A quiet bit of earth shattering news earlier this mornth shed new light on what NotAIDS! has been suggesting for years. Scientists have known for years intestinal parasite infections cause immune dysfunction.

The AIDS religious have spent the last 30 years telling the world that HIV is a disaster in and of itself, that singlehandedly, these tiny virii that we can't even truly isolate, mark an otherwise healthy person for death.

Those of us who the other side like to call "denialists" because we deny HIV that power over our lives, are mocked, ridiculed, and even accused of criminal negligenceand told we "better shut up" if we value our freedom.

Now, all these years and meds later, AIDS Healthcare Foundation, perhaps one of the most vociferous proponents of AIDS meds begins research into... yogurt and probiotoics to shore up the immune system and fight AIDS.

Here's what their release said.

"HIV infection is often marked by a state of chronic inflammatory response triggered by the leakage of Gram-negative bacteria from the intestines into the bloodstream."

This leakage is described in almost all parasite diagnoses, especially Candida infections - which also is from where the P24 antigenic protein signature derives that the AIDS people point at in their "GOTCHA!" moment to say "You got HIV / AIDS!!"

The release continues.

"This state of chronic inflammation is believed to leave CD4 cells more prone to infection and destruction by HIV."

Doesn't it seem like someone's trying to backtrack? They're conceding it's parasitic and intestinal bug-related, but because HIV finishes the job so you're still gonna get licked by HIV

But now the argument changes a bit due to economics. The article begins with a very important premise.

"Current drug regimens have allowed people with HIV infection to live longer; these drugs, however, can cost thousands of dollars per month and there is still no cure. Unfortunately, government programs to provide life-sustaining drugs to those who cannot afford them have been crippled by the weak economy, and tens of thousands of people are currently without access. The AHF is able to help some patients, but the size of the economic shortfall dwarfs citizens' current need.

"The AHF trial is believed to be the first-of-its-kind in the United States; while small clinical trials conducted in Africa have shown that probiotic yogurts can dramatically increase CD4 cell count in people (test subjects) with HIV infection.

"Researchers at the AHF hypothesize that probiotic consumption may reduce leakage of Gram-negative bacteria from the intestine, thereby reducing the resulting inflammatory response and destruction of CD4 cells."

The quotes are from the item in Medical News Today August 11, 2010.

Over fifty years ago, Rock Hudson, born Roy Scherer Jr. in 1925, was nominated for best Performance by an Actor in a Leading Role by the Academy of Motion Picutres, for his portrayal of Jordan 'Bick' Benedict Jr. in the epic film, Giant. George Stevens won the Oscar that year for Best Director.

In the United States, HIV/AIDS became a fashionable Hollywood cause celebre shortly before actor Rock Hudson died in 1985. The unfolding drama was thrust into the bright lights of the public eye when Mr. Hudson succumbed to a series of health complications widely reported as AIDS.

However, a review of available biographical data, and a privately-held, unpublished source, seem to indicate that his death was caused by other factors.

Rock Hudson had quadruple bypass heart surgery made necessary by a diet rich in animal fat, years of alcohol abuse, and a chain-smoking habit that continued even after the bypass surgery. His body's rejection of a blood transfusion given during the bypass, and an experimental AIDS drug called HPA23 given to him by physicians in Paris further eroded his precarious condition.

Despite having put AIDS on the list of Hollywood "cause celebs" and making an indelible mark on the world consciousness of HIV, Mr. Hudson actually tested negative for HIV one year before his death in 1985.

It is ironic that an experimental HIV/AIDS drug was partly responsible for his untimely death when the actor's immune deficiency was not caused by HIV.

Because AIDS is a syndrome, and there has been no irrefutable evidence that HIV causes AIDS, the answer to what causes immune deficiency is revealed in examples such as Rock Hudson's.

One of the irrefutable causes of immune deficiency is actually immune overactivation, which in Mr. Scherer's case, it was his body's rejection of foreign blood he received during a transfusion, added to the already compromised immune system due to alcoholism, a four-pack a day smoking habit, and a quadruple bypass open heart surgery.

Rock Hudson was a major motion picture star during the '60s, and in the '70s he became well-known on the small screen as the star of the television serial, "MacMillan and Wife." During the AIDS hysteria of the '80s, his cameo appearances on Dynasty that featured his character kissing a female costar made headlines.

Rock Hudson's role in Giant was a powerful example of his acting ability, and it was a craft he took very seriously. Perhaps the greatest disappointment towards the end of his life were the mediocre parts he landed both on the silver screen and television. His sexuality and the decline in health overshadowed nearly a half-century of acting.

Now that more than twenty years has passed, there is greater appreciation of his talent, preserved for the ages on film.

February 24, 2010

Just a reminder of how important it is to ask doctors plenty of questions. The US government says in a 'fact sheet' on HIV meds that

Twenty-one anti-HIV medications have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of HIV. These medications must be given in combination, and all of the drugs may cause negative side effects. Such side effects range from mild to life-threatening.

• Hepatotoxicity
• Hyperglycemia
• Hyperlipidemia
• Lactic Acidosis
• Lipodystrophy
• Osteonecrosis, Osteoporosis, Osteopenia
• Skin Rash

The fact sheet appears to be the latest.

In other news, the FDA has issued new warnings about Invirase and Norvir, drugs made by Roche and Abbot, potentially wreaking havoc on heart rythms whentaken together.

Another memo from the FDA on Invirase seems to indicate damage to the heart from Invirase under any circumstance.

And in point of fact, the dermatologists, when they looked back and began to see that there were a fair number of patients in their gay practices who had Kaposi's sarcoma but who ended up not having HIV. - Dr. John Ziegler

Remember PCP and KS, the scourge of gay men in cities across America? They were the face of AIDS. They WERE AIDS - later named HIV, said to be the underlying cause of AIDS.

What if they weren't AIDS? Would that beg the question, "What is AIDS anyway?"

Is it clear that what was referred to as PCP - an acronym for pneumocystis carinii pneumonia even related to AIDS? Kaposi's sarcoma, another early AIDS-defining illness, is now known to be NOT AIDS.

PCP, a fungal infection of the lungs, started as a small cluster of contagious infections under the tutelage of Los Angeles-based Dr. Gottlieb, who was in close touch with the Feds at CDC.

It eventually morphed first into GRID (gay-related immune deficiency) and then into "AIDS" in this concerted effort to see it not as any other cluster but as a homosexual cluster of immune dysfunction, as if therein lived the aetiology of the great and powerful mystery of gay men who fell ill.

No matter that almost every parasite harmful to humans causes immune dysfunction, and they are usually contagious.

As titillating as gay sex may be, and as feasible may it be that PCP or KS was a proximity-related fraternally infectious bubble, it still has never been proven that PCP, or KS, for another matter, was related to someone's testing positive for HIV.

The tests of course came later, after the initial PCP/ KS clusters had run their course when Gallo monetized the whole mess with the erstwhile "HIV test" marketed for gay men. Erstwhile, because if you've read the labels of any such test, they don't actually test for HIV.

History speaks volumes and it is instructional in this excerpt from interviews conducted in 1993 and 1994 by Sally Smith Hughes, Ph.D with Dr. John Ziegler.¹

Hughes:
In the early days, when it was pretty much you alone seeing AIDS patients at the VA, how did you deal with opportunistic infections? You presumably are not an expert on infectious disease. How did you handle patients with problems that really weren't in your territory?

Ziegler:
Well, they were partly in my territory, insofar as a chemotherapist renders people immunodepressed with cytotoxins. So as a profession, we have to deal with opportunistic infections. In fact, a lot of the early cases of Pneumocystis pneumonia were seen in leukemia patients who were treated with prednisone. So I was pretty familiar with the opportunistic infections, and we just treated them as part of our daily oncologic experience.

