Book Review — The Kingdom of Speech — Part II

Although Darwin held off writing up his ideas for 20 years, fearing the reaction he knew would come from the church, the criticisms that really bothered him the most were those of fellow intellectuals about the evolution of language. They began immediately after the Origin of Species came out in 1859, by linguists and later by Wallace himself. Even worse, one critic mocked him. The idea that language evolved from animal sounds was called the bow wow theory, or language arose from sounds that things made (the ding dong theory).

This is all detailed in pp. 54 – 87 of The Kingdom of Speech, about which I knew very little. If any real experts on the early history of evolutionary theory are out there and reading this and disagree, please post a comment. I am assuming that the facts as given by Wolfe are correct (I’ve already disagreed with him about his interpretation of some of them —

The real attack on Darwin’s ideas is that man’s mental capacities were so far above those of animals, that there was no missing link (particularly since there were lots or primates still around). By this critique man was so special, that a special act of creation (not evolution) was called for.  It’s theology getting in the back door, but of course this is essentially the claim of all theologies — special creation by a superior being(s).

In his later book “The Origin of Species and the Descent of Man” – 1871 (which I’ve not read), according to Wolfe Darwin made up all stories (many involving his beloved dog) to show the antecedents of all sorts of things in animal behavior — Darwin actually said that language originated with the songs birds sang during mating. Female protolanguage persists today in mothers cooing to their babies. Darwin spent a lot of time discussing his dog — how it recognized other dogs as a sign of intelligence. Religion came from the love of a dog for his master (Wolfe claims that Darwin said this in the book– I haven’t read the Descent of Man).

Darwin’s second book didn’t get much response. Postive reviews avoided his reasoning, and negative reviews said it was thin. In 1872 the Philological Society of London gave up on trying to find out the origin of language, and wouldn’t accept patpers about it. The Linguistic Society of Paris did this even earlier (1866).

Evolutionists basically stopped talking about language from 1872 to 1949.

As soon as Mendel’s work on genetics was discovered, evolution went into scientific eclipse. Here was something that wasn’t just armchair speculation about things happening in the remote past, something on which experiments could be done.
Mendel’s experiments with green peas took 9 years and involved 28,000 plants.

In a fascinating aside, Wolfe notes that Mendel actually sent his work to Darwin. Tragically it was found unread with its pages uncut in Darwin’s papers after his death. In all fairness to Darwin, he and his peers had no idea how heredity worked and there are parts in The Origin of Species in which Darwin appears to accept the inheritance of acquired characteristics (the blacksmith’s large muscles passed on to his son etc. etc.). I don’t think you can read the Origin without being impressed by the tremendous power of Darwin’s mind, and how much work he put in and how far he got with how little he had to go on.

Wolfe says Darwin’s ideas about the origin or language were mocked by Gould  one hundred years later (1972) as “Just So Stories”, fantastic bizarre explanations for why animals are the way they are — see I’m not so sure, the citation for this gives an article  Sociobiology which Gould and Lewontin (see later) relentlessly attacked. Gould himself saw what he wanted to see in his book “The Mismeasure of Man” — for details see —

As you can see,The Kingdom of Speech is full of all sorts of interesting stuff, and I’m not even halfway through talking about it.

Next up, linguistics, to include Noam  Chomsky and his admission that he doesn’t understand language or where it came from.

The energy of the future

Almost 60 years ago to the day, a group of Princeton freshman (including yours truly) were dazzled by a talk by Professor Lyman Spitzer, as he described the “Stellarator”, a machine designed to mimic the thermonuclear reaction of the sun. He said it would produce all the energy one could want using nothing more complicated than water (once it was broken down into hydrogen and oxygen). He described it as the ‘energy of the future’.

60 years later it still is.

An article in today’s Nature (vol. 537 pp. 14 – 15 ’16) describes the malfunction of the National Spherical Torus Experiment Upgrade (NSTX-U) at the Princeton Plasma Physics Laboratory (PPPL) founded by Spitzer himself. Apparently some component failed, and the machine will be taken offline for repairs. The machine was being upgraded to produce higher magnetic fields using new coils, and one of them failed.

Since a machine at MIT is being permanently shut down, this leaves US fusion physicists with just one functional machine for experiments.

Book Review — The Kingdom of Speech — Part I

If you’re interested in evolution, its history, English social and intellectual history, language, Chomsky and the origins of the journal Nature then Tom Wolfe’s “The Kingdom of Language” is the book for you. Fellow blogistas will be awed by the clarity and elegance of his writing, and how he easily carries the reader easily along. It’s very funny and sardonic as well. The review will be split into several parts because there’s so much in the book.

