There are two confusing but potentially important papers in the Jan. 25 2013 Science on long-term memory (LTM) formation in fruit flies:

Pierre-Yves Placais & Thomas Preat. To favor survival under food shortage, the brain disables costly memory. 339:440-441.

Yukinori Hirano et al. Fasting launches CRTC to facilitate long-term memory formation in Drosophila. 339:443-446.

These papers categorize long-term memory formation along three axes.

• Aversive vs. appetitive:  Actions that the brain interprets as helping it avoid something, vs. actions that help it attain something.
• Fasting-dependent (fLTM) vs. spaced training-dependent (spLTM):  fLTM is formed in a single learning episode, but only at the time that an organism first obtains food after a long fast. spLTM does not require fasting but requires repeated training.
• LTM vs. ARM: Memories that require protein synthesis (LTM) vs. "anesthesia-resistent memory" (ARM), which does not.  (The papers don't explain what ARM might correspond to in humans.)

The relationship between these is unclear, particularly as each of these three axes is claimed at various times to determine whether memory can be learned in a single training cycle (appetitive, fLTM, and/or ARM) or not (aversive, spLTM, and/or LTM).  But these things appear to be likely, or at least to be reasonable hypotheses, if these pathways are conserved in humans:

• How quickly you learn something depends on how much you've eaten recently.  You learn most quickly immediately after ending a long fast. Your brain thinks you just learned something that saved it from starvation. (But note that a 1-day fast for a fruit fly could be compared to a human fasting for months.)
• How quickly you learn something depends on whether your brain thinks that this knowledge is to avoid something bad (slow learning) or to attain something good (fast learning).
• Almost all of the mutations that extend lifespan in organisms from yeast to humans impact the FOXO3a vs. mTORc1 axis (to use the human analogs).  Expressing FOXO3a inhibits mTORc1 and extends lifespan in various ways; producing and assembling more mTORc1 inhibits FOXO3a and promotes protein synthesis, growth, reproduction, tissue repair, and immune response.  We already know that extending lifespan, in general, is antithetical to building muscle.  It may also be antithetical to forming long-term memories.  This makes sense.
• Learning rate can be increased by expressing or inhibiting  proteins involved in these responses.  Hirano et al. focus on activating a cAMP-regulated transcriptional coactivator (CRTC) by dephosphorylating it in order to invoke fLTM.  They were able to do this and enable flies to learn quickly without fasting followed by feeding.

I'd really appreciate it if somebody would do a literature review and a comparison of the pathways involved to those in humans, and summarize their findings.

This is hardly news, but this Guardian article reminded me of it - genes are really overrated, both among unwashed masses, and also here on Less Wrong.

I don't want to repeat things which have been said by so many before me, so I'll just link a lot.

Summary of evidence against genes being important:

• Almost no genes correlating with anything interesting been found. This is totally crushing evidence. If genes were important, Bayesian surprise of this lack of results would be in the land of impossible.
• Massive very fast changes of various supposedly highly hereditary characteristic with time in same populations. To name a few - Flynn effect, changes in people's height, obesity epidemic.
• Plenty of evidence of very large very reliable associations of various environmental factors with various important outcomes. For example unlike with genes and cancer where we get just noise, we know very well how much smoking increases chance of lung cancer.

Summary of evidence for genes being important:

• Some twin and adoption studies - which rely on very tiny highly atypical samples and a lot of statistical manipulation to get results they want. To make matters worse, results they got were wildly inconsistent.

And there's nothing more. Decades ago, before we had direct evidence of lack of correlation between genes and outcomes, it was excusable to believe genes matter a lot, even if it was never the best interpretation of data. Now it's just going against bulk of the evidence.

And in case you're wondering how could twin studies show high heredity when everything else says otherwise, I have two examples for you.

This one from a critique of twin studies by Kamin and Goldberger:

"A case in point is provided by the recent study of regular tobacco use among SATSA's twins (24). Heritability was estimated as 60% for men, only 20% for women. Separate analyses were then performed for three distinct age cohorts. For men, the heritability estimates were nearly identical for each cohort. But for women, heritability increased from zero for those born between 1910 and 1924, to 21% for those in the 1925-39 birth cohort, to 64% for the 1940-58 cohort. The authors suggested that the most plausible explanation for this finding was that "a reduction in the social restrictions on smoking in women in Sweden as the 20th century progressed permitted genetic factors increasing the risk for regular tobacco use to express themselves." If purportedly genetic factors can be so readily suppressed by social restrictions, one must ask the question, "For what conceivable purpose is the phenotypic variance being allocated?" This question is not addressed seriously by MISTRA or SATSA. The numbers, and the associated modeling, appear to be ends in themselves."

As the final nail in the coffin of heredity studies:

The Body-Mass Index of Twins Who Have Been Reared Apart

We conclude that genetic influences on body-mass index are substantial, whereas the childhood environment has little or no influence. These findings corroborate and extend the results of earlier studies of twins and adoptees. (N Engl J Med 1990; 322:1483–7.)

Or as paraphrased by a certain commenter on Marginal Revolution:

IOWs, the reason why white kids of today are much fatter than white kids of the 50s and 60s is due to genetic influences and environment has little or no influence

To summarize - heredity studies are pretty much totally worthless data manipulation. Once we accept that, all other evidence points for environment being extremely important, and genes mattering very little. We should accept that already.