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Genetic factors[ edit ] Genetic factors involved in depression have been Apple hypothesis to identify. Historically, candidate gene studies have been a major focus of study. However, as the number of genes reduces the likelihood of choosing a correct candidate gene, Type I errors false positives are highly likely.
Candidate genes studies frequently possess a number of flaws, including frequent genotyping errors and being statistically underpowered. These effects are compounded by the usual assessment of genes without regard for gene-gene interactions. These limitations are reflected in the fact that no candidate gene has reached genome-wide significance.
Two meta analyses reported null findings,   while a meta analysis with more liberal inclusion criteria reported a significant relaitonship. Apple hypothesis genes encoding for the 5-HTT and 5-HT2A receptor were inconsistently associated with depression and treatment response.
Polymorphisms in the tryptophan hydroxylase gene was found to be tentatively associated with suicidal behavior. Depression may be related to abnormalities in the circadian rhythm or biological clock.
For example, rapid eye movement REM sleep —the stage in which dreaming occurs—may be quick to arrive and intense in depressed people.
REM sleep depends on decreased serotonin levels in the brain stem and is impaired by compounds, such as antidepressants, that increase serotonergic tone in brain stem structures.
Prolonged wakefulness due to sleep deprivation  activates serotonergic neurons, leading to processes similar to the therapeutic effect of antidepressants, such as the selective serotonin reuptake inhibitors SSRIs.
Depressed individuals can exhibit a significant lift in mood after a night of sleep deprivation. SSRIs may directly depend on the increase of central serotonergic neurotransmission for their therapeutic effect, the same system that impacts cycles of sleep and wakefulness.
Exposure to light also targets the serotonergic system, providing more support for the important role this system may play in depression. Diurnal mood improvement was associated with activity of dorsal neural networks. Increased mean core temperature was also observed. One hypothesis proposed that depression was a result of a phase shift.
Synapses are gaps between nerve cells. These cells convert their electrical impulses into bursts of chemical relayers, called neurotransmitterswhich travel across the synapses to receptors on adjacent cells, triggering electrical impulses to travel down the latter cells.
Monoamines are neurotransmitters that include serotonindopaminenorepinephrineand epinephrine. The observation of this efficacy led to the monoamine hypothesis of depression, which postulates that the deficit of certain neurotransmitters is responsible for depression, and even that certain neurotransmitters are linked to specific symptoms.
The proponents of this hypothesis recommend choosing the antidepressant with the mechanism of action impacting the most prominent symptoms -- for example, they advocate that people with MDD who are also anxious or irritable should be treated with SSRIs or norepinephrine reuptake inhibitorsand the ones with the loss of energy and enjoyment of life—with norepinephrine and dopamine enhancing drugs.
The therapeutic effect of antidepressants is thought to arise from autoreceptor desensitization over a period of time, eventually elevating firing of serotonergic neurons. Green arrows means stimulation and red arrows inhibition.
Serotonin receptors are blue, norepinephrine orange, and dopamine yellow. Phospholipase C and adenylyl cyclase start a signaling cascade which turn on or off genes in the cell.
The 5HT-3 receptor is associated with gastrointestinal adverse effects and has no relationship to the other monoamine receptors. Initial studies of serotonin in depression examined peripheral measures such as the serotonin metabolite 5-Hydroxyindoleacetic acid 5-HIAA and platelet binding.
The results were generally inconsistent, and may not generalize to the central nervous system. However evidence from receptor binding studies and pharmacological challenges provide some evidence for dysfunction of serotonin neurotransmission in depression.
These emotional processing biases may explain the therapeutic gap. People with MDD have an increased reward response to dextroamphetamine compared to controls, and it has been suggested that this results from hypersensitivity of dopaminergic pathways due to natural hypoactivity.61 thoughts on “Hormesis: How Certain Kinds of Stress Can Actually Be Good for You”.
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. In mathematics, the continuum hypothesis (abbreviated CH) is a hypothesis about the possible sizes of infinite schwenkreis.com states: There is no set whose cardinality is strictly between that of the integers and the real numbers.. The continuum hypothesis was advanced by Georg Cantor in , and establishing its truth or falsehood is the first of Hilbert's 23 problems presented in