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Is your Hypothalamus up the creek?

andyguitar

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I'm only up to the Anterior Hypothalamus at the moment.
Anterior area is responsible for vasodilation. Posteria for vasoconstriction. Yin and Yang? Some texts on traditional chinese medicine describe a syndrome which is pretty similar to me/cfs. Deficient yin (and variants of it). Yin cools you down. Restrains yang which is hot. To much heat causes injury. Cold water therapy might be the solution here.
 

Rufous McKinney

Senior Member
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13,182
Do you mean that you had an MRI of your brain that showed inflammation in the central part of your brain? I apologize if you explained this elsewhere and I missed it!

I was referring to the 1 degree hotter tissue that Jared Younger observed in ME folks using MRI.

I don't know if my brain is exhibiting that or not. I just think its likely and possible.
 

Rufous McKinney

Senior Member
Messages
13,182
But I am thinking of a very simple structure, such as when you blow up a balloon and then try to let the air out via a collapsed "neck" of the end of the balloon. There's a glymphatic system, from what I read.

I think along similar lines....while its certain possible and likely we have a whole variety of- inflammation...I really wonder alot about the basic physical structure of the body, how it transmits messages via connective tissue, electrical impulses. How we have actual DUCTS which must SECRET things. We have collagen breaking down which is a form of structural support.

And every action requires an ATP to fire. Every Single Thing the body does- needs something to fire that.

So this lower brain stem- weakened ligaments holding the brain in place: thats very phsycial and I agree it could be a bit like your Balloon Analogy.
 

Rufous McKinney

Senior Member
Messages
13,182
Deficient yin (and variants of it). Yin cools you down
. Restrains yang which is hot. To much heat causes injury. Cold water therapy might be the solution here.

Yes- my chinese medicine main diagonsis is: severely Yin Deficient. So its all about being overheated and needing to cool down.

there are alot of dietary ways to reduce heat, and increase the Yin- feeding the Yin its called.
 

Pyrrhus

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Location
U.S., Earth
Apologies to @andyguitar if I have derailed your thread! Let me know if you want me to move my posts to a new thread...

Thinking about classic inflammation (heat, swollen tissues) is this why the structural issues, such as cranio cervical instability and lax ligaments might make sense in some cases?

I'm not as knowledgeable about CCI/AAI/TC spinal issues as @Hip is, so he may be better able to answer. But my best guess is that the cartilage destruction that appears to occur in some cervical issues is due to activation of mast cells in the cartilage.

Since mast cells are a tissue-resident immune cell, not a blood-borne immune cell, this mast-cell activation is actually closer to neuroinflammation than it is to classical inflammation. Maybe we could use a new word for this type of inflammation, such as "mastoinflammation". Or we could combine "mastoinflammation" and "neuroinflammation" into a single concept called "tissue-resident inflammation".

I do think that one under-appreciated issue related to cartilage destruction is the potential role of glycine deficiency. Glycine is an amino acid that is essential for making or restoring cartilage. The average dietary intake of glycine is roughly 1.5-3 grams per day.[1] This is not enough for the body's needs, so the body makes its own glycine to make up for the inadequate dietary supply. However, the way that the body makes new glycine is tied to the folate cycle, which means that glycine production can be slowed down by anything that slows down the folate cycle, such as B12 deficiency.[2]

One publication meticulously calculated the average glycine production and the average body's need for glycine. This paper found that the average body makes about 2.5 grams of glycine per day, but that the body needs a total of about 15 grams of glycine per day to sustain the amount of cartilage we had in early adulthood.[3] Although this is only one paper, their results are supported by the in vitro observation that large increases in glycine stimulate large increases in collagen synthesis.[4] (cartilage is made of collagen)

I keep thinking that an obstruction to the normal pathways to clear the byproducts of inflammation might keep that whole process going if the infection does its thing in the brain. But I am thinking of a very simple structure, such as when you blow up a balloon and then try to let the air out via a collapsed "neck" of the end of the balloon. There's a glymphatic system, from what I read.

You seem to have answered your own question. Yes, there is a lymphatic system in the brain that is responsible for clearing the byproducts of neuroinflammation, and the faster the byproducts are disposed of, the quicker the neuroinflammation might be able to resolve itself.

The flow through this lymphatic system is related to the normal fluid flow through the brain. Normally, there is a steady flow of fluid from the blood, into the cerebrospinal fluid (CSF), from the CSF into the brain, and then out of the brain into the lymphatic system. If blood flow to the brain is reduced, then lymphatic clearance of the byproducts of neuroinflammation will be similarly reduced.