Hughes:
I read of an NCI [National Cancer Institute] program called SEER [Surveillance, Epidemiology and End Results] which found that the incidence of KS prior to 1980 in various participating cities, San Francisco being one of them, was several times higher than in cities such as Atlanta and Denver where AIDS is relatively rare.

What does that mean?

Ziegler:
There's a long story around KS and its epidemiology. But the short version is that most people think that KS is caused by an infectious agent, not HIV, but an agent that is passed along with it, and that these were really two independent epidemics, both following pretty much the pattern of advanced promiscuity in the homosexual community in the seventies.

And in point of fact, the dermatologists, when they looked back and began to see that there were a fair number of patients in their gay practices who had Kaposi's sarcoma but who ended up not having HIV.

---

1. Excerpted from "The AIDS Epidemic in San Francisco: The Medical Response 1981-1984, Volume IV - An oral history conducted in 1993 and 1994" at the Regional Oral History Office, The Bancroft Library, University of California, Berkeley, 1997.

]]> http://notaids.com/de/maggiore 2009-11-05T20:42:35-06:00 2009-11-05T22:03:47-06:00 The Editor

NotAIDS! News
December 30, 2008, Updated November 5, 2009

by The Editor

The death of alternative AIDS activist Christine Maggiore came as a shock to me, not only because for 17 years she'd offered herself as living proof that a so-called "HIV-positive" diagnosis was not necessarily fatal but, more importantly, because she'd been a close personal friend for 15 years. Her death does not change any of the scientific facts that make the idea that HIV is the sole cause of AIDS not only wrong, but ridiculous; though supporters of the mainstream view of AIDS are exploiting it for propaganda, what it really underscores is the need for more basic research to document whether "HIV-positive" people who take the highly toxic AIDS medications actually live longer, healthier lives than those who don't. - Mark Gabrish, Conlan/Zenger's Newsmagazine^*

When the rabid AIDS promoters hit the media channels and the Internet gloating over the death of leading HIV "rethinker" Christine Maggiore, it will be in the sadistic manner of which only AIDS-lovers are capable, and they will twist the truth into a scary fable meant to coax you into taking your meds.

Yet, it would be prudent to resist any temptation to believe their false assumption that Christine Maggiore succumbed to an "AIDS-related" illness, specifically, HIV-related pneumonia. If she tested negative, after testing positive, and her son tests negative, how does her death from bacterial pneumonia prove she died from HIV infection? Even if she was HIV positive, on what basis is her death attributed to HIV?

In an international study of bacterial pneumonia outcomes, conducted in part by the University of Alberta, researchers concluded that pneumonia doesn't appear to harm HIV-positive patients any more than those who are HIV-negative.

There was also negligible difference in the mortality rate; total deaths among the HIV patients was 3.5 per cent (two of 58 patients), and 4.8 per cent (seven of 174) among the HIV-negative patients.

Mourners and revelers alike, consider the following, as noted on Medicine.net.

Currently, over 3 million people develop pneumonia each year in the United States. Over a half a million of these people are admitted to a hospital for treatment. Although most of these people recover, approximately 5% will die from pneumonia. Pneumonia is the sixth leading cause of death in the United States.

The latest numbers from the CDC put pneumonia as the 8th leading cause of death in the United States as of the last officially available government numbers from 2005.

]]>

NotAIDS! News
December 30, 2008, Updated November 5, 2009

by The Editor

The death of alternative AIDS activist Christine Maggiore came as a shock to me, not only because for 17 years she'd offered herself as living proof that a so-called "HIV-positive" diagnosis was not necessarily fatal but, more importantly, because she'd been a close personal friend for 15 years. Her death does not change any of the scientific facts that make the idea that HIV is the sole cause of AIDS not only wrong, but ridiculous; though supporters of the mainstream view of AIDS are exploiting it for propaganda, what it really underscores is the need for more basic research to document whether "HIV-positive" people who take the highly toxic AIDS medications actually live longer, healthier lives than those who don't. - Mark Gabrish, Conlan/Zenger's Newsmagazine^*

When the rabid AIDS promoters hit the media channels and the Internet gloating over the death of leading HIV "rethinker" Christine Maggiore, it will be in the sadistic manner of which only AIDS-lovers are capable, and they will twist the truth into a scary fable meant to coax you into taking your meds.

Yet, it would be prudent to resist any temptation to believe their false assumption that Christine Maggiore succumbed to an "AIDS-related" illness, specifically, HIV-related pneumonia. If she tested negative, after testing positive, and her son tests negative, how does her death from bacterial pneumonia prove she died from HIV infection? Even if she was HIV positive, on what basis is her death attributed to HIV?

In an international study of bacterial pneumonia outcomes, conducted in part by the University of Alberta, researchers concluded that pneumonia doesn't appear to harm HIV-positive patients any more than those who are HIV-negative.

There was also negligible difference in the mortality rate; total deaths among the HIV patients was 3.5 per cent (two of 58 patients), and 4.8 per cent (seven of 174) among the HIV-negative patients.

Mourners and revelers alike, consider the following, as noted on Medicine.net.

Currently, over 3 million people develop pneumonia each year in the United States. Over a half a million of these people are admitted to a hospital for treatment. Although most of these people recover, approximately 5% will die from pneumonia. Pneumonia is the sixth leading cause of death in the United States.

The latest numbers from the CDC put pneumonia as the 8th leading cause of death in the United States as of the last officially available government numbers from 2005.

It is disrespect of the lowest form; not giving time to honor a departed soul. Christine Maggiore was a tireless fighter, for what she believed in wholeheartedly. To hear the evil cackling on some blogs, such as Aetiology, is to hear the desperate rantings of those trying to convince themselves of their stories in the midst of so many questions of their position.

One blogger mocked Maggiore's death from pneumonia as an event extraordinarily rare and remotest of possibility, that a person unaffected by AIDS, HIV positive or not would endure.

It's not very difficult to consult the CDC website to find the top 15 causes of death in the USA, and to find pneumonia at numbers 6 and 8 for the two most recent national population studies.

It is curious that herpes is thrown in there as a cause of death. I don't find any evidence that herpes zoster or disseminated herpes causes death, in HIV seronegative or positive.²

• About 50 to 80 percent of American adults have oral herpes, which is commonly called cold sores or fever blisters.

• About one in five adults in the United States has genital herpes. However, most people don’t know they are infected because their symptoms are too mild to notice or mistaken for another condition.
• Herpes is most easily spread from genital-to-genital or oral-to-genital contact during an active outbreak or during prodrome -- the few days just before an outbreak.
• Oral and genital herpes can be uncomfortable, but they are generally not dangerous infections in healthy adults.
• Herpes does not affect the immune system. It is rare for adults to have any health problems from genital herpes.

The AIDS people often spout wild, baseless accusations of how many deaths AIDS-dissenters directly cause from their "dangerous" thoughts and words, based upon UN numbers that are faulty to begin with and bear no relation to reality. They speak as if Duesberg, or Culshaw, is running public health policy on a continent thousands of miles away.

Defending against this libelous accusations gives these bloggers unwarranted credit. Remember these are the same people who vilify those who advocate good nutrition, food and sanitation technology transfer, and parasite remediation, as "quacks".

One week they condemned the then South African public health minister and demanded her exit because she advised people to eat garlic and some local pomme de terre. The next week there was a prominent feature in an academic health journal discussing a study's newest findings about the far-reaching circulatory and immune function health benefits of garlic.

To say that the bloggers to whom I refer have a credibility problem is an understatement.

To respect their arguments and character is impossible, although this writer would never consider saying they should be silenced through any means. Unfortunately, many AIDS-lovers advocate this mafia-style threat to anyone who disagrees with them or dares to suggest that HIV is not the single cause of AIDS.

