The Van Lommel Lancet NDE paper

While I have read this paper in the past and read about this paper in the past I can’t say prior to re-reading it now that I recalled much specifically about particular criticisms. The following therefore represents solely my view based on my analysis that I’ve done over the last few days.
I’ve focussed only on certain elements in this post.

http://www.pimvanlommel.nl/files/publicaties/Lancet artikel Pim van Lommel.pdf

This first bit is simply a point form summary of the paper. It’s long so feel free to skip over it, but it might be useful to some so I’m leaving it in.

The summary section will be devided into two posts, then the third will have my analysis. Sorry about the formatting, I typed this up in Word.

Summary:

Two basic goals:

1) Establish the cause of the experience,
2) Assess factors that affected its frequency, depth and content

Method:

- Prospective: consecutive patients who were successfully resuscitated
- Patients had to be clinically dead as established by ECG records
- NDE defined as “the reported memory of all impressions during a special state of consciousness, including specific elements such as out-of-body experience, pleasant feelings, and seeing a tunnel, a light, deceased relatives, or a life review”
- Clinical death defined as “ period of unconsciousness caused by insufficient blood supply to the brain because of inadequate blood circulation, breathing, or both.”
- short, standardised interview with sufficiently well patients within few days of resuscitation
o asked whether patients recollected period of unconsciousness
o what did they recall
- 3 researchers coded the experiences according to the weighted core experience index
- Recorded:
o Date of cardiac arrest
o Date of interview
o Sex, age
o Religion
o Education
o Previous NDE? Heard of NDE?
o CPR inside or outside hospital?
o Previous myocardial infarction
o Number of times resuscitated
o Estimated duration of circulatory arrest and unconsciousness (say how?)
o Intubation?
o Type and dose of drugs before, during, after
o Assessed possible memory problems at interview after lengthy or difficult resuscitation
- patients resuscitated during electro physiological stimulation classed separately
- Interview:
o 2 year mark
§ Standardised/taped interview 2 yrs after CPR
§ Life-change inventory:
· Self-image
· Concern with others
· Materialism
· Social issues
· Religious beliefs and spirituality
· Attitude towards death
o At 8 year mark:
§ interviewed again
§ life-change inventory
§ medical and psychological questionnaire for cardiac patients
§ Utrecht coping list
§ Sense of coherence inquiry
§ Depression scale
- Control group:
o Resuscitated patients who had not reported an NDE
o Matched with patients who had had an NDE by age, sex and time interval between CPR and second and third interviews
Statistical analysis:
- Assessed causal factors for NDE with Pearson test for categorical and t test for ratio-scaled factors
- Mann-Whitney test to analyse factors affecting the depth of the NDE
- Spearman’s coefficient of rank correlation for ratio-scaled factors
- Mann-Whitney test to assess link between NDE and altered scores for life-change inventory
- Sums of individual scores used to compare the responses to the life-change inventory in 2nd/3rd interview
- All tests two-tailed with significance shown by p value less than 0.05

Results:
Patients
- 344 patients with 509 successful resuscitations
- Mean age 62.2 yrs
- 73% men/27% women
- 248 (74%) interviewed w/i 5 days of CPR
- Demographic info from first round insufficient for statistical analysis so used data from second
- 74 patients interviewed at 2 yr mark
- 86% were on their first heart attack
- Nearly all patients treated with:
§ Fentanyl
§ Synthetic opiod antagonist
§ Thalamonal
- 13% also received sedative drugs
- 11% given strong sedatives
- 68% resuscitated within hospital
o 81% resuscitated within 2 min of circulatory arrest
o 80% unconscious less than 5 min
o 30 patients electrophysiological stimulation with less than 1 min of circulatory arrest and less 2 min. unconsciousness
- 29% outside hospital, 3% both
o 80% more than 2 min circulatory arrest
o 56% unconscious more than 10 min
o 9% circulatory arrest more than 10 min
- 36% all patients unconscious longer 60 min.
o 37 had intubation + strong sedatives
o Interviewed later
o 24 of these showed memory defects
 
