The mechanism of dead-in-bed syndrome and other sudden unexplained nocturnal deaths


The mechanism of dead-in-bed syndrome (DBS), a rare but devastating condition that mainly affects young type 1 diabetes patients, remains mysterious. A new theory is proposed to explain this syndrome. This theory suggests that repeated episodes of hypoglycaemia-induced adaptation in orexin-A neurons cause (i) defective awakening and (ii) hypotonia of upper airway muscles during sleep. Consequently, due to the combined effect of these factors, long-term exposure of intermittent hypoxia occurs, leading to a combination of factors – such as depression of ventilation, increase in sympathetic tone, fluctuations in intrathoracic pressure and cardiac arrhythmias – these in conjunction with an underlying cardiovascular pathology (genetically inherited or acquired) cause cardio-respiratory failure and thus sudden death during sleep. This mechanism can be generalized to explain other cases of sudden unexplained nocturnal deaths including sudden infant deaths (SIDs).

 Orexin and sleep patterns

One group of researchers called these chemicals orexins and another, independent group of called themhypocretins.  Both names are used in the scientific literature. We prefer Orexin because it is shorter.

Orexins play a part in keeping people awake.  Like most of what goes on in the brain related to sleep and waking, there are mysteries and anyone who says they really understand every role that the orexin neurotransmitters play is lying.  But we know they are peptides – smallish proteins made in the body.  They also interact with other neurotransmitters in ways yet to be untangled, but they unquestionably appear to be involved in arousal and excitation of the brain.  The evidence suggests they form a part of the body’s overall sleep-wake regulation system by interacting with GABAergic sleep-promoting neurons and neurotransmitters like histamine, serotonin, melatonin, and acetylcholine. (More here:

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A potential role for adjunctive vitamin D therapy

Vitamin D is a prohormone with skeletal and extraskeletal properties that could potentially reduce the severity of these metabolic side effects.

High glucose levels could impair ferroelectricity in body’s connective tissues

Michelle Ma

News and Information

High sugar levels in the body come at a cost to health. New research suggests that more sugar in the body could damage the elastic proteins that help us breathe and pump blood. The findings could have health implications for diabetics, who have high blood-glucose levels.

Researchers at the University of Washington and Boston University led by Jiangyu Li andYanhang Zhang have discovered that a certain type of protein found in organs that repeatedly stretch and retract – such as the heart and lungs – is the source for a favorable electrical property that could help build and support healthy connective tissues. But when exposed to sugar, some of the proteins no longer could perform their function, according to findings published online April 15 in the journal Physical Review Letters.

“This finding is important because it tells us the origin of the ferroelectric switching phenomenon and also suggests it’s not an isolated occurrence in one type of tissue as we thought,” said co-corresponding author Li, a UW associate professor of mechanical engineering. “This could be associated with aging and diabetes, which I think gives more importance to the phenomenon.”

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Hemoglobinopathies May Distort HbA1C

Natasha Patel, PharmD Candidate, LECOM College of Pharmacy

Measuring glycated hemoglobin (HbA1c) gives us a patient’s long term average blood glucose levels.1

Since HbA1c measures the percentage of patients’ glycosolated hemoglobin, patients who possess variants of hemoglobin can exhibit false readings. Such variants, called hemoglobinopathies, can include inherited hemoglobin variants, elevated fetal hemoglobin, and hemoglobin S and E which are prevalent in people of Southeast Asia, Mediterranean, and African descent. 2 One variant of particular concern is the sickle cell trait. People with this trait have inherited biological differences affecting the formation of their hemoglobin and erythrocytes, which in turn affects their levels of glycated hemoglobin. 5

People who have the sickle cell trait have both normal hemoglobin A and hemoglobin S. In the U.S., African Americans are at a higher risk of having the sickle cell trait, and approximately 18.7 percent of African Americans who are 20 years and older have diabetes. 2 In people who have both the sickle cell trait and diabetes, about 1 million people in the U.S., using HbA1c to measure blood glucose levels can be prone to anomalies. People with these hemoglobin variants can have falsely low or high levels which can lead to improper treatment including: HbA1c readings that are different than expected; HbA1c levels that are extremely different from previous HbA1c readings; or low correlations between HbA1c and self-monitored glucose levels. 2

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