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Parenteral and Enteral Nutrition in Critical Illness
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Phase 2. The second phase of metabolic response and nutritional requirements begins as the body’s intrinsic capacity to produce fuel becomes impaired. This corresponds to a limited availability of substrate (i.e., freely mobilizable muscle) or a reduction in counter-regulatory hormones, possibly from adrenal fatigue. As endogenous glucose production declines, our therapeutic goal is to take over energy delivery to match the measured energy requirements. But it is important to note that the protein requirements remain as high as in the prior phase.
Managing Pain in the Presence of Autoimmune Disease
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Now when the body is stuck with cortisol running high at all times tested, this is called stage 1 adrenal fatigue.92 (I believe it is important for every physician to know that these terms and concepts have been described in the scientific literature for many decades. This reference here, in the British Medical Journal, is from 1950.) The hormone DHEA, like cortisol, will need to stay in an ideal level, or even increase temporarily, in order to allow the person to continue “running from the bear” even though they do not feel very well. If a bear is chasing you, you want to be able to keep running even if you don’t feel so well. Stop running and you are dead, or so your body thinks. But because the person is running 24 hours a day, 7 days a week, day after day, month after month, they are feeling worse and worse over time.
Medical imaging and the intrusive gaze
Published in Lesa Scholl, Medicine, Health and Being Human, 2018
A 2013 TV Ontario panel titled “More or Less Medicine” on current affairs programme The Agenda explored the changing complexion of healthcare. During the panel, Dr. Doug Weir of the Ontario Medical Association asserted that a serious issue with instrumental medicine is that it can create “false reassurance … that if it’s all clear, that somehow you’re in good health,” when this may not be the case, and may not reflect the patient’s experience. For example, in adrenal fatigue, tests may indicate normal adrenal function, while the patient experiences unexplained feelings of general unwellness. If the individual patient’s norm has dropped, they will notice the change, long before testing shows them outside the normal range. On the same panel, Dr. Danielle Martin, a family practitioner and Vice President of Medical Affairs and Health System Solutions at Toronto’s Women’s College Hospital, suggested, “perhaps we need to spend a little bit less time on the technology aspect of things and a little bit more time looking at the whole human being sitting in front of us.” Technologies have enticed doctors away from listening, a foundational skill for good patient care.
Fatigue in ANCA-associated vasculitis (AAV) and systemic sclerosis (SSc): similarities with Myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). A critical review of the literature
Published in Expert Review of Clinical Immunology, 2022
Charmaine van Eeden, Mohammed S. Osman, Jan Willem Cohen Tervaert
Individuals with ME/CFS often display symptoms associated with central nervous system abnormalities, including reduced cognitive function, increased pain syndromes such as fibromyalgia, and/or postural orthostatic tachycardia syndrome (POTS). Neuroendocrine studies into hypothalamic-pituitary-adrenal (HPA) function, and cortisol levels and serotonin transmission have, provided reproducible findings, suggesting physiological changes to stress response in ME/CFS [18,20,23]. ME/CFS patients appear to have a reduced HPA axis function resulting in adrenal insufficiency, which negatively affects immunological and neuronal homeostasis [96–98], individuals who suffer from adrenal insufficiency (e.g. Addison’s disease) resulting in low cortisol levels, display ME/CFS-like symptoms such as fatigue, arthralgia, myalgia, sleep disturbance, and mood disorders [23]. Glucocorticoid use is common in SARDS and is associated with adrenal suppression [99,100]. Low cortisol levels in SSc have been linked to symptoms of pain and depression and increased disease activity [101]. Adrenal fatigue is synonymous with POTS, and this condition is present in around 16% of individuals with autoimmune diseases [102].
The biology of burnout: Causes and consequences
Published in The World Journal of Biological Psychiatry, 2021
Adam Bayes, Gabriela Tavella, Gordon Parker
Burnout has been hypothesised to result from chronic (or repeated episodic) psychological stress which induces sustained activation of the autonomic nervous system and HPA axis, providing a ‘psychobiological explanation’ for development of the syndrome. Biological research has therefore predictably examined the HPA axis and cortisol. Findings have been inconsistent and sometimes contradictory, potentially due to heterogeneity in measurement of cortisol. Based on review of the studies and from clinical observation, we hypothesise that burnout is not simply marked by hypocortisolemia or hypercortisolemia. HPA dysfunction may evolve from an initial stress-induced hypercortisolism (as the individual faces stressors inducing burnout) to a later chronic hypocortisolemic picture – when burnout symptoms have evidenced (in Chow et al. 2018; Danhof-Pont et al. 2011; Fries et al. 2005). The concept of ‘adrenal fatigue’ as described by Wilson (2001) – involving hypofunction of the adrenal glands leading to hypocortisolism with concomitant fatigue, cognitive dysfunction and mood symptoms – appears consistent with such a process but the validity of this model has been challenged. (Cadegiani and Kater 2016). In addition, there would appear to be a number of other arenas of compromised biological functioning. DHEA-S, prolactin, thyroid hormones and BDNF have also been shown to be altered in burnout, but the limited studies make interpretation inconclusive.
Sex differences in the hypothalamic-pituitary-adrenal axis response following a single or multiple days of sleep restriction
Published in Stress, 2020
Katelyn N. Buban, Elizabeth A. Shupe, Stephen W. Rothwell, T. John Wu
Relative expression of 11β-hydroxylase, which is an enzyme involved in the biosynthesis of CORT via the conversion of deoxycorticosterone to the active corticosterone (White, Pascoe, Curnow, Tannin, & Rösler, 1992), was measured in the adrenal glands to assess for adrenal insufficiency following PSD. Adrenal insufficiency is a form of adrenal fatigue or exhaustion believed to be caused by a period of overactivation of the adrenal glands, whereby the adrenals are unable to produce CORT due to either a change in local enzymatic activity, or due to a disruption in higher level systems involved in CORT release (Guilliams & Edwards, 2010). 11β-hydroxylase expression, was increased in males but not females following both one and three days of sleep deprivation. While, females showed greater 11β-hydroxylase expression overall compared to their male counterparts. These findings suggests that it is not adrenal insufficiency caused by changes in enzymes that is responsible for the dysregulation in HPA axis reactivity, and that there might be sex-specific differences in baseline enzymatic activity that might contribute to overall sex differences in the HPA axis reported in the literature (Rao & Androulakis, 2017). Therefore, the alterations seen at the level of the adrenal glands might be due to changes in higher-order systems such as the adrenal-sympathetic system or they might be sex-specific strategies employed by the adrenals to combat disruptions elsewhere in the HPA axis.