Late addition (July 2019)
Please forgive this postscript, correction, “prescript”, correction, intrusion, added many years later – based on some 350 and more postings here and elsewhere.
That’s including some 7 years of my hands-on investigation into image-forming techniques, chosen to be credible with simple, indeed crude, medieval (14th century) technology etc etc.
(Oh, and yes, I accept the radiocarbon dating, despite it being restricted to a single non-random corner sample, making all the oh-so-dismissive, oh-so-derogatory statistics-based sniping totally irrelevant – a ranging shot being just that me dears- a single ranging shot, albeit subdivided into three for Arizona, Oxford and Zurich).
Sindonology (i.e. the “science” , read pseudoscience – of the so-called “Shroud ” of Turin) can be simply summed up. It’s a re-branding exercise, one designed to pretend that the prized Turin possession is not just J of A’s “fine linen”, described in the biblical account as used to transport a crucified body from cross to tomb.
Oh no, it goes further, much further, way way beyond the biblical account. How? By making out that it was the SAME linen as that described in the Gospel of John, deployed as final “burial clothes”. Thus the description “Shroud” for the Turin Linen, usually with the addition “burial shroud”. Why the elision of two different linens, deployed for entirely different purposes (transport first, then final interment)?
Go figure! Key words to consider are: authentic relic v manufactured medieval icon; mystique, peaceful death-repose, unlimited opportunity for proposing new and ever more improbable image-formation mechanisms etc. How much easier it is to attach the label “Holy” to Shroud if seen as final burial clothes, in final at-peace repose – prior to Resurrection- as distinct from a means of temporary swaying side-to-side transport in an improvised makeshift stretcher !
As I say, a rebranding exercise (transport to final burial shroud) and a very smart and subtle one at that . Not for nothing did that angry local Bishop of Troyes suddenly refer to a “sleight of hand” after allegedly accepting it when first displayed. Seems the script was altered, or as some might say, tampered with! It might also explain why there were two Lirey badges, not just one. Entire books could be written on which of the two came first… I think I know which, with its allusion (?) to the Veil of Veronica… yes, there are alternative views (the face above “SUAIRE” a visual link to the face-only display of the Linen as the “Image of Edessa” or as that on the then current “Shroud” per se.
Face shown (left) on mid- 14th century Machy Mould (recently discovered variant of the Lirey Pilgrim Badge) above the word “SUAIRE” (allegedly meaning “shroud”). Inset image on the right: one version among many of the fabled “Veil of Veronica” image. I say the two are related, and deliberately so, but this is not the time or place to go into detail.
No, NOT a resurrectional selfie, but instead a full size version of, wait for it, the legendary VEIL OF VERONICA , product of inital body contact – no air gaps- between body and fabric, but with one important difference. The Turin image was intended to look more realistic, less artistic.
How? By displaying a negative tone-reversed image implying IMPRINT (unless, that is, you’re a modern day sindonologist, in which case ‘resurrectional proto-photographic selfie” becomes the preferred, nay, vigorously proferred explanation assisted by unrestrained imagination, creation of endless pseudoscience etc etc, with resort to laser beams, corona discharges, nuclear physics, elementary particles, earthquakes etc etc – the list is seemingly endless!
Welcome to modern day sindonology.
Personally, I prefer no-nonsense feet-on-the-ground hypothesis-testing science, aided by lashings of, wait for it, plain down-to-earth common sense.
Updated 21st April 2012 with an “annotated” version in which I imagine myself to be Alan D Adler explaining his ideas in simpler terms, as if to someone on a web forum, while still trying to stay as close to his original version as possible in terms of content and interpretation (not always an easy task, even for this PhD biochemist). But first, the original version, with the annotated one tagged on the end:
Here is a passage from the revered STURP scientist Dr. Alan D. Adler (1931-2000). He is credited with having convinced many a wavering sceptic that it really is blood on the Shroud – albeit degraded blood in an unusual conformation, complexed with bilirubin. He proposed the latter to account, perhaps among other things, for residues still retaining their red colour after centuries of exposure to oxygen, moisture , microorganisms etc.