It is shameful how certain AIDS promoters used Christine's Maggiore's tragic and untimely death to advance their inference-based research. All the DNA markers in the world still don't elevate unsubstantiated mumbo-jumbo to a level of the proven science throughout history that has given us real medicine, and real cures.

The fascist style censorship evident on certain blogs is a disgrace to science, and the kind of morbid rejoicing from some corners creates a karma problem.

One nimrod even suggested putting Duesberg in prison for espousing his scientific opinion. Ah, Duesberg. I disagree with some of Duesberg's theories, to which he clings maddeningly and stubbornly. But Duesberg is an important scientific explorer and much of the field of biological science owes him a great debt, and a measure of respect. I'm quite certain that the sad excuse for a citizen who suggested that he be decommissioned is many things, but not a scientific explorer.

Of all the disciplines, the science people have and should continue to encourage dissent in the journey to uncover knowledge.

Voltaire, the French philosopher said in a letter to a contemporary, "I detest what you write, but I would give my life to make it possible for you to continue to write."¹ Those at the various HIV and AIDS promoting blogs should study this quote and put it to memory.

---

* "My Friend, Christine Maggiore"
by Mark Gabrish Conlan/Zenger's Newsmagazine ( mgconlan [at] earthlink.net ) Friday Jan 30th, 2009

1. Book of French Quotations (1963), Norbert Guterman suggesting that the probable source for the quotation was a line in a 6 February 1770 letter to M. le Riche. Thanks to http://swampbubbles.com, accessed 01/05/2009.

2. American Social Health Association http://www.ashastd.org/herpes/herpes_learn.cfm

]]> http://notaids.com/de/hon 2009-11-04T11:02:51-06:00 2009-11-04T14:36:15-06:00 The Editor

]]> http://notaids.com/de/tickbite 2009-08-08T15:53:33-05:00 2009-09-01T12:43:04-05:00 The Editor

It was over a year of symptoms increasing in severity, and more disabling with time, that culminated in profoundly depleted platelets. Platelets are the elements in blood that clot to prevent bleeding uncontrollably, either in the body or on the skin when cut.

My neck was stiff, and felt like muscles were twisted around a nerve, shooting electrial pulses of pain out to my shoulder. My lower back felt as if the cartilage was disintegrating and the lowest disks would grind and snap. It was difficult to stand up straight or walk if I dared to bend my back at all to pick something up off the floor.

My knee became arthritic, as did my left thumb joint which made gripping anything impossible.

But it was the second blood test that showed my platelets were dangerously low, and increasing difficulty walking that led me to take control of my own care, and figure out what was wrong with me. My ankles became swollen and painful, my and shins, (tibia) felt like someone had taken a sledgehammer to them. They were covered with red, hot patches that were strangely reminiscent of the migrating rash I had after the curious black blister over a year earlier.

Iin the absence of any medical staff I diagnosed myself finally, after 10 months of multiplying symptoms. I found a picture online of a blood engorged tick- it looked identical to the black blister I had taken a heat gun to last August because of the intense (there is no word adequate to describe it) itch that was deep below that blister. I had then washed the blister off with my hand and soap down the shower drain.

After the allergic reaction thatlasted 3 weeks with intense itching and microblistering, and oozing, the site of the blister finally healed and suddenly within days, a hot red blotchy patch with clearly demarcated, boundaries appeared under my arm ( I can't remember now if it was the left or right), and then disappeared quickly, and within hours, it reappeared on my neck. It felt like I had been branded with a hot iron. I believe this was the "migrating rash" that is described on many lyme disease web sites.

When my symptoms climaxed after months of feeling like I had morphed into an arthritic and crustry old man (I'm a young 39 who has never had any symptoms of back pain or any joint pain) I had to go to an emergency room armed with research, the photo of the engorged tick I found online, and specifically ask for a Doxycyclene prescription.

Most Doctors didn't believe i had been bitten by a tick or thougt I was being delusional and 3 docotrs at the local gay clinic told me it was HIV related, and even told me the low platelets were an HIV condition and if I only went on meds it would resolve. This is ludicrous as I told these doctors about my experience with a black blister that I think may have been a tick feasting on my stomach.

]]>

It was over a year of symptoms increasing in severity, and more disabling with time, that culminated in profoundly depleted platelets. Platelets are the elements in blood that clot to prevent bleeding uncontrollably, either in the body or on the skin when cut.

My neck was stiff, and felt like muscles were twisted around a nerve, shooting electrial pulses of pain out to my shoulder. My lower back felt as if the cartilage was disintegrating and the lowest disks would grind and snap. It was difficult to stand up straight or walk if I dared to bend my back at all to pick something up off the floor.

My knee became arthritic, as did my left thumb joint which made gripping anything impossible.

But it was the second blood test that showed my platelets were dangerously low, and increasing difficulty walking that led me to take control of my own care, and figure out what was wrong with me. My ankles became swollen and painful, my and shins, (tibia) felt like someone had taken a sledgehammer to them. They were covered with red, hot patches that were strangely reminiscent of the migrating rash I had after the curious black blister over a year earlier.

Iin the absence of any medical staff I diagnosed myself finally, after 10 months of multiplying symptoms. I found a picture online of a blood engorged tick- it looked identical to the black blister I had taken a heat gun to last August because of the intense (there is no word adequate to describe it) itch that was deep below that blister. I had then washed the blister off with my hand and soap down the shower drain.

After the allergic reaction thatlasted 3 weeks with intense itching and microblistering, and oozing, the site of the blister finally healed and suddenly within days, a hot red blotchy patch with clearly demarcated, boundaries appeared under my arm ( I can't remember now if it was the left or right), and then disappeared quickly, and within hours, it reappeared on my neck. It felt like I had been branded with a hot iron. I believe this was the "migrating rash" that is described on many lyme disease web sites.

When my symptoms climaxed after months of feeling like I had morphed into an arthritic and crustry old man (I'm a young 39 who has never had any symptoms of back pain or any joint pain) I had to go to an emergency room armed with research, the photo of the engorged tick I found online, and specifically ask for a Doxycyclene prescription.

Most Doctors didn't believe i had been bitten by a tick or thougt I was being delusional and 3 docotrs at the local gay clinic told me it was HIV related, and even told me the low platelets were an HIV condition and if I only went on meds it would resolve. This is ludicrous as I told these doctors about my experience with a black blister that I think may have been a tick feasting on my stomach.

Lucklily, the ER doctor knew about tick borne infections, and said he "was happy" to presecribe me what I requested. I was free of the leg and ankle symptoms and pain after 3 days of the Doxycyclene.

After 5 days, my lower back was pain free. After the full 12 days, the only symptom that persisted but was much improved nonetheless was my neck. Today it feels like the tendon or cartilage or muscle there is still a bit fragile, but most of the pain is gone.

After a couple of weeks though, I started feeling headachy and fatigued again. The platelts were exactly the same low number, 25,000, (>140 is normal) and my ankles and inner arches of my feet were starting to show the little red dots called petechiae and congealing areas of broken capillaries, the red and blue spotting known as purpura.

I went to a local hispanic clinic and after much pleading the doctor pffered to give me a bottle of doxycycline for $25 bucks plus the cost of my visit.

After 10 days of that, I am feeling better, and am hopful.

There is no sign of unusual brusing, and an accidental cut last week clotted within minutes. My head is clear, and my vision is no longer blurred. The headaches are so far absent.

I woke up this morning, and my eyes were not puffy. For the first time in over a year I feel like I'm going to be oK.