Prospective findings:
- 509 resuscitations: 12% resulted in NDE, 8% core experiences
- No distressing or frightening NDE
- Table re: classification of NDEs
- Table re: elements of NDEs
- “Denture man” account described – reported by a coronary-care unit nurse
- Table re: demographic, medical, pharmacological, psychological factors, frequency and depth of NDE
- Lengthy CPR = fewer reports of NDEs
- NDE patients higher mortality soon after stay than non-NDE patients
Longitudinal findings:
- 37 patients for 2nd interview
- All patients able to retell their experience almost exactly
- Of 17 patients low scores in first interview: 7 same score, 4 reevaluated on had positive emotions, 6 actually never had an NDE
- Control group selected
- 2 of them had positive emotion NDE, 2 actually had a core experience.
- Life change inventory: Significant differences in answers to 13/34 item between people with and without an NDE
- 8 yr follow-up:
o 23 patients with NDE at 2 yr Mark
§ Still recall almost exactly
o 15 patients from non-NDE group
o All patients had positive change:
§ More self-assured
§ Socially aware
§ Religious
o Various psychological conclusions
o Table life change inventory questionnaire
 
Summary cont-

Discussion:
- Medical factors cannot account for occurrence of NDE
- All patients clinically dead – most no NDE
- Seriousness of crisis not related to occurrence or depth of the experience
- If purely psychological factors resulting from cerebral anoxia caused NDE- most of patients should have had this experience
- Patient’s medication unrelated to frequency of NDE
- Psychological factors unlikely to be important as fear not associated with NDE
- They draw some conclusions about the true frequency of NDEs
- They compare some stats to other studies
- Good short term memory essential for remembering NDE.
- Study confirms transformational processes
- Takes several years to consolidate transformational process
- They presume the reason for this is due to society’s negative response to NDE
- Longlasting transformational effects of an experience that lasts for only a few minutes of cardiac arrest is surprising and unexpected
- They note that their sample might not be representative of all cases due to demographics
- Could be differences re: NDEs other causes
- Theories explain NDE:
o Did not show that psychological/neurophysiological/physiological factors caused experiences – not sure how they conclude this, whether true or not
o Describe Pam Reynolds case
o Conclude that neurophysiological processes must play some part in NDE
o Compare to similar experiences induced experiences:
§ electrical stimulation of temporal lobe
§ High carbon dioxide levels
§ Decreased cerebral perfusion/cerebral hypoxia
§ Hyperventilation
§ Ketamine-induced experiences/blockage NMDA receptor
§ Endorphins/serotonin.enkphalin
§ LSD/psilocarpine/mescaline
o These experiences can consist of unconsciousness, OBEs, perception of light, flashes or recollection from past
o Recollections consist of fragmented and random memories unlike panoramic life-review that can occur during NDE
o Transformational processes with changing life insight and disappearance of fear of death are rarely reported after induced experiences
o Induced experiences are not identical to NDE: unknown mechanism causes NDE by stimulation of neurophysiological and neurohumoral processes at subcellular level in the brain in only a few cases during critical situation such as clinical
o These processes might also determine whether the experience reaches consciousness and can be recollected
o Propose discussing whether consciousness and memories are located in the brain- sure, future study
o Propose relevant questions:
§ How could a clear consciousness outside one’s body be experienced at the moment the brain no longer functions during a period of clinical death with flat EEG? Good question but not one that the research methodology was designed to study
§ In cardiac arrest EEG usually flat in most cases within about 10s from onset of syncope: again, nothing in the research methodology geared towards this
§ Blind people described veridical perception during OBE at time of experience: again interesting but not related to the study methodology
§ NDE pushes at the limits of medical ideas about range of human consciousness and mind-brain relation: indeed- but not related to research methodology
§ Theory NDE might be a changing state of consciousness in which identity, cognition, emotion function independently from unconscious body but retain possibility of non-sensory perception: right, but again not related to the research methodology
o Suggestions for further research:
§ Concentrate on effort to explain scientifically the occurrence and content of NDE
§ Focus on specific elements of NDE
§ Theory and background of transcendence should be included as a part of an explanatory framework for these experiences
 
