#21 - Journalist: People whose diets contain a relatively

[AthenaDalton]

Hi mN2,

I think answer choice (A) is actually referring to removing genetics from the equation, not iron.

If we compare two groups of people -- those who are genetically pre-disposed to get Parkinson's disease, and those who do not have this genetic pre-disposition, and find that both groups eat about the same amount of iron, we can start to investigate the effects of iron independently of the effects of genetics.

If the situation were reversed, we would have real difficulty separating the effects of eating iron from pre-existing genetic factors. For example, if people who were already genetically pre-disposed to get this disease also ate three times the amount of iron as the rest of the population, it would be hard to tell whether these people developed the disease because of their genes, or because of their diets.

If, however, everyone in the gene pool eats about the same amount of iron, but the minority who eat really high amounts of iron are far more likely to develop the disease, we have a better case for arguing that the disease is linked to iron intake.

I hope this makes sense. Good luck studying!

Athena

[amacmill]

I'm not sure how this gets rid of an alternate cause. Even if people with a genetic predisposition to develop Parkinson's do eat more iron than the average person, does that really take away from the fact that people who don't have the genetic disposition but have high iron diets could be more at risk to develop the disease than those who have low iron diets?

[AthenaDalton]

Hi amacmill,

You're right that both genes and diet can be independent factors that increase the risk of getting this disease.

However, we're just looking for something that strengthens the journalist's argument that increased iron intake leads to an increased risk of Parkinson's.

If, hypothetically, everyone who developed this disease had both a high-iron diet and a genetic pre-disposition, we would not be able to deduce that increased iron intake was a risk factor. In such a case, it would be impossible to separate the effect of genetics from the effect of iron levels in the diet.

However, if we learn that the group of people who suffer from this disease includes both those with the genetic pre-disposition and those without it, then we can start to look at differences in diets to determine risk factors. Answer choice (A) just tells us that it's possible to isolate one variable from the other.

Best of luck studying!

Athena

[nlittle]

And that's why (A) strengthens.

I won't go through the rest of the answers since I imagine the difficulty here is understanding why (A) is right rather than why B-E are wrong. Tricky concept, but one well-worth knowing.

Good luck

This was very helpful in understanding. I had a tough time recognizing genetic predisposition was an alternative cause as even the mention of it seemed to be an unrecoverable weakening response because in stating that there are some who are genetically predisposed to it seemed to affirm that an alternative cause in fact existed, but I can definitely see how the test makers used it to (likely intentionally) avert me to choosing between the remaining answers (conditions being conducive to a disease does not mean those conditions were the cause, for example, what if "conditions" really just meant a heightened sensitivity to the actual cause, iron, and therefore the genetics themselves are not the cause). The elimination just seemed so subtle and at the same time counter intuitive... very tricky.

I will definitely be looking for these third element answer choices and critiquing whether they are being eliminated as a cause for these types of problems.

I agree that this technically is eliminating an alternate cause, given that genetic predisposition is different from actually having Parkinsons, but found it to be more easily understood in thinking of it as showing that the relationship is not reversed. If A were rephrased to "those more likely to develop Parkinsons are not more likely to consume an iron rich diet as a result" I would have been all over it.

Anyways, thanks for the thorough explanation!

[deck1134]

Perhaps this is splitting hairs, but could we determine that (A) is eliminating a reversal, (that is, ensuring that the relationship isn't reversed, as it were) instead of being an alternate cause?

I'm not sure why I found this to be so hard! Looking back it all seems so simple!

[Adam Tyson]

That's exactly how I would look at it, Deck. Nice job! If having Parkinsons (or at least, having a genetic predisposition to it) caused you to eat a lot of iron, that would hurt the claim that limiting iron intake would reduce the chances of getting the disease, because iron would be an effect rather than a cause. Answer A eliminates that possible reversed cause and effect, because those with the genetic predisposition are NOT eating more iron as a result. Good eye!

[AM4747]

What happens in the correct answer choice in #21 follows the same mechanism. In (A) we're told that people genetically prone to develop Parkinson's don't eat more iron than people without a genetic predisposition. In other words, a genetic predisposition to getting the disease--something that clearly is a cause--isn't related to the high-iron correlation noted in the stimulus, thus making iron, and not genetics, a more likely contributor. We've removed genetics from the equation and, in so doing, made iron's role more prominent. And thus the author's conclusion about iron --> Parkinson's more likely.



Hello, thanks for the response.

I just want to make sure I understood the explanation correctly.

- We have a correlation: people who consume a higher dosage of iron are more likely to develop Parkinson's disease.

- we pre-phrase an alternate cause; in this case genetic predisposition (GP)

- Answer A: "most people who have a GD to Parkinson's have no more iron in their diets than people without the GP".

Precisely, the question I have is how the answer eliminates the alternate cause. The way I understood it as follows: people with genetic predisposition either have equal iron or less iron in their blood than people who do not. The stimulus has already established that people with more iron are more prone to Parkinson's than people with less iron. So by saying that people with GP have less iron in their blood, in effect, we have brought them under the category of people, who according to the stimulus, are less likely to develop Parkinson's. It is this way that we eliminated the alternate cause.

Thanks in advance,
All best

[James Finch]

Hi AM4747,

It helps to think of the stimulus as referencing a study whose methodology is unknown--does the variable group (high iron in diet) also contain other potential confounding variables, such as a higher rate of people with genetic predispositions, or people who exercise less than the doctor-recommended amount, etc? If we can eliminate even one of these potentially confounding variables, then we've strengthened the argument in the stimulus.

The reason (A) works to eliminate an alternate cause is that it eliminates any potential of bias or statistical noise from genetic predisposition in the cause/effect relationship between iron in the diet and Parkinson's disease: if people with a genetic disposition to Parkinson's eat the same amount of iron as people who don't, meaning they aren't over-represented in the diet-high-in-iron group, and that group are still more likely to get Parkinson's, then we can eliminate genetic predisposition as a potential confounding variable for the causal link made by the stimulus. It doesn't strengthen it by a huge amount, as it is only one of a myriad of potential alternate causes, but as long as it strengthens the argument, it is correct.

Hope this clears things up!

[annabelle.swift]

Hi, I had a question regarding E.

I thought that E was eliminating the alternate cause of age. If younger people are eating more iron than older people and people who eat a lot of iron are more likely to develop Parkinson's, then we know that the cause for the greater incidence of Parkinson's amongst people who eat a lot of iron is NOT due to their more advanced age.

Where did I go wrong with this thinking?

[Adam Tyson]

A couple problems come up with that answer, annabelle. First, eating less iron as you age is just a comparison to when you were younger. You could still have some older people eating a lot of iron, even if they are eating less than they used to. Imagine someone who ate 10x the average amount most of their lives, and then began cutting back after 50, so now they only eat 8x the normal amount.

Second, the stimulus isn't indicating that iron is the only cause of Parkinson's. It's more of a "soft" causal factor - it increases the chances, rather than simply being the cause. So eliminating an alternate cause of age (if answer E did that, which it doesn't really do) doesn't strengthen the claim that iron might be a factor. We have to deal with that correlation between iron and Parkinson's and give more reason to believe that iron is a cause, rather than effect or just a coincidence.