Many people know what it’s like to dive headfirst into a captivating book. Sometimes fictional characters and emotions can feel completely real. But what happens in our brain when we devour page after page? How does this differ from its work during other moments of everyday life? And is there any difference at all?
These questions were partially answered by a team led by specialists from Carnegie Mellon University. They explored how we read literature using a machine learning algorithm.
How Scientists Study Brain Activity During Reading
The perception and comprehension of written text is an incredibly complex process. Early research tried to break it down into parts, focusing on each aspect separately. For instance, using functional magnetic resonance imaging (fMRI), they tracked which brain structures were involved in processing a single word or sentence.
However, these strictly controlled experiments barely resembled the actual process of reading. Sentences used as stimuli for brain activity were often out of context, crafted specifically for the research. While such studies provided useful information about certain aspects of text comprehension, they did not help form a complete picture.
Machine learning specialists took a different approach. Volunteers read a chapter from an engaging novel while scientists scanned their brains. The researchers then deconstructed the brain’s functioning process. According to the scientists, they created the first integrated model in the world that shows how our brain processes written words, grammatical structures, and stories.
The Study’s Process
Researchers gathered a group of eight volunteers and recorded their brain activity using an MRI scanner as participants spent 45 minutes reading a chapter from the book Harry Potter and the Philosopher’s Stone (specifically, the episode where the characters are learning to fly on broomsticks).
In the next stage, the scientists fed the data into a computer program they had written. Their algorithm looked for patterns of brain activity that occurred when participants read specific words, grammatical constructions, names of characters, and so on. There were 195 such “story elements” in total.
The program was able to determine which part of the chapter the participant was reading based solely on brain activity. To make these conclusions, the algorithm used models of brain activity that it had learned to associate with each story element. When researchers applied all these models at once, the program was able to identify which of two passages a person was reading with 74% accuracy, which is significantly higher than random guessing.
Finally, the scientists repeated the test for each type of story element in every brain region. This helped them discover connections between them and precisely determine which brain structures process different types of information. Some results aligned with the researchers’ expectations, while others were quite surprising.
Practical Implications of the Findings
As expected, the brain processes individual words through an initial stage in the visual cortex, which handles all visual information, and then through higher-level processing areas. These include gyri in the frontal and parietal lobes, which are involved in language, speech comprehension, interpretation of text, reflection, and more. But that’s not all.
When participants read descriptions of physical movements in the book, activity in the posterior temporal lobe and angular gyrus changed.
These brain regions are involved in perceiving real-life movements.
Different characters’ personalities correlated with neuron activity in the right posterior superior and middle temporal regions. These structures are important for speech perception, visual memory, and emotions.
Dialogues were linked to the right temporoparietal junction, a brain region critical for imagining the thoughts and goals of others.
Interestingly, some of the areas listed are not even considered part of the brain’s language system.
We use them daily when interacting with the real world, and now it turns out that they also engage when we imagine the perspectives of different characters in books.
This seems to confirm the existence of a phenomenon scientists call the “narrator perspective network.” In other words, it’s a network of brain areas that allows us to “become” the character of the story we’re reading.
If these hypotheses are correct, science could be on the path not only to creating a more accurate neural model of language processing but also to better understanding how and why this process can break down.
Scientists are interested in various ways that speech perception can be disrupted. With enough data, they may be able to understand how one brain, for example, that of a person with dyslexia, works differently from any other.
Researchers hope that such diagnostic tools will one day help create individualized neurological correction methods for dyslexia and other reading disorders. If these methods prove effective, many people may find it much easier to fully immerse themselves in a good book.
In our brain, these forms of love evoke different signals — clearly distinguishable patterns, as revealed by a study. They can be recognized by differences in the activated brain regions and intensity. For example, love between partners and towards children elicits strong reactions in our reward system and social circuits. Love for strangers, pets, or nature, on the other hand, shows different patterns.
Love is one of our most intense emotions — and one of the most diverse: It shapes erotic and romantic relationships, connects parents with their children, and forms the basis of friendships. Depending on its manifestation, very different hormones and physical sensations are involved in these feelings of love. In addition, there are other forms of love, for example towards a pet, nature, or generally towards our fellow human beings or the world as a whole.
How Do Different Forms of Love Manifest in the Brain?
“But when we love, is it neurologically the same whether this love is directed towards our child or, for example, nature?” ask Pärttyli Rinne from Aalto University in Finland and his colleagues. What differences does our brain make in these various types of love? Until now, the “neural fingerprint” of love has been studied almost exclusively for classic romantic love and parental love. However, not for other types of interpersonal and non-personal love.
“We now provide a more comprehensive picture of the brain activity associated with different types of love than previous research,” says Rinne. For their study, 55 test subjects listened to short scenes and stories about six different types of love while their brain activity was recorded using functional magnetic resonance imaging (fMRI). Immediately afterwards, the participants were asked to mentally recreate the respective form of love as intensely as possible.
In addition to the brain scans, all test subjects answered detailed questions. These included, for example, what feelings the stories about the six love variants evoked in them, how strongly they felt them, or how similar or different the reactions were. The six variants were love in relationships, parental love, love for friends, for strangers, for pets, or for nature.
Neural Fireworks for Parental Love and Partner Love
The result: Our brain generates very different neural “fingerprints” for the various forms of love. While all forms of this emotion are linked to parts of the reward system to some extent — like many pleasant experiences — which brain areas are involved and how intensely they fire varies greatly.
“The six different variants of love are linked to the reward centers and the centers for social cognition in different ways,” report Rinne and his team.
The brain reacts most intensely and extensively to love for a child and love for a partner. “When visualizing parental love, areas deep in the reward system of the striatum become active — we don’t see this with any other type of love,” reports Rinne. As with romantic love, areas in the brain stem, cerebellum, temporal lobes, and along the entire midline of the head are also active. “The subcortical areas of romantic and parental love include brain regions closely linked to reward, bonding, motivation, and reinforcement learning,” the team says.
