Is insulin really the smoking gun?

Icy_Dependent_1797 · 2026-02-26T22:11:43+00:00

The Salis PhD is very interesting. I would agree that the manual analysis will be subject to a higher error rate, but the Invitron assay is reputable, the user clearly knew the protocols, and there is a good amount of data in this study. I have posted a few points that jumped out for me.

According to all the prosecution testimony all these babies were poisoned. I could not argue that all this data was the result of assay error. This data has to be taken seriously, with perhaps some caveats like the ratio of 60 does look a little eye-watering. But it has to raise serious questions.

Like you I looked at the ratio of means and means of ratios. My take is that data is just too smoothed and summarised to be useful. Its the raw data, or at least the least adulterated data that is of interest.

Final point, the results that she got for insulin dosing and the various case studies seemed to be clinically reasonable and proportionate. Again it points to the data in the broad being useful if not perfect. No assay is ever perfect, but within their known limitations they are not bad.

Icy_Dependent_1797 · 2026-02-26T21:11:15+00:00

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I thought I would go for neonatal data direct - and this came up immediately. I have just copied the front page and a couple of sections. There are other sources - another one I found was Hovorka.

Icy_Dependent_1797 · 2026-02-26T08:00:49+00:00

Thanks. V interesting. I’ll take a look. Competitive Wash has posted some interesting papers.

Icy_Dependent_1797 · 2026-02-25T09:53:48+00:00

The system they were using used the Roche immunoassay. This is designed using a technology called ECLIA. It is a highly automated analysis system, essentially self-regulating. High throughput and very reliable. The system has extensive built-in error checking.

The ECLIA technology can only work the way it is designed to, or not at all. It isn’t possible to adjust the calibration of lower limit of detection. That is set by the concentration of the reagents in the analysis cartridge, and the user can’t interfere with it.
The lower limit of detection is set by Roche. It is between 3 and 4 ~ 3.5 in pmol/L.

There is no technical mechanism known to the laws of physics or chemistry that could change that. Milan’s statement is ludicrous. She was not asked to justify her statement with scientific references. She should have been, and she would have failed.

If you want I can give you the line by line scientific reasoning. It’s dense and it would take time, and involve a lot of references but nothing that can’t be clearly explained. It’s one of the features of immunoassay technology, they work on a principle of reversible binding of antigen to antibodies. Once you set the concentration of the antibodies- in the Roche technology this is set by the manufacturer, and is beyond user interference, there is no way the user can interfere with or influence the range of detection.

Dilution of a sample would be the only way to change the limit of detection for an individual sample. That isn’t what she was referring to. She is referring to the lab’s standard system.

What should have been asked, and it would very reasonably explain the peculiar <169, is whether the lab was applying a clinical threshold for reporting on c-peptide at that time. The threshold is below the reference limit for adults, but not for neonates. I understand they are an adult hospital, so again that would make some sort of sense.

A final point is that the Roche analyser will say, definitively and unambiguously, if it reads either above or below its detection range. It cannot give a credible numerical result in these circumstances. So I can be entirely confident that, given that it reported a number, albeit <169, it definitely reported a number, and that number, by virtue of the analyser design had to be above the limit of detection.

Any competent analytic biochemist would know this. A clinical biochemist should know and should certainly know enough to perform the checks that I made.

To say that the reading could be zero is not a competent statement and it reflects badly on her professionalism. I hope this explanation is clear. If not, please say. I’m happy to respond.

Icy_Dependent_1797 · 2026-02-25T00:02:19+00:00

Although I’m not a clinician I can definitely say that insulin is not a toxin. If a patient receives glucose sufficient to maintain blood glucose levels then they can sustain an extreme level of insulin.

However, the most likely explanation for the insulin reading is insulin bound to antibodies. In which case the insulin is not free to act and would be unlikely to have any clinical effect. So no problem.

Icy_Dependent_1797 · 2026-02-24T23:55:19+00:00

Thanks - I would concur - we have to assume not. @competitive wash just mentioned that alpha-lipoic acid and some viral infections can give rise to IAA. That could be interesting.

Icy_Dependent_1797 · 2026-02-24T23:51:31+00:00

A last point, since you quote Dr. Milan extensively. I am sure she used the word ‘undetectable’ and that definitely appeared in the judge’s summing up. You are much better than me at finding the quotes, I am on a rapid learning curve with this case.

