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From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.kids.health,sci.med,misc.health.alternative,misc.kids,
	uk.people.health
Subject: Re: Rumsfeld To Profit From Avian Flu Hoax
Date: 21 Oct 2005 13:41:23 -0700
Message-ID: <1129927283.557026.204410@g43g2000cwa.googlegroups.com>

john wrote:

> If you read the link below from Gilead, you'll discover Defense
> Secretary Donald Rumsfeld was made the chairman of Gilead in 1997.
>
> Since Rumsfeld holds major portions of stock in Gilead, he will
> handsomely profit from the scare tactics of the government that is
> being used to justify the purchase of $2 billion of Tamiflu.

COMMENT
Bzzt. And how EXACTLY do you know that?  While is true that Rumsfeld
was Chairman of the board of directors of Gilead and undoubtedly once
owned stock, it is also true that he divested himself of specific
investments and placed all assets in a blind trust when he entered
public service in 2001, as is required by law. Therefore, it's
extremely unlikely he owns any of Gilead, and in any case, since the
trust is blind, there's no way HE or YOU or anybody else but the
trustees has any idea what's in it. So you're "reporting" rumors you
have no way of knowing or checking, and scurrilous rumors at that.



> Ah there's the rub. 50% fatality rate sounds pretty scary to me. What
> Dr. Miller and the other experts fail to explain is how these numbers
> were derived. Did they examine everyone who contracted the avian flu
> and use those numbers or did they examine the sickest of the sick who
> had come down with the avian flu and determine the mortality from
> there?

COMMENT:

No, they examined everybody they could find with the disease. Even if
it was merely all flu cases who made it to the hospital, a mortality
rate of 60% would be shocking and rather frightening.

> This is shody science at best and beyond belief that any reputable
> scientist could get away with such nonsense.


COMMENT:
And just what makes you think you have any right to judge the standards
of science?  Are you a scientist?  Have any training, education or
credentials in science?  Did you bother to even find out the bare facts
behind the rhetorical questions you ask?  No.


> The avian flu epidemic hoax reminds me just how uncommon "common sense"
> is. Folks where is the sound basic science here?

COMMENT:
Since when did you ever believe in "sound basic science?"  In sound
basic science you attempt to find out some facts before you shoot your
mouth off.


> How do they make the
> giant leap of faith that 60 deaths will translate to 2 million or even
> 200,00 deaths in the US from a virus that does NOT readily spread from
> birds to humans or humans to humans?


COMMENT:
The figure is based on what would happen if the virus were to mutate so
that it was capable of doing this. Since the virus has already made 5
of the 10 required amino acid changes necessary to transform it into
the Spanish flu of 1918 (which was also a bird flu, as we know now),
we're already halfway to this disaster. The idea that we might go all
the way down a path which natural selection has taken us halfway down,
is not a "giant leap of faith." Rather, it's an example of a very
"common sense" type of fear. A well founded one, even if it doesn't
actually happen this year. Eventually, as in 1918, it will happen.



> Most of the people who acquired this infection were bird handlers who
> were in continuous contact with these sick birds. Does anyone in their
> right mind envision similar circumstances in the US?

COMMENT:
No, we envision a mutated virus which doesn't require this for
transfer. Duh.  Screw in your brain, John.




> Donald Rumsfeld to Profit Big Time
>
> So those 20 million doses the government has authorized will cost US
> Taxpayers 2 BILLION dollars.
>
> Defense Secretary Donald Rumsfeld will likely profit handsomely from
> the announcement the government is purchasing $2 billion of Tamiflu,
> the drug developed by Gilead Sciences when Rumsfeld was president of
> the company. He is reported to hold major portions of stock in Gilead


We've been over the part about "reported to own." And why should we
trust YOU, when you can't even tell the difference between the
president of a company and its board chairman? Gilead has a
president/CEO, but that position is not the chairman of the board of
directors, and never has been. So you can't even get simple facts
right.


> Not very different from his previous experience with aspartame where he
> was president of Searle and was able to get asparatame approved after
> being blocked by the FDA for more than a decade.


Aspartame was approved while Rumsfeld was at Searle. He had no
government post at the time. How is it that he is supposed to have
managed to get the FDA to do anything?  The FDA has a long history of
not giving a damn what the rest of the government thinks, and fights
between FDA and DoD, and between FDA and USDA, are legendary. The idea
that somebody working for a a private corporation outside of
government, could manipulate the FDA, is laughable. Even other
government agencies cannot manipulate the FDA.


> Now I think very few of us would mind if this drug actually worked and
> prevented even a few people from dying. But does it do that? Not
> really.

And your evidence for that statment is what?


> About all anyone can expect from this drug is that it might
> make the symptoms a bit less severe.


No. Tamiflu shortens the duration of symptoms in flu, and also their
severity, and also decreases incidence of secondary problems, including
pneumonia. Since the drug interferes with replication of the virus
itself, the decrease in symptoms is not due to some purely symptomatic
effect, but an effect on the disease process itself. The decrease in
pneumonia and secondary problems proves as much.


> On the downside (aside from
> setting you back $100) Dr. Tenpenny explained in her Flu Tele Clinic
> last week Tamiflu can actually cause the virus to mutate into a more
> dangerous and potent viral strain.

No, there is no evidence for that. Dr Tenpenny, if he said anything
like this, is wrong (in light of John's inability to deal with facts, I
am skeptical of his reports of anything anybody else said.) In any
case, this is factoid which requires a cite from a scientific study. I
cite a study below that concludes that mutations induced by Tamiflu
only affect resistance to Tamiflu and have no effect on the "potency"
of the virus (as expected-- resistance to antimicrobials does not make
microbes more virulent). And they affect its "dangerousness" only as
regards the fact that Tamiflu no longer works!


> Of course let us not forget the flu shots which many will use get when
> they confuse avian flu with the regular flu. Please understand even if
> you believe the flu shots work, the flu shot you can now purchase is in
> no way shape or form designed to protect you against the flu. They are
> completely different strains. (Avian flu is H5N1 strain).

COMMENT
A disingenuous argument from somebody who doesn't even think the flu
shot protects from the SAME strains. Liar.


> For more information about the avian flu you can obtain the Flu Tele
> Clinic I did last week with Dr. Tenpenny.

COMMENT:
For information, I suggest you pay no attention to anything some
ignorant sod like John says somebody told him over the telephone. Go to
the scientific literature and read some reviews of scientific studies.
Such as the two below.



1: Med Microbiol Immunol (Berl). 2002 Dec;191(3-4):165-8. Epub 2002 Sep
12.

Early therapy with the neuraminidase inhibitor oseltamivir maximizes its
efficacy in influenza treatment.

Gillissen A, Hoffken G.

St. George Medical Center, Robert-Koch-Hospital, Nikolai-Rumjanzew-Str. 100,
04207 Leipzig, Germany. adrian.gillissen@sanktgeorg.de

Influenza illness is an important cause of severe morbidity and mortality
in the population. Oseltamivir, the first oral neuraminidase inhibitor,
has proven efficacy. In children of 1 year and older (weight-dependent
dosing: 30 mg, 45 mg, 60 mg or 75 mg BID for 5 days) and adults (75 mg
BID for 5 days), oseltamivir reduces the duration and severity of acute
influenza. Furthermore, it decreases the incidence of secondary
complications such as otitis media, bronchitis, pneumonia and sinusitis.
Oseltamivir has been shown to prevent influenza when given for long-term
prophylaxis or for post-exposure prophylaxis. Because oseltamivir blocks
the neuraminidase, an enzyme crucial to influenza virion liberation from
the host cell, it is only effective during the replication phase.
Clinical benefits are only seen, when oseltamivir is applied within 48 h
after onset of symptoms, and clinical efficacy in acute influenza is
ighly dependent on the beginning of treatment.  Treatment within 12 h
after onset of symptoms reduces the duration of illness by an additional
74.6 h, and treatment within 24 hours an additional 53.9 h compared to
the benefit seen with an intervention at 48 h. In conclusion, clinical
efficacy of oseltamivir can be maximized by early start of treatment.
Resistance of influenza virus against oseltamivir has rarely been
observed and seems to be of no clinical relevance due to reduced
transmissibility and pathogenicity of mutants. Oseltamivir is generally
well tolerated. About 10% of the patients complain of transient upper
gastrointestinal events, which resolved within 1-2 days, and which could
be reduced when the medication was taken with a light snack.

Publication Types:
    Review
    Review, Tutorial

PMID: 12458353 [PubMed - indexed for MEDLINE]


2: Drugs. 2001;61(2):263-83.

Erratum in:
    Drugs 2001;61(6):775.

Oseltamivir: a review of its use in influenza.

McClellan K, Perry CM.

