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oemBiology oemBiology
wrote...
Posts: 1245
4 years ago Edited: 4 years ago, oem7110
Referring to following statement, I would like to know on how barometric pressure fluctuations can alter moods and trigger headaches in biological pathway.

"Barometric pressure fluctuations can alter moods and trigger headaches, some studies finding a link between low pressure and suicide."
http://theconversation.com/here-comes-the-sun-how-the-weather-affects-our-mood-19183

Does anyone have any suggestions?
Thanks in advance for any suggestions

Post Merge: 4 years ago

[Added] I would like to know on how altering atmospheric pressure influence serotonin metabolism, such as living on high-rise, people need to go up and down daily, and face with altering atmospheric pressure from high floor (lower pressure) to low floor (higher pressure).

"Atmospheric Pressure
There are several indirect reasons why atmospheric pressure may play a role in mood regulation. Several studies report that atmospheric pressure may influence serotonin metabolism, a major neurotransmitter involved in mood regulation and dysregulation. For instance, atmospheric pressure has been reported to explain a portion of the variance in platelet [3H]Paroxetine binding in normal volunteers [32], and in the ratio between the serotonin precursor L-tryptophan and the sum of the amino acids known to compete for the same cerebral uptake mechanism [5]. Furthermore, a negative correlation was shown between air pressure and CSF 5-HIAA [33], but this finding was not replicated at a second location with different climatic conditions [34]."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2651091/
Post Merge: 4 years ago

There is another example for diving, who also face with altering atmosphere pressure issue as well.

"At a depth of just 32.8 feet in the ocean, the hydrostatic pressure is equal to the pressure from the entire weight of the earth’s atmosphere as measured in pounds per square inch. In other words, at 32.8 feet, the total pressure, due to the weight of both the atmosphere and the water, is two atmospheres. At 65.6 feet it’s 3 atmospheres, and so forth."
https://midcurrent.com/science/the-pressure-myth/
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wrote...
Valued Member
Educator
4 years ago
"Barometric pressure fluctuations can alter moods and trigger headaches, some studies finding a link between low pressure and suicide."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684554/ Study here shows a correlation between migraines and atmospheric fluctuations -- but only in people who already experience migranes.

It is generally accepted that migraines can be caused by blood flow changes resulting from blood vessel dilatation associated with the influence of the changes in the physical load that atmospheric pressure imposes on the body. This may be particularly relevant in Japan, which has four seasons and is often hit by typhoons and cyclones. In this study, we investigated the relationship between migraine attacks and barometric pressure changes. Specifically, we report the range of pressure changes associated with migraine and we discuss methods for preventing migraines that develop in response to variations in barometric pressure.

In the same report, they discuss:

Bolay and Rapoport (2011) noted that low atmospheric pressure is associated with warm weather, winds, clouds, dust, and precipitation, and suggested that low pressure alone does not trigger migraine. They also proposed that high altitude may complicate the association of low atmospheric pressure with the triggering of migraine. In addition, they suggested that cortical spreading depression (CSD), an intrinsic brain event, activates prevascular trigeminal nerve fibers and may induce migraine (Bolay et al. 2002). On the other hand, Pun (2012) proposed that altitude-triggered migraine and high-altitude headache are likely due to hypobaric hypoxia rather than low atmospheric pressure.

High-altitude means less oxygen -- leading to headaches (not pressure).

On rats:

Messlinger et al. (2010) used a climate-controlled room to evaluate the effect of low atmospheric pressure on rats, specifically investigating whether rapid reduction of the ambient pressure to a level comparable to that during a typhoon would induce neuronal activity in the trigeminal nucleus caudalis. Their results indicate that rapid changes in barometric pressure activate trigeminal afferents, followed by an increase in arterial blood pressure. They found that such alteration of barometric pressure did not trigger trigeminovascular neurons with receptive fields from dura mater or from both dura mater and cornea; even prior sensitization with a nitric oxide donor did not alter the response to low atmospheric pressure.

