CSF norepinephrine levels found to be elevated in those with PTSD. This is one of the few, if not only study, that has looked at epinephrine concentrations in PTSD. Plasma norepinephrine levels were found to not be associated with PTSD.
Study finds that low estrogen, assuming estradiol, higher FSH, low epinephrine, higher norepinephrine are associated with severe hot flashes. Of interesting note, Cortisol and Testosterone were not associated with symptom severity.
Thyroid hormone increased localized norepinephrine production and liposlys resulting in decreases SQ adipose tissue compared to hypothyroid. This study showed a localized effect of adipose tissue by thyroid hormone.
Progesterone increased MAO in prior estrogen treatment. Without prior treatment, Progesterone did not increase MAO and decrease the monoamine neurotransmitters norepinephrine, serotonin, and dopamine.
Interesting case study of ED presenting in man with pheochromocytoma. Only abstract here; yet the cause is the high norepinephrine and the effect it exerts on the corpus cavernosum.
Animal study points to methylB12 as the cause of an increase in adrenal medulla norepinephrine production. This has significant implications in individuals with hypertension.
SAMe increased hippocampal serotonin levels by 300% in rat brain model. Methylation is known to play a major role in serotonin, dopamine, and norepinephrine.
appears that PTSD results in divergent catecholamine and cortisol levels as patients age. The catecholamines (norepinephrine) will elevate and the cortisol will progressive decrease. Additionally, this is revealed in salivary cortisol testing
Treatment of exercise-associated hyponatremia with hypertonic IV infusion to correct plasma sodium levels is also a standard and accepted use of IV fluid infusions
athletes who present for medical care with hypernatremia who cannot tolerate oral fluids can benefit from IV fluids
Vaporization of sweat accounts for 80% of heat loss in hot, dry atmospheric conditions. This mechanism of water loss is the major contributor for exercise-associated dehydration
The rate of water loss can be quantified through measurement of sweat rate
Pre- and postexercise body weight measurements are the most common means to estimate overall water loss but are condition specific
It appears that 1% to 2% body weight loss is well tolerated by the exercising athlete
Dehydration, defined as greater than 2% loss of body weight, can negatively affect performance
In highly trained endurance athletes, plasma volume and sodium serum concentration were preserved despite a 5% body weight loss
In Ironman triathletes, dehydration to 5% body weight loss did not correlate with occurrence of medical complications
hydration should begin hours prior to exercise, especially if known deficits are present, and fluids should be consumed at a slow, steady rate, with 5 to 7 mL/kg taken 4 hours prior to exercise
Sodium concentration did not produce significant changes in the rate of absorption but was primarily dependent on carbohydrate concentration
Replacing 150% of body weight loss over 60 minutes has been tolerated without complications
IV treatment of severe dehydration (>7% body weight loss), exertional heat illness, nausea, emesis, or diarrhea, and in those who cannot ingest oral fluids for other reasons, is clinically indicated
A recent survey of the National Football League teams revealed that 75% (24 of 32) of the teams utilized IV infusion of fluids for prehydration in at least some otherwise healthy individuals
In the National Football League, an average of 1.5 L of normal saline was administered approximately 2.5 hours prior to competition
after 2 hours of exercise, the rectal temperature was 0.6° higher in the group not receiving IV infusion. Also, stroke volume and cardiac output were 11% to 16% lower in the control group versus the IV infusion group.
Recent evidence suggests the etiology of EAMC is related to muscle fatigue and neuronal excitability
no correlation between hydration status or electrolyte concentrations with EAMC
there may be a subset of muscle cramping that is associated with a loss of both body fluid and sodium
Glycerol is the primary agent for oral hyperhydration
elevation of plasma volume by 200 to 300 mL via dextran infusion resulted in 15% increase in stroke volume, 4% increase in VO2 max, and an increase in the exercise time to fatigue
Neither the tonicity nor mode of hydration resulted in improved speed of rehydration, greater fluid retention, or improved performance
There are beneficial anecdotal reports of EAMC treatment in elite and professional-level athletes with IV hydration during the course of an event
Plasma volume was better restored during rehydration with IV fluids at preexercise and 5 minutes of exercise. At 15 minutes, there was no difference between IV and oral rehydration
More rapid restoration of plasma volume was accomplished in the IV treatment group with no advantages over oral rehydration in physiological strain, heat tolerance, ratings of perceived effort, or thermal sensations
No difference was found in exercise time to exhaustion. IV and oral rehydration methods were equally effective. Heart rates were statistically higher in the oral rehydration group through 75 minutes of exercise, and there were higher increases in norepinephrine plasma concentrations
No significant differences between the groups were found for time to recovery, number of days with pain, number of days with stiffness, sleep disturbance, fatigue, rectal temperature, and loss of appetite
The current data suggest that IV rehydration is faster than oral
There may be physiological benefits of decreased heart rate and norepinephrine in athletes rehydrated via IV route
Postexercise blood 1 hour and 24 hours showed no differences in circulating myoglobin or creatine kinase
The use of IV fluid may be beneficial for a subset of fluid sensitive athletes
this should be reserved for high-level athletes with strong histories of symptoms in well-monitored settings.