One caveat: I’ve made no attempt to check any of the historical statements in the book. Hopefully they are all true. If you think any of it is incorrect, please post a comment.

Although the book has a lot to say about language, it doesn’t get into this until nearly 1/3 of the way through. It starts with Alfred Russell Wallace in 1858 lying in a sickbed with Malaria in the Malay peninsula coming up with the idea of natural selection, survival of the fittest (his term) and the origin of species. He writes an essay of 20+ pages and sends it off to Darwin, in the hopes that Darwin will pass it to Sir Charles Lyell (who Wallace didn’t know) who might find it worthy enough to publish.

Darwin gets it in June and is floored. The ideas that he’s been working on since 1838 (in silence for fear of what the religious establishment will say) are all laid out by what was called a ‘flycatcher’, someone making their living by going off to the colonies and sending back exotica for British Gentleman back home.

Tom Wolfe has always been fascinated by social class and distinctions between them (about this much more in part II).

British Gentlemen were landed gentry, who inherited land and wealth (if not noble titles). Darwin’s history went back to Erasmus Earle who was an attorney for Cromwell in the mid 1600’s. He made so much money, that no one in the succeeding EIGHT generations had to work. Robert Darwin, Charles’s father) nonetheless did — he was an M. D. but was more a businessman. He also attained even more money by marrying Wedgewood’s daughter.

Fortunately Robert had lots of money, as Charles was something of a slacker. He started by studying medicine at Edinburgh, but dropped out. He then went to Christ’s College Cambridge to become a clergyman — he dropped this as well, graduating eventually from Cambridge without an honor to his man. So Robert paid to have Charles to on a 5 year voyage of exploration on the Beagle. On return, Robert bought Charles a amLL pied a terre in the country (Down House) with 8 – 9 servants. (Did you know any of this).

The idea of species change was not new. Erasmus Darwin (Darwin’s grandfather) in 1794 and Lamarck in 1800 thought present day species had evolved from earlier ones.

Lamarck’s rather blasphemous thinking was saved by his heroics in battle at age 17 (as a private). His unit was decimated, all officers killed, Lamarck took command somehow and held their position until reinforcements arrived.

There’s a lot in the book about how Darwin Lyell and Hooker screwed out of the priority of thinking of evolution and natural selection first. Here Wolfe gets things seriously wrong, while Wallace was first into print, his thinking lagged Darwin’s by 20 years. However, Darwin, not wishing to be attacked by the clergy kept things to himself, only telling Lyell about is in 1856.

Most of the readership is probably fully engaged with work, family career and doesn’t have time to actually read “The Origin of Species”. In retirement, I did,and the power of Darwin’s mind is simply staggering. He did so much with what little information he had. There was no clear idea of how heredity worked and at several points he’s a Lamarckian — inheritance of acquired characteristics. If you do have the time I suggest that you read the 1859 book chapter by chapter along with a very interesting book — Darwin’s Ghost by Steve Jones (published in 1999) which update’s Darwin’s book to contemporary thinking chapter by chapter.

Wolfe also gets evolution wrong, saying there is no evidence for it. E.g. no one has seen a species change, etc. etc.  Perhaps, but the biochemical evidence is incontrovertible for descent with modification, otherwise you couldn’t replace a vital yeast protein gene with the human homolog and have it work.

Do you know what the X club is? It was a group of 9 naturalists (including Thomas Huxley and Hooker) who met monthly to defend Darwin’s ideas. They also created the journal we know today as Nature.

This actually explains a lot of stuff there that I’ve read over the years — the correct interpretation of evolutionary doctrine receives a great deal of space — punctuated evolution, group selection, kin selection, what is the proper unit of selection etc. etc.

The attacks that bothered Darwin the most, were those about language. That’s the subject of the next part of the review.

The world’s longest allosteric effect

I think there is some very interesting protein physical chemistry to be discovered/worked out based on a recent report [ Nature vol. 537 pp. 107 – 111 ’16 ]. It involves a long (2,200 Angstrom) coiled coil protein called EEA1 (Early Endosome Antigen 1). It contains 1,400 amino acids 1,275 of which form a coiled coil.

If you are conversant with the alpha helix and how two of them form a coiled coil, jump to ****. Otherwise here is some background and links to pictures which should help.

