Lizard Blood Kills Lyme Disease Bacteria

At least two lizards in California have a protein in their blood that kills borrelia, which has slowed (but not stopped) its spread. When I left PA in the late 90s, I felt like I was escaping Lyme disease - one group of trail runners I knew estimates the prevalence of Lyme in its ranks at 70% - but by the mid-teens I had already started seeing cases of Bell's palsy caused by Lyme - it's here. But still not as bad.


From microbenotes.com. Note that the classic target lesion occurs in only about 50% of cases, meaning that just because you never saw a target lesion, doesn't mean it's not Lyme.

No word on whether therapeutics are being based off this protein but it seems like an obvious move.

Biomass and Toxicity Responses of Poison Ivy (Toxicodendron Radicans) to Elevated Atmospheric CO2

Of interest to trail runners and hikers. Just passing along this paper, by Mohan et al 2006.

From the abstract: "Furthermore, high-CO(2) plants produce a more allergenic form of urushiol. Our results indicate that Toxicodendron taxa [which includes poison oak] will become more abundant and more "toxic" in the future, potentially affecting global forest dynamics and human health."


Biomass and Toxicity Responses of Poison Ivy (Toxicodendron Radicans) to Elevated Atmospheric CO2. Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9086-9. Mohan JE, Ziska LH, Schlesinger WH, Thomas RB, Sicher RC, George K, Clark JS.

New Podcast: Trail Doc Vlog

By John Onate of UC Davis, and medical director of the Western States 100.

Here's episode 2 - Ultramarathons during a Pandemic, a discussion with Ultramarathon Medical Directors.

Calculating the Limits of Endurance - Intensity versus Time

Thurber et al in Herman Pontzer's lab at Duke used the Race Across USA (what dummies!) to look at metabolic rate relative to basal metabolism. Over an arbitrarily long period, humans can only sustain effort at 2.5x resting metabolism. In a marathon it's almost 16x (for less than 1 day), in the Tour de France it's almost 5x (for 23 days) and for someone crossing Antarctia it's 3.5x for 95 days. Lay article here, paper here.

Altitude Plus Exertion (Including Associated Poor Sleep and Dehydration) Interact to Produce Cognitive Deficits

Outside Magazine summary here, PLOSOne study here. I strongly suspect that poor sleep at altitude is a (the?) major contributor to this, but in a multi-day climb like Kilimanjaro, I see no solution - wearing an O2 mask when you go to bed in your tent? Yeah, that sounds like the solution to restful sleep!

Additional Evidence for the Central Governor Hypothesis: No Claudication-Like Symptoms With Sustained Maximal Effort

Two theories have emerged to explain a maximal exertion limit in exercise.

1. Catastrophic failure. This is the "common sense" idea that limitations of local physiology set the maximum exertion - e.g., oxygen supplied to muscle, muscle fiber recruitment, and metabolite accumulation; and
2. The Central Governor model (CGM), where some central regulator sets the limit. This regulator is often assumed to be in the central nervous system, and has been explained either as active limitation of exertion, and also as depletion of neurotransmitters during exercise.

For a more detailed explanation of these models, I refer you to Ament and Verkerke (2009.) They primarily defend the catastrophic failure model, and while they do give a fair shake to CGM, they also have some interesting arguments against it, as well as an excellent reference section (with references to Tim Noakes, probably the best-known proponent of CGM.)

It should be said that nothing in biology is ever simple, so I would agree with Ament and Verkerke that at the very least it's worthwhile distinguishing between slow- and fast-twitch muscle fibers. In pointing that out, they imply but don't really defend the point that BOTH of these models may be correct, i.e., CGM in Type I slow-twitch muscle fiber, and catastrophic failure in Type II fast-twitch. It also seems that CGM proponents like Noakes are mostly interested in slow-twitch (he's an endurance runner) and I'm interested in this model for the same reason.

A bit of circumstantial evidence to bolster the CGM argument, at least for slow-twitch fibers is the phenomenon of claudication. Long story short, claudication is what happens when you have a blockage in a peripheral artery in your leg. Some blood may still be getting through, but not enough - and the problem is revealed with activity, so that when the person tries to run or even walk, they get extreme tiredness, pain and cramping, often in a matter of blocks, and at a very consistent distance. It's basically the peripheral analog to chest pain on exertion (stable angina) though in that case it's because of a blockage in a coronary artery in your heart. In some cases, especially in diabetic people whose circulation is damaged by the disease, skeletal muscle can actually be infarcted - that is, severe damage to muscle cells occurs causing tissue necrosis much like in a myocardial infarction.

