Q20 - In a recent study of stroke patients

[ManhattanPrepLSAT1]

This is a fun one, thanks!

The argument concludes that glutamate leaking from damaged or oxygen-starved nerve cells is a cause of long-term damage resulting from strokes. Whoa! That's a mouthful. And so specific everywhere! In fact too specific. The argument shows how glutamate could cause long-term damage, but there could be glutamate present for many other reasons than the argument concluded.

Perhaps the glutamate came from somewhere other than leaking out of damaged or oxygen-starved nerve cells. If that were the case, the argument's conclusion would definitely be undermined. Answer choice (D) defends the argument from this dangerous possibility.

Incorrect Answers
(A) supports a premise, rather than the argument.
(B) weakens the argument by providing a potential alternative cause.
(C) is too weak. Those other neurotransmitters haven't been linked, as has glutamate, to nerve cell damage.
(E) is out of scope. Whether those damaged, leaking cells survive is irrelevant. The leaked glutamate will still kill surrounding nerve cells.

#officialexplanation

[crocca]

I originally got this question wrong, but then correctly answered it upon blind review. I was only able to get to the correct answer by POE and am still unsure why D is correct. If someone could explain the argument and why D strengthens it, it would be greatly appreciated.

Thank you in advance!!

[bswise2]

D is correct for the following reasons.

The only empirical evidence that the argument offers to link glutamate to the deterioration of the stroke patients' cells after the stroke is the high level of glutamate in their blood. We are not told where this glutamate necessarily comes from. All we are told is a theory regarding how this could make sense, in light of the fact that glutamate has the potential to kill nerve cells if leaked from damaged or oxygen-starved nerve cells. That is not much to go on considering there is no guarantee that this high level of glutamate in their blood even came from these cells.

One thing to note is that the conclusion is very specific--"glutamate leaking from damaged or oxygen-starved nerve cells is the cause of long-term brain damage resulting from strokes." Not "glutamate from the new medication the patient was put on" or "glutamate from an increase in brain activity", etc. The conclusion is very specific about where the glutamate came from. But this specificity is not warranted, considering there could be numerous causes of this high level of glutamate.

What if the high level of glutamate came from the new diet they were put on after their stroke or the medication they were given? That would destroy the entire argument. D eliminates any other potential source of glutamate, forcing us to recognize these damaged cells as the source of glutamate, thus allowing us to strengthen the causal relationship asserted by the conclusion.

[andrewgong01]

I wanted to add my thoughts as I think i understand this now finally,

I understand "D" now; didn't pay attention to the context in the first sentence and the conclusion was specific on where the glutamate is leaking from ( i thought it just meant glutamate - regardless of its source- causes the damage)

C seemed attractive because in other LR questions with corr/cause you tend to want to eliminate other causes and "C" does eliminate every other neustransmitter but it does not go far enough since "C" is only about leaks from damaged nerve cells but in stroke patients are there other ways for higher levels of neurotransmitter ( including Glutamate) - that seems to be what "D" is saying

[MingL143]

I have difficulty in choosing between C and D.

This is a causation argument,
The premise is " Stroke people has high level of G, and G can kill surrounding nerve cells if it leaks from damaged or oxygen-starved nerve cells."
The conclusion: "G is a cause of long term brain damage resulting from strokes."

The thinking process should be two-pronged prephrase. The answer choices seem fall into the category of objection to "other ways to explain".

C rules out other possible neurotransmitter that might kill surrounding nerve cells

D, rules out G presents in the blood in cells other than damaged or oxygen-starved nerve cells.

What's the take away of this question?

[ohthatpatrick]

This is indeed a Causal Argument: the author presents a curious fact and then concludes some causal interpretation of what happened.

CURIOUS FACT:
Why did the stroke patients whose nerve cells got worse even after the stroke also have the highest levels of glutamate in their blood?

AUTHOR'S CAUSAL INTERPRETATION:
Glutamate was causing the nerve cells to get worse (glutamate is a cause of long-term brain damage)

What's the author's evidence for this interpretation?

If glutamate leaks from damaged or oxygen-starved nerve cells, it can kill surrounding nerve cells.


Our two pronged prephrase for causal arguments:
1. Is there some OTHER WAY to explain the curious fact?
2. How plausible is the AUTHOR'S WAY of explaining it?

When we're strengthening, we'd either want to rule out some other way to explain the curious fact, or we'd want to bolster the AUTHOR'S WAY of explaining it

If we ask ourselves whether there is some other way to explain why the patients with continuing nerve cell damage were also the patients with the highest levels of glutamate, we can consider the usual suspects:

REVERSE CAUSALITY? Instead of the high glutamate leading to deteriorating nerve cells, maybe deteriorating nerve cells led to high glutamate. We'd like an answer that said "when nerve cells deteriorate, they do NOT emit glutamate"

THIRD FACTOR? Maybe there's some other factor that causes people to have high glutamate in their blood stream that ALSO causes people to have longer than average damage from strokes. Say, for example, that drinking lots of white wine causes high glutamate in the blood and causes nerve cells to be especially punished by strokes. Maybe the stroke patients with the long lasting nerve damage were just heavy white wine drinkers, and that's why they also had lots of glutamate in their blood. We'd like any answer ruling out that sort of story.