The alpha helix is a type of protein secondary structure in which the protein backbone assumes the shape of a coiled spring. There are 3.64 amino acids per turn. A single turn is 5.4 Angstroms high and 11 Angstroms wide. The alpha helix is right handed. That is to say, that if you orient the chain so that your thumb points from the N terminal to C terminal amino acid, the chain will twist in the direction of the fingers of the right hand as it rises. For some reason I can’t provide a link to a very large number of images for you hit. However, when I go to Google and type images of alpha helices you see them immediately — you’ll have to do the same to get there.

Coiled coils have two alpha helices winding around each other. This means that for secure interactions, the same types of amino acids must repeat again and again. A 7 residue periodicity (abcdefg)n in the distribution of nonpolar and charged amino acid residues is a feature characteristic of proteins which form alpha helices coiled about each other (coiled coil molecules). The 7 amino acids are lettered a – g from amino to carboxy. Positions a and d are usually hydrophobic amino acids (Leu, Ile, Val, Ala), positions e and g are usually polar or charged. The nonpolar a and d side chains associate by means of complementary knobs into holes packing. Each individual alpha helix is right handed, but the two helices wind around each other with a left handed turn. There are 3.64 amino acids per turn of an alpha helix, so for a regular repeating structure an amino acid should appear at the same position in space on the alpha helix (which forms a rigid rod). To see all the pictures you want — go to Google and type “Images of the Alpha Helix”.

To get the number of amino acids down so there are 3.5 per/turn (so the structure can repeat exactly every 7 amino acids –e.g. after 2 alpha helical turns) left handed supercoiling of each helix occurs (it’s a chicken and the egg situation). The helices are at an angle of 18 degrees to each other, and every 3.5 amino acids still form a 5.4 Angstrom (when one helix is viewed in isolation), but due to the tilt, they take up 5.1 Angstroms. This means that the same type of amino acid is found at positions 1, 8, 15, 22 etc. All intermediate filament proteins (keratin, neurofilaments, vimentin, etc.) contain a coiled coil structure. So to see all the pictures you could want — go to Google and type “Images of coiled coil proteins”

So the 1,275 amino acids of EEA1 divided by 3.5 and multiplied by 5.1 give you a coiled coil of fairly enormous length for a protein (1,858 Angstroms) — average protein diameter (if there is such a thing) is under 50 Angstroms

Functionally, EEA1 seems to be used as a tether with one end free and the other end hooked to a target membrane which wants to ‘catch’ the early endosome. The target membrane isn’t specified in the paper. Apparently EEA1 when not binding the endosome, is in a fully extended state, at around 2,000 Angstroms.

A protein called Rab5 is found on the early endosome membrane, and when EEA1 contacts it, the long coiled coil helix collapses, dragging the endosome toward the target membrane.  This is entropy in action, there being far more configurations of a collapsed protein than a rigidly extended one. To feel entropy for yourself, just pull on a rubber band, entropic effects just like this one are what you feel pulling back.

The collapse of EEA1  is an allosteric effect and a very long one, although the authors note long range allosteric effects are “not uncommon among coiled coil proteins”.

EEA1 is more complicated than initialy described. It contains amino acids which disrupt the 7 amino acid periodicity of the coiled coil (making it a jointed structure). The authors then made an EEA1 protein without the joints (so it was a perfect very long coiled coil). Binding of this protein to Rab5 on an endosome doesn’t result in collapse. So clearly normal EEA1 collapses at the ‘joints’.

The authors talk about some hypotheses as to how this happens in the Supplementary material (but I was unable to find).

So here’s a good research proejct for an enterprising grad student: either find out why and how a protein with multiple joints should exist in a fully extended configuration, or figure out how binding of Rab5 at one end of EEA1 produces such profound allosteric changes through this long linear protein. Happy hunting and thinking.

I must say it’s a pleasure to get back to chemistry after writing about the neurologic and medical issues of the presidential candidates.

Addendum 29 September — I wrote one the following to one of the authors (Dr. Grill) sending him the post above

Dr. Grill

Greatly enjoyed the paper.  I could never find the discussion of possible mechanism in the supplementary material.  You might enjoy the following post written about the paper

He replied as follows:

“Dear Luysii thank you very much for the kind words, and I really like your title!

