Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Thursday, May 25, 2017

Gut Microbiota Potential for a Unifying Hypothesis for Prevention and Treatment of Hypertension

This would be cool because of the side effects of hypertension medications.
YanFei Qi, Seungbum Kim, Elaine M. Richards, Mohan K. Raizada, Carl J. Pepine
Despite major advances in pharmacological and device-based therapies, systemic hypertension (HTN) continues to be the major, modifiable risk factor for most cardiovascular disease and a leading cause of morbidity and mortality. Treatment resistant HTN (RH) is present in ≈15% to 20% of hypertensive patients, with few treatment options. These facts provide an opportunity to develop novel hypotheses to advance this field.
Over 60 years ago, Irvine Page1 proposed a mosaic theory where interplay of multiple factors integrate to increase blood pressure (BP). This fostered establishment of cellular, molecular, and physiological mechanisms altered in HTN. However, how these diverse factors integrate to impair BP control remains a challenge. Furthermore, why some factors are prohypertensive in one individual and not in another, and where prohypertensive signals originate, remains an enigma.
In this Viewpoint, we propose that the gut and gut microbiota could be one missing link and provide a potential unifying concept. We summarize most recent evidence for involvement of gut microbiota in BP control and HTN. We present our thoughts on the current state and relevant knowledge gaps to be addressed to determine whether targeting gut microbiota and related pathology would be a next frontier in HTN therapeutics.

Are HTN or RH Associated With a Unique Gut Microbial Signature?

Gut dysbiosis and microbial functions contribute to pathological effects beyond the gastrointestinal system. Gut microbiota play a role in BP regulation, and gut dysbiosis has been observed in multiple animal models of HTN.25 Our group was among the first to document HTN-associated gut dysbiosis and an increased Firmicutes/Bacteroidetes ratio.2,3 This was associated with a decrease in acetate- and butyrate-producing bacteria and an increase in the lactate-producing bacteria. High-fiber diet and acetate supplementation correct gut dysbiosis, increase the abundance of acetate-producing bacteria, and are associated with lower BP in DOCA-salt mice.5 Stroke-prone spontaneously hypertensive rats exhibit gut dysbiosis, and fecal microbiota transplant (FMT) from stroke-prone spontaneous hypertensive rats to Wistar–Kyoto normotensive rats increases BP.4 Furthermore, we noted that HTN is associated with profound pathological changes in the gut and increases brain–gut transmission in animal models of HTN.6
Microbial dysbiosis has also been observed in patients with high BP.2,3 Interestingly, subjects with HTN or pre-HTN demonstrate similar characteristic changes in gut microbiota composition.7 In a RH patient, antibiotic treatment resulted in BP under control with only an angiotensin-converting enzyme inhibitor, suggesting possible involvement of gut microbiota in the pathogenesis of RH as antibiotics alter gut microbiota.8 Future work will be needed to determine whether a unique microbial signature in the gut, gut pathology, and increased brain–gut–bone marrow connection are present in patients with RH.

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