In this Special Feature, we examine a potential link between sleep apnea, hypertension, and gut bacteria. Although a link between the three may seem unlikely on the surface, scientists are unraveling the connections.
Before taking a look at the bonds between these three seemingly unconnected things, we should start with an explainer: What is sleep apnea?
Sleep apnea is a condition where an individual stops breathing for periods throughout the night. Obstructive sleep apnea (OSA), the most common form, occurs when throat muscles temporarily relax and block the airways.
Central apnea, which is relatively rare, occurs when the brain does not send appropriate signals to the muscles engaged in breathing. The issue here lies within the central nervous system, rather than a physical obstruction of the airway.
OSA
Hypertension needs no introduction. It is even more prevalent than sleep apnea, affecting
Although treatment for hypertension is available, the drugs do not work effectively for some individuals. It is not always clear why this is the case, but OSA is
Also, research suggests that there is a dose-response relationship between sleep-disordered breathing and hypertension. In other words, individuals with more severe breathing difficulties at night have an increased risk of developing hypertension.
Scientists are still exploring the mechanisms involved in the link between OSA and hypertension.
If this article had appeared 20 years ago, we might have needed to explain the importance of gut bacteria. Today, though, with the microbiome featuring prominently in both scientific research and yogurt marketing campaigns, most people will be familiar with the concept.
In brief, we harbor up to
Historically famous for helping us digest certain components of our food, scientists now suggest associations between these microbes and a wide range of health conditions, including obesity, diabetes,
Studying the interactions between our microbial residents and our health is notoriously challenging, and many questions remain. What we do now know for certain is that we would be far worse off without them.
The link between our intestinal residents and disease will take some unpicking, but one of the key factors seems to be dysbiosis, an imbalance or reduction in microbial diversity.
In oversimplified terms, changes to the bacteria’s environment might, for instance, hinder “good” bacteria while giving “bad” bacteria an opportunity to thrive.
Now, to the matter in hand.
The question remains: How could bacteria in our gut play a role in sleep apnea-related hypertension?
A review in the Journal of Clinical Sleep Medicine (JCSM) outlines one theory as to how disordered breathing during sleep might influence bacterial populations.
Sleep apnea causes intermittent hypoxia or low levels of oxygen in the blood throughout the night. This hypoxia produces periodic decreases in the partial oxygen pressure gradient inside the tubes of the gastrointestinal system.
Consequently, bacteria that can only grow in low oxygen environments — obligate anaerobes — and those that can thrive with or without oxygen — facultative anaerobes — get a boost. As with any finely balanced ecosystem, when certain populations receive a leg up, they might push others aside.
In one
Specifically, the study notes an abundance of Firmicutes and a reduction in Bacteroidetes and Proteobacteria compared with control mice.
An increase in Firmicutes with a reduction in Bacteroidetes is considered a
Some people refer to Bacteroidetes as good bacteria because they produce short-chain fatty acids (SCFAs) — we will hear much more about the importance of SCFAs later. Conversely, some think of Firmicutes as bad because they have a negative influence on glucose and fat metabolism.
These two bacterial phyla, or types, make up around
In animal studies, researchers have shown that a shift in bacterial populations can cause the degradation of mucins in the gut. Mucins help keep the gut lining or epithelium healthy. If they suffer damage, the epithelium can become more permeable or “leaky” as the damage disrupts junctions between epithelial cells.
Also, good bacteria, which produce SCFAs from dietary fiber, are in shorter supply.
SCFAs are a source of nutrition and energy for the epithelium. With the limited production of SCFAs, the epithelium takes a second hit. Again, this can cause dysfunction in the epithelium.
On top of the mucin degradation and drop in SCFAs, intermittent hypoxia itself can physically
Here, we have outlined how disordered breathing at night can cause damage to the intestinal epithelium through mucin breakdown, reduced levels of SCFAs, and physical damage through hypoxia.
But we must ask again, what has this got to do with hypertension?
A damaged intestinal epithelium or “leaky gut” allows increased traffic from the gut into the blood. Compounds that the gut would normally trap and excrete from the body can now enter the blood and travel to distant organs and systems.
Another effect of dysbiosis is an increase in bacterial species that produce toxins. A healthy epithelium might block these toxins, but an overly permeable epithelium allows these compounds to slip into the blood.
Once they are in circulation, the body mounts a low-grade inflammatory response. Here, finally, we meet the intersection of OSA, gut bacteria, and hypertension.
Inflammation occurs with a wide range of conditions, including
Inflammation also appears to play a role in the development of
To summarize, intermittent hypoxia experienced during the night disturbs the microbiome. This bacterial disturbance makes the gut epithelium leaky and allows toxins to leach into the blood. This sparks inflammation and, therefore, increases the risk of hypertension and other cardiovascular problems.
As the authors of the JCSM review conclude:
“OSA animal models confirmed that [intermittent hypoxia during sleep] and sleep fragmentation […] are associated with worsening gut microbiota profile with the emergence of species negatively influencing the gut through damage to the epithelial cells and producing endotoxins leading to a state of ‘low-grade systemic inflammation.’”
This, they explain, “may contribute to the pathophysiologic mechanisms for many chronic inflammatory, cardiovascular, and neoplastic disorders.”
Source: Medical News Today
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