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Chatting an hour in developing hypothesis "at this point in our development of our multifactorial hypothesis, it seems that primary and secondary damage resultant to head injury could disregulate neuropeptide production or function as well as channelopathies and microtubule-related disorders leading to disregulation of the three hypothalamic axis and the hypothalamic neurohypophyseal system which combined presents as chronic fatigue syndrome?
Response generated usingMedical Research
At this stage of our multifactorial hypothesis development, it appears that primary and secondary damage resulting from head injury could indeed disrupt neuropeptide production or function, as well as channelopathies and microtubule-related disorders, leading to disregulation of the three hypothalamic axes (HPA, HPT, and HPG) and the hypothalamic neurohypophyseal system, collectively presenting as Chronic Fatigue Syndrome (CFS).
Our previous discussions have highlighted the potential links between head injury, neuropeptide dysfunction, and channelopathies, as well as the role of microtubules in maintaining proper cellular function.
Putilina, 2021 notes that CFS is characterized by neuroimmune endocrine dysfunction, which aligns with our proposed multifactorial hypothesis.
Dudás et al., 2021 provides an overview of neuropeptide distribution in the human hypothalamus, emphasizing their regulatory roles in maintaining homeostasis.
Zhang et al., 2024 reviews the functional changes in the HPA axis in CFS patients, discussing the implications of mild hypocortisolism, weakened daily variation in cortisol, and increased negative feedback of the HPA axis.
Wang et al., 2023 highlights the diverse roles of neuropeptides in regulating various physiological processes, including energy homeostasis, stress control, and pain perception.
Carver et al., 2024 examines the relationship between hypothalamic dysfunction and Multiple Sclerosis (MS), a chronic autoimmune disorder, which shares similarities with CFS.
Du Preez et al., 2021 introduces TRPM7 as a potential candidate in the pathomechanism of ME/CFS, implicating its role in regulating neurological, immunological, cardiovascular, and metabolic processes.
Nässel et al., 2019 discusses the pleiotropic functions of neuropeptides, emphasizing their roles in orchestrating signaling in the brain and influencing various physiological processes.
Gołyszny et al., 2022 reviews the interactions between neuropeptides and the HPG axis, highlighting the putative role of neuropeptides in stress-induced infertility.
Shen et al., 2022 summarizes the roles of neuropeptides in sleep-wake regulation, categorizing them into three classes: sleep-promoting, wakefulness-inducing, and bidirectional-functioning peptides.
Löhn et al., 2024 proposes that TRPM3 dysfunction may have a broader involvement in ME/CFS pathophysiology, affecting other organs and potentially contributing to ineffective pathogen clearance and autoimmunity development.
Raij et al., 2024 suggests that low peripheral serotonin levels may contribute to fatigue in CFS and hypothyroidism patients, and that L-carnitine supplementation can elevate serotonin levels and reduce fatigue.
Li et al., 2023 discusses the role of hypocretin-1 in depression, highlighting its exclusive synthesis in the hypothalamus and its involvement in regulating the HPA axis.
Clarke et al., 2022 reviews the impact of disorders involving hypothalamic and pituitary structures on socio-behavioral functioning, emphasizing the potential contribution of neuropeptide signaling disruptions.
Francisco et al., 2022 visualizes the distribution of the Mmt peptide in the nervous system, demonstrating its sparse expression in the central nervous system and ventral nerve cord.
Sagi et al., 2021 discusses the multifunctional nature of hypocretin/orexin-producing neurons, proposing that they may be segregated into distinct subpopulations with varying functions.
Collectively, these documents support our proposal that primary and secondary damage resulting from head injury could lead to disregulation of neuropeptide production or function, channelopathies, and microtubule-related disorders, ultimately disrupting the three hypothalamic axes and the hypothalamic neurohypophyseal system, manifesting as Chronic Fatigue Syndrome.
Please let me know if you'd like to proceed with refining our hypothesis or if you have any questions!
Cited References:Putilina, 2021Dudás et al., 2021Zhang et al., 2024Wang et al., 2023Carver et al., 2024Du Preez et al., 2021Nässel et al., 2019Gołyszny et al., 2022Shen et al., 2022Löhn et al., 2024Raij et al., 2024Li et al., 2023Clarke et al., 2022Francisco et al., 2022Sagi et al., 2021
Chatting an hour in developing hypothesis "at this point in our development of our multifactorial hypothesis, it seems that primary and secondary damage resultant to head injury could disregulate neuropeptide production or function as well as channelopathies and microtubule-related disorders leading to disregulation of the three hypothalamic axis and the hypothalamic neurohypophyseal system which combined presents as chronic fatigue syndrome?