Mentioned further down in the report:

In our study, patients with MA had a higher incidence of migraine attacks than patients with MOA (migraine without aura). This is consistent with the idea that small atmospheric changes trigger migraine via the following mechanism (Welch et al. 1993; Lauritzen 1994; Lance et al. 1983; Silberstein and Silberstein 1990): (1) first, a small decrease in barometric pressure causes dilatation of cerebral blood vessels, leading to serotonin release from platelets, (2) increased levels of blood serotonin induce vasoconstriction and the onset of aura, and (3) finally, the subsequent decrease of serotonin causes rapid dilatation of cerebral blood vessels, thereby triggering migraine. This is consistent with the common observation that the temporary decrease in cerebral blood flow during CSD is caused by constriction of both the superficial and parenchymal blood vessels, whereas the post-CSD rise in cerebral blood flow is primarily related to the dilatation of parenchymal blood vessels. Considering that migraine patients were more susceptible to small atmospheric changes than controls, it is plausible that the sympathetic nervous system of patients with migraine is more sensitive to barometric perturbations and the pain threshold may be lower than that of controls.

Hope this helps clear up the first question.
oemBiology Author
wrote...
4 years ago
Thank you very very much for detailed finding :>

Please see following questions as shown below

(1) first, a small decrease in barometric pressure causes dilatation of cerebral blood vessels, leading to serotonin release from platelets,

Q :  How do dilatation of cerebral blood vessels leading to serotonin release from platelets? Would it be direct cause (dilatation of cerebral blood vessels) and effect (serotonin release from platelets) relationship between them?

(2) increased levels of blood serotonin induce vasoconstriction and the onset of aura,

Q : vasoconstriction seems contradiction with question (1), dilatation of cerebral blood vessels lead to increase serotonin, but increasing serotonin cause vasoconstriction, How do body balance between 2 forces (dilatation vs vasoconstriction) ?

(3) finally, the subsequent decrease of serotonin causes rapid dilatation of cerebral blood vessels, thereby triggering migraine.

Q : Do you mean that decrease of serotonin causes rapid vasoconstriction of cerebral blood vessels instead of dilatation?

Do you have any suggestions?
Thank you very much for any suggestions (^v^)
wrote...
Valued Member
Educator
4 years ago
(1) first, a small decrease in barometric pressure causes dilatation of cerebral blood vessels, leading to serotonin release from platelets,

Serotonin (5-HT) acts as a vasoconstrictor. It induces constriction of peripheral collateral blood vessels. Now, what signals the platelets to release serotonin, I'm not sure.

According to Wikipedia, in high concentrations, serotonin acts as a vasoconstrictor by contracting endothelial smooth muscle directly or by potentiating the effects of other vasoconstrictors.

Quote
(2) increased levels of blood serotonin induce vasoconstriction and the onset of aura,

The body responds to vasodilation by release serotonin. Negative feedback cycle. I think you misunderstood the role of serotonin here.

Quote
(3) finally, the subsequent decrease of serotonin causes rapid dilatation of cerebral blood vessels, thereby triggering migraine.

When serotonin isn't present, there's no mechanism to stop the dilation.
oemBiology Author
wrote...
4 years ago Edited: 4 years ago, oemBiology
A small decrease in barometric pressure causes dilatation of cerebral blood vessels, leading to serotonin release from platelets. What would happen to cerebral blood vessels as increasing barometric pressure? would it cause vasoconstriction of cerebral blood vessels as well?

If yes, when people face with altering atmosphere pressure,  would the signals to serotonin release from platelets would become altering as well? which would mess with co-ordinating the nervous system, would it be correct?

Do you have any suggestions?
Thank you very much for any suggestions (^v^)

Function of Serotonin
"Serotonin is used to transmit messages between nerve cells, it is thought to be active in constricting smooth muscles, and it contributes to well being and happiness, among other things. As the precursor for melatonin, it helps regulate the body's sleep-wake cycles and the internal clock.

It is thought to play a role in appetite, the emotions, and motor, cognitive, and autonomic functions. However, it is not known exactly if serotonin affects these directly, or if it has an overall role in co-ordinating the nervous system.

It appears to play a key role in maintaining mood balance. Low serotonin levels have been linked to depression."

https://www.medicalnewstoday.com/kc/serotonin-facts-232248



Post Merge: 4 years ago

During decreasing in barometric pressure, I would like to know on what happen on following case as shown below

Case 1: there is not enough serotonin release from platelets.
Case 2: there is too much serotonin release from platelets.
wrote...
Valued Member
Educator
4 years ago
A small decrease in barometric pressure causes dilatation of cerebral blood vessels, leading to serotonin release from platelets. What would happen to cerebral blood vessels as increasing barometric pressure? would it cause vasoconstriction of cerebral blood vessels as well?