]]> http://notaids.com/de/Misdiagnosis%21 2009-07-05T13:41:42-05:00 2009-07-05T13:58:39-05:00 The Editor

]]> http://notaids.com/de/thrombo 2009-07-04T12:25:03-05:00 2009-07-10T12:34:20-05:00 The Editor

NotAIDS! Blog
July 4, 2009

HIV gets blamed a lot. From anemia to dementia, wasting, lymphomas, and fungal infections, it is also blamed for TB, pneumonia, KS, "wasting", obesity, and yes, even car accidents in some countries.

I recently had a strange migrating red rash on my shins, and ankles. The red patchy areas were hot and my ankles and calves, and shins were extremely tender, painful, and felt like they were atrophying.

I went to the clinic where I get my labs, saw a doctor who said I injured myself, did I maybe go on a drinking or drug binge and not remember what happened. I was sent on my way with a grin and a nod.

I had my labs done a few days later, 5 or whatever tubes of blood were taken.

My legs seemed like they were healing, at least the red hot patches were going away.

The HIV doctor at the clinic where I have my labs done called me on a Tuesday morning. There was an abnormal result on my labs, did I have time to talk for a few.

He said I had 25,000 platelets per microliter. Under 20,000 you can have dangerous nosebleeds and under 10,000 you can have a spontaneous brain or stomach bleed - and die.

Doc told me to make an appointment right away to start AIDS drugs, and that should take care of my low platelets. I asked about other more specific causes and he couldn't name one. My appointment day I declined the Prednisone, and declined the HIV drugs. I would wait 10 days and retest and then make my decision.

I read a paper about low platelets - thrombocytopenia - and they said this condition frequently occurs in HIV+ people. Then it quoted a study where only 3% of a random HIV+ cohort had thrombocytopenia. Most studies show a prevalence of about 20% of all HIV+ populations with clinically insignificant low platelet counts (higher than 20,000).

My research showed about 140 causes of thrombocytopenia. Here are just a few items that caught my attention.

]]>

NotAIDS! Blog
July 4, 2009

HIV gets blamed a lot. From anemia to dementia, wasting, lymphomas, and fungal infections, it is also blamed for TB, pneumonia, KS, "wasting", obesity, and yes, even car accidents in some countries.

I recently had a strange migrating red rash on my shins, and ankles. The red patchy areas were hot and my ankles and calves, and shins were extremely tender, painful, and felt like they were atrophying.

I went to the clinic where I get my labs, saw a doctor who said I injured myself, did I maybe go on a drinking or drug binge and not remember what happened. I was sent on my way with a grin and a nod.

I had my labs done a few days later, 5 or whatever tubes of blood were taken.

My legs seemed like they were healing, at least the red hot patches were going away.

The HIV doctor at the clinic where I have my labs done called me on a Tuesday morning. There was an abnormal result on my labs, did I have time to talk for a few.

He said I had 25,000 platelets per microliter. Under 20,000 you can have dangerous nosebleeds and under 10,000 you can have a spontaneous brain or stomach bleed - and die.

Doc told me to make an appointment right away to start AIDS drugs, and that should take care of my low platelets. I asked about other more specific causes and he couldn't name one. My appointment day I declined the Prednisone, and declined the HIV drugs. I would wait 10 days and retest and then make my decision.

I read a paper about low platelets - thrombocytopenia - and they said this condition frequently occurs in HIV+ people. Then it quoted a study where only 3% of a random HIV+ cohort had thrombocytopenia. Most studies show a prevalence of about 20% of all HIV+ populations with clinically insignificant low platelet counts (higher than 20,000).

My research showed about 140 causes of thrombocytopenia. Here are just a few items that caught my attention.

• Infection with T. Cruzi -also known as Chagas' disease - an intestinal bug common among those in the developing countries, and in gay men, causes dramatic platelet decline. Could there be a connection between high rates of intestinal parasite infections in these populations and the relatively high incidence of thrombocytopenia? These connections are never made. In science and biomedicine, it's like one hand doesn't know what the other is doing.
  

  Strong thrombocytopenia is observed during acute infection with Trypanosoma cruzi, the parasitic protozoan agent of American trypanosomiasis or Chagas' disease. The parasite sheds trans-sialidase, an enzyme able to mobilize the sialyl residues on cell surfaces, which is distributed in blood and is a virulence factor. Since the sialic acid content on the platelet surface is crucial for determining the half-life of platelets in blood, we examined the possible involvement of the parasite-derived enzyme in thrombocytopenia induction. We found that a single intravenous injection of trans-sialidase into naïve mice reduced the platelet count by 50%, a transient effect that lasted as long as the enzyme remained in the blood.¹

• Bacteremia in general have extreme depressive effects on platelet count and can cause transient thrombocytopenia which reverses upon treatment of the underlying infection. The interesting conclusion of this research, aside from the non-HIV causes of low platelet count was the fact that mortality and morbidity (incidence and prevalence of disease in a population) were not at all influenced by taking AIDS drugs (HAART).
  

  Patients in the HAART-era had more comorbidity (41/72 vs 4/31), more frecuently neutropenia (13/72 vs 1/29), pneumococcal vaccine administration (38/63 vs 4/31)and prophylaxis with TMT-SMX (18/66 vs 2/31) than patients in the pre-HAART era. No statistically significant differences were observed between the pre-HAART and the HAART-era in the isolated germs, origins of bacteraemia, mean CD4 cells count, global mortality (7/31 vs 18/72) nor related to bacteraemia mortality (4/31 vs 13/72).
  ...
  The incidence, etiology, origin and mortality of bacteraemia in HIV patients have remained stable. Patients in the HAART era had more frequently associated comorbidity, pneumococcal vaccine administration an prophylaxis with TMT-SMX than those in the pre-HAART era.²

Then I found the culprit for my case of low platelets. It all started last fall when I suffered a tick bite. (I wonder if some AIDS lovers out there may want to get government funding to fabricate some garbage research on "HIV-related tickbites". That would be funny.)

I remember the telltale sign of tick-borne bacterial illness, the migrating rash, red and hot to the touch, moving around to different areas of the skin. I alerted an HIV doctor to the bite at this clinic I go to for my labs - allergic reaction on my stomach the reason for my visit. They told me the hot, red oozing patch was an HIV-related fungal infection and gave me an antifungal cream. Obviously it didn't make it better, only worse.

My symptoms subsided as the bacteria seemed dormant, but was establishing itself in my body- in the muscle tissue, in cartilage, over the last few months causing symptoms such as arthritis in my knee, neck stiffness and pain in the cartilage, ankle pain, and swelling, a recurrence of the migrating rash on my lower legs, painfully tender and stiff calves and shins.

I declined my doctor's recommendation to go on steroids (Predispose pills) and HIV drugs. I would do another blood screen and evaluate then.

That Sunday the migrating rash appeared in another spot above my ankle, and armed with my research results, I motored over to a local hospital emergency room. I told them about the tick bite, informed them of my HIV status, explained my doubt of an HIV cause of my thromobcytopenia.

The general medicine doctor immediately evaluated the hot red patch on my leg and said it wasn't caused by low platelets, but rather the low platelets and the leg / ankle symptoms were caused by a systemic illness, and that likely could be tick borne bacteria, which absolutely have a dramatically depressive effect on platelet count.

I'm on Doxyclycleine for 10 days at the time of this update. My legs are already clear of any rash. My calves are no longer tender. My neck is at least 75% better. Ankle swelling is completely resolved, and the stiffness in my joints, as well as the pain my knee are gone. I feel like my life force has returned.

An emotional ordeal that started out with a measure of self-doubt, the horror that I could have been wrong to doubt the AIDS doctrine, and a sudden fear of dying of AIDS, has ended with more resolve than ever to share the knowledge I have about the dishonesty of the HIV diagnosis.

What is unforgivable is the malpractice in the treatment of those of us who are gay, and those who live in the developing world, who were naive enough to take an HIV test, and unlucky enough to have the few antibodies at the time of the test that passes for a death-diagnosis.

