Lucy Letby: summary of evidence

This is a summary of the main evidence used to convict Lucy Letby, with links to many other documents relating to the case and more in-depth articles examining the severe shortcomings in the scientific evidence which led to the conviction. Much of the material comes from the website of the organisation Science on Trial The material in (now offline, but preserved at was presented to the defence team during the trial but was not used due to rules which prevent the introduction of new expert evidence once a UK criminal trial is underway.

This summary was written by Tom Gibb and Kate Nickalls and reproduced here with their permission (some minor corrections made by Richard Gill).

Lucy Letby (LL) was convicted and sentenced to spend the rest of her life in prison for murdering seven babies and attempting to murder six others between June 2015 and May 2016. The summary of evidence below is organised in rough chronological order to also explain how the investigation against her was conducted. It is accompanied by commentary to explain why both the investigation and evidence collected were flawed:

1) The Statistical Evidence.

In 2016, consultants at the Countess of Chester Hospital (CoCH) became suspicious that LL always appeared to be on duty when babies collapsed or died. These suspicions were later summarised into a data chart of nurses’ shifts produced by the police which, the jury was told, showed that LL was the only nurse present at all 8 deaths (one murder charge was dropped by the court prior to the trial), and 17 incidents of sudden collapses on the unit which were listed in the chart. This gave the very misleading impression to the jury of a correlation that was too much to be coincidence. In fact, there were many more deaths which should have been included in the chart; and most likely very many collapses too.

  • The 25 incidents in the Police chart only represented those included in the investigation. Hospital records (obtained by a freedom of information request) show that there were an additional 9 neonatal deaths during this period, for which LL was not charged and when she was not on duty. So, the police table showed only a partial subset of data representing less than half the deaths on the unit. During the trial, no proof was given at all that Lucy had done anything wrong or was in any way the cause of those 25 events.
  • The statistical evidence about the 16 non-fatal collapses is even more misleading. The collapses were selected by the hospital consultants because they deemed them suspicious. They did this retrospectively after they had agreed LL herself was suspicious, and the list was restricted to incidents occurring during Lucy’s shifts making it statistically meaningless. The shift data chart does not show any non-fatal incidents/collapses which occurred when Lucy was not on shift. In fact, nobody can say how many such incidents occurred because neither the hospital nor NHS systematically registers incidents/collapses requiring quick action by nurses or doctors.
  • Statistics weren’t explicitly used by prosecution, because no detailed statistical analysis was ever carried out; instead they insinuated a statistical correlation via the shift data chart.
  • The lack of any formal statistical analysis made it impossible to conclude whether LL’s presence could have been the result of chance. A number of factors would point to a coincidental relation. While other staff indicated on the data chart worked part time, LL worked overtime, often at nights (when babies are more likely to collapse). The neonatal unit Lucy worked on cared for poorly and premature babies requiring more intensive care.
  • Professional statisticians have since performed statistical assessments that demonstrate a) there remains a systemic cause of infant still-birth and neonatal death at the COCH even when the so-called murder cases are removed from the data; and b) that the police table representing LL presence for all the events is a statistically normal artefact. 
  • A Royal Statistical Society (RSS) report, produced before the LL trial, laid out the standard methods from medical statistics and epidemiology which should be used to analyse such data in this and similar alleged serial killer nurse cases. It drew on the experience obtained from earlier cases, for example, that of Lucia De Berk, a nurse in a children’s hospital in the Netherlands, who was initially convicted because of a faulty statistical analysis. Lucia’s conviction was only overturned after analysis showed that the notion that her presence at so many deaths and other incidents could not be a coincidence had contaminated the medical judgements of medical experts called to give their opinion on individual events. Numerous recommendations of the RSS had already been grossly violated during the police investigation into the case of Lucy Letby by. the time the report was published. No statistical analysis of the roster data was performed at all.

2) Other possible causes of the neonatal deaths. The limited scope of the investigation.

No direct evidence implicating Lucy Letby was produced. No one saw her doing anything wrong. Instead, the jury was told that she must be guilty because all other possible causes of unexpected collapse and death had been investigated and eliminated, and that LL was the only link between the 25 incidents. This is untrue. There never was a wider, independent investigation by outside experts with the relevant scientific expertise. Indeed, a 2017 report by the Royal College of Paediatrics and Child Health (RCPCH) into the unit at the CoCH criticised the lack of systems in place in the hospital for reviewing such serious incidents. The report identified a series of problems in the unit, where the number and acuity of patients had expanded faster than resources available to look after them. These included significant understaffing, with gaps in doctor and nursing rotas, poor decision-making and insufficient senior consultant cover provided by paediatricians (the unit had no neonatologist), and lack of coordination to transfer very sick babies to the nearest Neonatal Intensive Care Unit (NICU). It recommended a wider independent expert and forensic investigation to look at possible medical causes of the unexplained deaths and collapses and the rashes some of the infants exhibited. Instead of this happening, the police were called in to conduct a criminal investigation which focused narrowly on looking for evidence that LL was a possible mass murderer. The main investigator and prosecution expert witness, Dr Dewi Evans, is a decade-long retired paediatrician, (not a forensic scientist or neonatologist specialising in intensive care neonates) who volunteered his services, and who has neither the expertise nor experience to make the scientific claims he made. Far from eliminating all other possible causes, alternative avenues of medical and scientific inquiry which could have pointed to different explanations for the deaths, were not followed up.

  • At the time of their deaths, autopsies were performed for six of the babies. A natural cause of death was listed by a pathologist for 5 of them, and one cause of death was un-ascertained. These conclusions were overturned by the police investigation, even though there was no new evidence, with no explanation as to why.
  • All but one of the children were born pre-term, several very pre-term. This makes them extremely vulnerable to infection. All the babies in the case showed many signs of viral or bacterial infection and all were listed as having “suspected sepsis”. Some of the babies had rashes and discolouration that the doctors said they had never seen before. The prosecution presented this as evidence that the babies were deliberately injected with air, based on a single scientific paper from 1989 which was not applicable to the babies in the LL case (see below). Viral or bacterial infections (including antibiotic resistant bacterial infections) and sepsis, which can also cause rashes and skin discolouration, were not presented as possible explanations to the jury.
  • The police investigation did not include independent infectious diseases experts, forensic neonatal pathologists or toxicologists; no independent, scientific forensic investigation took place. Most worrying, there was no systematic investigation into possible viral or bacterial infections, even though the pattern of collapses and deaths fits an outbreak of infection. A nearby hospital had experienced a similar cluster of deaths within a short period just prior to events at CoCH. It was determined not to be the result of criminal action, with the deaths deemed to be natural. It is well known by epidemiologists and statisticians that clusters of unexpected deaths do occur within hospital settings, often due to outbreaks of unidentified infections.
  • At the time of the collapses and deaths of the infants, enterovirus and parechovirus had been reported in other hospitals. There is a history of outbreaks of these viruses in neonatal wards in hospitals around the world. They especially harm preterm infants who do not yet have a functioning immune system. It is reported that many parents of the infants were concerned that their ward had a virus (as was Lucy). To date we have seen no evidence to show the hospital did any viral testing and, if they did, what the results were.
  • At the same time as the increase in deaths in the CoCH neonatal unit, there was also a spike in stillbirths (often infection related) in the adjacent maternity unit.
  • Both the maternity unit and the Neonatal unit at COCH had repeated raw sewage spills, providing an obvious explanation as to how a pathogen like an enterovirus (which is highly contagious through faeces) could have spread in the hospital.
  • All the babies in the case were presented to the jury as being stable, before an unexpected and unexplained sudden collapse. This was highly misleading. All of the babies had “suspected sepsis” in the notes, with clear signs of an undiagnosed infection. They required resuscitation, mechanical ventilation and intubation. This was a very sick group of babies.
  • Evidence from less well-resourced settings shows that death would be a normal and common outcome for babies in this category. Many would be expected to die after a sudden deterioration. Low staffing levels, leading to poor monitoring and poor infection control, are globally the big killers of preterm babies. In developed world settings babies are only kept alive by expert intensive care, with high staff-to-patient ratios and a focus on infection prevention. In this context, the low staffing levels at CoCH and the sewerage leaks are highly significant. While the death rate at CoCH was slightly higher than normally expected in the UK, it was much lower than the global average.
  • The neonatal unit at CoCH was a level 2 unit offering mid-level specialist care for babies with severe health issues and prematurity. The prosecution claimed that neonatal deaths decreased after Lucy was taken off the unit. But in fact, the hospital, at the same time, downgraded the unit to level 1 (no longer taking in such sick babies), increased senior consultant cover and repaired the sewage spillage from the drains. This easily explains the decrease in neonatal deaths.

