Cognitive abilities can be influenced by components of the diet. Foods low on the glycemic index appear to improve alertness, memory, and functional capacity, while foods high in simple sugars are associated with difficulties concentrating and paying attention. The brain requires a steady supply of amino acids for the synthesis of neurotransmitters, particularly serotonin and catecholamines.
Low levels of serotonin have been linked to decreased learning, thinking, and memory. The quality and type of dietary fat can also affect intellectual and mental performance. High consumption of saturated fat has been linked to cognitive decline, while consumption of polyunsaturated fatty acids (docosahexaenoic acid) has positive effects in prevention.
It is advisable to consume diets with an adequate ratio (5:1) of omega 6:3 fatty acids (Mediterranean diet) as they are associated with better memory performance and a lower risk of cognitive impairment. Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron, and iodine have a neuroprotective effect and improve mental performance. In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein, and zeaxanthin) play a very important role in warding off oxidative stress associated with mental decline and in enhancing cognition.
Currently, there is a high consumption of diets high in saturated fats and refined sugars and low intakes of fruits, vegetables, and water that can negatively impact cognitive performance. Proper nutrition is necessary to optimize brain function and prevent cognitive decline.
DOES DIET AFFECT COGNITIVE FUNCTION?
Nutrition affects many facets of your life. A healthy diet gives you the energy to stay active, protects you from infection and helps you look your best. Healthy foods also benefit your mind as they nourish the cells in your brain that enable cognitive functions by remembering information, learning, and perceiving the world around you. Adequate nutrients in your diet support cognitive function, while nutrient deficiencies or a poor diet impair cognition.
FAT AND PROTEIN
Adequate intake of fat and protein in your diet helps maintain cognitive function. Proteins provide you with a variety of amino acids, including tyrosine and tryptophan. Your body uses both amino acids to make brain-signalling chemical neurotransmitters needed for cognition. Healthy Fats also help with cognitive function. Omega-3 fatty acids, unsaturated fats found in fish, and some nut and seed oils promote brain function. Low levels of these fats in your body can impair cognitive function and cause neurological disorders like depression that threaten your mental health.
A varied diet rich in vitamins also helps the brain function properly to support cognition. Several B vitamins, including vitamins B3, B6, and B12, help your body convert tryptophan into neurotransmitters. Vitamin B12 also keeps brain cells covered in myelin, a fatty substance that helps nerves communicate effectively. Vitamins C and E may also help maintain cognitive function as we age, reports the Franklin Institute. Vitamins help fight dementia, a condition characterized by decreased cognition and personality changes.
Cognitive function also depends on the minerals in your diet. Sodium, potassium, and calcium help brain cells generate action potentials, small electrochemical signals that carry information between nerve cells. Magnesium also contributes to cognition. Like vitamin B12, magnesium helps maintain the myelin sheath. It also activates the enzymes your brain cells need to produce usable energy, giving the cells responsible for cognitive function access to the fuel they need to function.
EATING FOR COGNITIVE FUNCTION
Because so many nutrients contribute to cognitive function, you should focus on eating a healthy, balanced diet that includes all the nutrients you need for cognitive function. Some foods are particularly high in cognition-friendly nutrients. Salmon, for example, contains many nutrients necessary for cognition, protein, omega-3 fatty acids, B vitamins, vitamin E and potassium.
Kale also contains nutrients for cognition, providing protein, B vitamins, and calcium. If you’ve noticed a deterioration in your cognitive function, be sure to talk to your doctor about your symptoms. Cognitive impairment can develop for a variety of reasons, and a trained physician can identify the underlying cause and prescribe appropriate treatment.
COGNITIVE AND EMOTIONAL DYSFUNCTIONS ARE A GROWING BURDEN IN OUR SOCIETY.
The precise factors and underlying mechanisms that trigger these disorders remain to be elucidated. In addition to our genetic makeup, the interaction between specific environmental challenges that arise during well-defined developmental periods seems to play a role. Interestingly, such brain dysfunctions are more common in metabolic disorders (e.g., obesity) and/or poor eating habits; Obesity and poor diet can have adverse health effects, including cognitive and mood disorders, suggesting a strong interaction between these elements.
