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Red Light Improves Mental Function

Also see:
Light is Right
Fat Deficient Animals – Activity of Cytochrome Oxidase
Glucocorticoids, Cytochrome Oxidase, and Metabolism
“Curing” a High Metabolic Rate with Unsaturated Fats
PUFA, Aging, Cytochrome Oxidase, and Cardiolipin
Blue Light, Cytochrome Oxidase, and Eye Injury
Get a “Chicken Light” and Amp Up Your Energy!
Using Sunlight to Sustain Life

BR40 250W Bulb and 10'' Metal Brooder

“Getting a generous amount of light on the head has beneficial effects on mental function, by increasing the activity of cytochrome oxidase (Rojas, et al., 2012) and reducing inflammation.” -Ray Peat, PhD

J Alzheimers Dis. 2012;32(3):741-52. doi: 10.3233/JAD-2012-120817.
Low-level light therapy improves cortical metabolic capacity and memory retention.
Rojas JC, Bruchey AK, Gonzalez-Lima F.
Cerebral hypometabolism characterizes mild cognitive impairment and Alzheimer’s disease. Low-level light therapy (LLLT) enhances the metabolic capacity of neurons in culture through photostimulation of cytochrome oxidase, the mitochondrial enzyme that catalyzes oxygen consumption in cellular respiration. Growing evidence supports that neuronal metabolic enhancement by LLLT positively impacts neuronal function in vitro and in vivo. Based on its effects on energy metabolism, it is proposed that LLLT will also affect the cerebral cortex in vivo and modulate higher-order cognitive functions such as memory. In vivo effects of LLLT on brain and behavior are poorly characterized. We tested the hypothesis that in vivo LLLT facilitates cortical oxygenation and metabolic energy capacity and thereby improves memory retention. Specifically, we tested this hypothesis in rats using fear extinction memory, a form of memory modulated by prefrontal cortex activation. Effects of LLLT on brain metabolism were determined through measurement of prefrontal cortex oxygen concentration with fluorescent quenching oximetry and by quantitative cytochrome oxidase histochemistry. Experiment 1 verified that LLLT increased the rate of oxygen consumption in the prefrontal cortex in vivo. Experiment 2 showed that LLLT-treated rats had an enhanced extinction memory as compared to controls. Experiment 3 showed that LLLT reduced fear renewal and prevented the reemergence of extinguished conditioned fear responses. Experiment 4 showed that LLLT induced hormetic dose-response effects on the metabolic capacity of the prefrontal cortex. These data suggest that LLLT can enhance cortical metabolic capacity and retention of extinction memories, and implicate LLLT as a novel intervention to improve memory.

“Rats had a bright red laser beam shined on their heads for 15 minutes and then the respiratory enzymes of the Krebs cycle was studied. The changes were consistent with enhanced respiration. (A.T. Pikulev, et al., Radiobiology 24(1):29-34, 1984).” -Ray Peat, PhD

Radiobiologiia. 1984 Jan-Feb;24(1):29-34.
[Enzyme activity of glutamic acid metabolism and the Krebs cycle in the brain of rats laser-irradiated against a background of altered adrenoreceptor function].
[Article in Russian]
Pikulev AT, Dzhugurian NA, Zyrianova TN, Lavrova VM, Mostovnikov VA.
In the in vivo experiments it was demonstrated that the effect of a helium-neon laser (lambda = 632.8 nm), at the background of altered functional status of adrenoreceptors, changes the activity of some enzymes of the glutamic acid metabolism and the Krebs cycle. This may be attributed to both the direct effect of laser radiation and the indirect effect via the adrenergic system.