As elated as I am about my recovery from the nasty tick-bite, I am saddened that so many people worldwide probably will never learn the biological truths that I have discovered by connecting disparate research results, my own experiences with the system, to what I believe is the worst and most long-standing boondoggle of science in the history of intelligent life.
##

---

1. The trans-Sialidase from Trypanosoma cruzi Induces Thrombocytopenia during Acute Chagas' Disease by Reducing the Platelet Sialic Acid Contents by
María Virginia Tribulatti,1 Juan Mucci,1 Nico Van Rooijen,2 María Susana Leguizamón,3 and Oscar Campetella1*
Instituto de Investigaciones Biotecnológicas, Universidad Nacional de General San Martín,1 Departamento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina,3 Department of Molecular Cell Biology and Immunology, Faculty of Medicine, Free University, Amsterdam, The Netherlands2

Infection and Immunity, January 2005, p. 201-207, Vol. 73, No. 1 0019-9567/05/$08.00+0 doi:10.1128/IAI.73.1.201-207.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

2. A prospective study of bloodstream infection in HIV-positive patients during a 15-year period by
J. Garc´?a Rodri?guez, H. Alvarez, B. Buno, A. Marino, M. Rodr?guez, P. Sesma (Ferrol, ES)].

17th ECCMID / 25th ICC, Posters 1998(?)

]]> http://notaids.com/de/malnutrition 2009-05-24T16:02:25-05:00 2009-05-25T03:35:27-05:00 guest

by Ulrich E. Schaible*, Stefan H. E. Kaufmann

I am not interested in the bloody system! Why has he no food? Why is he starving to death?                                          - Bob Geldof in The Observer, 1985

Activation and sustenance of immune responses during infection requires increased energy consumption. Protein energy malnutrition (PEM) is a critical, yet underestimated factor in susceptibility to infection, including the “big three” infectious diseases: HIV/AIDS, tuberculosis, and malaria. In this article, we discuss current concepts and controversies surrounding the complex influences of malnutrition on infection and immunity, and point to practical consequences of countermeasures in acute malnutrition.

We call for new strategies to overcome worldwide morbidity and mortality caused by chronic malnutrition in impoverished countries and by the newly emerging public health threat of overnutrition in industrialized societies.

Background 

In response to infection, the immune system first executes innate and then subsequently acquired host defense functions of high diversity. Both processes involve activation and propagation of immune cells and synthesis of an array of molecules requiring DNA replication, RNA expression, and protein synthesis and secretion, and therefore consume additional anabolic energy. Mediators of inflammation further increase the catabolic response. Studies in a simple system, involving measurement of the survival of malnourished bumblebee workers, showed that the energy cost of immunity further impairs fitness [1].

Consequently, the nutritive status of the host critically determines the outcome of infection.

Apart from deficiencies in single nutrients, such as vitamins, fatty acids, amino acids, iron, and trace elements, undernourishment based on PEM greatly increases susceptibility to major human infectious diseases in low-income countries, particularly in children [2–4].

Malnutrition is responsible, directly or indirectly, for 54% of the 10.8 million deaths per year in children under five and contributes to every second death (53%) associated with infectious diseases among children under five years of age in developing countries [5]. Infection causes energy loss on the part of the individual, which reduces productivity on the community level and perpetuates the alarming spiral of malnutrition, infection, disease, and poverty (Figure 1).

]]>

by Ulrich E. Schaible*, Stefan H. E. Kaufmann

I am not interested in the bloody system! Why has he no food? Why is he starving to death?                                          - Bob Geldof in The Observer, 1985

Activation and sustenance of immune responses during infection requires increased energy consumption. Protein energy malnutrition (PEM) is a critical, yet underestimated factor in susceptibility to infection, including the “big three” infectious diseases: HIV/AIDS, tuberculosis, and malaria. In this article, we discuss current concepts and controversies surrounding the complex influences of malnutrition on infection and immunity, and point to practical consequences of countermeasures in acute malnutrition.

We call for new strategies to overcome worldwide morbidity and mortality caused by chronic malnutrition in impoverished countries and by the newly emerging public health threat of overnutrition in industrialized societies.

Background 

In response to infection, the immune system first executes innate and then subsequently acquired host defense functions of high diversity. Both processes involve activation and propagation of immune cells and synthesis of an array of molecules requiring DNA replication, RNA expression, and protein synthesis and secretion, and therefore consume additional anabolic energy. Mediators of inflammation further increase the catabolic response. Studies in a simple system, involving measurement of the survival of malnourished bumblebee workers, showed that the energy cost of immunity further impairs fitness [1].

Consequently, the nutritive status of the host critically determines the outcome of infection.

Apart from deficiencies in single nutrients, such as vitamins, fatty acids, amino acids, iron, and trace elements, undernourishment based on PEM greatly increases susceptibility to major human infectious diseases in low-income countries, particularly in children [2–4].

Malnutrition is responsible, directly or indirectly, for 54% of the 10.8 million deaths per year in children under five and contributes to every second death (53%) associated with infectious diseases among children under five years of age in developing countries [5]. Infection causes energy loss on the part of the individual, which reduces productivity on the community level and perpetuates the alarming spiral of malnutrition, infection, disease, and poverty (Figure 1).

Malnutrition and Infection

Malnutrition increases risk of infection PEM is a common cause of secondary immune deficiency and susceptibility to infection in humans (Table 1). This causal relationship is further supported by animal studies. Severe PEM in children is clinically defined as less than 70% weight-to-height and/or the appearance of pitting edema on both feet, described as either marasmus, a chronic wasting condition, or kwashiorkor, characterized by edema and anemia.

Children with kwashiorkor often suffer from marked skin infections. Severe malnutrition during childhood affects thymic development, which compromises immunity in children by a long-term reduction of peripheral lymphocyte counts [6].

This immunodeficiency represents a key factor in susceptibility to infections and has therefore been termed nutritionally acquired immunodeficiency syndrome [7].

In severely malnourished patients, both acquired immunity—i.e., lymphocyte functions—as well as innate host defense mechanisms—i.e., macrophages and granulocytes—are affected.

Diminished immune functions render undernourished patients more susceptible to infections, notably those by opportunistic pathogens commonly prevalent in patients with HIV/AIDS [2–4,8,9].

The opportunistic fungus Pneumocystis carinii, frequently diagnosed in patients with AIDS, was repeatedly identified in malnourished children after the Second World War [9].

Noma is an opportunistic infection in children between one and four years with PEM, which occurs worldwide, but is most common in sub-Saharan Africa. The infection evolves from gingival inflammation to orofacial gangrene and is commonly preceded by other infections such as measles, malaria, severe diarrhea, and necrotising ulcerative gingivitis.

Noma coincides with the period of linear growth retardation in malnourished children [10]. In addition to promoting acute and chronic infections, PEM impairs the linear growth of children, leading to a further reduction in food intake, nutrient absorption, direct or catabolic nutrient losses, and increased metabolic requirements. It has been suggested that acute phase response and proinflammatory cytokines directly affect the bone remodelling required for longitudinal growth [11].

Correlation of malnutrition and growth retardation allows assessment of the individual nutritional state, which is usually measured as mid-upper arm circumference or body mass index (BMI).

BMIs are given either as weight-for-height to indicate acute PEM (wasting), or as weight-for-age (underweight) or height-for-age (stunting), correlations for chronic PEM.

A study in Kenya found a significant association between HIV infection and lower mid-upper arm circumferences and serum albumin concentration, another measure of malnutrition, but found no such association with BMI [12]. Independent of HIV, socioeconomic factors and severity of tuberculosis are important correlates of acute PEM or wasting [12].

Infection itself contributes to malnutrition. The relationship of malnutrition on immune suppression and infection is complicated by the profound effects of a number of infections on nutrition itself.

