People surprised by positive HIV-tests sometimes ask for help. At last, Rethinking AIDS has assembled a list — all too short! — of medically qualified practitioners who do not subscribe to HIV/AIDS dogma: Rethinking AIDS Medical Professionals List
Archive for the ‘Alternative AIDS treatments’ Category
Posted by Henry Bauer on 2015/01/09
Posted by Henry Bauer on 2014/05/30
A film by Andi Reiss and Joan Shenton
Positive Hell is the story of five individuals who have defied their doctors and lived on for nearly thirty years with a diagnosis of death. The film highlights a network of people diagnosed HIV Positive in the province of Galicia in Northern Spain.
Some of them, like physician Dr Manuel Garrido, have never taken any antiviral drugs. He’s been swimming against the tide of medical orthodoxy for three decades.
Raquel has had two children who are fit and well and are HIV negative and her husband, Pablo is also HIV negative.
Others like Manoel took antivirals for a while and found they made him feel so ill he stopped taking them. How can this be? Haven’t we been told that everybody who tests positive is sure to die? Dothese people have a special magic gene that protects them against HIV? Or could it be that this death sentence has been mistaken all along?
The five protagonists describe their struggle to survive when faced with a death sentence, their experiences as social pariahs, their battles with doctors and the medical orthodoxy and their absolute conviction that the science behind AIDS is cruelly wrong.
Posted by Henry Bauer on 2014/05/11
When “HIV-positive” gay men who have long been healthy then become sick with an “AIDS-like” illness, perhaps they are experiencing idiopathic CD4-T-cell lymphopenia and not “HIV/AIDS”.
* * * * * * * *
The “AIDS” era had begun as GRID: gay-related immunedeficiency. As John Lauritsen pointed out as early as 1985, that naming stemmed from a bizarre, unique, misleading classification scheme which masked the fact that the prime risk factor for illness was not being gay, the prime risk factor was abusing drugs as part of a blatantly unhealthy lifestyle .
When Africans, Haitians, and drug injectors were seen to have the same illnesses, GRID was re-named AIDS: acquired immune deficiency syndrome of unknown cause, characterized by low CD4 counts. In 1984, the cause of this immune deficiency was prematurely and mistakenly attributed to a retrovirus claimed to have been discovered by Robert Gallo who subsequently reported detecting “HTLV-III” in “18 of 21 patients with pre-AIDS … [and] 26 of 72 adult and juvenile patients with AIDS” , a rate of detection that is anything but convincing proof of cause. The evidence has continued to accumulate that this “HTLV-III”, subsequently re-named “HIV”, was and is not the cause of “AIDS”, which therefore remains an immune deficiency of unknown or unspecified cause.
By 1993 so many cases of “HIV-negative AIDS” had come to official attention that these were attributed to yet another newly minted condition: Idiopathic CD4-T-cell Lymphopenia, ICL or ITCL: immune deficiency of unknown cause associated with low CD4 counts.
But this is precisely the original definition of AIDS before the red herring of “HIV”. Therefore AIDS Rethinkers and HIV Skeptics, given their understanding that “HIV” does not cause “AIDS”, might logically conclude that “AIDS” is indistinguishable from ICL/ITCL.
* * * * * * * *
What really matters, of course, is not names but illnesses and deaths, and the reasons for those have been thoroughly confused and obscured by several official re-definitions of “AIDS” and by corollaries of the mistaken treatment of “HIV-positive” individuals with toxic “antiretroviral drugs” instead of treatment of manifest illnesses and symptoms, typically opportunistic infections.
None of those manifest illnesses were new or unique to “AIDS”. They were brought about in different ways in the four original (early 1980s) risk groups:
(1) In drug abusers, immune deficiency is brought about directly by the drugs, resulting in “AIDS”-like diseases that were noted already in the 1960s .
(2) In Africans, immune deficiency is brought about by malnutrition and periodic infections by a multitude of endemic diseases .
(3) Haitians were soon removed from the list of risk groups to which they had been added prematurely.
(4) In gay men — in only a small proportion of gay men, it is not emphasized often enough — immune deficiency had been brought about by drug abuse as part of a blatantly unhealthy lifestyle [1, 5]. The only “AIDS disease” unique to gay men was identified, also mistakenly, as Kaposi’s sarcoma; it was not actually a sarcoma, it was damage to blood vessels caused by ingestion of volatile nitrites, “poppers” .
