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The Somerton Man and what may have ailed him

I’ve lifted Byron Deveson’s comment from Cipher Mysteries, certain that Byron won’t mind – with Nick we’ll have to see – but information such as this is too valuable to lose amongst the thousands of comments and dozens of threads he runs over there, not to mention the invaluable assistance Dusty is giving to those on shaky ground.

Read on, and thanks BD.



The examination of SM’s body by Paul Lawson revealed two uncommon, even rare, features. First, SM’s hand were soft and smooth. Paul was an amateur wrestler a so he would have the experience required to recognise that SM’s skin was abnormally smooth and soft. Paul would have grappled with enough normal skin in his wrestling days.

Second, SM’s calf muscles were both raised and enlarged. I have previously mentioned that these features can occur with connective tissue disease (CTD), particularly Ehlers-Danlos syndrome (EDS). It is unfortunate (for those with EDS of course, but incidentally also for us Taman Shuders) that the ins and outs of connective tissue diseases are still being thrashed out. Because connective tissues are a major component (35%) of our bodies the symptoms associated with CTD can be very diverse.

Ehlers-Danlos syndrome

There are many connective tissue syndromes known at present and my research suggests that this might increase ten fold as the “100,000 genomes” projects in Britain and Australia bear fruit. I suspect/hope more countries will launch their own “100,000 genomes” projects in the near future. In med speak connective tissue diseases are “protean diseases”, which means they display great diversity or variety (indeed a constellation) of symptoms. Protean refers to Proteus, the mythological master of disguise. OK, that’s the classical studies input for the day.


We know from the post mortem findings that SM had the following noteworthy signs additional to those noted by Paul Lawson:

– an enlarged spleen containing a strange pigment. Some EDS syndromes can cause calcification of a wide range of body tissues; almost any organ can be calcified. Maybe the pigment was calcified material (it’s rare so that might be why it was not identified)
some peculiarity with the liver tissue, the liver lobules (calcification? As above)
– hypodontia. EDS is known to be associated with ectodermal dysplasias.
– paralysis of the heart muscles with an otherwise apparently normal heart. EDS can cause a “right bundle branch block with a high risk for sudden death with a normal heart” says the literature

– relatively tall with broad shoulders and a narrow waist. This body type is relatively common with some variants of EDS.

– pronounced gastric bleeding (known to be associated with some EDS variants)
– abnormal pupils of his eyes – smaller than normal and with an uneven edge (iris coloboma?). Known to occur with some variants of connective tissue disease.
– large hands but normal sized feet (Known to occur with some variants of connective tissue disease)

There are some additional possible unusual features that we can infer about SM
he was over dressed for the day (Raynaud’s syndrome?). Raynaud’s syndrome often occurs with EDS.

Raynard’s syndrome

– he wore jockey shorts and these were not commonly worn in Australia at the time (a large scrotum/testicles needing good support can be associated with connective tissue disease). (No way anyone’s getting an image here.)
He seems to be very clean shaven for somebody who died in the late evening. A scanty beard can be a symptom of connective tissue disease. 

OK, so how might this illuminate anything associated with the SM case?

Well, firstly, EDS is rare with an incidence of about one in 5 to 10,000. We now know that SM’s mitochondrial haplogroup is H4a1a1a but unfortunately there isn’t much relevant mtDNA available at present and we will have to wait for more data. It is possible that SM’s mtDNA carries additional mutations over and above those that required by the H4A1A1A haplogroup.

It is possible, even likely, that these additional mutations (variants) could narrow down SM’s maternal ancestral line to a small family group. In my own case my mtDNA (H1ag1) is uncommon but my additional mtDNA variants are sufficient to make my mtDNA unique to my immediate family and known maternal line forbears at present.

The bottom line is that SM’s mtDNA mutations (over and above those required to place him in the H4a1a1a sub-clade) will probably be specific enough to identify SM’s maternal line when enough mtDNA data becomes available. We would have to be lucky at present but mtDNA data is becoming rapidly more available, so, fingers crossed, a total match might emerge in the next couple of years.
When we have a match then it will be possible to see if any of the families have a history of EDS or other connective tissue disease.

SM’s mtDNA haplogroup, H4, is very common in Iceland (9% prevalence) and occurs all over Europe so it is not particularly useful in nailing down SM’s place of origin. However, maybe there are some additional clues.

I think that SM’s face is remarkably hairless and Paul Lawson commented that SM had sparse body hair. I think the most likely explanation is that SM was one of those uncommon western European men who have negligible facial hair. I note that 30% of males with EDS have hypogonadism and this can eventually render them more or less beardless. EDS can also be associated with hypothyroidism which can cause hair loss (and beard loss?). A possible double whammy.

It has previously been suggested that connective tissue disease would preclude ballet but I have recently discovered that this is not the case.

“Interpretation of generalised JHM (joint hypermobility) is not always straightforward and needs a holistic perspective. In fact, JHM is often experienced as an asset for some occupational and sport activities, such as ballet, gymnastics, and playing instruments. At the same time, generalised JHM is the physical marker of various HCTDs. Distinguishing between benign, asymptomatic JHM and an HCTD is of utmost importance for preventing potential life-threatening complications and/or early detecting and managing long-term disability.”