3) The insulin evidence.

Soon into the police investigation, doctors discovered an entry in the notes of two babies who had died two years earlier, showing high levels of insulin and low levels of C-peptide. This was later presented to the jury and wider public as the key breakthrough which proved there was someone committing deliberate harm in the unit. Cheshire Police, in media reports like the Panorama programme, said this was the point that they focused all their efforts into a murder investigation. LL was accused of injecting insulin into the feeding bags of the two babies. These two hormones both derive from proinsulin, produced by the pancreas, leading to an expectation of related levels unless insulin has been injected, (although C-peptide levels can be higher as it has a slower clearance rate). Expert witnesses testified that deliberate poisoning with insulin was the only possible explanation. The defence accepted this as “established fact”, based on the testimony of the prosecution’s expert witnesses. This meant no defence expert witness was called to rebut this claim. However, the weight of expert opinion consulted since the trial is that there are better, innocent explanations for the two test results recorded in the notes, which were not presented to the jury. Guidelines for levels of evidence required in insulin poisoning cases were ignored.  Other experts in the field say that two isolated tests with no possibility of follow-up or confirmation, were wholly inadequate for a murder conviction. (See also the section “opinions of other scientists re insulin” at the end of this post).

  • The immunoassay lab tests used to establish the insulin and C-Peptide levels, are complicated and can give false results for many different reasons, one being the false-negative hook effect. One of the tests had such a high insulin level (4657 pmol/L), that lab specialists say this would almost certainly lead to a false negative for C-peptide, and so explain the discrepancy in recorded results. For an Insulin level of 4656 pmol/L, the predicted C-peptide concentration would be 99,277 pmol/L, which exceeds the parameters of the test. There is a hook effect at C-peptide concentrations that exceed 60,000 pmol/L. (The manufacturer of the blood test kit is “Coba”.)
  • The Insulin assay test used is not designed to discover or measure the presence of injected insulin. Indeed, the lab where the tests were carried out states clearly on its website that its insulin assay tests are not designed “to measure exogenous insulin”, which would require a more precise (mass-spectrometry) test at an entirely different lab (Guildford RSCH Peptide Laboratory). This mass-spectrometry test was not carried out.
  • Instructions from the forensic science regulator about the use of measurements like this in criminal prosecution were ignored. These state that there “must” be repeat samples, including a baseline blood sample taken before treatment starts; and further testing should have been required in order to confirm the values at a specialist laboratory. There must be reporting of possible sources of error and the likely sizes of errors, as well as a reporting of alternative explanations of anomalous outcomes. This was not done, so the tests should not have been accepted as forensic evidence. In many countries these assay tests are not accepted as forensic data for criminal prosecution because of all the possible errors from the collection of samples to procedures in the lab.
  • The sample for baby F was not collected at the right time to diagnose exogenous insulin. This should have been done at the first episode of hypoglycaemia, prior to treatment. The blood sample was taken after multiple dextrose treatments; the insulin levels AFTER dextrose (glucose) were significantly raised. Multiple attempts to rectify the blood sugar would have increased the plasma insulin and suppressed the C-peptide. The babies should have been fasting three hours prior to the blood tests, which did not happen in this case.
  • In neonates, there are a number of possible natural explanations for an unusual ratio of insulin to C-peptide, for example, autoimmune insulin syndrome (AIS), which were not presented to the jury. This is a highly specialist area requiring outside expert opinion, which was not sought during the investigation.
  • A mother of one of the two babies was reported to have diabetes; therefore, the baby is more likely to have higher and less stable production of insulin as well as periods of low blood sugar (hypoglycaemia) shortly after birth, and during the first few days of life. (33.7% of all preterm neonates experience hypoglycaemia during this period – Sharma et al 2017). Likewise, clearance rates of insulin and C-peptide can vary much more in preterm babies than in children or adults, as organs like the liver may not be yet working properly.
  • The link to Lucy Letby was conjecture. She was never seen injecting a baby, there is no direct evidence. The test for baby F was taken some 10 hours after LL’s shift ended, and after the TPN (intravenous feeding) bag had been changed. Baby L continued to have hypoglycaemia for a further 24 hours after LL left the ward.
  • Expert witnesses testified that LL only needed to have injected a small amount of insulin into the TPN bag to reach the levels reported in the tests. These calculations have been challenged by other experts as they appear to be based on calculations for muscular rather than intravenous insulin injection. Intravenous fusion would require much higher doses of insulin.
  • Both babies survived. Baby F tested a very high blood insulin concentration of 4657 pmol/L, C-peptide was 169 pmol/L and a blood glucose reading of 1.3 mmol/L. Within two hours of the blood test the baby’s blood sugar level was ~4 mmol/L. Normal glucose levels range between 1.5 and 6 mmol/L – so these readings are not particularly out of the ordinary. They are, however very surprising if the high blood insulin level recorded was accurate and a result of deliberate injection. Indeed it would be very surprising for the babies to have survived such an attack.

4) The evidence of deliberate injection of air

After mistakenly believing they had proved through the insulin evidence that there was a killer on the loose, police and doctors then looked for explanations as to how LL could have killed the other babies. She was accused of injecting them with air. She was also accused of pulling out ventilation tubes.  But no direct evidence was presented for either claim. Indeed, the investigation did not follow normal scientific methods and once again there are much better explanations for the evidence presented. Indeed the evidence for air injection, which was claimed as the main murder method, totally ignores a large body of contradictory evidence.

  • No forensic pathologists were involved in this investigation. Instead, it was carried out years after the deaths by Dr Dewy Evans, who is not qualified in this very specialist area. He approached the investigation like a doctor looking for a possible diagnosis, not like a scientist or pathologist looking for firm evidence. The jury, however, were told by the judge that they could trust his opinion as firm evidence.
  • Conventional methods for investigating air embolism were not followed. These require specific post-mortem techniques, which were not carried out. Instead, two x-rays, taken more than 30 minutes after death and showing air in major blood vessels, were presented as evidence.
  • One 1989 scientific paper was cited by Dr Evans to back up his theory. This paper was totally inapplicable to the case as it related to babies on aggressive ventilation treatments used at the time. The paper explicitly says post-mortem x-rays taken more than 30 minutes after death must not be used to determine air embolism, but in this case both the x-rays were performed beyond this time limit. “In 75% of reported cases the radiographs were taken antemortem. Post-mortem radiographs need to be interpreted with caution as intravascular air may appear as early as 25 minutes after death.”, (page 2 of paper). Relevant scientific papers were not included or presented to the jury.
  • There are many other explanations for air in the veins after death which were not presented to the jury. A 2015 study, for instance, showed the majority of new-borns who had been resuscitated with CPR and subsequently died, had air embolism (Halbertsma et al) which showed up in scans taken after death. The babies in the Lucy Letby case, almost all received CPR. Air in the great vessels is also a common side effect from having tubes inserted into the baby’s umbilical lines and from intravascular injections.
  • Another possible explanation for the radiological appearance of gas is sepsis. Jurors were told that Prof Owen Arthurs, radiologist at London’s Great Ormond Street Hospital, had been instructed to review X-rays taken of Child A – when alive and after death – as well as other babies in the investigation. He concluded that a line of gas in front of the spine was an “unusual finding” in a post-mortem x-ray which would be unlikely in deaths by natural causes, and which could be explained by air having been administered. But, he said, it has also been seen in road traffic accidents and cases of sepsis infection.

5) The “Confession” Note

Police found a handwritten note in LL’s home stating “I am Evil […] I did this” – which was presented to the jury as evidence by the prosecution.

