neuroscience-corner

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Since the beginning of the pandemic many people have noticed how much they miss physical touch and connection with other people. Being forced to be alone has had a deteriorating effect on people’s mental health. Why so? One of the reasons could be the decreased levels of oxytocin, or so-called “love hormone”.

Oxytocin is a hormone (check out my previous post to find out what it is!) that is secreted by the hypothalamus (a small region in the brain). It acts as a neurotransmitter (chemical communicator) in the brain. It is often referred to as “love” or “cuddle hormone” and the reason for it is that it is being actively released during hugging and orgasm. Mainly, however, it is involved in childbirth and lactation. During labour, it causes contractions in the muscles of the uterus, and as the cervix is widening, oxytocin is released, causing more contractions to occur. Oxytocin can also be prescribed as a drug or be used in a form of injections to stimulate birth, only under medical supervision as it can cause excessive bleeding, rapid heartbeat or, if used too rapidly, rapture of the uterus.

Oxytocin and lactation

During breast-feeding, the production of oxytocin is achieved by nipple stimulation. The oxytocin causes the muscles around the milk-making glands in the breast to contract. When the glands contract, they squeeze the breast milk into the milk ducts. Research shows that breastfeeding has a positive effect on a mother's physiological and psychological states, buffering depression and anxiety, as well as enhancing positive feelings when mothers see their infants' facial expressions. One study has suggested that oxytocin can aid emotion recognition in mothers. A study by M.Matsunaga et al. (https://royalsocietypublishing.org/doi/10.1098/rsbl.2020.0139) has examined the effects of endogenous (produced by the body itself) oxytocin fluctuation via breastfeeding on emotion recognition in mothers. Among mothers who breastfed daily, those who increased levels of oxytocin showed recognised more positive adult facial expressions, while the recognition of negative ones was reduced.

Oxytocin and romantic attachment

Well, what about love? A study conducted in 2012 has attempted to assess the role of oxytocin in romantic attachment. Participants included newly formed couples (3 months after they started dating) and “singles”. Couples were observed in their interactions and interviewed regarding relationship-related thoughts and behaviours. Levels of oxytocin were significantly higher in couples than singles and did not decrease in 6 months. Oxytocin levels during the first assessment differentiated couples that stayed together longer than 6 months from those who separated before that. Findings suggest that oxytocin might play an important role in early romantic attachment, as well as support the evidence that parental and romantic attachments might share some of the behavioural mechanisms.

Oxytocin and sex

Sexual activity has shown to stimulate the release of oxytocin, yet the process is not fully understood. Some studies found the correlation between the orgasm intensity and oxytocin levels.

Oxytocin and emotions

Oxytocin has an effect on emotional regulation and processing as well. It helps to regulate pro-social behaviors, including trust, empathy, gazing, positive memories, processing of bonding cues, and positive communication. Recent studies confirm that high levels of oxytocin lead to more accurate emotion recognition and processing, irrespective of the emotion type. This particular area of oxytocin functions is a popular topic for research as more data may lead to practical implications to aid people with various diseases. For example, oxytocin has been used to lower anxiety symptoms and help with social skills (such as making eye contact and recognising emotions) for autistic people. Here is a nice article where you can read more about the relation between autism and oxytocin: https://www.spectrumnews.org/news/the-connection-between-oxytocin-and-autism-explained/

Oxytocin and Fatherhood

Despite playing a significant role in childbirth and lactation, oxytocin in men and women actually facilitates many of the same mechanisms, such as bonding with children, romantic attachment, and reproduction for both sexes. Emory University study has shown that men after receiving boosts of oxytocin had an increased activity in the brain areas associated with reward and empathy when viewing photos of their toddlers. In general, oxytocin in fathers facilitates physical contact with their children during play and the ability to synchronise their emotions with kids.

Sources:

https://www.medicalnewstoday.com/articles/275795#the_love_hormone

https://royalsocietypublishing.org/doi/10.1098/rsbl.2020.0139

https://pubmed.ncbi.nlm.nih.gov/27071915/

https://www.sciencedaily.com/releases/2017/02/170217095925.htm

https://www.psycom.net/oxytocin

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At some point in life our brains begin to deteriorate, the cortex shrinks, causing cognitive decline. This is a normal part of ageing. The thin layer of grey matter is the outermost layer which is essential for higher-order cognitive functions, such as thinking and memory.