Unique Patterns Also for Friendship Love and Love for Animals
Comparing these two closest and most intense forms of love to friendship love and love for strangers revealed that while all these interpersonal emotions are similar in terms of some brain areas — the regions responsible for social behavior and parts of the reward system are active in all — the activity is weaker in friendship love and even more so in empathetic love for strangers, and encompasses fewer areas of the brain, as Rinne and his colleagues determined.
In contrast, non-personal love for nature or pets activates the reward system but not the social areas of our brain — with one exception: People who own pets themselves react differently. In their case, thoughts about pets or stories about pets evoke similar reactions in the brain as love for fellow humans. “The activity of these brain areas linked to sociality therefore reveals whether a person has a pet or not,” says Rinne.
“Wonderful Complexity of Human Love”
According to the researchers, the neural fingerprints of love in our brain reflect the diversity of the feeling we summarize as love. “From the perspective of functional neuroarchitecture, we see how the wonderful complexity of human love arises,” state Rinne and his colleagues.
Anyone suffering from migraines has undoubtedly heard the term “trigeminal nerve” from their doctor. This comes up when physicians explain how the agonizing, persistent pain in the head occurs. The trigeminus is a cranial nerve that connects the forehead, face, and chewing muscles to the brain. It sends faulty signals to blood vessels in the meninges, according to the currently prevailing theory. This is supposed to release inflammatory substances that cause the vessels to dilate, become more permeable, and thus begin the vicious cycle of pain.
New data from the United States now challenges this idea: While they also attribute a prominent role to the trigeminus in migraines, researchers led by neurobiologist Maiken Nedergaard from the University of Rochester, New York, have managed to show that it’s not about misdirected nerve signals. They demonstrate something previously considered far-fetched: In migraine patients, the trigeminal nerve has a hole at its brain-side end.
The work was published in the journal Science. The hole is located between the trigeminal nerve cells that process signals from the face and the brain. More precisely, its membrane. This allows cerebrospinal fluid to reach the cluster of nerve cells. This explains why a pain attack follows a migraine aura.
A migraine aura can be auditory hallucinations, numbness, but most often visual disturbances, temporary blindness, flashes of light, blinding circles, or “shooting stars.” These symptoms typically occur five to 60 minutes before the headache. It’s estimated that one in 10 people suffers from migraines, and in about a quarter of these cases, the headaches are preceded by an aura.
At that moment, a loss of voltage occurs at the level of brain cells. The cells, which normally build up electrical voltages across their membranes, “depolarize.” This means they can no longer build up electrical voltage and, thus, can no longer communicate. Most frequently, the depolarization event occurs in the visual processing center of the cerebral cortex, resulting in the visual symptoms that first announce an impending headache.
The substances that enable the voltage difference literally wash away, leading to the loss of voltage.
Nedergaard and her colleagues at the University of Rochester and the University of Copenhagen are pioneers in understanding fluid flow in the brain. In 2012, their laboratory was the first to describe the “glymphatic system”: Both the brain and spinal cord are surrounded by fluid-filled sacs. In emergencies, the system uses this fluid to flush out toxic proteins in the brain.
This also occurs spontaneously in migraine patients. In the process, proteins are released again as alarm signals, indicating that the voltage situation isn’t working properly.
Previously, it was assumed that the end of the trigeminal nerve rests outside these membranes, and the biological barrier there strictly controls which molecules can enter and leave the brain.
However, in experiments with mice where they artificially generated the fluid wave, the researchers found a previously unknown gap in the barrier. Through this, fluid could escape from the brain and flow directly to the nerve cell node at the tip of the trigeminus.
The nerves would then be exposed to a cocktail of alarm proteins.
The brain itself cannot generate pain when something is wrong. The trigeminal nerve can. And it’s precisely with pain that it reacts to the wave of fluid from the brain.
The discovery of alarm proteins is also somewhat novel. In total, they identified twelve proteins whose concentration increases sharply during a depolarization event and which simultaneously bind to receptors on the sensory nerves in the trigeminal end. A new class of medications already targets Calcitonin Gene-Related Peptide (CGRP), one of the proteins. These CGRP inhibitors prevent migraine attacks in advance.
Others of the alarm proteins identified in the Rochester study are already known from other pain studies. They suffer from neuropathic pain. Nedergaard and her colleagues now anticipate the development of effective pain blockers at this stage. They should prevent the proteins from triggering a pain signal at the trigeminus.
“In this study, we describe how the central and peripheral nervous systems interact with each other in migraine,” Nedergaard says in a press release from her university. “These findings provide us with many new targets for medications. We can devise strategies to avert nerve activation or migraine altogether.
The connection with the fluid wave in the head also explains why so many migraine patients have unilateral pain: There is one trigeminal end on each side of the head. The researchers observed that the transport of proteins released on one side of the brain primarily reaches the nerves on the same side.
The higher risk of Alzheimer’s disease in women compared to men may be due to a difference between the sexes that manifests as a protein shift in the brain. Specifically, it is found that C3 protein changes occur more often in female dementia patients than in male ones. This immune protein leads to synaptic atrophy when it undergoes a change.
Proteins adapt to their new environment in part because estrogen levels diminish after menopause.
Nearly 4 million women are among the more than 6 million Americans aged 65 and over who have Alzheimer’s disease. About twice as many females as males are afflicted. Nobody knows for sure what causes this neurological illness. The usual plaques in the brain are known to be formed by misfolded amyloid beta proteins. Moreover, tau protein filaments, or fibrils, develop inside the nerve cells. Both are known to increase the risk of brain cell death and subsequent cognitive decline. However, additional systems that are poorly known seem to be implicated in the illness as well.
Post-translational changes
Researchers from China’s Changchun University of Chinese Medicine, led by Hongmei Yang, have shifted their focus to other processes that may contribute to Alzheimer’s disease. Post-translational changes were investigated by the team studying the human brain. These are protein extensions that can change how the protein works.
S-nitrosylation (SNO) is one example of such a change. In this situation, a nitric oxide group serves as the appendage. The potential involvement of this alteration in neurodegenerative illnesses was suggested by previous research. Yang and his colleagues looked into the brains of 10 men and women who had died with and without Alzheimer’s disease to see whether there were any differences between the two groups.