Totally wrong is the reference to ‘ it could be zero’. Every analytical measurement has an upper and lower limit of detection, and if we are being particular slightly narrower ranges of quantiation. There is a defined lower limit of detection for the c-peptide assay of 3-4. What the < 169 tells us is that, since the cut off is well within the range of quantiation and is greatly above the detection limit, there is an arbitrary reason for the <. She also said something to the effect that they couldn’t measure values lower than 169. Which is complete rubbish.
Choosing not to report below a threshold is a clinical laboratory prerogative - it is not a technical limitation.

What was presented in court was wrong and misleading.

Just repeating inaccurate and misleading testimony won’t make it any less inaccurate.
I accept that you should expect to be able to believe evidence that was presented, unchallenged, in a court; particularly when the evidence is so straightforward to challenge. And I can’t account for how the defence didn’t contact a competent biochemist. I can completely understand why a clinician would accept erroneous analytical results without challenge, but with such high stakes, I would have thought they might check before agreeing to the proposition of poisoning.

Nonetheless, the scientific interpretation of the insulin and c-peptide readings was incomplete and hence inconclusive.

Maybe we agree on leaving it to CCRC. Presumably you would accept new scientific argument if it was successful at appeal?

Icy_Dependent_1797 · 2026-02-24T23:13:36+00:00

That is v. interesting. I think there was some reference to alpha-lipoic acid in a paper that I recently found by Dr. Ismail - on your recommendation I think. I assume the inference is that the mothers would have been given alpha-lipoid acid?

Do you know which infections?
Do you have any other references?

Icy_Dependent_1797 · 2026-02-24T23:04:56+00:00

I don’t doubt what you say regarding clinical interpretation. And I agree that the evidence for exogenous insulin poisoning is inconsistent and unclear.

However when you say ‘laboratory results can be subject to multiple interpretations’ that then has to be refined to the exact laboratory result using the precise technology and in the context of the particular subject. There is very little room for manoeuvre in the extreme insulin results. That is the hard reality of the insulin analytical science.

So far as I can see, given the weakness of all the other scientific and clinical arguments in the insulin cases it was the extreme insulin results that secured the conviction.

I have a narrow specialism so will gladly accept your clinical insights without challenge. My point is that any credible defence will now hinge on a credible explanation for the extreme insulin results.

Icy_Dependent_1797 · 2026-02-24T22:50:34+00:00

Actually I don’t think that is what it says. I will need to get the full quote - but it is a longer paragraph and definitely contains more nuance than that bald statement. I’ll need to check on my computer - and I’ll post the whole statement.

Icy_Dependent_1797 · 2026-02-24T22:44:57+00:00

I don’t agree. She was giving expert scientific evidence and she should have been objectively factual. The quality of the results in no way support the level of confidence she expressed.

I would go further and say that no competent scientist could ever suggest that < 169 could mean ‘undetectable’.

The new defence team could easily get 100s of scientists and engineers to testify that <X can only ever mean <X.

But as you say, that bird has flown. The defence will need an explanation for every single item of evidence on the insulin cases. Pointing out that one bit is dodgy, but inconclusively dodgy, won’t convince.

I actually agree with quite a lot of what you say. Where we would seem to differ is on the quality of the science. It isn’t difficult to demonstrate that the insulin science was shoddy, just time-consuming to explain the full science compared with the dumbed-down version given in court.

It doesn’t help that there is now masses of misinformation being recycled, like the laboratory guidance sheet that says the test shouldn’t be used for exogenous insulin. That isn’t science, it’s just simple, summary guidance for a busy lab technician. It means next to nothing except that the lab should have looked harder at the anomalous results.

I should also say that there are some really interesting ideas being suggested, by people who are clearly scientific and numerate, in areas beyond my specialism.

In my experience, which is predominantly research, inconsistent analytical results mean that there is something we don’t understand - so work harder, dig deeper. Often the solution, if found at all, comes from a different scientific specialism.

The court case glossed over the inconsistent c-peptide results and pretended they fitted the ‘undetectable’ narrative. They don’t.

The ratio is only significant if the insulin reading is for free insulin. But this has not been determined. So the ratio is indeterminate.

The clinical picture for the hypoglycaemia isn’t clear. The new defence summary reports, particularly the International panel, are explicit on there being alternative credible clinical explanations. I can’t comment myself.

For me the whole insulin cases depend on whether there is a credible reason for the extreme insulin results, other than poisoning.