Adis International, Mairangi Bay, Auckland, New Zealand.
demail@adis.co.nz

Oseltamivir is a prodrug of oseltamivir carboxylate (Ro 64-0802, GS4071),
a potent and selective inhibitor of the neuraminidase glycoprotein
essential for replication of influenza A and B viruses.  Studies in
volunteers with experimental human influenza A or B showed that
administration of oral oseltamivir 20 to 200 mg twice daily for 5 days
reduced both the quantity and duration of viral shedding compared with
placebo. Subsequent assessment of the drug at a dosage of 75 mg twice
daily for 5 days in otherwise healthy adults with naturally acquired
febrile influenza showed that oseltamivir reduced the duration of the
disease by up to 1.5 days and the severity of illness by up to 38%
compared with placebo when initiated within 36 hours of symptom onset
(earlier initiation of therapy was associated with faster resolution).
The incidence of secondary complications and the use of antibacterials
were also reduced significantly in oseltamivir recipients. A liquid
formulation of oseltamivir (2 mg/kg twice daily for 5 days) has been
shown to be effective in the treatment of children with influenza, and
data presented in abstracts suggest that the drug may also be of use in
high-risk populations such as the elderly or those with chronic cardiac
or respiratory disease. In addition to treatment efficacy, the drug has
demonstrated efficacy when used for seasonal or household prophylaxis.
Oral oseltamivir (75 mg once or twice daily for 6 weeks) during a period
of local influenza activity significantly prevented the development of
naturally acquired influenza by >70% compared with placebo in
invaccinated otherwise healthy adults. The drug also demonstrated
efficacy when used adjunctively in previously vaccinated high-risk
elderly patients (92% protective efficacy). Short term administration of
oseltamivir (75 mg once daily for 7 days) may significantly reduce the
risk of illness in household contacts of infected persons when
administered within 48 hours of symptom onset in the infected person.
Oseltamivir 75 mg twice daily for 5 days was well tolerated in clinical
trials in healthy adults and high-risk patients, with nausea and vomiting
being the most commonly reported events.  Gastrointestinal events were
mild and transient and both nausea and vomiting were less likely when
oseltamivir was taken with food. Conclusions: Oseltamivir is a well
tolerated orally active neuraminidase inhibitor which significantly
reduces the duration of symptomatic illness and hastens the return to
normal levels of activity when initiated promptly in patients with
naturally acquired influenza. It therefore represents a useful
therapeutic alternative to zanamivir (especially in patients who prefer
oral administration or who have an underlying respiratory disorder) and
the M2 inhibitors amantadine and rimantadine (because of its broader
spectrum of anti-influenza activity and lower likelihood of resistance)
in patients with influenza. In addition, although annual vaccination
remains the best means of influenza prevention, there may be a place for
oseltamivir in providing household prophylaxis or adjunctive prophylaxis
in high-risk vaccinated patients during an outbreak of the disease or for
use in patients in whom vaccination is unsuitable or ineffective.

Publication Types:
    Review
    Review, Tutorial

PMID: 11270942 [PubMed - indexed for MEDLINE]



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.kids.health,sci.med,misc.health.alternative,misc.kids,
	uk.people.health
Subject: Re: Rumsfeld To Profit From Avian Flu Hoax
Date: 21 Oct 2005 13:59:47 -0700
Message-ID: <1129928387.202959.44190@o13g2000cwo.googlegroups.com>

john wrote:
> Now I think very few of us would mind if this drug actually worked and
> prevented even a few people from dying. But does it do that? Not
> really. About all anyone can expect from this drug is that it might
> make the symptoms a bit less severe. On the downside (aside from
> setting you back $100) Dr. Tenpenny explained in her Flu Tele Clinic
> last week Tamiflu can actually cause the virus to mutate into a more
> dangerous and potent viral strain.


COMMENT:
You know, flu viruses do mutate into more dangerous and potent
strains, all by themselves. Drugs are not required. Such a thing
happened in 1918, when a bird flu virus jumped to humans and killed 20
million people. We'd rather this didn't happen again.



> Review the simple lifestyle measures I outlined earlier this year that
> will serve to boost your immune system to not only address any form of
> the flu but also other infectious illness like the cold. When you have
> a healthy lifestyle and follow basic steps of the Total Health program,
> for the most part you just don't get sick.


Unless you happen to get the wrong virus. In which case, you die
anyway. In 1918-9, many of the victims came from groups which aren't
supposed to die of flu. It decimated soldiers in basic training, for
example. These were young men selected to fight in war, who had already
had the unhealthy men of their age screened out, and who were in the
best physical shape of their lives. The Spanish flu-- an avian flu--
killed them anyway.

Learn from history, John-boy.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.kids.health,sci.med,misc.health.alternative,misc.kids,
	uk.people.health
Subject: Re: Rumsfeld To Profit From Avian Flu Hoax
Date: 21 Oct 2005 16:03:35 -0700
Message-ID: <1129935815.055684.259080@g14g2000cwa.googlegroups.com>

C.Health wrote:
> To Sbharris,
>
> It was just reported that a 48 year old Thai man contracted the avian flu
> after eating an infected chicken. Prior to this report, I heard that it was
> not transmitted through diet. Is this report correct? It was on the news. I
> have friends traveling to China and they are concerned about eating chicken
> there. Thanks.


COMMENT:

I have no way of knowing if the report is correct. I can tell you that
cooking meat kills viruses quite effectively. Before the meat is
cooked, you could in theory get meat juice on your hands, touch your
nose or mouth somehow before you wash up, and there you are. If you eat
chicken in china, I recommend dim sum style :).

Avian or "bird" flu bugs are probably where most new strains of the
"flu" as we know it, come from. But ordinarily, strains of the bird flu
pass through pigs first, and in the process, recombine with human flu
viruses that also infect pigs, and acquire enough mutations that when
new strains finally go back from pigs to humans, then from humans to
humans, they aren't terribly deadly. All viruses generally become less
deadly as they have time to adapt to the new host species, over time.
The longer the virus has been in the new species, the less disease it
causes. Viruses don't want to kill you, remember. Killing you means
they've screwed up and pulled the wrong switches--- something likely to
happen only in a new and "wrong" species.

The scary thing about the 1918 flu is that we know now (having
completely revived it under strict quaranteen in a P3 lab at the CDC)
that it's basically a bird flu virus that made the jump directly to
humans without ever going through pigs. This caused some confusion last
year when it was found to be an H1 virus (a "human" or swine type), not
an H5 or H7 strain of the type seen in birds (this caused some
confusion when the virus was first sequenced, since it was EXPECTED to
be a bird virus). But now we know it's a mutant, and a big part of its
mutation is in that H gene. It still kills bird embryos in bird eggs,
just like the Asian bird flu does. Human and swine flus don't do that--
in fact we still culture them in bird eggs to make the vaccines. If
they killed bird embryos, we couldn't do it that way. But these average
flu viruses have already adapted away from their bird hosts enough that
we can make them in eggs.

But the 1918 flu, an "H1" N1 flu, had an H1 hemagglutinin gene which
was subtly different from the normal bird virus H5. The glyoprotein
produced by the 1918 virus H1 not only binds to bird cells, but the
sialic acid of human cells as well. That difference is a key one that
allowed it to spread from human to human in 1918. The 1918 virus has
all the lethal characteristics of a bird virus. It is extremely
pathogenic to mice-- infected with it, their lungs fill up with blood
and they drown, which is pretty much what happened to people in 1918.
(The idea that dying from the flu is always due to some kind of poor
condition or nutritional deficiency, is nonsense. If you're unlucky
enough to encounter Ebola or SARS or some other strain that has just
made the jump from animals to humans, you may not survive no matter how
healthy you are.)

The question is whether the H5 (a typical bird subtype) in today's
Asian bird flu will mutate enough that it becomes equivalent to the
"H1" in the 1918 Spanish/bird flu which allowed it to go from human to
human. If it does, there's every reason to imagine that it might become
as transmissable as the 1918 flu. And we already know it's as lethal
when it does get into humans.

Will today's vaccines protect against an H5 N1 Asian bird flu virus
which manages to mutate to an "H1" N1 type and thus re-create the 1918
bird flu?  Maybe. I've read reports that H1 N1 vaccines do protect mice
from the 1918 flu, even though (other than its H1 glycoprotein) it is
basically an avian flu virus. And there is an H1 N1 human strain in the
vaccine this year (which I'm doubly glad I just got). It may work.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med.nutrition,sci.med,talk.politics.medicine,
	misc.health.alternative
Subject: Re: Speaking of the pneumonia vaccine ...
Date: 23 Oct 2005 16:18:15 -0700
Message-ID: <1130109495.476631.173350@f14g2000cwb.googlegroups.com>

Mr-Natural-Health wrote:
> Annual Flu Deaths: The Big Lie
> http://thinktwice.com/flu_lie.htm
>
> "By Neil Z. Miller
>
> The Flu Vaccine: Safety & Efficacy
>
> Avian Flu: Quarantine vs. Vaccine
>
>        Every year, just prior to the impending "flu season," the CDC
> and their acquiescent media pawns terrorize the American public with
> false claims regarding annual flu deaths. The CDC boldly asserts that
> 36,000 people die every year from the flu. Such scare tactics are
> calculated to increase flu vaccine sales. However, according to the
> CDC's own official records documented in National Vital Statistics
> Reports, only a few hundred people die from influenza (flu) on an
> average year.

COMMENT:
That's because the flu is not a legally reportable disease in any
state, so usually isn't reported to the CDC. You are quoting the few
cases that do get reported *anyway.* Which isn't many. Duh. So you get
numbers which are meaningless. As well try to find out from the CDC how
many people died because they were smokers.