Examples of how infections can contribute to malnutrition are: (1) gastrointestinal infection can lead to diarrhea; (2) HIV/AIDS, tuberculosis, and other chronic infections can cause cachexia and anemia; and (3) intestinal parasites can cause anemia and nutrient deprivation [13].

Stimulation of an immune response by infection increases the demand for metabolically derived anabolic energy and associated substrates, leading to a synergistic vicious cycle of adverse nutritional status and increased susceptibility to infection.

Under inflammatory conditions such as sepsis, mediators increase the catabolic disease state characterised by enhanced arginine use. Furthermore, arginase is induced during infection and uses up arginine as substrate. It has been suggested that depletion of this amino acid impairs T cell responses [14], and exceeding the body’s arginine production leads to a negative nitrogen balance [15].

A study in Nigeria found that the severe metabolic demands made during acute measles infection further deteriorated the condition of malnourished children, leading to further weight loss, wasting, and reduced serum levels of essential amino acids [16]. Increased energy consumption due to immune responses may also affect the efficacy of live attenuated vaccines in populations ridden with PEM.

Arginine treatment has been shown to improve nitrogen balance and lymphocyte function and stimulate arginine transport in the liver. These benefits have made arginine an essential constituent of immunonutritive formulas currently in use for critically ill patients. PEM is an important health determinant for critically ill patients and increases susceptibility to infections in malnourished elderly patients and patients with anorexia.

A large and strictly controlled inpatient study in France pinpoints malnutrition as an independent risk factor for nosocomial infections, which account for 6%–10% of all in-hospital deaths worldwide [17]. Accordingly, nutritive management has to become an elementary part of intensive health care. In summary, nutritional quality and composition are pivotal for anti-infectious immunity.

Malnutrition Affects Immunity

Severe protein malnutrition in newborns and small children causes atrophy of the thymus with reduced cell numbers and subsequently ill-developed peripheral lymphoid organs, i.e., lymph nodes and spleen [6].

This causal chain leads to long-lasting immune defects characterized by leucopenia, decreased CD4 to CD8 ratio and increased numbers of CD4/CD8 double-negative T cells, and, therefore, the appearance of immature T cells in the periphery.

Malnourished children suffer in greater proportion from respiratory infections, infectious diarrhea, measles, and malaria, characterized by a protracted course and exacerbated disease. These malnourished children present with diminished functional T cell counts, increased undifferentiated lymphocyte numbers, and depressed serum complement activity (Table 1).

Reduced antibody responses to polysaccharide antigens of encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae exacerbate susceptibility to these pathogens [2,4,18]. Moreover, immune defense at the epithelial barrier of the undernourished host is compromised due to altered architecture of the gut mucosa, such as flattened hypotrophic microvilli, reduced lymphocyte counts in Peyer’s patches, and reduced immunoglobulin A (IgA) secretion [7].

Availability of complement components is restricted by malnutrition, thereby affecting the capacity of professional phagocytes to engulf and eliminate pathogens. In mice with experimental PEM, phagocytosis and production of reactive oxygen intermediates (ROIs) and reactive nitrogen intermediates (RNIs) by macrophages is diminished, as is antigen presentation to T cells by dendritic cells [19].

Temporary PEM in mice challenged by experimental peritonitis resulted in impaired immune cell migration and extravasation, as indicated by reduced numbers of CD11b/CD18-positive cells at the site of infection, probably involving lower concentrations of the chemokine MIP-2.

Peripheral T lymphocytes from infected children with PEM had lower expression of the activation marker CD69, and predominantly showed an intermediate (CD45RAlow/CD45ROlow) rather than a memory phenotype (CD45ROhigh) when compared to healthy donors [20,21].

These T cells were biased towards type 2 T helper cell (Th2) responses, represented by decreased IFN-?/IL-2 (type 1 T helper cell [Th1]) and increased IL-4/IL-10 (Th2) production [22].

Experimentally undernourished weanling mice had predominantly T cells of the naïve quiescent phenotype (CD45RA+/CD62L+) [23,24]. In these mice, IFN-?- responses were depressed and IL-10 and the Th2-associated antibody, IgE, were increased, while IL-4 production remained normal [25]. These findings, however, should not be taken to suggest that PEM generally biases towards Th2 responses. Rather, PEM appears to alter immune responses, thus hampering protective immunity of any type.

Protective T cell responses against helminth infections are predominantly of the Th2 type comprising IL-4 production, expansion of eosinophils, and IgE secretion.

However, malnourished children are deficient for protective IgE antibodies against Ascaris lumbricoides [26,27]. By suppressing such responses in mice, PEM increases susceptibility to infection with the intestinal parasite, Heligmosomoides polygyrus [28].

Malnourished children suffering from helminth infections have high concentrations of total IgE. Yet these antibodies are neither worm-specific nor protective, and their memory T cells do not recognize helminth antigens [27,28].

Malnutrition and Tuberculosis: Yesterday and Today

Malnutrition is generally appreciated as a major risk factor in the onset of active tuberculosis [9]. This notion is largely based on historical reports but also on more recent experimental animal studies. One of the major disease burdens globally, tuberculosis is a well-documented example of the way in which malnutrition leads to worse disease outcomes.

During the First World War, Denmark was affected by a tuberculosis epidemic similar to that prevailing in countries at war. The Danish tuberculosis epidemic could be explained by widespread malnourishment, since the export of meat, fish, poultry, and dairy products meant that food was scarce inside the country. This tuberculosis epidemic plummeted once the German blockade of Denmark was established and food became available to the Danish population again, but the epidemic continued in other countries [9].

A comparative radiographic survey of prisoners of war held in German camps during the Second World War under similar living conditions found a tuberculosis prevalence of 1.2% versus up to 19.0% among the British and Russians, respectively, with more severe outcomes in the latter.

This difference in prevalence and severity is probably a direct consequence of the fact that only the British prisoners received—in addition to the regular prison diet—a Red Cross supplement of 30 grams of protein and 1,000 kilocalories per day. This causal relationship is in line with the positive correlation of below average BMI with increased risk of pulmonary tuberculosis [9].

More contemporary reports provide further support that malnutrition has an impact on the clinical outcome of tuberculosis [29]. A statistically significant number of patients with tuberculosis were malnourished in a recent study in Sri Lanka and skin test reactions for tuberculosis were negatively affected by malnutrition [30,31].

Hence, in poor settings, nutritional measures should be considered as an adjunct to anti-tuberculosis drug treatment. Animal experiments, mainly in the guinea pig tuberculosis model, document detrimental consequences of chronic PEM on immunity to Mycobacterium tuberculosis. In these experiments, lymphocyte stimulation as well as secretion of the Th1 cytokines IL-2, IFN-?, and TNF-?, involved in control of M. tuberculosis, were significantly reduced in animals with PEM [9].

Moreover, macrophages from such animals produced more transforming growth factor ? (TGF?), which further suppresses T cells and inflammation [32,33].

A study in murine tuberculosis reached similar conclusions and additionally found that malnourished mice showed hampered production of RNIs, which act as critical effectors against tuberculosis in mice. Consequently, malnourished mice suffered from higher bacterial burdens and died earlier of infection [34].

Finally, efficacy of BCG vaccination against tuberculosis was profoundly reduced in malnourished guinea pigs as compared to normally fed animals, due to impaired T cell priming and function [9,35]. Malnutrition, Leptin, and Immunity Top Leptin is a central mediator connecting nutrition and immunity. Levels of the pleiotropic hormone leptin, which regulates satiety, are reduced in patients with PEM.

Leptin concentrations correlate with body fat mass and are quickly reduced by fasting [36]. Leptin is a 16 kDa ?-helix type protein similar to the cytokines IL-6 and IL-12, and is mainly secreted by adipose tissue.