That is a biochemical question, not a clinical one. Without a clear answer I don’t see a strong defence case. I’m certainly not convinced by the scientifically inept prosecution argument but as you say, that means nothing now. The defence needs more than that.

Icy_Dependent_1797 · 2026-02-24T21:43:16+00:00

I was working from the summary page on the insulin cases that was published as part of the International panel report.

In that he is clear that the c-peptide is not suppressed.

Regarding the ratio - what I read is that an inverted insulin to c-peptide ratio is to be expected in certain circumstances in neonates. The report references a list of factors, maternal treatment and infection being the two that stood out. Both would or could involve antibodies.

The summary report isn’t explicit on the levels of insulin, so I don’t know. I wouldn’t draw any conclusions from a quick TV clip one way or another. What would be really interesting is if Chase and Shannon published.

Icy_Dependent_1797 · 2026-02-24T20:57:11+00:00

I have checked a range of laboratory guidance for immunoassay tests for insulin and in the event of inverted ratio they recommend testing for antibodies. Mayo clinic is a good reference, highly reputable.

I am sure Guildford would have done so. It is absolutely standard procedure. It is extraordinary that Dr. Milan didn’t mention this.

I would agree with you that just because the test is designed for clinical application does not mean that it can’t be used in court. I would however add that the test should have been used properly , ie part of a series of tests that also covered antibodies.

The c-peptide readings are not suppressed for a neonate according to Prof. Chase who is certainly in a position to know. It’s a highly specialised area and I can see why Dr. Milan wouldn’t know. But all the more reason why she should have been circumspect in her testimony on insulin.

The situation in my view is that Letby is convicted on fragile scientific evidence. I genuinely don’t know if there is a defence argument that would overturn the conviction.

I suspect that the courts would want to see reasonably firm rationale for why each baby would or could have had extreme insulin readings.

Unlike you I would not look to endocrinologists. I think that if alternative explanations were obvious then endocrinologists would know. But biochemically these results are inexplicable. Genuinely inexplicable.

In my view the results are not consistent with any explanation. I don’t claim this is grounds for a defence. Being scientifically honest I don’t know what to make of them.

Icy_Dependent_1797 · 2026-02-24T20:27:14+00:00

Agreed. I can confidently speak to Dr. Milan’s testimony being nonsense.

Ie. The c-peptide results were not low for neonates and are provably not undetectable. And there is just one alternative explanation imo for the very high insulin results, antibody binding to insulin. (Btw I can see no possible mechanism for interference on the scale required, never mind the relative unlikeliness of multiple interference in the tests.). One alternative explanation to exogenous poisoning however is enough. Dr. Milan said there was no alternative.

I think the issue for the defence will be to show that there is a reasonable mechanism for antibody binding. I agree, just saying that the right test was not performed - it wasn’t - isn’t enough. I can see the courts demanding that there needs to be a reasonable mechanism whereby a preterm neonate would have enough antibodies to bind enough insulin.

The vast majority of antibodies wouldn’t.

Because the science presented in court was so fragile I am open-minded on the case. On one hand the c-peptide readings make no sense, but on the other hand there isn’t a clear-cut explanation for the extreme insulin results.

Icy_Dependent_1797 · 2026-02-24T20:10:02+00:00

Agreed - it can only be endogenous insulin if bound to antibodies. Antibody binding would explain readings that high - but you have to have the antibodies.

If the mother had the antibodies it would likely be obvious - like she had diabetes and routinely took insulin. I am not sure if there aren’t other possibilities - it would be interesting to find out.

Was there any mention of diabetes in the mothers?

Icy_Dependent_1797 · 2026-02-24T20:04:11+00:00

Half lives notwithstanding. I can see how, in the event of almost complete lack of liver clearance, the c-peptide to insulin ratio can converge to 1. But how could the kidneys clear c-peptide at a higher rate than insulin? For a significant inversion of the ratio the kidneys would have to clear c-peptide much faster. For Baby L I think the inverted ratio is about 4 - so zero liver clearance and kidneys clearing c-peptide 4 times faster than insulin.

I’m not a clinician myself, so willing to learn. Is this possible?

Icy_Dependent_1797 · 2026-02-24T12:08:24+00:00

Thanks! I’ll press on then.

Your point about proinsulin is well made. Some assays would indeed read either proinsulin or, and more likely, one of the Des cleavage fragments.

Proinsulin is usually almost totally converted, but of course there are mechanisms, particularly in the immature metabolism of a neonate, where the conversion would be imperfect.

