#hippocampus is in charge of higher thought and memory.

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not sorry i really do believe you have to be fundamentally stupider than the average person to believe in religion and religious teachings.

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18 Amazing Benefits of Yoga, According to Science

Yoga is becoming more mainstream in western cultures as those who practice it realize the numerous physical, mental, and emotional benefits that come with the ancient art. Science has proven that yoga can have a transformative effect on the body, resulting in everything from lowered blood pressure to disease prevention. Here are some of the many health benefits of yoga, as proven by science. 1. Regular Yoga Practice Relieves Stress and Anxiety Almost every benefit that comes from regularly practicing yoga stems from the activity’s proven stress-reducing properties. Stress has become the norm in our everyday society. With high-pressure careers, children’s demanding schedules, and little time to focus on self-care, more adults than ever are experiencing dangerously high levels of stress. Those who experience frequent stress and anxiety are at a higher risk for clinical depression, high blood pressure, chronic disease, insomnia, and a host of other problems. When the body becomes regularly anxious or stressed, it may never get the signal to return to normal functioning. This can lead to a prolonged ‘fight or flight’ response that is incredibly draining on the body and the mind. Preliminary research shows that practicing yoga can have the same stress-reducing effects as exercise and relaxation techniques, which makes sense because it is essentially the combination of the two. The controlled breathing that is inherent in practicing yoga is probably the biggest factor in reducing stress. When focused on breathing, participants have little room to engage in irrational fear, worry, or other obsessive thoughts, many of which are contributing to their stress levels. Yoga also helps increase mindfulness and the focus on gratitude, both of which help to ease anxiety. When we take the time to practice yoga, we are taking time to care for ourselves. This has taken a back seat in our current culture, and yoga can teach us to get back to basics. Focusing just 20 to 30 minutes a day on the self-healing practice of yoga can then lead to other beneficial activities. It can be a gateway to a more calm, focused life. Bottom Line: Yoga can help reduce stress and anxiety by focusing on breathing and increasing mindfulness and focus on gratitude. 2. Practicing Yoga Improves Cardiovascular Health Heart health is crucial to our overall wellness. Hypertension and coronary blockage leads to hundreds of thousands of deaths every year. Relaxation is incredibly helpful when it comes to heart health as it relaxes the blood vessels and reduces blood pressure while increasing blood flow to the heart. Because of its combination of breathing, meditation, and slow controlled movement, yoga is one of the most relaxing exercises on the planet. Yoga, especially the more energetic forms, also increases the heart rate. This makes it as beneficial to your heart as any other form of exercise. In fact, yoga may actually lower the risk of heart disease as much as traditional exercise such as brisk walking. Those who are interested in the cardio benefits of yoga should try out the more active forms such as ashtanga yoga, which provide more of a bump in heart rate than other forms. They might also consider pairing a vigorous form of yoga in the morning with a relaxing form in the evening to provide more stress-reducing and sleep benefits. Individuals who have suffered a heart attack or are recovering from other heart-related issues also benefit from yoga. Because they are unable to perform more strenuous exercises such as jogging or bicycling, the low-key and less strenuous poses of yoga give them the exercise they need without taxing their already strained heart muscle. In addition, those who have suffered a cardiac event also benefit from the stress-reducing effects of yoga. Having a life-threatening heart attack or stroke can induce acute emotional stress, which continues to have a negative effect on the heart even after the event is over. Those who have heart-related illnesses often have to face the fact that they have a life-altering condition. This can often cause grief or depression, both of which are proven to be eased by yoga. Bottom Line: Yoga improves cardiovascular health by lowering blood pressure, offering relaxation benefits, and increasing blood flow to the heart. It’s also beneficial for those recovering from a heart attack. 