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289907/
“More in detailed studies showed that SIVs from chimpanzees and gorillas have crossed the species barrier on at least four occasions leading to HIV-1 group M, N, O and P in humans [6,23]. The different HIV-2 groups are the result from at least nine independant transmissions of SIVs from sooty mangabeys in west Africa [6,23,24].”
That would have been a very bizarre coincidence in Africa around 1930 which 50 years later lead to an epidemic among homosexuals in the USA.
Until today there is no animals model for HIV. Apes don't get AIDS.
I have someone sitting beside me who has full blown AIDS with less than 50 CD4 cells. He tried following a natural path as you suggest and that has taken him to place from which he might have permanent damage. He started meds last week and has already seen significant improvement. I have seen this happen literately hundreds of times. I worry that more people will follow what you say and may occur permanent damage like may have happened to my friend.
https://www.medpagetoday.com/hivaids/hivaids/104326
“ Mysterious White Blood Cell Disorder Not Just 'AIDS Without HIV.”
It’s an interesting article. I wanted to share here. I would very much like to be in contact with you to share my story. I don’t know how to facilitate that. I know Celia for many years. I’ve been involved with the issues you write about here for many years. And I am desperately looking to share my story. If there is a way to reach out and communicate with you I would very much appreciate it.
You have done a masterpiece.
With regards chemical imbalance and MH there is one but it is not serotonin nor dopamine you are correct - researchers looked at the metabolites in the cerebrospinal fluid and found the levels all over the place - it's between glutamate and gamma- Aminobutyric Acid being as GABA is synthesized from glutamate decarboxylase and the active form of B6 pyridoxal 5′-phosphate. Tip - if anyone suffers from anxiety you'll find the active form of B6 helpful, It can also stop akathisia at high dose.
https://pubmed.ncbi.nlm.nih.gov/15554771/
For those who do not know the condition which causes suicide ideation, suicide, violence upto homicide is called Akathisia there are over 100 drugs that can cause it including almost all psych drugs. It's a massive scandal that has been going on for decades. It's going on because the doctors and coroners can hide it under the guise of serious mental illness. There are thousands of people who die from akathisia every year.
Sorry I wasn't clear I'm asking Rebecca for her email address