  • There were a multitude of handwritten notes. This was not unusual, as nurses are encouraged to journal as a component of their training.
  • In the notes, LL also writes, “I’ve done nothing wrong […] how has this happened? […] Please help […] I feel very alone and scared […] no hope”. The guilt she expressed was clearly stated as worry that she might not have been “good enough” in her role as a nurse to save the babies who died while in her care.
  • On BBC’S Panorama, Professor Emeritus criminologist David Wilson explained that these notes were not a confession but that they were instead “the ramblings and outpourings of someone under extreme psychological pressure and stress”, due to the nature of the accusations against her. He suggested that she could have meant that, “it is alleged I am evil […] It is alleged I did this”, referring in her notes to the serious accusations made against her by the doctors and the police.
  • David Wilson stated that, in his experience of criminal cases, it is very common to see these types of notes written by people who in fact transpired to be innocent.
  • Neonatal nurse Lucia de Berk and Kathleen Folbigg both had similar handwritten notes shown to the jury by the prosecution. Both were convicted and sentenced to life imprisonment, but years later both were exonerated after new medical, scientific and statistical expert evidence revealed their wrongful convictions.
  • The code LD in her notes means “Long Day”, text commonly used by nurses to record shift notes.

A detailed analysis of the main “post-it note” shown to the jury is posted below. It demonstrates clearly that the note does not contain a confession.

6) The prosecution ignored the rules governing the use of Scientific experts and there was a lack of expert defence witnesses

The scientific experts used in the case did not behave as scientific expert witnesses must behave, according to the rules of CPS criminal prosecution. They are supposed to be strictly neutral (despite who is paying them) and they are supposed to always give alternative explanations and to mention scientific (and statistical) uncertainties. They did not do this. And they also spoke about scientific matters in which they have limited expertise. This applies not only to Dr Dewy Evans. Prof Hindmarsh has no expertise in forensic science in neonates. He also clearly did not know the relevant scientific literature concerning insulin poisoning, a specialist area which would not be in the knowledge of most practicing doctors. The defence appear to have accepted at face value the neutrality and expertise of the prosecution’s scientific witnesses and for some reason did not seek their own experts to challenge central conclusions of the case. Much of the material above, plus more analysis, was presented to the defence team before the end of LL’s trial. There was also an attempt made to present it to the judge as a “friend of the court”. But both were unsuccessful because rules prevent the defence calling new expert witnesses after a trial has started. So the jury never had the benefit of this evidence.  In particular, no defence experts testified regarding strong evidence of a differential diagnosis of infection in every case and what that could mean. This left all the prosecution’s expert witnesses essentially unchallenged. While this could be dismissed by putting the blame on the defence team, this misses the point. In a case which relies on highly specialised medical and scientific evidence, it is perhaps unreasonable to expect solicitors, barristers, judges and other legal professionals to be able to evaluate the quality of evidence and find the right experts. Defence barristers also complain that it is often very difficult to find expert defence witnesses willing to testify in cases involving children. This points to much deeper systemic deficiencies related to the use of complex scientific and medical evidence in criminal cases. The same is true for the police and prosecution investigation. The very obvious and alarming errors in the investigation are not necessarily the result of a deliberate cover-up or bad intent. Rather they result from the lack of understanding of scientific processes and investigation and a lack of understanding of how to judge and grade the reliability of medical evidence. There is a more detailed discussion of these aspects below.

The wider implications of the Lucy Letby case for the use of science in criminal trials and the need for reform.

Scientific evidence today plays an increasingly important role in obtaining convictions in the criminal justice system. However, the use of deeply flawed science in the Lucy Letby case raises worrying questions as to how scientific evidence is assessed and presented to juries, and whether the whole system needs modernisation and reform if miscarriages of justice are to be avoided.

Normally scientific evidence is peer reviewed by a panel of suitable and carefully identified experts, before it is published. This is a vital step, not only to iron out mistakes, but also to ensure correct scientific methods are followed and that the evidence published is robust enough to justify any conclusions that are reached. Peer review is used because scientists are the only ones with sufficient knowledge and expertise to evaluate the work of their peers.

In terms of medical evidence there is then a further process of independent grading before producing guidelines for doctors and other medical practitioners to follow. Grading provides a guide for doctors, who are often not experts in scientific methodology or statistics, so they can evaluate how reliable evidence is. The process usually starts with a systematic review of all the literature about the topic. If the review does not show up relevant studies or clinical trials from which to draw firm conclusions, a panel of experts will make recommendations for medical practice based on their experiencer. This expert opinion is considered low quality evidence, and any recommendations will be heavily qualified, because panels of top medics are rarely unanimous in their opinions and are often shown to be wrong when more rigorous scientific studies are carried out.

Relevant observational studies, where researchers simply observe and record the impact of potential treatments in a systematic way, get a higher grade. The gold standard for evidence are Randomised Controlled Trials (RCTs), which are carefully designed experiments used to prove or disprove a particular theory. These have built in methods to remove the inevitable bias of the researchers, as well as the doctors and other medical staff actually involved in treating patients in the study, and to work out detailed estimates of potential benefit and harm. To get the highest grade of evidence, RCTs need to be big enough so that the results are statistically significant and could not be the result of chance. And their results need to be replicable and relevant to the wider target group of patients. Often medical practitioners will not accept a single RCT as a basis upon which to change practice, in case there were errors in the way it was conducted. There are sometimes prolonged debates with serious differences of opinion among expert opinion before new treatments are adopted, because even the conclusions of RCTs can turn out to be wrong.

In the legal system, too often none of this happens when scientific or medical evidence is presented to juries who are likely to have much less understanding of the scientific process than doctors. Investigations are often police led and may not follow a scientific process. The trial then relies on both prosecution and defence to find their own expert witnesses, in a process where there are few criteria set down for vetting the suitability of experts beyond how well they will come across to a jury. The judge and jury, who are bound to be out of their depth in terms of scientific knowledge, are left to assess the relative strength of evidence when witnesses disagree with each other, with little chance to pose questions. Within this adversarial courtroom process, it is extremely difficult for non-scientists, to evaluate where the weight of scientific opinion might lie, or the reliability of the evidence presented. In the Lucy Letby case, the jury and the legal professionals involved were clearly not equipped to understand the reliability (or lack or it) of the evidence presented in the prosecution case.

Because of the adversarial nature of the process, it is also very difficult for legal teams to find scientists willing to act as expert defence witnesses. Academics are worried about a public process where hostile lawyers may try their best to discredit them – not necessarily focusing on the quality of evidence or the science. And the process provides no mechanisms for experts watching from outside, to input their knowledge when they see mistakes being made. Indeed, once a trial has started new expert evidence or expert witnesses cannot be introduced.

The Lucy Letby case demonstrates clearly many of the most serious weaknesses of the criminal justice system with regard to scientific evidence. After a series of unexplained deaths in a public hospital, there should have been a broad independent science-led investigation to evaluate how serious a spike this represented and probable causes. Instead, after the police were called in, the investigation tunnelled into a criminal investigation focusing only on gathering enough evidence to prosecute Lucy Letby. Doctors working on the ward became the principal advisors to the investigation and then “expert” witnesses in the trial.

The prosecution investigation, led by a retired paediatrician, should never have been presented to the jury as reliable scientific evidence. Doctors and scientists have very different methods for carrying out an investigation. A doctor will come up with a differential diagnosis, listing all the possible causes of a patient’s symptoms. They will then work through the list, eliminating all the possibilities, often by trying different treatments, until they reach a diagnosis. Often this turns out to be wrong, which does not matter as long as the doctor keeps an open mind, is prepared to consult with colleagues who make have more specialist knowledge, and to change course in the face of new evidence. This not a scientific method. Medicine is often as much an art as a science and has to confront many aspects of disease where we are still fundamentally ignorant. This is especially true when working with neonates, who cannot talk or indicate what hurts and what their symptoms are.

The Lucy Letby investigation was led by doctors and carried out using this method. Dr Dewy talked about his “diagnosis” that the babies were killed by air embolism. It was a diagnosis reached after the event, without ever being able to examine the babies. It may have been his honest opinion, but it was not scientific at all and should never have been presented to the jury without very strong caveats and warnings about its inevitable limitations.