In absence of any known ways to strengthen immune systems, early cases of AIDS among gay men were handled by treating, or by prophylactic measures against, the specific opportunistic infections. Following the mistaken attribution of AIDS to HIV, about 150,000 deaths were then brought about by administration of the supposedly “antiretroviral” AZT . After the replacement of monotherapy by less toxic combinations of AZT-like and other types of drugs (cART or HAART), mortality declined, but it seems to have leveled off since about 1998 at roughly 15,000 annually in the USA  (15,529 in 2010 ). How much of that mortality is attributable to the drugs cannot be estimated because too many pertinent data are lacking (mortality as a function of length of time on antiretroviral drugs, type of drugs, specific causes of death).
* * * * * * * *
This factual history is a preamble to further consideration of the conundrum addressed in two recent posts : the puzzle of delayed illness in “HIV-positive” gay men. Commentaries to those postings made me realize that “AIDS” is really ICL/ITCL. When “HIV-positive” gay men who have been healthy for long periods without antiretroviral treatment then become ill and have low CD4 counts, the cause cannot be “HIV” because “HIV” does not cause illness and may not even exist; therefore the cause of “AIDS-like” illness must be idiopathic CD4-T-cell lymphopenia. Hence it is worth considering what mainstream science has to say about that condition, two decades after its discovery. If successful treatments for ICL had been found, perhaps those could also work for cases of delayed illness in “HIV-positive” gay men. Unfortunately, I have not come across reports of successful treatments for ICL. Nevertheless, some aspects of ICL may allow for a different approach to cases of delayed illness in “HIV-positive” gay men, in particular recognition of the wide range of possibly associated manifest illnesses, the good probability of recovery from those illnesses, and the occasional observation that ICL reverses itself — CD4 counts sometimes increase, for as mysterious a reason as that for their initial decline.
There are no reliable data about the population-wide prevalence of ICL, because counting CD4 is not part of routine testing. Therefore almost all cases of ICL have been identified following manifest illness later diagnosed as brought on by CD4-specific immune deficiency. Thus it is not known how many people with “low” CD4 counts never become ill. What is known, though, is that CD4 counts in themselves are not valid markers of good or bad health .
So when “HIV-positive” gay men who have long been healthy then become sick with an “AIDS-like” illness, not only is “HIV-positive” a red herring, so too is CD4 count. No doubt something specific is at the root of the newly experienced illness, but it isn’t “HIV” and it may not have anything to do with the CD4 level, and it may not be the same “something” in all such cases.
Perhaps most striking in the literature on ICL is the lack of regularities — other than that there is no identified cause for the low CD4-count. A recent review of 258 cases from all over the world  found that ICL had been diagnosed at ages ranging from 1 to 85, with a very broad distribution (standard deviation of 19 on a mean of 41). As would be expected from the manner in which cases typically come to light, most had infections “including AIDS-defining illnesses”, but about 1 in 8 were healthy despite low CD4 count. Where illness was present, it ranged over various kinds of mycobacterial and cryptococcal infections as well as candidal and herpes (Varicella zoster); nearly 1 in 5 had a malignancy, and 15% had some sort of autoimmune disease. Only 4 patients had family members who also had low CD4 counts.
Etiology (cause) of ICL remains mysterious, but it has been “hypothesized that abnormally increased microbial translocation through the intestinal wall may be an underlying etiology” — consistent with the intestinal dysbiosis hypothesis in “HIV/AIDS” . Low CD4 counts can also be caused by the manifest infections themselves.
It is encouraging that nearly 4 out of 5 of the described cases survived the manifest illness  (but for how long was not reported). Furthermore, “Transient CD4 lymphocytopenia is common and has been estimated to occur in healthy HIV-negative individuals . . . [at rates of] from 0.4-4.1%” [emphasis added], consistent with the literature that reveals CD4 and health to be independent of one another . According to one report, CD4 counts normalized spontaneously in 7 of 39 ICL patients after an average of 31 months . It is further reassuring though puzzling that “Patients with cryptococcal infection and ICL have . . . favorable prognosis . . . [despite] an increased likelihood of developing dermatomal zoster” .
There is no agreed general way to treat ICL, but some data “support IL-2 as a relatively safe and potentially effective treatment for ICL patients with opportunistic infections, especially when combined with conventional treatment regimens” .