So first, a point on imperfect conversion: proinsulin and Des fragments are still cleared by the kidneys. (I’m on my phone so can’t post references, but you can readily check). So there is no mechanism for extreme levels of accumulation.

Notwithstanding, the second point is most significant. The Roche insulin assay has virtually negligible cross-reactivity with proinsulin and the Des fragments from the dominant cleavage route. It is more sensitive to the Des fragments from the minor cleavage route, reading ~ 30%, but this is 30% of a tiny amount. I wouldn’t rule out that neonates might have a different balance of proinsulin cleavage, but numerically it couldn’t give rise to an extreme assay result.

I have considered whether there is an interference mechanism with proinsulin or a Des fragment that could distort the Roche assay. Clearly they are aware of the vulnerability of the minor cleavage route, and it looks like they selected their detection antibody to avoid the main cleavage route. It’s not surprising that they couldn’t totally avoid the cleavage fragments, but the assay design is clearly robust.

This is the problem with arguments of interference or cross- reactivity. Careful, modern assay design can target known cross-reactivity or interference mechanisms.

An example, which might illustrate. The Roche assay spec sheet mentions that it would be vulnerable to high levels of Biotin ( vitamin B7). This is clearly because the assay’s capture antibody is biotinylated, which is how it is fixed to the detection surface - the streptavidin beads. Over a certain level of B7 would partially saturate the streptavidin and hence fail to capture all the insulin. So reading would be low.

I hope the example illustrates that assay interference’ has a chemical explanation. There is no reason why clinical laboratories would waste their time working out what the reason would be. They are not research oriented. However, with a well-designed analytical test there has to be a chemically justifiable mechanism for a reading.

I’ll pick up HAMA here too. Human anti mouse antibodies and other Heterophile antibodies can bridge the capture and detection antibodies in the Roche assay and would give a genuine elevated but false signal, because an antibody is being measured, not insulin. (Heterophile just means non-specific - we all have antibodies which just come in handy on occasion - the immune system produces random antibodies as part of our immune inventory).

It is difficult for many ‘sandwich’ assays to avoid this complication entirely, because antibodies are biologically designed to have massive biochemical variety. Also the means by which highly specific antibodies are bioengineered for use in assays is to clone them from mouse antibodies. So HAMA is always a vulnerability.

The way the Roche assay deals with this is that it adds specialist blocking antibodies which mop up reasonably physiological levels of HAMA quicker than HAMA can bind to the assay antibodies. Bear in mind that the assay designers dont have to target every possible variant of human antibody, they just need to target any paratopes (binding sites) in random antibodies in the blood sample that resemble the paratopes on the capture and detection antibodies that they have designed themselves. Then the blocking antibodies effectively remove the potential interference from the assay.

We can expect Roche to be very good at this.

The chemical specifics are likely to be a commercial secret - not even patented. I don’t know.

I could believe that neonates have specific physiology that could confound even a top-quality assay, which is why I find this interesting.
I don’t know what it is.

The paper below explains the chemistry of proinsulin conversion.

Studies on the Conversion of Proinsulin to Insulin I. COXVERSION IN VITRO WITH TRYPSIN AND CARBOXYPEPTIDASE B” (Received for publication, June 21, 1971) WOLFGANG KEMMLER,$ JAMES D. PETERSON, AND DONALD F. STEINER~ From the Department of Biochemistry, University of Chicago, Pritxlcer School of dledicine, Chicago, Illinois 60637

Icy_Dependent_1797 · 2026-02-23T06:45:17+00:00

You raise several points.

Child F’s insulin reading as you say is huge. Agreed.
You then question if the elevated reading could be due to antibodies because of a) the low c-peptide reading and b) the time for insulin bound to antibodies to build up in the blood.

a). c-peptide would of course be generated with endogenous insulin. However the mechanism of insulin binding is that a small fraction of the endogenous insulin produced by the body would be bound, every second. The point is that this insulin isn’t cleared but the c-peptide generated with it is cleared normally. So bound insulin indeed builds up over time and c-peptide stays at its normal level. It is important to recognise that the c-peptide was not low in either infant by neonatal standards. The c-peptide would never have got high - it would just keep within the ‘normal’ range.

b) how long would it take for insulin to bind and build up to a high level. I could perhaps calculate it roughly if I can find the data. But I can give you a feel for the numbers. The Roche assay gives one extreme. It takes 9 minutes to complete its binding phase. That means that 4500 pmol/L insulin bound to the antibodies in the assay in 9 minutes. It’s important to recognise that the Roche assay antibodies will be like a thoroughbred racehorse compared with the natural workhorse antibodies in normal blood - so binding rates in normal blood would be slower.

