Creatine and increased brain performance

I just took creatine monohydrate yesterday with caffeine and I actually noticed an improvement in brain performance.

I've tried different stuff but most of them doesn't work.
Only things so far that has worked on me:
Creatine monohydrate mixed with apple juice
Caffeine
Zinc
Omega 3 fats.

What should I take in addition to creatine to get a even better cognitive effect?

Creatine requires a loading phase of about 5 days to work more effectively, and then a small daily maintenance dose,
its best taken with some simple carbohydrates to enhance absorption

most studies say that caffeine and creatine should not be taken at the same time as they compete against each other

I was a vegetarian/vegan for 10 years, and both my physical and cognitive abilities gradually declined towards the end of that period
I have been supplementing with creatine mono for the last few weeks and I have noticed a remarkable increase both my physical and
cognitive abilities. I have also noticed an improvement in my general sense of well-being

I have tried nearly all of the racetams and to be honest they didn't do much for me, some of them made my symptoms worse

creatine fuels both the muscles and the brain, try it, you might be surprised

Interesting thread... made me reconsider supplementing with creatine. Altough I dont like the weight gain from the water retention.

There is 2010 paper showing that creatine monophosphate reduces the BOLD response by 16% incrases memory span by 26% (And these were not vegetarians). They supplemented with 20 g/day for five days, followed by two additional days at a dose of 5 g/day and then run the MRIs.

I wonder whether this means that the brain has a higher "anaerobic" capacity. E.g. beneficial for people that are often exposed to hypoxic conditions e.g. smokers, people that inproperly breath while working out and so on... Maybe it generally reduces oxidative stress because it gives the mitochondria a break?

"Dietary supplementation of creatine monohydrate reduces the human fMRI BOLD signal"

Creatine monohydrate is an organic acid that plays a key role in ATP re-synthesis. Creatine levels in the human brain vary considerably and dietary supplementation has been found to enhance cognitive performance in healthy individuals. To explore the possibility that the fMRI Blood Oxygen Level Dependent (BOLD) response is influenced by creatine levels, BOLD responses to visual stimuli were measured in visual cortex before and after a week of creatine administration in healthy human volunteers. The magnitude of the BOLD response decreased by 16% following creatine supplementation of a similar dose to that previously shown to increase cerebral levels of phosphocreatine. We also confirmed that cognitive performance (memory span) is increased. These changes were not found in a placebo group. Possible mechanisms of BOLD change are considered. The results offer potential for insight into the coupling between neural activity and the BOLD response and the more immediate possibility of accounting for an important source of variability during fMRI analysis in clinical studies and other investigations where between-subjects variance is an issue.

In order to verify previous reports of cognitive enhancement following Cr supplementation we also measured performance on the Backwards Digit Span (BDS) [28] and Raven's Advanced Progressive Matrices (RAPM) [24] prior to each scan. The BDS comprises a set of number sequences of increasing length with two different sequences of each length. Subjects were required to repeat each sequence backwards. The test was terminated when the subject failed to repeat two sequences of the same length. Different number sequences were used for the two testing sessions. Subjects were required to complete as many items of the RAPM as possible in 5 min. Since the RAPM tests are ordered in terms of difficulty, odd-numbered and even-numbered tests were administered on weeks 1 and 2 respectively. Whilst we did not counterbalance administration of odd and even-numbered tests, the differential difficulty between contiguous tests is small and our analyses revealed that there was no significant difference in performance in the placebo condition across weeks (t = 0.773, df = 10, p = 0.457), nor was there a significant difference in performance between creatine and placebo groups in week 1 (t = 0.187, df = 20, p = 0.854).