If the catastrophic failure model is correct, then athletes pushing themselves and only being limited by peripheral metabolism in their muscles would sometimes infarct their muscles like this, and yet it doesn't happen. If CGM is correct, you would expect that the Governor keeps us out of trouble by keeping us away from the limit - except in people whose vascular systems have undergone rapid pathological deterioration (not just deconditioning), at a rate which perhaps the feedback system to the Governor can't adjust fast enough to take into account. Not only that, the experience of maximal exertion during exercise is not at all like claudication or muscle infarction. (Admittedly I don't have a satisfying mechanism for the peripheral vasculature's feedback to the Governor, but it is very interesting that anatomically nerves and vessels do tend to travel together in bundles.)

The most tempting possible objection to using the lack of claudication or infarction events as support for CGM is to say that catastrophic failure is correct, but the cardiopulmonary system is the constraint that sets maximal exertion, not the peripheral muscle. That is, in a runner, the quads are nowhere near their "theoretical limit" but the heart-lung system is at its maximum (whether it's cardiac output or diffusion-limitation, as occurs in a very few elite athletes.) But this just moves the site of the potential infarction, since now we would be infarcting our hearts instead of our limbs if that's where the limitation is, with no outside governor, and again, this never (or almost never) happens. (A very few elite athletes are diffusion limited, where cardiac output is so great that blood is moving so fast through the lung's capillaries that there's not enough time for oxygen to get into the blood, but this is certainly not the case for the vast majority of humans.)

A second possible objection is to say that catastrophic failure is true because at sustained maximal exertion there IS infarction, e.g., after a marathon, runners sometimes show CK values on the order of 10,000 to 100,000. Yes, but a) CK levels in infarcts from diabetes are actually much lower, in the low thousands; b) chronic mechanical damage to muscles would produce the same effect; c) these runners don't describe acutely feeling part of their quad suddenly dying like an infarct - it's a gradual process, and d) such elevations would happen in acute exercise as well. But they do not.

I suspect that the final correct answer will be that there is a CGM for slow-twitch muscle and not for fast-twitch, and this is why things like neurological changes e.g. after surgery or trauma, placebos, motivation, and anecdotally SSRI use have an effect on endurance sports but not as much in acute strength-and-speed events.

Exercise More Important Than Obesity or Age as a Risk Factor for Knee Osteoarthritis

Osteoarthritis (OA) is the wear-and-tear kind. A recent study discussed in JAMA looked at skeletal remains and found that even after controlling for weight and age, if you were born in a developed country after WWII, you're more than twice as likely to have OA of the knee.

That is to say: a two hundred pound man born in 1945 and who died at 70 is twice as likely to have OA of the knee than a two hundred pound man born in 1900 and who died at 70.

What changed since WWII? Wealth plus automation = less exercise. This is quite consistent with the work done already showing that runners are slightly LESS likely to have knee problems than non-runners. (This should shut up those annoying people telling you you're going to mess up your knees.) As the JAMA editorial states, it's also consistent with evolutionary medicine - that if we behave as evolution designed us to behave - i.e., running around all the time doing stuff and not sitting at home in front of glowing screens - that we're more likely to be healthy.

Where Should You Live? Critter Fatalities By State From 1900

Added later: a NYT article shows that we do indeed spend too much time in the U.S. worrying about things with venomous things and things with big teeth, as opposed to dogs and wasps. And even considering wiki statistics, based on Wiki statistics from the 2010s for snake bite deaths and population, a person in Australia is indeed more than 11 times as likely to be killed by a snake in Australia than the U.S. - but even in Australia you still didn't even have a 1 in 13 million chance of being a victim from 2011 until today. Your morning commute is far more dangerous than living in Australia.

Also added later: here's a guy screwing up my statistics who was also bitten by a shark in Hawaii just a month after being attacked by a bear in Colorado. If I were this guy I would have business cards made up that said this.


In light of the recent seasnake that washed up on a beach in Oxnard (pleasantly, a few days after we were swimming across the channel from there), I looked up the statistics for snakebite fatalities in the U.S. (No recorded seasnake fatalities.) Interestingly, at the bottom of the wiki article for snakebite fatalities, they have links to mountain lion, bear, alligator, and shark fatalities because they know there are people like me running around loose who will look those up next anyway. (Hereinafter these five types of animals are referred to collectively as "critters".)