With the supplementary discussion, besides the method part there is an additional supplement file on the Nature website that is easy to miss…I attach it here for you. We discuss this a bit more, but I must admit that this is not very satisfactory at the moment. We just don’t know how this works, and much of our efforts at the moment are dedicated to understand”
So for other readers of the original paper who also can’t find the supplement with the authors’ speculations as to what is going on– here  is what he sent.

” A key question is how Rab5 can induce such a long-range global molecular transition in flexibility of EEA1. Indeed, long-range allosteric effects have been observed for other coiled-coil proteins. In the case of myosin, the presence of discontinuities in the coiled-coil heptads drive structural changes to flexibility. Other tethering factors may bend through large breaks in coiled-coil structure acting as joints, although it remains to be shown whether and how conformational changes are triggered by Rab binding, as shown for EEA1.

Furthermore, a dynamically flexible coiled-coil is mostly extended, provided its ends are free60. However, when the ends of this coiled coil are tethered, bent, or when torsion is locally applied, compensatory structural changes are propagated and even amplified through the length of the structure. Our results suggest that a change in intrinsic static curvature may contribute but is not the major cause for the reduction in end-to-end distance. However, a more rigorous assessment would require visualizing the thermal fluctuations of the bound and unbound EEA1 very rapidly and in three dimensions.

Force generation due to entropic effects plays a key role in many processes in biology ranging from DNA cytoskeletal filaments to motor proteins. Switching a molecule from stiff to flexible could be an effective and general mechanism of many coiled-coil proteins for generating an attractive force, thereby pulling two objects together or allowing reactions otherwise hindered by polymer rigidity. Future experiments will test to what extent the entropic collapse is a general mechanism used not only by membrane tethers but also in other biological processes.”


Hillary’s health — you can see a lot by looking

Last night’s debates should put two suggestions about Hillary’s health to rest and gives some evidence for two others. First, she does not have Parkinson’s disease. Second, she does not have epilepsy. Third, her eye movements still show some residua from the stroke of December 2012. Fourth, she may have a mild proximal myopathy.

Now to elaborate.

Parkinson’s disease: Two great things happened in September 1970 — I finished my two years in the Air Force and L – DOPA was released for use in the USA. American neurologists had been reading about the great things it was doing for the disease in Europe for almost 10 years. So when I went back to complete the last two years of my residency, the chief put me in charge of the L – DOPA clinic he’d just set up. So until retirement in 2000, I treated lots of people with it.

As the chief said — Parkinson’s disease is a Yellow Cab disease. If you see a Yellow Cab on the street, you don’t write down the license number, go down to city hall and find that it was registered as a Yellow Cab. You look at it and say “that’s a Yellow Cab”.

Parkinsonians have a rather immobile face (masklike) — Hillary’s face is quite mobile. Their speech lacks the normal musicality of speech (prosody), Hillary’s speech has normal inflection. Parkinsonians have a slow, stiff gait with difficulty initiating it. Hillary has none of this. Finally there is no sign of any tremor.

Epilepsy: Videos of purported seizures are out and about on the internet, particularly one during an interview. I thought that the ones I saw looked rather edited, as though some individual frames had been deleted from the videos. Fortunately last night we had an opportunity to see for ourselves. Toward the end of the debate, she had another episode, during which she shook her head and her shoulders for a few seconds. This happened in real time, so we could run the video recording backwards and forwards. At no time did she appear to be out of contact, and she then continued on with what she was saying without pause. So it’s just something she voluntarily does. It isn’t epilepsy.

Eye movements: Recall that after the stroke in December 2012, Hillary had double vision and had to wear Fresnel lenses to correct it for a few weeks afterwards — pictures of her testifying in congress January 2013 show this. So last night there was a 90 minute opportunity to watch the way her eyes move. They aren’t quite normal – on looking to her left the right eye lags and doesn’t bury the white. Even though Trump was to her right, she turned her head rather than her eyes to look at him, so I only saw her look to her right on a few occasions, but when she did her eyes appeared to move together. No other residua of a brainstem stroke were present such as slurred speech (dysarthria), facial weakness, facial asymmetry.

Proximal muscle weakness: The internist referred to in a previous post noted the following:

“There were shots a month or so ago of her needing help to get up outdoor stairs and also needing a small step-stool to get up into a Secret Service Suburban. My wife and I hop in and out of a Yukon and do not need any step device (they are of comparable age). After a photo of her doing that was published, she started getting in and out of vehicles on the side away from cameras and was also switched to a taller van with a step mounted on the vehicle. In February, press was forbidden by her staff from filming her climbing the stairs to board her private jet.”