References
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627940/#idm139934315659552title
[2] https://pubmed.ncbi.nlm.nih.gov/19179765/
[3] https://pubmed.ncbi.nlm.nih.gov/20093739/
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6153947/
 

Rufous McKinney

Senior Member
Messages
13,182
The flow through this lymphatic system is related to the normal fluid flow through the brain. Normally, there is a steady flow of fluid from the blood, into the cerebrospinal fluid (CSF), from the CSF into the brain, and then out of the brain into the lymphatic system. If blood flow to the brain is reduced, then lymphatic clearance of the byproducts of neuroinflammation will be similarly reduced.

Super interesting @Pyrrhus ....

This washing of the brain- is impaired in us, I"m just sure of it. Thanks for those links. That likely can affect the hypothalamus- somehow. as well.
 

HABS93

Senior Member
Messages
485
Yes foods that generate heat can give some a quick boost. But it's a bit like taking money out of a bank account that is overdrawn. You pay for it later.
I feel I am too in the impaired washing of the brain. I worded in my own head like there's not enough blood flow . Which is just causing all sorts of problems. When I smoked weed I would feel like I couldn't load the high like loading a saved file in a video game
Instead of it loading and resuming play. I was trapped in this loaded play that's glitching out(symptoms increased). I like your description of yin and yang. Maybe there's truth to that. I'll have to buy some grapefruit.
 

ahmo

Senior Member
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4,805
Location
Northcoast NSW, Australia
I had good results from hypothalamus glandular. I was having severe reactions when going out into heat. After a bit of research, I started on hypothalamus. Withing hours I was no longer hyperventilating when going out into heat. I suded it for several years. Also used pituitary, which seemed to help my sleep, and I continue to use adrenal glandular twice daily to support my poor adrenal health. Good luck.
 

andyguitar

Moderator
Messages
6,581
Location
South east England
I had good results from hypothalamus glandular.
I see that on your profile you say that foot baths helped. Were they cold water ones? To cut a long story short I'm now of the opinion that the sort of things people report as being what started their me/cfs have caused Hypothalamus dysfunction and thats what needs to be treated. Infection (that causes raised temperature) is a often reported beginning of me/cfs for many. The higher incidence of me/cfs among women might be due to temperature fluctuation during the monthly cycle. So if something causes Hypothalumus dysfunction at the start then those temperature changes would aggravate it.
 

Marylib

Senior Member
Messages
1,139
Thanks @Pyrrhus. Very interesting.

Yeah, the good old question - are we actually able to absorb the needed amino acids and other nutrients through the digestive process? Elsewhere on this forum I have, I think, noted my own quite notable response to IV nutrition. (the usual B vitamins, amino acids, minerals, including delicious-feeling-sleep-inducing magnesium sulfate, and good old glutathione)

Ages ago, when I first had symptoms of whatever this all is - before PEM, I was sent to a doc, who measured the amino acids in a blood test. He said he had never seen such low levels before, except in a corpse.

So I have never been one to assume I can get what is actually needed through the digestive process, but IV nutrition is far too pricey. Grapefruit or no grapefruit, glandular extracts or no glandular extracts - it's all one wacky dysfunctional system!

I have had somewhat of a response to verapamil, which begs the question posed in the current research out of NCNED at Griffith University in Australia, regarding the problem with the calcium ion channels and the possibly broken receptors, NK cell degradation, etc. The main response I have is increased blood flow - probably somewhat of a correction of a genetic or epigenetic defect. It helps my POTS. Apparently the use of a calcium channel blocker creates a reservoir that holds the calcium for a time, so that the cells have access to it.

Some say, "Oh but that is impossible, because that means if you carry that defect, you would have had ME/CFS from birth! My money is on the metabolic trap hypothesis."

Methinks it's not that simple. It seldom is.
 

Pyrrhus

Senior Member
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4,172
Location
U.S., Earth
Yeah, the good old question - are we actually able to absorb the needed amino acids and other nutrients through the digestive process?

That is a question that I keep returning to. I have repeatedly noticed that I can get a greater effect from a given dosage in supplemental form than the exact same dosage in food form.

The first couple of times that I noticed this, I reasoned that there must be something special about the formulation of the supplement that made it more bioavailable than the food form. But I have now noticed this discrepancy with a wide variety of types of supplements, which means a new explanation is in order.

The most obvious explanation is that low-level inflammation in the gastrointestinal tract prevents full digestion of food, limiting absorption of food nutrients. But how exactly would that work?

Another explanation is that the autonomic nerves that release digestive enzymes into the intestines fail to release sufficient enzymes, resulting in incomplete digestion, also limiting absorption of food nutrients.

A third explanation is that the autonomic nerves that regulate stomach acid fail to release sufficient stomach acid for the proper breakdown of food before it reaches the intestines, which makes it harder for the intestines to digest and absorb food nutrients properly.

Or some combination of the above...