And of these critters, how many deaths do you think they've caused in the U.S. since the turn of the last century? 226, over the last 115 years. Not even two a year, not many! Compare that to the about 31 deaths per year caused by dogs (actually, 42 in 2014). And of course (being responsible) if you're out in the wild you are much much much more likely to be killed or injured by falls, drowning, exposure to heat or cold, dehydration, or other people than by wild animals. Of course drowning doesn't have pointy poisonous teeth that rush at us from the darkness, so our dumb Type-1-error making brains pay less attention to rushing water rising around our ankles than a twig snapping in a forest.

Still, I decided to compile absolute critter fatalities by state. In calculating this, I took out BS ones (i.e. snake handlers and dummies who keep non-native poisonous snakes at home don't count as a legitimate bite. Come on guys.) Interestingly, Texas has fatalities from the most types of critters (four of the five) - they finally got a gator fatality on the board this summer - and in fact Texas is the only state where the range for all five critter types overlaps because there are sharks and gators on the Gulf Coast, snakes all over, mountain lions in the west, and bears in the Big Bend part of the state. (Come on guys, you can do it!) There are 22 states with no fatalities from these critters since 1900. If all these critters scare you, then the biggest contiguous area with no critter fatalities stretched from Minnesota, to the west of Missouri and down to Louisiana. (To be honest I have difficulty believing no one died from a snake bite in the southern part of this range since 1900, and if this omission from my data here offends you I'd like to invite you to go dig for the stats yourself.) Northern Iowa/Southern Minnesota is the only place safe from all five, which no doubt is why the Mayo Clinic was placed there, as there's no other reason to want to be in Rochester Minnesota.

Ranked in order, the states with the most critter fatalities in absolute terms are:



However: the absolute number of critter-victims in each state is lacking as a risk indicator. Why? Look at California and Alaska, which are tied. There are a lot of people in California, and not so many in Alaska, and yet critters have managed to get the same number of people in each state. Concretely speaking, there are 38 million people in California, and not even a million in Alaska, so walking around in Alaska it's actually *76* times more likely that critters will get you! So if we weight for population (i.e. critter fatalities per person in the state) what does it look like? Now, Hawaii, which somehow manages to keep its shark attacks very quiet (I wonder why?) comes out on top, so I adjusted the rates to express the others in terms of how many Hawaiis-worth of critter risk they represent:



Interestingly, Hawaii has only ONE type of the five critters, but apparently in Hawaii that one type of critters eats well. In this analysis, California drops from #3 to #13. An also-ran! Even New Jersey is per capita more dangerous than California! (Granted, this is owing to the black-swan/white-shark event of the Matawan Maneater.)

People in Hawaii are in the water a lot, which reminds me that I once calculated statistics showing that people in Florida were 3 times more likely to get attacked by a shark, but people in California were 3 times more likely to be killed by one. (Which is to say, once you're attacked, you're 9 times more likely to get killed in California than in Florida. Because we have great whites and they have coot widdle tigers and bulls.) But again this statistic still understates the danger, because Florida has a lot more accessible coastline (California is mostly cliffs) and it's warm, so lots more people go in the water, therefore a LOT more exposure to shark attacks in FL. And still more fatalities in CA? That is to say, once you're in the water in CA, you're much more likely to be attacked and killed - but I don't have ocean bather-numbers to back that up.

And a good day to you.




Above: the head of the Hawaiian Tourism Development Board. He advises that all tourists bring Worcestershire sauce and perhaps tuck a sprig of parsley behind the ear before swimming. From animaltime.com.

The Mortality of Aircraft Wheel-Well Stowaways

Cross-posted to my cognitive science blog.

The FAA gives a report of 11 known stowaway incidents from 1947-1993.

Of these 11, 6 died. 2 of them had definitely frozen to death. 3 more fell after the plane made it to cruising altitude, and could have frozen to death. Another fell on takeoff. This means that you have a 55% chance of dying if you attempt this, and if you die the chance is 33-87% that you will freeze to death.

Of course it's likely that other fatalities occurred but were not discovered because the plane was over water or the body landed in an unpopulated area; it is also likely that people stowed away and were not discovered, so it's hard to say which way the sample is biased.

The mechanism cited as probable pathway to fatal hypothermia at altitude seems very likely to be the same one that explains the strange behavior of high altitude mountain climbers who succumb to a similar fate, and are found having taken off most or all of their layers. Under conditions of low ambient O2, the hypothalamus becomes hypoxic and can longer thermoregulate. In climbers, their frontal lobes are hypoperfused, and they feel hot and can't reason themselves out of/inhibit themselves from taking their clothes off in the middle of a glaciated mountain. Stowaways are crammed in and can't move anyway.

