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Glucose and ADD


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#1 chrono

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Posted 03 September 2010 - 05:30 PM


It is well established that ADD is the result of decficit metabolism in central regions of the brain and that stimulant rectify this problem through increased dopamine. Hence carbos are causing a tranisent ADD.

ADD is not caused by 'decficit metabolism,' and eating a heavy meal causes nothing like its dopaminergic deficiency.

OTOH, if it is indeed 'well established,' feel free to post some references.


[this topic split from How about insulin and cognitive ability?]

Edited by chrono, 10 September 2010 - 12:45 PM.


#2 NR2(x)

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Posted 03 September 2010 - 10:15 PM

Fair enough, just dumped some material

http://grande.nal.us....&therow=228518
QUOTE
The stimulation of D1 and D2 dopamine (DA) receptors by selective agonists produced large increases in brain glucose concentrations. D2 receptor stimulation also produced large increases in blood glucose.

Dopamine agonist treatment ameliorates hyperglycemia, hyperlipidemia, and the elevated basal insulin release

Serotonin mediates rapid changes of striatal glucose and lactate metabolism after systemic 3,4-methylenedioxymethamphetamine (MDMA, “Ecstasy”) administration in awake rats
http://www.sciencedi...bfaa53cbdf97794
QUOTE
A single dose of MDMA (2–10–20 mg/kg i.v.) evoked a transient increase of interstitial glucose concentrations in striatum (139–223%) with rapid onset and of less than 2 h duration, a concomitant but more prolonged lactate increase (>187%) at the highest MDMA dose and no significant depletions of striatal serotonin. Blood glucose and lactate levels were also transiently elevated (163 and 135%) at the highest MDMA doses. The blood glucose rises were significantly related to brain glucose and brain lactate changes. The metabolic perturbations in striatum and the hyperthermic response (+1.1 °C) following systemic MDMA treatment were entirely blocked in p-chlorophenylalanine pre-treated rats, indicating that these effects are mediated by endogenous serotonin


Regional brain glucose metabolism: Correlations to biochemical measures and anxiety in patients with schizophrenia
http://www.sciencedi...d5b71a231922bcd
QUOTE
In all subjects, positive correlations were found between the level of anxiety and the regional glucose metabolism.

http://www.ncbi.nlm..../pubmed/8489322
QUOTE
Global or absolute measures of metabolism did not statistically differ between groups, although hyperactive girls had a 17.6% lower absolute brain metabolism than normal girls. As compared with the values for the controls, normalized glucose metabolism was significantly reduced in six of 60 specific regions of the brain, including an area of the left anterior frontal lobe (P < .05). Lower metabolism in that specific region of the left anterior frontal lobe was significantly inversely correlated with measures of symptom severity (P < .001-.009, r = -.56 to -.67).

http://www.ncbi.nlm....pubmed/11513813
QUOTE
Quote:
At least some forms of ADHD may be viewed as cortical, energy-deficit syndromes secondary to catecholamine-mediated hypofunctionality of astrocyte glucose and glycogen metabolism, which provides activity-dependent energy to cortical neurons. Several tests of this hypothesis are proposed.

Relationship between personality trait and regional cerebral glucose metabolism assessed with positron emission tomography
http://www.ncbi.nlm....pubmed/12270587
QUOTE
There have been no studies systematically investigating relationships between biogenetic temperament dimensions and patterns of brain glucose metabolism. Nineteen healthy subjects were evaluated regarding the biogenetic temperament using Cloninger's Temperament and Character Inventory (TCI). In addition, [18F] fluorodeoxyglucose (FDG) positron emission tomography (PET) was used to measure regional brain glucose metabolism. Voxel-based correlation analysis was used to test correlations between regional brain glucose metabolism and scores on the TCI. We identified that each temperament dimension, such as Novelty Seeking, Harm Avoidance, and Reward Dependence, was significantly correlated with specific brain regions. The majority of correlations were observed in the areas of paralimbic regions and temporal lobes. The current study provides evidence linking each biogenetic temperament dimension with specific brain areas and provides a promising base for future personality research.

here is evidence that patients with major depression have reduced blood flow and metabolism in the prefrontal cortex, particularly when they exhibit psychomotor retardation. Abnormalities are also found in the anterior cingulate gyrus and the basal ganglia

Mood disorders may be associated with global and regional changes in cerebral blood flow and metabolism. The accumulated functional neuroimaging findings in mood disorders were reviewed in order to examine a proposed neuroanatomic model of pathophysiology. Global cerebral blood flow and glucose metabolism appear normal, but may be decreased in late-life depression. Regional cerebral blood flow and glucose metabolism deficits are present, and may be indicators of brain regions participating in neuroanatomic circuits involved in mood disorders. Decreased pre-frontal cortex blood flow and metabolism in depressed unipolar and bipolar patients are the most consistently replicated findings, and correlate with severity of illness. Basal ganglia abnormalities have been found in depressed unipolar and bipolar patients, involving decreased blood flow and metabolism. Temporal lobe abnormalities are present in bipolar disorder patients, and perhaps unipolar depression. There is conflicting evidence of abnormalities in other limbic regions. Cognitive impairment may correlate with decreased metabolism in frontal and cerebellar areas. The relationship between functional neuroimaging findings and clinical course, and therefore state and trait characteristics, has not been systematically investigated. Antidepressant medications, but not ECT, seem to reverse some of the identified functional brain changes in the depressed state. The structural, neurotransmitter and neuropathological correlates of these functional abnormalities are yet to be determined. Functional abnormalities in frontal, subcortical and limbic structures appear to be part of the pathoph

