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.
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.
– 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 Ethlers-Danios.com.
“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).”