“Adult onset” immunodeficiency  may be akin to ICL in some respects, but it is not associated with low CD4 counts. Instead, the opportunistic infections were associated with the presence of anti-interferon-γ auto-antibodies, and a hereditary or genetic predisposition was suggested. Since autoimmune conditions were also found in about 15% of ICL cases , it would seem reasonable to look into possible autoimmune conditions whenever ICL is diagnosed or suspected — including cases of “HIV-positive” gay men who have long been healthy but then become ill.
Although ICL is said to be rare, this may only be because little population-wide data on CD4 counts are available and ICL is only identified in the presence of manifest illness. It also complicates matters that “ICL lymphopenia” might actually be owing to the manifest illnesses. Similarly, cases of “HIV-positive” gay men who have long been healthy but then become ill may seem to be rare just because they become known only serendipitously through anecdotal reports when the affected individuals choose to bring their situation to wider attention.
Note that many or most of the manifest diseases associated with ICL are or could be classified as “AIDS-defining”. Therefore an “HIV-positive” gay man who has long been healthy and who then “acquires” ICL — cause unknown — would naturally suspect that HIV/AIDS theory might be correct after all, and he might infer that “HIV” had been long latent and was now making him ill, and he would likely then experiment with antiretroviral drugs. Short courses of antiretroviral drugs have indeed been effective in some instances, but an alternative might be to experiment with speculative possible treatments for ICL: IL-2, probiotics, perhaps steroids which can help against autoimmune diseases, for example Hashimoto’s encephalopathy .
In any case, it is worth knowing that nearly 80% of ICL patients recovered from their manifest illness and that in some cases the low CD4 count reversed itself after as much as 3 years.
 John Lauritsen, “CDC’s tables obscure AIDS-drug connection”, reprinted as chapter I in The AIDS War (ASKLEPIOS, 1993)
 Gallo et al.,. “Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS”, Science, 224 (1984) 500-3
 P. 103 f. in Neville Hodgkinson, AIDS: The Failure of Contemporary Science, 1996.
 Robert S. Root-Bernstein, Rethinking AIDS — The Tragic Cost of Premature Consensus, 1993; especially chapter 9
 For descriptions of that “fast-lane’ life-style, see the sources cited in section 126.96.36.199 of The Case against HIV
 John Lauritsen & Hank Wilson, Death Rush: Poppers and AIDS, 1986
 Section 5.1.5 of The Case against HIV
 Figure 3, p. 21 in Deaths Among Persons with AIDS through December 2006, HIV/AIDS Supplemental Report, 14 #3
 Statistics Overview, “Deaths of persons with an AIDS diagnosis”, updated 23 April 2013;
 The Lazarus Effect in HIV/AIDS; The Lazarus Effect and the puzzle of delayed illness in “HIV-positive” gay men
 David Crowe, “Predictability of a CD4 count”, July 2012;
 Dina S. Ahmad, Mohammad Esmadi, and William C. Steinmann, “Idiopathic CD4 Lymphocytopenia: Spectrum of opportunistic infections, malignancies, and autoimmune diseases”, Avicenna Journal of Medicine, 3 (#2, April-June 2013): 37-47
 See sections 188.8.131.52 & 184.108.40.206 of The Case against HIV
 Zonios et al., “Idiopathic CD4 lymphocytopenia: natural history and prognostic factors”, Blood, 112 (2008) 287-94)
 Zonios et al., “Cryptococcosis and idiopathic CD4 lymphocytopenia”, Medicine (Baltimore), 86 (#2, 2007) 78-92
 S. K. Browne et al., “Adult-Onset Immunodeficiency in Thailand and Taiwan”, New England Journal of Medicine, 367 (2012) 725-34
 When doctors can’t tell you what’s wrong (updated); Encephalitis and Hashimoto’s Encephalitis
Posted in Alternative AIDS treatments, antiretroviral drugs, HIV does not cause AIDS, HIV risk groups, HIV skepticism | Tagged: AIDS as Idiopathic CD4-T-cell Lymphopenia, delayed illness in “HIV-positive” gay men | 3 Comments »
Posted by Henry Bauer on 2014/05/06
Recent comments from CJ and some digging into the past (Reminiscing; not much new under the sun; why gay men and Africans are the predominant victims) brought to the forefront of my mind what has been lurking in the background for quite a long time, the puzzle that is of literally vital importance to some unknown number of gay men: those who are aware of the lack of proof that HIV causes AIDS, who are both “HIV-positive” and healthy for a long time, but who then suffer illness which, for one reason or another, is ascribed or ascribable to “HIV”.