Management: don't be in a plane at cruising altitude outside a warmed and pressurized cabin.

Safety and Efficacy of Caffeine in Exercise

Boing Boing has a nice post about caffeine and energy drink use in distance running events, and associated mortality. It's not huge, but it's still worth reading. The best part of it is the actual peer-reviewed references. One shows that marathon runners (highly-trained or recreational) reap a 1% boost in their marathon times by using caffeine; so if you run a 3:30 marathon, now you'll run 3:28. Another shows a similarly modest boost in high-impact exercise, as long as you're not already a caffeine junkie with a developed tolerance.

Beers Most Implicated In Emergency Room Visits

Done at Johns Hopkins. They should've adjusted the list by per capita consumption, although I bet it still wouldn't change much.

A Paleo *Cognitive* Regimen

This is cross-posted to Cognition and Evolution.

Paleo dieters avoid post-agricultural foods. The argument is that agriculture is a product of culture and so it introduced sources of nutrition that our genes haven't caught up with, especially grains, refined sugar, and other concentrated carbs. By eating vegetables and lean meats (so the argument goes) we are more in tune with paleolithic humans and therefore should be healthier.

There are any number of problems with that argument (not least of whic is that adherents often seem disinterested in empirical testing of it), but an interesting question is: couldn't we apply similar arguments to our cognition? The way we think about the world, or possibly even, that we think about the world, started undergoing profound changes about 40,000 years ago. Of note, this time corresponds with humans leaving Africa, developing specialized tools, hunting larger game that required team planning, and the spread of the current form of the FOXP2 gene and subsequent use of language and the cognitive modernization of humans; it marks the boundary between the upper and lower paleolithic. That is to say, until about 40,000 years ago, we solved problems in a primitive, isolated way, and knowledge could be shared only at a much more basic level. Suddenly we have language, reasoning, and mountains of cultural transmission in the form of tools and worldviews so that what we achieve in working memory can be expanded across a whole lifetime, or indeed indefinite lifetimes (i.e., among other things, the idea of an alphabet, hit upon by some clever Phoenician twenty-five centuries ago, allows us to more easily share these ideas right now). This has profoundly changed our physical environment in ways that have outrun our genes' ability to respond - including agriculture.

Therefore, shouldn't a person making the paleo argument for diet also make a similar argument for post-paleo (or at least post-lower paleo) cognition? That is to say, if you're really concerned that agriculture-based food is a threat to the fluorishing of H. sapiens because of its newness and alienness, aren't things like reasoning and systematic institutional research just as bad, if not profoundly more dangerous? Shouldn't we be approaching problems with blunt emotions and a vague memory of some chance association from last time we were in this part of the world with no way to obtain or share knowledge from others? Shouldn't the males of the species be getting in fights with people that look different from us or look at our woman for a second too long, with a resulting homicide rate of 30%? (The actual number for some hunter-gatherer groups.) This is what we're adapted for - our cognitive environment for thousands of centuries. How can the alien world we've built for ourselves in cognitive modernity not be hurting us?

In extension you could even make a Nagel-like argument here that paleo defeats itself, that if you think paleo is the way to go because profoundly biologically novel activities are threatening to an animal's well-being, then you should also eschew reasoning, and therefore eschew paleo, which was arrived at with a very un-paleo process (reasoning, communicating about it with large groups of people, and institutional research).

Pronation Doesn't Matter For Injuries

A Danish study just published in the British Journal of Sports Medicine investigated the received wisdom that under- or over-pronating runners are more subject to injury than "neutral" runners. They found that this was not the case. (The study is well-summarized in the New York Times.)

Study design: 927 male and female runners from 18 to 65, prospectively evaluated as under- or over-pronator or neutral, given light-weight NON-motion-controlling shoes, and left alone to run as they please for a year.


From 5k Fashionista.

So what happened? There was no difference between the under/over-pronators and the neutral runners overall; but in fact among higher-mileage runners the over-pronators had a slightly but significantly lower chance of injury than neutral runners. Higher-mileage here is >600 miles a year, which isn't even 12 miles a week, so not very high mileage; "injuries" here were any medically-confirmed back or leg complaint that caused the subject to stop running for at least a week.