He wondered if she could have something like limb girdle dystrophy.

Well, such a dystrophy is certainly possible. Although Hillary  had no difficulty standing for 90 minutes, at the end, she appeared to waddle as she walked toward the moderator.. There wasn’t really enough time to definitely say that she waddled.  It’s worth carefully watching the way she walks in the future.

Why is waddling a sign of mild weakness of the muscles of the pelvic girdle? Believe it or not the buttocks are not a secondary sexual characteristic. The main buttock muscle (gluteus maximus) is so big because it has so much work to do.

Think about what you do when you take a step forward with your right foot. To remain stable, your entire upper body weight must  be strongly plastered to your left hip. You need a strong, large muscle to do this (the gluteus maximus). What happens if the muscle is weak? Your upper body would fall to the right. How would you prevent this? By throwing your upper body to the left, putting its center of gravity there, so it presses on the left hip with greater force. A similar thing happens when stepping forward with the left foot. The net effect is that you waddle, which is what Hillary appeared to do.

It’s worth watching her walk in the future.

Stamina: she was under 90 minutes of stress, and showed no sign of fatigue.

Now, hopefully, back to the science, with a very long (over 1,000 Angstroms) allosteric effect.

Trump’s health

Here is a link to an article containing the full text of the letter by Trump’s personal physician Harold Bornstein M. D. -=-

Trump’s lipids could be better (total 232) and he is currently taking a lipid lowering agent (a statin). Aside from this, his labs are good (perfect in fact). He does take care of himself, and has annual physicals.

It isn’t clear why he had a transthoracic echocardiogram 2 years ago. Otherwise aside from that every test performed is pretty standard for a man his age.

Despite being overweight his blood pressure is excellent (particularly for man his size).

The indications for low dose aspirin aren’t stated, but yours truly has taken much more for decades based on a reading of the literature while in practice showing that doses of two adult aspirin a day reduced the recurrence rate of stroke by 33%.

So his main health problem is weight and mildly elevated lipids (even on medication).

His BMI (Body Mass Index) is stated to be 29.5. So it’s time for you to calculate your own — don’t worry that BMI is usually based on weight in kilograms and height in meters — the following site lets you put in your weight in pounds, and your height in inches — To get started, calculate your own BMI– A 6 footer would have to weigh 222 pounds to be obese (BMI over 30).

So is Trump’s BMI of 29.5 bad? Overweight is defined as a BMI over 25. So is a BMI over 25 bad? Not if you’re interested in mortality (death) as opposed to morbidity (things like heart attack and stroke). It turns out that the BMI with the lowest mortality at 70 is over 25 — e.g. 26. e.g. in the overweight range as currently defined. I don’t think there are good statistics on overall morbidity vs. BMI (there probably is for heart attack and stroke separately).

Now it gets interesting. That statistic cited above is based on the following data on 3 million people in 97 different studies [ J. Am. Med. Assoc. vol. 309 pp. 71 – 82 ’13 ].

At 6 feet 1+ (which I used to be) a weight of 190 puts me at 24.69. To be obese (BMI over 30) I’d need to weigh 228 (which I almost did 54 years ago).

When you plot BMI vs. probability of death you get a U shaped cure, with the very thin and the very fat showing increased risk of dying (mortality). The paper is interesting as it shows 6 curves for people at ages 20, 30, 40, 50, 60, 70. As one might expect, the curves for each age lie below the next oldest. All of them rise with BMIs under 20 and over 30, so there’s no argument about whether obesity (BMI over 30) is bad for longevity.

Well, if the curve is U shaped, it has a minimum. The excitement comes in because the healthiest weight (the minimum) is a BMI of just over 25 for those in their 60s and around 26 for those in their 70s. Also in ALL 6 age groups the curve is pretty flat between 25 and 30, rising on either side of the range.

Naturally people who’ve invested their research careers in telling everyone to diet and that weight is bad, don’t like this, and a symposium involving 200 unhappy people convened 20 February at the Harvard School of Public Health is described, along with a lot of the back and forth between the authoress of the study (Flegel) and Willett of Harvard who didn’t like it one bit. The best comment IMHO is from Robert Eckel “We’re scientists. We pay attention to data, we don’t try to unexplain them.” Read the article, it’s well written and there’s a lot more.