Obesity is a global phenomenon, with approximately 38% of adults and 18% of children and adolescents worldwide being classified as overweight or obese. Even without obesity, poor dietary habits are commonplace, for example eating lots of foods that are highly processed and lack important polyphenols and antioxidants or contain far below recommended levels of omega-3 polyunsaturated fatty acids (PUFAs).
Overeating, obesity, acute consumption of a high-fat diet, poor diet at a young age, or adversity at a young age can provoke an inflammatory response in peripheral and central immune cells and affect the blood-brain interface and circulatory factors that regulate satiety. Peripheral pro-inflammatory molecules (cytokines, chemokines, danger signals, fatty acids) can signal immune cells in the brain (most likely microglia) via blood, humoral, and/or lymphatic pathways. These signals can sensitize or activate microglia, leading to the de novo production of pro-inflammatory molecules such as interleukin 1beta.
PERINATAL NUTRITION DISRUPTS LONG-TERM COGNITIVE FUNCTION, A ROLE FOR MICROGLIA
Poor nutrition in utero and during early postnatal life can cause long-lasting changes in many aspects of metabolism and central function, including impairments in cognition and accelerated brain aging, but look. Maternal gestational diabetes and even a junk food diet in non-diabetics can lead to metabolic complications such as diabetes and obesity in the offspring. It can also lead to changes in reward processing in children’s brains, so they grow up to prefer foods high in fat and sucrose.
Similarly, early introduction of solid foods in children and high consumption of fatty foods and sweetened beverages in childhood can accelerate weight gain and lead to long-term metabolic complications that may be associated with poorer executive functioning. On the other hand, some dietary supplements may positively affect cognition, as observed in infant formula supplementation with omega-3 long-chain polyunsaturated fatty acids, which improve cognition in infants. In these randomized controlled trials (RCTs), an omega-3 PUFA-enriched formula started shortly after birth or 6 weeks of breastfeeding significantly improved the performance of 9-month-old infants on a problem-solving task.
Animal models show that the effects of diet in early life are far-reaching. Even obesity in rats (which play no role in raising offspring) results in pancreatic beta cell dysfunction in female offspring that can be passed on to the next generation. Obesity and high-fat diets in rat and mouse mothers during gestation and lactation induce changes in several mood tests, including those that model depressive and anxious behaviour, as well as adversely affect cognition. Postpartum nutrition may be affected by weaning have an impact on similar behaviours.
In addition to the effects of prenatal feeding, excessive consumption of breast milk during the first 3 weeks of life of a rat result in long-term obesity in both males and females. This neonatal overfeeding also impairs cognitive function. For example, new born overfed rats perform poorly compared to control rats on the novel object recognition test and the Win shift delayed spatial radial arm maze as adults.
These results are interesting to compare with the effects of poor diet in adults where a higher-fat diet is required over the longer term (about 20 weeks in the rat) and/or a high-fat diet associated with a prediabetic phenotype to induce cognitive dysfunction. While there are no differences in post-learning synaptogenesis (synaptophysin) or apoptosis (caspase3) to explain the effects observed in overfed new-borns, these rats have an altered microglial response to the learning task.
Microglia are one of the main populations of immune cells in the brain. During development, they are essential for synaptic pruning, while their main function in an adult animal is to trigger a pro-inflammatory immune response and to phagocytose pathogens and injured brain cells.
Hyper activated microglia can lead to cognitive dysfunction through excessive production of pro-inflammatory cytokines that cause impaired long-term potentiation induction, reduced production of plasticity-related molecules, including brain-derived neurotrophic factor and insulin-like growth factor1, and reduced synaptic plasticity. However, an appropriate microglial response may also be essential for effective learning.