The evidence that HIV does not cause immunedeficiency and AIDS is powerfully strong in a number of ways (The Case against HIV). What first convinced me personally was the accumulated data on “HIV-positive” tests: what those tests detected is neither infectious nor correlated with AIDS (The Origin, Persistence and Failings of HIV/AIDS Theory).
But that is overall. Could some small proportion of all the cases nevertheless conform to the mainstream view? Is it possible that HIV is after all what the mainstream says it is, but is responsible for only a small proportion of AIDS cases?
That seems awfully unlikely. Similar arguments apply as against the possibility that data from “HIV-positive” tests might be invalidated by contamination of samples or false positives (p. 39 ff. in The Origin, Persistence and Failings of HIV/AIDS Theory): the data show extraordinary regularities with respect to sex, age, and race, at all levels of average “HIV-positive” prevalence. There seems no room for a “real HIV” to be lurking in the mass of mistaken “HIV”: if there were, then one or more of those correlations should break down at low prevalence.
Further: Everything the mainstream says about HIV has turned out to be wrong: that it targets T-cells and somehow destroys them indirectly by some occult mechanism, that it’s sexually transmitted, that it hides somewhere during a latent period of a decade or so.
So it seems impossible that the mainstream view could be valid in a tiny proportion of all instances when it is definitely wrong in almost all cases.
If Duesberg is right and HIV is a “passenger” virus, could it be almost always harmless as Duesberg claims and yet harmful to some people some of the time?
If de Harven is right and “HIV” tests pick up circulating DNA and things from endogenous retroviruses (HERVs), could one of those HERVs occasionally become functional, active, harmful?
Such speculations seem unlikely to be true. What an astounding coincidence it would be that everything the mainstream claims has been shown to be unfounded or ill-founded in innumerable instances and yet could be correct in a tiny proportion of instances, so tiny that all the observed correlations are not significantly affected.
I can’t see it.
Doesn’t the lifesaving cART or HAART demonstrate that the mainstream is basically correct?
Not at all. Antiretroviral drugs are not life-saving (Section 7.1.3 in The Case against HIV), indeed the drugs are incredibly toxic. That mortality rates declined almost immediately when HAART was introduced showed not that HAART is good but that it is not as highly toxic as what it replaced (Section 5.1.6 in The Case against HIV).
Moreover, what HAART replaced continues in use, albeit in lower doses, within HAART. Components of that — AZT and its cognate NRTIs and probably NNRTIs and the other kinds of antiretroviral drugs — destroy bone marrow and mitochondria (among other nasty effects) to produce long-term, cumulative, damage, albeit perhaps so gradually that consumers might live for quite a long time, though uncomfortably and in increasingly fragile health.
The Lazarus Effect is hyped by mainstream propagandists as proof that antiretroviral drugs work and transform illness into health: there have been a number of anecdotal accounts over the years of people seriously ill with “AIDS” rising vigorously from their sick-beds within a day or two of starting antiretroviral drugs.
But the Lazarus Effect actually speaks against HIV/AIDS theory, not for it.
HIV is not claimed to cause any direct harm (Section 1.3 in The Case against HIV), only indirectly by supposedly destroying the immune system and allowing opportunistic infections to get a foothold. Antiretroviral drugs are designed to prevent replication of HIV, and there is no reason to expect that such an effect could bring rapid recovery from an illness. Rather, the “antiretroviral” is evidently acting against whatever opportunistic infection or inflammation a somehow weakened immune system allowed. Antiretroviral drugs are known to be magnificently toxic to living cells, and the Lazarus Effect actually demonstrates the antibiotic action of “antiretroviral” drugs. As Drs. Koehnlein and Sacher have pointed out, this gives grounds for prescribing antiretroviral drugs for short periods when it has not been possible to identify the specific cause of an illness. In no way does the Lazarus Effect support HIV/AIDS theory or the use of antiretroviral treatment over extended periods of time (let alone for so-called pre-exposure prevention, PrEP — see Poisonous “prophylaxis”: PrEP [Pre-Exposure Prevention]).