Alan D. Adler is, or rather was, an acknowledged expert in the field of porphyrins, which, when complexed with ferrous (Fe++) iron and linked to globin proteins, constitute the red pigment of oxygen-transporting erythrocytes (red blood cells).
I do not intend to comment here on the post, but invite those with some knowledge of blood chemistry and trauma physiology to ask themselves the question posed in the title. Is this science? In other words, I intend to take a back seat for now, but welcome questions, discussion and, most of all, informed comment.
“… The next test we did was to take micro-spectrum photometry of the non-birefringent red-coated fibrils from the Shroud. It was obvious that the spectrum it produced did not match the spectrum of methemoglobin, at least as it is given in the standard references, which is a solution spectrum of blood. But in a film of hemoglobin there is a confirmation (sic) change ;it no longer remains in the “met”form but goes to the para-hemic form. It is known now that there is a certain species which will spontaneously go the para-hemic form if there is not enough turnover in the spleen and liver to process the blood fast enough. We found a spectrum that was characteristic of only one known group of compounds -the so-called high spin, high iron porphyrin. So instead of being wrong, the spectrum peaks were in the right place. What we were seeing was the breakdown products of hemoglobin – bilirubin and biliverdin. And one began to make sense out of all of this. There is an extraordinarily high bilirubin count, almost as high as the methemoglobin. Now how does one account for such a high bilirubin in a person? One possibility is that the person had a severe malaria, but this does not seem very likely. But a torture, scourging and crucifixion leading to shock – that would produce a tremendous hemolysis. In less than 30 seconds the hemolyzed hemoglobin would run through the liver, building up a very high bilirubin content in the blood. If that blood then clots, an exudate forms, and all the intact cells with bilirubin stay behind, only the hemolyzed hemoglobin goes out along with the serum albumin which binds the bilirubin. So what one ends up with is on the cloth is an exudate which has an enhanced bilirubin with respect to the hemolyzed hemoglobin.You now mix bilirubin which is yellow-orange with methemoglobin in its para-hemic form which is an orangey-brown and you get blood which has a red color.
In fact, we have been able to simulate the spectrum in the laboratory by the process described above. This very strongly suggests that the blood stains are of a man who was severely beaten. No one would have ever dreamed when we first started doing the analysis that the chemistry would provide corroborating evidence to what the pathologists concluded long ago about the Shroud figure. The blood has no cells, is very low in potassium, and has the right color and composition for the blood of a man who was severely flogged and crucified. This is entirely consistent with the forensic evidence…”
Now for that annotated version (see preamble added 21st April):
“… The next test we did was to take micro-spectrum photometry of the non-birefringent red-coated fibrils from the Shroud.
We selected for study the smallest fibre components of the Shroud that were red, in other words stained with what one assumed was blood. (Some have asked why ancient blood should still be red – instead of black). We applied a scanning technique that measures characteristics like absorption spectrum of near uv and visible light, since blood components have characteristic spectra (e.g. the so-called Soret absorption band of heme proteins at 400nm).
(ed: it’s not immediately clear to me why the selected fibres had to be non-birefringent, since birefringence is simply a property of highly ordered arrays of cellulose, and I don’t see why a fibril cannot be blood stained and have ordered cellulose).
(ed: The birefringence test was a reference, I now realize, to the iron oxide debate, not cellulose)
It was obvious that the spectrum it produced did not match the spectrum of methemoglobin, at least as it is given in the standard references, which is a solution spectrum of blood.
In fresh blood which is usually bright red (a little darker if de-oxygenated) the hemoglobin (ed: I shall stick with Adler’s US spelling) has iron in its ferrous form , i.e. Fe ++. On ageing, the iron oxidises to the ferric (Fe+++) form, and the blood stain becomes dark brown. The hemoglobin is now in the “methemoglobin” form. So why did the “blood” from the Shroud not show the expected absorption spectrum of methemoglobin? How can one hope to convince anyone that it is blood if it does not look and behave like textbook methemoglobin, i.e. oxidised blood?
But in a film of hemoglobin there is a confirmation (sic) change ; it no longer remains in the “met”form but goes to the para-hemic form.
