- Could we perhaps agree to disagree as a group, rather than turning this into a mud-slinging match?
- Could those advocating a low-K approach to orchid nutrition in culture consider accumulating more evidence (with the proviso that lots of anecdotes are not the same as evidence)?
- Could those people who are positive this is madness wait for such evidence?
- Could we note that people are free to do whatever they want with their own plants?
And could those of us (like me) who are interested in the outcomes wait for 2) above?
Quote:
Originally Posted by Leafmite
Discus, very nice post. Loved it!
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Thanks
Quote:
Originally Posted by Fabian24
Potassium chloride injections being lethal to humans.
Another laughable statement when used in relation to K uptake in orchids. Even more laughable when one considers that thousands of people with high blood pressure consume lite-salt which generally contains 50% potassium chloride.
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I am pretty sure I pointed out that I was NOT using this example as having any bearing on the current topic of discussion, but rather one of simply tangentially related academic interest.
Since you bring it up (and with the proviso we mutually agree what I am discussing in the remainder of this post has *NOTHING* whatsoever to do with the nutrition of orchids):
Eating a chemical is quite different to injecting a solution of it directly into your heart or circulatory system.
Another thing to consider is that the
amount of low sodium salt a person normally sprinkles on their food doesn't have anything near the dose of potassium used in a lethal injection (something in the region of 8 grams for an adult, I believe, which has to be administered within a fairly short time-period); my quick reading online now suggests that elevating the blood K level >8mEq/l is the lethal level, with the lethal dose being 100mEq, with normal blood K being around 5-10mEq/l (in the case of K, mEq == mmol).
100mEq/mmol of KCl is:
39.098+35.453=74.551 g/mol
-> 74.551 *0.1 = 7.4551g. (because 100mMol = 1/10th of a mole == 0.1). If you say low sodium salt is 50% KCl, that means you would need to rapidly infuse something like 15g of it into your profoundly disliked human. I have stuck some of it on my tongue before and it tastes quite unpleasant compared to "normal" salt. Good luck getting me to eat 15g of it (I was one of those inquisitive kids that would taste things to see what the fuss about. I quickly learnt that artificial sweeteners should be left in peace, and that low Na salt was horrid).
Even if you got that dose there, I am not sure how quickly it would be absorbed into the blood stream; in my reading, it was suggested that the dose would have to be delivered "within 5 hours" if done by IV drip; for lethal injection this is inevitably done quickly. Of course, K+ is a pretty small ion, so it tends to diffuse through tissues relatively easily; the interesting question is how quickly it's absorbed, and how quickly your body's homoeostatic processes might be able to act to sustain the right levels of K. So I looked this up.
It appears the "
lowest lethal dose" by ingestion is around 0.51mmol/kg - (74.551/1000 = 1mmol in weight [g]). Let's assume an adult weight of 80kg - that would mean a lethal dose would be anything
upward of about 40.8mmol - 3.04g (just over 6g of low-Na salt, assuming 50% by molar mass). Of course, this is in medicine where you *don't* want people to die, rather than where you're
actively trying to ensure their death, which I guess goes some way to explaining the discrepancy between the ~8g lethal dose by injection and the need to eat anything over about 3g at a time to possibly die. Either that or inmates on death row are considerably heavier than 80kg. Even then, I don't think many people will find 6g of low-Na salt at a time in any way palatable. It is also the "lowest" lethal dose, suggesting that
likely and
certainly lethal doses lie some way above this. For perhaps obvious reasons, the lethal dose rates of things in humans are not well studied; although obviously not directly applicable, LD50 for rats is around 2600mg/kg and for mice it's 363mg/kg (if we scale it up to our hypothetical 80kg human that's around 29g-208g of K; what's not stated is if this is molar mass of K alone; I suspect so, which means a really huge about of low-K would be required). Remember also that this is LD50, not lowest lethal dose, which goes some way toward explaining the larger magnitude.
This probably also assumes that these people don't then feel a raging thirst come on and drink a huge amount of water as a result and then urinate copiously to flush the K out. It also
appears that we have mechanisms that note the amount of K ingested and do something about it (by regulating uptake by tissues and excretion through kidneys).
One thing that is a little confusing here is that a "normal" western diet contains "approximately 70mmol of K a day"(according to that paper). That is of course over the course of 3 or so meals, so that's about 23mmol per meal - still that's uncomfortably close to the lowest lethal dose - but again, the circumstances around LLD were not explained in the reference I read, and again, that's the lowest lethal dose.
In any case, I think we can agree that sprinkling a bit of low-Na salt on your food is clearly nowhere near the level that might cause a problem in the long term culture of humans.
I would like to point out that I'm not attacking you personally here, but pointing out that 1) my initial point on lethal injection had
nothing to do with plants (and this was noted in the post) and 2) you did make a somewhat specious claim that this was being taken as the case and was being advocated as "for the defense of the low-K hypothesis", which I felt the need to point out, lest this be co-opted into the discussion as a serious point in the long term (which it should not be).
---------- Post added at 12:11 PM ---------- Previous post was at 11:47 AM ----------
Quote:
Originally Posted by ALToronto
This is about as scientific as a home experiment can get, given that I don't want to lose any plants, so I'm not pushing any boundaries.
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Hi ALToronto, thanks for your post.
"Home experiments" can get quite sophisticated. Some points for you to consider quickly considering some basic experimental design questions:
1) how were seedlings allocated to each sample group? Was it truly random?
2) how big is your sample size? (how many plants in each treatment, across how many pots? Which variety where?)
3) which of these is your "control" (or are you actually running two uncontrolled experiments in parallel)?
4) why are you using different pots (this should be uniform across treatments, or you're introducing more variables)? How have they been assigned across the two groups?
5) how will you try and minimise the effects of variables such as light exposure, water amounts, temperature, airflow etc.? A fairly simple system to ensure relatively fair controls on some of these is a so-called "latin square" design of your plant experimental layout. Pots *must* be allocated randomly. With water, it would be sensible to deliver a measured amount to each pot each time.
6) how will you account for your own (possible) bias toward/against one of the treatments? (i.e. can you do something in the trial to make it "double blind" with respect to the treatments, perhaps by getting a 3rd party to create and maintain an A and B stock solution you then use for the tests, without revealing which is which until after it is concluded). Is there something about either treatment that makes this blinding impossible (colour, smell?)?
I hope you find these questions useful.
Thanks again for your willingness to experiment and report on your plants.
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