“Cytochrome oxidase in the brain can also be increased by mental stimulation, learning, and moderate exercise, but excessive exercise or the wrong kind of exercise (“eccentric”) can lower it (Aguiar, et al., 2007, 2008), probably by increasing the stress hormones and free fatty acids.” -Ray Peat, PhD

Neurosci Lett. 2007 Oct 22;426(3):171-4. Epub 2007 Sep 4.
Mitochondrial IV complex and brain neurothrophic derived factor responses of mice brain cortex after downhill training.
Aguiar AS Jr, Tuon T, Pinho CA, Silva LA, Andreazza AC, Kapczinski F, Quevedo J, Streck EL, Pinho RA.
Twenty-four adult male CF1 mice were assigned to three groups: non-runners control, level running exercise (0 degrees incline) and downhill running exercise (16 degrees decline). Exercise groups were given running treadmill training for 5 days/week over 8 weeks. Blood lactate analysis was performed in the first and last exercise session. Mice were sacrificed 48 h after the last exercise session and their solei (citrate synthase activity) and brain cortices (BDNF levels and cytochrome c oxidase activity) were surgically removed and immediately stored at -80 degrees C for later analyses. Training significantly increased (P<0.05) citrate synthase activity when compared to untrained control. Blood lactate levels classified the exercise intensity as moderate to high. The downhill exercise training significantly reduced (P<0.05) brain cortex cytochrome c oxidase activity when compared to untrained control and level running exercise groups. BDNF levels significantly decreased (P<0.05) in both exercise groups.

Neurochem Res. 2008 Jan;33(1):51-8. Epub 2007 Jul 6.
Intense exercise induces mitochondrial dysfunction in mice brain.
Aguiar AS Jr, Tuon T, Pinho CA, Silva LA, Andreazza AC, Kapczinski F, Quevedo J, Streck EL, Pinho RA.
There are conflicts between the effects of free radical over-production induced by exercise on neurotrophins and brain oxidative metabolism. The objective of this study was to investigate the effects of intense physical training on brain-derived neurotrophic factor (BDNF) levels, COX activity, and lipoperoxidation levels in mice brain cortex. Twenty-seven adult male CF1 mice were assigned to three groups: control untrained, intermittent treadmill exercise (3 x 15 min/day) and continuous treadmill exercise (45 min/day). Training significantly (P < 0.05) increased citrate synthase activity when compared to untrained control. Blood lactate levels classified the exercise as high intensity. The intermittent training significantly (P < 0.05) reduced in 6.5% the brain cortex COX activity when compared to the control group. BDNF levels significantly (P < 0.05) decreased in both exercise groups. Besides, continuous and intermittent exercise groups significantly (P < 0.05) increased thiobarbituric acid reactive species levels in the brain cortex. In summary, intense exercise promoted brain mitochondrial dysfunction due to decreased BDNF levels in the frontal cortex of mice.

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Light therapy and muscle endurance.

Photochem Photobiol. 2010 May-Jun;86(3):673-80. doi: 10.1111/j.1751-1097.2010.00732.x. Epub 2010 Apr 16.
In vivo low-level light therapy increases cytochrome oxidase in skeletal muscle.
Hayworth CR, Rojas JC, Padilla E, Holmes GM, Sheridan EC, Gonzalez-Lima F.
Low-level light therapy (LLLT) increases survival of cultured cells, improves behavioral recovery from neurodegeneration and speeds wound healing. These beneficial effects are thought to be mediated by upregulation of mitochondrial proteins, especially the respiratory enzyme cytochrome oxidase. However, the effects of in vivo LLLT on cytochrome oxidase in intact skeletal muscle have not been previously investigated. We used a sensitive method for enzyme histochemistry of cytochrome oxidase to examine the rat temporalis muscle 24 h after in vivo LLLT. The findings showed for the first time that in vivo LLLT induced a dose- and fiber type-dependent increase in cytochrome oxidase in muscle fibers. LLLT was particularly effective at enhancing the aerobic capacity of intermediate and red fibers. The findings suggest that LLLT may enhance the oxidative energy metabolic capacity of different types of muscle fibers, and that LLLT may be used to enhance the aerobic potential of skeletal muscle.

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