The lead author concluded that runners are better off paying attention to "things like body mass, training, behavior, age and previous injury in order to prevent running-related injuries." Admittedly, I'm posting this because what I don't want to hear from the super-paleo "all shoes are bad" crowd is that this study supports their conclusion; it just leans us further toward "follow your natural stride type". And to that end, some of us, your blogger included, are obligate 21st century runners whose build, foot shape and size, stride length, and running habits requires us to wear a well-cushioned (if not motion-controlling) shoe. And I've never had a use injury in 22 years of running with no warm-ups, or stretching, or proper build-ups to big events. And this paper is telling us all that our natural stride/strike is a-okay!

Running Surfaces and Your Knees

The next time someone brings up the old canard that running is bad for your knees, now you'll have evidence to the contrary. Running is not only not bad for your knees, it's actually better than not running, in terms of developing osteoarthritis, the wear-and-tear kind of arthritis. (2008 Stanford study here;(1) 2011 Australian meta-analysis here).(2)



I also wanted to see if there was a controlled study comparing running on pavement to running on soil or sand, in terms of osteoarthritis or acute injuries. In this I admit I was partly motivated by my snooty trail-runner's disdain for the very roadist culture of the San Diego running community.

Surprisingly at least to me, no such study has been done. Common sense (and expert opinion, i.e. orthopedic surgeons) say soil is better. Unfortunately in medicine, the weight of expert opinion isn't as good as good old data, and it's labelled as mere Class C evidence; in contrast, the Australian meta-analysis above is by definition Class A, because it draws from multiple controlled studies. That said, the Australian study is somewhat limited because it looks at anatomy correlates of knee damage, rather than at the clinical manifestations of osteoarthritis (as in the Stanford study), which is what we care about. That is to say, sure there are osteophytes, but how much more or less often do runners' knees hurt than non-runners'? This looks like a sports medicine study waiting to happen! (Incidentally, here's another post with some more information but which still found the same lack of data on this question.)

I had been coached in high school track that running frequently on sand was bad for your knees, and I'd long stuck with this belief. But I recently revisited that belief based on a conversation with a long-time distance runner patient of 70 years who prefers running on the beach, and whose knees are none the worse for it. There's no study there either, so again for now we'll have to provisionally go with common sense/weight of opinion, and I've now updated my belief that sand is bad for your knees, to sand is probably at worst neutral and maybe better than pavement.


1. Long Distance Running and Knee Osteoarthritis: A Prospective Study. Eliza F. Chakravarty, MD, MS, Helen B. Hubert, PhD, Vijaya B. Lingala, PhD, Ernesto Zatarain, MD, and James F. Fries, MD. American Journal of Preventive Medicine. 2008 August; 35(2): 133–138.

2. What is the effect of physical activity on the knee joint? A systematic review. Urquhart DM, Tobing JF, Hanna FS, Berry P, Wluka AE, Ding C, Cicuttini FM. Medicine and Science in Sports and Exercise. 2011 Mar;43(3):432-42.

Prevention and Treatment of Lightning Injuries

Mark Tanaka helpfully posts a link to a review paper, with evidence classifiers. (If lightning hits you, it's doubtful you'll end up as lucky as this guy.) In SoCal it might not be as scary as in the Colorado mountains in the summer, but it's still useful to know if you spend time outside. You might be the one to save someone's life!

Neat Bits from Medical Journal Article about Crocodile Attacks

From an article in Wilderness and Environmental Medicine (Caldicott DG, Croser D, Manolis C, Webb G, Britton A., "Crocodile attack in Australia: an analysis of its incidence and review of the pathology and management of crocodilian attacks in general." Wilderness Environ Med. 2005 Fall;16(3):143-59.)

Crocodilian hemoglobin has 12 unique bicarbonate binding sites, allowing far more oxygen to be released from the molecule for a given oxygen tension than from the human equivalent. A hybrid human-crocodilian hemoglobin (Hb-Scuba) has been developed and has potential as a synthetic hemoglobin.


In the only reported Australian series to date,77 cause of death was attributed to either decapitation or truncal transection (Figure 2). It should be assumed that massive blood loss90 and drowning are the cause of death in a large number of crocodilian attacks. Assessing the actual cause of death can be complicated by the fact that bodies are sometimes not found, have been eaten, or are decomposed to an extent that makes cause of death difficult to ascertain. Mercifully, death appears to be swift, with little or no bruising seen on postmortem examination.


The power and size of some animals are such that, if not lethal in the first instance, injuries can be as severe as those seen in major road trauma or in the military arena.

I am an Alpha-Actinin 3 Knock-Out Homozygote

I just found this out today when I reviewed my DNA test results. To learn why that's significant for distance runners, go here.