Critical diaphragm failure in sudden infant death syndrome

Siren, Pontus M. A.; Sirén, Matti

doi:10.3109/03009734.2010.548011

Cited by 23 publications

(32 citation statements)

References 105 publications

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“…Newborns and infants born prematurely are especially prone to oxidative stress and have reduced antioxidant defense mechanisms. Since young infants exhibit transient melatonin deficiency for the first 2-4 months of life and pineal dysfunction and impaired melatonin metabolism have been associated with SIDS, the role of the tryptophan-serotonin-melatonin pathway in the etiology of SIDS should be investigated in the future (Siren et al, 2011).…”

Section: Sepsis and Septic Shockmentioning

confidence: 99%

Melatonin as a stabilizer of mitochondrial function: role in diseases and aging

Carrasco

Rodríguez²,

Pariente³

2015

Turk J Biol

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It is now almost 60 years since the discovery of melatonin and new physiological functions of the indole continuously appear in the most recent studies worldwide. Experimental evidence emphasizes its importance as a stabilizer of the mitochondrial bioenergetics, which could be related to the prevention of development of aging and several diseases. In the next years, conscientious investigation about this topic should be undertaken by scientists of different research areas to achieve a better understanding of the molecular mechanisms implied. This will ultimately allow the development and clinical application of efficacious treatments.

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Section: Sepsis and Septic Shockmentioning

confidence: 99%

Melatonin as a stabilizer of mitochondrial function: role in diseases and aging

Carrasco

Rodríguez²,

Pariente³

2015

Turk J Biol

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“…The sudden infant death syndrome (SIDS)–critical diaphragm failure (CDF) hypothesis was first published by Siren and Siren in 2011 (1). Since its publication, the hypothesis has continued to generate interest and several colleagues have contributed perspectives and insights to it (2–5).…”

mentioning

confidence: 99%

SIDS–CDF Hypothesis Revisited: Cause vs. Contributing Factors

Siren¹

2017

Front. Neurol.

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The sudden infant death syndrome (SIDS)–critical diaphragm failure (CDF) hypothesis was first published by Siren and Siren in 2011 (1). Since its publication, the hypothesis has continued to generate interest and several colleagues have contributed perspectives and insights to it (2–5). The basic premise of the hypothesis is that the diaphragm is a vital organ that must continuously generate adequate force to maintain ventilation, and that CDF is a terminal event and the cause of death in SIDS. I have argued in two follow-up articles that all SIDS factors either increase the workload of the respiratory muscles, the diaphragm being the primary muscle affected, or reduce its force generating capacity (6, 7). The SIDS–CDF hypothesis posits that SIDS has many contributing factors but only one cause, namely, the failure of the vital respiratory pump. There are several known SIDS factors, such as the prone sleeping position, non-lethal infections, deep sleep, gestational prematurity, low birth weight, cigarette smoke, male gender, and altitude, but of these, some such as the prone sleeping position more significantly both impact diaphragm function and correlate with SIDS. However, SIDS cases are multifactorial and as such can be caused by different combinations of factors. An infection combined with a prone sleeping position and elevated room temperature could lead to SIDS, whereas in other circumstances, low birth weight, cigarette smoke, prone sleeping position, and altitude could result in CDF and SIDS. The SIDS–CDF hypothesis also posits that SIDS does not have a congenital or genetic origin, and that efforts to identify significant genetic anomalies in SIDS victims are unlikely to be successful (8–11).

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“…The 2011 publication of Siren and Siren (1) and the subsequent letter to the editor (2) focus on critical diaphragm failure as a possible cause and provide plausible evidence. However, these articles do not explore the metabolic basis for this critical diaphragm failure.…”

mentioning

confidence: 99%

“…Siren and Siren's (1) comment that REM sleep inhibits intercostal muscles compounded by diurnal rhythms in blood phosphate could explain why SIDS strikes during night-time REM sleep. Also, phosphate has a seasonal rhythm with lows in the winter which could explain a higher prevalence of SIDS in this season, and 2,3-DPG is lower in infants exposed to cigarette smoke which could explain a higher incidence of SIDS in houses of smokers (23,24).…”

mentioning

confidence: 99%