Defence lawyers, the judge and the jury cannot be expected to understand complex scientific and medical evidence – and the processes by which it needs to be gathered in order to be reliable.  This is why in the LL case they accepted as scientific fact what was actually medical opinion, most of which would never have got through a scientific peer review. The defence team accepted that the insulin tests showed there was deliberate poisoning as “established fact”. The judge allowed evidence into the court that was not based on properly conducted forensic methods and told the jury they could trust an expert witness, who was a retired paediatrician and not qualified to make the statements he made. If it were graded, all of the evidence presented would have struggled to even be classified as “low quality” expert opinion, because no systematic review was carried out, and the expert witness was not qualified in the area where he gave testimony. It was a long, long way from proving guilt “beyond all reasonable doubt”.

And it was not only the legal professionals who were out of their depth. The journalists covering the case also had no idea of the correct questions that needed to be asked. Panorama produced a documentary which did not challenge the flawed scientific evidence relating to insulin and air embolism.  While it would be easy to blame everyone involved for not doing their jobs – this misses the point. Rather the whole case shows the difficulties faced by non-scientists in evaluating complex medical and scientific evidence, if they are not trained to do so. It is the system which is at fault.

Neither is the case unique. There have been a series of other cases both in the UK and other countries where medical professionals have been convicted on evidence which would not have stood the scrutiny of a peer review process within the scientific community – leading to innocent people spending years in jail.

So is it time for a change? What kind of reform would be necessary?

The most basic tenets of our legal system lay down that a defendant is considered innocent until found guilty beyond all reasonable doubt by a jury of their peers. It is of fundamental public interest, not only that this happens, but that it is seen to happen. In terms of complex scientific evidence, perhaps the word “peer” needs to be extended to include a role for “peer review” and grading of scientific evidence before it is presented to a lay jury, to make sure that it is indeed up to standard to reach a threshold of “beyond all reasonable doubt”.

This would not require major changes in the way the criminal justice system works. It would also allow scientists to be consulted and input their expertise, without becoming part of such an adversarial courtroom drama, making it more likely that more scientists would agree to be involved. And it would mean that all this evaluation happens before the massive expense and potential damage of a criminal trial.

Without reform, there is a real danger not only of serious miscarriages of justice, but also that the criminal justice system is brought into disrepute, as some of the country’s leading scientific and academic minds start to question the basis for criminal convictions.


1) The Statistical Evidence.

Links to SoT articles:

RSS Report:

Data obtained from FOI requests:

See especially,

2) Other possible causes of the neonatal deaths. The limited scope of the investigation.

Links to SoT articles:

RCPCH Report:

NHS Sepsis symptoms:

Neonatal sepsis:,with%20poor%20perfusion%20and%20shock

Cluster of human parechovirus infections as the predominant cause of sepsis in neonates and infants, Leicester, United Kingdom, 8 May to 2 August 2016

3) The insulin evidence.

Links to SoT articles:

Forensic Science Regulator: code of practice

Insulin assay test kit instructions:

A Nurse’s report of insulin: see attached file

C-peptide Suppression During Insulin Infusion in the extremely Preterm infant is associated with insulin sensitivity:

4) The evidence of deliberate injection of air

Links to SoT articles:

1989 Air embolism paper, see (page 2)

Prevalence of systemic air-embolism after prolonged cardiopulmonary resuscitation in newborns: A pilot study, (Halbertsma et al, 2015)

Systemic Air embolism secondary to respiratory therapy in the neonate, (Marvin S Kogutt)

Lucy Letby trial: Expert says ‘line of gas’ in post-mortem X-ray was ‘unusual’ but not diagnostic of air having been administered:

Normal perinatal and paediatric postmortem magnetic resonance imaging appearances:

5) The “Confession” Note

6) The lack of expert defence witnesses

This is a link to the complete evidence presented to the defence team before the end of the trial.

Opinions of other scientists and specialists which back up the insulin research:

  • “Among all the tests performed by clinical labs, immunoassays have the highest inaccuracy. In addition to intrinsic inaccuracy being based on immunological interactions, numerous drugs and conditions could influence the data produced by immunoassays.” Adel Ismail, retired Head of Clinical Biochemistry and Director of Pathology Services, Pinderfiels and Leeds Teaching Hospitals, West Yorkshire. Area of speciality in laboratory medicine is in ensuring the diagnostic accuracy of measurements and interpretation of laboratory results.
  • In his paper “Hypoglycaemia: accidents, violence and murder. Part 2, Prof V. Marks states, “Contrary to dogma, an inappropriately high plasma insulin and a low C-peptide concentration –especially in the presence of hypoglycaemia – though highly suggestive, is not pathognomonic of exogenous insulin administration,” Professor Vincent Marks, Emeritus Professor of biochemistry and leading authority on insulin in criminal law. In discussing the Letby case with Science on Trial, Prof Marks insisted that assay tests used in the Liverpool laboratory have no forensic value and should have been judged inadmissible by the court.
  • In his paper “Forensic aspects of Insulin,” Prof V. Marks states, “A sample of venous blood must be collected, before any treatment is given, and separated into plasma or serum immediately, or as soon as practicable, and stored at -20 °C until analysed or discarded. At least one further blood sample should be collected, preferably about 1h after restoration of normoglycaemia, and stored alongside it.” In the case of both babies with hypoglycaemia, repeat insulin measurements were not taken.
  • Marks (2005): “Cases that come to court and depend exclusively on the results of a single insulin assay should always be suspect as the methods of measurement employed generally do not meet forensic standards and/or their interpretation is questionable”.
  • Vincent Marks claims a fatal dose of insulin for an adult human being is around 1000 units.
  • Alan Wayne Jones (2023) says: “Analytical methods utilizing immunoassay, such as RIA, EMIT and ELISA, are mainly intended as presumptive, diagnostic, or screening tests for presence of drugs. In forensic toxicology, positive immunoassay results need to be verified by re-analysis with a more specific confirmatory method, such as GC-NPD, GC- MS or LC-MS/MS”.
  • Alan Wayne Jones (2023) has almost the same statement as Vincent Marks: Practical Diabetes Int 2005; 22(9): 352–358, “Hypoglycaemia: accidents, violence and murder. Part 2”

Links to scientists’ research papers:

Insulin analogues as a new example of interference in insulin assays

Adult hypoglycaemia; a narrative review on forensic aspects

Hypoglycaemia: accidents, violence and murder. Part 1

Hypoglycaemia: accidents, violence and murder. Part 2

A W Jones (2023): Insulin murder and the case of Colin Norris.

Forensic aspects of Insulin

Scientific working group for forensic toxicology, (SWGTOX) standard practices for method validation in forensic toxicology. J Anal Toxicol (2013), 37, 452 -447.

Links to other articles and blogs/books:

In 2020, Doctors at The Countess of Chester Hospital missed chances to save Olly Thornton who died from sepsis after they discharged him from hospital. He received inadequate care; they didn’t screen him for a bacterial infection he had which led to sepsis. He exhibited the same rash on his body as did the babies Lucy is accused of killing.

Professor Richard Gill’s blog:

Unlucky Numbers: Richard Gill is fighting the shoddy statistics that put nurses in prison for serial murder. Science, Vol 379, Issue 6629, 2022.

Dr David Robert Grimes, scientist and author:

Two thirds of maternity units are dangerously substandard:

Matthew Syed, British journalist and author of “black box thinking” book. From a review: “In Black Box Thinking, Matthew Syed argues that learning from failure drives human progress. Namely, our politics, courts, and hospitals stigmatise failure and perpetuate a culture of false exceptionalism that prevents them from improving. If we neglect to improve our stagnating institutions, they’ll continue to take the lives of innocents—whether it’s death due to preventable medical error or wrongful conviction that leads to life in prison. ”

Peter Elston, statistician, “Chimpinvestor” blog:

Scott McLachlan’s Law Health and Tech blog: LL Part 0: Scepticism in Action: Reflections on evidence presented in the Lucy Letby trial.

Anonymous nurse “report”: please see attached file

Lawrence George report of baby F and baby L : please see attached file.

The state of forensic science in the UK.  “The UK’s forensic science used to be considered the gold standard, but no longer. The risk of miscarriages of justice is growing. And now a new Westminster Commission is trying to find out what went wrong. Joshua talks to its co-chair, leading forensic scientist Dr Angela Gallop CBE, and to criminal defence barrister Katy Thorne KC.”

