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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.

proteus-e1543713484904.jpg

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.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3512326/

“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).”

And again:

http://danceinjuryrecovery.blogspot.com/2010/01/grand-battement-problems-with-hips-in.html

eds3.jpg

 

12 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 Ancestry.com might be interested in funding the testing. What a story it would make! Perfect publicity. Are you listening Ancestry.com? 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 Ancestry.com? 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
  6. Angela May Syvret-Jones #

    I have MtDna H4a1a1a and family came from Liverpool and involved with shipping on father’s side descendant’s of Joseph Williamson of Liverpool Tunnels fame. I am currently with genebase.com but having a 2nd test with Living Dna to find relatives. I know I have similar features to this person despite being a female. Also have abnormal pupils (but larger). Cup shape tissue beneath and to side of knees. Also have syndactyly (not pronounced but can be missed). Grandmother died from 5 problems one of which was a liver issue. Incidentally I cut my labels out of clothes because they irritate me so much.

    September 13, 2019
    • Byron Deveson #

      Angela, thank you!
      from memory syndactyly can be associated with connective tissue disease. H4a1a1a is inherited from your mother (and her mother and exclusively on the maternal side. It is not passed on by the father) so you would have to trace your female side back as far as possible and then trace all the female descendants until you have a complete a list as possible of all females born 1860-1890 (to cover all possibilities. SM was born in the period 1898-1908) if you want to see if you are related by blood to Somerton Man. Then you have to find all the sons of these women and hope that SM is one of these sons. It could be done but is very time consuming and the efficiency is low due to missing records (speaking from experience). There are better and much easier and cheaper ways to achieve the same end. Genealogical autosomal DNA tests (as opposed to a mtDNA test) will probably give you thirty thousand or more DNA matches and 250 or so fourth cousins or closer matches. I have 33,000 DNA matches and 260 of those are at the fourth cousin or closer level and there is no reason why you would not have a similar number of matches. Ancestry.com currently have autosomal DNA results for 15 million customers and that number is increasing at a truly staggering rate.
      Bottom line? We (you and us in general) need to trace your maternal line but the only practical way of doing this at present is by you taking an autosomal DNA test. I note that you have tested with GeneBase (mtDNA test?) and you are awaiting the results of a LivingDNA test which is an autosomal DNA test. There are several Genealogical DNA sites that will allow you to upload your LivingDNA test data and this will increase the number of your DNA matches.
      By the way, are your parents or grand parents Canadians Keith and Jessie Syvret? I assume that your maiden name is Syvret and you live in Canada? I note that the surname Syvret is quite rare and there are only about 500 people with this surname worldwide. The surname is most prevalent in Canada (257 people) and has the highest density in Jersey, Channel Islands (29 people). See: https://forebears.io/surnames/syvret
      In the 19th Century the surname was essentially only found in the Channel Islands. However, it is your maternal line that is of interest because it is this line from whence you inherited your H4a1a1a mtDNA.
      Thank you for your interest and I look forward to hearing from you.

      September 14, 2019
      • Angela May Syvret-Jones #

        Will try to respond in clear fashion. Lots about me is v.unique and I have been trying to “fit in” and be normal. As u may be able to figure I have given up trying to do that.
        I joined Genebase.com now dnaacess.com about 17 yrs ago and only last year managed to be updated to the new Phylo tree where CRS has been moved to its rightful place on H2, which moved me from 1438a to its current position in H4a1a1a which is firm.

        DNA-All family older than me that is known about are dead.

        Father…Unfortunately I have only a watch left from father which has not been cleaned that I may be abe to get Dna from. I have a half brother from him (uk) and we have met once.

        Mother is different as I have my own Dna and a half sister in UK. There are 2 other half brothers and that is another can of worms.

        Health Issues

        Father. Half brother has some Aspergers and v.high IQ not sure where.

        Mother. Half brother (1) (youngest male sibling) youngest has Aspergers, Crohn’s and connective tissue probs noticed as a child especially in ankles and knees. So he was home schooled until he went to Montessori school in South Australia. Parents (mother and stepfather) come out from UK about 1979/80. IQ high…Chemistry year 11 when he was young. Wrote programming age 5. Is a subsitute IT manager at Uni when needed.

        Mother. Half sister (only and 2nd oldest sibling in UK has ‘delicate’ constitution and son has Aspergers. Looks exactly like my mother except for Jewish nose. Strawberry blonde hair.

