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. Author manuscript; available in PMC: 2012 Jan 13.
Published in final edited form as: Nutr Health. 2011;20(3-4):165–169. doi: 10.1177/026010601102000401

Collaborative effects of diet and exercise on cognitive enhancement

Fernando Gomez-Pinilla 1
PMCID: PMC3258096  NIHMSID: NIHMS347663  PMID: 22141190

The brain has a remarkable capacity for plasticity, which can be enhanced by appropriate stimulation. Growing evidence indicates that aspects of lifestyle encountered in our daily routine can determine the capacity of the brain to fight diseases and react to challenges. For example, now we know that certain types of dietary factors, such as omega-3 fatty acids and curcumin, can stimulate molecular systems that serve synaptic function, while diets rich in saturated fats do the opposite. In turn, exercise, using similar mechanisms as healthy diets, displays healing effects on the brain such as counteracting the mental decline associated with age (Hillman et al., 2008) and facilitating functional recovery resulting from brain injury and disease (Griesbach et al., 2004). Diet and exercise are two noninvasive approaches that can be used to enhance neural repair (Chytrova et al., 2009). Omega 3 fatty acids and curcumin elevate levels of molecules important for synaptic plasticity such as brain-derived neurotrophic factor (BDNF), thus benefiting normal brain function and recovery events following brain insults. BDNF is a neurotrophin that, in addition to regulate the survival, growth, and differentiation of neurons during development (Zuccato and Cattaneo, 2009), stimulates synaptic and cognitive plasticity in the adult brain (Nagappan and Lu, 2005). BDNF modulates the efficacy of synaptic transmission and hippocampal long-term potentiation (Nagappan and Lu, 2005), and learning and memory in animals (Lu et al., 2008) and humans (Egan et al., 2003). Recent findings that BDNF is associated with energy homeostasis are offering new possibilities to understand the action of diet and exercise on the brain, as diet and exercise are intimately related to energy metabolism. For example, recent evidence indicates that exercise-induced BDNF influences hippocampal synaptic plasticity by modulating cellular energy metabolism(Gomez-Pinilla et al., 2008).

The action of select nutritional factors in the brain

Omega-3

One of the most important forms of omega-3 fatty acids, docosahexaenoic acid (DHA) is a key component of neuronal membranes at sites of signal transduction at the synapse, such that its action is vital to brain structure and function (Gomez-Pinilla, 2008). Evidence suggests that DHA serves to improve neuronal function by supporting synaptic membrane fluidity (Suzuki et al., 1998), and regulating gene expression and cell signaling (Salem et al., 2001). Because the inefficiency of mammals to produce DHA, consumption of dietary DHA is critical for proper neuronal function and promoting resistance to neurological disorders (Wu et al., 2004, Wu et al., 2007, Ma et al., 2009). The capacity of DHA to increase molecules associated with synaptic function such as the BDNF system and to normalize oxidative stress appear crucial for the healing effects of DHA after brain disorders (Wu et al., 2007, 2008).

Curcumin

Curcumin is a major component of turmeric (Curcuma longa) and a commonly used spice in Indian meals. Substantial evidence from in vitro studies indicates that curcumin has antioxidant, anti-inflammatory activities (Menon and Sudheer, 2007). Curcumin as well as DHA has been shown to attenuate degenerative events in Alzheimer's disease mice model with advanced amyloid accumulation (Ma et al., 2009). In addition, curcumin dietary supplementation has been shown to reduce the effects of experimental concussive injury on cognitive function tasks involving the action of BDNF on synaptic plasticity (Wu et al., 2006). In addition, an important aspect of the healing power of curcumin seems to rely on its capacity to normalize energy homeostasis that is disrupted under trauma conditions (Sharma et al., 2009).

