2014-02-01

Science Fiction

We humans are storytellers. When we want something to be memorable and meaningful, we make it into a story that can be interpreted causally. Our brains are just made that way [1], [2]. That may be why adding dramatic anecdotes to a book or article can make it more popular and persuasive than sticking solely to claims that have gone through rigorous tests. This can lead us to believe more strongly in a hypothesis than the evidence merits.

In Apologia we describe how we try to mitigate errors in our work by tracing our sources of evidence. We aim to at least label our hypotheses as such, and to point out when evidence we used comes only from observed correlations.

Beyond anecdote, there are other ways that storytelling is used in science: the plausible mechanism, and the evolutionary story. Both types are used in two ways: to explain an observation, or to lend weight to an hypothesis. A characteristic of this “science fiction” is that it can be argued against by making a different, more compelling story. The best narrator wins! Like any other hypothesis, though, an hypothesis supported by plausible mechanisms or evolutionary stories might be disproven by experimental evidence.

Plausible mechanisms

Plausible mechanisms are stories that involve chains of known scientific facts, integrated together into an expected result.


Here's an example of plausible mechanism that we used in a post a couple of years ago:

  1. "[BCAAs] are known to have positive effects on muscle growth and recovery.
  2. "One important effect of keto-adaptation is a dramatic increase in circulating BCAAs."
  3. "Therefore it is quite plausible that [...] a ketogenic diet will improve muscle growth and recovery relative to a glycolytic diet, something already anecdotally reported."

(We're glad to see that we drew attention to the type of argument we were making, with the word plausible, even as we threw in anecdote for good measure.)

A counter-story might go along these lines:

  1. Muscle growth is stimulated by insulin.
  2. Ketogenic diets lower insulin.
  3. Therefore muscle growth will be retarded on a ketogenic diet in comparison with a glycolytic diet.

We could spend a lot of energy expounding on one story or other, but only replicable, randomised, controlled trials can finally lay a story to rest.


Evolutionary stories

Evolutionary stories are stories that make plausible hypotheses about why certain adaptations could have been selected. They can be used to argue that a certain trait is adaptive, or, more subtly, that an organism has a certain trait.


Here's an example of an evolutionary story:

  1. Ketogenic metabolism is an adaptation to cope with conditions of scarcity.
  2. We get fat because our genes are thriftily hanging on to excess calories to use in famines.
  3. Therefore ketogenic diets must send stress signals to the body, indicating imminent famine.

We recently read a counter-story described by Anna of the blog “lifeextension”.

We can't do that whole post justice, so we recommend you read it. It's not long, and it contains citations supporting the premises. The gist of the story goes like this:

  1. We adapted to a diet largely consisting of meat.
  2. When meat is plentiful, our bodies keep fat at optimal levels for peak fitness and ability.
  3. Eating starch or fiber sends a strong stress signal, mediated by gut microbiota which are sensitive to small changes in diet, indicating that famine is imminent.
  4. This starts a cascade of fat storage.
  5. That is, starch digestion is an adaptation to cope with conditions of scarcity.

We could add more to that story. For example,

  • There is a follow-up post about work that demonstrates that amylase activity is a biomarker of stress.
  • We could point out that no other species responds to abundance by getting fat. Instead they reproduce more.

But these are just embellishments to one of the stories. The right question to ask is:

What kind of evidence could let us discriminate between these two stories?

One way to do that would be to understand stress, how to measure it, and how to tell when it is healthy and when it is detrimental.

Tune in next time for “Ketogenic diets, Cortisol, and Stress, Part II”: The Ketogenic Diet's Effect on Cortisol Metabolism, in which we provide evidence that ketogenic diets have a beneficial effect on cortisol metabolism.

Further Reading

  1. Darwin's Dangerous Idea by Daniel Dennett

    In which we are warned against “Just So Stories”—evolutionary stories that are plausible (at least to some people), and that would explain some observations, but that may or may not be true.

  2. Just So Stories by Rudyard Kipling

    Stories explaining how animals came to be the way they are, such as “How The Leopard Got His Spots”.

  3. The Black Swan by Nassim Nicholas Taleb

    In which we are warned against “The Narrative Fallacy“—the tendency to rely on explanations because they make good stories.