Distinct variations
Researchers found a total of 1,450 SNO-modified proteins across all human brain tissues. Despite the fact that Alzheimer’s brains had just slightly more SNO proteins, their composition was very different from brains without Alzheimer’s.
They utilized statistical techniques to figure out which proteins were more likely to be S-nitrosylated in Alzheimer’s brains.
The researchers used this information to create a ranking of proteins that may have a role in Alzheimer’s disease. They discovered alterations in proteins associated with autophagy, a cellular mechanism that eliminates unnecessary or broken pieces. This finding has the potential to shed light on previously unrecognized mechanisms through which Alzheimer’s progresses.
Alzheimer’s dementia is exacerbated by mutations in the immunological protein C3, which accelerate the aberrant destruction of synapses in the brain. (Credit: Scripps Research Institute)
The majority of these alterations concern females
The so-called complement factor C3, a protein with a crucial function in the innate immune system, showed the most dramatic modifications. The investigation revealed that altered C3 proteins were mostly found in the brains of females with Alzheimer’s disease. Female brains with Alzheimer’s disease exhibited a 34-fold increase in SNO-C3 compared to the brains of women without Alzheimer’s disease. Male Alzheimer’s brains increased just 5.6-fold.
Although C3 has been implicated in the pathogenesis of Alzheimer’s disease, its S-nitrosylation and differential distribution between the sexes were previously unknown. Scientists used human stem cells to show that the altered C3 proteins increase neuronal deterioration by leading immune cells to erroneously attack healthy synapses.
Beta-estradiol could shield premenopausal women
The data demonstrated that beta-estradiol, a female sex hormone, may inhibit C3 modification, a process critical to the proper functioning of the immune system. This may explain why postmenopausal women have a higher risk of developing Alzheimer’s than men do.
The findings imply that beta-estradiol could shield premenopausal women against S-nitrosylation of C3.
However, this defense diminishes when estrogen levels decline after menopause. Therefore, C3 proteins in women’s brains undergo greater pathogenic alteration, making women more likely to develop Alzheimer’s disease. Together, these discoveries improve our capacity to comprehend Alzheimer’s disease’s progression and, maybe, to design more effective strategies for early diagnosis and treatment.
The startling similarity between us vertebrates and the invertebrate octopus is that little snippets of RNA may play a critical role in the formation of huge brains. This is due to the fact that octopuses’ nerve tissue and brains contain more active microRNAs than those of any other invertebrate.
Indeed, their collection of these proteins is the third greatest in all of life. This may be the key to understanding the extraordinary intelligence shown by these cephalopods.
No other animal group has the same genetic structure as the octopus, and no other invertebrate has developed such a sophisticated neurological system or as much intellect. Sea creatures like the octopus, squid, and cuttlefish have remarkable cognitive abilities. They are numerate and handy with tools. Octopuses have more neurons and neurological connections than rats and canines, respectively.
Typical of squid like this young octopus, they have enormous lenticular eyes, a massive brain, and a complicated neurological system.
Utilizing miRNAs as a Target
But why squid have developed such enormous, sophisticated brains, and how, is still only partly known. Researchers headed by Grygoriy Zolotarov of the Max Delbrück Center have therefore explored a particularly specific component of the cell biology of the sick: microRNA. Unlike messenger RNA, which contains genetic instructions for making proteins, these RNA fragments do not. However, they can bind to this mRNA and control how much of its information is translated into proteins.
Researchers Zolotarov and colleagues examined miRNA expression in 18 tissues from O. vulgaris, the common octopus, and O. bimaculatus, the California two-spotted octopus. What this showed was that there was something remarkable going on in the octopus tissues, where over 138 different families of microRNAs were all actively working. In addition, 90 of these microRNA families were previously unknown.
The number of microRNAs in the neural tissue of an octopus is higher than that of any other invertebrate.
MiRNA Repertoire Growth Is Exponential
After that, they compared the octopuses’ microRNA repertoire to that of the primordial, low-intelligence mollusk Nautilus and the dwarf squid Euprymna scolopes. The researchers report discovering 90 novel microRNA families, 12 of which were also present in Nautilus and the dwarf squid, and are therefore representative of the core cephalopod repertoire. 35 microRNA families were solely found in octopuses, whereas 43 were present only in octopuses and dwarf squid.
The research found that the amount of microRNAs has expanded drastically throughout the history of evolution, from primitive cephalopods like Nautilus to complex, high-functioning squid with a massive brain. This is the biggest microRNA family growth outside of vertebrates, and the third largest in the animal world overall. No other invertebrate animal has such a vast amount of microRNAs.
Squid, which are classified as invertebrates like chickens, actually contain more microRNA families (138 in all) than chickens do.
Active Primarily in Brain and Nerve Tissue
This leads scientists to wonder whether the octopuses’ huge brains and extraordinary intellect have anything to do with the remarkable growth of their microRNA repertoire. To elucidate this, Zolotarov and coworkers looked at the octopuses’ microRNAs and where they are active. Of the 43 octopus-specific miRNAs examined, 34 were determined to be functional in nervous system tissues. The average expression level in neural tissues was 13-fold higher than in other types of tissue.
Accordingly, microRNAs very certainly serve an important function in the maturation of brain and neural tissue. Researchers conclude that the rapid expansion of the squid’s microRNA repertoire supports the idea that microRNAs and the specific neuronal processes they regulate are important to the formation of sophisticated animal brains.
High-resolution brain scans have recently shown that migraine not only presents itself in the form of frequent headache episodes but also shows up on the brain. There are permanent alterations. The results indicate that those who suffer from migraines tend to have noticeably larger cavities surrounding the blood vessels in certain brain areas.
They also tend to have more microlesions, or minute holes, in their blood vessels. Those who suffer from migraines may have a neural lymphatic system malfunction, according to the findings of the study.
Mild darkening of the brain’s central white matter is indicative of abnormally enlarged fluid-filled gaps surrounding blood vessels, as shown in this migraine sufferer above.