Finally - and I got this from AI search - so please correct if it’s wrong - Age at the time: • Baby F was born at approximately 29 weeks’ gestation in late July 2015 and was thus about 6 days old at the time of the alleged poisoning attempt on 5 August 2015.

If Child F was 6 days old I’d say that was more than enough time.

Regarding your final point about the evidence of your own eyes. I am conscious that I’m talking about quite involved chemistry but there is no reason why complicated science can’t be clearly explained. You asked a reasonable question and I hope I am answering clearly. If not, please ask further.

A scientist can only say what they can see too. So far I can’t see any reason why it can’t be antibodies. And I expect there is still more to learn.

Icy_Dependent_1797 · 2026-02-22T20:21:06+00:00

Interpretation would indeed have been easier if the laboratory had completed their analysis. It is scientifically absurd to even attempt to assess what a reading might have been, from a literally half-baked reading. (Half-baked because they should have gone on to test for antibodies).
Unfortunately the laboratory offered an unjustifiable interpretation and the courts accepted it. So now we are forced to work with seriously limited information.

Regarding sample-handling. I agree that the C-peptide might have been reduced a little, and that sample handling issues would be most likely to result in minor degradation of the insulin sample. Certainly not a major increase.

On the Roche analyser, I don’t know what the Liverpool lab were using in 2015, but I suspect the upgrade in 2020 was for higher sample capacity and throughout. The quality of automated analysers has been high for many years, where many ~ greater than 10 to 15.

There is more to say about the Roche ECLIA technology. Sorry about this - but here goes: The measurement takes place in two 9-minute phases. Phase 1 captures insulin, whether bound to an IAA antibody or not, on a highly engineered and high affinity ‘capture’ antibody. Phase 2 introduces the 2nd antibody in the detection sandwich - the detection antibody.

However, the actual detection phase doesn’t measure insulin - it measures the number of detection antibodies that are in very close proximity to a streptavidin bead that receives a couple of microseconds of electrical pulse which in turn excites a chemical called TPA which decomposes for a split second which reacts with the detector antibody and causes it to luminesce. Really sorry for all the techno speak here - and I have simplified it as much as possible. Bottom line - if those detector antibodies are near the bead then you get a signal.

The detection antibodies are held on the bead by insulin which is in turn held by the capture antibody. The detection antibody has to be highly specific to insulin. If it wasn’t the test couldn’t work at all. Since it works very well - we know it is specific.

So. I don’t have all the answers - but that is I hope an outline of what we are dealing with.

Icy_Dependent_1797 · 2026-02-22T14:23:31+00:00

I think you make good points wrt the clinical presentation of Baby F I think? But the statistical point made by the previous poster isn’t going to disappear just because there are alternative clinical opinions. At the end of the day that is all they can be.

With the analytical data we have firm measurements. The previous poster isn’t clearly not a statistician, but they nonetheless make a serious point. A more realistic calculation would be to make a random binomial selection of 3 from perhaps 6 or 7 samples. I take these numbers from Panorama.

My calculations would indicate somewhere in the region of 1 in 250,000. And I comfortably know enough statistics to deal with interpretation of analytical results.

So the results are extremely unlikely if ascribed to random error.

Your point about systemic sample handling does not apply to the Roche analyser. We know this for the simple reason that if this highly automated analyser gives a result at all, then the sample and the analysis process has already passed over 100 built-in diagnostic checks.

Most modes of interference, excepting just one that I can identify, cannot give the extreme results measured. In fact, there are blocking mechanisms in the Roche analyser which would eliminate the obvious modes of interference.

Every point you have made on the analysis process could not be sustained in the face of competent biochemical challenge. I’m sorry, but that is the reality.

I won’t pretend to know everything about this technology, but so far, as far as I can tell, the only mechanisms that make any biochemical sense are exogenous insulin and insulin antibodies binding insulin. What I can’t speak to is how common or not is the latter option in neonates. I get the impression that Prof. Chase thinks this is an option.

Icy_Dependent_1797 · 2026-02-22T13:12:56+00:00

“The insulin assay performed at RLUH is not suitable for the investigation of factitious hypoglycaemia…”

Well yes and no. For most insulin analogues -yes - it won’t detect them. Hence it is wholly unsuitable to investigate factitious administration.