> And many of these deaths occur in people with preexisting
> conditions, weakened immune systems, and the elderly.

COMMENT:
LOL.  Please remember both of the above arguments, next time you report
on iatrogenic deaths in the US. Sort of shot yourself in the foot
there, didn't you?


> To rationalize this discrepancy between the true number of deaths
> caused by influenza every year (as documented in the CDC's own National
> Vital Statistics Reports) and the outrageously exaggerated bogus number
> of flu deaths promoted by the CDC, officials claim that flu often leads
> to pneumonia and that many deaths from pneumonia are really deaths
> caused by flu. Apparently the CDC has a secret formula for estimating
> how many pneumonia deaths (officially listed in the CDC's own National
> Vital Statistics Reports as deaths from pneumonia, not flu) are really
> deaths caused by flu.


COMMENT:

SECRET FORMULA??  It's only secret to people who can't use a library or
data retreival system. Which I'm afraid includes you, Gohde, and
apparently also the doofus author of the above article.  I suppose the
world tends to be a pretty secret place to you-all, then. Scary, too.

But for the rest of you reading, the full description of how the CDC
made this estimate is detailed in the following article, from which the
US 36,000 flu deaths a year comes. Basically, viral survailance of
specific areas is used to how much more likely a person who enters the
hospital from influenza infection is to die, vs. a control group of
similarly aged persons who entered for pneumonia which did not start
out as influenza. That gives a death rate attributable to the flu
itself, and not just age and pneumonia. It can be checked to see if the
deaths attributable to flu match flu infection rates over the yearly
cycle (which it does) and if the figures match the known increase in
pneumonia deaths during flu season (which they do). A similar analysis
can be carried out for other viruses, such as RSV. Attributable death
analyses can be carried out for any disease which you can diagnose with
a good test, so long as a control without the problem (in this case,
flu infection) is available, to keep you honest. Influenza cases are
usually diagnosed serologically, from antibody titers.

I was going to say "just thought you'd like to know, John" but I
realized that you really don't like to know anything new. If you did,
you'd work harder to check your drivel.


JAMA. 2003 Jan 8;289(2):179-86.

Comment in:
    JAMA. 2003 Jan 8;289(2):227-9.
    JAMA. 2003 May 21;289(19):2499-500; author reply 2500-2.
    JAMA. 2003 May 21;289(19):2499; author reply 2500-2.
    JAMA. 2003 May 21;289(19):2500; author reply 2500-2.

Mortality associated with influenza and respiratory syncytial virus in
the United States.

Thompson WW, Shay DK, Weintraub E, Brammer L, Cox N, Anderson LJ,
Fukuda K.

Influenza Branch, National Center for Infectious Diseases, Centers for
Disease Control and Prevention, Atlanta, Ga 30333, USA. wct2@cdc.gov

CONTEXT: Influenza and respiratory syncytial virus (RSV) cause substantial
morbidity and mortality. Statistical methods used to estimate deaths in
the United States attributable to influenza have not accounted for RSV
circulation.
OBJECTIVE: To develop a statistical model using national mortality and
viral surveillance data to estimate annual influenza- and
RSV-associated deaths in the United States, by age group, virus, and
influenza type and subtype.

DESIGN, SETTING, AND POPULATION: Age-specific Poisson regression models
using national viral surveillance data for the 1976-1977 through
1998-1999 seasons were used to estimate influenza-associated deaths.
Influenza-and RSV-associated deaths were simultaneously estimated for
the 1990-1991 through 1998-1999 seasons.

MAIN OUTCOME MEASURES: Attributable deaths for 3 categories: underlying
pneumonia and influenza, underlying respiratory and circulatory, and
all causes.

RESULTS: Annual estimates of influenza-associated deaths increased
significantly between the 1976-1977 and 1998-1999 seasons for all 3 death
categories (P<.001 for each category). For the 1990-1991 through
1998-1999 seasons, the greatest mean numbers of deaths were associated
with influenza A(H3N2) viruses, followed by RSV, influenza B, and
influenza A(H1N1). Influenza viruses and RSV, respectively, were
associated with annual means (SD) of 8097 (3084) and 2707 (196)
underlying pneumonia and influenza deaths, 36 155 (11 055) and 11 321
(668) underlying respiratory and circulatory deaths, and 51 203 (15 081)
and 17 358 (1086) all-cause deaths. For underlying respiratory and
circulatory deaths, 90% of influenza- and 78% of RSV-associated deaths
occurred among persons aged 65 years or older. Influenza was associated
with more deaths than RSV in all age groups except for children younger
than 1 year. On average, influenza was associated with 3 times as many
deaths as RSV.

CONCLUSIONS: Mortality associated with both influenza and RSV
circulation disproportionately affects elderly persons. Influenza
deaths have increased substantially in the last 2 decades, in part
because of aging of the population, underscoring the need for better
prevention measures, including more effective vaccines and vaccination
programs for elderly persons.

PMID: 12517228 [PubMed - indexed for MEDLINE]



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 13:50:11 -0800
Message-ID: <1130968211.304779.68470@f14g2000cwb.googlegroups.com>

fresh~horses wrote:
> Tamiflu being pushed with little evidence it mitigates flu for more
> than a few hours, and that only in certain populations and at great
> cost;

COMMENT:

Yeah, "certain populations" like healthy adults and vaccinated elderly
are protected (70% and 92% respectively, as compared with placebo
controls) from getting the flu *at all* by Tamiflu, in post-exposure
prophylaxis. Which would be damned useful in an outbreak of a killer
virus for which there is no effective vaccine.

In children over 12 months old (they didn't test it on younger),
Tamiflu not only decreases flu duration and severity, but secondary
symptoms like bacterial bronchitis and pneumonia. There is no reason to
imagine the same would not happen in populations of adults who get the
same problems (ie, the elderly) but this hasn't been explicitly tested,
AFAIK.

In healthy non-elderly adults, Tamiflu decreases flu duration and
severity. But this is testing in adults who are infected with a
non-killer flu virus, so there aren't/weren't enough cases of secondary
bronchitis and pneumonia to assess impact.

However, in *animals* exposed to a strain of flu which produces high
mortality in the model, Tamiflu *greatly* decreases mortality. As well
as disease duration and severity in animal which survive. All this is
backed up by a very great deal of knowledge of the effect of Tamiflu on
replication of flu virus in culture, which is how the drug was first
developed.

Now, given all that information, what do you think? Just hype?  Well,
you (and your government) are welcome to bet against the odds with your
own life. Bon chance, les Canucks. But then, "Dans les champs de
l'observation le hasard ne favorise que les esprits préparés."
(Pasteur) If you're not prepared to look, you won't see the monster
till it eats you. Get out the mighty monster song, cause one
rendition's all you get, before the coughing fit makes you stop.

> and who profits from this scam should just be kept quiet. Is that
> what you're saying Carey?

COMMENT
Who profits is irrelvant, so long as they're not making the government
decisions, as regards this drug. Which there is no reason to think the
US Secretary of Defense is. That's just paranoid nonsense.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 14:21:28 -0800
Message-ID: <1130970088.524585.210810@o13g2000cwo.googlegroups.com>

fresh~horses wrote:
> "Well, you (and your government) are welcome to bet against the odds
> with your own life. Bon chance, les Canucks."
>
> This is such a childish response Steve. I fail to see where this is an
> issue of my government against your government.  But if you want to go
> with the paranoia theme...


COMMENT:

Sigh. The US government is stockpiling Tamiflu and paying a lot of
money to do it (unlike Canada, which isn't). You start a thread with an
article which insinuates that a US political appointee is profiteering
from said decission, and you post this on "can.politics."  THEN, you
now call ME "childish" for wondering how this might *possibly* be seen
as a "government vs government" issue? Say what?

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 15:45:08 -0800
Message-ID: <1130975108.753722.69930@z14g2000cwz.googlegroups.com>

fresh~horses wrote:
> Like everyone else I am trying to determine the value of these drugs.
> To me, and to anyone. Why are we being told, virtually, that we must
> use them?


COMMENT:

You're not being told that, at present. Not by any competent
professional. We are talking about two completely separate cases: 1)
ordinary flu season, and 2) a bird flu epidemic with attendent VERY
MUCH HIGHER THAN NORMAL mortality profile.

For Case #1, the analysis you post below is entirely reasonable (and in
fact contains much of the info I already noted). In normal flu seasons,
90% of the deaths are in people over 65, and most of the rest are in
people who are chronically ill, and can be identified as so,
beforehand. Tamiflu is useful for those groups and people *in those
groups* who are exposed to a known flu case. As for others, probably
it's not worth the money, and especially isn't worth using up
stockpiles of a drug in short supply, as this one will be for the next
couple of years. I wouldn't take my *own* stockpile of Tamiflu for the
ordinary kind of flu, if I came down with it. I've been vaccinated, and
if I get the flu, then amantidine, aspirin, and the good old hot tub is
going to have to do. I might try some ribivirin since I happen to have
a lot of it on hand, and know more about the "guts" of why it's not a
presently recommended flu drug (bottom line-- this was an FDA screwup,
for fully political reasons). But there are things I'd do for myself
that I'd never prescribe, and that's one of them.