Cortex thinning is also seen in Alzheimer’s disease - one of the most widespread types of dementia in the world, affecting memory, thinking and behaviour, overtime leading to inability to perform basic daily tasks.

Cortical asymmetry is a phenomenon of one side of the cortex being thicker than another one. It is allegedly a good thing, allowing our brain to function properly and have necessary optimal balance. It was assumed that both left and right sides age at the same right, but the new findings show that the part that was thicker in a 20-year-old deteriorates faster.

Trying to connect it with Alzheimer's disease, researchers measured the thickness of all areas of the cortex using brain scans from over 2600 healthy people across Europe and the US, and in an Australian sample with dementia. The findings showed that cortical asymmetry is actually lost with age, and in the same brain regions as in normal ageing, the left side of the brain shrinks faster in people with Alzheimer’s disease.

It was consistent throughout the study that the decline started at around age 30 with acceleration around age 60, but the process was accelerated in those with Alzheimer's disease.

“The implication is that at least some brain-changes associated with Alzheimer’s disease may play out over extended periods of the lifespan, possibly on the order of decades, and may show high overlap with those occurring gradually in normal ageing,” the lead author of the study James Roe says.

Source:

https://www.sv.uio.no/psi/english/research/news-and-events/news/left-and-right-brain-age-differently.html

https://www.nature.com/articles/s41467-021-21057-y#Sec8

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Synapses are sites of neuron-to-neuron connections. They are spaces between a presynaptic (giving information) neuron and a postsynaptic (receiving information) neuron. The synaptic connections between neurons and skeletal muscle cells are generally called neuromuscular junctions, and the connections between neurons and smooth muscle cells or glands are known as neuroeffector junctions. Neurotransmitters are brain chemicals that communicate information via electrical impulses throughout our brain and body. They relay signals between neurons (nerve cells), transmitting signals across a chemical synapse from one neuron to another "target" neuron. This process is called neurotransmission.

Source: https://www.semanticscholar.org/paper/Neurotransmitter-Receptors-in-the-Postsynaptic-Stephenson-Hawkins/6148a8948a3145d1cfe6de61a3d161235bffe9bd

Action potential travels down the axon (check out the post about the structure of a neuron). When depolarized, the signal arriving releases pre-made neurotransmitters into the synaptic cleft (space that separates 2 neurons). It happens in the following way. Neurotransmitters are packed into vesicles that fuse into the membrane. Those vesicles then become part of the membrane and the molecules of neurotransmitters are released into the synaptic cleft. They diffuse across the cleft and bind to specific molecules called receptors on the postsynaptic terminal. Ionotropic receptors (e.g., ligand-gated ion channels) open as soon as the right neurotransmitter is binded, while metabotropic receptors (G protein-coupled receptors) cause a complex chain of actions.

Neurotransmittors have been shown to have a range of different effects on human behaviour, such as mood, sleep, sexual arousal or mental illness. In Antonova’s study, male participants were asked to take part in a double-blind study, meaning that the participant and the researcher were not aware of which group they were a part of. The participants were randomly allocated to either the scopolamine group or the placebo saline solution group. The participants were then placed into an fMRI in order to read their brain activity. They were told to play a few rounds of a virtual reality game with a joystick in order to become familiar with the controls. The game consisted of the participants being dropped in the middle of an arena and told to find a special landmark. Each round of the game started them at a different location within the arena. After a few rounds, the researchers recorded their brain activity in the next few rounds.

The participants were asked to come back after 3 to 4 weeks where they repeated the procedure. The researchers found that when participants were injected with scopolamine, they demonstrated a significant reduction in the activation of the hippocampus compared to when they received a placebo. This shows that the scopolamine actually blocked the receptors on the neuron for acetylcholine and prevented neurotransmission from taking place, thus impairing the participants’ ability to create spatial memories. It appears that acetylcholine could play a key role in the encoding of spatial memories in humans, as well as in rats.