Physiologically, high barometric pressure is associated with vasoconstriction. It constricts blood vessels, which hinders blood flow, while low pressure expands blood vessels, making it more difficult for the heart to pump blood. I'm assuming the brain would shut off the mechanism that releases serotonin.

If yes, when people face with altering atmosphere pressure,  would the signals to serotonin release from platelets would become altering as well? which would mess with co-ordinating the nervous system, would it be correct?

Certainly. It wouldn't mess with it in that sense. Instead, the homeostatic mechanism controlling the balances in the body would have to adjust.

During decreasing in barometric pressure, I would like to know on what happen on following case as shown below Case 1: there is not enough serotonin release from platelets. Case 2: there is too much serotonin release from platelets.

Neither case would happen naturally, but if blood vessel dilation occurs for a prolonged period of time, you'd faint due to low internal blood pressure. You'd become lightheaded and likely die. Same reason why they don't use nitroglycerin as a permanent fix for heart conditions.
oemBiology Author
wrote...
4 years ago
Decreasing in barometric pressure causes dilatation of cerebral blood vessels, leading to serotonin release from platelets.  I would like to know on how many hour the effect of serotonin is last to constrict smooth muscles within cerebral blood vessels.

Do you have any suggestions?
Thank you very much for any suggestions (^v^)


wrote...
Valued Member
Educator
4 years ago
Without having researched it thoroughly, I'd say almost instantly. Reason why is b/c our body's homeostasis control center reacts instantly to cold/hot temperature conditions -- for example, you sweat when you're hot right away.

I read that serotonin amplifies the vasoconstrictor responses to other vasoactive substances. So maybe it doesn't act directly on the blood vessels, but influences other hormones to work more effective -- https://www.ncbi.nlm.nih.gov/m/pubmed/2931729/

Another great source found here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310484/
oemBiology Author
wrote...
4 years ago
Thank you very much for your reference, I would take time to look into it.

It is an important issue on how many hour the effect of serotonin is last to constrict smooth muscles within cerebral blood vessels.  Body cannot react instantly with serotonin, that is why SAD occur during winter.

Do you find any related materials about this issue on serotonin ?
Thank you very much for any suggestions (^v^)
wrote...
Valued Member
Educator
4 years ago
https://www.ncbi.nlm.nih.gov/pubmed/2931729 -- 1985

Serotonin causes contraction of the vascular smooth muscle cells in most blood vessels studied in vitro. This contraction is mainly due to activation of S2-serotonergic receptors. The monoamine can cause relaxation through activation of serotonergic receptors, different from the S2-serotonergic receptor and located on endothelial cells, or through an inhibitory effect on adrenergic neurotransmission. In certain blood vessels, the contractile effects can be markedly enhanced by hypoxia or moderate cooling. At low concentrations serotonin amplifies the vasoconstrictor responses to other vasoactive substances. Ultimately the effect of serotonin on vascular constriction is defined by the balance between these different actions. In the intact organism under normal conditions serotonin may play a modulatory role but exacerbation of the contractile effects because of hypersensitivity of the smooth muscle cells, local physical or humoral factors or loss of the relaxatory ability may lead to abnormal tissue responses. Thus, serotonin-induced vasoconstrictor responses may play a role in the etiology of vasospasm and peripheral vascular diseases, in particular at sites of endothelial lesions. Both the vasoconstrictor and the platelet aggregating effects of serotonin combined with its accelerated turnover may be important in the induction and maintenance of the augmented peripheral vascular resistance in arterial hypertension.

https://link.springer.com/chapter/10.1007/978-1-4615-9471-0_6 --1987

Reaffirms the segment written above.

I'm assuming both of these documents discuss the S2-serotonin pathway in more detail, but I do not have access to either of them. If the pathway is discussed, the timing is also discussed. I'm assuming it's relatively quickly, and so is not the cause of SAD. The association you're making is this:

In the winter, we experience low barometric pressures. Low barometric pressure is associated with dilation of blood vessels. Serotonin found in the platelets counteract this dilated blood vessels but causing vasoconstriction.
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