Migraines cause severe headaches, sensitivity to light, and nausea for around 15% of the world’s population (1.1 billion people) and around 11.4% in the US. We still don’t fully understand what sets off this illness, which has a weak hereditary component, or how it shows itself in the brain. But it does seem that migraines have other, non-headache-related manifestations.
Between headache episodes, migraineurs exhibit anomalies in brain activity, cerebral cortex structure, and specific membrane lipids in the blood.
A picture of a brain with migraine
An additional characteristic of migraines has been found by a team led by Wilson Xu of researchers at the University of Southern California in Los Angeles. They scanned the brains of 25 patients: 10 people with chronic migraine, 10 people with episodic migraines, and 5 healthy control participants.
The researchers doing this MRI scan were especially interested in the minuscule alterations near the brain’s vascular system.Regional white matter compression was also more common in migraine sufferers. (Credit: RSNA/ Wilson Xu)
This is the first research to our knowledge to employ ultra-high-resolution MRI images to investigate microvascular alterations in the brains of migraine sufferers. Pain during a migraine episode has long been thought to be caused by a disruption in blood flow to the brain. Now, Xu and his team sought to see whether these shifts could be detected outside of the context of sudden strikes.
The group did, in fact, uncover its target. Migraine sufferers, both those who experience them often and seldom, tend to have alterations in the perivascular spaces. These are lymphatic drainage channels located around the brain’s blood vessels.
The presence of degenerative changes or inflammation of the vessels is sometimes accompanied by the symptom of dilated blood vessels.
The findings showed that the perivascular spaces were most enlarged in the so-called centrum semiovale in the migraine sufferers. White matter, which consists mostly of nerve conduits, is primarily located in this area of the brain between the cerebral cortex and the central ventricles. This crescent-shaped region of the brain is located on both sides, and the researchers detected an increased number of microlesions and other microscopic, concentrated regions there due to tiny breaches in the brain’s blood vessels.
The brain’s waste disposal system
Migraines, as Xu and his colleagues see it, may be related to an underlying dysfunction in the glymphatic system, the network of tubules, cavities, and drains responsible for removing waste from the brain. The perivascular spaces contribute to the brain’s waste management system. More research on their role in the development of migraine might aid in understanding the disorder’s complicated causes.
However, it is still unknown if the current alterations seen are a result of migraines or the cause. Researchers are hoping to learn more about this by conducting bigger investigations over longer periods of time.
Instinctive fear keeps us alive; without it, our species likely would have perished a long time ago. However, fear may sometimes take on a life of its own and make us physically unwell. Because once panic takes over our minds, there’s no stopping the terrible cycle: when we fear fear, we feel even more fear. But what exactly is fear? How did it get here, and what harm does it cause? This emotion originates in a very small region of the brain, yet it has an enormous influence on human behavior.
Fear and panic take control of our minds, bodies, and lives when the normal communication between the brain’s various regions and its neurotransmitters breaks down. However, once an anxiety condition has been identified, effective treatment options are available for people suffering from it.
The mutable nature of fear
We’ve all experienced it, whether it’s the dread of walking through a shadowy alley on our own, the fright of hearing a rattling sound on the balcony late at night, or the fear we felt as kids when we dared not stand in front of the bed, convinced that a hand would snap down suddenly and grab our bare ankles. Fear is often nothing more than an irrational thought that stays with us until it’s rationalized away. However, despite the fact that our irrational apprehensions seldom have any bearing on reality, they continue to linger in our thoughts anyway.
A healthy dose of fear saves lives
And that’s a good thing, since fear serves a useful purpose. To put it simply, it is one of the finest defense mechanisms our bodies have, and without it, the human race likely would have perished a long time ago. Within seconds of being startled, we are on high alert. The human organism is geared up and ready to function at its peak when it enters the “fight or flight” state. Instantaneously, the subconscious mind takes control of the body, and it is only after a little pause that the conscious mind intervenes to assess the situation. When things get rough, though, we turn tail and flee for our lives.
The human brain is crucial to this process. Primitive instincts are kept there, and they help us respond to certain perilous circumstances in the same way that our ancestors did thousands of years ago. Contrarily, it has a high capacity for learning; this is necessary for it to create new anxieties in response to the evolving threats of each new era. This means that our brain is able to identify and evaluate potential threats in both familiar and novel contexts without prior direct experience with them. The suffocating emotion then frequently leads us to automatically give these situations a wide berth.
But fear can be illogical
Many people are afraid of heights. (Image: Pascal Reusch (CC BY-SA 3.0))
Fear may take various forms and is usually hard to escape. It might be logical or illogical, and it often manifests when confronted with situations involving spiders, snakes, tests, heights, or small places. There are three basic kinds of fear: The kind of existential panic that comes from seeing an imminent fear of one’s physical or mental well-being. We worry more about being embarrassed in social anxiety than in performance anxiety. Anxiety is an irrational and meaningless emotional state, but fear describes a real and present threat.
Between healthy anxiety and anxiety disorder
All these fears have a comparable symptom set, although one with varying intensities and specifics. This occurs when several brain regions become active and then tell the body to take action. Most of the symptoms, including a rapid heartbeat, a suffocating sensation, sweaty hands, and stiffness, are well known.
However, anxiety may develop into panic attacks, which bring on physical symptoms such as chest tightness, shortness of breath, nausea, and dizziness. Anxiety disorders are diagnosed when what was once a normal emotion becomes a reoccurring panic that has lost all connection to the actual risk. There’s a fear that this may escalate to the point where the anticipation of another panic attack triggers it. Pathological anxiety is the term used by professionals to describe a condition in which a person’s normal activities are so impaired that they may benefit from treatment.
Where fear arises: Amygdala
The amygdala, our fear center. (Image: Life Science (CC BY-SA 2.1 jp))
Anxiety may have several physical manifestations, including but not limited to a rapid heartbeat, profuse perspiration, and elevated blood pressure. Like elevated blood pressure or enlarged bronchial tubes, many of these effects are so subtle that we scarcely even recognize they’re happening. This is due to the fact that the body’s response to acute danger is predicated not only on the fact that our conscious mind recognizes the circumstance as threatening, but also, and perhaps more importantly, on the fact that our unconscious mind can respond with lightning speed.
