Food has often been seen as a means of energy, macros to hit or just plain things we eat, break down, and use to build muscle and recover from training. Let’s change the lens for which we currently see food as just being a source of energy to highlight foods ability to prevent against disease and dysfunction.
It is an exciting time for the field of neuroscience, as the past 5 years have revealed evidence of the influence of our diet on the integrity of brain function and cognition. But before we get into the exciting stuff, lets define a few key terms and concepts that will be important to know:
Cognition: Mental processes that include thinking, learning, perceiving, and remembering.
Synapse: A junction between two nerve cells that allows a signal to pass from one neuron to the next.
Synaptic Plasticity: The ability of synapses to strengthen or weaken over time in response to increases or decreases in their activity.
Brain Derived Neurotrophic Factor (BDNF): A protein that induces survival, development and function of neurons.
Animal Models: On average, the protein-coding regions of the mouse and human genomes are 85 percent identical; some genes are 99 percent identical while others are only 60 percent identical. (1) Due to similarity in genomes, we can understand why human and animals suffer from a lot of the same diseases such as cancer, atherosclerosis, and neurodegenerative diseases. This is not to say that mice, rodents, drosophila flies, rabbits, and other animals used in researched are an exact model, but they do allow scientists to make implications on what treatments may or may not work in humans. We often have to test a hypothesis treatment in animals multiple times before humans can even be brought into clinical trials.
Now that we have taken care of the semantics, let’s dive in…
I’ll start of by saying that this will be much shorter and more summarized than I’d like it to be, but this email would be about 20 pages long if I went into the deep details, so I have provided a list of sources at the end of this email in case you really want to go down the rabbit hole!
Diet and exercise play a crucial role in shaping the brains cognitive capacity. Our brains have evolved alongside food-derived signals that influence energy metabolism and synaptic function (communicative signals between nerve cells). This can be implied by looking at skull sizes from thousands of years ago. The size of an Australopithecus man-ape skull from 2-3 million years ago, is much smaller than the modern day homo sapien skull we find in cadavers today. Therefore, we see that humans brains have evolved with access to more food. (2)
Feeding Effect on Emotion and Cognition
We can probably attest from an anecdotal standpoint the effect of food on cognition and emotion. We’ve all felt that “hangry” state where literally everything and everyone is dead to us until we get our dang food. Before we even begin eating, all it takes is the sensory inputs of sight and smell of food to affect our emotional status.
Food also triggers peptides and hormones like insulin, leptin, ghrelin, glucagon-like peptide which all serve as visceral signals that can modulate cognition and body physiology through the hypothalamic-pituitary axis (HPA). The vagus nerve which originates at the brain and innervates the gut, sending neurotransmitters both ways, and enables gut activity to influence emotions and cognition. Overall, evidence seems to show that the 2 main ways food can affects cognition is through the neural pathways through the vagus nerve and the release of certain gut peptides into our bloodstream. (2).
Vagus Nerve – Mental Health is Gut Health, Olive Retreat Blog. October 11, 2018
Your brain requires A LOT of energy, relative to the rest of your body. So you can imagine that the energy transfer from foods to your brain cells is fundamental to its function and WHAT we feed ourselves is important for this reason. Quality of synaptic function can either insult or enhance metabolic energy of the brain. BDNF is a protein that serves as a great example of how molecules can affect both energy metabolism and synaptic function(3). We can find this protein in areas of the brain that are associated with cognitive and metabolic regulation(main). BDNF can also influence appetite suppression (4,5), insulin sensitivity, and glucose(6) and fat metabolism(7).
Now let’s talk nutrients…
This one may be beating a dead horse but we have all heard a time or 10 of how important getting our omegas in is for our brain. You can typically find our instagram foodie hash-tagging #brainfood when posting pictures of things like certain fish, salmon, and avocados.
Dietary deficiency of omega-3 fatty acids in humans has been associated with increased risk of several mental disorders, including ADHD, dyslexia, dementia, depression, bipolar disorder and schizophrenia, (2,8–12).
The Omega 3 fatty acid DHA is a particularly important component of the cell membrane, but our body’s are fairly inefficient at making DHA for itself, so we are reliant on dietary DHA. Dietary supplementation of DHA has been found to elevate levels of hippocampal BDNF. DHA might also act through its effects on metabolism, as DHA stimulates glucose utilization (13) and mitochondrial function(14), reducing oxidative stress.
For the sake of context, I will also mention that in rodent studies the effects of obesogenic foods, characterized by high contents of fat and sucrose, have shown a decline in cognitive performance and reduced levels of BDNF after only 3 weeks of consuming an obesogenic diet (15). These findings suggest that the diet had a direct effect on neurons that was independent of insulin resistance or obesity.
Folate and folic acid – AKA most of your green veggies
Folate or folic acid is found in various foods, including spinach, oranges and yeast. Adequate amounts of folate are essential for brain function, and folate deficiency can lead to neurological disorders, such as depression(15) and cognitive impairment. Folate supplementation either by itself (16,17) or in conjunction with other B vitamins (18,19) has been shown to be effective at preventing cognitive decline and dementia during aging (20). It is also worth the mention that a recent randomized clinical trial has shown that a 3-year folic acid supplementation can help to reduce the age-related decline in cognitive function.