My take:
I think this is certainly an interesting paper and quite a useful one. I can see why it was accepted for publication in the Lancet as I think it certainly contributes in a valuable way to the research base on NDEs.
As stated, the authors were investigating two major things in this paper:
1) Establish the cause of the experience,
2) Assess factors that affected its frequency, depth and content
Let me start with 2. Here is where I think the paper shines and where I think it is most valuable: The paper seems to me to do a good job of identifying factors involved in the NDE and most particularly giving some insight into how having an NDE can effect a person on a psychological basis under the categories listed. Comparing to the group without NDEs (minor quibbles over the ones that snuck into the wrong group aside) seems to me to be an effective way to gage this. The paper doesn’t seem to overreach in its conclusions here and the methodology leads to the conclusions reached.


Moving on to (1): the cause of the experience: Here, I can’t see how we can consider this a controlled study in that the controls to me see very geared to (2) but I can’t see the strong link to (1). I don’t think its fair to say but I’m not saying that as a criticism because I don’t think the authors suggest otherwise. To me, the research methodology is less related to determining the cause of the experience and the conclusions drawn (tentative as they are) are much less related to the controlled aspects of the study.

The authors state that the study did not show that psychological/neurophysiological/physiological factors caused experiences. I agree that it didn’t show that, but it also didn’t show they weren’t involved. I’m not sure how the methodology could really allow us to draw any conclusions about that, one way or the other. I am having trouble seeing how the research design – geared so strongly to answering (2) gives us that much insight into (1).

For example, they state: “If purely physiological factors resulting from cerebral anoxia caused NDE, most of our patients should have had this experience’ Regardless of whether anoxia could be involved in causing NDEs I don’t see how anything in the research protocol could help assess whether or not we should expect them all to have had one especially when they also conclude that good short-term memory seemed to play a role.. I don’t see how the research methodology they laid out can help draw the conclusion that if the NDE were physiological in nature most patients should remember it.

The literature review is interesting.. Here I think there is a link to the results in stating that the experience in the NDE varies from these induced experiences. I don’t think we can call it controlled (since what was done was compare the controlled findings of this study to findings they’d read in other studies) but I think the conclusions are fair – there seem to be some pretty clear differences and I think the study does help us understand that. But what I don’t think the protocol gets at is whether similar brain processes are involved in the NDE. I can’t see how the protocol is geared at answering this question at all. I don’t know why one would expect if similar processes were going on in the brain between the induced and the NDE why we should expect them to be identical if they were triggered differently, in different combinations, etc. That said, I don’t think the authors go so far as to make this claim anyway. They note that there are differences, but do not state that similar processes couldn’t be going on. What they do is suggest further research and set out a bunch of questions which are perfectly reasonable.

In conclusion, I think the paper as a whole is reasonably good. The only conclusion that I think is somewhat overstated they don’t focus that much on. The controlled aspects of the study produce some good insight into several factors involving NDEs and the non-controlled parts raise interesting questions for further research.

I think a bigger issue for this paper is how some people have interpreted it: ie: concluding for example that this paper demonstrates strongly that NDEs aren’t physical. I don’t think it does. It’s a controlled study, but not on the elements that are most hotly debated here – that of whether NDEs are brain based or not.
 
I just read over the paper myself before reading this review, and the anoxia comment stands out to me as odd. There is a fair point that everyone should be having this experience if the answer was that simple.

I remember my own experience going under anesthesia for the first time, I was wondering if it would feel like anything since the family has had "NDE-ish" experiences before under anasthasia; I heard the EKG beep in the background and by the time it took effect to the time everything was over it sounded like the machine hadn't even skipped a beat. It seems odd to me that if both parents have had similar experiences, I would have a null experience, since that would indicate there is something other than a simple genetic answer to this problem.