Only two nerve tracts and a small area
Here we see the autonomic nervous system at work, which controls our body’s internal processes independently of our awareness. That way, our bodies can adjust to the ever-shifting environments outside. When faced with an immediate threat, the body’s sympathetic nervous system activates to help bring all available resources to bear. The parasympathetic nervous system is in charge of recharging our bodies during rest and sleep, while the sympathetic nervous system is in charge of getting us pumped up for action.
The amygdala is the region of the brain that processes emotions associated with fear, and this has been recognized for some time. Limes are part of the brain’s limbic system, which is characterized more by its function than its physical location. This encompasses a wide range of activities, such as dealing with one’s feelings.
The woman without fear
This little functional unit in our brains, the origin of our fear, is starting to paint a fairly ominous picture. Imagine a world free of fear and trepidation.
This is the case when the amygdala has been damaged, preventing the maturation of a fear response. Another example of this is a very unusual clinical scenario in which the patient, dubbed “S.M.” by the medical staff, shows very little fear. Her amygdala has calcifications on both sides, impairing its ability to operate normally.
The scientists did not subject her to any of the following: spiders, snakes, a dungeon of horrors, or a marathon of psychological thrillers. Not a single iota of fear crept in. The researchers are rather amazed that the test subject S.M. is still alive, despite the fact that it is very “cool” not to sense fear in the scenarios indicated. Usually, fear serves as an alarm system, ensuring our safety as we go about our everyday lives.
What fear does to us
But how does the body function, exactly? Let’s role-play a potentially perilous scenario. On your trip, you see a snake in the middle of the road. The brain receives and stores a signal, including a picture of the snake. There, it first reaches the thalamus, the brain’s sensory control hub. That’s where all the information from our senses goes on its way to our brain. The thalamus then relays the information in two ways: swiftly to the amygdala and considerably more slowly to the cerebral cortex.
The subconscious mind thinks for us
When the amygdala receives a signal and determines that it poses a threat, it works quickly to alert other parts of the brain. Subsequently, the body releases hormones, including cortisol, adrenaline, and noradrenaline, which help activate the autonomic nervous system by stimulating the sympathetic nervous system and depressing the parasympathetic nervous system. Evolution thinks for you. As soon as you’re in danger, you’re already responding.
After being startled, the body goes through a short period of shock. During this limited window, a thorough assessment of the perilous situation may be made. This is because the prefrontal cortex, a region of the brain, is also performing at peak efficiency and assessing the issue at this moment. This is where much of our awareness takes place. To put it another way, while our conscious mind is still “thinking,” our subconscious mind is already doing.
A crude, unintentionally assessed “situation sketch” is also sent to the cerebral cortex from the amygdala. We’re at the point when people start thinking about whether to run away or fight. The scenario is only “defused in the mind” if the prefrontal cortex relays back to the amygdala that there is no risk or that the danger has been averted, like when we understand the snake is a fake and laugh at our fear. According to LeDoux, it is this loop that allows for the experience of conscious fear.
When the messengers go on strike
Neurotransmitters play a crucial role in signal transmission because they act as messengers in the brain. They serve as intermediaries between the synapse of many types of neuronal nerve cells.
Certain types of neurotransmitters are more active in certain parts of the brain. Most people only know dopamine as a happy messenger, yet it is one of the most well-known neurotransmitters and responsible for a variety of functions. The amygdala, on the other hand, uses it to create fear. A higher level of dopamine release in the amygdala correlates with a more intense fear reaction.
Serotonin is another neurotransmitter that has been discovered. Anxiety, concern, and fear develop when this neurotransmitter fails to “get through” or is missing during anxiety formation, which takes place in the brainstem. As a result, low levels of serotonin might contribute to feelings of depression and irritability.
Other neurotransmitters, like GABA and norepinephrine, also contribute to the emergence of fear. It’s not only the amount of information that matters, but also whether or not the neurons and synapses receive and process it. Mood swings, as well as shifts in behavior and thought, may have many different origins.
Anxiety disorder: The enemy in your own head
Anxiety and panic disorder symptoms may strike anywhere, including the metro, the theater, and the grocery store checkout line. In doing so, the worry multiplies like a virus, invading and eventually taking over even more aspects of daily life. If anxiety attacks become too severe, people may start avoiding the triggers altogether. However, the more people isolate themselves, the worse their anxiety gets, until finally, for many, their own homes become their only refuge.
Discordant spirit
We talk about an anxiety disorder when rational thought is replaced by irrational fear. Approximately one-quarter of the population experiences such pathological anxiety at some point in their lives; women are more likely to be affected than males. They often manifest in the early adult years in response to a stressful event, whether it is an accident, the death of a loved one, or “just” stress. In our daily lives, we don’t need to be scaredy-cats for any of them to increase our susceptibility to anxiety-inducing events.
It’s common for the phase to end on its own. Repeated episodes of unwarranted worry over an extended period of time only serve to exacerbate the situation. As much as possible, they steer clear of anything that can set off their anxiety. Anxiety episodes and generalized avoidance put a significant damper on daily life, making it difficult to take any kind of action. It’s possible that a variety of clinical presentations of persistent anxiety disorder might emerge: Some examples of these conditions include social phobia, particular phobia, and panic disorder.
Wide range of phobias
Everyone is familiar with the hundreds of different types of phobias. There are both logical and irrational phobias, as well as particular and social phobias of things like certain locations or animals. Hippopotomonstrosesquippedaliophobia is the fear of really long words, and the term is a scientific joke. Simply letting people know about the illness might send people into a state of complete and utter panic.
The majority of phobias seem rather ridiculous, no? The inability to fit in socially is a major challenge for those with anxiety disorders. Because fear is such a personal sensation, we frequently dismiss the fears of others or believe that our own fears are met with good-natured laughter. However, phobias lose all of their comedic value if they begin to control a person’s daily life. This occurs when people attribute negative emotions to situations that provide no real threat. Agoraphobia, the fear of locations or circumstances from which there is no easy escape, is a common phobia.