Glycolysis regulates the induction of lactate utilization for synaptic potentials after hypoxia in the granule cell of guinea pig hippocampus.
http://www.ncbi.nlm....pubmed/15567484
QUOTE
Lactate is considered an alternative substrate that is capable of replacing glucose in maintaining synaptic function in adult neurons. But, we found recently that lactate could be utilized for maintenance of synaptic potentials only after the activation of NMDA and voltage-dependent-calcium channel during glucose deprivation. To clarify more on the relationship between glycolysis and induction of lactate utilization, we tested lower concentration of glucose with hypoxia to induce a relative shortage of anaerobic energy production. Population spikes are not maintained with lactate following hypoxia in 10 mM glucose medium, but are maintained at their original levels with lactate after exposure to hypoxia in lower concentration (5 mM) of glucose. Hypothermia during low glucose-hypoxia, bath application of the NMDA channel blocker and the voltage-sensitive calcium channel blocker, as well as the omission of extracellular calcium prevented the induction of the lactate-supported population spikes. ATP levels in the tissue slices are relatively preserved in the conditions that block the induction of lactate-supported population spikes. From these observations, we propose that the energy source for maintenance of synaptic function in adult neuron changes from adult form (glucose alone) to immature one (glucose and/or lactate) after short of glucose supply.
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#3 chrono

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Posted 10 September 2010 - 10:21 AM

Fair enough, just dumped some material

Thanks for being willing to post some refs supporting your claim, it's honestly greatly appreciated. The two pubmed articles are perhaps the most compelling, along with the one linking dopamine and glucose. I wasn't aware that there was such a direct link, but it suggests an obvious mechanism (beyond the slight dopamine boost) for why ALCAR has been shown to be beneficial for ADD.

However, based on this, I still don't think it's reasonable to say that it's generally accepted that ADD is the result of deficient metabolism. The review lists several indications before the one you quoted, which I'm certain have other possible contributing etiologies.

Edited by chrono, 10 September 2010 - 12:46 PM.


#4 NR2(x)

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Posted 10 September 2010 - 11:50 AM

Ill get back to this thread in the next day and right up the direct linkage between the energy metabolism and dopamine. Also I will show that most neurological disease are typified by deficit metabolism, bring us to the chicken and egg dilemma. But it should provide a context to understand how and why various nootropics work although often indirectly

#5 medievil

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Posted 10 September 2010 - 11:56 AM

On mind and muscle there recently was a thread discussing the link with glucose/oxygen and several mental disorders, there's a massive list of references in there.

http://www.mindandmu...showtopic=42450

There ARE glucose problems in ADHD but as references show D2 agonism for example increases glucose uptake, as we've seen ADHD patients have a dopamine and norepinephrine defiency:

J Clin Psychopharmacol. 2008 Jun;28(3 Suppl 2):S39-45.
Catecholamine dysfunction in attention-deficit/hyperactivity disorder: an update.
Prince J.

Department of Child Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. jprince@partners.org
Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous disease that affects children, adolescents, and adults. Genetic research has confirmed that there is a large hereditary component to this condition and has helped identify some of the genes associated with it. Among these are several genes associated with the catecholaminergic system including the dopamine receptor genes (DRD4 and DRD5), the dopamine transporter gene, and the gene for dopamine beta-hydroxylase, which catalyzes conversion of dopamine to norepinephrine. Attention-deficit/hyperactivity disorder is believed to be a result of abnormalities in the frontal regions of the brain, particularly the prefrontal cortex and associated subcortical structures and circuits. Underpinning these abnormalities are disturbances of catecholamine neurotransmission. Studies have demonstrated that patients with ADHD have depleted levels of dopamine and norepinephrine thought to be largely the result of dysfunction of their respective transporter systems. The efficacy of stimulant agents confirms that the neurotransmitter abnormalities seen in ADHD are primarily catecholaminergic in origin. This article focuses on the catecholaminergic networks of higher cognitive functions such as attention and focus and of motor functions that may be associated with such networks, reviewing both the physiology of such functions and the pathophysiology of ADHD. Researchers are currently investigating whether other neurotransmitter systems may be partially involved and are investigating whether agents that affect these other systems will prove complementary to currently used treatments.

This defiency in dopamine and norepinephrine can indirectly cause problems in glucose uptake and thus show a association between glucose and ADHD, however that doesnt mean that ADHD is caused by a deficit in glucose.

The dopamine receptor genes (DRD4 and DRD5), the dopamine transporter gene, and the gene for dopamine beta-hydroxylase have been associated with ADHD, indicating that glucose utilisation isnt the cause of ADHD but rather just a downstream effect.

Edited by medievil, 10 September 2010 - 12:44 PM.

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#6 Pike

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Posted 10 September 2010 - 06:23 PM

so ADHD could actually be a glucose problem that leads to the major irregularities in the prefrontal cortex?

this is definitely an interesting topic for me. i really hope this thread develops. once my renewed ID goes through, i'll have access to my libraries database subscriptions again and i'll see what i can dig up on this.

#7 chrono

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Posted 11 September 2010 - 01:35 AM

If you haven't, I'd definitely recommend checking out the thread medievil linked to. keroloydi did some excellent research summaries that may give you some starting points.

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#8 NR2(x)

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Posted 11 September 2010 - 02:53 AM

The Mind and muscle post is excellent, I scavanged that material from there. Im hoping to show the biochemical pathways involved and how it all joins together, which that post doesnt quite do.
It would be nice to have a singlar rationale to base regieme design on.

I was told that when you exercise there is a substantial electrical energy transfer from the brain to the body. Estimates were over twenty percent of mechanical work being derived from the brain. So brain fitness maybe a real concept.




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