New-born overfed rats have more microglia in the CA1 region of the hippocampus, i.e., the day after birth. That is, while they still have access to excess breast milk and experience accelerated weight gain. These microglia also have a larger soma and retracted processes, indicating a more activated phenotype. When these rats reach adulthood, there remains an increase in the dentate gyrus area immunolabeled with the microglial marker Iba1. In overfed new-borns, the microglial response to a learning task is less robust than in controls.
This effect is associated with a suppression of cell proliferation in control animals compared to overfed new-borns, potentially preserving existing neural networks, and minimizing new inputs while learning occurs. Interestingly, global inducible microglial and monocyte depletion can lead to improved performance in Barnes maze, suggesting that deprivation of microglial activity at specific learning stages is important for learning. These findings implicate microglia on the long-term effects of early overfeeding on cognition, suggesting that normal microglia should be able to respond robustly to learning tasks and that overfeeding in new-borns impairs their ability to do so.
Neuroinflammatory processes, including the role of microglia, can clearly be influenced by neonatal nutrition and represent at least one mechanism that contributes to how cognitive function is affected. Neuroinflammation and microglia can also be influenced by other early life events and play an important role in how developmental stress alters long-term physiology.
EARLY LIFE STRESS (ES) PROGRAMS SUSCEPTIBILITY TO COGNITIVE DISORDERS
ES alters brain structure and function throughout life, leading to increased susceptibility to developing emotional and cognitive disorders, as evidenced by multiple preclinical and clinical studies. The precise underlying mechanisms for such programming remain elusive. There is extensive pioneering work suggesting a key role for sensory input from the mother and neuroendocrine factors (e.g., stress hormones) in this programming; however, it has recently been suggested that these factors may act synergistically with metabolic and nutritional elements.
In fact, SSC is associated with an increased susceptibility to developing metabolic disorders such as obesity, most often associated with cognitive deficits, and both SSC and an unfavourable early dietary environment result in strikingly similar cognitive deficits later in life. Elements could be some of the effects of ES on the Teach brain structure and function.
The brain has very high nutritional needs at this early stage, and nutritional imbalances interfere with normal neurological development, resulting in long-lasting cognitive deficits. Understanding the role of metabolic factors and specific nutrients in this context is key to developing effective peripheral (e.g., dietary) intervention strategies. A chronic SE mouse model with limited litter and nesting material during the first postnatal week has been shown to result in abnormal maternal caregiving, leading to cognitive impairment in SE offspring.
The hippocampus, a key brain region for cognitive function, is permanently altered in structure and function in these ES-exposed puppies. In fact, the hippocampus is particularly sensitive to the early life environment as it continues to develop in the postnatal period. Adult neurogenesis (AN) is a unique form of plasticity that occurs in the hippocampus and consists of the proliferation of neuronal progenitor cells that differentiate and mature into fully functional neurons that subsequently integrate into existing hippocampal circuitry. These newly formed neurons are involved in various aspects of hippocampus-dependent learning and memory. AN is permanently influenced by ES, and more specifically, while exposure to ES initially increases neurogenesis (i.e. proliferation and differentiation of new-born cells) at the 9th day after birth, at later time points (150th day after birth) the survival of the new-born cells is reduced, for example with an increase in CD68 (phagocyte microglia expression) in adulthood .
Overeating at a young age can permanently sensitize the brain’s neuroinflammatory response to challenging stimuli, leading to lifelong cognitive and immunological dysfunction. ES alters brain function through metabolic and nutritional factors to increase susceptibility to developing emotional and cognitive disorders. Short- and long-term consumption of foods high in saturated fat in adulthood produces a sensitized inflammatory phenotype in the hippocampus through elevated glucocorticoids, leading to learning and memory deficits.
The imbalance of omega-3 and omega-6 polyunsaturated fatty acids contributes to neurodevelopmental disorders by altering microglial activation, resulting in abnormal network formation and neuronal activity. Finally, eating fruits and vegetables high in polyphenols can prevent and reverse age-related cognitive deficits by reducing oxidative stress and inflammation.