There is a number of plausible mechanisms by which increased Cr levels may reduce the BOLD response. Three possibilities are (1) Cr elevation reduces metabolic demand (by elevating PCr) and the stimulus-related change in CBF is consequently reduced. However, there is considerable evidence to suggest that such a straightforward coupling of CBF and neuro-metabolic activity is unlikely [1] and [2]. (2) Cr influences the mechanisms of the vascular response with no attendant change in metabolic demand. This is akin to suggesting that Cr increases basal perfusion whilst not affecting neural activity. It is possible that Cr's effect on astrocyte metabolism could yield relatively direct vascular changes [14] and there is good evidence that the BOLD response is modulated by basal state [6]. Thus we cannot rule out the possibility that our results reflect an increase in basal perfusion and no, or a proportionately smaller, change in BOLD response. However, studies of the relation between basal state and BOLD magnitude have used hypercapnic and other manipulations that exclusively modulate perfusion. Cr's ubiquity and physiological properties render it unlikely to have an exclusively vascular effect. (3) Cr enhances the normally relatively low uptake of available O₂ (thus reducing the ratio of oxy- to deoxy-haemoglobin). Cr may lead to an increase in CMRO₂ by providing a more direct and abundant energetic pool for oxidative glycolysis, reducing O₂ levels and therefore the BOLD response. If this is the case, our results represent an increase in aerobic metabolic activity coupled with a decrease in the BOLD response and imply that the amount of freely available ATP in the brain is not tightly coupled with the haemodynamic response. This interpretation of the BOLD reduction is plausible since (1) Cr is known to increase oxidation in skeletal muscle [8] and (2) there is considerable evidence for a decoupling of CBF and metabolic rate [1] and [2]. However, other plausible possibilities exist such as a more direct neuromodulatory effect, since Cr has recently been implicated in modulation of both glutamatergic and GABAergic function [26] and [17], and further work will be required to resolve the issue.
Regardless of the underlying cause, the substantial reduction in the BOLD response following Cr supplementation may have general consequences for the interpretation of fMRI data. Endogenous levels of PCr and ATP vary across the brain and oral Cr supplementation has been shown to yield region-dependent elevation in Cr levels [21] and [10]. The coupling of BOLD to Cr supplementation that we find suggests that meaningful comparison of responses in different areas of the brain requires consideration of the relative levels of PCr across regions. Indeed, it has recently been reported that similar changes in energy metabolism in the lentiform nuclei and visual cortex result in substantially lower BOLD response in the former sub-cortical region [1] and that levels of PCr in the striatum are substantially lower than in cortical areas [21]. Moreover, dietary dependent [11] and independent [3] variations in Cr levels may well be a major source of between-subjects variance in fMRI. If so, careful control could potentially yield real benefits in terms of across-subject statistical signal detection, particularly in studies that compare BOLD responses in different populations. Differences in the shape of the BOLD signal across subjects have often been observed [16] and, given that Cr acts as both a spatial and temporal buffer for ATP, it is conceivable that dietary intake of Cr might contribute to such differences in temporal dynamics as well as response amplitude.
The Cr-induced reduction in BOLD may also bear upon clinical intervention and interpretation in Alzheimer's disease (AD). It has previously been suggested that Cr may hold promise in the treatment of AD [7] and our current results are certainly encouraging in this respect. The effects of Cr administration we find in healthy humans – reduced BOLD response and enhanced memory – are the reverse of those found in pre-symptomatic humans at high risk of developing AD by virtue of carrying the APOE e4 allele [5] and [4]. Whether Cr supplementation will have any significant therapeutic effect in Alzheimer's is unknown. However the current results, together with Cr's lack of toxicity and low cost make it an attractive potential therapeutic agent, and investigation of this therapeutic potential and its ability to inform clinical interpretation is clearly a priority.
In summary, we have shown that Cr supplementation reduces the fMRI BOLD response by 16% whilst increasing memory span by 26%. The cause is unknown, but a possible mechanism is an increase in cerebral glucose oxidation or basal perfusion. Whilst it is generally assumed that the larger the BOLD response, the greater the underlying neural activity, our reasoning suggests that a reduction in BOLD may occur in response to an increase in oxidative glycolysis. If so, the amount of freely available ATP in the brain may not be tightly coupled with the haemodynamic response. Regardless of the precise mechanism of action, variation in brain Cr may explain some of the between-subjects variance in BOLD responses across a wide range of studies and holds great promise as a probe compound for investigating the nature of the BOLD signal.

Edited by Jim Morrison, 28 July 2013 - 08:33 PM.

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