Mainstream shibboleths in relatively recent times have come to include the presumption that “HIV” can somehow cause damage directly to organs including the brain: publications refer to “HIV-associated” dementia, lipodystrophy, arthritis, and more. But those ailments have been “HIV-associated” only since the advent of antiretroviral treatment, and they are actually caused by the antiretroviral drugs (Section 4.3.4 in The Case against HIV); those drugs have legions of toxic effects and are anything but “life-saving” (Section 5 in The Case against HIV).
Another possible explanation for the Lazarus Effect is hormesis: Substances and types of radiation that are harmful at larger doses may actually be beneficial at low doses — the dose-response curve is U- or J-shaped. Thus an initial or short-term “antiretroviral” treatment might appear as life-saving. A common explanation for hormesis is that the poisonous stimulus brings the immune system into action to a degree that more than outweighs the poisonous effect.
The phenomenon of hormesis has been controversial, but it is being increasingly recognized as genuine. A useful review is “Defining hormesis” by Calabrese and Baldwin (Human & Experimental Toxicology, 21  91-7 ). A specialist society is dedicated to the study of hormesis: the International Dose-Rresponse Society which has published a journal for more than a decade.
A personal speculation: some of the adjuvants used in vaccines might work because of hormesis since such adjuvants as squalene and aluminum salts have been reported as harmful at large doses.
* * * * * * * *
How then to comprehend cases of gay men who have been both “HIV-positive” and healthy for a long time and who then suffer illness which, for one reason or another, is ascribed or ascribable to “HIV”?
Taking the dissident stance that “HIV” is not the cause of immunedeficiency, one recalls that there are innumerable possible cause for immunedeficiency (described comprehensively by Root-Bernstein in Rethinking AIDS—The Tragic Cost of Premature Consensus, Free Press, 1993).
Furthermore, it is not only “HIV-positive” gay men who experience illness that their doctors cannot diagnose specifically (When doctors can’t tell you what’s wrong). It is not impossible, after all, that when gay “HIV-positive” men become ill, that the illness has nothing to do with being gay or with being “HIV-positive”. As we go through life, all of us — women and men, heterosexual and bisexual and homosexual — sooner or later lose health and die.
Still, there is at least one reason why “HIV-positive” gay men may be especially prone to illness: the Nocebo Effect.
It has become generally understood that the Placebo Effect is very real, albeit its mechanism is not understood: Belief that one is being cured can in itself effect a cure *.
It is less widely understood that the same not-understood mechanism can have the opposite, nocebo, effect: Belief that one is going to become ill or to die can in itself bring about illness or death. Not widely enough understood, especially by doctors, is that what a doctor says to a patient can be very damaging when the doctor is simply trying to be straightforward and truthful about conveying bad news **.
This is clearly of great relevance with “HIV/AIDS”, as discussed in The AIDS Cult by John Lauritsen & Ian Young (ASKLEPIOS, 1997), and is clearly pertinent to the puzzle of “HIV-positive” gay men who consider themselves HIV/AIDS dissidents and have been healthy for a long time but then become ill with symptoms associated with AIDS.
It cannot be easy to thoroughly believe the dissident view if one is not a doctor or scientist widely read in the copious technical literature. Most gay men surely find themselves in the dilemma of having to choose who to believe, mainstream doctors and scientists or dissident doctors and scientists. It cannot be easy, when one’s own health and life are at stake, to make such a choice, to believe one group or the other without fully understanding the technical issues, having to take opinions on faith by trusting the expertise and honesty of people who are not known on a personal level.
Surely most gay dissidents have at least occasional doubts, perhaps only subconscious, that perhaps the mainstream could be right after all. That sort of doubting, worrying, would be prime ground for generating stress and a nocebo effect.
* * * * * * * *
This is an attempt to clarify the dreadful dilemma faced by some number of gay men.
In recent correspondence made available for wider distribution, one man in this situation wrote that antiretroviral drugs were effectively treating his cytomegalovirus and toxoplasmosis, at the cost of such “side” effects as : nausea, pain / headache (to the point of continual moaning and pacing), itchy groin/feet (scratched until I bled), insomnia, fatigue, bags under my eyes, bloated, swollen ankles, calves and thighs, diarrhoea, tingling hands, feeling cold”.
