"David C. Ullrich" wrote:
>
> On Fri, 15 Jun 2001 15:23:03 +0100, Paul Jones
> <[EMAIL PROTECTED]> wrote:
>
> >"David C. Ullrich" wrote:
> >>
> >> But analyzing it this way simply makes no sense. Those
> >> "trials" you're talking about are _far_ from independent;
> >> each "trial" is associated with a particular person, and
> >> there will be a very strong correlation between various
> >> "trials" for the same person at different hours.
> >
> >Okay then, how should it be analysed?
>
> I've explained at least twice why I do not believe it
> is _possible_ to draw the sort of inference you want
> to draw from the data you've given us. You must
> be reading _some_ of those posts or you wouldn't
> keep replying.
>
Well, although I've agreed with most of your complaints about trying to
derive any information from the scanty data shown, there is *something*
we can notice about the data set which has some relevance.
Let's say we look at a sampling of 100 people who have both had heart
attacks within the last year and have smoked an aspirin an average of
once a week during that year.
Now, without knowing what the average percentage of people who smoke
aspirin each year, and the average percentage of people who have heart
attacks each year without smoking aspirin, these numbers alone would be
pretty useless.
But if 95% of the people in the data set had their 1 heart attack inside
of 1 minute after smoking an aspirin, you'd have some reason to further
examine the hypothesis that, for some segment of the population, smoking
an aspirin could trigger a heart attack. (Of course it could also be
that impending heart attacks bring on the desire to smoke aspirin, or
some other hypothesis that correlates the two phenomena).
One the other hand, one would expect if there were no immediate
correlation between smoking aspirin and heart attacks, the average time
between smoking aspirin and heart attack would be more like 1/2 week.
This would then indicate that it was not particularly worthwhile to
investigate an immediate link between asprinin smoking and heart
attacks.
That seems to be the type of correlation that was reported here - some
distribution of MJ smoking, and its *temporal* correlation with heart
attacks.
Now, that says exactly nothing about whether MJ use increases or
decreases the liklihood of having a heart attack in general (it could in
fact in general *decrease* heart attacks, even in our data set); but
instead would say, there is a segment of the population for whom MJ use
is followed by a high liklihood of a heart attack.
Would those people have had a heart attack anyway? Is this some small
segment of the population that reacts this way? These questions would
still remain without any further figures.
Even in the abscence of this data, though, one might want to take some
precautions during the hour following MJ usage, for those with an
otherwise high liklihood of heart attack, such as: be near medical
facilities, etc.
Cheers - Chas
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