4000 year old Assyrian tablet has a prenup that addresses infertility:

https://www.dailysabah.com/history/2017/11/09/first-infertility-diagnosis-made-4000-years-ago-discovered-in-cuneiform-tablet-in-turkey

Hey, looky here!  Turns out our old friend Ancel Keys did a huge randomized controlled trial with a coworker on people in nursing homes and asylums trying to show that polyunsaturated fats would reduce heart attacks relative to saturated fats.  Then when the actual data showed there was no benefit - cholesterol was reduced, but as many or more people died - he never published the results.  But the truth got the last laugh, after he and a coworker died.

https://www.statnews.com/2016/04/12/unearthed-data-challenge-dietary-advice/

... I run to the drugstore instead of walking because I'm in a hurry, rather than because I need the exercise.

Somehow I missed this when it came out.  Calorie restriction has previously been shown to extend lifespan in a wide variety of animals from microbes to rats.  Now that result has been extended to primates - specifically, rhesus monkeys.  A 30% calorie restriction resulted in about a 20% increase in lifetime when looking only at age related deaths, and about a 10% increase in lifetime when other causes of death were included.

Caloric restriction (CR) without malnutrition increases longevity and delays the onset of age-associated disorders in short-lived species, from unicellular organisms to laboratory mice and rats. The value of CR as a tool to understand human ageing relies on translatability of CR’s effects in primates. Here we show that CR significantly improves age-related and all-cause survival in monkeys on a long-term ~30% restricted diet since young adulthood.

http://www.nature.com/ncomms/2014/140401/ncomms4557/full/ncomms4557.html

Apparently there's a kerfluffle between various ancestral health diet blogs about a mutation found in most coastal Inuit and almost no one else, and what its implications are regarding whether the Inuit were in ketosis most of the time, and whether they are a good model for the effects of long term ketosis in people without the mutation.  The information is sufficiently interesting that I thought I'd post a summary here.

The mutation is in the CPT1 gene, which is ultimately responsible for oxidation of long chain fatty acids.  The associated enzyme activity was reduced by a factor of roughly 17 in people homozygous for the mutation - that is, that had the mutation on both strands of their DNA - and appears to inhibit ketosis on modern diets.  Out of 422 consecutive infants screened from one affected region, 70% were homozygous for the mutation and another 24% were heterozygous - had the mutation on one of their two DNA strands.  A significant proportion of the affected people are in hypoketotic hypoglycemia - that is, have low blood sugar, but without the normal response of going into ketosis - and there were at least 10 infant deaths out of the 422 screened.

http://www.ncbi.nlm.nih.gov/pubmed/19217814

So basically we have a mutation that seems to kill a noticeable percentage of infants, but which has actually been selected for, rather than against, in coastal arctic Inuit populations.  The question is, why?

Petro Dobromylskyj, who writes the Hyperlipid blog, has an explanation that hangs together pretty well.  He notes that the coastal inuit's precontact diet was extremely high in fat and had virtually no carbohydrate.  He argues that with such a diet, the free fatty acid concentration in the body would increase to the point where even the small residual activity from the enzyme from the mutated CPT1 gene would be sufficient to allow adequate levels of long chain fatty acid metabolism.  This would explain why the mutation didn't get rapidly selected out of the gene pool, for this population.

There remains the question of why there was selection in favor of the mutation.  Dobromylskyj notes that normally, when the energy from oxidative metabolism is no longer needed, the enzyme from the CPT1 gene is inhibited by malonyl-COA.  The enzyme from the mutated CPT1 gene is not inhibited by malonyl-COA, so long chain fatty acid oxidation would continue even when the energy was not needed for normal functions:  the energy would simply be dissipated as heat when it wasn't powering muscles or other tissue activity.  In addition, the increased free fatty acid concentration would mean that this elevated level of metabolism could be sustained for much longer than in people without the mutation.  In the arctic areas where the mutation is found, the extra body heat would be adaptive:  for example, it could keep you alive through a cold night or rest period where normal humans would die of hypothermia.

http://high-fat-nutrition.blogspot.com/2014/11/coconuts-and-cornstarch-in-arctic.html

What does this mean for the paleo diet, and for the argument that the Inuit are a model for a sustained ketogenic diet?  Well, it does mean that they metabolized an extremely high fat, virtually zero carb diet slightly differently from most of us.  The differences mean that such a high fat diet won't give most of us quite the ability to survive the arctic wilderness that it gave the Inuit.  On the other hand, the extra free fatty acid metabolism that the Inuit have on such a diet would mean that they would see a bit more oxidative stress than most of us on such a diet.

Ultimately, though, they were still likely in long term ketosis.  And, if anything, a long term ketogenic diet, outside of the arctic wilderness, is likely more healthy for us than for the Inuit, given our lower levels of oxidative stress on such a diet.

I've previously observed that while men can easily lose excess weight on paleo, women have a lot more difficulty.  More recently, I've noticed that of the two or three cases of successful substantial weight loss in women - by which I mean 30 lb or more - all seemed to be operating in ketosis.  So, I theorized that the reliable way to use paleo for weight loss for women was to use ketostix and stay in ketosis.

My wife, who had previously not been in ketosis and had been having trouble losing her most recent pregnancy weight, recently changed jobs, saw her weight increase due to the temptation of a candy bowl that was kept near her new cube, and got serious about losing weight.  This gave me an opportunity to confirm my theory.

I suggested she start using the ketostix at least daily to ensure she got into ketosis, and she did.  Within the first week, she lost the expected six or seven pounds of water weight.  Since then, she has been losing a pound or two per month, though of course it is as always somewhat obscured by changes due to the monthly cycle - during one part of the cycle she loses a pound a week, and during the rest of it she stays flat.

It looks like ketosis, measured through ketostix, may be the way to go for women who really want to lose substantial amounts of weight.

Apparently yes.  Next time a vegetarian talks about all the cuddly animals your paleo diet is killing, refer him to this video:

https://www.youtube.com/watch?v=fGLABm7jJ-Y

Plants' physical reactions can be inhibited by anesthetization with ether, and burning a leaf results in the propagation of electrical signals in the plant.