Woerlee mentioned something about a heart condition which also occurs in the same rough block of people (~20% or so) that seemed like an oddly close correlate; I don't remember which condition it was he brought up to investigate that though. (I'm not a Woerlee fan, but leads are leads.)
 
Woerlee mentioned something about a heart condition which also occurs in the same rough block of people (~20% or so) that seemed like an oddly close correlate; I don't remember which condition it was he brought up to investigate that though. (I'm not a Woerlee fan, but leads are leads.)

Woerlee has been refuted over and over again. I am not going to expand on that, because I have already had too many fights with him on this and other cases (the Dentures man, and the Pam Reynolds cases - see, for example the respective Journals of Near-Death Studies, wherein mine and his articles were published). I am fed up with his rants.

As for Arouet's take on this particular study, on the other forum I promised to send his comments to the authors. One of them, R.van Wees, has responded. I will translate it shortly.
 
I just read over the paper myself before reading this review, and the anoxia comment stands out to me as odd. There is a fair point that everyone should be having this experience if the answer was that simple.

The issue I was looking at was not whether anoxia causes the NDE or plays a role in the NDE but rather whether the research protocol that the authors set up was geared towards answering that question. I can't see how it was.

It may be true that if anoxia were involved then everyone should have an NDE - or it may not. Anoxia may be involved in full or in part. The brain processes involved in anoxia may be involved in full or in part. It may be part of the cause or none of the cause. It may be that everyone should remember it or not. These to me are reasonable hypotheses to explore - but I think the paper simply raises them as hypotheses - I don't think this study can be said to have explored it in any controlled manner. The controlled elements are simply geared towards answering different questions. And the controlled elements seem to indicate that memory does play a role in how these things are reported which suggests that there probably are people who have had NDEs who don't remember them.

As I suggest above there may be nothing simple about how the NDE comes about. I don't think we should assume it is ONE cause - such as anoxia. I think what the comparisons to the induced experiences show is that the brain is capable of quite diverse experiences in various situations. some which involved elements of NDEs and that study is needed to investigate these processes. But in terms of this study I'm not sure we can say that the protocols used helps us answer these questions. Or if it can perhaps someone could help me better understand it.
 
Woerlee has been refuted over and over again. I am not going to expand on that, because I have already had too many fights with him on this and other cases (the Dentures man, and the Pam Reynolds cases - see, for example the respective Journals of Near-Death Studies, wherein mine and his articles were published).

I'll look them up; do you have the article titles on hand?

I end up shoving both the proponent and skeptic articles in to JabRef and marking them as related; it helps track what I've already read, and I can trace the lineage of an argument through that to see what is worth paying attention to.

The issue I was looking at was not whether anoxia causes the NDE or plays a role in the NDE but rather whether the research protocol that the authors set up was geared towards answering that question. I can't see how it was.

I think the basis of the argument is that under anoxia, 100% of patients will die if the situation is not remedied within five to ten minutes. If an NDE was "only" a product of anoxia, then there shouldn't be a wide division between those who have an NDE and those who do not. So it does not explicitly set out to test that, but derives that conclusion from speculation. Parnia demonstrates that if adequate steps are taken it is still possible to preserve and revive someone beyond this five-to-ten minute period (his primary topic) but it does not appear to change what percentage of these recoveries report NDEs.
 
I would be pretty surprised myself if anoxia were the only cause of NDEs - my point was that other than speculation as you point out the study was not designed to determine whether anoxia or brain processes similar to those caused by anoxia were involved. There may be various ways to trigger certain brain processes.
 
There may be various ways to trigger certain brain processes.

Well, there are NDEs that are claimed from only the perception of danger. I'm not sure how we can really test those, without getting back in to the nebulous area of studying people who can induce OBEs.
 
