I've heard that the brain's energy requirements represent about 20-25% of an individual's basal metabolic rate.

I'd like to know how much energy thinking/learning/reasoning requires. I would imagine it's significant at high levels of cognition due to the amount of energy it takes to reset a neuron. I would also imagine it varies greatly.

I've searched Entrez for related research articles, but I haven't been able to find any.

I've been able to find studies relating macronutrient consumption to cognitive performance, but that's not what I'm looking for.

Does anyone have any information that could help me?

...found this at

http://www.popsci.com/popsci/science/61994...ecbccdrcrd.html

By Melissa A. Calderone | July 2006


Need to lose some flab? Sit your big butt down with a math book—and feel the burn. The human brain is a 24-hour workhorse. While you’re thinking, millions of neurons fire messages back and forth to each other and to the various tissues in the body. These neurons need fuel, consuming a full 75 percent of the blood sugar from the liver and 20 percent of the body’s total used oxygen. Here’s how your neurons feed: Astrocytes—the cells near the capillary walls in your brain—suck energy-rich glucose from the bloodstream and convert it into a form that the neurons can soak up. The neurons then use it to fuel the production of neurotransmitters and, eventually, conscious thought. “The more energy an area of the brain wants, the more glucose that part of the brain will break down,” explains neurologist Harry Chugani of the Children’s Hospital of Michigan. “So yes, if you’re thinking really hard and really struggling with your thoughts, the neurons in the frontal lobes of your brain will be burning a lot more glucose.”

Simply to survive, your brain requires a tenth of a calorie per minute. Compare this with a walk to the doughnut shop, when your body burns approximately four calories a minute. Kickboxing zaps 10 calories a minute. And when you’re hunched over a crossword puzzle? Your brain is blasting through a respectable 1.5 calories a minute. Pass the Cheetos.

Here is an interesting one

The selfish brain: competition for energy resources. Prog Brain Res. 2006;153:129-40.

Although the brain constitutes only 2% of the body mass, its metabolism accounts for 50% of total body glucose utilization. This delicate situation is aggravated by the fact that the brain depends on glucose as energy substrate. Thus, the contour of a major problem becomes evident: how can the brain maintain constant fluxes of large amounts of glucose to itself in the presence of powerful competitors as fat and muscle tissue. Activity of cortical neurons generates an "energy on demand" signal which eventually mediates the uptake of glucose from brain capillaries. Because energy stores in the circulation (equivalent to ca. 5 g glucose) are also limited, a second signal is required termed "energy on request"; this signal is responsible for the activation of allocation processes. The term "allocation" refers to the activation of the "behavior control column" by an input from the hippocampus-amygdala system. As far as eating behavior is concerned the behavior control column consists of the ventral medial hypothalamus (VMH) and periventricular nucleus (PVN). The PVN represents the central nucleus of the brain's stress systems, the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). Activation of the sympatico-adrenal system inhibits glucose uptake by peripheral tissues by inhibiting insulin release and inducing insulin resistance and increases hepatic glucose production. With an inadequate "energy on request" signal neuroglucopenia would be the consequence. A decrease in brain glucose can activate glucose-sensitive neurons in the lateral hypothalamus (LH) with the release of orexigenic peptides which stimulate food intake. If the energy supply of the brain depends on activation of the LH rather than on increased allocation to the brain, an increase in body weight is evitable. An increase in fat mass will generate feedback signals as leptin and insulin, which activate the arcuate nucleus. Activation of arcuate nucleus in turn will stimulate the activity of the PVN in a way similar to the activation by the hippocampus-amydala system. The activity of PVN is influenced by the hippocampal outflow which in turn is the consequence of a balance of low-affinity and high-affinity glucocorticoid receptors. This set-point can permanently be displaced by extreme stress situations, by starvation, exercise, hormones, drugs or by endocrine-disrupting chemicals. Disorders in the "energy on request" process will influence the allocation of energy and in so doing alter the body mass of the organism. In this "selfish brain theory" the neocortex and the limbic system play a central role in the pathogenesis of diseases, such as anorexia nervosa, obesity and diabetes mellitus type II. From these considerations it appears that the primary disturbance in obesity is a displacement of the hippocampal set-point of the system. The resulting permanent activation of the feedback system must result in a likewise permanent activation of the sympatico-adrenal system, which induces insulin resistance, hypertension and the other components of the metabolic syndrome. Available therapies for treatment of the metabolic syndrome (blockade of alpha- and beta-adrenergic receptors, insulin and insulin secretagogues) interfere with mechanisms, which must be considered compensatory. This explains why these therapies are disappointing in the long run. New therapeutic strategies based on the "selfish brain theory" will be discussed.

Thanks Ironslave! Great article.

Here's the DOI:
http://dx.doi.org/10.1016/j.neubiorev.2004.03.002

lol then I blame my brain on why I am having trouble gaining weight at the gym