Let’s emphasise that we are restricting comment now to a “film” of blood, so that what follows should not necessarily apply to what you may read about the “typical” properties of blood in situations where it has not dried out to a thin film. Oops., “confirmation” is a typo. That should have read ”conformation”. So, when blood dries to a film, the methemoglobin undergoes a further change to what I call the para-hemic form. It’s a subtle change, and one that you may have difficulty in finding elsewhere in the literature, since it is a species of methemoglobin that I have discovered through my own extensive researches, and have decided this is the appropriate time to release into the public domain.
It is known now that there is a certain species which will spontaneously go the para-hemic form if there is not enough turnover in the spleen and liver to process the blood fast enough.
In fact, it’s a little more complicated than that. The change from methemoglobin to my “para-hemic” form is not just because blood has dried into a film, as my emphasis on “film” might suggest (ed: film being the only italicised word in the original). This para-hemic entity is something that is generated even before the blood escapes from an external wound. It is produced when the spleen and liver, which break down old red blood cells, are overloaded, giving time for methemoglobin to adopt this new conformation that I have christened the “para-hemic” form. You may ask why physiological considerations are intruding on what initially seemed a straightforward business of deciding if red stains on the Shroud were those of blood or not. But I want you to understand that there is “blood” and there is “blood”. The blood on the Shroud would be different from just any old blood, as I am about to describe.
We found a spectrum that was characteristic of only one known group of compounds -the so-called high spin, high iron porphyrin. So instead of being wrong, the spectrum peaks were in the right place.
The spectrum was wrong for blood. But there is an extensive chemical literature on the components of blood porphyrins in different oxidation states with which I am intimately familiar, and I was able to find a class of porphyrins in which the central iron atom was in precisely the right kind of electronic configuration to match, or at any rate resemble, the “wrong” spectrum in Shroud blood. Ipso facto, the Shroud blood was not just any old blood, but a very special kind that I call “high spin, high iron porphyrin”. (The literature is highly specialized, so do not imagine you can simply google that term and find pages full of returns. In fact you may find none at all, given the abstruse nature of porphyrin chemistry).
What we were seeing was the breakdown products of hemoglobin – bilirubin and biliverdin. And one began to make sense out of all of this.
Apologies for introducing an extra dimension of clinical chemistry so abruptly. You see, one has now to consider what the body does to get rid of oxidised haemoglobin. Well, it’s a long story, but basically what happens is this. The haemoglobin is stripped of its globin and iron to leave the porphyrin, which is a cyclic tetrapyrrole. The ring is then opened, first to make a green linear tetrapyrrole called biliverdin, and that is then reduced to bilirubin, which is yellow or orange, depending on concentration.
There is an extraordinarily high bilirubin count, almost as high as the methemoglobin.
There’s a lot of bilirubin in those blood spots, based on the purple color one gets with the Ehrlich diazo reagent. But please don’t ask me to put a figure on it. (Or waste time in discussing the units for bilirubin and methaemoglobin, whether in old-fashioned milligrams, or the SI (molar) units which are supposed to be standard in clinical chemistry in order to make any kind of sense to a chemist, but which are still slow to be adopted in certain parts of the world). Let’s not forget either that one is not dealing here with blood by the syringe- full, as normally arrives at the path lab, but tiny scrapings of blood that have had to be made soluble with specialist chemical reagents like hydrazine. There is also a tiny question mark over the specificity of the Ehrlich reagent – substances other than bilirubin can also give a purple color – but let’s not get too bogged down in detail.
Now how does one account for such a high bilirubin in a person?
I trust I have not lost you there. I suppose I should have said a “hypothetical” person who has left a stain on fabric that has a special kind of methemoglobin which arises when red blood cells are being broken down faster than the liver and spleen can cope with, producing an excess of bilirubin that in turn is being produced too fast for the liver and kidneys to excrete. Remember: we are dealing with some scrapings that are being related to a hypothetical scenario – one that might be described as acute haemolytic trauma. We are into new territory here – going boldly where no man has gone before – at least in the context of the Man on the Shroud….
One possibility is that the person had a severe malaria, but this does not seem very likely.