Having a fear of having a fear
The trouble with anxiety disorders is that it’s possible to develop a fear of fear itself, a condition known as phobophobia. There is a domino effect that leads to further problems. It’s possible for this to occur since our brains readily generalize our fears. What’s meant to keep us safe in a world full of new threats has the potential to become a mental illness.
When someone has had a panic attack, for instance, they may worry that the fear may happen again in a similar setting. The other three options are that (1) no panic occurs when a comparable circumstance develops, and (2) everything works out. Or maybe we manage to dodge them altogether. Or maybe the impending fear inspires the next assault. In this case, the fear might become a self-fulfilling prophecy, manifesting itself in ever-increasingly threatening circumstances, from which there is no real way of escaping.
Even if such fears are difficult to ignore, it may be years before a person is diagnosed with an anxiety condition. The reason is that the onset of physical symptoms in a panic disorder may be sudden and severe. A person with this disorder may experience a wide range of symptoms, from an incorrect diagnosis to the firm conviction that they are about to die. Because of the nature of a brain-based illness, victims often see a succession of medical professionals without resolution.
Insufficiency and excess in mental processing
It’s common for people to freak out despite the obvious lack of threat. However, why is it that the conscious mind has long understood that a certain circumstance is harmless, while the subconscious mind continues to fail to accept it as such? With anxiety disorders, two things go wrong in the brain: the amygdala speeds up, while the prefrontal cortex slows down. What this implies is that our subconscious’s fear center is always overactive, sending the body the message that it is in a hazardous circumstance even when there is none. That it isn’t, the prefrontal cortex at that time doesn’t recognize it, therefore it doesn’t tell the amygdala to relax.
Numerous neurotransmitters in the brain are likely playing a role, since they are out of whack. A panic attack may be triggered by a variety of factors, including an imbalance in neurotransmitters, exposure to a stressful event, persistent stress, or an unhealthy way of life. Patients with panic disorders, for instance, have lower levels of anxiety that trigger GABA.
The gene responsible for fear
Anxiety is a complex emotion, and its intensity is influenced by a wide range of factors. One’s own lifestyle and attitude, a traumatic event, and even one’s own genetics may all play a role in exacerbating an existing fear and turning it into a phobia. For the simple reason that our ancestry already tells us whether or not we would be vulnerable to fear-based disorders.
The probability of inheriting an anxiety condition is three- to six-fold greater in some families. Gene variations often change the brain’s messenger system in a manner that makes us more vulnerable to fear disorders. Numerous variations in this kind of gene have previously been discovered. However, they are not independent factors; rather, they are the result of a number of genes interacting in a complicated manner, leading to a condition known as a complex genetic illness. Genetic risk is the result of several genes interacting in complex ways.
Still, having a genetic predisposition doesn’t guarantee that the illness will manifest. The fact remains, nevertheless, that they are a necessary requirement. An estimated 50 percent of the onset of affective and schizophrenia illnesses may be traced back to genetics. Many aspects of one’s way of life, such as the use of alcoholic beverages, contribute to the remaining 50%.
Patterns in education influence us
In addition to our genetic makeup, our development may be shaped by the experiences we encounter as children. This is because children often mimic their parents’ behaviors and attitudes. In the case of a lack of fear of heights, for instance, this trait may be imparted to offspring by seeing their parents’ own attitudes and actions. They may teach their child to fear heights by reacting wildly and panicking when exposed to dangers like cliffs and other vertical surfaces.
Is fear inherited?
Is it also possible to pass on a learned fear? In 2013, American researchers found that mice were able to pass on their acquired fear to their offspring. Researchers Brian Dias and Kerry Ressler from Emory University School of Medicine in Atlanta used electric shocks to teach mice to develop a fear response to the aroma of cherry blossoms. After mating the animals, they created hybrids. It turned out that the smell of cherry blossoms sent fear into the hearts of the next two generations as well.
The biological inheritance of experiences is shown here, at least in mice. The epigenome is responsible for this. These tethers to DNA regulate gene expression in numerous ways. It was shown that chemical modifications to the genes responsible for odor recognition in mice might affect the gene’s activity. Extensive investigation is still needed to see whether the same holds true for people. This, however, would imply that parents aren’t the only ones passing on their fear to their children.
How to face fear?
Concerning anxiety disorders, the prognosis is typically quite excellent. The first step in getting help for anxiety disorders is realizing that you have a problem and trying to fix it on your own if you can. But if it doesn’t work, or if their anxiety is so bad that regular living is difficult or impossible, they should see a therapist or psychiatrist.
Realize the significance of your way of life. It follows that if a person’s pathological anxiety worsens, making adjustments to their regular routine might be helpful. First, it’s important to minimize stress; regular exercise, even for 30 minutes a day, may help a great deal. A balanced diet and avoiding using substances like alcohol or drugs to numb one’s fears are also crucial.
Anxiety patients might utilize the tactic of “desensitization” to target and lessen their episodes of anxiety. Similar to how the immune system learns to stop responding to an allergen, facing a fear may teach the brain to minimize the reactions. It’s necessary to confront fears and actively seek out “dangerous” circumstances, however. Psychotherapy takes advantage of this as well.
Hold your ground rather than run away
Sitting it out is the best option if the anticipated fear materializes. The best thing to do if you’re scared of the seemingly hopeless scenario on the train is to stay seated and keep going till your nerves calm down. Getting out of there doesn’t imply you’re a failure or have to quit. It’s best to give it another go once you’ve had a chance to collect your thoughts and the initial worry has worn off. In most cases, the human body just can’t withstand prolonged exposure to high levels of stress. Slowly but surely, calmness settles in, and the first step is made.
Our amygdala, the fear center of the brain that monitors threats, eventually concludes that we are safe. This is due to the fact that the fear memory has a high learning capacity; otherwise, anxiety disorders wouldn’t exist. An area of the brain reconditions the individual by writing over the previous pattern. Eventually, the brain “perceives” the once unpleasant circumstance as neutral, and the panic response to it fades.
When life is a constant minefield
It’s time to seek professional aid after you’ve exhausted all other options for resolution. The sooner an anxiety problem is identified, the better it may be treated, but for many individuals, this comes much too late. Additionally, there are additional positive indicators of achievement. Psychotherapy and medicine are often used together to treat patients. Using cognitive-behavioral therapy, one may also face their fears head-on.