3. Yoga Strengthens Brain Activity As we age, our brains change. Certain parts, such as the prefrontal cortex and hippocampus, shrink. Because these areas are crucial to our learning, memory, planning and other mental activities, This can lead to frustrating memory lapses, inability to focus, and a struggle to retain new information. In extreme cases, in can even lead to neurological diseases such as Alzheimer’s or dementia. Not surprisingly, yoga promotes a more focused, calmer mind through its controlled breathing and focus on relaxation. What may come as a surprise, though, is that yoga can actually change the physical makeup of your brain matter. Using MRI scans, scientists have detected more cells in certain brain areas of those who practiced yoga regularly. Yoga practitioners had larger brain volume in their somatosensory cortex, visual cortex, hippocampus, precuneus and posterior cingulate cortex. These areas are in charge of visualization, concept of self, and directing attention. Scientists attribute these benefits to the focused breathing in yoga, which maximizes oxygenation and blood flow to the brain. These benefits also led to fewer depressive symptoms and increased memory performance in practitioners. The happier and more positive thoughts that flow from yoga can also help change the chemical composition of the brain and ‘rewire’ it to focus more on positive thoughts. When we break the habit of reacting to stressful events with anxiety and negative thoughts, which yoga helps us do, we encourage the mind to embrace more beneficial thinking. This helps us embrace the present moment and let go of harmful anxiety. Bottom Line: Yoga helps increase brain matter in various areas of the brain, leading to better memory, less depression and more focus. It also helps rewire the brain for positivity and promotes a calm mind. 4. Practicing Yoga Can Lower the Risk of Cancer Cancer remains one of the leading causes of death in the United States. In fact, one of four deaths in the U.S. can be attributed to some form of cancer. Practicing yoga may prevent the genetic mutation from expressing in those who have a family history of cancer. This means that it can have powerful cancer prevention properties. It can also help reduce fat stores in the body, which reduces the likelihood of cancer developing and spreading. Chronic stress, which yoga helps to reduce, weakens your immune system and leaves you more susceptible to diseases like cancer. It can also enable cancer cells to grow and spread as it increases negative hormones and certain growth factors. The stress-busting quality of yoga can boost your immune system and regulate hormones, both important cancer-fighting tools. In addition to cancer prevention, a regular yoga practice with the soothing music from yoga DVDs can also help those who are battling cancer by lowering inflammation, boosting energy, and lifting the mood. One study showed that regularly practicing yoga for three months was effective in improving thenegative moods of those undergoing treatment for breast cancer. Cancer treatments can also cause fatigue and zap strength in those undergoing them. Yoga has proven beneficial in combating these symptoms and can improve range of motion in patients and help them stay limber and active. Bottom Line: Yoga can help prevent cancer by reducing fat stores and preventing genetic mutation expression. It can also assist those undergoing cancer treatments by keeping them limber and boosting energy. 5. The Deep Breathing and Poses of Yoga Improve Digestion Devotees of yoga believe that all health begins in the gut. If we are digesting food, air, water, and energy properly, every other part of the body and mind suffer. Yoga improves our body’s internal rhythms, which assist in how we digest and detoxify. Even if you don’t currently suffer from any outward signs of impaired digestion, increasing our body’s ability to remove toxins is extremely beneficial. Many people suffer from poor digestion and constipation. Not only is it uncomfortable, but it can also lead to colon cancer and other diseases. Still others have developed chronic digestion disorders, such as irritable bowel syndrome or Crohn’s disease. These disorders can have a serious impact on our quality of life. Relying on laxatives or other interventions is not a good way to combat digestive issues, and many find that a high fiber diet is not enough to resolve their issues. That’s where yoga can come in handy. Deep breathing, the cornerstone of all yoga practices, is like a mild massage for the digestive tract. Breathing brings life force into the body, and helps cleanse it of dangerous toxins. There are also a number of different poses, such as the peacock and nauli, that are designed specifically to get waste moving through and out of your body. Many of these are best done in the morning on an empty stomach and after a glass of warm water with lemon. In addition to being helpful for improved digestion on its own, the practice of yoga also encourages individuals to take care of themselves with a healthier diet, more rest, and fewer processed foods and beverages. The increase in self-care helps not only with digestion, but with feeling good as a whole. Bottom Line: Yoga helps move toxins through the body with deep breathing and specific poses aimed at improving digestion. 