There may be any number of reasons why a blood sample has an elevated level of bilirubin. Malaria, a disease in which red blood cells are destroyed by parasites, is just one of them. Let’s discount that straight away.
But a torture, scourging and crucifixion leading to shock – that would produce a tremendous hemolysis. In less than 30 seconds the hemolyzed hemoglobin would run through the liver, building up a very high bilirubin content in the blood.
This is that hypothetical situation to which I was referring a minute ago. Any insult to blood and red blood corpuscles can cause the cells to burst and release their haemoglobin “(hemolysis”) which for reasons stated results in a rise in plasma bilirubin levels. Let’s not get bogged down in figures for now: there are values in the literature for raised bilirubin (hyperbilirubinaemia) in a range of different haemolytic and non-haemolytic states. When I say “very high” bilirubin content I mean very high relative to normal healthy bilirubin content, possibly multiples, tens of multiples (who knows?)
If that blood then clots, an exudate forms, and all the intact cells with bilirubin stay behind, only the hemolyzed hemoglobin goes out along with the serum albumin which binds the bilirubin.
It now gets a little tricky, so bear with me. We are now trying to imagine a scenario that would result in a blood stain that had so much bilirubin relative to methemoglobin (the special variety) that the spectrum one would expect of methemoglobin is replaced with an entirely different one.
The first step is to have the liquid blood with its high level of bilirubin and special methemoglobin form a solid blood clot. After that has happened, one can then envisage a separation process. Any red cells that are intact will stay put, along with their associated bilirubin. (OK, some would argue that most bilirubin in blood is attached to serum albumin, not red blood cells, but there are times one has to think out of the box). But there is an exudate that leaks out – which will be free hemoglobin that has escaped from busted red blood cells, and serum albumin with attached bilirubin. Yes, I know, it’s getting a bit complicated now, but let’s soldier on…
So what one ends up with is on the cloth is an exudate which has an enhanced bilirubin with respect to the hemolyzed hemoglobin. You now mix bilirubin which is yellow-orange with methemoglobin in its para-hemic form which is an orangey-brown and you get blood which has a red color.
I trust you see my point. You now have that high-spin methemoglobin – bilirubin complex that can explain why the blood still looks red after centuries of exposure to air etc. It’s the result of some very special physiology (trauma/acute hemolysis/liver overload etc etc) generating a very special and unusual kind of chemistry – special methemoglobin, masses of bilirubin – which under the mechanical straining influences of clot formation are forced together to make a chemical adduct that instead of looking brown, like old blood, is still bright red. (This adduct must also have exceptional chemical stability so as not to undergo further oxidation and degradation, but we’ll leave the details of that to another day).
In fact, we have been able to simulate the spectrum in the laboratory by the process described above.
We can reproduce in the test-tube what we think is happening in that sequence of events I have just hypothesised. Ipso facto, that sequence events explains why the ancient blood stains are red.
This very strongly suggests that the blood stains are of a man who was severely beaten.
It’s been a long and perhaps tortuous route between cause and effect, but we are now finally there. The ancient blood stains are red because they are from a man who was severely beaten.
No one would have ever dreamed when we first started doing the analysis that the chemistry would provide corroborating evidence to what the pathologists concluded long ago about the Shroud figure.
The Shroud investigators interpreted the markings as those from a man who had undergone severe trauma, but were unable to explain why the blood stains were still red. I have explained why the blood stains are still red, by devising a physiological scenario that begins with a man who has undergone severe trauma. Begging the question? No, there is a solid chain of reasoning here that depends on an intimate acquaintance with all possible oxidation states of free porphyrins, allied to a an enhanced form of jaundice physiology seen in athletes etc that causes mild elevations in bilirubin, greatly magnified here to take account of the multiple traumas of a flogged and crucified victim.
The blood has no cells, is very low in potassium, and has the right color and composition for the blood of a man who was severely flogged and crucified. This is entirely consistent with the forensic evidence…”
The explanation here can neatly account for some otherwise unexpected features of the blood stains, like their showing no red blood cells, like being low in potassium. It’s all to do with that complex clotting/exudation scenario I was talking about earlier.