        Mother. Half brother (2) (Oldest sibling who happens to be male) High IQ 175.

        Mother. Me. 2nd oldest sibling, oldest girl. Do not look at all like my mother. I am the one who looks like the bust of S.Man. I am v.strong. Pronounces calf muscles and front muscles. Strange pad/sacs below and inner side of knee. Scoliosis (mild), vertical spine due to shape of vertebrae. Hair was blond front top and darker behind. V.sensitive to wool, labels and irritation from fibres. Aspergers. Syndactyly which causes probs now I am older and prevents my long walking. I used to climb, not extreme, mountains.

        I have one family photo from Victorian times of close family with a row of boys that would have been S. man age. A clothing historian would probably be able to work out date and since the family was well known in Liverpool because of my mother’s fathers family line there may be some history somewhere.

        LivingDna.com…sent off my specimen a couple of weeks ago after some communication with them. I explained that I had another test done and sent them my report. They assured me that they could put me in touch with an extended string of relatives up to 16? Have to wait many weeks for that. Probably around 12. The report will be published in a book format.

        There are a lot of other health issues for everyone including me.

        Family trees based on marriage and NOT Dna that I know, or have and/or can locate.

        Father . David Syvret Jones…His father Welsh. His mother (my grandmother) Mary Ann Syvret…..I have her family history back to about 1640 on paper. The Jersey wikipaedia has all my rellies and I uploaded most of mine to LDS many years ago. I was brought up for a few years in the family home Les Cinq Verges, Rue de Corvee. St.Ouen. Jersey. Name probably come from Latin child of Severus…which would be Severit then changed over the years. Family Crest similar to Richard the Lionheart. Lion (Rampant) over heart with blue background from Civray in France to Caen to Jersey. Came from same area as Jeanne D’Arc. The name of town in Normandy is St. Ouen and probably given land in Jersey for loyalty.

        Regarding your query Mother’s line. I do have dates somewhere. Too many pieces of paper right at the moment. Born in Wallasey, now Birkenhead, as was her mother (my grandmother) and her mother (my GGM). Dates, approx, as I am now too lazy to get out (this is giving my head a pain) Patricia Williamson 6 Dec 1925, Emily Constance Lewis 1901, and her mother smith around 1875/6.

        I was planning to get all female certificates after Living Dna results and putting those into order.

        All siblings except one were conceived with other partners by my parents during and outside marriage. I was not expecting a Dna match with anyone as Genebase could not find me a match. I found S.man quite by accident and was piqued by the book of Omar K. as my mother would go into raptures about it. When I saw to bust and some of the details I knew, without a doubt that we are/were related through my mother.

        The last detail. My grandfather on my mother’s father side, Joseph Williamson, was a descendant of Josiah Williamson who owned much of Liverpool and built streets of houses. He also built tunnels underneath Liverpool that used to connect a variety of these. The Williamson square is named after him. My grandmother was a Chemist and worked in the Liver Building. Her husband Joseph Williamson was a bit of a philanthropist and helped Jewish families. The country home is not in a distant relatives hands.

        One of my mother’s nephews by marriage in the head of Roche Chems somewhere in Scotland.

        I don’t mind doing the hard yards. My IQ is off the charts and an outlier SMILES. At the moment my current loo reading is learning Latin one page at a time.

        Incidentally, Byron Deveson, you do not say much about yourself. Pls tell if u have time. I like lots to read even in one paragraph.

        My last job in Gov…Department of Justice, Tasmania..all departments, courts, prisons, labs, corrections BDM,Supreme Court Library, directorate, Consumer Affairs and Fair trading and ended up in Policy and Legislation.

        I haven’t yet located my mothers photo, but I will do at some stage. After reading the versed I must say that some of the letters refer to the style of the lines. Where 3 lines rhyme and one doesn’t the book actually has incorrect info in it if you look up the expected rhyming of the quatrains and what is actually stated so some of the written letters is putting that correct. I was confused by it at first until I investigated the rhyming type and then I realised that S.man and partner had picked up on it themselves. I probably think it may have come about as a translation error in the original translation.

        One idea…ships coming to australia around S.Man’s teens from Liverpool with the last name Lewis.

        Have a look at my Facebook page. Boys middle front in the family photo in my profile

        September 17, 2019
  7. Byron Deveson #

    Thanks Angela, it is much appreciated. I have started tracing your maternal line and thus far I have got back to Mary Melling born 1710 at Upholland, Lancashire, England. Father: John Melling. Mother: Unknown.