For Case #2, all bets are off. Who you use Tamiflu on THEN, depends on
who's doing the dying. If it's 1918 again, that might be people age 20.
Previously done risk analysis only applies very losely to this
situation, except that it's very reasonable to believe that a drug
which ameliorates lesser flus, and almost completely prophylaxes
against lesser flus, will do so also against a killer bird flu (which
we know will use the same mechanisms that this drug works against).

>If I dismissed it out of hand, I wouldn't be asking. Asking
> involves searching. Searching, for me, involves sharing what I find,
> especially when it begins to follow a pattern. Why are there such scare
> tactics being used? I find more and more hype that is typical of how
> another class of drugs was and is pushed.


Scare tactics in medicine are used mainly on people who don't seem to
"get it" any other way. Know any?

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 17:04:09 -0800
Message-ID: <1130979849.769952.3910@g44g2000cwa.googlegroups.com>

fresh~horses wrote:
> Steve Harris wrote:
> > fresh~horses wrote:
> > > Like everyone else I am trying to determine the value of these drugs.
> > > To me, and to anyone. Why are we being told, virtually, that we must
> > > use them?
> >
> >
> > COMMENT:
> >
> > You're not being told that, at present. Not by any competent
> > professional. We are talking about two completely separate cases: 1)
> > ordinary flu season, and 2) a bird flu epidemic with attendent VERY
> > MUCH HIGHER THAN NORMAL mortality profile.
>
> Please show me any evidence that TAMIFLU has efficacy against Avian
> Flu.

COMMENT:

In people?  None exists because there have been too few cases. There
has even been a report of a resistant strain isolated from one person.
Too few of any of these to do stats with. In mice, the drug works
reasonably well. The virus is essentially 100% lethal without it.
However, the flu is worse in mice than it is in people. I think that
has to do with our respiratory reserve. Humans are runners with lots of
reserve, and it takes a more lung problem to kill us than any mammal
but the dog.

You can do your own medline searches, you know.



1: J Infect Dis. 2005 Aug 15;192(4):665-72. Epub 2005 Jul 15.

Virulence may determine the necessary duration and dosage of oseltamivir
treatment for highly pathogenic A/Vietnam/1203/04 influenza virus in
mice.

Yen HL, Monto AS, Webster RG, Govorkova EA.

Department of Infectious Diseases, St. Jude Children's Research Hospital,
Memphis, Tennessee 38105-2794, USA.

BACKGROUND. Control of highly pathogenic avian H5N1 influenza viruses is
a major public-health concern. Antiviral drugs could be the only option
early in the pandemic.METHODS. BALB/c mice were given oseltamivir (0.1,
1, or 10 mg/kg/day) twice daily by oral gavage; the first dose was given
4 h before inoculation with H5N1 A/Vietnam/1203/04 (VN1203/04) virus.
Five- and 8-day regimens were evaluated.RESULTS. Oseltamivir produced a
dose-dependent antiviral effect against VN1203/04 in vivo (P<.01). The
5-day regimen at 10 mg/kg/day protected 50% of mice; deaths in this
treatment group were delayed and indicated the replication of residual
virus after the completion of treatment.  Eight-day regimens improved
oseltamivir efficacy, and dosages of 1 and 10 mg/kg/day significantly
reduced virus titers in organs and provided 60% and 80% survival rates,
respectively (P<.05). Overall, the efficacy of the 5- and 8-day regimens
differed significantly (death hazard ratio, 2.658; P<.01). The new H5N1
antigenic variant VN1203/04 was more pathogenic in mice than was
A/HK/156/97 virus, and a prolonged and higher-dose oseltamivir regimen
may be required for the most beneficial antiviral effect.CONCLUSIONS.
Oseltamivir prophylaxis is efficacious against lethal challenge with
VN1203/04 virus in mice.  Viral virulence may affect the antiviral
treatment schedule.

PMID: 16028136 [PubMed - indexed for MEDLINE]

2: Antimicrob Agents Chemother. 2001 Oct;45(10):2723-32.

Comparison of efficacies of RWJ-270201, zanamivir, and oseltamivir
against H5N1, H9N2, and other avian influenza viruses.

Govorkova EA, Leneva IA, Goloubeva OG, Bush K, Webster RG.

Department of Virology and Molecular Biology, St. Jude's Children's
Research Hospital, 332 N. Lauderdale, Memphis, TN 38105, USA.

The orally administered neuraminidase (NA) inhibitor RWJ-270201 was
tested in parallel with zanamivir and oseltamivir against a panel of
avian influenza viruses for inhibition of NA activity and replication in
tissue culture. The agents were then tested for protection of mice
against lethal H5N1 and H9N2 virus infection. In vitro, RWJ-270201 was
highly effective against all nine NA subtypes. NA inhibition by
RWJ-270201 (50% inhibitory concentration, 0.9 to 4.3 nM) was superior to
that by zanamivir and oseltamivir carboxylate.  RWJ-270201 inhibited the
replication of avian influenza viruses of both Eurasian and American
lineages in MDCK cells (50% effective concentration, 0.5 to 11.8 microM).
Mice given 10 mg of RWJ-270201 per kg of body weight per day were
completely protected against lethal challenge with influenza A/Hong
Kong/156/97 (H5N1) and A/quail/Hong Kong/G1/97 (H9N2) viruses. Both
RWJ-270201 and oseltamivir significantly reduced virus titers in mouse
lungs at daily dosages of 1.0 and 10 mg/kg and prevented the spread of
virus to the brain.  When treatment began 48 h after exposure to H5N1
virus, 10 mg of RWJ-270201/kg/day protected 50% of mice from death. These
results suggest that RWJ-270201 is at least as effective as either
zanamivir or oseltamivir against avian influenza viruses and may be of
potential clinical use for treatment of emerging influenza viruses that
may be transmitted from birds to humans.

PMID: 11557461 [PubMed - indexed for MEDLINE]

3: Antiviral Res. 2000 Nov;48(2):101-15.

The neuraminidase inhibitor GS4104 (oseltamivir phosphate) is efficacious
against A/Hong Kong/156/97 (H5N1) and A/Hong Kong/1074/99 (H9N2)
influenza viruses.

Leneva IA, Roberts N, Govorkova EA, Goloubeva OG, Webster RG.

Department of Virology and Molecular Biology, St. Jude Children's
Research Hospital, PO Box 318, 332 N. Lauderdale, Memphis, TN 38105-2794,
USA.

In 1997, an H5N1 avian influenza A/Hong Kong/156/97 virus transmitted
directly to humans and killed six of the 18 people infected. In 1999,
another avian A/Hong/1074/99 (H9N2) virus caused influenza in two
children. In such cases in which vaccines are unavailable, antiviral
drugs are crucial for prophylaxis and therapy. Here we demonstrate the
efficacy of the neuraminidase inhibitor GS4104 (oseltamivir phosphate)
against these H5N1 and H9N2 viruses. GS4071 (the active metabolite of
oseltamivir) inhibited viral replication in MDCK cells (EC(50) values,
7.5-12 microM) and neuraminidase activity (IC(50) values, 7.0-15 nM).
When orally administered at doses of 1 and 10 mg/kg per day, GS4104
prevented death of mice infected with A/Hong Kong/156/97 (H5N1),
mouse-adapted A/Quail/Hong Kong/G1/97 (H9N2), or human A/Hong
Kong/1074/99 (H9N2) viruses and reduced virus titers in the lungs and
prevented the spread of virus to the brain of mice infected with A/Hong
Kong/156/97 (H5N1) and mouse-adapted A/Quail/Hong Kong/G1/97 (H9N2)
viruses. When therapy was delayed until 36 h after exposure to the H5N1
virus, GS4104 was still effective and significantly increased the number
of survivors as compared with control. Oral administration of GS4104 (0.1
mg/kg per day) in combination with rimantadine (1 mg/kg per day) reduced
the number of deaths of mice infected with 100 MLD(50) of H9N2 virus and
prevented the deaths of mice infected with 5 MLD(50) of virus. Thus,
GS4104 is efficacious in treating infections caused by H5N1 and H9N2
influenza viruses in mice.

PMID: 11114412 [PubMed - indexed for MEDLINE]



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 16:35:54 -0800
Message-ID: <1130978154.670538.36730@g14g2000cwa.googlegroups.com>

(PeteCresswell) wrote:

> So, either way, 20 million doses doesn't sound even remotely adequate - in fact
> it sounds laughable.
>
> Have I made some unrealistic assumption?
> Have I slipped a decimal point somewhere?
>
> Somebody point out the flaw(s) to me, and I'll feel a *lot* better.
> --
> PeteCresswell


No, your math is good. Obviously 20 million doses is not enough for the
population for prophylaxis. And is only enough to treat the 1 million
sickest people who get the flu-- or may twice that (we don't know if
people behave like mice). If you can figure out who those are. The
problem is the stuff only works when given early, and in the early
stages, people aren't yet ill enough to tell if they're "the sickest."
Thus, you end up giving the drug to all high-risk people in early
stages. And we have roughly 30 million people over 65 or at special
risk, in this country. If a third of them get the flu and need Tamiflu
for 10 days we end up with need for 200 million doses. Or 100 million
for 5 days. Which is indeed 5 times our supply.