Toxic doctors put patients at risk, says NHS Watchdog. From sepsis to maternity, the ombudsman says he is shocked by failings every day,

Announcement follows campaign by parents of Martha Mills, 13, who died in hospital after developing sepsis

Bad stats overturn medical murders podcast

The insulin question

This story focusses on two tests performed at the “Clinical Laboratory Medicine” lab of Royal Liverpool and Broadgreen University Hospitals NHS Trust,, see their “instruction sheet” (reproduced as jpeg image above).

Two babies are supposed by the prosecution to have received a huge unauthorised amount of insulin. Moreover, it was alleged that Lucy was the perpetrator of this, though how she had done it is totally unclear. For reasons which are still unclear, Lucy’s defence did not contest the first claim, obliging Lucy herself to agree with the prosecution that there must have been a murderer on the ward.

These two cases are the only cases where the jury (though reduced in size to only 11 persons) was unanimous in accepting the charges made by the prosecution. Together with the infamous post-it note confession and the infamous spreadsheet showing that Lucy was always there whenever the prosecution alleged that she had murdered or attacked babies (it would have been very surprising if that had not been the case!) these three pieces of evidence seem to be the ones which sway most people’s minds.

I recently came across a long analysis of the two insulin cases on one of the FaceBook pages devoted to the Lucy Letby trial. I believe it has been written by someone in the nursing profession. They appear to me to be extremely knowledgeable. I will reproduce the text verbatim, in a moment.

Notice that the insulin attacks are supposedly proved by the results of blood test which were requested by a doctor who apparently never looked at the result. These results were discovered either by Dr Breary or by Dr Dewi Evans (they both claim to have been the one who did this) in 2018, after the police investigation had been ongoing for a year. Note that that investigation had started almost immediately with Dewi Evans’ analysis of the medical notes on 32 incidents (deaths and resuscitations) in 2017.

The blood test was performed by laboratory of the Royal Liverpool Hospital. The image featured at the top of this post is the information officially provided by the hospital about this particular assay. Note that it explicitly says that the test is not appropriate for the purpose it is now being used for, namely to use a high ratio of insulin to C-peptide in the blood (relatively too much insulin) as an indicator that excess insulin has been administered.

Part 2, September 21

Part 1, September 1



The now infamous INSULIN CASES.

Novel alert!

Sorry, it can’t be helped as there’s so many places to go with this. Promise I’ll try and keep some structure and attempt not to miss anything.

But you may need a drink and a comfortable seat. Let’s go.

I’ll start with some scene setting:

In August 2015 and April 2016, two separate blood test results revealed instances of two neonates who had high levels of insulin and low levels of  C-peptide, in blood samples taken at the Neonatal Unit at the Countess of Chester Hospital.

The children concerned were referred to as Child F and Child L as part of the trial of Lucy Letby, due to the court-imposed reporting restrictions, protecting the identity of the babies and their families.

They are now 8 and 7 years old respectively.

The ‘insulin’ charges are considered the ‘smoking gun’ evidence against Lucy.

This is because in the majority of cases where high insulin levels are secreted naturally by the body, there will be an accompanying level of C-Peptide.

However, C-Peptide levels are not influenced by exogenous insulin levels or ‘injected’ insulin.

Hence the conclusion drawn by the prosecution.


1. Where insulin antibodies are present, transiently (from for example a diabetic mother in utero) or chronically the test used will also report in the same way.

2. There are other conditions that can also generate a misleading conclusion of ‘facticious hyperinsulinism’ from this testing.

3. They include infection, primary or secondary adrenal suppression (Addison’s), genetic variants and liver issues. We do not know how much or how often.

5. The test is also unreliable in some other circumstances, including chronic kidney disease, consumption of certain drugs and alcohol as well improper sample storage/processing.

We are told that the blood results were not noted until the police investigation – with the discovery taking place at some point in 2018, a year into the enquiries by Cheshire Police.

This is important because it makes no sense and is contradicted in testimony. But let’s pretend we believe it.

How this came to pass is in itself a changing story, with both Dr Brearey and Dr Evans claiming they spotted it in 2018.

I’ve asked before what a party in the investigation, if it was conducted as robustly as the police claim in the ‘Operation Hummingbird’ documentary, who therefore should have been a suspect at this point, was doing reviewing and preparing files for the police and supposedly impartial expert witness, but this is one of many extraordinary aspects to this case.  

But let’s get back into the testing.

A key point to note first is that we have no idea of how many other babies could have had the same results, as that information is not shared as part of the case put before the court.

These are not standard tests done from the off and were an external test conducted by the lab at the Royal Liverpool.

They are only ordered with persistently low blood glucose values and have to be requested by a consultant.

In neonates, hyperinsulinism as it’s known, when there is a high insulin reading, NOT related to administration of synthetic insulin, is considered rare, accounting for 1:25k births according to official data.

Although blood glucose issues more broadly are extremely common in premature babies (as confirmed by the prosecution’s chief witness himself, Dr Dewi Evans, in his post-trial interview – nice when we agree on something 😂).

Causes vary and we do not know how many others would present like this, given as per the note above, insulin and C-peptide levels are not recorded in every instance, as the resulting hypoglycaemia can resolve before it gets to that stage.

Where they are, it may not result in a diagnosis of anything – as we see in these cases, if it has corrected.

That said, it is also more common in multiples or in a sibling of a child who has also had the condition; and both of these cases relate to twins.

In both cases their sibling also had issues with maintaining stable blood glucose values.

NOTE, As a result of this, both Child F and his twin brother E were also previously prescribed insulin as part of their care.

We know from research that Transient Hyperinsulinism is often diagnosed in infants of diabetic mothers or mothers with gestational diabetes.

We know this is the case for Child L (& M), whose mother was T1, but do not know if relevant for the other set of twins.

We do not know if she is a carrier of insulin auto antibodies, or another cause for her Diabetes, such as GAD – but if this is the case, the antibodies would have been present in the twins for up to several weeks post-delivery. And alone fully explain L’s Insulin and C-Peptide ratio.

Re F, the risk of developing gestational diabetes is generally higher in people carrying twins or multiples than those carrying a single fetus, so could well be a factor for his mother.

This is because carrying multiple babies places additional stress on the body and increases the demand for insulin. The risk may also be higher due to increased placental hormones. So, it could be a factor there too.

Transient Hyperinsulinism can also occur in association with perinatal stress, which leads to Hyperinsulinism by uncertain mechanism(s).

Factors associated with perinatal stress Hyperinsulinism may include; Intrauterine growth restriction, cesarean section delivery, infection and birth asphyxia.

They also have less well-defined co-morbid test values, because there is not a singular aetiology.

We don’t know how many cases have been noted with corresponding low C-Peptide. And repeat tests can look very different given said transient nature.

Despite this – the ratio of high insulin and low C-peptide has been used to implicate many a healthcare ‘killer’, given exogenous insulin is a more common, researched explanation.

But because of these and other factors, several convictions have also been overturned on appeal. The case of Colin Norris might well become yet another example.

Both the cases for F&L would be classed as ‘transient’ as they self-corrected over time.

(Which enables us to rule out genetic causes.

So, I won’t discuss that here. Even though such tests were not completed either, but it’s more likely it would have been lasting, in all but a couple of known variants – even with treatment).

We were not given much of any comment on the risk factors in the babies involved in court, as the witnesses suggested the C-Peptide made other causes near impossible, but there are known / confirmed relevant factors, in both cases summarised:

*CHILD F* was an identical twin (to Child E) born by caesarean section (✔️) on July 29th, 2015, 10 weeks early.

Child F was just 1.434kg on delivery and had blood sugar issues from the off, before Lucy Letby was anywhere near him. He also needed resuscitation at birth and significant support with breathing thereafter (✔️).

He was being treated for an infection and ‘suspected sepsis’ (✔️). He also had ‘some jaundice’.

*CHILD L* (Twin brother of Child M) was also born by c-section on April 8 2016, seven weeks premature (✔️).

Type 1 diabetic mother (✔️).

Although closer to term that E&F, he only weighed 1.465kg, and was delivered early because the twins had stopped growing properly (✔️). Mum had been admitted two weeks prior to monitor this complication.