    Your direct maternal line is as follows:

    Emily Mary Constance Williamson nee Lewis 1901-1964 m Joseph Willimson
    Edith Maud Lewis nee Stowell 1872-?
    Ann Stowell nee Burrows 1845-?
    Mary Burrows nee Rushton 1816-1888
    Ellen Rushton nee Rawsthorne 1790-1852
    Nancy Rawesthorne nee Scarisbrick 1760-1832
    Ann Scarisbrick nee Simpson 1732-1794
    Mary Simpson nee Melling 1710-?

    I have started tracing all the female lines (= mitochondrial DNA = H4a1a1a) but this is laborious and will take more than a few cut lunches to complete:(

    I haven’t come across any associations with Australia or any obvious Scandinavian ancestry thus far. H4a1a1a is common in Finland but the connection to Finland could be a long way in the past.
    I will post updates as interesting results come up and I will deal with your other question in a later post.
    Thanks again. Byron

    September 18, 2019
  8. Angela May Syvret-Jones #

    Connection would be as a sailor. Both sides of family involved with trading, dockers union, insurance etc. Someone was given george medal for rescuing someone in liverpool harbour. Not at all sure about stowell..I was told it was smith. Am going to get full certificates which show occupation. Where are you located? If u r in SA then u probably know my half brother.

    September 18, 2019
  9. Byron Deveson #

    Thanks Angela,
    the 1911 British Census gives the following details for Emily Mary Constance Lewis and her parents. I am assuming that this is your grand mother because the details fit OK.

    Name: Emily Mary Constance Lewis
    Age in 1911: 9
    Estimated birth year: abt 1902
    Relation to Head: Daughter
    Gender: Female
    Birth Place: Liscan
    Civil Parish: Hoylake cum West Kirby
    County/Island: Cheshire
    Country: England
    Street address: 36 Orrysdale Rd West Kirby
    Marital status: Single
    Occupation: School
    Registration district: Wirral
    Registration District Number: 451
    Sub-registration district: Woodchurch
    Household Members:
    Name Age
    Henry James Lewis 40
    Edith Maude Lewis 38
    Emily Mary Constance Lewis 9

    Name: Edith Maude Lewis
    Age in 1911: 38
    Estimated birth year: abt 1873
    Relation to Head: Wife
    Gender: Female
    Birth Place: New Brighton, Cheshire, England
    Civil Parish: Hoylake cum West Kirby
    County/Island: Cheshire
    Country: England
    Street address: 36 Orrysdale Rd West Kirby
    Marital status: Married
    Occupation: Insurance Agent
    Registration district: Wirral
    Registration District Number: 451
    Sub-registration district: Woodchurch
    ED, institution, or vessel: 11
    Piece: 21952

    Name: Henry James Lewis
    Age in 1911: 40
    Estimated birth year: abt 1871
    Relation to Head: Head
    Gender: Male
    Birth Place: Liverpool, Lancashire, England
    Civil Parish: Hoylake cum West Kirby
    County/Island: Cheshire
    Country: England
    Street address: 36 Orrysdale Rd West Kirby
    Marital status: Married
    Occupation: Clerk (tobacco Warehouse)
    Registration district: Wirral
    Registration District Number: 451
    Sub-registration district: Woodchurch
    ED, institution, or vessel: 11
    Piece: 21952

    1901 Census:

    Name: Edith M Lewis
    Age: 28
    Estimated birth year: abt 1873
    Relation to Head: Wife
    Gender: Female
    Spouse: Henry J Lewis
    Birth Place: New Brighton, Cheshire, England
    Civil Parish: Liscard
    Ecclesiastical parish: Liscard St Mary
    County/Island: Cheshire
    Country: England
    Street address: 13 Wimbledon St.
    Occupation: Clerk, Dock Board.
    Condition as to marriage: Married
    Registration district: Birkenhead
    Sub-registration district: Wallasey
    ED, institution, or vessel: 11
    Neighbors: View others on page
    Piece: 3402
    Folio: 119
    Page Number: 25
    Household schedule number: 156
    Household Members:
    Name Age
    Henry J Lewis 30
    Edith M Lewis 28

    England and Wales, Civil Registration Marriage Index, 1837-1915
    Edith Maud Stowell married Henry James Lewis 1895 July-Sept. At Toxteth Park, Liverpool.

    I think the above suggests that your maternal great grandmother was Edith Maud(e) Stowell born circa 1872-73.

    September 19, 2019

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