One final point, which might explain why the minima of the curves shift to higher BMIs at older age — which the article didn’t contain. People lose height as they age, yet the BMI is quite sensitive to it (remember the denominator has height squared). The great thing about BMI is that it’s easily measured, and doesn’t rely on what people remember about their weight or their height. Well as a high school basketball player my height was 6′ 1”+, now (at age 78) it’s 6’0″. So even with constant weight my BMI goes up.

Well it’s time to do the calculation to see what a fairly common shrinkage from 73.5 inches to 72 would to to the BMI (at a constant weight). Surprisingly it is not trivial — (72/73.5) * (72/73.5) = .9596. So the divisor is 4% less meaning the BMI is 4% more, which is almost exactly what the low point on the curve does with each passing decade after 50 ! ! ! This might even be an original observation, and it would explain a lot.

Well, that’s the take of this neurologist on Trump’s health —’s pretty good. I’m going to pass this post on to the very smart internist (whose comments about Hillary you can read in — for his take, as there really isn’t anything in the history suggest a neurologic problem. Unlike Hillary, he hasn’t fainted twice in the past 4 years, and hasn’t had a neurologic deficit persisting for a month.

The impeccable timing of the New York Times — take II

Reality keeps intruding. I’d much rather be posting about a marvelous paper (see the end), but the Sunday New York Times of 18 September 2016 had 3 articles telling us all how deplorable, irrational and islamaphobic we are, the day after 3 separate attacks on the citizenry (the Chelsea and Seaside Park bombs and the knife attack in Minnesota).

Two were on the opinion page — one comparing the Jews of the 30s trying to escape the Nazi’s with the mideast refugees, another concerned “England’s Forgotten Muslin History”. Well, we all know what a bunch of terrorists the Jews of the 30s were.

On p. 13 “Level of Hate Crimes Against U. S> Muslims Highest Since After 9/11” “Some Tie Attacks to Trump’s Statements” It couldn’t possibly be anything they’ve done.

For your enjoyment, here’s the post of just 3 months ago (13 June)

The impeccable timing of the New York Times

After putting ex-Weatherman Bill Ayers on page 1 saying he wished he’d ‘bombed more’ the day of the attack on the World Trade Center in 2001, the New York Times kept its unenviable timing record intact by posting “Dreams of my Muslim Son” about Islamophobia on the editorial page the day of the Orlando massacre. Usually they run their invariable innocent Muslims fearing hate crimes by American rednecks story a day or so after the latest atrocity.

Unfortunately Orlando can’t be camouflaged as workplace violence or the response to some video or other a la Benghazi. The perp was far too explicit. Nor can it be blamed on the failure of ‘the MidEast Peace Process’ or Israel, although undoubtedly some will try.

If I were the Muslim leadership in this country, I’d try to put together a Million Muslim March on Washington to protest the Orlando, San Bernadino, Boston etc. etc. massacres, as blots on the name of Islam. ISIS would probably try to kill a few, but it’s time for them to stand up, assuming there are large numbers of US Muslims that actually think this way.


You could not have a better example of how totally out of touch elite opinion is and the placement and timing of these articles is exactly an expression of elite opinion.

I had thought that the terrorists would be lying low until after the election, as terrorist acts work in Trump’s favor. But as a friend said about another Muslim group — they never miss an opportunity to miss an opportunity.

The paper I’d planned to write about is Nature vol. 537 pp. 107 ’16 (1 September 2016 Issue).

Now on to Trump’s health information.

Thank God for the internet, warts and all

Here’s the New York Times Monday reporting on Hillary’s fainting spell the previous day — “Clinton Treated for Dehydration and Pneumonia”, “Falling Ill at 9/11 Event”. Then it states that she ‘had to be helped into a van by Secret Service Agents”.

Still on the first page, “about 90 minutes after arriving there (Chelsea’s apartment) Mrs.Clinton wearing sunglasses emerged from the apartment” She is then quoted as “I’m feeling great” “It’s a beautiful day in New York” On the front page there’s a picture of her at the 9/11 service before anything happened. Inside there’s a picture of her leaving the apartment looking just wonderful and smiling.

The Times does mention the video, and noted that it captured ‘what appeared to be her legs buckling’.

Back in the day when the NYT controlled the news, you’d think nothing much happened. However, anyone looking at the video can see her passing out and nearly hitting the pavement, until she was caught by her handlers.

As I predicted in an EMail to some friends, the Times in its letters to the editor today had a letter praising Hillary as a typical plucky lady who carried on no matter what. For a paper that routinely headlines articles dumping on the church (the front page of 14 Sep has an article concerning how Putin is using the Russian Orthodox Church to extend Russian power abroad) they certainly love one of its institutions (the amen corner — aka letters to the editor).