Volume expanders may also be beneficial for some athletes
the reduction in BP within the first 10–20 min may be primarily attributed to a direct vasodilatory physiological effect, described as venodilation
BP reduction observed after 70–90 min is likely attributable to pharmacokinetically plausible vitamin C absorption and vasodilation because of nitric oxide release
Pharmacokinetic studies of IVC administration observed peak plasma levels within the first 90 min, with plasma levels reaching 13350 μmol/l for 50 g of IVC
Essential hypertension, associated with endothelial dysfunction because of an impaired nitric oxide/l-arginine pathway and impaired vasodilation can be restored by vitamin C
marked increase in BP response when IVB12 is administered
The mean BP increased significantly up to 12–16 mmHg systolic and diastolic independent of the dosage of vitamin B12
The production of norepinephrine, which can stimulate angiotensin-II production, which in turn influences BP, has been suggested as a possible mechanism for the increase in BP with IVB12
excess norephinephrine levels stimulate the sympathetic nervous system, leading to increased cortisol production, which has also been linked to increases in BP
Animal studies have found higher serum levels of norepinephrine (noradrenaline) in the adrenal medulla of rats receiving methylcobalamin (methyl-vitamin B12)
IV vitamin C in mostly normotensive patients (> 30 grams) reduced blood pressure. Some of the patients were pre-hypertensive. Vitamin B12 increase the blood pressure.
It is now well recognized
that the disease manifestation is reduced in pregnant women with
relapsing-remitting MS
This occurs particularly during the
third trimester when levels of estrogens (estradiol and estriol) and
progesterone (see Table 2) are elevated
up to about 20 times
This seems
well correlated with a decrease in active white matter lesions detected by MRI
This clinical improvement is
however followed by temporary rebound exacerbations at post-partum, when the
hormone levels decline
a shift from Th1 to Th2 immune response, expansion of
suppressive regulatory T lymphocytes and decrease in the number of circulating
CD16+ natural killer (NK)-cells
Th2 cytokines are
associated with down-regulation of Th1 cytokines and this Th2 shift is believed
to provide protection from allograft rejection during pregnancy as well as from
Th1-mediated autoimmune disease
it is
worth noting that the levels of other hormones with anti-inflammatory activity
(1,25-dihydroxy-vitamin D3, norepinephrine, cortisol) also increase
by 2 to 4 times during late pregnancy
1,25-dihydroxy vitamin D3
induces regulatory T-cell function important for development of self-tolerance
breast-feeding does not alter the
relapse rate in women with MS
Leptin is a pleiotropic
hormone produced primarily by adipocytes but also by T lymphocytes and neurons
Several lines of evidence indicate that leptin
contributes to EAE/MS pathogenesis, influencing its onset and clinical severity,
by acting as a proinflammatory cytokine which promotes regulatory T cell (Treg)
anergy and hyporesponsiveness, resulting in increased Th1 (TNFalpha, INFgamma)
and reduced Th2 (IL-4) cytokine production
circulating leptin levels are increased in relapsing-remitting MS
patients (men and women analyzed together) while the
CD4+CD25+Treg population decreases
As the leptin plasma concentrations are
proportional to the amount of fat tissue, obese/overweight individuals produce
higher levels of leptin
Nielsen et al found that estradiol and progesterone exert
neuroprotection against glutamate neurotoxicity, while MPA antagonizes the
neuroprotective effect of estradiol and exacerbated neuron death induced by
glutamate excitotoxicity
The typical onset of TS occurs at 6–7 years of age and is characterized by the appearance of simple, recurrent motor tics, followed by the manifestation of phonic tics after several months [12]. In most children, TS symptoms undergo a progressive exacerbation, which reaches its zenith at the beginning of puberty (11–12 years of age), and is then followed by a gradual remission in the majority of patients
30–40% of TS-affected children retain their symptoms in adulthood
Multiple neurotransmitters have been implicated in TS, including dopamine (DA), serotonin, norepinephrine, acetylcholine, glutamate and γ-amino-butyric acid (GABA)
ample evidence supports the involvement of DAergic dysfunctions in TS
male gender is a major risk factor for TS (with a male:female prevalence ratio estimated at ~4:1)
the typical age of onset coincides with adrenarche (6–7 years old); symptoms increase in severity until the beginning of puberty (12 years old) and then undergo a spontaneous amelioration, which becomes apparent with the end of puberty (at 18–19 years of age)
TS is diagnosed later in females than males
female gender may predict greater tic severity in adulthood
a number of clinical observations showed that tics in TS patients could be exacerbated by anabolic androgens
steroidogenic enzymes and androgen receptors may serve as putative therapeutic targets for this disorder
Unlike males, tic severity is typically increased after puberty in females
26% of females were found to experience exacerbation of tics in the estrogenic phase of the menstrual cycle, and this phenomenon was found to be correlated with increased tic severity at menarche
biochemical hallmark of adrenarche is the acquisition of 17,20 lyase activity by cytochrome P450 C17 (CYP17A1)
increased synthesis of dehydroepiandrosterone (DHEA) and androstenedione, which leads to the growth of axillary and pubic hair as well as enhancement in the oiliness of the skin
interesting read on hormones and tourette's.. Proposed that 5 alpha reductase activity is involved in worsening of tics. This makes sense as Testosterone in men with low T is known to increase dopamine and dopaminergic dysfunction is known to play a role in tourette's; the clinical presentation of girls vs boys is very different. The authors of this article propose that 5 alpha reductase activity controls a back door method where by progesterone is converted to androgens.