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The structure of one’s brain is not set in stone. It is actually quite the opposite, as our brains have the ability to change due to different things we experience. This is called brain plasticity, or neuroplasticity. Neuroplasticity is the brain's ability to reorganise itself by forming new neural connections. It allows us to learn new things, enhance our cognitive abilities, aid recovery from strokes and various brain injuries. Neuroplasticity allows neurons in the brain to compensate for injury (for instance, by strengthening some areas to compensate for damaged ones) or to respond to changes in the environment. When neurons fire continually as a result of stimulation in the environment, the neurons sprout new dendrites – known as dendritic branching.  This increases the number of synapses available for the behaviour. On the contrary, neurons that are not in use eventually die out - that is why as adults we have twice as less synapses as we did in childhood. This process is called synaptic pruning.

Dendritic branching as a result of stimulation in the environment is seen in a study by Maguire. The aim of the study was to see if neuroplasticity would be seen in the brain of London taxi drivers due to the amount of time that they had been driving the streets of London. As the study was conducted back in 2000, at that point in time taxi drivers needed to pass a test called “The Knowledge”, which required them to memorise the location of key places and routes in the city. This led to a hypothesis that repeated use of the brain for spatial memory would result in neuroplasticity and a denser hippocampus. Hippocampus is a complex brain structure embedded into the temporal lobe that plays a major role in learning and memory.

Source: https://www.simplypsychology.org/hippocampus.html

Maguire used 16 healthy right-handed males who were licensed taxi drivers. She compared the taxi drivers to 50 healthy right-handed males who were not taxi drivers. An MRI was used to detect changes in the structure of the brain as a result of their experience. The results showed that the taxi drivers had larger posterior hippocampi compared to the controls and that the controls had larger anterior hippocampi compared to the taxi drivers. Also, there was a positive correlation between the number of years the participants had been taxi drivers and the size of the posterior hippocampus, but a negative correlation with the size of the anterior hippocampus. Maguire argued that this demonstrates the plasticity of the hippocampus in response to environmental demands and that the posterior hippocampus stores a spatial representation of the environment and that in the London taxi drivers the volume of the posterior hippocampus expanded because of their high reliance on navigation skills and spatial memories. This is a good example of how repeated, constant use of knowledge causes your brain to adapt to better serve its functions.

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Neurons, or nerve cells are the fundamental units of one’s nervous system, both central (consisting of a brain and a spinal cord) and peripheral (neurons and parts of neurons outside the CNS). Nervous system allows us to experience the world that surrounds us by receiving and sending signals. Scientists distinguish between sensory, motor and interneurons. Sensory neurons help us to get information about what is happening inside our bodies and outside in the environment. This information gets sent to CNS for processing. Motor neurons, on the other hand, get information from other neurons and send commands outside the CNS, to your muscles, glands and internal organs. If you touch something very hot, your sensory neurons will ensure your brain is aware it is hot and your motor neurons will send a command to your hand muscles to quickly get your hand off it. Interneurons exist only within the CNS, connecting one neuron to another. They receive information from other neurons (either sensory neurons or interneurons) and transmit information to other neurons (either motor neurons or interneurons). Summing up, neurons have 3 basic functions: receiving, integrating and communicating signals.

Neurons consist of the following parts:

Soma is a cell body, where you can find the nucleus of a neuron, holding all of its DNA. Protein synthesis also takes place in the soma.

Dendrites are short branches that receive and process incoming information. Those signals may be inhibitory, or preventing the neuron from firing, or excitatory, generating an electrical impulse. As one neuron has a lot of dendrites, whether the firing will take place depends on the net sum of all the inputs.

Axons are long branches along which the signal travels. Towards the end, an axon splits into several branches, each ending in an axon terminal that connects to a target cell to pass on a signal.

Myelin sheath is an insulating substance that covers an axon to aid in conveying the impulse more rapidly.