As for Arouet's take on this particular study, on the other forum I promised to send his comments to the authors. One of them, R.van Wees, has responded. I will translate it shortly.

Here is the response of Ruud van Wees (one of the four authors of the article in the Lancet - aka the Van Lommel paper, which is stricly incorrect):

"Arout says that in our article he looked in vein for proof of causes of NDE's. That's correct. The problem with the absence of (proof of) causes of the NDE also has to do with our assumption of a transcendant consciousness. For the forum of mainstream science this transcendence kan only be proven indirectly: by excluding all immanent causes (fysiological, psychological etc). This "via negativa" is the way that we and the various other researchers/authors have followed" (and still follow - Smithy).
 
Here is the response of Ruud van Wees (one of the four authors of the article in the Lancet - aka the Van Lommel paper, which is stricly incorrect):

"Arout says that in our article he looked in vein for proof of causes of NDE's. That's correct. The problem with the absence of (proof of) causes of the NDE also has to do with our assumption of a transcendant consciousness. For the forum of mainstream science this transcendence kan only be proven indirectly: by excluding all immanent causes (fysiological, psychological etc). This "via negativa" is the way that we and the various other researchers/authors have followed" (and still follow - Smithy).

Thanks Smithy. While I believe that this answer supports my analysis I do want to mention that in my post I was not looking for proof of causes of NDEs. Rather I was looking at the methodology used in the study and seeing if I could link them to answering the question of what causes NDEs.

But on his point about excluding all physiological, psychological causes - I also don't see how this study does that. Our understanding of the physiological causes of what's going on in the brain is still in its infancy. The Lancet study itself highlights a number of induced experiences that give hints at what the brain can produce. We have very little knowledge about how exactly such experiences work and whether elements of them are involved in NDEs. We might know that a particular experience can be triggered through anoxia but do we know whether it could be triggered otherwise? If certain chemical reactions are triggered during a certain induced experience do we know if they can be triggered otherwise.

I'm not suggesting these are easy questions to answer - but I think they have to be answered before we reach the conclusion that we've excluded all mundane causes.

In any event, thanks again Smithy!
 
I'm not suggesting these are easy questions to answer - but I think they have to be answered before we reach the conclusion that we've excluded all mundane causes.

Ultimately, all of the mind /= brain lines of questioning will be in a massively healthier shape when it can move out of relying on negatives. Something that makes me uncomfortable about the dualist mindset is that it is very much a "in the gaps" line of arguing in its current state.

Easier said than done, I know.
 
Would it be appropriate to call it the "Lommel et all. (2001)" paper? This is what my citation managers call it, because there are four authors and he's marked as the first one.

Actually, it would not be fully appropriate, because as I said before in the other forum, all four authors of the Lancet paper were equally important. It would thus be better to call it the Merkawah paper, as the study was done under the auspices of Merkawah Foundation aka IANDS The Netherlands. In terms of the law it is Merkawah who is the legal owner of the study.
But I realize that since Van Lommel is the first name appearing in the list of authors, it is indeed better to call it the Van Lommel et al (2001) paper.
 
I also found the anoxia comment from van Lommel strange, coming from a physician. It would be like saying that aspirin can't have any effect, otherwise, all those who take aspirin would never have heart attacks.

Regardless, it's irrelevant because the study does not look at anoxia or any other physiologic parameters anyway.

Linda
 
Ultimately, all of the mind /= brain lines of questioning will be in a massively healthier shape when it can move out of relying on negatives. Something that makes me uncomfortable about the dualist mindset is that it is very much a "in the gaps" line of arguing in its current state.

Easier said than done, I know.

Oh sure - it would indeed be much better if we could stop relying on negatives. But as someone already indicated, the whole of NDE research is still in its infancy, despite being on the map since 1975 (Moody...)

And as long as the "Hard Problem" (of consciousness - Chalmers!) has not been solved, I am afraid NDE-research will remain in its infancy...
 
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