Creatine has been sought after for its effects on depression, due to the significant changes occurring in brain morphology and neuronal structure associated with depression and low brain bioenergetic turnover in depression, perhaps related to abnormal mitochondrial functioning, which reduces available energy for the brain. The general association of low or otherwise impaired phosphate energy systems (of which creatine forms the energetic basis of) with depression, has been noted previously. Due to associations with cellular death and impaired bioenergetics with depression, creatine was subsequently investigated.
Oral ingestion of 1-1000mg/kg bodyweight of creatine in mice was able to exert an anti-depressive effect, which was blocked by dopamine receptor antagonists. A low dose of creatine (0.1mg/kg) was able to enhance the dopaminergic effects of dopamine receptor activators, suggesting supplemental creatine can positively influence dopamine signalling and neurotransmission.
Mechanically, creatine may exert anti-depressant effects via mixed dopaminergic and serotonergic mechanisms. The exact mechanisms are not clear at this time
Anti-depressive effects have been noted in humans, where 5g of creatine monohydrate daily for 8 weeks was able to augment the efficay of SSRI anti-depressants. Benefits were seen at week two and were maintained until the end of the 8 week trial. These effects were noted before in a preliminary study of depressed adolescents (with no placebo group) showing a 55% reduction in depressive symptoms at 4g daily when brain phosphocreatine levels increased. Other prelimnary human studies suggest creatine might lessen unipolar depression and one study on Post-Traumatic Stress Disorder (PTSD) noted improved mood as assessed by the Hamilton Depression Rating Scale.
It is possible that females could benefit more than males due to a combined lower creatine kinase activity as well as having altered purine metabolism during depression, but no human comparative studies have been conducted yet. One rat study noted that creatine monohydrate at 2-4% of feed had 4% creatine able to exert anti-depressive and anxiolytic effects in female rats only.
Intervention studies with creatine supplementation and depression show promise, but only one well conducted study (used alongside SSRI pharmaceuticals) has been done, while other studies have flaws. Promising, but no conclusions can be made at this time.
Okazuje się również, że kreatyna wywiera działanie neuroprotekcyjne i potencjalnie może wpływać na neurogenezę.
Creatine, through its ability to act as an energy reserve, attenuates neuron death induced by the MPTP toxin that can produce Parkinson’s Disease-like effects in research animals, reduces glutamate-induced excitotoxicity, attenuates rotenone-induced toxicity,L-DOPA induced dyskinesia, 3-nitropropinoic acid, and preserves growth rate of neurons during exposure to corticosteroids (like cortisol) which can reduce neuron growth rates. Interestingly, the energetic effect also applies to Alzheimer’s Disease, where creatine phosphate per se attenuates pathogenesis in vitro, yet creatine per se did not.
These effects are secondary to creatine being a source of phosphate groups and acting as an energy reserve. The longer a cell has energy, the longer it can preserve the integrity of the cell membrane by preserving integrity of Na+/K+-ATPase and Ca2+-ATPase enzymes. Preserving ATP allows creatine to act via a nongenomic response (not requiring the nuclear DNA to transcribe anything), and appears to work secondary to MAPK and PI3K pathways.
A protective effect on neurons by creatine, secondary to its ability to donate phosphate groups, exists and appears to be quite general in its protective effects
When assessing the antioxidant effects of creatine, it does not appear to sequester superoxide and may not be a direct antioxidant. Additionally, creatine failed to protect neurons from H2O2 incubation to induce cell death via pro-oxidative means. These results are in contrast to previously recorded results suggesting creatine as a direct anti-oxidant.
Some reports exist that creatine may be a direct anti-oxidant, but these have failed to be replicated. Creatine most likely does not possess anti-oxidant potential
The concentration of creatine that increases mitochondrial respiration in skeletal muscle (20mM) and this concentration also appears to work similarly in hippocampal cells. This promotes endogenous PSD-95 clusters and subsequently synaptic neurogenesis (thought to simply be secondary to promoting mitochondrial function).
Mitochondrial function per se appears to promote neuronal growth and proliferation, and at least in vitro, creatine is known to do the same and promote growth.
Reasumując- uczęszczasz na siłownię i bierzesz SSRI? Kreatynę możesz nie tylko bez obaw brać, ale wręcz powinieneś.