I have had somewhat of a response to verapamil, which begs the question posed in the current research out of NCNED at Griffith University in Australia, regarding the problem with the calcium ion channels and the possibly broken receptors, NK cell degradation, etc. The main response I have is increased blood flow - probably somewhat of a correction of a genetic or epigenetic defect. It helps my POTS. Apparently the use of a calcium channel blocker creates a reservoir that holds the calcium for a time, so that the cells have access to it.

That's great that you seem to benefit from Verapamil! The effects of calcium channel blockers are indeed myriad and complex. We still don't know exactly how the calcium channel blocker gabapentin works for pain. Calcium ions (Ca2+) are used in so many different ways throughout the body, and there are so many uses for calcium channels, it's hard to know for certain why a given drug works for a given symptom.
 
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ahmo

Senior Member
Messages
4,805
Location
Northcoast NSW, Australia
I see that on your profile you say that foot baths helped. Were they cold water ones? To cut a long story short I'm now of the opinion that the sort of things people report as being what started their me/cfs have caused Hypothalamus dysfunction and thats what needs to be treated. Infection (that causes raised temperature) is a often reported beginning of me/cfs for many. The higher incidence of me/cfs among women might be due to temperature fluctuation during the monthly cycle. So if something causes Hypothalumus dysfunction at the start then those temperature changes would aggravate it.

Footbaths were warm, used for varieties of detox. Cold therapy is not my cuppa tea.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
Let's not forget Warren Tate's theory on the paraventricular nucleus of the hypothalamus:

A compromised paraventricular nucleus within a dysfunctional hypothalamus: A novel neuroinflammatory paradigm for ME/CFS (Mackay and Tate, 2018)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6291860/

Discussion:
https://forums.phoenixrising.me/thr...-and-limbic-system-theory.62675/#post-1021106

Excerpt:
Mackay and Tate 2018 said:
A neuroinflammatory paradigm is presented to help explain the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The hypothalamic paraventricular nucleus (PVN) is responsible for absorbing and processing multiple, incoming and convergent ‘stress’ signals, and if this cluster of neurons were affected (by neuroinflammation), the ongoing hypersensitivity of ME/CFS patients to a wide range of ‘stressors’ could be explained.

Neuroinflammation that was chronic and fluctuating, as ‘inflammatory-marker’ studies support, could reflect a dynamic change in the hypothalamic PVN’s threshold for managing incoming ‘stress’ signals. This may not only be a mechanism underpinning the characteristic feature of ME/CFS, post-exertional malaise, and its associated debilitating relapses, but could also be responsible for mediating the long-term perpetuation of the disease.

Triggers (sustained physiological ‘stressors’) of ME/CFS, such as a particular viral infection, toxin exposure, or a traumatic event, could also target the hypothalamic PVN, a potentially vulnerable site in the brains of ME/CFS susceptible people, and disruption of its complex neural circuitry could account for the onset of ME/CFS.

In common with the different ‘endogenous factors’ identified in the early ‘neuroinflammatory’ stages of the ‘neurodegenerative’ diseases, an as yet, unidentified factor within the brains and central nervous system (CNS) of ME/CFS patients might induce both an initial and then sustained ‘neuroinflammatory’ response by its ‘innate immune system’. Positron emission tomography/magnetic resonance imaging has reinforced evidence of glial cell activation centred on the brain’s limbic system of ME/CFS patients. Neuroinflammation causing dysfunction of the limbic system and its hypothalamus together with a consequently disrupted autonomic nervous system could account for the diverse range of symptoms in ME/CFS relating, in particular to fatigue, mood, cognitive function, sleep, thermostatic control, gastrointestinal disturbance, and hypotension.
 
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Pyrrhus

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U.S., Earth
And for anyone interested in a review of research into the Hypothalamic-Pituitary-Adrenal Axis in ME/cfs, there is the 2013 review by Cara Tomas, Julia Newton, and Stuart Watson:

A Review of Hypothalamic-Pituitary-Adrenal Axis Function in Chronic Fatigue Syndrome (Tomas, Newton, & Watson, 2013)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4045534/
Excerpt:
Tomas et al 2013 said:
Hypothalamic-pituitary-adrenal (HPA) axis dysfunction has been found in a high proportion of chronic fatigue syndrome (CFS) patients and includes enhanced corticosteroid-induced negative feedback, basal hypocortisolism, attenuated diurnal variation, and a reduced responsivity to challenge. A putative causal role for genetic profile, childhood trauma, and oxidative stress has been considered. In addition, the impact of gender is demonstrated by the increased frequency of HPA axis dysregulation in females.

Despite the temporal relationship, it is not yet established whether the endocrine dysregulation is causal, consequent, or an epiphenomenon of the disorder. Nonetheless, given the interindividual variation in the effectiveness of existing biological and psychological treatments, the need for novel treatment strategies such as those which target the HPA axis is clear.