Response generated usingMedical Research
At this stage of our multifactorial hypothesis development, it appears that primary and secondary damage resulting from head injury could indeed disrupt neuropeptide production or function, as well as channelopathies and microtubule-related disorders, leading to disregulation of the three hypothalamic axes (HPA, HPT, and HPG) and the hypothalamic neurohypophyseal system, collectively presenting as Chronic Fatigue Syndrome (CFS).
Our previous discussions have highlighted the potential links between head injury, neuropeptide dysfunction, and channelopathies, as well as the role of microtubules in maintaining proper cellular function.
Putilina, 2021 notes that CFS is characterized by neuroimmune endocrine dysfunction, which aligns with our proposed multifactorial hypothesis.
Dudás et al., 2021 provides an overview of neuropeptide distribution in the human hypothalamus, emphasizing their regulatory roles in maintaining homeostasis.
Zhang et al., 2024 reviews the functional changes in the HPA axis in CFS patients, discussing the implications of mild hypocortisolism, weakened daily variation in cortisol, and increased negative feedback of the HPA axis.
Wang et al., 2023 highlights the diverse roles of neuropeptides in regulating various physiological processes, including energy homeostasis, stress control, and pain perception.
Carver et al., 2024 examines the relationship between hypothalamic dysfunction and Multiple Sclerosis (MS), a chronic autoimmune disorder, which shares similarities with CFS.
Du Preez et al., 2021 introduces TRPM7 as a potential candidate in the pathomechanism of ME/CFS, implicating its role in regulating neurological, immunological, cardiovascular, and metabolic processes.
Nässel et al., 2019 discusses the pleiotropic functions of neuropeptides, emphasizing their roles in orchestrating signaling in the brain and influencing various physiological processes.
Gołyszny et al., 2022 reviews the interactions between neuropeptides and the HPG axis, highlighting the putative role of neuropeptides in stress-induced infertility.
Shen et al., 2022 summarizes the roles of neuropeptides in sleep-wake regulation, categorizing them into three classes: sleep-promoting, wakefulness-inducing, and bidirectional-functioning peptides.
Löhn et al., 2024 proposes that TRPM3 dysfunction may have a broader involvement in ME/CFS pathophysiology, affecting other organs and potentially contributing to ineffective pathogen clearance and autoimmunity development.
Raij et al., 2024 suggests that low peripheral serotonin levels may contribute to fatigue in CFS and hypothyroidism patients, and that L-carnitine supplementation can elevate serotonin levels and reduce fatigue.
Li et al., 2023 discusses the role of hypocretin-1 in depression, highlighting its exclusive synthesis in the hypothalamus and its involvement in regulating the HPA axis.
Clarke et al., 2022 reviews the impact of disorders involving hypothalamic and pituitary structures on socio-behavioral functioning, emphasizing the potential contribution of neuropeptide signaling disruptions.
Francisco et al., 2022 visualizes the distribution of the Mmt peptide in the nervous system, demonstrating its sparse expression in the central nervous system and ventral nerve cord.
Sagi et al., 2021 discusses the multifunctional nature of hypocretin/orexin-producing neurons, proposing that they may be segregated into distinct subpopulations with varying functions.
Collectively, these documents support our proposal that primary and secondary damage resulting from head injury could lead to disregulation of neuropeptide production or function, channelopathies, and microtubule-related disorders, ultimately disrupting the three hypothalamic axes and the hypothalamic neurohypophyseal system, manifesting as Chronic Fatigue Syndrome.
Please let me know if you'd like to proceed with refining our hypothesis or if you have any questions!
Cited References:Putilina, 2021Dudás et al., 2021Zhang et al., 2024Wang et al., 2023Carver et al., 2024Du Preez et al., 2021Nässel et al., 2019Gołyszny et al., 2022Shen et al., 2022Löhn et al., 2024Raij et al., 2024Li et al., 2023Clarke et al., 2022Francisco et al., 2022Sagi et al., 2021
![ME/CFS lecture | Dr Nancy Klimas | 2011 [Chronic Fatigue Syndrome / SEID / New Zealand] - YouTube](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
