fetal pain | 🧠 + 🫀 | life
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Joined July 2019
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Either-or is sometimes just a fact. We can't always have it all. Good vs evil is a real thing, especially at the margins.
But in between, this paradigm is an adversarial, zero-sum, false worldview that only one can matter; only one can be true:
- saint vs sinner
- God vs man
- mother vs baby
- truth vs grace
- faith vs science
- forgiveness vs boundaries
- individual vs community
- freedom vs responsibility
- fetal pain vs right to life
This adversarial paradigm accords with the Theory of Evolution (survival of the fittest) and Marxism (class struggle).
But it does not fit with Christianity, which is abundance, both-and:
- saint AND sinner
- God AND man
- mother AND baby
- truth AND grace
- faith AND science
- forgiveness AND boundaries
- individual AND community
- freedom AND responsibility
- fetal pain AND right to life
Each one matters maximally.
Zero-sum, either-or only applies at the margins.
It's the exception that the "vs" advocates would generalize into a rule. the abortion edge cases--pregnant 12-year-olds, etc.
"Hard cases make bad law."
it's almost always both-and, not either-or
what does @jordanbpeterson say--"when all the options are bad, the solutions are upstream."
that's where we should put our energy for those edge cases.
You can and must, actually. To support abortion, you can and must insist on at least two contradictory things at once. Every lie, every injustice requires this dissociation.
Anti-intelligent design arguments concede the basis of ID arguments.
Namely, that intelligent design can be recognized. Their arguments are expressly theological, not scientific. "God wouldn't have done it that way."
But ID simply recognizes the scientific hallmarks of intelligence and leaves theology to theologians.
"Is pregnancy irreducibly complex? case for and against."
share.google/aimode/eaHVpVwG…
I've heard that "A woman's work is never done," but the burden of carrying a dead fetus to term is...interminable.
Debating lipidology in between deadlifts.
What do you think:
1) do we need to know a mechanism before we can harness an effect
2) do atherosclerosis & MACE demonstrably arise from LDL, ApoB, non-HDL, and Lp(a)
We don't need to know the mechanism before we can harness the effect. General anesthesia; sleep; placebo effect; paracetamol; gravity. No demonstrable mechanisms.
But we do know the mechanism of elevated LDL, non-HDL, ApoB, and Lp(a) in atherosclerosis: retention, oxidation, foam cells; stenosis, plaque formation, emboli. MACE.
Thoughts?