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FOXP2, or forkhead box protein P2, is a protein that is encoded, in humans, by the FOXP2 gene. It has been widely referred to by the media as “the language gene”. But is it really that simple? Well, the simple answer is no and it could never be so. We do not know where our ability to communicate and recognise speech arise from but what we do know is that the system is much more complicated than just one language gene. There is not a place in the brain responsible for language, it is most likely due to the specific relationships between the parts involved. However, this gene is the first gene to be associated with language disorders. The mutated version of FOXP2 was found in the family whose 15 members (3 generations!) had trouble generating and comprehending speech.

The human version of FOXP2 gene differs from animal’s (mice’s) only by 2 amino acids, but the practical differences are significant. In striatum (part of the brain related to habit formation) the scientist saw longer dendrites (extensions from the neuron's body that are used by neurons to communicate with each other). In general, those neurons were also better at forming new synapses (connections between neurons). Overall, the mice with humanized version of the gene were better at any activity that required turning memories into habits. The protein encoded by FOXP2 gene has an ability to turn on/off other genes. Together, these changes are believed to help the brain to adapt to speech and language acquisition.

Sources:

https://news.mit.edu/2014/language-gene-0915

https://www.sciencedirect.com/science/article/pii/S096098221831546X

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Melatonin is one of the natural hormones that is produced by the pineal gland located in the brain. Melatonin is considered one of the central parts of the body’s sleep-wake cycle. It helps regulate and orient our circadian rhythm while synchronising our sleep-wake cycle with night and day. Apart from circadian rhythms, melatonin levels have a seasonal (or circannual) rhythm, with higher levels of melatonin produced during winter and autumn due to longer nights and, therefore, more darkness. In some animals melatonin is vital for regulating season-dependent activities, such as reproduction, change of fur colour, coat growth and behaviour.

Production of melatonin is prompted by the darkness and is stopped by the light. Exogenous melatonin can be made synthetically in a laboratory and is used as a dietary supplement that helps with such things as sleep disorders in children, sleep regulation in blind or jet lag.

Source: https://ib.bioninja.com.au/standard-level/topic-6-human-physiology/66-hormones-homeostasis-and/melatonin.html

Scientists assume that melatonin has other bodily functions, except being important for sleep regulation. A study conducted in Denmark in 2011-2012 by Hansen et al. confirms the idea. The aim was to investigate whether melatonin could lower the risk of depressive symptoms in women with breast cancer in a three-month period after the operation and whether it would influence subjective parameters, such as anxiety, sleep, general well-being, fatigue, pain, etc. The study was a double-blind (meaning neither participants nor researchers knew which group a particular person belonged to), randomised study. Women aged 30-75 years without any signs of depression according to Major Depressive Inventory were put into a melatonin or a placebo group one week before the surgery. They received 6 mg oral melatonin or a placebo for three months.

As a result, the melatonin group showed significantly lower risk of developing depressive symptoms, but there was no significant difference in subjective parameters. This study has shown that melatonin is not only vitally important for sleep-wake cycle regulation but can also potentially have an effect on depressive symptoms.

Sources:

https://www.yourhormones.info/hormones/melatonin/

https://www.sleepfoundation.org/melatonin

https://www.mayoclinic.org/drugs-supplements-melatonin/art-20363071

https://www.nccih.nih.gov/health/melatonin-what-you-need-to-know

https://pubmed.ncbi.nlm.nih.gov/24756186/

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Hormones are chemical substances that act like messengers in the body. They are produced by glands, ovaries and testes, and released into the bloodstream. From the blood they can reach any of their target destinations, where they serve different purposes, including regulating long-term behavioural patterns. They can affect such things as growth, development, reproduction, sexual function, metabolism, mood, etc.

Here is a diagram of how hormones move through the body. From the secreting cell hormone enters the bloodstream and moves along it to further enter the target cell. There can be multiple target cells for just one hormone.

When reaching the target cell, hormones bind to receptors. Receptors are proteins embedded into the plasma membrane that are shaped to fit specific molecules (substrate-specific receptors). Later some other reactions take place producing second messengers. In the end, those messages activate various cellular responses. This diagram demonstrates the work of water-soluble hormones that are unable to pass through the membrane that has hydrophobic layers. Fat-soluble hormones pass through the cell membrane directly and produce their effect by binding to receptors inside the cell.