Due to the fact that the brain has such a high metabolic load, it is very susceptible to oxidative stress or the imbalance of the production of free radicals (harmful) and the body’s ability to detoxify itself from them. ANTI oxidants are compounds that help to keep this balance and mitigate high levels of free radicals. Berries, for example, have been shown to have strong antioxidant capacity through the polyphenols they contain.
Alpha lipoic acid, which is found in meats such as kidney, heart and liver, and vegetables such as spinach, broccoli and potatoes, is a coenzyme that is important for maintaining energy homeostasis in mitochondria (21). Alpha lipoic acid has been shown to reduce cognitive decay in a small group of patients with Alzheimer’s disease (22). Vitamin E, has also been implicated in cognitive performance, as low levels of vitamin E were associated with poor memory performance in older individuals (23).
Curcumin is a strong antioxidant that seems to protect the brain from lipid degradation (24) and other free radicals (25).
The table below is a short list of nutrients and their effect on the brain, as well as their food sources.
Table 1 – Brain Foods: the effect of nutrients on the brain (2)
This very short and rather “watered down” synopsis on the numerous studies that have been done looking at foods affect on the brain hopefully points to the fact that not only quantity but quality of food plays a major role in our body’s ability to utilize micronutrients to either hurt or help the healthspan of our brain and cognitive abilities. Micronutrient rich foods provide your metabolism with many more tools to reduce oxidative stress and maintain overall health than something that was 90% sucrose. While having certain foods in moderation can be key to adhering to an overall whole food/nutrient dense diet, it is important to remember that macronutrient quality affects micronutrient availability.
Thanks for reading! We hope you learned a thing or two about how to better feed your biology!
– Karina at Team LoCoFit
National Human Genome Research Institute (NHGRI). (2019). Importance of Mouse Genome. [online] Available at: https://www.genome.gov/10001345/importance-of-mouse-genome/ [Accessed 15 Feb. 2019].
Gómez-Pinilla, F. (2008). Brain foods: the effects of nutrients on brain function. Nature reviews neuroscience, 9(7), 568.
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Tonra JR, et al. Brain-derived neurotrophic factor improves blood glucose control and alleviates fasting hyperglycemia in C57BLKS-Leprdb/leprdb mice. Diabetes. 1999;48:588–594. [PubMed]
Tsuchida A, et al. Brain-derived neurotrophic factor ameliorates lipid metabolism in diabetic mice. Diabetes Obes Metab. 2002;4:262–269. [PubMed]
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Peet M, Laugharne JD, Mellor J, Ramchand CN. Essential fatty acid deficiency in erythrocyte membranes from chronic schizophrenic patients, and the clinical effects of dietary supplementation. Prostaglandins Leukot Essent Fatty Acids. 1996;55:71–75. [PubMed]
Hibbeln JR. Fish consumption and major depression. Lancet. 1998;351:1213. [PubMed]
Horrobin DF. Schizophrenia: the illness that made us human. Med Hypotheses. 1998;50:269–288.[PubMed]
Freeman MP, et al. Omega-3 fatty acids: evidence basis for treatment and future research in psychiatry. J Clin Psychiatry. 2006;67:1954–1967. [PubMed]
Pifferi F, et al. (n-3) polyunsaturated fatty acid deficiency reduces the expression of both isoforms of the brain glucose transporter GLUT1 in rats. J Nutr. 2005;135:2241–2246. [PubMed]
Flachs P, et al. Polyunsaturated fatty acids of marine origin upregulate mitochondrial biogenesis and induce β-oxidation in white fat. Diabetologia. 2005;48:2365–2375.
Molteni R, Barnard JR, Ying Z, Roberts CK, Gomez-Pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience. 2002;112:803–814. [PubMed]
Corrada M, Kawas C, Hallfrisch J, Muller D, Brookmeyer R. Reduced risk of Alzheimer’s disease with high folate intake: The Baltimore Longitudinal Study of Aging. Alzheimers Dement. 2005;1:A4.[PMC free article] [PubMed]
Fioravanti M, et al. Low folate levels in the cognitive decline of elderly patients and efficacy of folate as a treatment for improving memory deficits. Arch Gerontol Geriatr. 1997;26:1–13. [PubMed]
Nilsson K, Gustafson L, Hultberg B. Improvement of cognitive functions after cobalamin/folate supplementation in elderly patients with dementia and elevated plasma homocysteine. Int J Geriatr Psychiatry. 2001;16:609–614. [PubMed]
98. Ramos MI, et al. Low folate status is associated with impaired cognitive function and dementia in the Sacramento Area Latino Study on Aging. Am J Clin Nutr. 2005;82:1346–1352. [PubMed]
Fava M, et al. Folate, vitamin B12, and homocysteine in major depressive disorder. Am J Psychiatry. 1997;154:426–428. [PubMed]
Liu J. The effects and mechanisms of mitochondrial nutrient α-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: an overview. Neurochem Res. 2008;33:194–203.[PubMed]
Holmquist L, et al. Lipoic acid as a novel treatment for Alzheimer’s disease and related dementias. Pharmacol Ther. 2007;113:154–164. [PubMed]
Perkins AJ, et al. Association of antioxidants with memory in a multiethnic elderly sample using the Third National Health and Nutrition Examination Survey. Am J Epidemiol. 1999;150:37–44. [PubMed]