The paper of record in Northampton described the event has Mrs. Clinton becoming “Unwell”, With Hillary in seclusion and unable to campaign, the lead story on Yahoo yesterday, concerned an attack ad of Hillary’s on Trump, not anything he said or did.

The internet and the blogosphere is often scatological, misleading, irritating and biased. But there’s such massive coverage on the internet that it has broken the monopoly of the mainstream press. Thank God for them warts and all.

Now, hopefully back to the science.

Hillary’s fainting spell

And I thought I’d retired as a neurologist. What is there to say about the video that shows Hillary Clinton being held up by a woman on her left, later by others, and then collapsing sufficiently that her head is at most 3 feet from the pavement in one frame. You don’t have to go to medical school to call this a fainting spell.

As to what caused the episode, we can only speculate. I see no reason to trust what the campaign is putting out, that she had ‘pneumonia’ for the previous two days. Since I’ve already gone on record that she had a stroke in December 2012 ( ), not due to head trauma sustained in what was said to another fainting spell, people have asked me what the event could be neurologically.

But I’m a neurologist not an internist, so I talked to a very smart one for his take.

“Somewhat oddly, her campaign now reports that pneumonia had been “diagnosed” as of two days before her collapse. However, she was not acting as if she is infectious, going out into crowds and getting close to small children. The Clintons are known for lawyerly parsing of phrases carefully, so it may matter what the meaning of pneumonia “is.” Therein may lie a clue which puts the chronic non-productive cough of many months duration, along with apparent decreased stamina and a carefully tuned and truncated schedule over a similar period into perspective.

Chronic lung disease, particularly a mildly progressive idiopathic pulmonary fibrosis/interstitial pneumonia could fit that picture. It would also be technically true as a diagnosis. Whatever pulmonary condition she has does not appear to be acute.”

He also had an interesting observation on the way the faint was handled. “There must be some chronic known condition, as she has two attendants with her now at all times–large black male and heavyset white woman. Her collapse was handled as if it were familiar territory. Hustling a woman of her age into a van and driving to her daughter’s apartment is a highly unusual way to handle such a loss of consciousness in a 68-year old woman, particularly when there had to be a number of emergency vehicles loaded with EMT’s on the scene and well as several hospitals at least as close as her daughter’s apartment.” To which a friend noted that the secret service is trained to react immediately to situations like this, going through dry runs of all sorts of eventualities etc. etc.

Taking her to her daughter’s apartment is quite strange, given the way the secret service was acting 40 or so years ago. Back then, a neurosurgeon in Billings Montana told me that the secret service had called him up and asked him to be available in the coming weekend as the president would be visiting Yellowstone, a mere 140 miles away by the nearest road. It seems likely that some hospital close by was on alert that Hillary was in the neighborhood.

The internist has been watching her a lot more closely than I have and noted the following “There were shots a month or so ago of her needing help to get up outdoor stairs and also needing a small step-stool to get up into a Secret Service Suburban. My wife and I hop in and out of a Yukon and do not need any step device (they are of comparable age). After a photo of her doing that was published, she started getting in and out of vehicles on the side away from cameras and was also switched to a taller van with a step mounted on the vehicle. In February, press was forbidden by her staff from filming her climbing the stairs to board her private jet.” He wondered if she could have something like limb girdle dystrophy — watching her walk and stand during the upcoming debates will be helpful for determining that.

Finally he noted — “There are also a number of cardiovascular causes (transient arrhythmia for starters) as well as pulmonary microemboli which can cause collapse like that.”

Now for the neurologic possibilities.

There are peculiar videos purporting to show Hillary having a ‘seizure’ during a press conference. They look doctored to me. She appears to be compulsively laughing. Such seizures are called gelastic epilepsy. They are rare but I’ve seen them. They arise from the hypothalamus and the temporal lobes. Nothing in the current video is suggestive of a seizure. Loss of consciousness at this age rarely is due to a seizure. Cardiovascular causes are far more likely.

Another possible cause is a brainstem transient ischemic attack (TIA), since we have been told that the clot of 2012 was in a draining sinus of the posterior fossa (we have no pictures of any sort from that episode). Recovery in 90 minutes is consistent with either syncope or TIA.