Source: https://oakcrestapbio.wordpress.com/endocrine-system/how-hormones-work/

Hormones are very powerful - very little amount is needed to perform its function. That is why any discrepancies from the normal levels are dangerous. For example, high levels of oestrogen (e.g. from taking birth control pills) can put you at higher risk of blood clots, stroke and even thyroid dysfunction, while low levels of it interfere with sexual development, can cause more frequent UTIs, irregular menstrual cycles and many more.

Some signs of hormonal imbalance include low libido, insomnia or poor-quality sleep, unexplained weight gain, headaches, fertility problems, skin problems, weak bones, mood swings, heavy and painful periods, etc. It is always best to consult a specialist if you experience one or more of those to get an accurate diagnosis, because many of those can be caused by other diseases as well.

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Resources about Parkinson's disease

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An interesting discovery has been made by scientists at King's College London and the University of Athens Medical School. They have provided evidence for malfunction in the brain years before the onset of the disease. The main feature of Parkinson’s disease has been an impairment of dopamine systems. However, these brain scans show that the first thing that becomes affected is actually a serotonin system. Serotonin (“hormone of happiness”) is another neurotransmitter that is involved in the brain, that stabilizes mood and helps with sleeping and digesting. In the brain it is almost exclusively produced by raphe nuclei (located in the brainstem).

To read the brain scans, we need to know the basics - the colour here means the changing level of activity, with blue being the lowest, and white being the highest. As you see, in the health brain, both substantia nigra (white spot) and raphe nuclei (red areas in the midbrain) function perfectly. Before symptoms of Parkinson’s disease occur, we can see the massive decline in serotonin production (the red area in the midbrain has turned into green), while dopamine still remains at some levels of activity. After the symptoms, none of the systems work on an acceptable level.

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There is no full picture of brain structures that are affected by Parkinson’s disease, and it is yet to be determined the connection between them and the cause of such diverse symptoms, but by looking at the specific symptoms, it is possible to determine some of the structures involved. For instance, symptoms affecting memory and thinking can be linked to the presence of Lewy’s bodies in the cerebral cortex (one of the largest brain’s areas) and limbic system.

Limbic system can also be involved in emotions and pain-related symptoms, together with amygdala - structure in the brain that is believed to be involved in mental disorders, like PTSD. The olfactory system is responsible for smell and is actually one of the earliest structures involved.

Then, the disease travels up the brainstem, through medulla oblongata, pons and midbrain, all are places where cranial nerve synapses before going into the cortex. Hypothalamus is located right next to the midbrain and is a control centre for autonomic nervous system, and its parasympathetic component - “rest and digest” - can be responsible for sleep dysfunction in patients with Parkinson’s disease. Dorsal thalamus can be involved as well, because it participates in a circuit together with basal nuclei’s components. As soon as the disease goes all the way up and reaches the neocortex (“the new cortex’), some higher functions begin to be impaired. That can include language, perception, cognition. At this point, it is spreading all over the cortexes, causing dementia. Finally, it reaches the area involved in memory.

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Parkinson’s disease is a neurodegenerative (meaning it affects cells of the central nervous system causing them to stop functioning and eventually die) disease and the second most common type of dementia (with first being Alzheimer’s disease). It usually occurs after the age of 50 (normal onset), and all the cases occurring between ages 21-50 are referred to as “early-onset”. The symptoms patients experience can be divided into 2 groups - motor and non-motor symptoms. 

The primary motor symptoms are:

Tremor - shaking in limbs, especially when they are at rest

Bradykinesia - gradual slowing down of spontaneous movements

Rigidity - an abnormal stiffness in limbs or other parts of the body

Postural instability - impaired balance, difficulty standing/walking

The secondary motor symptoms differ from case to case, but can include speech difficulties, micrographia (abnormally small handwriting), “masked” face expression. 

The motor system is controlled by the structure in the brain called basal nuclei, or basal ganglia, which is affected in Parkinson’s disease. Direct pathway through basal nuclei facilitates appropriate motor programmes (if something is wrong, the person is unable to initiate normal habitual behaviours, like walking). Indirect pathway inhibits competing motor programmes (if something is wrong, a person experiences unwanted motions, like tremor). Looking at the symptoms of Parkinson’s disease, we can claim that both are affected in one way or another. 