Lifted from

“Joint hypermobility, one of the most prevalent symptoms across multiple types of Ehlers-Danlos syndromes (EDS) and hypermobility spectrum disorders (HSD) can be advantageous in certain sports and activities. And researchers have observed a high prevalence of joint hypermobility among dancers and gymnasts. (Briggs, et al. 2009

However, hypermobility can sometimes come at a cost. From susceptibility to injuries to myriad related health challenges, those living with Ehlers-Danlos or hypermobility spectrum disorders are likely to face considerable challenges as they reach for most elite levels of ballet, gymnastics, and other athletic endeavors where flexibility is seen as a competitive advantage (Briggs, et al. 2009).

Hypermobility is often seen as advantageous for these athletes, literally giving dancers, gymnasts, acrobats, and skaters a “leg up” on their competition. However, the early advantages may quickly become challenges, as serious joint hypermobility may lead to joint instability, frequent dislocations, chronic pain—and a whole host of EDS/HSD symptoms and related conditions. Indeed, recent research demonstrates that hypermobile athletes may become injured more often—and take longer to heal, too often preventing advancement or leading to early retirement (Schmidt, et al. 2017).”

And again:



6 Comments Post a comment
  1. Byron Deveson #

    Could somebody please ask Paul about the canasta bag and accessories?

    December 3, 2018
  2. Clive #

    I’m sure if I ask Paul about a Canasta bag, he’ll give me a good hand!

    December 3, 2018
  3. Are you planning to have another chat with the old lad, Clive?

    April 29, 2019
  4. MPowell #

    I was just Googling my mtDNA H4a1a1a when I came across this post. Then, to my astonishment, I realized it was about a mystery man I had previously inquired about ages ago but have since lost track.
    I did a bit more searching and looked at tamamshud.blogspot and saw the references to Russia and such and thought yet again that I MAY be related to this man. All the connective tissue talk here, which I suspect I suffer from but get ignored due to my bone issues, which include something called “Melorheostosis, also known as Leri disease, is an uncommon mesenchymal dysplasia manifesting as regions of sclerosing bone…” which you speak of something like it as well, seem to support my theory as well, but I guess I just didn’t ‘fit the bill’ when I inquired previously. I remember being ignored and deciding to let it go, but I seem to be getting led back so here I am again… Who do I speak with? Or has this mystery been solved? I should add that the tamamshud page is set up in a way that I just can’t process due to my being on the Spectrum. So I skimmed it as best I could and picked up what seemed important. So if I am missing anything please forgive me!

    June 22, 2019
    • No, MPowell, the mystery has not been solved … but we know he wasn’t wearing striped trousers, that’s for sure. I’ve passed your comment to ByronD .. he has The Knowledge.

      June 22, 2019
  5. Byron Deveson #

    M Powell, Thank you.

    Prof. Abbott’s team has established that SM’s mtDNA haplogroup is H4a1a1a and I suspect that the team might have been able to extract at least a part of SM’s autosomal DNA. Given that you have LWD and that this can sometimes cause calf enlargement (an otherwise fairly rare feature and a notable feature of SM) then Prof. Abbott might be interested in testing your mtDNA and maybe your autosomal DNA as well. And might be interested in funding the testing. What a story it would make! Perfect publicity. Are you listening And the exhumation of SM requires about A$20,000 funding. That’s only US$14,000 and it would almost certainly throw up 2nd or 3rd cousin matches to SM which would be easy to trace. The identification of SM and the subsequent discovery of the events of his life, and his death under suspicious circumstances, with possible Cold War espionage, atom bomb testing and a possible exotic poison thrown in, what’s not to like? The story would make a great mini series. What about it Are you game?

    M Powell, do you have an family connections to Australia or New Zealand? Even 5th or 6th cousins would be worth checking because it is not difficult to trace the descendants (most, there are always some that disappear into thin air, but a 50% to 75% success rate is possible in tracing all of the male descendant born 1898-1908 (SM’s estimated birth) from present 5th or 6th cousin matches.
    The things that I think are important to note in relation to Somerton Man possibly having Leri-Weill Dyschondrosteosis (LWD) are: 1) LWD is an extremely rare condition so tracing LWD genealogies would be easier than usual in so much that the number of people suffering from this condition is very small. However, when we are conceived we all get ten to thirty new mutations that don’t come from our parents, so LWD disease or even the causative mutations may not be present in the forbears of a patient with LWD.
    In any case trying to work backwards from a handful of LWD cases and concomitantly working forward from all of collateral lines would not be feasible at present (but it maybe possible in 10-20 years time). However, if we have a possible identification of SM then it might pay to look at the SOXH and SOXHY genes in the putative relatives.
    2) The genetic causes of LWD are not fully known but most are due to very rare variants (mutations) in the SOXH and SOXHY genes.
    3) LWD is a very variable disease and carriers may not exhibit most, or indeed any, of the physical symptoms. That complicates diagnosis from historical data.
    4) I note that overgrowth (hypertrophy) of the calf muscles can occur with LWD.

    M Powell, if you want to contact me Pete will give you my email address. Cheers. Byron

    June 22, 2019

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