Confusing theories with observations
A recurring pet peeve of mine is ubiquitous in alt health discussions. Here's the pattern:
- Someone has a cluster (C) of unhappy symptoms.
- Those symptoms reliably go away with treatment approach (A).
- A theory, or hypothesis (H) is developed for why A might treat C.
- People get excited about H and mistakenly assume that 2. is proof of H!
- (Bonus fallacy) It becomes common wisdom that lack of / opposite of H causes C.
- People hearing 4. and 5. reject A because they think it's predicated on H rather than inital observations, and they recognise 4. and 5. as preposterous. Or at least light on logic.
I've seen this again and again in the Carnivore world. Here are some examples of proposals people have made for why Carnivore "works" to relieve so-called autoimmune conditions.
- anti-nutrients in plants cause intestinal permeability
- depletion of excess vitamin A
- depeletion of linoleic acid
- depletion of deuterium
- repletion of conditionally essential amino acids
Some of these are more plausible to me than others. Nonetheless, they are all untested hypotheses.
If you tell someone that there are many cases of Carnivore apparently putting arthritis into long-term remission, you are speaking factually.
If you tell people Carnivore puts arthritis into remission because it eliminates vitamin A toxicity, you're confusing theories with observations and making a quackery of it.
If you tell someone that Carnivore frequently puts arthritis into remission, and that you think it may be attributable to reduction in subclinical hypervitaminosis A (and have good reasons why that you're ready to discuss), you're being honest and moving the scientific dialogue ahead.
An example of the latter strategy from my own writing on the topic of arthritis and intestinal permeability is in the "plausible mechanisms and prior probabilities" section of this post