Another thing connecting basal nuclei and Parkinson’s disease is dopamine - a neurotransmitter (brain chemical), whose lack is one of the main features of Parkinson’s disease. It is produced in substantia nigra (part of basal ganglia) and travels through the brain via several pathways, one of them being nigra-striatal pathway (striatum is also a part of basal nuclei, whose function includes receiving input from several areas of the cerebral cortex and from the dopaminergic cells of the substantia nigra). It is unknown that causes the death or impairment of neurons producing dopamine (so-called dopaminergic neurons), but it’s clear that it leads to motor dysfunction.

The presence of Lewy’s bodies is another main feature of Parkinson’s disease. Lewy’s bodies are unusual clumps of protein alpha-synuclein, that appear on neurons in the brain in Parkinson’s disease and another dementia type, called Lewy’s body dementia. Those clusters of protein prevent neurons from maintaining normal synaptic activity, which in some way contributes to the symptoms, but the actual normal and abnormal functions of this protein is unknown.

The non-motor symptoms include dementia (gradual cognitive decline), swallowing problems, mental disorders (like depression and anxiety), smell and sleep dysfunction, blood pressure changes. 

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Resources about ADHD

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While some might be surprised, it is a general trend in society that it is much harder for women to get diagnosed with ADHD. The reason for that lies primarily within the fact that symptoms of ADHD in women differ greatly from those experienced by men, and therefore primary care physicians, teachers and other adults surrounding young girls are having a harder time diagnosing it. 

Based on information retrieved from “A Review of Attention-Deficit/Hyperactivity Disorder in Women and Girls: Uncovering This Hidden Diagnosis” (Patricia O. Quinn, Manisha Madhoo, 2014) I would like to provide a simplified overview of ADHD representation in women.

Statistics show that there is higher prevalence in childhood ADHD diagnosis in boys than girls, but prevalence becomes more comparable in adulthood. This raises a question - can it be that ADHD symptoms are just being overlooked in girls in their childhood? There are reasons to assume it can be possible.

Many professionals in different areas that work with kids are trained or are generally familiar with the ways to identify ADHD, but what they consider ADHD is actually its externalising and hyperactive subtype, predominant in boys. On the other hand, girls experience internalising predominant symptoms and inattentive subtype. It makes symptoms more subtle and hard to notice, especially for those unfamiliar with the details. Another common feature for girls experiencing ADHD is presence of various comorbidities, or diseases that are present at the same time with ADHD, such as psychiatric disorders (depression and anxiety that often do not respond to usual treatment), obsessive-compulsive disorders. Many of the girls with undiagnosed ADHD are also considered “gifted kids” in their educational environment as it is common to experience perfectionists behaviour as well. Girls with ADHD usually do now show externalised aggression or typical “classroom disruption” behaviours. Their “aggression” is internalised and results in low self-esteem, inattention, difficulty building interpersonal relationships, promiscuous behaviours, and eventually development of coping mechanisms, such as “work harder”.

Neuroendocrine factors, or the effect of hormones, can play a role in expression of ADHD symptoms in women. Some studies show estrogen hormones play an important role in the development and plasticity of midbrain dopamine neurons. Dopamine is often called a “happy hormone” as its high levels result in feelings of well-being and happiness. One study has also shown that there is a correlation between ovarian hormones and activity in brain areas responsible for decision-making, emotional and social behaviours. It might be then assumed that fluctuations in those hormones can regulate those pre-existing behaviours associated with ADHD in women.

Thyroid hormones can also have an effect on ADHD symptoms, as it has been shown in a study that kids having higher levels of thyroid-stimulating hormones (still within the normal range) had a higher risk of exhibiting ADHD symptoms. There is also evidence of the role of thyroid hormones in brain development and function. Considering the higher incidence of thyroid disorders in women than in men, the possibility of those hormones having an effect on expressing ADHD in women has to be researched. 