The most typical answer for boosting plausibility of the author's story is a covariance "control group" answer: we'd like an answer that said "when the glutamate went back to normal levels, the nerve cell deterioration stopped".

(C) does seem to rule out the possibility that the long-term nerve cell damage was caused by any other neurotransmitter that leaked out (although it's not like we KNOW that a neurotransmitter is causing the damage, so ruling out the possibility of some other neurotransmitter causing the damage isn't especially crucial)

(D) rules out the possibility that glutamate is high in the blood for some other reason. (i.e. there's no third factor, like the white wine example, that could cause glutamate). Conditionally, this says "If you see glutamate in the blood, then it leaked from damaged or oxygen-starved nerve cells". We could chain this new idea to the conditional we saw in the argument:

gluta in blood -> leaked from damaged nerve cells -> kills surrounding cells

Since we found glutamate in the blood of these patients, we know from this chain that the glutamate could be killing surrounding nerve cells.

This ends up ruling out other sources of glutamate and triggering a conditional chain that greatly increases the plausibility of the author's story.

Ultimately, I think the takeaway for this problem is more about the conditional logic premise than the causal argument template.

Strengthen and Weaken very rarely use conditional logic. But if we see some, it's important. We know that gluta can kill nerve cells IF it leaks from damaged cells.

Okay, but do we know for these stroke patients that the gluta in their blood leaked from damaged cells?

We do not. So choice (D) triggers that conditional, which allows the author to say that "gluta was killing surrounding cells".

To see another example of a Strengthen question in which the correct answer essentially functions by "activating a conditional" that the author assumes is being triggered, check out this one:
https://www.manhattanprep.com/lsat/foru ... -t678.html

[abrenza123]

For a covariance group such as "when glutamate levels went down to normal, nerve cell deterioration stopped," couldn't that still imply that a third factor was associated with both higher glutamate levels and nerve cell deterioration, and it was actually the third factor that was eliminated?? Or is the point that even though it doesn't guarantee the casual relationship, it strengthens the possibility that the casual relationship is there??

[ohthatpatrick]

You nailed it with that last thought.

Causality is forever a very fuzzy world. We really could never PROVE one thing caused another unless there were some way to rule out all other possible causes and establish that this remaining thing was a possible cause.

So LSAT is mainly mad at their causal authors for being too sure of themselves in the conclusion.

Correlations DO strengthen the notion of causality. They never prove it, but they're not value-less.

If we had a correlation like,
"When glutamate levels went down to normal, the nerve cell deterioration stopped"

then LSAT would consider this a valid conclusion:
"Thus, there is some reason to think that glutamate causes nerve cell deterioration"

but would not consider this a valid conclusion:
"Thus, glutamate clearly causes nerve cell deterioration"

Hope this helps.

[StratosM31]

Wondering why nobody found (E) tempting...

If we negate it (nerve cells can't suffer enough damage to leak glutamate before being destroyed themselves), it basically rules out the possibility that the nerve cells leak glutamate before they are destroyed themselves.

Can we assume that nerve cells can leak glutamate even after being destroyed themselves?

There is also another issue: why can't (E) be treated as ruling out an alternative cause (=nerve cells destroy themselves instead of being destroyed by glutamate)?

Edit: to answer my own question, I finally accepted to live with the fact that (D) is strengthening the argument in a way more obvious way than (E) does (and the questioon asks what MOST strengthens the argument).

I can't think of any plausible reasons to still cast doubt on the argument if (D) is true, whereas I can do it in case (E) is true:

- Who says that nerve cells can't leak glutamate AFTER being destroyed?
- Even if they couldn't: according to the stimulus, not only damaged, but also OXYGEN-STARVED cells can leak glutamine. So, even if the self-destruction the cells and not the glutamate leaked from the damaged cells appears to be the cause, there is still a possibility that the source of the glutamate leakage are oxygen-starved cells, which still contribute to the destruction of surrounding nerve cells and therefore are indeed a cause of long-term brain damage!

[Laura Damone]

I would argue that "without being destroyed" is a non-issue. Maybe they leak glutamate as they are being destroyed. Or maybe they leak it, which makes their future destruction imminent. As long as damaged or oxygen-starved nerve cells can leak glutamate at some point, this argument is fine. It really doesn't help to establish that they can leak glutamate without being destroyed.

I would also say that E doesn't rule out an alternate cause explicitly enough to be a strengthener. It doesn't imply that maybe nerve cells can continue to deteriorate after the stroke because they are self-destructing, and there isn't any reason to believe this could be the case. We're trying to explain continued nerve deterioration, and "it just keeps happening" isn't really an alternative explanation.

Hope this helps!