But you do what you can. I don't think there are 200 million doses in
the world right now.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 17:17:55 -0800
Message-ID: <1130980674.963721.161710@z14g2000cwz.googlegroups.com>

fresh~horses wrote:
> Steve Harris wrote:
> > (PeteCresswell) wrote:
> >
> > > So, either way, 20 million doses doesn't sound even remotely adequate - in fact
> > > it sounds laughable.
> > >
> > > Have I made some unrealistic assumption?
> > > Have I slipped a decimal point somewhere?
> > >
> > > Somebody point out the flaw(s) to me, and I'll feel a *lot* better.
> > > --
> > > PeteCresswell
> >
> >
> > No, your math is good. Obviously 20 million doses is not enough for the
> > population for prophylaxis. And is only enough to treat the 1 million
> > sickest people who get the flu-- or may twice that (we don't know if
> > people behave like mice). If you can figure out who those are. The
> > problem is the stuff only works when given early, and in the early
> > stages, people aren't yet ill enough to tell if they're "the sickest."
> > Thus, you end up giving the drug to all high-risk people in early
> > stages. And we have roughly 30 million people over 65 or at special
> > risk, in this country. If a third of them get the flu and need Tamiflu
> > for 10 days we end up with need for 200 million doses. Or 100 million
> > for 5 days. Which is indeed 5 times our supply.
> >
> > But you do what you can. I don't think there are 200 million doses in
> > the world right now.
> >
> > SBH
>
>
>
> Do not let facts get in your way Steve. Prophylaxis occurs before
> someone already has the flu. By definition.


COMMENT:

Yes.  So?  The question of whether the drug is useful for prophylaxis
is entirely separate from the question of whether we have enough of it
for the purpose at this time.  Clearly we don't. At least, not for
everyone who might need it, in the worst case. Or even a bad case.  We
need to make more, if we do want it for this use, and various routes to
doing so, are being explored. The issue changes as I type. So?

It's a complicated issue, even when it comes to drugs. There are three
other drugs which should work on H5N1, one of which (Relenza) has been
proven to work in animals, and the other (ribavirin) which works on
most A and B flu strains, and should also work here (looking at
mechanism of action). Also the classic amantidine may work in some
cases, since not 100% of bird viruses are yet resistant to it (just
many of them, due to discussed Chinese use of the drug in
chickenfeed--- idiots).


> Your argument makes me wonder what stake you have in this?


What statement??

>You did say your lab tests pharmaceuticals. Does that include flu vaccine?


My, paranoia attack again?  No, we do no vaccine or antimicrobial work.
We're interested mostly in lipid soluble drug delivery. Recent projects
have been general anesthetics and nutritional supplements.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 18:08:04 -0800
Message-ID: <1130983684.818908.253880@f14g2000cwb.googlegroups.com>

fresh~horses wrote:
>> Hmmm. 14 days and counting and Roche still hasn't come across. I'll bet
> you a book of your choice, through Amazon, if I'm right and they
> refuse, or even waffle.
>
> Deal?

Deal if the terms are that they do (or don't) license it out to at
least two other companies, by end of next year (2006). That's 13
months.

Naturally there's going to be some very heavy bargaining here. The
generic guys know they have Roche by the cojones, due to public
sentiment and the chance of other countries bolting. There's even
precident for the US breaking US patents in the name of public safety.
Against this, consider that it's a difficult drug to make, and Roche no
doubt has considerable "black art" experience which isn't IN the
patents. Which it doesn't have to give up if it doesn't want to. Nobody
can force an expert to be a full expert; that takes heart. The best you
can do is force an expert to ACT like a full expert. Not the same.


> I liked this part best:
>
> "Tamiflu is not a cure for the flu, but it can lessen the flu's
> severity or cut the chances of spreading the disease if taken before
> symptoms develop.
>
> Even still, despite the rush to stockpile the drug, some experts warn
> that uncertainty remains around how effective it will be in a
> real-world bird flu pandemic.
>
> H5N1 infects more quickly and enters a broader range of lung cells than
> do other more common flu strains, Michael Osterholm, MD, an infectious
> disease expert and Department of Homeland Security official, cautioned
> earlier this week. The infection causes the body to release a rush
> chemicals that attack the immune system, and there is little evidence
> showing how well Tamiflu can stop or lessen the release, he told
> reporters.
>
> "Frankly we just don't know," Osterholm said.


COMMENT:

You never know how the human trials are going to come out, till they
come out. But there's a world of difference between "We don't know" and
"We have no clue." Don't watch what Feds SAY, watch what they DO.
That's what they guess and more or less believe.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 17:53:37 -0800
Message-ID: <1130982817.562942.189160@f14g2000cwb.googlegroups.com>

fresh~horses wrote:
> A 25 mm socket wrench as analogy for effectiveness of TAMIFLU? Oh snort
> Steve. Now you're dead on.
>
> Each about as useful as a tit on a boar.


Depends. If you have a 25 mm bolt you really need out, the correct
wrench is very useful. Otherwise, not.  It's really very much the same
with drugs.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 18:11:28 -0800
Message-ID: <1130983888.719630.268680@f14g2000cwb.googlegroups.com>

fresh~horses wrote:
> Right. But to know what size socket wrench will remove your 25mm bolt
> you don't just stand back and throw socket wrenches at it until you
> find the one that fits.

Actually, that's close to what usually happens. It never says on the
bolt, and it's usually down there in a greasy hole. You try the socket
you *guess* will fit, and if it's too large or two small, you get it
the next time.

Either that, or (here in the US) you realize it's a metric/English
problem, and then you curse and get the other set.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 22:56:29 -0800
Message-ID: <1131000989.389209.67070@z14g2000cwz.googlegroups.com>

fresh~horses wrote:
> Steve Harris wrote:
> > fresh~horses wrote:
> > > Right. But to know what size socket wrench will remove your 25mm bolt
> > > you don't just stand back and throw socket wrenches at it until you
> > > find the one that fits.
> >
> > Actually, that's close to what usually happens. It never says on the
> > bolt, and it's usually down there in a greasy hole. You try the socket
> > you *guess* will fit, and if it's too large or two small, you get it
> > the next time.
> >
> > Either that, or (here in the US) you realize it's a metric/English
> > problem, and then you curse and get the other set.
> >
> > SBH
>
>
> Oh. No. Steve. I want experts. Someone who knows a 10 mm socket wrench
> from a 25mm.

No need for that. Anybody can tell a 25 mm drive socket from a 10 mm.
The hard part is telling whether you need a 24, 25, or 26 for a job,
just by looking at the nut. Or whether it's really a 1 inch nut.


>An expert. Remember? As in the Vioxx experts and the
> Baycol experts. My auto expert, and my drug expert, better know which
> socket wrench won't strip the bolt or I'm going somewhere else.


He won't know until he tries them for fit.


> Which brings me to the "We don't know" quote from your WebMd post,
> which said, basically, that first of all the drug really isn't very
> effective (at flu; making money for investors is another issue) AND
> it's going to strip our bolts too. And very likely cause our motors to
> seize:
>
> ~~~~~~~~~~~~~
>
> "The infection causes the body to release a rush {of) chemicals that
> attack the immune system, and there is little evidence showing how well
> Tamiflu can stop or lessen the release..."
>
> ~~~~~~~~~~~~~
>
> That's a pretty damn serious problem don't you think?



No. It's somebody noodling over biochemistry, when we know the outcome
of it all: the drug saves the lives of infected animals. Obviously it
helps the cytokine cascade there, or they'd die.  Whether this
constitutes "little evidence" or not that it will do the same in
humans, considering that the drug obviously does some of this in humans
infected with other flu viruses (or else it wouldn't decrease pneumonia
and bronchitis), is just skepticism for the sake of skepticism. As I
said before, look what the government does, not what it says. They are
buying Tamiflu.

Also, never trust any quote by a journalist. I don't care if they're
writing for "WebMD."  Peer review and multiple layers of
science-professional editing, with physical text change *by the
originator of the quote* (not by whatever some fact-checking doofus may
or may not read to the quotee over the phone, and may or may not chance
as a result), and finally covered by a written and signed letter to the
journal by the quotee, protects scientific journals from misquotation.
Newpapers and most news magazines (pubished on the web or not) haven't
got the least idea about any of this. It's as foreign to them as the
calculus of variations.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 2 Nov 2005 23:19:25 -0800
Message-ID: <1131002365.832661.46270@g44g2000cwa.googlegroups.com>

notritenoteri wrote:
> SO you are applying the good old ATC rule,  "give it a green and see what
> develops"? THis is part of the medical science armoury?


COMMENT:

Of course it is!  How the hell can you imagine not?  What kind of
simplified and mechanistic universe do you think you inhabit??

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med
Subject: Re: Not one single case
Date: 2 Nov 2005 21:53:16 -0800
Message-ID: <1130997196.401477.163990@g43g2000cwa.googlegroups.com>

Steven Bornfeld wrote:
> 	So, Steve--with all respect...
> 	Why should this be different than the demographic course SARS has
> taken?  That was gonna kill everyone too.  Were we just lucky?
>
> Steve


COMMENT:

Oh, this particular small outbreak we're having now may turn out to be
a SARS-like flash in the pan--- controllable with isolation,
quaranteen, and public health measures.  Most zoonoses are, because the
virus that has made the species jump isn't very comfortable or
infectious.

What makes Avian flu different is that we've had at least two nasty
Avian flu outbreaks which became full epidemics-- the 1918 flu, and
also the 1997 Hong Kong flu, which was a H5N1 virus like the one
killing people now. Both these epidemics were far worse than SARS. If
we've had two, it's only a matter of time till #3.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 3 Nov 2005 13:06:35 -0800
Message-ID: <1131051995.260800.150740@o13g2000cwo.googlegroups.com>

fresh~horses wrote:
> Skeptic wrote:
> > "notritenoteri" <coldasfire@hades.com> wrote in message
> > news:BUgaf.1638$XR4.5120@newscontent-01.sprint.ca...
> > > So what evidence is in existance that Tamiflu is effective against the
> > > suspected but as yet undefined bird flu? could the answer be "we don't
> > > know"?
> >
>
>
>
> > Are you saying that it is not effective or that we need more information?
> > Based on available literature and an understanding of its mechanism of
> > action, it seems there would be no reason it would not have clinical
> > utility.
>
>
> There's a limit to the number of qualifiers you can have in a sentence
> and expect credibility.
>
> Tamiflu efficacay is a couple hours, in a study covering a
> cherry-picked population for a four weeks; about half the average flu
> course. Read BMJ up-thread.


Read the entire literature, not some abstract of a bad BMJ review
(remind to tell you what I think of the politics of the BMJ). Tamiflu
reduces illness time by 3 to 5 days, and reduces pneumonia in children
(a high risk group). It cuts mortality in avian flu infected mice in
half. From this, you are required to *make an inference.* Yes, perform
logical induction, like a human being. Yes, I know some people aren't
up to it. Perhaps including the "cost efficacy" skeptics writing for
the BMJ. Not my problem. I can lead you to water. Socialists will have
to decide when it's okay for the public "as a whole," to drink.  Sheep
that they are. That probably won't happen for quite a while, and after
a lot of people have died. That's the way of it with herd animals.



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 3 Nov 2005 20:01:34 -0800
Message-ID: <1131076894.721992.248240@f14g2000cwb.googlegroups.com>

notritenoteri wrote:
> Yah yah. So your trying to say what works for mice is absolutely 1000%
> transferable to people.


COMMENT:

That rather depends on the drug. Antimicrobials which work in animal
models transfer very well to people, since they aren't really working
on the animal at all, but the microbe (which is often the same). In
this case, it is.

Occasionally a successful antiomicrobial in animals will get nixed in
people due to some special toxicity problem of the drug in people. But
Tamiflu's already been though human trials.

Nothing in life's 100%.  But then that's true even of drugs what DO
work in people. Skeptics always then ask "Yes, but where's the proof
they work in my sex? Or my age group?  Or my ethnic group?  Or my
knitting circle?  What the proof they work in people with my particular
genetics (ie, myself and my twin). Or just me, if I don't have a
twin...."

Because there no formal proof of any inductive propostion (rather, just
more and more evidence for it), you can deny there exists proof all you
like for any one of them, and not technically be wrong.  But you will
also likely wind up dead.

Besides, it's dishonest. Few people go about refusing to eat new foods
unless they have prior proof they won't be deathly allergic to them.
Life is about taking reasonable chances.

-- Hume

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,talk.politics.medicine,can.politics
Subject: Re: rumsfield's growing stake in TAMIFLU
Date: 3 Nov 2005 20:26:30 -0800
Message-ID: <1131078389.966405.115000@z14g2000cwz.googlegroups.com>

fresh~horses wrote:
> Here you go Dr. Skeptic:
>
>
> ttp://bmj.bmjjournals.com/cgi/content/full/331/7524/1041?ehom
>
> "I would like to know what evidence there is that Tamiflu actually
> alters mortality," {Joe Collier, professor of medicines policy at St
> George's Hospital Medical School, London, and former editor of the Drug
> and Therapeutics Bulletin} said.
>
> "And if it doesn't then what are we doing? What it certainly does is
> shorten the illness by a day, but the question is-does that matter?"


Talking here about ordinary flu strains.  Not talking about a killer
strain. And not talking about prophylaxis, since obvious a flu case
prevented, is a flu case which won't have a chance to kill you. Limited
drug is available for this purpose, but one group there is enough for
is paramedics, hospital workers, and other people who will have to deal
directly with people who have the flu, in an epidemic.

Tamiflu does matter in animals infected with the killer strain. If it
didn't matter in humans infected with the same killer strain, it would
be a remarkable thing indeed, given how the drug works. We've been over
this.

> On the other side of the Atlantic Canada's federal health minister,
> Ujjal Dosanjh, told listeners to an interview on a Canadian
> Broadcasting Corporation radio programme ("The Current," 27 Oct) that
> oseltamivir did not prevent infection with the flu virus....


It certainly prevents the clinical disease, if used before infection.

> The full article on TAMIFLU in BMJ:
> http://bmj.bmjjournals.com/cgi/content/full/326/7401/1235
>
> "The results of our systematic review show that treating otherwise
> healthy adults and children with zanamivir and oseltamivir reduces the
> duration of symptoms in the intention to treat population by between
> 0.4 and 1.0 days and provides 29% to 43% relative reduction in the odds
> of complications requiring  antibiotics when these are given within 48
> hours of onset of symptoms. The results were less conclusive in the
> high risk population (as defined in the methods) though these were
> based on fewer patients. Caution is required when comparing the results
> because the definition of symptoms assessed for alleviation in the
> treatment trials varied among trials of the two compounds,  and between
> adults and children for each compound. Moreover, the time to event
> outcomes were measured on different scales (days and hours). Also, the
> rates of flu positive (=49%) individuals who were enrolled in the
> trials may be higher than the rates identified routinely in clinical
> practice. Thus, the  treatment effects estimated for the ITT trial
> populations may not be achievable in routine practice.
>
> The data on complications reported above were not ideal because they
> relied primarily on pooled marginal analyses and thus did not take into
> account any heterogeneity between trials.19 20 It is not clear how well
> complications requiring antibiotics correlate with the incidence of
> more serious complications of flu.


COMMENT:

It may not be "clear." but it's a good assumption there's a high
correlation, since secondary bacterial infection (including bacterial
pneumonia) is a major cause of flu-related mortality.

The kind of medical skepticism you see here falls into the category of
"bloody minded." Following this logic, we should considering
withholding antibacterials from flu victims with secondary bacterial
pneumonia, as well. For while these have been proven to decrease
mortality in primary pneumonia, nobody has ever proven them to decrease
mortality in secondary bacterial pneumonia FROM THE FLU. Same exact
argument, QED.

But methinks the writer would be shocked at that suggestion, because he
takes as given that these things are "required."  Basically,  he's just
a reactionary, trying to figure out ways to keep from using a new and
expensive drug.  It was the same when antibiotics themselves came out.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,can.politics,sci.med.pharmacy
Subject: Ribavirin and Avian Flu (Re: TAMIFLU effectiveness questioned: 
	shortens illness one day
Date: 5 Nov 2005 18:07:11 -0800
Message-ID: <1131242831.549577.70550@o13g2000cwo.googlegroups.com>

fresh~horses wrote:
> http://bmj.bmjjournals.com/cgi/content/full/331/7524/1041?ehom
>
> "I would like to know what evidence there is that Tamiflu actually
> alters mortality," {Joe Collier, professor of medicines policy at St
> George's Hospital Medical School, London, and former editor of the Drug
> and Therapeutics Bulletin} said.
>
> "And if it doesn't then what are we doing? What it certainly does is
> shorten the illness by a day, but the question is-does that matter?"
>
> On the other side of the Atlantic Canada's federal health minister,
> Ujjal Dosanjh, told listeners to an interview on a Canadian
> Broadcasting Corporation radio programme ("The Current," 27 Oct) that
> oseltamivir did not prevent infection with the flu virus and that at
> best it would reduce the severity of the illness.
>
> `````````````````````````````
>
> The full article on TAMIFLU in BMJ:
> http://bmj.bmjjournals.com/cgi/content/full/326/7401/1235
>
> "The results of our systematic review show that treating otherwise
> healthy adults and children with zanamivir and oseltamivir reduces the
> duration of symptoms in the intention to treat population by between
> 0.4 and 1.0 days and provides 29% to 43% relative reduction in the odds
> of complications requiring  antibiotics when these are given within 48
> hours of onset of symptoms. The results were less conclusive in the
> high risk population (as defined in the methods) though these were
> based on fewer patients. Caution is required when comparing the results
> because the definition of symptoms assessed for alleviation in the
> treatment trials varied among trials of the two compounds,  and between
> adults and children for each compound. Moreover, the time to event
> outcomes were measured on different scales (days and hours). Also, the
> rates of flu positive (=49%) individuals who were enrolled in the
> trials may be higher than the rates identified routinely in clinical
> practice. Thus, the  treatment effects estimated for the ITT trial
> populations may not be achievable in routine practice.
>
> The data on complications reported above were not ideal because they
> relied primarily on pooled marginal analyses and thus did not take into
> account any heterogeneity between trials.19 20 It is not clear how well
> complications requiring antibiotics correlate with the incidence of
> more serious complications of flu. Little evidence exists either on
> serious complications requiring admission to hospital or causing death
> or on adverse events. Both of these are evidently rare (at least in
> otherwise healthy individuals) but are potentially important in the
> evaluation of treatments; the trials were underpowered in terms of such
> outcomes. Insufficient data are available from clinical trials to
> assess adequately the risk of emergence of resistance to neuraminidase
> inhibitors.
>
> A lack of evidence exists for use of neuraminidase inhibitors for
> preventing flu in children and in frail elderly people in residential
> care. We found that neuraminidase inhibitors given for flu prevention
> led to a relative reduction of 70% to 90% in the odds of developing
> flu, depending on the strategy adopted and the population studied.
>
> In conclusion, although evidence from randomised controlled trials
> consistently supports the clinical effectiveness of both oseltamivir
> and zanamivir for the treatment and prevention of flu, evidence is
> limited for the treatment of high risk populations and for all
> prevention strategies. Research is needed into the comparative
> effectiveness of neuraminidase inhibitors with one another and the
> potential "added value" of these drugs compared with or in combination
> with flu vaccine."