As it is necessary to be referred to a physician to get diagnosed, and most of the adults only focus on the stereotypical representation of ADHD, many girls go into adulthood without being diagnosed, which leads to a lot of problems and inconveniences throughout their lives. Symptoms persist into adulthood, and result in higher anxiety levels, unhealthy coping mechanisms, emotional reaction to stress, disorganization, sleep difficulties and even somatization, or experiencing physical symptoms without a particular cause. Those symptoms include headaches, stomach aches and musculoskeletal problems. 

To conclude, for a successful ADHD diagnosis it is important to look at gender-specific representations. Therefore, greater awareness amongst professionals and health-care providers is needed. Academic achievements should not come in the way of a diagnosis, as they can be a result of developing coping mechanisms that regulate symptoms of ADHD in women.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195638/

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Breaking down claims about brain training apps being "backed up by science" and what is actually beneficial for the brain. I found the video really interesting!

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as per usual, a TED talk

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We have all heard about the benefits of exercise for literally every part of our body at least once. But what about the brain? Dementia is a concern for many, and brain training and reducing the risk of dementia is a very active field of research. However, the role of brain training remains controversial, but what we know for sure is that physical exercise can help your brain maintain its health for longer, and there is some scientific evidence to back it up.

What are some benefits of exercise for the brain?

There are many, but amongst the main ones are decreased stress and “brain fog”, decreased social anxiety, improved emotional processing, increased focus, attention and memory, and potential prevention of ageing and dementia!

How can exercise actually benefit the brain?

Firstly, by promoting cardiovascular health. Regular exercise was also shown to improve the blood and oxygen flow to the brain. Steady blood flow helps to deliver vitamins, glucose, amino acids and other nutrients that are essential for the mental sharpness of your brain. It also helps get rid of waste materials such as carbon dioxide faster. Any aerobic activity that increases your heart rate will do! Other ways to benefit the brain health is to reduce inflammation and lower cortisol (stress-hormone) levels. Meditation and yoga were shown to help with that.

It could be that exercise may provide physical benefits to your brain itself, too, through improving neuroplasticity (or the ability for the brain to adapt to changes), increase the thickness of the cerebral cortex and improve the integrity of white matter.

What about the evidence?

In a study done in 2019 older adults underwent yearly medical check ups and cognitive tests for 20 years, and they agreed to donate their brains for research when they die. They were also given equipment to track their activity, like accelerometers. Those who moved more throughout their day scored better on memory and thinking tests. The researchers also reported that increased physical activity was associated with a 31% lower risk of dementia (remember to be critical - this is a correlation but not yet a causation). 

A study on greek participants with amnestic MCI* showed that those who were randomly allocated to engage in 1 hour of ballroom dancing twice a week for 10 months improved in multiple areas of brain function, their mood and behaviour. 

In another study on MCI patients researchers offered participants to engage in aerobic exercise (three times a week for 45 minutes per session), eat a heart-healthy Dietary Approaches to Stop Hypertension (DASH) diet, combine exercise and diet or receive health education. Over a six-month study, it was seen that those who followed the DASH diet alone didn’t improve on assessments of executive function (which is responsible for tasks like planning, problem-solving and multitasking), while the health-education group’s brain function worsened. Those who exercised, on the other hand, showed improvements in thinking and memory, and those who combined exercise and the DASH diet improved even more, the researchers reported.

When it comes to how much exercise you actually need, scientists recommend to aim for 15 minutes of 3 days per week of vigorous aerobic activity or 30 minutes of mild one 5 days per week.

Some research shows that even a little bit of extra activity you can get can be beneficial. In one recent study researchers concluded that each hour of light-intensity physical activity and achieving 7,500 steps or more daily was associated with higher total brain volume, even in people who didn’t meet the activity guidelines. Researchers claimed it was “equivalent to approximately 1.4 to 2.2 years less brain aging.”

*MCI stands for mild cognitive impairment which is considered to be a pre-dementia state, where cognitive decline is noticeable but doesn’t interfere as much with day-to-day life. Amnestic means referring to memory. I actually wrote an extended essay on this so I am thinking of introducing this concept in the later posts!

Sources: