Serotonin does in fact cross the blood brain barrier.

[Outdoctrination]

I've been struggling with this concept in my head given my own experience with dramatically improved mood with antibiotics which lower gut serotonin. The official narrative has been and continues to be that gut serotonin and brain serotonin are completely separate and that serotonin itself does not cross the blood brain barrier, and thus gut serotonin has no impact on mood.

Well. An immunohistochemical analysis of SERT in the blood–brain barrier of the male rat brain - Histochemistry and Cell Biology

"The interaction of 5-HT with the BBB has been studied previously, but in different ways such that our understanding of the biological role of 5-HT in using the BBB to cross to and from the CNS, as well as cause changes in how other substances traverse the BBB, has been spotty.

Work on 5-HT and the BBB has been done in both immortalized culture lines and the whole animal. Studies nearly 50 years ago showed that 5-HT can move from brain to blood. The application of intravenous 5-HTP, 5-HT, and 5-HIAA to the rat increased levels of these substances in the brain (Bulat and Supek 1968). A decade later, Westergaard (1975, 1978) demonstrated that 5-HT itself modified the plasma membrane of endothelial cells within arterioles, venuoles, and capillaries, enhancing the transfer of vesicles and protein within the brain. These studies were done before the discovery of monoamine transporters, and Brust and colleagues were the first to demonstrate mRNA and functional expression of SERT in the rat brain endothelium. Another step in our understanding came when Nakatani et al. showed that 5-HT crosses the BBB from brain to periphery. They administered 5-HTP intravenously to male rats, and subsequently observed increased levels of 5-HT in the frontal cortex (Nakatani et al. 2008). In a second experiment, they surgically removed the gastrointestinal tract and kidneys and then inactivated the liver by destroying the portal vein and bile duct in male rats. This effectively eliminated all sources of 5-HT production within the periphery. Intravenously administered 5-HTP elevated brain levels of 5-HT twofold from baseline, and elevations in peripheral 5-HT could be measured. This movement appears to require SERT given that administration of the SERT inhibitor fluoxetine in the surgically modified rats prevented the significant increase in 5-HT levels in the brain. These data support that 5-HT can move from periphery to brain and brain to the periphery, and thus, SERT, at least under the collective experimental conditions of the studies reported, can function in both directions. All of these studies lend support to our identification of SERT in the BBB of the male rat brain, but ours is the first in-depth study in which the location of SERT is thoroughly investigated. These studies are important because they challenge the commonly held idea that 5-HT cannot enter the CNS. This finding makes it such that we have to consider 5-HT entering the CNS from the periphery as one means by which 5-HT could influence blood pressure, just as we observed in the chronically infused rat (Diaz et al. 2008). This present study does not intend to answer the biological question of 5-HT crossing the BBB to change blood pressure, but rather raise the possibility."

This is huge!

The other massive caveat to this theory is that serotonin itself increases the permeability of the BBB Changes in blood-brain barrier and cerebral blood flow following elevation of circulating serotonin level in anesthetized rats

"An infusion of 10 μg per kg body weight for 10 min significantly increased blood-brain barrier (BBB) permeability to Evans blue and 131I-sodium measured in whole brain. Regional BBB determinations with labelled 131I-sodium showed that the permeability to this compound was increased in the cerebral cortex, hippocampus, caudate nucleus, hypothalamus, colliculus and the cerebellum but not in the pons and the medulla oblongata. Regional blood flow was reduced in the same parts which showed BBB abnormality tested with 125I-labeled microspheres. Pretreatment with cyproheptadine, a 5-HT2 receptor antagonist, prevented the BBB increase and the regional blood flow was near normal values."

More fraud and lies from the serotonin shills.

 

[RobertMichael]

What if somebody feels nothing from antibiotics/cyproheptadine?

 

[SonOfEurope]

Fast transit time is key, any dietary combos that slow down digestion should be out.

 

[haidut]

I've been struggling with this concept in my head given my own experience with dramatically improved mood with antibiotics which lower gut serotonin. The official narrative has been and continues to be that gut serotonin and brain serotonin are completely separate and that serotonin itself does not cross the blood brain barrier, and thus gut serotonin has no impact on mood.

Well. An immunohistochemical analysis of SERT in the blood–brain barrier of the male rat brain - Histochemistry and Cell Biology

"The interaction of 5-HT with the BBB has been studied previously, but in different ways such that our understanding of the biological role of 5-HT in using the BBB to cross to and from the CNS, as well as cause changes in how other substances traverse the BBB, has been spotty.