At least six receptors representing different splice forms encoded by one gene are broadly distributed on different cell types. The isoform is not only full-length ObRb expressed in the hypothalamus, but is also prevalent on lymphocytes and macrophages [36,37].

Leptin binding activates immune cells via the to ObRb JAK-2/STAT-3 and the MAPK pathway and induces TNF-?, IL-6, and IL-12 secretion in macrophages.

Leptin stimulates naïve T cells (CD45RA+) but blocks proliferation of memory T cells (CD45RO+). Concomitantly, leptin promotes IFN-? secretion by memory T cells, inhibits Th2 responses [38,39], and induces activation markers (CD69, CD25, and CD71) [40]. Apart from inducing lymphopoiesis, leptin seems to deliver survival signals to T cells by upregulating anti-apoptotic proteins T-bet and Bcl-xL [36].

Active tuberculosis is associated with cachexia, weight loss, and low serum concentrations of leptin [41–44]. Moreover, leptin-deficient mice are more susceptible to M. tuberculosis than wild-type mice, and T cell numbers, including those producing IFN-?, are reduced in infected lungs, suggesting that leptin contributes to protection against tuberculosis [45].

However, a causative correlation between severity of tuberculosis and leptin is not fully established, and leptin concentrations do not predict wasting in human tuberculosis [44]. Malnutrition causes immunosuppression through a variety of mechanisms, including the involvement of leptin and the hypothalamic-pituitary-adrenal axis.

PEM reduces leptin concentrations and increases serum levels of stress hormones, i.e., glucocorticoids [2,4,46–48]. Thus, it is likely that the hypothalamic-pituitary-adrenal axis plays a critical role in malnutrition-associated immune deficiency. In well-nourished people, infection and inflammation increase leptin levels in an IL-1-dependent manner and increase glucocorticoid concentrations, which subsequently can control inflammation [40,49,50]. Under conditions of PEM and low leptin concentrations, glucocorticoids impair macrophage functions by decreasing NF-kB translocation into the nucleus [49]. Macrophages from mice with experimental PEM are less sensitive to activation with lipopolysaccharides, partly due to decreased NF-kB translocation. Their ability to engulf pathogens and to produce cytokines and ROIs is impaired [51–54]. However, the suggestion that malnutrition suppresses macrophage functions due to elevated glucocorticoid levels was not supported by a recent study [55]. Further experiments are required to identify the mechanisms connecting PEM and immunosuppression.

More contemporary reports provide further support that malnutrition has an impact on the clinical outcome of tuberculosis [29]. A statistically significant number of patients with tuberculosis were malnourished in a recent study in Sri Lanka and skin test reactions for tuberculosis were negatively affected by malnutrition [30,31]. Hence, in poor settings, nutritional measures should be considered as an adjunct to anti-tuberculosis drug treatment.

Animal experiments, mainly in the guinea pig tuberculosis model, document detrimental consequences of chronic PEM on immunity to Mycobacterium tuberculosis. In these experiments, lymphocyte stimulation as well as secretion of the Th1 cytokines IL-2, IFN-?, and TNF-?, involved in control of M. tuberculosis, were significantly reduced in animals with PEM [9]. Moreover, macrophages from such animals produced more transforming growth factor ? (TGF?), which further suppresses T cells and inflammation [32,33]. A study in murine tuberculosis reached similar conclusions and additionally found that malnourished mice showed hampered production of RNIs, which act as critical effectors against tuberculosis in mice. Consequently, malnourished mice suffered from higher bacterial burdens and died earlier of infection [34]. Finally, efficacy of BCG vaccination against tuberculosis was profoundly reduced in malnourished guinea pigs as compared to normally fed animals, due to impaired T cell priming and function [9,35].

Outlook Top

Extrapolating the studies discussed, malnutrition can be considered a major risk factor for morbidity and mortality worldwide due to infections with bacterial, viral, and protozoal agents [2,8,9]. This causal relationship was suggested in the US Surgeon General’s Report in 1988 [71]. With more than 842 million chronically malnourished people worldwide [72], we agree with the notion that “…malnutrition may account for a greater population-attributable risk of tuberculosis than HIV infection, and certainly a much more correctable one” [9].

In the context of what is known as the 10/90 gap (10% of global health research funding is being targeted to health problems that account for 90% of the global disease burden) [73,74], research on infection and malnutrition are highly warranted for scientific, economic, and ethical reasons [75].

To conquer malnutrition, cost-efficient and practical approaches need to be established. Measures to counteract acute malnutrition are now available and were successfully applied in 2005 when Niger was affected by a famine. The crisis did not come as a surprise to the consortium of stakeholders, i.e., the government of Niger, its international partners, and the Famine Early Warning Systems Network of the US Agency for International Development. To avoid disturbance of the market and long-term development goals, food was sold to starving people for too high a price instead of being freely distributed. The catastrophe became apparent as vast numbers of malnourished children were brought to medical stations. Ready-to-use therapeutic food was delivered by doctors from Médecins Sans Frontières as an outpatient measure (community therapeutic care) with enormous success [76].

Usually children are hospitalized under such circumstances and given milk products as therapeutic food. Outpatient treatment during emergencies, however, decreases (1) duration of maternal absence from the family, thereby limiting children’s risk of malnourishment, (2) time needed to establish treatment centers, and (3) risk of spreading nosocomial infections among hospitalized children in a limited number of overcrowded places. New therapeutic food formulations with balanced contents of macro- and micronutrients, which are ready to use and do not need a clean water supply for their preparation, are important prerequisites for such rapid aid measures. In the past, life-threatening respiratory infections, diarrhea, and malaria were frequent complications requiring short-term inpatient anti-infectious treatment. Under the emergency conditions of the Niger famine in 2005, the measures employed by Médecins Sans Frontières kept child mortality at the rate of non-famine periods. Thus, there is a precedent of effective interventions for acute malnutrition in an emergency to avoid subsequent infections.

This measure, however, is unlikely to minimize mortality and morbidity due to chronic malnutrition worldwide. Further research and development in diverse areas ranging from biomedicine to public health are required to stop the downward spiral of chronic malnutrition, infection, disease, and reduced economic productivity in impoverished societies with the consequences of migration and economical and political instability or war (Figure 1). Diseases resulting from overnutrition in industrial societies are of equal concern and similar conditions are already spreading to developing countries. Under- and overnutrition and diet-related chronic diseases represent a critical risk factor for more than half of the world’s diseases and incur hundreds of millions of dollars in public expenditure [5], requiring the immediate attention of biomedical science and public health agencies alike.

 

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]]> http://notaids.com/de/1981 2009-05-22T12:27:32-05:00 2009-05-22T12:27:32-05:00 The Editor

NotAIDS! Essay
December 22, 2006 (updated May 22, 2009)
UPDATE: New evidence indicates that KS may be related to intestinal parasites. More to come on this story.
Why did the U.S. National Institutes of Health (NIH) and Centers for Disease Control (CDC) look for a singular agent underlying uncommonly occurring illnesses afflicting 5 Los Angeles gay men, and 12 other men in New York and San Francisco, in 1981?

It was 1981 when Dr. Michael Gottlieb reported five patients to the Centers for Disease Control (CDC) because each had an uncommonly intensive infection.

The men had Pneumocystis Carini pneumonia (incorrectly identified as PCP, now known to be Pneumocystis Jiroveci); they also suffered from cytomegalovirus (CMV) infections, and intestinal and/or oral Candida Albicans overgrowth. Kaposi's Sarcoma lesions were reported at other clinics, in New York and San Francisco, and noted on the page following Dr. Gottlieb's report.