Collaborative effects of diet and exercise

Exercise has the capacity to enhance learning and memory under a variety of conditions, from counteracting the mental decline that comes with age (Hillman et al., 2008) to facilitating functional recovery after brain injury and disease (Vaynman and Gomez-Pinilla, 2005). Much like a healthy diet, physical activity can benefit neuronal function by increasing BDNF levels and reducing oxidative stress. More specifically, exercise plays an important role in the maintenance of the synaptic structure (Vaynman et al., 2004), axonal elongation (Molteni et al., 2004), and neurogenesis in the adult brain (van Praag et al., 1999). Exercise applied after experimental traumatic brain injury has also been shown to have beneficial effects but these effects seem to depend on the post-injury resting period and the severity of the injury(Griesbach et al., 2007).

Given the ability of exercise to augment BDNF levels, exercise may be an effective adjuvant therapy to balance the effects of dietary choices. In particular, it has been found in rats that exercise counteracts the decrease in hippocampal BDNF, synaptic plasticity, and cognitive function due to the consumption of a diet high in saturated-fat and sucrose (Molteni et al., 2004). In turn, the effects of the combined application of a healthy diet and exercise can promote enhanced beneficial effects on brain healing and plasticity than when either option is implemented by separate. For example, exercise is capable of boosting the healthy effects of omega-3 fatty acids on synaptic plasticity and cognition (Wu et al., 2008). The combination of experiences and various types of nutrients is a common attribute of our daily living. It is remarkable that new advances in molecular biology indicate that nutrients and experiences share common mechanisms that seem to have complementary effects on brain function. The challenge is how to take advantage of this capacity in order to boost brain health and plasticity as well as to counteract the source of neurological disorders.

Acknowledgements

This work was supported by National Institute of Health Grants NS50465 and NS56413.

