Unlike other mammals, human infants are born with significant fat stores. This fat provides essential nutrients like DHA and a source for ketones, which are the preferred fuel for the developing brain, especially in the first few weeks of life.
While caffeine is administered to preterm infants primarily to stimulate their underdeveloped respiratory drive, clinical trials have revealed a significant side effect: durable improvements in cognitive function that last into childhood.
While BDNF is associated with exercise's brain benefits, the BDNF produced in muscles doesn't readily cross into the brain. Instead, lactate produced during intense exercise enters the brain and acts as a signaling molecule, stimulating local BDNF production and improving hippocampal function.
While cooling is effective for newborns with brain injuries, trials in adults haven't shown the same benefit. However, preventing hyperthermia (fever) is crucial. A fever increases the brain's metabolic demand when its energy supply is already compromised, worsening the injury.
A study requiring participants to perform a grueling HIIT protocol (4 sets of 4 minutes at 85-95% max heart rate) three times a week resulted in significant improvements in hippocampal structure and function. Remarkably, these benefits were maintained for several years after the trial ended.
People who are bilingual consistently outperform monolinguals on tasks requiring executive function, such as response inhibition. This cognitive advantage is thought to stem from the lifelong, unconscious practice of actively suppressing one language while speaking another, effectively training the brain's control networks.
Sensory decline, like hearing loss or cataracts, is linked to a higher risk of dementia, likely due to reduced brain stimulation and social engagement. However, this risk appears to be reversible. Interventions like cataract surgery or hearing aids restore sensory input, effectively eliminating the added risk.
To drive neuroplasticity—the process of building new neural connections—the brain needs to recognize a gap between its current capacity and a desired outcome. This gap is most clearly revealed through mistakes. Activities where you never fail or push your limits do not provide the necessary stimulus for adaptation.
Gum disease (periodontitis) is a significant risk factor for dementia, as harmful bacteria can enter the bloodstream and contribute to brain inflammation. Studies show that xylitol, found in certain gums and mouthwashes, improves the oral microbiota by inhibiting these specific harmful bacteria, offering a low-risk preventative measure.
Clinical trials show that supplementing with either B vitamins (to lower homocysteine) or omega-3s alone has little effect on cognitive decline. However, when combined, they significantly improve brain atrophy rates. Adequate methylation, supported by B vitamins, is required for DHA to be incorporated into brain cell membranes.
Exercises that require constant adaptation to a changing environment (open-skill), such as dancing, martial arts, or team sports, provide greater cognitive benefits than closed-skill activities like jogging. The added cognitive challenge of complex motor skills and reaction time yields superior improvements in brain structure and function.
Over short periods, sleep deprivation's main cognitive effect is a reduction in processing speed, not accuracy. The quality of work remains the same; it just takes longer. Mood is affected far more significantly than actual performance, a useful insight for managing expectations after a poor night's sleep.
Auguste Deter, the first patient described with Alzheimer's, lacked the genetic risk factors for the disease. Retrospective analysis suggests her presenile dementia, which featured amyloid plaques similar to Alzheimer's, may have been caused by neurosyphilis or other factors, challenging the historical foundation of the disease's definition.
While PET scans show lower glucose uptake in Alzheimer's brains, this may not be due to insulin resistance ("type 3 diabetes"). Studies show these brains can absorb glucose normally when cognitively stimulated. This suggests the issue is a lack of demand from inactive brain regions, not a failed supply mechanism.