The final possibility is that the event is a warning of an impending second stroke. If you look again at the post about the events of 2012, you’ll see that I speculated that the ‘faint’ occuring in the week of 9 December could have been a transient warning of the cerebral venous thrombosis she suffered that month. I don’t think this likely, but when I examined for the Neurology boards, fellow examiners always wanted to see how many possibilities for diagnoses the candidates can muster.

So what do I think it was? A fainting spell (syncope if you want to be impressive). Her blood pressure dropped for some reason or other, the brainstem which maintains alertness didn’t get enough fresh blood and she passed out nearly. The people with her did NOT help by keeping her erect, which kept the brainstem from getting the blood (and the oxygen it delivers) it needed. In fact holding someone up who has fainted is the perfect crime, as the brain deprived of oxygen long enough begins to die, and no marks will be found on the body.

Why out of the thousands there, on a warm but not excessively hot day, she was the only one to pass out can only be the subject of speculation until more details are forthcoming. The health of a possible future president is simply too important not to speculate about.

What neuropharmacology can’t tell us about opiates and addiction

A friend’s wife had some painful surgery and is trying to get by with as little opiates as possible, being very worried about becoming an addict, something quite reasonable if all she had to go on was the popular press with lurid stories of hapless innocents being turned into addicts by evil physicians overprescribing opiates (it’s the current day Reefer Madness story). Fortunately her surgeon wisely told her that her chances of this happening were quite low, since she’d made it past 50 with no dependency problems whatsoever. Here’s why he’s right and why neuropharmacology can’t tell us everything we want to know about opiates and addiction.

Back in the day, disc surgery required general anesthesia, dissection of the back muscles down to the spine, sometimes chipping away at the bones of the spine to remove a bone spur (osteophyte) and/or removal of the offending herniated intervertebral disc. This meant a hospital stay (unlike my ophthalmologist who had a microdiscectomy as an outpatient a few years ago). This was the era of the discovery of the protein receptor for morphine and other opiates, and we were all hopeful that this would lead to the development of a nonAddicting opiate (narcotic). Spoiler alert — it hasn’t happened and likely won’t.

Often, I was the neurologist who diagnosed the disc and told the surgeon where it was likely to be found (this was in the preCT and later the preMRI era). I’d developed a relationship with most of those I’d referred for surgery (since it was never recommended, without a trial of rest — unless there were compelling reasons not to — trouble controlling bowels and bladder, progressive weakness etc. etc.). I was their doc while they tried to heal on their own.

So post-operatively I’d always stop by to see how the surgery had worked for them. All were on a narcotic (usually Demerol back then) as even if the source of their preoperative pain had been relieved, just getting to the problem had to cause significant pain (see above).

If the original pain was much improved (as it usually was), I’d ask them how they liked the way the demerol made them feel. There were two types of responses.

#1 I hate feeling like this. I don’t care about anything. I’m just floating, and feel rather dopey. I’m used to being in control.

#2 I love it ! ! ! ! I don’t have a care in the world. All my troubles are a million miles away as I just float along.

Love it or hate it, both groups are describing the same feeling. Neuropharmacology can help to tell us why opiates produce this feeling, but it can’t tell us why some like it (about 5%) and the majority (95%) do not. This clearly is the province of psychology and psychiatry. It’s the Cartesian dualism between flesh (opiate receptor) and spirit (whether you like what it does). It also shows the limitation of purely physical reductionism of the way we react to physical events.

The phenomenon of a small percentage of people becoming addicted to a mind altering substance is general and is not confined to one class of drug. We were told never to prescribe chronic benzodiazepines (valium, etc. etc.) to a recovered alcoholic. People who get hooked on one thing are very likely to get hooked on another.

I realize that some of this could be criticized as blaming the victim, but so be it. Medical facts are just that, like what they say or not.

Addendum 11 Sep ’16 — I’m not saying that you won’t become physically dependent on opiates if you get them long enough and at high enough doses. We all would. Even if this happened to you. When you no longer needed them for pain and went through medically supervised withdrawal, you wouldn’t crave them, and do crazy things to get them (e.g. you were physically dependent but never addicted to them — it is important to make the distinction).

Example — when I was in the service ’68 – ’70, we had half a million men in Vietnam. Everyone I’ve talked to who was over there says that heroin use among the troops was 25 – 50% (high grade stuff from Thailand was readily available). As soon as they got back to the states, the vast majority gave them up (and with minimal withdrawal requiring my attention – I think I saw one convulsion due to withdrawal).