They had more mild breathing issues, but issues all the same (✔️).

Note Child E and F were also a set of twins for which twin-twin transfusion syndrome (TTTS) was identified.

TTTS is a rare, serious condition that happens when identical twins share a placenta (monochorionic).

Abnormal blood vessel connections form in the placenta. They allow blood to flow unevenly between the fetuses. the recipient twin receives too much blood, it can thicken.

Thicker blood is harder to pump, so the baby is at risk for developing soft tissue swelling and heart failure, and may even die in utero.

Meanwhile, the donor twin is at risk for organ failure, including the kidneys, because of inadequate blood flow.

This could be a factor in the accuracy of any blood tests taken from Child F and also a huge additional factor of perinatal stress and complications.

It’s fair to say in most reported / research cases, hyperinsulinemia is congenital (present at

birth) and is genetic.

However, children do develop the condition later and it can be transient or more lasting depending on an array of differential factors and cause.

In any case, Child F had needed insulin almost immediately after birth.

We have less accurate data regarding these cases, as they mostly self-correct. So, the numbers could also be higher than anyone actually realises.

And in fact in the neonatal period, acquired forms are usually associated with conditions like perinatal stress as noted in both babies or maternal gestational diabetes and are often transient see [6, 7] in the attached article.,transient%20%5B6%2C%207%5D.

Also note from the research paper linked to below:

The defining laboratory value of hyperinsulinism is not always a measurable elevation of insulin.

« Insulin levels fluctuate greatly because of the short half-life of 4 to 5 minutes and because it is rapidly cleared by the liver before it reaches the peripheral circulation »

As also seen in these babies. But put down to very different circumstances by the Expert Witnesses, with very little to back this up, years after the event.

Two important studies also ref in this paper discuss the level of plasma insulin during hypoglycemic states in large groups of patients with transient HI.

The first study noted that 22 of 27 (81%) of infants diagnosed with transient HI had elevated plasma insulin levels.

In the second study, plasma insulin levels were elevated in only 11 of 24 (46%) of neonates with transient HI.

These cases were diagnosed with hyperinsulinism on the basis of other evidence, including lack of ketosis in the setting of hypoglycemia, elevated glucose requirements, and glycemic response to glucagon.

Meaning others could fly under the radar and tests taken very close together can vary greatly.,by%20uncertain%20mechanism(s).&text=Factors%20associated%20with%20perinatal%20stress,section%20delivery%2C%20and%20birth%20asphyxia.

But also is very important because of the prosecution’s allegations about why the insulin levels were high and the method they theorise exogenous insulin was administered.

So what was the cause in these babies, how was it determined, confirmed and is it as clear cut as the prosecution make out, for their lynchpin cases or ‘ah ha moment’ as they’ve put it prior.

The fact is – we don’t know. And I’ll tell you why.

The clinical pathology is not there conclusively with the testing they did and then onwardly didn’t do (esp. with the compounding factors I’ve outlined above) and well their version of events from a bigger picture perspective makes even less sense.

We have discussed this a lot from different perspectives, but I wanted to share my own personal observations – along with a video, showing that after the trial, the key parties don’t seem to be able to make their minds up how they even came across this information and who interpreted it.

Firstly – We are supposed to believe that even by the first incident, but certainly by the second, ‘the doctors’ were highly suspicious of either grave incompetence (in addition to their own – well documented in a series of reports and in court testimony) or nefarious activity by LL.

Yet astonishingly they want us to believe in the next breath, that on neither occasion the test results highlighting raised insulin levels were escalated to senior consultants.

So let’s get this straight:

They have ordered the tests for both children. They were supposedly concerned they had mistakenly or purposefully been given insulin or had some apparent disorder / wider issue with their blood glucose, endocrine system or genetics even, to have done so, over and above the standard testing at the hospital … but they didn’t think it in any way important to review the results properly at the time. 🤯

“None of us regrettably realised two babies had been poisoned by insulin, so we didn’t have the full picture”

A statement made Dr John Gibbs in court and widely shared in the media.

I’m sorry … that does not wash with me.

Nor is this what happens in clinical practice. Or rather, in any case should happen.

Talking about the first incident relating to Child F, we were told that the long and short of it is:

A blood sample was sent to the Royal Liverpool Hospital for analysis which confirmed the insulin detected was not naturally produced.

Dr Gibbs said in court on the 24NOV22 the insulin c-peptide reading should be at 20,000-40,000 to correlate with the insulin reading in his test (4657).

And so Child F had been given a pharmaceutical form of insulin administered, and he “should have never received it”.

A bold statement.

Yet Gibbs or any other prosecution witness has provided absolutely no conclusive evidence that this was the case as I’ve said.

Other than a test that does not record the type of insulin or differentiate from the insulin produced naturally by the body. Just an indicator in C-Peptide to insulin ratio, that further testing is required to investigate the cause.

Exogenous insulin one cause. Yes, the most common cause. But not the ONLY cause.

And both babies had significant risk factors for other causes as I have outlined.

So, no. That is absolutely not what the test said. Or measured. It’s a total misrepresentation.

In fact, the lab themselves suggested further testing to conclusively determine this in the results provided.

More so, (see video, link to be added later), even test interpretation notes suggest insulin autoantibodies as a potential cause.

It’s important we deal in facts, not opinions here. Especially in matters of such importance.

And we actually heard days and days of testimony re these two babies. But also, insulin and TPN, from various witnesses.

Whilst I’ll go as far as to say some of them over played their hand and made it sound like it was the only explanation, some of the experts did give a more rounded representation when pushed, a ‘most experts agree’ type statement – insinuating that there are other causes and possibilities. Even if they were presenting what they believed to be the most likely explanation (according to the prosecution case).

It’s fair to say though, no real detail was covered re other causes of Transient Hyperinsulinism in neonates, with low accompanying C-peptide, nor medical history of the mother to confirm or discount transient insulin auto immunity or great detail about the reliability of the testing when used alone to be diagnostic.

But I’ll be clear here. That is not what they were there to do.

They were hired to theorise and explain the how. The why had already been decided.

More so they brought in other experts to expand on their theory – with scientific calculations, pertaining to half-life & most likely method of administration as a result (TPN bags they claimed), but again with no real evidence that seems to stand up when you take a step back.

1. There were no TPN bags tested or retained.

2. There are many practical flaws to this. Including TPN being changed when LL was not even working a shift – with the clinical state continuing. This had them theorising that she must have ‘spiked’ stock in the ward fridge, using the bag ports.

Professor Hindmarsh for the prosecution said that insulin could be added “fairly easily” through a portal that’s located at the bottom of the feed bags.

He also told the court that in his opinion, to produce the blood glucose levels detected, around at least three or potentially four bags could have been contaminated.

Forgetting to mention that the same stock bags were being used for other babies on the ward.

It would be a starting coincidence that only one baby would have received all of the contaminated bags, eh?

Crucially though, remember they have not and couldn’t discount other causes with actual testing, or confirm if it was indeed exogenous, incl. the brand/type/chain to confirm it was the same that was held in the ward fridge, as they didn’t bother to do it, and so have no actual conclusive proof of their theorised accounts.

However much they double down.

This is the test they would require to confirm the aspect of their theory that it was exogenous or manufactured insulin and which type:

LC-MS/MS testing.

This would have not only identified if the beta chain was synthetic, but also the manufacturer of that synthetic insulin.

If negative; other avenues should have been explored, including genetic, auto immunity of various types. Transient or chronic.

But they didn’t even repeat the first test. Let alone do more.

Let summarise so far:

CHILD F had significant risk factors for congenital hyperinsulinism.

As did CHILD L, which I’ll get to shortly in a little more detail.

These risks were actually increased by over 300% due to their size and weight according to various studies.

But the prosecution claims a murderous serial killer nurse was far more plausible, despite being many times rarer on a population level than congenital hyperinsulinism. Even without the elevated risk factors.

Not even 1:300k in the U.K.

And other staff had to select the supposedly spiked TPN, for the same babies, in each case, consistently around 3 times, when LL was not on shift.


But that’s not even it.

This is where it gets very interesting re F.

Child F collapsed on the 5th August.