COMMENT:

Here, for the record, is the NEJM / WHO review--- everything you wanted
to know about bird flu. The New England Journal, BTW, thinks use of
Tamiflu and Relenza is entirely reasonable as treatment in humans.

http://content.nejm.org/cgi/content/full/353/13/1374

The NEJM also mentions ribavirin, a nucleoside antiviral presently used
for hepatitis C and RSV virus in children. Ribavirin was invented at
ICN in the early 1970's and its patents as an antiviral have long since
expired.  Early on it was discovered that ribavirin protects mice from
influenza death, but ICN could not get the FDA to approve it for this
use in humans. ICN had jumped the gun and misbranded the drug for use
in both RSV and flu, and the rumor is the FDA "punished" the company by
refusing to approve it for flu use, EVER, until the patent ran out.
Ostensibly the FDA simply chose to believe human studies finding the
drug had NO effect in humans, but not studies showing it did. And yet
the drug is as active against influenza in culture as it is against
RSV, a virus it's approved for (in inhaled form).

The ribavirin fight has had many twists and turns. When ICN (through
Schering Plough) wanted to market ribavirin capsules in the US, as part
of a combo treatment for hepatitis C, there was a problem. The FDA knew
that once the capsules had been approved for ONE use, they could be
used for any other (like flu). So it allowed Schering to get around the
long expired oral ribavirin patent by marketing the combo treatment
with interferon-- nothing anybody with flu would be able to afford.
People who wanted ribavirin capsules have had to purchase it as ICN's
"ribavirina" (trade name Vilona) in Mexico, and import it. A difficult
process.

The fact that ribavirin had long been off patent, but was still being
controled by Schering in the US, led to patent fights between ICN,
Schering, and various generic companies who wanted to make generic
ribavirin. One of those fights was won by Three Rivers Pharmaceuticals
in 2003 (http://www.hivandhepatitis.com/hep_c/news/071803a.html), but
the FDA has dragged on approving generic ribavirin until last month.
"Ribasphere" the generic ribavirin capsule will finally be marketted by
Par Pharmaceuticals, which licenses it from Three Rivers:

http://biz.yahoo.com/prnews/051024/clm015.html?.v=25

http://www.drugs.com/ribasphere.html


Indication will only be for treating hepatitis C, but once released,
the drug can be used for anything, including influenza.

It may be no coincidence that the FDA has finally acted on this matter
now, with bird flu starting us in the face. Ribavirin is considerably
easier to produce than is oseltamivir (Tamiflu), and many generic
companies will have no difficulty with it.  It adds one more badly
needed weapon to the armamentium against avian flu, which is already
usually resistant to the amatidine-class drugs, and has even been
reported in a strain resistant to Tamiflu.

Steve Harris



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: misc.health.alternative,misc.kids,misc.kids.health,sci.med,
	sci.med.nursing
Subject: Re: Bird flu hype
Date: 5 Nov 2005 18:34:11 -0800
Message-ID: <1131244451.328921.162510@o13g2000cwo.googlegroups.com>

Ra♥ïⁿg L♂♀♫iε wrote:
> Avian flu has been around for a very long time. ... It has crossed over
> many times.
>   Aside from us NOW being sensitized to 'bird flu', specifically ...
>       ... What has changed?


COMMENT:

What has changed is we found out very recently from full analysis and
reconstruction of the live virus, that the great killer flu of 1918,
the worst flu infectious epidemic in history (20 to 40 million dead
globally in one year) and the worst epidemic of all time after the
black plague, was a bird flu.

Previously (before resuscitation this year) the 1918 bug had been known
to be an H1N1 type, and on that basis, was thought to be a human flu.
But now that we have reconstructed it into infectivity (in ultra
quarantine) and can study all its features, we know it was Avian, and
had little human component in it (it had made the jump directly without
going through pigs).

So things have gotten a lot scarier since then.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,sci.med.nutrition,misc.health.alternative
Subject: Re: Americans were lining up for vaccines: the flu virus simply 
	disappeared
Date: 28 Nov 2005 20:53:15 -0800
Message-ID: <1133239995.418582.227920@o13g2000cwo.googlegroups.com>

fresh~horses wrote:
> Wall Street Journal
>
> November 28, 2005
> DEJA VU
> By CYNTHIA CROSSEN
>
> Political Action, Folly Greeted the Outbreak Of Swine Flu in 1976
>
> November 28, 2005; Page B1
>
> It looked like the flu pandemic the world had been dreading for 50
> years: A virus, seen only in animals for several decades, had made the
> leap to humans and, more ominously, had passed from person to person.
> Yet for the first time in history, scientific knowledge and government
> funding might be able to stop the flu in its tracks, saving a million
> lives at risk. Within months, Americans were lining up to be vaccinated
> against the virus. Then, in another triumph of nature's
> unpredictability over human planning, the flu virus simply disappeared.
>
> Incubated in pigs but not seen in humans since the 1920s, swine flu
> broke out in February 1976 at an Army base in New Jersey. The medical
> community quickly became alarmed. The swine-flu virus was incurable,
> potentially lethal, and very few people had natural immunity to it.
> Although scientists couldn't pin a number on the probability of a major
> swine-flu outbreak, all agreed it was greater than zero. As David
> Sencer, then director of the Centers for Disease Control, said, "If we
> believe in preventive medicine, we have no choice" but to try to
> immunize the entire country.
>
> However noble the sentiment, the National Swine Flu Immunization
> Program, announced by President Gerald Ford just a month after the
> virus had been identified, became a public-health debacle that probably
> cost more lives than it saved. It also illustrated the massive
> logistical hurdles involved in trying to produce, test and deliver a
> vaccine to millions of people of all ages, classes and medical
> conditions.


COMMENT:

Sigh. Another story told in breathless "you are there in history," told
by a bunch of journalists who either don't have the later facts, or
chose not to bother with them, because it made a better "establishment
screws up" story. Journalists love to write such stories because
journalists are forever pissed off that they're not running things.
Generally, they think they're smart enough that they should be. If only
they knew enough....

Yes, in 1976 it looked like the swine flu was some terrible pandemic
that might be a repeat of 1918. But since then, we've come to
understand flu a lot better. What we've found out since is that it is
bird and not pig flus that are the most dangerous to humans. In short:

1) Most new significant yearly new epidemic flus ARE "swine flus," in
the sense that they've been incubated in pigs and passed to humans, and
that's where "new" and very pathogenic flu strains come from. They
don't come from Mars. In pigs, influenza picks up genes from bird flus
(which pigs also easily get), and the new recombinant virus has new
genes from waterfowl influenza and pigs. Pigs are thus the normal
intermediate vector between humans and the true mother of all influenza
gene reservoirs--- which is migratory ducks. However, usually only
parts of the bird virus is passed to humans in this way, because the
bird influenzas have trouble infecting people directly, and when they
do, aren't (usually) passed from person to person (The great 1918 flu
being an exception). Pigs have receptors to both bird and human flu
viruses, though, so they get both kinds of flus. Through pigs, humans
pick up new bird flu genes. These genes "hide out" in birds, being
passed to humans about once a generation, as a few crop of
non-resistant humans is born.

2) The great 1918-19 flu was thought (mistakenly) in 1976 to be a
"swine" flu because it was an H1N1 virus, which is the most common type
of flu virus in pigs (at least in the US).  In 2005 we finally have the
whole 1918 virus and know it wasn't a swine-type virus, but entirely
(or almost entirely) an avian virus, with a few swine-flu like
mutations and antigens allowing it to infect AND be contagious in
humans. We know know that whole bird flus are the big "pandemic"
danger, and swine flus are merely the "normal" background epidemic flu
danger.