The fundamental unresolved problem is how to strengthen a weakened immune system, and medical science seems to offer no help in that direction: “I’ll wean myself off the medications over the coming year, but getting my immune system (specifically my cell-mediated immunity) operating well has been problematic. Let’s see if I succeed the third time around!”.
Dr. Christian Fiala commented that antiretroviral drugs are certainly effective against bacteria, more so than regular antibiotics, and also against viruses, “However you have to be careful that they kill the virus before they kill the patient”. Dr. Claus Köhnlein emphasized that antiretroviral drugs can be useful in extreme cases, but “HIV theory is still the reason for a massive overtreatment because most patients are being treated prophylactically”.
Clarification is needed, I believe; but what’s really needed is help in finding ways to strengthen immunity and to diagnose the actual underlying cause of the weakened immunity in each of these individual cases. That’s where research is needed most desperately.
* Howard Brody with Daralyn Brody, The Placebo Response: How You Can Release the Body’s Inner Pharmacy for Better Health (Harper Perennial, 2001); Arthur K. Shapiro and Elaine Shapiro, The Powerful Placebo: From Ancient Priest to Modern Physician (Johns Hopkins University Press, 2000); Anne Harrington (ed.), The Placebo Effect: An Interdisciplinary Exploration (Harvard University Press, 1997).
** For a review of studies, see Nocebo phenomena in medicine: Their relevance in everyday clinical practice by Winfried Häuser, Ernil Hansen, & Paul Enck, Deutsches Ärzteblatt International, 109 (2012) 459-65 (in English). The Skeptic’s Dictionary gives a useful summary (nocebo and nocebo effect). A few anecdotes are cogently recounted on YouTube by Helen Pilcher (The nocebo effect — Helen Pilcher — nothing event).
Posted in Alternative AIDS treatments, antiretroviral drugs, HIV as stress, HIV does not cause AIDS, HIV risk groups, HIV skepticism, HIV/AIDS numbers | Tagged: delayed illness in “HIV-positive” gay men, hormesis, Lazarus effect | 24 Comments »
Posted by Henry Bauer on 2014/04/08
The Centers for Disease Control & Prevention has ballyhoo-ed “PrEP: A New Tool for HIV Prevention” because Truvada has been approved by the Food and Drug Administration for preventing HIV infection. Truvada — tenofovir (TDF) plus emtricitabine (FTC) — had been earlier approved (in 2004) for treating HIV infection.
The 4-page CDC Fact Sheet contains no adequate warning of toxicity; the closest is this recommendation: “Disclose to women that safety for infants exposed during pregnancy is not fully assessed but no harm has been reported”.
Media coverage included “Gay men divided over use of HIV prevention drug”; but the reported division was not over the feeding of toxic drugs to healthy people but over whether such prophylaxis might induce people not to use condoms. The story said nothing about the toxicity of Truvada.
But the official Treatment Guidelines, freely available from the National Institutes of Health, have much to say about toxicity:
Adverse Effects of Antiretroviral Agents (Last updated February 12, 2013; last reviewed
February 12, 2013)
Adverse effects have been reported with use of all antiretroviral (ARV) drugs; they are among the most common reasons for switching or discontinuing therapy and for medication nonadherence. . . . However, because most clinical trials have a relatively short follow-up duration, the longer term complications of ART can be underestimated. In the Swiss Cohort study, during 6 years of follow-up, the presence of laboratory adverse events was associated with higher rates of mortality, which highlights the importance of adverse events in overall patient management (page K-7). [In clearer language: these are deadly drugs that can and do kill]
TDF may cause kidney injury in some patients, particularly in those who have pre-existing renal disease or are receiving concomitant nephrotoxic drugs. In addition, TDF induces a greater decline in bone mineral density than other ARV drugs (page F-2).
Renal impairment, manifested by increases in serum creatinine, proteinuria, glycosuria, hypophosphatemia, proximal renal tubulopathy, and acute tubular necrosis, has been associated with TDF use. . . .
participants receiving TDF/FTC experienced a significantly greater decline in bone mineral density than ABC/3TC-treated participants page (F-14).