Dr Gibbs, now famous here for his ‘memory’ lapses, (that only he’s allowed), conceded in his testimony to the court that insulin was given far later than originally represented in his statements (the night of the 4th August – a bolus he says) to said baby.

He had originally stated that Child F had last been prescribed insulin on the 29th July.

This was repeated by multiple professionals, each stating that none was administered since the 29th July.

Which for me makes all of this completely nul and void. Their records were a mess. How do we know that any of it was reliable.

The child had insulin.

More so, F’s brother, Child E WAS prescribed insulin too.

Child E had sadly passed the prior day, but obviously has the same surname.

Was this a matter of incompetence?

Is it not more plausible that IF the result was indeed due to synthetic insulin, that Gibbs did only give a bolus overnight if we can believe his latest conclusion.. that further doses could have been given in error, to a child with the same surname, right next to F?

Especially on a chaotic ward making an exceptional number of mistakes, that have been well documented.

To make this seem unlikely … it was represented to the court that there were no other children on the ward, in receipt of insulin at the time. Technically correct, but also misleading on account of this information.

So, what about the sequence of events relating to the results?

Evidence was also given to the court that the results for Child F were phoned through to the Countess of Chester’s biochemistry lab on August 13. (It is a delayed result).

By that stage Child F’s blood sugar had stabilised and he had been moved to a different hospital closer to his parents’ home.

So, NOTHING was followed up.

A doctor involved in the care of Child F said she was “at a loss” to explain the blood test findings.

The medic, who could not  be identified for legal reasons (convenient eh!), told Manchester Crown Court:

“This is something we found very confusing at the time because (Child F) had only been prescribed insulin five days previously (on July 31). AGAIN even though Gibbs changed his story on this date.

Contrary to the account of Dr Gibbs and Dr Brearey, the unnamed doctor said it was looked at to see if anyone else at the time was prescribed insulin in the whole neonatal unit. Investigated for a possible ‘accidental administration’, when the results came back.  But there were no other babies at that time. No further action was taken.


Gibbs claimed that ‘I was not thinking at the time that someone might have administered insulin. The results showed that, but unfortunately the junior doctors who read them didn’t realise the significance’.

Seemingly contradicting her. She clearly DID understand the potential significance.

So what was it … Who is telling the truth?

They need to get their story straight.

But from this we can infer they did know … or why did they check the other prescriptions?

And so Gibbs and his bolus aside, if they had this information, why didn’t they follow the advice to understand WHY these tests came back as they did?

So let’s get to Child L, where denials and excuses become even more astonishing. By now we are in APRIL 2016.

The doctors were in full ‘blame Lucy’ mode and had been in conflict with management.

A blood sample taken from Child L was again sent to the Royal Liverpool for the tests.

That too showed a high level of insulin which the prosecution and the media tell us ‘had been given to the patient’ again with absolutely no evidence, other than some clever sounding, educated theory that it was the case.

For all the same reasons it’s disingenuous to claim otherwise..

Even more so with Child L’s mothers T1 diabetes. There was even more likelihood of a biological rationale for the events.

YET AGAIN – The result was phoned through to the Countess of Chester on April 14 and entered on the computer system – with no further action taken that was tangible or followed the next steps suggested by the lab.

Crucially again … it’s Doctors ordering these tests. They don’t order themselves and procedure states that they have to be both requested and interpreted by a consultant.

Why were we not given more specifics here?

Who did this.

Why were we not given the name of the doctor that both ordered and interpreted the tests?

Why was this and procedure glossed over?

Why were doctors allowed to make inaccurate statements unchallenged?

The media happily minimise phrases like “it significance did not appear to be appreciated as the child’s condition had improved”.

Ummm, not good enough. And highly misleading.

Now let’s briefly discuss the numbers for each baby. As it opens another worm hole.

For Child F the insulin level was provided to the court as 4657. I am presuming this is pmol/mL – as despite this being INSANE, any alternative unit measurement is worse.

Note, 4000 anything insulin, is enough to put grown man in a coma.

It would not be unreasonable to conclude this is likely to be inaccurate. And would call for repeat testing.

In fact, generically neonatal blood tests often read inaccurately high, on account of low blood volume and potential newborn hemolysis, so often need to be repeated.

Confirmed now by several doctors.

Where there is TTTS even more so.

For Child L, it was far lower.

1,099. With a smaller C-Peptide disparity (recorded as 264).

Remember this is the child with a type one diabetic mother.

Given the values are not just significantly lower, but in another stratosphere – would it not make more sense to conclude that they were not the result of the same set of circumstances. And that this is more likely the cause of the hyperinsulinism with low C-Peptide?

Now blood sugars.

In both cases some of the many values given were not even indicative of poisoning.

Levels of 0.2 or lower – would be expected.

In Child L, they never fell below 2.0. Not once.

In F, the lowest reading was 0.8. But others were much higher.

I’m not going to go too much into the chain of evidence as it’s a lesser factor. But we don’t know what happened in transit to the lab. Bloods without this clearly documented can become inadmissible evidence in any case.

That’s before we get to both the TPN and insulin. Even after its arrival on the ward from all over the contentent and via various hospital departments, the entire ward staff had access to it. Yet of course, if it went as told, it had to be LL. I won’t even give this any more time. 🥴

And let’s get back on to Dr Evans and the police now.

The police claim that Dr Evans reviewed all files relating to collapses and deaths of babies covering the period in question (June 2015-July 2016, when Lucy was removed from the ward) to determine which were ‘suspicious’.

However, Dr Evans claimed in his post-trial interview, that he only saw the files for F&L, because their siblings were “harmed in other ways”.

So … why were their collapses not included in the original bundle?

Is it because Lucy Letby was not on shift in the most part, so the files had been ‘pre sifted’, to only include babies that collapsed or died when Lucy was on shift?

Can we reasonably infer from this that they were ever only investigating incidents they could associate with Letby being on shift, despite their claims to the contrary?

Which also makes their so called ‘strongest evidence’ their potential undoing. Well, the undoing of their narrative in any case.

Especially since as no information was provided in discovery as to the other up to 10 deaths (numbers vary from different sources as we have previously discussed, which in itself is a 🚩) and unknown number of other collapses in the same 12-month period.

Or indeed what really differentiated these from the others – with the very vague and unshared methodology of ‘unexpected and unexplained’.

Despite all the cases linked to the charges, having many, many factors that regularly cause death and collapse in premature infants.

The police want us to believe that deaths and collapses in neonates is exceptionally rare.

10 others on the same ward and statistics re mortality by gestational age (see my prior posts), also prove this a fallacy. Even if these comorbidities did not exist.

In what sort of alternate reality is this acceptable?




The insulin debate.

First, let’s repeat the beginning of the Part 1.

Discordant Insulin to C-peptide results being an absolute indication of factitious insulin administration is an entirely false assumption.

Not only that, the results proposed are beyond insane.

There are several reasons for that, it’s complex and multifactorial.

Let’s try and break it down somewhat.

• The test showed that the insulin concentration was 4657/pmol/L, the C-peptide was 169 pmol/L and the glucose was 1.3 mmol/L.  Within two hours of the blood test the baby’s blood sugar level was ~4 mmol/L, which is normal.

• When there’s is a concern of neonatal glucose issues, the best standard of care would be to take C peptide/Insulin levels from cord blood at birth or at first recognition of an abnormal blood sugar, or when there is known diabetic mother either – Type1/2 or gestational. It’s a right away job. Not a ‘when shit hits the fan’ job.

• Second from that, the test to prove exogenous insulin is preferably done fasting, though ovbiously impossible in neonates,  it can also be done in the first instance of sudden, unexpected hypoglycaemia. This would be differentiated as a ‘fasting’ result and a ‘stimulated’ result.

• However, what you don’t do, what you absolutely avoid doing, if you want any accuracy or legitimacy in the results, you later use to infer attempted murder – You do not start treating the hypoglycaemia, then take the C peptide/ to insulin test. A test taken after treatment has commenced, is completely compromised.  

• Because treatement of hypoglycaemia raises the insulin and suppresses the C peptide, therfore you get abnormal results.

• The hypoglycaemia was treated with IV dex MULTIPLE times over several hours, prior to this test being considered, returning an odd result. If it were to be considered a legitimate result.   It would insinuate invalidity, due to not being taking prior to treatment.  Those results could be partially explained by the repeated IV dex prior to the test, which stimulates the Insulin release and supresses the C peptide.

