forbigoneamanda

strep throat
eat infections
asthma machine
--went to camp upstate in middle school, got hpylori infection-
sleep disorder started in middle school

lice for a long time (shampoo treatment between 6-7th grade (middle school)(several of these are neurotoxins possibly inhaled through steam))
pneumonia
scarlet fever
heliobacter pylori - middle school (iv of sedative for scope)

posture: hunching when walking

strattera: might have helped but said it was expired (few weeks taking, not sure of dosage)

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DXM - makes feel relaxed
alcohol - knock out

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low stimulating stuff
high sleepiness stuff

overdose of stimulating stuff = permanent damage (increased sleepiness gland or smaller stimulating gland)

"Narcolepsy is due to a decrease in orexin. It is hypothesised in narcolepsy the reduced level of orexin means that the switch between the VLPO and the arousal system is destabilised [9] resulting in sudden switches from wakefulness to sleep; the characteristic symptom of narcoleptics."


-locus coeruleus <- lateral hypothalamus (orexin producer)
TAAR1:
 p-tyramine ? PEA ? octopamine ? m-tyramine ? dopamine ? tryptamine ? histamine ? serotonin ? norepinephrine.

BDNF / exercise
hippocampus atrophy
In animals, injections of IL-1ß and TNF-a result in increased non-REM sleep time and slow wave activity during the non-REM sleep.37 In humans, increases in inflammation following the administration of interferon-alpha in hepatitis C patients is predictive of decreases in self-reported sleep quality assessed by the Pittsburgh Sleep Quality Index.38 Lower self-reported Pittsburgh Sleep Quality Index scores are also associated with an increased inflammatory response to stress.39 As a whole, this suggests a negative feedback loop in which sleep, inflammation and depression interact and progressively worsen. The results of the current analysis, along with our previous findings in this sample,21, 24 suggest that exercise may be resetting this negative feedback loop.
Our results also implicate BDNF in improvements in sleep quality following exercise, as decreases in BDNF were associated with decreased hypersomnia. This finding is in contrast to our initial hypothesis that improvements in sleep would be related to increases in BDNF. Our intial hypothesis was based on previous research that demonstrated BDNF-dependent changes in sleep quality. In animals, intracerebroventrical injections of BDNF increase both non-REM and REM sleep40 and increased slow wave activity during non-REM sleep.9 In humans, non-REM sleep slow wave activity was higher during recovery sleep in Val/Val genotype compared with Val/Met genotype.41 Finally, ketamine treatment of MDD has been found to result in associated increases in BDNF and non-REM slow wave activity.42 The discrepancy between our results and our initial hypothesis may be owing to the unique biological underpinnings of hypersomnia and help further highlight the possible differential biomarker associations between hypersomnia and insomnia.

tyrosine

Adrenocorticotropic hormone

Metabotropic_glutamate_receptor
Excitatory amino acid receptor antagonist

hypocortisolemic disorders
glucocorticoid resistance
Adrenal insufficiency , addisons , ALD , Cushings
diseases of the HPA axis
poems syndrome/castlemans
low CRF, ACTH, cortisol

AMPD1

low hypocretrin in cerebrospinal fluid
improvement with corticosteroid (hypothalamus lesion after encephalomyelitis)
sustained damage to hypothalamis/pituitary regions
blunted cortisol awakening response and hippocampal atrophy

In contrast, atypical
depression state of hyperphagia, hypersomnia, enhanced affected responsiveness to
external stimuli, lethargy and fatigue would be based upon increased levels of
corticosteroids and decreased levels of CRH

cortisol: Caffeine may increase cortisol levels
Sleep deprivation
Intense (high VO2 max) or prolonged aerobic exercise, cortisol declines to normal levels after eating

high oxytocin? vitamin c

lymes disease

vitamin e deficiency
vitamin b12 deficiency
iron deficiency