Steve Hays has a good post titled “A catalogue of evils“. His post is in response to secular philosopher Michael Tooley over the argument from evil. It’s worth reading.
I’d like to tack on the following piece (below) to Steve’s post. It was originally meant to be a comment in his post, but it became too long to post as a comment. So I’ll post it here:
I think I could provide reasonable responses to each of Tooley’s dysteleological examples, but regrettably I don’t have the time to do so. I’ll only respond to one of Tooley’s objections for now, though perhaps I’ll try to respond to more in the future:
Men and women differ in various ways. One interesting way, recently discovered, involves a gene called gastrin-releasing peptide receptor – or GRPR for short – which is linked to abnormal growth of lung cells. It had been noted by earlier medical researchers that women were more likely to develop lung cancer than men, without smoking more, and it turns out that the explanation is that while the GRPR gene in not active in men unless they smoke, it is active in 55% of non-smoking women. (The reason for this is connected with the fact that the gene is on the X chromosome, of which women have two, and men only one.) So greater susceptibility to lung cancer is programmed into women.
1. To my knowledge, the correlation between GRPRs and gender-related susceptibility to lung cancer is still debated. For instance, DeVita is the gold standard textbook for oncology (at least in the United States), but the most recent edition of DeVita notes: “Although many other serum markers have been proposed to have prognostic significance, including neuron-specific enolase, chromogranin, and precursors of gastrin-releasing peptide, none have been strong and reliable enough to warrant general use.”
2. It’s interesting what Tooley leaves out. He leaves out more established genetic associations with lung cancer. For example, he doesn’t mention that the most common tumor suppressor genes in lung cancer are p53, RB1, and p16. Nor that the most common oncogenes in lung cancer are KRAS, HER-2, BCL-2, and EGFR.
3. In particular, let’s take note of EGFR (epidermal growth factor receptor). EGFR is important in gender-related differences in lung cancer. It’s been well-established that (activating) EGFR mutations are more commonly found in women who have never smoked (especially East Asian women who have never smoked) than in men who have never smoked. This is significant because EGFR mutations are predictive for a favorable prognosis and survival outcome in lung cancer! That’s because oncologists can specifically target EGFR mutations with certain kinds of cancer drugs (i.e. EGFR-TKIs). See here for more information: “These mutations increase the kinase activity of EGFR, leading to hyperactivation of downstream pro-survival signaling pathways”.
In short, all things equal, a person with an EGFR mutation has a better (not worse) prognosis when it comes to lung cancer! And EGFR mutations are more common in women who have never smoked than in men who have never smoked. So it would seem some genetic mutations are advantageous, thanks to how cancer drugs can target these genetic mutations.
Will Tooley ever be willing to argue some genetic mutations might be evidence of good design? Or at least that some genetic mutations aren’t necessarily evidence of poor design? For one thing, it would seem serendipitous that our cancer drugs align with certain genetic mutations.
Or would Tooley chalk that up to human ingenuity in spite of having to work with poor design? If so, then we’d have to look into the details. If one builds a key that just so happens opens a lock, would human ingenuity or a happy coincidence be able to explain it all if the lock is highly complex, etc.?
4. If we have to single out a single group, then black men have the highest incidence rate when it comes to lung cancer in general. Would Tooley therefore conclude being a black man is evidence of poor design? Of course not. That’d be absurd.
5. If we want to delve deeper, there are different types of lung cancers. Broadly, there are two main types of lung cancers: small cell lung cancers (SCLCs) and non-small cell lung cancers (NSCLCs). NSCLCs can be further subdivided. The most common NSCLCs are squamous cell carcinomas, large cell carcinomas, and adenocarcinomas.
SCLCs and squamous cell carcinomas are more common in men than women. However, adenocarcinomas are more common in women than men. And adenocarcinomas are the lung cancer that is least correlated with smoking.
Given all this, it seems reasonable to presume Tooley is referring to adenocarcinomas, since he framed his argument in the context of “non-smoking women”.
If so, what’s interesting is GRPRs aren’t common in NCLCs (which, as mentioned, include adenocarcinomas). Rather, GRPRs are most common in SCLCs. As such, it would seem there’s some tension or conflict in Tooley’s argument.