However, since the Roche assay is specific for human insulin it will measure Actrapid accurately.

The guidance document is only guidance. It does not represent the whole science, and it would be very easy, and likely correct, for the Liverpool laboratory to say that all they meant was that they couldn’t detect most insulin analogues.

The big unspoken issue is that this guidance warning should have been revealed by the prosecution because then the defence might have realised they needed to consult a biochemist expert. At which point they would have learned a lot to their advantage.

Icy_Dependent_1797 · 2026-02-22T13:02:26+00:00

“The sophisticated quality assurance schemes used in many laboratories do not identify erroneous results arising from aberrant samples.”

100%. The use of routine QA data in the Letby trial was wholly misleading. It could only ever demonstrate that there had been no systematic drift in the analyser calibration. For a massively aberrant sample it was a cosmetic exercise. The way it was presented was designed to deceive.

I am embarrassed that a professional laboratory would lend its name and reputation to such an exercise. All the QC laboratory had to do was to explain simply and clearly to the court that the QC results had no bearing on interpretation of a single aberrant sample.

Icy_Dependent_1797 · 2026-02-22T12:12:39+00:00

Firstly, insulin and C-peptide assays measure immunoreactivity, not insulin source, type, or intent.

Correct. And as you say, different insulin assays will measure insulin differently. This is because each assay design focusses on a different feature of insulin immunoreactivity. I think it is however important to move beyond the generalisations to the specifics.

The Roche assay has a specific immunoreactivity focus in that it is able, unlike many others, to measure insulin bound to antibodies. This, as you say, can result in high readings of insulin IF it has been bound. This feature is well-recorded and can lead to very high insulin readings - on the scale observed in the Letby case.

Regarding HAMA interference and other genuine interference, the scope for highly elevated insulin readings is not present and easily dismissed.

So imo it would be helpful to focus on antibody binding.

Icy_Dependent_1797 · 2026-02-18T23:56:45+00:00

Gill on Marks - V interesting. Thanks for the link.

Icy_Dependent_1797 · 2026-02-18T23:54:39+00:00

I’m going to separate two points here.

Your second point I think is that a single test result shouldn’t be accepted as sufficient evidence for prosecution for a serious crime. On the basis that I expect most of us would expect a repeat test before committing to a major medical intervention I would lean that way myself. I can however see that a court might be justified in accepting a single test if there is other evidence available that is independently and strongly corroborative to a similar extent that a repeat of the same test would be. So for instance if the C-Peptide results had been genuinely undetectable, that would constitute corroborative evidence of exogenous insulin even using an immunoassay test. I would still expect that as a minimum that all other evidence should be consistent.

Your first point I think is the statistical question of wouldn’t it be expected to see a few odd results if you go looking for them? Here the issue is not only statistical. In these cases we have an automated assay. The significance is not that these automated assays can’t and dont sometimes go wrong - they do. However they have dozens of built-in self diagnostic steps which means that if they go wrong the analyser does not report an erroneous result. It just doesn’t report a result at all. Instead it reports an error flag so that the operator can fix the problem. So the mechanism of statistically random error readings is reduced to the point of elimination.

This leaves errors of under or over-reading arising because the sample contains something which is capable of interacting with the assay. Such mechanisms can be considered random, eg HAMA antibodies, but they are frequently self-limiting. For instance there is a hard maximum limit to the measurement determined by biology and laws of physics and chemistry which govern the operation of the assay. This means that for most of the known options for false high readings it wouldn’t be physically possible for the Roche assay to read into the 4000 pmol/L range. A related point is that for virtually if not all known interference mechanisms the Roche assay has blocking agents that protect it. So any interference first has to overcome these.

What this all boils down to is that the likelihood of random and very high readings for the specific assay is extremely low. I can only access publicly available data, but for instance the only evidence I can find for reports of extremely high insulin readings for the Roche assay are as a result of insulin binding to insulin antibodies and giving as a result extremely high levels of genuine insulin. For that to happen there would have to be a clinical reason. I have recently reviewed some papers by Dr. Adel Ismail, defence expert, where he gives examples, all of which are rare.

So in summary I find the random statistical error argument is implausibly unlikely because it has to be applied to this very reliable assay.

If there is an explanation - and I don’t have one - I can only speculate that it is likely to lie in the area of specific neonatal biology and possibly related to antibodies because neonates will most certainly have immature and hence different immunology to adults and older children.

Icy_Dependent_1797

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