Dr. Gottlieb's Los Angeles report, and the KS "outbreak" in NYC and San Francisco, spurred a race among epidemiologists at the CDC and NIH - and simultaneiously at the Pasteur Institute - to find a cause celebre, a 'bug' that was making gay folk sick, even though the reasons for these illnesses caused by the mens' immunocompromised state was plainly attributable to behavioral causes.

The late seventies were characterized by a mentality of free-flowing sex, love, drugs, and rock and roll, and sex. In the late seventies and early eighties, there were thousands of other gay men who were dealing with irritable bowel syndrome (IBS) - caused by parasites and candida overgrowth, sometimes severe or entrenched enough to cause wasting and other so-called "rare" illneses.

Dr. Michael Gottlieb described these infections in his 1981 report to the CDC on five patients of his Los Angeles office. What is not in the report is the setting of this medical drama about to unfold on center stage for the next 30 years.

]]>

NotAIDS! Essay
December 22, 2006 (updated May 22, 2009)
UPDATE: New evidence indicates that KS may be related to intestinal parasites. More to come on this story.
Why did the U.S. National Institutes of Health (NIH) and Centers for Disease Control (CDC) look for a singular agent underlying uncommonly occurring illnesses afflicting 5 Los Angeles gay men, and 12 other men in New York and San Francisco, in 1981?

It was 1981 when Dr. Michael Gottlieb reported five patients to the Centers for Disease Control (CDC) because each had an uncommonly intensive infection.

The men had Pneumocystis Carini pneumonia (incorrectly identified as PCP, now known to be Pneumocystis Jiroveci); they also suffered from cytomegalovirus (CMV) infections, and intestinal and/or oral Candida Albicans overgrowth. Kaposi's Sarcoma lesions were reported at other clinics, in New York and San Francisco, and noted on the page following Dr. Gottlieb's report.

Dr. Gottlieb's Los Angeles report, and the KS "outbreak" in NYC and San Francisco, spurred a race among epidemiologists at the CDC and NIH - and simultaneiously at the Pasteur Institute - to find a cause celebre, a 'bug' that was making gay folk sick, even though the reasons for these illnesses caused by the mens' immunocompromised state was plainly attributable to behavioral causes.

The late seventies were characterized by a mentality of free-flowing sex, love, drugs, and rock and roll, and sex. In the late seventies and early eighties, there were thousands of other gay men who were dealing with irritable bowel syndrome (IBS) - caused by parasites and candida overgrowth, sometimes severe or entrenched enough to cause wasting and other so-called "rare" illneses.

Dr. Michael Gottlieb described these infections in his 1981 report to the CDC on five patients of his Los Angeles office. What is not in the report is the setting of this medical drama about to unfold on center stage for the next 30 years.

Intravenous drug use, exotic pills, 8 or 12 hour sex parties, and the many sacrificed meals and lost nights of sleep set up an environment favorable to mycobacteria (CMV), fungal organisms (Candida, PCP), and viral antigens like Kaposi's sarcoma, a human herpes virus. All of these organisms are present in a majority of humans but don't typically manifest in illness, under the immune system's capable control.

Some of the sexual activites gay men enjoy, like rimming, are unfortunately high-risk for parasites, which commonly travel the fecal-oral route. In Africa, due to the lack of water filtration systems, this route is quite common. Less than half of the sub-Saharan population has access to clean drinking water.

Research has repeatedly shown that parasitic infections over time damages the immune system, restricts absorption of nutrients from food, and settle in organs beyond the digestive tract, in the lungs for example. It is notable that pneumocystis pneumonia is a fungal parasite.

Candida overgrowth, another fungal infection, occurs routinely in the intestines post-antibiotics. It is no surprise, then, that IBS was common. In the gilded age of gay liberation, sex was carefree; it was as easy to find antibiotic pills as it was to get laid, if you caught something from your midnight snack.

Despite the wild sex parties of the time, these "CDC five" who are the subject of Dr. Gottlieb's infamous report, hadn't had direct sexual contact with each other - an interesting sidebar despite the "sex kills" mentality coming out of the AIDS madness.

One wonders if there were 5 straight people, not having had direct sexual contact with each other, presenting with pneumonia, CMV and IBS candida overgrowth, would they have not been reported to the CDC, and might we never have had AIDS?

The fact is that the only "unusual" thing about these men is that they preferred sex with men - note the wording in the CDC report: "all active homosexuals." (When the CDC refers to heterosexuals, are they qualified by their "active" sex life?)

Statistics indicate that around 60% of the general population would test positive for the CMV bacteria. As stated, all of the other offending organisms also are common but not commonly fatal. Therefore, a diagnosis of immunodeficiency is a no-brainer, but a prognosis of "eat well" and "get some rest" was apparently not exciting enough for the public health establishment, and certainly too boring for the career epidemioligist.

As anyone knows, when the body gets run down, illness is likely to follow. It is a known fact that protracted parasitic infections cause AIDS symptoms. So there is in fact nothing unusual at all about these five men getting sick given each of their behaviors leading to their illness.

Kaposi's sarcoma (KS) that afflicted other cohorts of men from New York and San Francisco was also blamed on the imaginary "AIDS virus," but a 1990 study concluded that KS had nothing to do with HIV.

"Differences in clinical findings, CD4+ and CD8+ cell counts, and P24 antibody and antigen levels indicate that the occurrence of KS may be independent of HIV induced severe immunodeficiency."²

Research shows that KS was and is directly attributable to the the hepatitis B vaccine. An experimental formulation of the hepatitis B vaccine was administered to thousands of gay men in New York, San Francisco, between 1979 and 1981 - the year a "gay related immune deficiency" syndrome called GRID was described in the media, later to become known as AIDS.

When all the facts are considered, the response of the CDC was fatefully overwrought in 1981. The sexual proclivities of gay men became a hot topic and maybe was titillating to certain repressed NIH / CDC epedemiologists. But beyond some gay men's choice of recreational activity, and the reaction of overzealous government employees and entrepreneurial medical workers like Robert Gallo who saw dollar signs in other people's suffering, not much else was unusual about some guys getting sick from partying and playing too much.

Nope, there was nothing unusual at all about what was to become AIDS, and what would curse generations of gay men, and consign them and later, sub Saharan Africa to the longest running pharmaceutical and human surveillance experiment in history.

The dose of trimethoprim sulfa is too high. It was the dose that we were taught to give, but we recognized fairly early, probably by '83 at least, that this was too high a dose...because it was toxic, yes. People got too sick on this high dose.

Early in the epidemic, people with KS had a better prognosis than later, after the first couple, three years of the epidemic. This was because the oncologists were just blasting the KS patients with chemotherapy and further depressing their immune system, and so their life expectancy went down.

So there was this dip in the life expectancy of KS patients. In fact, the early response, despite what the dermatologists and oncologists may say, was to overtreat these patients with chemotherapy. This hurt patients in terms of their life expectancy, because they were treated aggressively for their visible KS lesions.¹

- Dr. Stephen Follansbee

See page 2 of the MMWR report on the New York and San Francisco KS outbreak.Essay by Kirk Cordell, ©2006.

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1. The San Francisco AIDS Oral History Series;The AIDS Epidemic in San Francisco: The Response of Community Physicians, 1981-1984, Volume II. Stephen Follansbee, M.D., Infectious Disease Practitioner in the Early AIDS Epidemic. With an Introduction by Donald I. Abrams, M.D. Interviews Conducted by Sally Smith Hughes, Ph.D. in 1996. Copyright © 2000 by The Regents of the University of California
2. Epidemiology and natural history of Kaposi's sarcoma (KS) and Pneumocystis carinii pneumonia (PCP).. Winkelstein W, Fusaro RE, Sheppard HW. Int Conf AIDS. 1990 Jun 20-23; 6: 281 (abstract no. Th.C.627). University of California, Berkeley, California, USA

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