And now Part 2 really begins –

• DR Gibbs states the patient is peripherally shut down. And blames possible infection or stress. Yet that is also a consequence of Hypoglycaemia. Hypoglycaemia induces a reduction in peripheral circulation, which in turn affects circulating blood volume for tests. Slow difficult blood draws often read Insulin inaccurately high.

• A C Peptide of “under 169 P/Mol” being considered ‘undetectable’ is also, complete randomness. 169 is not a low C – Peptide result, under 94 is the beginning of low 94 – 300 is an ‘indeterminate’ number. 300 + is high.

• It’s widely assumed that a supressed C peptide from insulin would be very low, much lower than 94, never mind 169. p/mol/l.

Though this varies in neonates,

Recent studies show that 5 out of 9 c peptide results were low, 4 out of 9 was high, after insulin administration. (it is not an exact science in the most complex creatures in this world)

• The test itself is unfortunately difficult to trust, as the standards prior to it arriving frozen, rely on it being centrifuged and frozen within 30mins of being taken. As a nurse who has worked in 4 hospitals in various departments, The likelihood this happened at 5.30am in a busy acute hospital is almost 0. I would be flabbergasted if even a good hospital managed that.

•  Even if it was handed straight to the lab, it would sit amongst the ED bloods that come every 5 to 10 mins, where 1 or 2 members of staff would slowly work through them.

• Unless it was sent on a bed of ICE, the sample would have already started to degrade, it wasn’t sent on Ice, there is no Ice in the woman and children’s building.  If it was centrifuged (plasma separated) after 6 hours, it would be non-diagnostic, totally void. They only confirm it arrived frozen and was processed within 24 hours. No one has confirmed it was treated and frozen within the expected 30 mins.

• On top of that, it was sent to Liverpool, who state they cannot diagnose exogenous insulin in their 2012 protocol, but on this day, on the C peptide page, have returned to their 2010 protocol which has no mention of their inability to detect exogenous insulin. (Good PR for the trial not to fully annihilate your credibility, eh?)

• The people who should be doing this test – Guilford,  who they considered forwarding the sample too, but didn’t, as they had ‘confidence’ in the tests accuracy despite working off a much older set of standards for preservation.

• Guilford had a different set of standards, for neonates especially. They request the blood test of neonates to be heparinised, as there is normally a much lower blood volume and this maximises the plasma for testing.

• Had the test went to the right lab, to verify what this test is supposed to be proof of, it wouldn’t have even been in the same vial, never mind every other error up until that point.


1. The test wasn’t done at the time needed to diagnose exogenous insulin. First episode of hypoglycaemia, prior to treatment.

2. Multiple attempts to rectify the blood sugar, would have increased the plasma insulin and supressed the c peptide.

3. The test was taken from a peripherally shut down patient who had issues with cannulation and multiple IV infusions of dex

4. The test would have needed to come from a non-IV line infusion arm or limb. Though failed cannulas would likely have meant there was no IV free limb.

5. The test needs to be kept at 4’ min immediately, centrifuged within 30 mins and frozen to -20, to stop degradation as the hospital and Liverpool lab were still using the less stable testing protocol of gel tubes. Despite there being a testing protocol that allows 24*s stability at ambient temperature.

6. If it was delayed 6 hours + prior to the centrifuge, the results were degraded and absolutely unable to be used in court. Even if they arrived to Liverpool ‘frozen’

7. They were sent to a lab unable to conduct the proper testing that would have actually evidenced exogenous insulin, the lab that accurately determines that was Guilford, the test didn’t go there. We are relying on Liverpool’s interpretation, despite them not having the proper assays to be used credibly, like to accuse someone of murder.

8. Had there have been some initiative in sending the test to the right lab in the first instance, the Guildford lab would have advised that neonatal bloods specifically, were taken in a ‘red top’ no preservative, heparinised, then separated, as neonatal blood tests cannot be treated the same way as adults.

9. HOWEVER despite all of that – 4657/pmol/l cannot be the result, it is not possible.  Not on the proposed 0.6ml Of insulin added to a slow bag which is another fallacy entirely. That same result was found on attempted suicide patients who injected over 200 Units of insulin, and who were in a coma in the ICU for several days.

10.  The insulin may have already been high from all the IV Dex infusions, likely a degraded, partially haemolysed sample from inability to follow the strict protocol, taken too late, from a peripherally shut down neonate, it wasn’t heparinised, as expected for neonates and small blood volumes, yet Liverpool ran it anyway.

A blood test with very serious consequences, requires it to be done properly and to the letter. Then be properly analysed considering the results make 0 sense even if insulin was added, the C peptide would have been less, the patient would have been very much dead or dying – Not recovering to a Blood sugar of 4 0 –  2 hours later

11. The C peptide result of 169 P/Mol/l is not low for neonates. It doesn’t come under the bracket of low, yes it’s lower than expected for an insulin level that high, maybe in adults?  but once you start treating the issue, you supress the C peptide, so it may even have been normal, prior to all the increasing dex infusions.

Would this be good enough for your life?

#Weegie RN

Angelidi, A.M., Filippaios, A. and Mantzoros, C.S. (2021). Severe insulin resistance syndromes. Journal of Clinical Investigation, 131(4). doi:

Cryer PE, Axelrod L, Grossmann AB et al. Evaluation and management of adult hypoglycaemic disorders: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2009;94:709-728. This identifies 0.2 nmol/L (0.6 μg/L) as the critical concentration below which C-peptide should be suppressed during hypoglycaemia.

ECLI (2019). C Peptide (Plasma) / Blood Sciences Test / Exeter Clinical Laboratory International. [online] Available at:

McDonald, T.J., Perry, M.H., Peake, R.W.A., Pullan, N.J., O’Connor, J., Shields, B.M., Knight, B.A. and Hattersley, A.T. (2012). EDTA Improves Stability of Whole Blood C-Peptide and Insulin to Over 24 Hours at Room Temperature. PLoS ONE, [online] 7(7), p.e42084. doi:

Sacks DB, Arnold M, Bakris GL et al. Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. Diabetes Care 2011;34:e61-e99.

Venugopal, S.K., Mowery, M.L. and Jialal, I. (2020). C Peptide. [online] PubMed. Available at: (n.d.). C peptide measurement helps to determine the cause of hypoglycemia. [online] Available at: [Accessed 21 Sep. 2023]. (n.d.). Causes of spurious results – Biochemistry. [online] Available at:

Yamamoto, J.M., Corcoy, R., Donovan, L.E., Stewart, Z.A., Tomlinson, G., Beardsall, K., Feig, D.S. and Murphy, H.R. (2019). Maternal glycaemic control and risk of neonatal hypoglycaemia in Type 1 diabetes pregnancy: a secondary analysis of the CONCEPTT trial. Diabetic Medicine, 36(8), pp.1046–1053. doi:

MedicineNet. (n.d.). What Is a High Insulin Level? [online] Available at:

Introduction to the case: R. v. Lucy Letby

Here I will introduce the first project which our foundation is going to tackle. Our aim is to disseminate reliable information about the case, in particular concerning the science which could (and in our opinion, should) have been brought to bear on it, both medical and statistical. Perhaps even also insights from history, sociology, psychology. We, the founders of Science for Justice – NL, are scientists, but not medical scientists. One of us is a statistician with long experience in the use of statistics in medical science and in forensic science. He has been deeply involved in several past serial killer nurse cases.

Certainly, the similarities with the famous case of Lucia de Berk in the Netherlands are large, and once one knows more about both cases, horrifying. For the time being we must refer the reader to a blog post by one of the two founders of Foundation Science for Justice – NL:

Foundation Science for Justice NL

I will write more about our history, explain who we are, and in particular, publish the statutes of our foundation, in the coming weeks, … Right now there are very pressing things to do, related to our first project, Freedom for Lucy Letby.

Several more projects are in the pipeline.

We are interested in truth and justice and interested in achieving Justice through uncovering the truth as much as possible. Science gives us tools for that purpose. The purpose of Science is to get a closer understanding of the truth about the world around us through the use of scientific methodology and the powers of reason.