3) Swine and humans share flu viruses all the time, and the result
isn't usually pandemic, though it does cause many yearly deaths. Since
1977 a swine-type H1N1 virus has been circulating in humans most places
on the globe every year, and there was a "swine flu" type H1N1 virus
strain included in the flu shot for the US this year and last year. The
great ramping up of the vaccine industry to produce large (millions of
doses) of a swine-type virus has happened many times since 1977. It's
not new! In fact it's now the NORM. Most years recently the flu shot
has had a two A strains: an H1N1 "swine-like" stain and an H3N2
"human-like" strain. Note that the H3N2 caused the "Hong Kong" 1968
outbreak, following which there were worldwide problems from humans
passing it to swine. This was a case of a new virus which was a bad one
for both pigs and people.

4) Yes, a new H1N1 swine flu showed up in Fort Dix in 1976, but it's
not true, as the article says that swine flus hadn't been seen since
the 1920s. H1N1 viruses were the main human yearly flus up until the
"Asian flu" (H2N2) outbreak of 1957. It was the 23 year gap between
1954 and 1977 that made the "Russian Flu" of that year so scary,
because the Russian flu was also an H1N1 type swine flu. But only
people younger than 23 got it, so it never become a big deal. Had swine
flus been a new thing not seen since the 1920's, the Russian flu of
1977 would have been a far bigger problem, because everyone under 50
would not have been immune, instead of just everyone under 23.

5) There was something still not understood about the H1N1 New Jersey
swine strain that was made the basis of the vaccine that year (1976-7)
which caused a larger number of Guillain-Barre syndrome that year.
Whatever it was, it was difficult to tease out, because the normal
baseline Guillain-Barre incidence is a few hundred cases per year (in
non vaccinated people), which was about the same number of additional
cases the vaccine probably caused in 1977. If you want a taste of the
difficulty of the problem I suggest:

http://www.hsph.harvard.edu/Organizations/DDIL/swineflu.html

In any case, we haven't seen anything like this since, even though as
noted, a number of "swine flu" type strains have been made into
vaccines, and increased incidence of Guillain-Barre has been looked
for. There's no reason to think that any particular short cuts in that
year led to the problems. Nothing particular was done in 1976 that
hasn't been done many times since, without problem. Including (as
noted) this year and last year. The only think different is the New
Jersey/Fort Dix flu strain, which (for obvious reasons) hasn't been
used as the basis of a vaccine since.

6) 1976 was notable for having a virus strain which wasn't as bad as
expected, and a vaccine made from it which had problems. However, the
vaccine was worse than the disease perhaps for the first and only time,
that year. We know that in an average year the flu leads to 36,000
deaths at year, mostly in the elderly. The 500 or so cases of
Guillain-Barre caused by the 1976 vaccine led to about 25 deaths. The
flu, even in in non-pandemic years, kills 1000 times more people in the
US than the "swine flu" vaccine of 1976.  Did this particular virus
"disappear?"  Well, the particular strain never made it out of the Ft.
Dix area where it probably hopped from swine to humans. But if not for
the mass-vaccination campaign, it might have. How bad would it have
been, if it had?  We'll never know. In any case, while this strain is no
longer with us in humans, many similar strains are.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,sci.med.nutrition,misc.health.alternative
Subject: Re: Americans were lining up for vaccines: the flu virus simply 
	disappeared
Date: 29 Nov 2005 12:21:20 -0800
Message-ID: <1133295680.580723.284550@z14g2000cwz.googlegroups.com>

Del Cecchi wrote:
> Would you address then why the "swine flu" of 1976 led to such a major
> panic and public health effort, if the virus itself was no big deal?
> Did the feds lie to us?  Did CDC lie to us?  Or is there more to the
> story than your narrative suggests?


Never ascribe to malice and deceit what can more easily be explained as
simple ignorance and/or stupidity.

No, it was more a matter of an imcomplete knowledge in 1976 of how the
flu "works".  We knew then that zoonoses (animal infections that pass
to humans) are particularly nasty--- when a virus jumps species, it
takes a while to adapt, and in the interim it's very deadly (which is
bad for both host AND virus). In 1976 it wasn't recognized that
pig->human flu transmission is very common, and that's the normal
source of "new" flu bugs. Which is why most of them seem to come out of
Asia where pigs wallow in rice paddies where they catch duck viruses.

The swine flu of 1976 also faked some people out by appearing in young
healthy soldiers at Ft. Dix, and killing one of them. Also, as noted,
in 1976, it was thought the 1918 bug was a swine flu because it hadn't
at that time been fully "resurrected" and studied. So some people in
1976 thought that maybe the 1918 pattern (unusual virulence in young
healthy soldiers) was being repeated.

Today we've brought the 1918 bug back, and know it's really an avian
flu that probably hadn't ever passed through pigs. So we know it's
*those* bugs that are really the dangerous ones.

In 1976 I don't think there was a full appreciation that the big flu
virus reservoir is wild migratory birds, which get all the kinds of flu
bugs that humans do, plus many, many more. All the flu genes that
exist, are in waterfowl. They just sit there in one giant mobile pool,
trying to get out. The way they normally do that is by mixing with
swine flu in pigs, then passing to humans, in parts (since they have a
hard time infecting humans directly, and when they do, have a hard time
jumping person to person). We know now that the truly deadly flus, like
the 1918 bug, are those that make the jump from birds directly to
humans AND manage to mutate enough then for human-human transmission.
Swine flus are business as usual.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,sci.med.nutrition,misc.health.alternative
Subject: Re: Americans were lining up for vaccines: the flu virus simply 
	disappeared
Date: 30 Nov 2005 20:04:06 -0800
Message-ID: <1133409845.966798.205550@g49g2000cwa.googlegroups.com>

Pizza Girl wrote:
> Funny how it is always the young, healthy, physical,
> soldiers that seem to die from these viruses.
>
> I wonder how many vaccines they receive to get
> enlisted?


In 1918?  Maybe typhus vaccine, but not until they went overseas. The
flu killed them everywhere.  It also killed young adults
preferrentially in cities--- most of whom of course in 1918 hadn't had
any vaccines of any kind.

Bird flu kills partly because of an overtuned host immune response
(inflammatory response). That's worse in the young and healthy. This is
not typical of influenza, but it is typical of bird flus when
transmitted directly to people. They also kill mice in the same
fashion-- an overwhelming lung autoimmune response causes drowing.
Vaccines have nothing to do with it.

SBH



From: Steve Harris <sbharris@ix.netcom.com>
Newsgroups: sci.med,sci.med.nutrition,misc.health.alternative
Subject: Re: Americans were lining up for vaccines: the flu virus simply 
	disappeared
Date: 1 Dec 2005 14:19:44 -0800
Message-ID: <1133475584.400971.68450@g44g2000cwa.googlegroups.com>

(PeteCresswell) wrote:
> Per bae@cs.toronto.no-uce.edu:
> >As for why young soldiers in training sometimes die of these diseases
> >that might otherwise just give them a week or two of feeling miserable,
> >there are social and psychological factors involved.  We occasionally
> >hear of young healthy soldiers dropping dead of dehydration, heat
> >stroke, or even exhaustion.
>
> when I was in Basic Training, we had three guys die for no apparent
> reason at all - although I'd venture that doing hand-clap pushups in
> 100+ degree temps and who-knows-how-high humidity might have had a teeny
> little role.
> 
> Also, when people were sick, the treatment wasn't all that wonderful.
> One guy, reputed to have jaundice (hot, feverish, noticeably yellow)
> wound up getting thrown down a flight of stairs by the so-called medics
> because he couldn't get out of bed and they sure as hell weren't " gonna
> carry your malingering ass down them stairs....".


COMMENT:


There are many stupidities associated with the training in military
basic training, not least of which is failing to account for the fact
that men start out in very different states of aerobic fitness, and
there's no point at all in driving every person past their training
limit. It's simply not true that the harder any given person trains,
the faster they progress. For every person there's a well-understood
limit, which any exercise physiologist can approximately define for you
in terms of heart rate, acidosis, and maximal oxygen consumption.

That being said, it's impossible to eliminate sudden death and heat
stroke in all situations in which groups of people are training hard.
Sudden deaths in spring-training camps in professional sports are
well-known, and they're not all drug-related, even though we all like
to find a villain.

THAT being said, the 1918 flu virus deaths spread very well in military
camps due to the close communal sleeping conditions, BUT they continued
to have a predilection for young adults after moving to the cities, and
the "Spanish Flu" killed young women about as easily as young men. You
don't have to be Albert Einstein to see that this pretty much
eliminates any condition associated with military-training, or physical
training stress, as a contributing cause to the odd epidemiology of
this epidemic .

The idea that the ordinary flu can be deadly in a young man training
very hard, whereas the same person would do fine otherwise, sounds
reasonable on the face of it. Except I know of no evidence for it, and
it stands as a simple assertion without factual basis. The doctors
doing the autopsies of these flu victims weren't stupid. The avian flu
fills up the lungs with a rapid autoimmune exudative fluid and you
drown. It doesn't look at all like heat stroke or whatever it is that
kills training recruits. Nor is there any particular reason why hard
physical training should make people have an exaggerated immune
reaction to a virus in the lungs. If anything, the opposite should be
the case.

The behavior of the 1918 flu in the cities once it left the military
bases, confirms this idea.

SBH


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