Work on 5-HT and the BBB has been done in both immortalized culture lines and the whole animal. Studies nearly 50 years ago showed that 5-HT can move from brain to blood. The application of intravenous 5-HTP, 5-HT, and 5-HIAA to the rat increased levels of these substances in the brain (Bulat and Supek 1968). A decade later, Westergaard (1975, 1978) demonstrated that 5-HT itself modified the plasma membrane of endothelial cells within arterioles, venuoles, and capillaries, enhancing the transfer of vesicles and protein within the brain. These studies were done before the discovery of monoamine transporters, and Brust and colleagues were the first to demonstrate mRNA and functional expression of SERT in the rat brain endothelium. Another step in our understanding came when Nakatani et al. showed that 5-HT crosses the BBB from brain to periphery. They administered 5-HTP intravenously to male rats, and subsequently observed increased levels of 5-HT in the frontal cortex (Nakatani et al. 2008). In a second experiment, they surgically removed the gastrointestinal tract and kidneys and then inactivated the liver by destroying the portal vein and bile duct in male rats. This effectively eliminated all sources of 5-HT production within the periphery. Intravenously administered 5-HTP elevated brain levels of 5-HT twofold from baseline, and elevations in peripheral 5-HT could be measured. This movement appears to require SERT given that administration of the SERT inhibitor fluoxetine in the surgically modified rats prevented the significant increase in 5-HT levels in the brain. These data support that 5-HT can move from periphery to brain and brain to the periphery, and thus, SERT, at least under the collective experimental conditions of the studies reported, can function in both directions. All of these studies lend support to our identification of SERT in the BBB of the male rat brain, but ours is the first in-depth study in which the location of SERT is thoroughly investigated. These studies are important because they challenge the commonly held idea that 5-HT cannot enter the CNS. This finding makes it such that we have to consider 5-HT entering the CNS from the periphery as one means by which 5-HT could influence blood pressure, just as we observed in the chronically infused rat (Diaz et al. 2008). This present study does not intend to answer the biological question of 5-HT crossing the BBB to change blood pressure, but rather raise the possibility."

This is huge!

The other massive caveat to this theory is that serotonin itself increases the permeability of the BBB Changes in blood-brain barrier and cerebral blood flow following elevation of circulating serotonin level in anesthetized rats

"An infusion of 10 μg per kg body weight for 10 min significantly increased blood-brain barrier (BBB) permeability to Evans blue and 131I-sodium measured in whole brain. Regional BBB determinations with labelled 131I-sodium showed that the permeability to this compound was increased in the cerebral cortex, hippocampus, caudate nucleus, hypothalamus, colliculus and the cerebellum but not in the pons and the medulla oblongata. Regional blood flow was reduced in the same parts which showed BBB abnormality tested with 125I-labeled microspheres. Pretreatment with cyproheptadine, a 5-HT2 receptor antagonist, prevented the BBB increase and the regional blood flow was near normal values."

More fraud and lies from the serotonin shills.

Very good find, thanks!
Yep, another medical myth that cannot die soon enough and I always make sure to mention that myth in podcasts when the topic of serotonin is brought up. I think the myth grew out of the claim that another neurotransmitter - GABA - being a similar, charged aino-acid molecule cannot cross the BBB. The GABA myth was also sponsored by Big Pharma as it realized nobody would take a benzo drug if they just can pop instead a cheap, widely available and safe amino acid (GABA). The GABA myth/claim was debunked years ago (though it is still pervasive in the medical field), but the serotonin myth has been aggressively defended by medicine since a huge industry of SSRI drugs depends on it and it is also at the core of mind control the govt has been pushing since the 1940s. Namely, medicine knows there is strong evidence that elevated peripheral serotonin is bad, hence the Pfizer trials with the drug serotonin antagonist terguride to prevent and even reverse fibrosis, as well as the recent human trials with peripheral TPH (TPH1) inhibitors to treat obesity and diabetes. When concerns were raised decades ago (when it became common knowledge that high peripheral serotonin is bad) that if serotonin is bad peripherally it can't be that good for the brain either the defense had always been that "the dose makes the poison" and that serotonin at lower levels (as found in the CNS and synthesized only locally by TPH2) is very good for us and peripheral levels/synthesis is irrelevant since they cannot affect the brain. If this ability of serotonin to cross the BBB becomes more widely known it would be the end of the SSRI industry, and likely most of psychiatry as so much of it depends on the serotonin lie.