  4. Thrifty genes for obesity and the metabolic syndrome — time to call off the search?

  5. Salivary alpha-amylase in biobehavioral research: recent developments and applications.

Notes

[1]

The Neurology of Narrative

Kay Young, Jeffrey L. Saver
From: SubStance Issue 94/95 (Volume 30, Number 1&2), 2001 pp. 72-84

"Abstract

Narrative is the inescapable frame of human existence. Thinkers as diverse as Aristotle, Barthes, and Bruner have recognized the centrality of narrative in human cognition, but have scanted its neurobiologic underpinning. Recent advances in cognitive neuroscience suggest a regionally distributed neural network mediates the creation of narrative in the human central nervous system. Fundamental network components include: 1) the amygdalo-hippocampal system, responsible for initial encoding of episodic and autobiographical memories, 2) the left peri-Sylvian region, where language is formulated, and 3) the frontal cortices and their subcortical connections, where individuals and entities are organized into real and fictional temporal narrative frames. We describe four types of dysnarrativia, states of narrative impairment experienced by individuals with discrete focal damage in different regions of this neural network subserving human self-narrative. Patients with these syndromes illustrate the inseparable connection between narrativity and personhood. Brain- injured individuals may lose their linguistic or visuospatial competencies and still be recognizably the same persons. Individuals who have lost the ability to construct narrative, however, have lost their selves."

[2]

Causal coherence and memory for events in narratives

John B. Black Hyman Bern
Journal of Verbal Learning and Verbal Behavior. Volume 20, Issue 3, June 1981, Pages 267–275

"Causally related events in narratives were remembered better than events that were not causally related. In Experiment 1, subjects recalled sentences from stories when given the sentences that immediately preceded them as cues. Cued recall was better when the two sentences were causally related than when they were not. In Experiment 2, subjects free recalled the same stories. Again, recall was better for the sentences when they were part of a causally related pair. Also subjects were more likely to combine two sentences into one during recall when they were causally related."

11 comments:

  1. Let's amalgamate 2 hypotheses in circulation: 1) Our ancestors were naturally in ketosis and intermittent fasting was a norm 2) Foraging led to consumption of resistant (indigestible) starch in far higher quantities than typical today. We can emulate and "have our cake and eat it" - so have our ketones, BCAAs AND our SCFA. In a nutshell - ketogenic eating, and "supplementation" with potato starch.

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    1. Well, that's a different story, because It would be incompatible with the hypothesis that starch signals stress (unless you are going for a hormetic story). Seems like it could be tested, though.

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    2. This is more an "appendix" to your story - and we are not talking about digestible starch. The evidence with resistant starch contradicts the stress story - fasting glucose drops significantly, for example. hardly indicative of a 'cascade of fat storage'.

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    3. I agree it could be different. Does amylase respond to ingesting it? About BG dropping, is that in keto dieters, or glycolytic ones? If glycolytic, it still supports the "rescue" hypothesis. It would be very interesting to see trials in keto dieters.

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    4. Any way to set up email alerts on your comment sections? ;)

      I doubt an amylase response, since RS is a kind of "depth charge" (anyone who ramps up the dose too soon will know what I'm talking about!) - so indigestible, but "fermentable" by beneficial bacteria in the colon.

      There is evidence for BG lowering in both ketotic and glycolytic individuals - Steve Cooksey is an example of an ex Type 2 diabetic who has followed a strict ketogenic programme for years. For details of his (recent) experiments with RS, take a look at his blog, but I think his FBG was typically around 85, and RS dropped it over 10 points.

      I don't see the rescue hypothesis relevant for RS, but I like it as a powerful argument against the concept of "safe starches" (except the indigestible ones).

      Love your blogs and FB posts - keep it up!

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    5. Bill, tick "notify me" under the comment box.

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    8. Doh! Thanks Oliver Magoo :)

      I'm personally trialling RS (potato starch - 40g in cold water on rising).

      I'm only in my 3rd week, but have noticed a curious side effect - I sleep a lot better, and also I am getting a lot of vivid dreams - the latter seems to be a common observation.

      I'm beginning to wonder if gut biota mediate health benefits via a much "higher" function - i.e. HPT axis, neurotransmitter balance etc. Why else the psychic effects?

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  2. This goes along the line:

    Vitamin C is known to partially block the effects of fructose to induce this metabolic phenotype (26). Importantly, as fruit ripens towards the end of the summer season, the vitamin C content falls whereas fructose content increases (27). Hence, fruits are an important food source not only for their energy intake, but for their metabolic effects to increase fat stores. In addition, fruits are the most lipogenic at the end of summer, prior to seasonal cooling and a reduction in food availability.
    ...
    fructose inhibits vitamin C synthesis in mammals that are capable of synthesizing vitamin C (34). Hence, vitamin C may be considered an antidote to the effects of fructose to stimulate fat storage.


    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917125/

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    1. That story is explicitly crafted to support the thrifty gene hypothesis; in particular, the modern-age-as-perpetual-autumn version. The hypothesis IIUC is that the simultaneous inability to create vitamin C and degrade uric acid augments the tendency of fruit to make us fat. No good test comes immediately to mind — perhaps some variations in gene knock-outs in other animals could explore that.

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