Medications assist in altering the brain’s neurological circumstances in such a manner that there are fewer pure physical fear impulses if patients are unable to manage their anxiety via behavioral changes. Drugs like antidepressants and benzodiazepines are widely used and well understood. Both medications elevate levels of the relevant neurotransmitters.
Medicine as treatment
Although these medications are often the last choice for patients with severe anxiety, many patients report limited effectiveness and significant adverse effects. Researchers are always looking for novel treatments, but no effective psychopharmaceutical has been created as of yet. But gradually, some researchers are starting to focus on something “different”: the components of various drugs of abuse.
Because psychotropic mushrooms and ketamine, two common hallucinogens, may provide fresh promise in the treatment of anxiety disorders. Many years ago, the use of these chemicals was outlawed in the field of drug development. Yet researchers are examining them in depth to see whether they may really help people get well. Tiny dosages of ketamine given intravenously may benefit very ill individuals. It has come a long way, but it has not yet been widely recognized as a legitimate medical treatment. Looking into adverse reactions and addiction will need more study time and resources over the next several years.
It’s an old saying that laughter is good for you. People report feeling healthier and stronger after a good laugh. However, might there possibly be any truth behind this? What happens when you are stressed and not in the mood to laugh? What good does smiling do for you? Does it make you live longer? As early as the Bible, people recognized the healing power of humor and laughing. A laughter’s remedial powers continue to be covered extensively in both the scientific and popular press. However, only a fraction of this subject has been systematically investigated.
Suppressing pain and stimulating the immune system
Nonetheless, it’s widely accepted that a good belly laugh stimulates our immune system. Scientists discovered this with 52 willing participants in a 2001 study. Several types of immune cells, including killer cells crucial for warding off illness, were substantially more active in the blood when the young men had just viewed a comedic film and laughed.
Intense bouts of laughing have been shown to alleviate pain. British scientists found that this was due to the fact that it prompted the body to produce its own opioids, hence reducing the body’s production of pain-signaling molecules. Researchers found that participants with a history of laughing had a greater pain tolerance than those who had not recently experienced laughter.
Yet another way in which laughing may alleviate stress is by lowering blood levels of the stress hormone cortisol, which is often elevated when people are under pressure. The levels of cortisol, however, fall significantly following a bout of laughing. This means that laughing immediately mitigates the stress response. Laughing also counteracts the suppressive impact of stress on the immune system.
Put on a forced smile and you’ll see results
Okay, but what about smiling? After all, it’s not often that you can laugh heartily and for an extended period when under pressure. According to the preliminary research that even a forced laugh or smile might have an impact. 22 participants were prompted to laugh, smile, or howl like wolves at various points during the research.
All participants were interviewed and given tests to measure their emotional states before and after each of these occurrences. The results showed that howling did not have any effect on the test subjects’ moods, but that forced laughing and smiling had a considerable positive effect.
The mere act of raising the corners of your mouth
Even when you merely raise the corners of your mouth in an artificial smile, it still helps. This is what a group led by psychologist Tara Kraft from the University of Kansas discovered. Scientists were curious to know whether or not the mere act of contorting the facial muscles in a smile had any beneficial effects, regardless of the test participants being conscious that they were smiling.
Kraft accomplished this by subjecting 169 test volunteers to stress by having them hold chopsticks with their lips while completing computer-based activities under time constraints. Half of the volunteers were instructed to smile while the other half were told to keep a neutral expression throughout the experiment. The reason for this was that everyone had to reflexively bend their lips and facial muscles as if they were smiling, to maintain the chopsticks in their mouths.
The findings of this study demonstrate the physiological effects of smiling, even when we are unaware of doing so. This is because throughout the stress activities, the heart rates of all participants who had previously held chopsticks stayed much lower than those of control subjects who had done the tasks without chopsticks. Facial muscle contractions reduced not just objective measures of stress but also subjective assessments of it.
Try forcing a smile the next time you’re stuck in traffic or going through any other stressful situation. This helps counteract the bodily manifestations of stress, in addition to enhancing your public persona right away.
What makes chocolate so addictive? Chocolate, in any of its many forms (dark, milk, or white), is a food that is consistently well-liked by a large number of people. It shouldn’t come as a surprise that, for many people, chocolate is inextricably linked to happiness. They feel the urge to consume at least one portion of this delectable delight by melting it in their mouths each day. They turn into “chocoholics” (chocolate addicts).
According to a study, those who are susceptible to chocolates may go through similar physiological changes to those who become dependent on substances like alcohol or drugs. Similarly, people who are addicted to chocolate have an unquenchable desire for it that nothing can fill.
More than 40 percent of women and 15 percent of men have a craving for chocolate that is comparable to addiction. In more severe cases, people may consume chocolate in secret or in large quantities, similar to the way that some people do it with alcohol.
People who are addicted to chocolate state that they become irritable when they are unable to indulge in their habit. The desire for chocolates is very comparable to these more common types of addiction. But it’s not clear if these similarities are enough to show a link between chocolate and the complex physical and mental effects of addiction.
Simply Having a Sweet Is Not Sufficient
So, why is it that chocolate is so hard to turn down? There are a lot of hypotheses about it, but there isn’t much evidence to back them up, and there isn’t much agreement among specialists. Some researchers believe that the addictive qualities of chocolate are caused by the high amount of sugar that is contained in it. A preference for sweet foods is hardwired into the human brain, as well as the brains of many other animals. This is likely due to the high amount of energy that is contained in sweet foods.
However, 75 percent of people who identify as chocoholics claim that other types of sweets are unable to satisfy their cravings.
Some people may base their addiction on the typical flavor of chocolate, which can be described as the way it melts on their tongue. Other people may base their decision on the texture of the chocolate.
But for this to be true, white chocolate should be able to satisfy the needs of chocoholics too. Because its consistency is identical to that of cocoa, and it lacks cocoa’s flavor and, possibly, the elements of cocoa that are beneficial to the body’s physiological function. Experiments have been carried out to prove this theory. According to that, white chocolate temporarily reduces cravings for chocolate, but the effect is only temporary.