TDF/FTC — Potential for renal impairment, including proximal tubulopathy and acute or chronic renal insufficiency (Table 6)
[TDF and FTC are both NRTIs (nucleoside reverse transcriptase inhibitors)]
Table 13. Antiretroviral Therapy-Associated Common and/or Severe Adverse Effects
Hepatic effects — reported for most NRTIs
Lactic acidosis —NRTIs
Nephrotoxicity/urolithiasis — TDF: ↑ serum creatinine, proteinuria, hypophosphatemia, urinary phosphate wasting, glycosuria, hypokalemia, non-anion gap metabolic acidosis
Osteopenia/osteoporosis — TDF: Associated with greater loss of BMD than with ZDV, d4T, and ABC.
Even Truvada’s own website acknowledges the serious risks of taking this drug:
“IMPORTANT SAFETY INFORMATION
What is the most important information I should know about TRUVADA?
TRUVADA can cause serious side effects:
Too much lactic acid in your blood (lactic acidosis), which is a serious medical emergency. Symptoms of lactic acidosis include weakness or being more tired than usual, unusual muscle pain, being short of breath or fast breathing, nausea, vomiting, stomach-area pain, cold or blue hands and feet, feeling dizzy or lightheaded, and/or fast or abnormal heartbeats.
Serious liver problems. Your liver may become large and tender, and you may develop fat in your liver. Symptoms of liver problems include your skin or the white part of your eyes turns yellow, dark “tea-colored” urine, light-colored stools, loss of appetite for several days or longer, nausea, and/or stomach-area pain.
You may be more likely to get lactic acidosis or serious liver problems if you are female, very overweight (obese), or have been taking TRUVADA for a long time [emphasis added. PrEP implies extended use, but the CDC Fact Sheet says nothing about long-term use increasing the risk of iatrogenic harm]. In some cases, these serious conditions have led to death. Call your healthcare provider right away if you have any symptoms of these conditions.
Worsening of hepatitis B (HBV) infection. If you also have HBV and take TRUVADA, your hepatitis may become worse if you stop taking TRUVADA. Do not stop taking TRUVADA without first talking to your healthcare provider. If your healthcare provider tells you to stop taking TRUVADA, they will need to watch you closely for several months to monitor your health. TRUVADA is not approved for the treatment of HBV.”
“Serious side effects of TRUVADA may also include:
New or worsening kidney problems, including kidney failure. Your healthcare provider may do blood tests to check your kidneys before and during treatment with TRUVADA. If you develop kidney problems, your healthcare provider may tell you to take TRUVADA less often, or to stop taking TRUVADA. [But the CDC Fact Sheet warns that failure to take Truvada consistently may vitiate its PrEP benefit]
Bone problems, including bone pain or bones getting soft or thin, which may lead to fractures. Your healthcare provider may do tests to check your bones.
Changes in body fat can happen in people taking HIV-1 medicines.
Changes in your immune system. If you have HIV-1 infection and start taking HIV-1 medicines, your immune system may get stronger and begin to fight infections. This may cause minor symptoms such as fever, but can also lead to serious problems. Tell your healthcare provider if you have any new symptoms after you start taking TRUVADA.
The most common side effects of TRUVADA are:
In people taking TRUVADA with other HIV-1 medicines to treat HIV-1 infection, common side effects include: diarrhea, nausea, tiredness, headache, dizziness, depression, problems sleeping, abnormal dreams, and rash.
In people taking TRUVADA to reduce the risk of getting HIV-1 infection, common side effects include: headache, stomach-area (abdomen) pain, and decreased weight.
Tell your healthcare provider if you have any side effects that bother you or don’t go away”.
And of course there is the usual
“You are encouraged to report negative side effects of prescription drugs to the FDA. Visit http://www.FDA.gov/medwatch, or call 1-800-FDA-1088”.
The ultimate purpose of this statement is to safeguard a drug’s manufacturer against lawsuits stemming from the drug’s toxicity, by pretending concern for patients.
A drug with known serious toxic effects,
which become more serious over time,
is being recommended for continuous use
and unlimited use in healthy people.
This would be bad enough
if HIV were actually an infectious agent causing serious illness,
which however it isn’t (see The Case against HIV)
Posted in Alternative AIDS treatments, clinical trials, experts, HIV absurdities, HIV risk groups, Legal aspects, sexual transmission, uncritical media | Tagged: Pre-Exposure Prevention of HIV infection (PrEP), PrEP risks, tenofovir toxicity, toxic antiretroviral drugs for prophylaxis, Truvada toxicity | 19 Comments »