Traumatic brain injury impairs hormone production, disrupting sleep, cognition, and memory

[Milo]

This is an article of a paper that is yet to be published.
View here.

More than 2.5 million people in the United States alone experience a traumatic brain injury, or TBI, each year. Some of these people are plagued by a seemingly unrelated cascade of health issues for years after their head injury, including fatigue, depression, anxiety, memory issues, and sleep disturbances.

A collaborative team, led by Dr. Randall Urban, The University of Texas Medical Branch at Galveston’s Chief Research Officer and Professor of Endocrinology, has spent the past 20 years investigating this post-TBI syndrome. The team has learned more about how a TBI triggers a reduction in growth hormone secretion and why most TBI patients improve after growth hormone replacement treatment.

The studies led to the definition of the syndrome as brain injury associated fatigue and altered cognition, or BIAFAC, as recently described in a commentary published by Drs Urban and Brent Masel, UTMB Professor of Neurology, in the Journal of Neurotrauma. Detailed information on the team’s two most recent advances also in the Journal of Neurotrauma

There is much more to the article, discusses a trial with growth hormone.

The team has been building on the discovery that TBI triggers a long-term reduction in growth hormone, or GH, secretion that is linked with BIAFAC. Most TBI patients experience dramatic symptom relief with GH replacement therapy, but the symptoms return if the treatment stops. The researchers are trying to better understand BIAFAC and exactly how and why GH replacement works so well in order to develop new interventions.

BIAFAC stands for brain injury associated fatigue and altered cognition.


It makes me wonder, how many of us had a genuine concussion prior to getting sick? I got one maybe 6-7 years prior to getting sick. While the CT scan showed no injury, i had over 9 months of headaches. I was hit by a car while i was riding my bike. I went over the hood and cracked my helmet.

 

[Hutan]

It's interesting.

They seem to be suggesting that the TBI causes intestinal dysfunction and changes in nutrient utilisation (along with changes in fecal bacterial communities). And this causes changes in hormonal patterns, specifically a long term reduction in growth hormone. They claim that most TBI patients experience dramatic symptom relief with growth hormone replacement therapy.

Which may all be right. But the studies discussed in the article don't prove that.

They examined 18 people with a history of mild TBI and inadequate GH secretion.

So they didn't take just any TBI patients. They took TBI patients with 'inadequate GH secretion' and found that GH replacement therapy helped. Which is not surprising.

We compared the fecal microbes of 22 moderate/severe TBI patients residing in a long-term care facility with 18 healthy age-matched control subjects....The results suggest that the people with TBI-related fatigue and altered cognition also have different fecal bacterial communities than the control group

. And this study might just be reflecting the quality of food in this single long-term care facility.

 

[ScottTriGuy]

"...these symptoms can manifest months to years after the initial injury and as this cluster of symptoms hasn’t been previously grouped together, it often goes unidentified in the medical community."

Slight aside...I just published an interview with a woman who had 100+ ECT (aka shock therapy, where they zap the brain into seizure) - she said research shows electrical injury effects manifest in the brain 2 - 10 years after ECT (and ECT is not regulated or standardized).

For her, symptoms showed about 7 years after she stopped ECT (against psychiatrists' advice).

(Spoiler: turns out her psychiatric symptoms were a result of ammonia and other toxins 'marinating' her brain. Once that was addressed, the years of 24 / 7 voices telling her to kill herself disappeared.)

 

[Arnie Pye]

Surely it should be obvious that Traumatic Brain Injury will often damage the hypothalamus and the pituitary. These two organs are responsible for controlling the release of or actually releasing a huge number of hormones that affect the entire body. This isn't new "news".

 

[mariovitali]

FWIW, i added TBI on the software framework i am using. It receives a high ranking for its relevance to ME/CFS symptoms :

The system suggests that the proposed mechanism may involve glutamate metabolism. More importantly : TBI can affect the Liver and Bile acid metabolism

Hepatic alterations are accompanied by changes to bile acid transporter-expressing neurons in the hypothalamus after traumatic brain injury

Some excerpts :

Bile acid transporters are central to maintaining bile acid circulation and homeostasis37, and specific transporters carefully regulate entry and removal from the CNS. Blood brain barrier (BBB) breakdown can facilitate bile acid entry into the brain38. Once in the brain, bile acids can be beneficial39 or detrimental32,38depending on the physiological conditions, as well as the type and location of the receptors to which they bind40. Bile acids receptors may be cell-surface or nuclear, and have tissue-specific effects related to cholesterol synthesis, bile acid synthesis, and other g-protein mediated effects41,42.

Briefly, we pose that the increase in IL-1β, IL-6 and TNF-α after TBI results in activation of the hepatic APR. The APR precedes hepatic inflammation and altered bile acid release. Because a TBI results in blood brain barrier breakdown, bile acids enter the brain in concentrations outside of the typical regulation by the bile acid transporters. Thus, dysregulation of brain bile acid homeostasis after TBI may contribute to detrimental neurological outcomes.

Within the hypothalamus, we found ASBT+ neurons in medial and lateral portions of the preoptic area, the dorsal medial nucleus and the lateral hypothalamus. The dorsal medial nucleus is involved in regulating circadian rhythm, feeding, and drinking behavior, as well as body metabolism64,65. Considering that sleep cycles are often altered following TBI, it is possible that dysregulation of the bile acid system in this nuclei is involved in this alteration. Interestingly, the lateral portions of the preoptic nuclei, and the lateral hypothalamus, have also been shown to be involved in sleep onset66,67. Considering that we observed ASBT+ neurons in these hypothalamic nuclei, it is possible that bile acid system changes after TBI might be involved in sleep and/or circadian deficits after TBI.

 

[wastwater]

Hi I wondered do you have a link to this story
Spoiler: turns out her psychiatric symptoms were a result of ammonia and other toxins 'marinating' her brain. Once that was addressed, the years of 24 / 7 voices telling her to kill herself disappeared.)

 

[Sly Saint]

didn't know where to put this