I am interested in Sudden Infant Death Syndrome [SIDS] and the role of the neurones in the brainstem that process serotonin.
I am not a researcher or a scientist but I have stumbled on a scientific puzzle.
My friend Paula might have ended up a SIDS casualty, but she survived. She was born in France and in 1955, babies slept on their backs, tightly wrapped in swaddling cloths. Maybe this is why she survived. Today ,parents are counselled to avoid putting infants, in their first year, to sleep on their tummies, to lessen the occurrence of sudden infant death.
Paula was born not breathing [she got stuck in the birth canal-her Mom had had Rickets and crooked bones], she swallowed meconium, she was suctioned, resuscitated [hyperoxia] and then had to be transfused and the she was fine, completely normal…..
Twenty years ago, we took a first aid class for work and she and I found out that her breathing rate at rest was only 3 breaths per minute [with active exhaling] . We have been trying to figure this out since then. We eventually learnt that her tidal volume is normal at .5 L. This however means that her minute ventilation is only 1.5 L., not the assumed 6-8 L stated in textbooks.
Her HCO3 and O2 [pulse oximetry] are completely normal.
Hence the scientific mystery.
Her breathing rate does not increase with physical illness [a cold or flu]. Her breathing rate rises only sluggishly when she does exercise. Instead the other systems of the body work harder. Her vital signs [except for breathing rate] are normal in health.
When ill, her BP rises a lot [perhaps to perfuse the brain?], her HR also goes up and there are lots of intermittent murmurs, palpitations and the like, her body temperature decreases [mild hypothermia] and her hands, feet, lips get cold , pale, even a little blue. If really sick, she gets neurologically confused in a quiet unseen way [because she cannot talk much due to shortness of breath she cannot describe and remains unseen due to her too slow manner of breathing. She loses her appetite, loses weight and generally looks unwell.
She got really unwell after the hormonal changes during menopause.She looked like she was having a bout of depression [instead of a bout of quiet delirium due to hypercapnia] and was given many medications but only one brought back her normal mental function and memory. I helped her test her ability to remember personal details like her own address and postal code, daily.
A serotonin agonist [Paxil] was the only medication to begin to help her to remember her address, so we chose that one. It was slow, had side effects [mania], and it took 18 months to recover her memory enough to be able to function more or less normally. It really took 10 years to completely recover her mental status and to reliably remember her address and much more.
She is back to better than normal now and we are discussing her experience every day in this blog.
It is interesting that a serotonin agonist helped Paula so much [albeit slowly and at first, with significant side effects]. And it seems interesting that sudden infant death syndrome could be associated with alterations in serum 5HT levels, as discovered below:
Something to think about further,I think.
Abstract
Sudden infant death syndrome (SIDS), the leading cause of postneonatal infant mortality, likely comprises heterogeneous disorders with the common phenotype of sudden death without explanation upon postmortem investigation. Previously, we reported that ∼40% of SIDS deaths are associated with abnormalities in serotonin (5-hydroxytryptamine, 5-HT) in regions of the brainstem critical in homeostatic regulation. Here we tested the hypothesis that SIDS is associated with an alteration in serum 5-HT levels. Serum 5-HT, adjusted for postconceptional age, was significantly elevated (95%) in SIDS infants (n = 61) compared with autopsied controls (n = 15) [SIDS, 177.2 ± 15.1 (mean ± SE) ng/mL versus controls, 91.1 ± 30.6 ng/mL] (P = 0.014), as determined by ELISA. This increase was validated using high-performance liquid chromatography. Thirty-one percent (19/61) of SIDS cases had 5-HT levels greater than 2 SDs above the mean of the controls, thus defining a subset of SIDS cases with elevated 5-HT. There was no association between genotypes of the serotonin transporter promoter region polymorphism and serum 5-HT level. This study demonstrates that SIDS is associated with peripheral abnormalities in the 5-HT pathway. High serum 5-HT may serve as a potential forensic biomarker in autopsied infants with SIDS with serotonergic defects. High serum serotonin in sudden infant death syndrome, Robin L. Haynes, et al. PNAS July 18, 2017 114 (29) 7695-7700; https://doi.org/10.1073/pnas.1617374114
In the 1900’s, Dr Emile Kraepelin described the same ventilatory defect/injury that Paula has in THOUSANDS of unmedicated patients in the asylums. What he found fascinating is despite too slow breathing during the depressive insanity episodes – they remained alive….[they were mostly young adults when they first got sick and they probably had normal lungs]. When they occasionally became manic, their breathing became too fast and even periodic, for months, still they [mostly] remained alive.He noted that they were the only patients to spontaneously remit and leave the asylum for years, before submitting to another attack. The problem was that these attacks could last months, years decades before spontaneously lifting.
He understood that supportive medical treatments of the 21 st century would help these patients recover faster. And he knew that successful treatments would help them recover their intellect completely, not just sedate them- as doctors often do today.
Alas, Kraepelin’s work has been forgotten, in part, because – as is the case with Paula- no one believes in autonomic nervous system damage affecting the movement of air in and out of the body- is important in manic depressive insanity, because the patients are unaware of their respiratory rate at rest when awake and do not complain. Doctors never measure respiratory rate or minute ventilation. We have tried to tell doctors what we have learnt and there is a lot of resistance. You would think they would be excited to find that they might be able to help these patients, but no…when it comes to ventilatory defects….they are terrified.
Anyway, please think over what we are saying.We think that this hypothesis is easy to prove or disprove and Krapelein’s work is easy to replicate [or not]. So far no one is interested and we have talked to researchers and doctors [in person and through emails] all over the world.
It is easy to imagine that genes are turned on and off differently when the transition of a baby to their first exposure to air and fuel is an initial failure.
Also, Paula’s parents lived in a very polluted industrial area in Paris France, in a poorly ventilated apartment heated by a coke oven…..It kind of makes sense for the brain stem to exchange less air.
But all this is speculation and much work needs to be done, I think, to explain what we found [Paula] and what Kraepelin found.
These are original findings, unknown, [or- in the case of Kraepelin-neglected and forgotten], unless one has received one of my emails or read my blogs.
By the way, before covid, I would measure people’s respiratory rates for fun. The baseline range was very wide, and I think the extremes [too fast, too slow] indicate an increased risk of delirium or dementia due to unseen hypercapnic ventilatory failure. PCO2 is not measured in ambulatory patients. Yet CO2 is a deliriant, intoxicant and asphyxiant, depending on levels in the blood. And it is a normal byproduct of cell metabolism and effects are completely reversible.
I find this fascinating.
I do not understand why I have so much difficulty getting others to be fascinated too.
Plus, there are lives at stake.
Please discuss with others; and ignore the resistance of doctors and find out for yourself.
Of Sound Mind 