Can probiotics lower blood pressure?
Recently, multiple animal and human studies have examined the relationship between the gut microbiome and blood pressure. These studies demonstrated a significant decrease in microbial richness and diversity in the presence of hypertension. If gut bacteria truly do have the power to produce hypertension, does this mean probiotics can affect blood pressure?
Affecting more than one billion people worldwide, hypertension is a global public health problem and is considered the most prevalent modifiable cardiovascular disease risk factor. The pathogenesis of hypertension is known to involve a diverse range of risk factors, both genetic and environmental.
Changes in microbiome linked to development of chronic diseases
Although the gut and blood pressure might not seem like obvious companions, the connection is hardly surprising. Many of the factors that increase the risk of hypertension, such as the consumption of salty food, enter the body through the digestive system. Moreover, changes in the microbiome are increasingly linked to the development of several chronic diseases, including hypertension. Although evidence is mounting, most of the studies to date have been observational.
Association between the gut microbiota and high blood pressure
Numerous human gut microbiome studies have reported an association between a higher abundance of gram-negative microbiota (including Klebsiella, Parabacteroides, Desulfovibrio, and Prevotella) and higher blood pressure. Indications of a cause-and-effect relationship come from research with germ-free mice that received faecal matter from a hypertensive human donor; the mice developed elevated systolic and diastolic blood pressure after eight weeks. Conversely, faeces from mice without hypertension transplanted into mice with hypertension results in a reduction in blood pressure in the hypertensive mice.
Possible mechanisms
The gastrointestinal tract hosts a number of processes that have the potential to play a role in hypertension. This role involves the production of metabolites and hormones and establish a direct connection with the nervous- and immune system.
For example short chain fatty acids in the gut (SCFA’s) can enter the bloodstream and stimulate SCFA-receptors in the kidney that play a role in regulating blood pressure. Some scientists hypothesize that increased sympathetic nervous activity in the gut could result in increased gut permeability, gut inflammation, and dysbiosis. This possibly contributes to chronic inflammation and sustained hypertension. It is very well possible that the relationship between dysbiosis and hypertension is bidirectional or amplifying.
Restoring the balance
Lifestyle factors shape and are modulated by the microbiome, modifying the risk for hypertensive disease. For example the Dietary Approaches to Stop Hypertension (DASH) regime is one of the interventions used to reduce blood pressure. This diet is rich in fruits and vegetables. It is possible that components (e.g. high fiber, dairy) of the diet alter the microbiota favourably and contribute to its blood pressure-lowering effects. Additionally, in both humans and mice, higher salt intake appears to lead to a decrease in the amount of lactobacilli and to an increase in blood pressure. In contrast, administering probiotic lactobacilli to mice improved salt-sensitive high blood pressure.
A systematic review published in the American Heart Association journal ‘Hypertension’ showed that Lactobacillus-containing probiotics are effective, if used in sufficiently high doses (109-1012 CFU) and for at least eight weeks. Multispecies probiotics lowered blood pressure more than those with a single bacteria.
The future
Despite preliminary advances in understanding the role of the microbiome in the regulation of blood pressure, it is essential to elucidate how environmental factors affect this nexus. To advance the field and begin to address whether the microbiome can be targeted or manipulated to influence the prevalence or progression of hypertension, studies that can establish causation and uncover mechanisms are urgently needed.
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