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From the Original Article
One of the most widely used animal models of hypertension are spontaneously hypertensive stroke-prone (SHRSP) rats, a line of rats that develop hypertension at six weeks of age, much earlier than control animals. Like hypertensive humans, these rats show gut dysbiosis.
To investigate whether gut dysbiosis contributes to the development of hypertension, the researchers transferred gut microbiota from SHRSP rats to rats with normal blood pressure. The previously healthy rats to develop high blood pressure, pointing towards a causal relationship between gut dysbiosis and hypertension.
Could changing the feeding pattern through fasting reduce the blood pressure of the SHRSP rats?
To test this, the researchers split the SHRSP rats into two groups: one group had unlimited access to food, while the other group was fed only every other day. After nine weeks, the rats that had unlimited access to food had developed high blood pressure, as is expected for the SHRSP model. In contrast, rats that were fed only every other day did not develop high blood pressure.
Faecal Transplant Experiments further demonstrate the causal nature of the Gut Biome
The researchers observed that germ-free rats that had received microbiota from the fasting SHRSP rats had lower blood pressure than germ-free rats that had received microbiota from normal-fed SHRSP rats. With this, the researchers discovered that modulating the gut microbiota
- Exactly what is the gut dysbiosis, which species?
- Is there a similar difference between normotensive and hypertensive humans?
- Does alternate day fasting affect human BP the same for hypertensives?
- Does the same dysbiosis affect normotensive humans? Could it be an identifiable risk factor/ predictor?
- Hypertension is strongly age related in humans ==> therefore ==> Is dysbiosis age related?
Researchers have conducted a review of studies analyzing how disruptions to maternal and infant microbiomes may increase the risk of certain illnesses later in life.
The microbiome refers to the tens of trillions of microorganisms that live in our intestine, respiratory tract and on our skin.
There is increasing evidence that disruptions to a person’s microbiota in early life may influence the likelihood of developing certain illnesses later in life. Earlier this year, for example, a study reported by Medical News Today found that an increase in richness of gut bacteria at 3 months of age was associated with reduced risk for food allergies at 1 year of age.
“Disturbed microbiota could potentially contribute to a wide range of childhood diseases including allergies, asthma, obesity and autism-like neurodevelopmental conditions,” notes Dr. Meropol.
However, she points to a number of recent studies that suggest a number of factors that may aid a child’s microbiome development, including breastfeeding, vaginal birth and skin-to-skin contact straight after birth.
Growing evidence that microbiota development begins before birth
Popular notion holds that the development of microbiota begins at birth and that the womb is a sterile environment. However, recent studies have challenged this idea, suggesting that gut microbiota development begins before birth. Dr. Meropol and colleagues discuss this theory, pointing to a review that assesses the growing evidence that a child’s microbiota development starts in the womb.
In a review titled “Microbial Programming of health and disease starts during fetal life,” Petya T. Koleva, of the University of Alberta in Canada, and colleagues cite research that found the offspring of mothers with allergies have greater abundance of Enterobacteriaceae bacteria in their earliest stools, which may raise their risk of later-life respiratory problems.
“This means that not only do we have to consider the microbiome of the child but also that of the mother,” notes Dr. Meropol, “and the irony is that some of our modern medical practices, through their effect on these early microbiota, could have unintended consequences, interfering with normal development of children’s immune, metabolic, and neurologic systems.”