This suggests that either a biologically active component or the typical aroma of chocolate plays a role in the development of chocolate addiction.
Effects of Chocolate Addiction Are Comparable to Those of Cannabinoids
Anandamide.
Researchers who specialize in the study of addiction note that chocolate contains several substances that affect a person’s body and mind. Among them are the precursors of anandamide, which is a molecule with an action in the brain that is analogous to that of the narcotic that can be found in cannabis. The coffee stimulants include caffeine, tyramine, and phenylethylamine, among others.
The euphoria you experience from eating chocolate may be due to the increased levels of anandamide in your brain. On the other hand, the physiologically active components of the chocolate may work together to produce this effect. There has been no investigation into whether or not this is the case. It is still unknown whether these substances found in chocolate are indeed sufficient to cause a biological impact.
Nevertheless, it is undeniable that the cravings that are reminiscent of chocolate addiction are real, even if the exact mechanism of action is unknown. Medical professionals and nutritionists need to take this into account when attempting to alter the eating behaviors of their patients, especially those who are overweight.
A person’s intellect is not very noteworthy if their IQ falls between 85 and 115. That puts the person in the middle of the pack or on the ability spectrum. Conversely, you need to have an IQ of 130 or more to be considered among this elite group of brilliant individuals. However, only around one person in every 50 reaches such a level. Can intelligence be inherited? Or, is there a way to improve it via training?
The brain-exercising
There are no solid scientific assertions pointing in this direction. Intelligence is one of those traits that remains surprisingly consistent over a person’s lifespan. There is no way to improve upon the underlying talent pool. However, the brain is capable of adapting to new challenges. Improvements in memory performance or the capacity to spatially orient taxi drivers are two examples. So it needs consistent effort and concrete benefits to greatly enhance a skill.
There are several brain-exercising apps available today. But what do they even do? All of the best brain exercise programs test your patience and resolve by putting you in sticky situations where you have to come up with a solution on the fly. Most of the programs also need lateral thinking and the development of intricate answers.
This also encourages creative thinking and prevents individuals from falling into the same ruts of thinking in the same ways over and over. The term “brain exercise” refers to a set of techniques used to improve cognitive performance. Many specialists, however, are uncertain as to whether or not this also results in a rise in IQ.
Intelligence levels among young individuals are continually evolving
However, whereas adults’ IQs don’t seem to fluctuate much over the course of a lifetime, children and teens’ do. Researchers have shown that there is still room for significant IQ differences among them. The research found that between the ages of 12 and 16, individuals may experience both declines and gains of up to 20 points. Changes in IQ are caused by structural changes in the brain.
However, experts are baffled as to what causes these IQ spikes. Since it can’t be ruled out that education plays a role, this means that intelligence can be taught, at least in young people.
Prematurely dismissing those who were formerly seen as poor achievers is unwise since their intelligence may have increased dramatically in only a few short years. There is a widespread practice, common in many nations, of deciding a child’s future educational trajectory from an early age.
Logic games on the computer are good for your brain
The idea that playing video games might help young people develop higher intelligence is a relatively recent discovery. This, however, does not apply to all video games but rather to specialized programs designed to improve reasoning.
According to the study, children who were trained in this way both outperformed their peers on IQ tests over time and also saw their academic performance increase dramatically during the same period.
Are they also smarter in everyday life?
The benefits of having a high IQ in the classroom and the workplace are obvious. Yet, are there not also practical benefits to having a powerful brain? It is not always true that people with high IQs are also “smarter” in other areas of life.
Highly endowed individuals often do not learn to utilize their exceptional skills strategically. It is of little benefit to understand the precise mechanics of how the nail must be driven into the stone and what happens to the metal while it does so. You just have to precisely strike the nail with the hammer.
How is it possible to accustom ourselves to enjoy a flavor that previously had a repulsive taste? There is a widespread consensus among coffee consumers that coffee has an unpleasant flavor, especially when first sipped. Despite this, they identify themselves as coffee enthusiasts. Then they will tell you, “You just have to get accustomed to the taste.” “You learn to enjoy the taste,” even if it’s something unpleasant like a bitter alcoholic beverage, a hot dish, or the smell of cigarettes. But how does it even work? How can we overcome our dislike for flavors that are unpleasant?
Humans have the most bitter taste receptors, with around 25 distinct ones identified. Sweets, on the other hand, only have one receptor. Frogs have roughly 50 bitter receptors, coelacanth fish have about 70, while penguins only feel salty and sour flavors.
A defensive purpose
To begin, the ability to detect bitter flavors serves a defensive purpose. Poisonous or inedible plants are often bitter, which almost immediately discourages humans from consuming them. As a result of this, this protective reflex is still very potent in children, who tend to put a lot of items in their mouths as they investigate their surroundings. Despite this, there are a lot of individuals who really like things that make other people grimace. Coffee, for example, has a taste that is at first revolting, but most people grow to appreciate its flavor after giving it some time to grow on them.
It is about experience and time
For one thing, it’s all a question of becoming used to an unpleasant taste; the more often we are exposed to it, the less it affects us after the first few times we experience it. This is mostly because the first warning becomes less effective over time, assuming that the sour flavor does not result in unfavorable experiences. If you felt queasy after drinking just a little bit of coffee, you probably won’t ever get accustomed to the taste of coffee.
Positive reinforcement is what matters
However, the concept known as positive reinforcement is the most significant factor in determining behavior. The mere absence of a bad experience is insufficient to make the flavor desirable on its own. On the other hand, if an occurrence is followed by a beneficial result, then the response to the occurrence will supersede the unpleasant warning signal. Caffeine, which is found in coffee, for example, is what causes this energizing effect. This reinforcement may also happen when the activity is done with other people, like when you have coffee and cake with friends or family.
How it works?
To put it another way, our brain is capable of learning two different things. To begin, the flavor isn’t all that horrible. Second, the flavor has pleasant after effects on the person. The initial aversion is gradually transformed into something else entirely in the end.