References

  1. Chytrova G, Ying Z, Gomez-Pinilla F. Exercise contributes to the effects of DHA dietary supplementation by acting on membrane-related synaptic systems. Brain Res. 2009 doi: 10.1016/j.brainres.2009.05.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Egan MF, Kojima M, Callicott JH, Goldberg TE, Kolachana BS, Bertolino A, Zaitsev E, Gold B, Goldman D, Dean M, Lu B, Weinberger DR. The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function. Cell. 2003;112:257–269. doi: 10.1016/s0092-8674(03)00035-7. [DOI] [PubMed] [Google Scholar]
  3. Gomez-Pinilla F. Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci. 2008;9:568–578. doi: 10.1038/nrn2421. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Gomez-Pinilla F, Vaynman S, Ying Z. Brain-derived neurotrophic factor functions as a metabotrophin to mediate the effects of exercise on cognition. Eur J Neurosci. 2008;28:2278–2287. doi: 10.1111/j.1460-9568.2008.06524.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Griesbach GS, Gomez-Pinilla F, Hovda DA. Time window for voluntary exercise-induced increases in hippocampal neuroplasticity molecules after traumatic brain injury is severity dependent. J Neurotrauma. 2007;24:1161–1171. doi: 10.1089/neu.2006.0255. [DOI] [PubMed] [Google Scholar]
  6. Griesbach GS, Hovda DA, Molteni R, Wu A, Gomez-Pinilla F. Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function. Neuroscience. 2004;125:129–139. doi: 10.1016/j.neuroscience.2004.01.030. [DOI] [PubMed] [Google Scholar]
  7. Hillman CH, Erickson KI, Kramer AF. Be smart, exercise your heart: exercise effects on brain and cognition. Nat Rev Neurosci. 2008;9:58–65. doi: 10.1038/nrn2298. [DOI] [PubMed] [Google Scholar]
  8. Lu Y, Christian K, Lu B. BDNF: a key regulator for protein synthesis-dependent LTP and long-term memory? Neurobiol Learn Mem. 2008;89:312–323. doi: 10.1016/j.nlm.2007.08.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Ma QL, Yang F, Rosario ER, Ubeda OJ, Beech W, Gant DJ, Chen PP, Hudspeth B, Chen C, Zhao Y, Vinters HV, Frautschy SA, Cole GM. Beta-amyloid oligomers induce phosphorylation of tau and inactivation of insulin receptor substrate via c-Jun N-terminal kinase signaling: suppression by omega-3 fatty acids and curcumin. J Neurosci. 2009;29:9078–9089. doi: 10.1523/JNEUROSCI.1071-09.2009. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Menon VP, Sudheer AR. Antioxidant and anti-inflammatory properties of curcumin. Adv Exp Med Biol. 2007;595:105–125. doi: 10.1007/978-0-387-46401-5_3. [DOI] [PubMed] [Google Scholar]
  11. Molteni R, Zheng JQ, Ying Z, Gomez-Pinilla F, Twiss JL. Voluntary exercise increases axonal regeneration from sensory neurons. Proc Natl Acad Sci U S A. 2004;101:8473–8478. doi: 10.1073/pnas.0401443101. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Nagappan G, Lu B. Activity-dependent modulation of the BDNF receptor TrkB: mechanisms and implications. Trends Neurosci. 2005;28:464–471. doi: 10.1016/j.tins.2005.07.003. [DOI] [PubMed] [Google Scholar]
  13. Salem N, Jr., Litman B, Kim HY, Gawrisch K. Mechanisms of action of docosahexaenoic acid in the nervous system. Lipids. 2001;36:945–959. doi: 10.1007/s11745-001-0805-6. [DOI] [PubMed] [Google Scholar]
  14. Sharma S, Zhuang Y, Ying Z, Wu A, Gomez-Pinilla F. Dietary curcumin supplementation counteracts reduction in levels of molecules involved in energy homeostasis after brain trauma. Neuroscience. 2009;161:1037–1044. doi: 10.1016/j.neuroscience.2009.04.042. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Suzuki H, Park SJ, Tamura M, Ando S. Effect of the long-term feeding of dietary lipids on the learning ability, fatty acid composition of brain stem phospholipids and synaptic membrane fluidity in adult mice: a comparison of sardine oil diet with palm oil diet. Mech Ageing Dev. 1998;101:119–128. doi: 10.1016/s0047-6374(97)00169-3. [DOI] [PubMed] [Google Scholar]
  16. van Praag H, Christie BR, Sejnowski TJ, Gage FH. Running enhances neurogenesis, learning, and long-term potentiation in mice. Proc Natl Acad Sci U S A. 1999;96:13427–13431. doi: 10.1073/pnas.96.23.13427. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Vaynman S, Gomez-Pinilla F. License to run: exercise impacts functional plasticity in the intact and injured central nervous system by using neurotrophins. Neurorehabil Neural Repair. 2005;19:283–295. doi: 10.1177/1545968305280753. [DOI] [PubMed] [Google Scholar]
  18. Vaynman S, Ying Z, Gomez-Pinilla F. Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition. Eur J Neurosci. 2004;20:2580–2590. doi: 10.1111/j.1460-9568.2004.03720.x. [DOI] [PubMed] [Google Scholar]
  19. Wu A, Ying Z, Gomez-Pinilla F. Dietary curcumin counteracts the outcome of traumatic brain injury on oxidative stress, synaptic plasticity, and cognition. Exp Neurol. 2006;197:309–317. doi: 10.1016/j.expneurol.2005.09.004. [DOI] [PubMed] [Google Scholar]
  20. Wu A, Ying Z, Gomez-Pinilla F. Omega-3 fatty acids supplementation restores mechanisms that maintain brain homeostasis in traumatic brain injury. J Neurotrauma. 2007;24:1587–1595. doi: 10.1089/neu.2007.0313. [DOI] [PubMed] [Google Scholar]
  21. Wu A, Ying Z, Gomez-Pinilla F. Docosahexaenoic acid dietary supplementation enhances the effects of exercise on synaptic plasticity and cognition. Neuroscience. 2008;155:751–759. doi: 10.1016/j.neuroscience.2008.05.061. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Wu A, Ying Z, Gómez-Pinilla F. Dietary Omega-3 fatty acids normalize BDNF levels, reduce oxidative damage, and counteract learning disability after traumatic brain injury in rats. J Neurotrauma. 2004;21:1457–1467. doi: 10.1089/neu.2004.21.1457. [DOI] [PubMed] [Google Scholar]
  23. Zuccato C, Cattaneo E. Brain-derived neurotrophic factor in neurodegenerative diseases. Nat Rev Neurol. 2009;5:311–322. doi: 10.1038/nrneurol.2009.54. [DOI] [PubMed] [Google Scholar]

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