6. Those Who Practice Yoga Are More Aware of What’s Going on in Their Bodies The term ‘body awareness’ can take many forms, each of which can be enhanced by the practice of yoga. As we grow into adults, most of us start losing touch with our bodies as matters of the mind take over. We focus so much on our thoughts and feelings, we forget about the mind-body connection and how powerful it is. This can lead to a reduction in the enjoyment of simple pleasures such as the feel of the sun on our face, or the warm breeze across our skin. It can also lead to a disconnection between ourselves and our bodies. As we age, this disconnection becomes more pronounced, which is why we often hear of seniors experiencing more falls and accidents than their younger counterparts. When we’re aware of and connected to our bodies as we step into our yoga pants, we’re able to better enjoy the present moment and understand what impact it has on us both physically and mentally. Yoga brings body awareness to the forefront. Each pose is focused on one or more body parts and as we breathe in and out, we are only only aware of that breath but also of the part of the body we are currently stretching. Yoga is also based on being aware of what your body is and is not capable of. Because no pose should be forced, those who are practicing yoga must listen to their body and make adjustments based on what it is telling them. Bottom Line: Yoga helps increase the mind-body connection. This enhances enjoyment of the present, and also encourages us to be more in tune with how our bodies move. 7. Yoga Practice Lowers Sugar Levels in the Blood, Decreasing Diabetes Symptoms Diabetes is an epidemic that is becoming quite common in the United States. A condition that is triggered by high blood sugar, either due to lack of insulin production in the body or the body’s lack of response to insulin, diabetes can lead to a dependence on medication, amputations, or even death. Type 1 diabetes tends to develop in childhood or early adulthood and is usually genetic while type 2 diabetes usually develops in adulthood and is often a product of an unhealthy lifestyle. Along with lowering blood pressure and keeping weight in check, yoga helps with diabetes by reducing the levels of sugar in the blood, all of which help slow the rate of progression and lessen the severity of complications. Though it’s a more gentle form of exercise than most people are used to, yoga still provides a workout. The boost in heart rate experienced by yoga practitioners can improve glucose metabolism and increase insulin sensitivity, both beneficial to diabetes sufferers. Cravings for sweets is a common symptom of diabetes, and the ensuing consumption of sweets only aggravates the problem. Deep breathing, yoga positions, and meditation can help reduce these cravings. When we become more aware of the mind-body connection through the practice of yoga, we can identify what our bodies really need and make healthy decisions about what we put in our body. Bottom Line: Regular practice of yoga can decrease blood sugar levels, keep weight in check, and reduce stress, all of which help improve diabetes symptoms. 8. The Practice of Yoga Can Help Regulate Your Adrenal Glands Adrenal fatigue syndrome can cause lack of energy, disrupted sleep, anxiety, and a number of other symptoms that are triggered by a sustained ‘fight or flight’ response in the body. This can result from prolonged levels of stress, a traumatic event, or a stressful living situation. When your adrenal glands are not functioning correctly, too much cortisol is released into your body and it compromises your immune function. Those who have adrenal fatigue syndrome get sick more often and have a lowered level of energy to deal with the sickness. They are also more susceptible to osteoporosis and high blood pressure, and tend to gain more fat in the abdomen area. Mastering the breathing that is the center of all yoga practices is a key element in managing stress levels. Because high stress is the main contributing factor to adrenal issues, it makes sense that this type of breathing will lower cortisol levels and lessen the symptoms of adrenal fatigue syndrome. When we practice yoga, we also give our minds a chance to quiet down and take a break from any negative our repetitive thoughts that often take over when our adrenal glands are overwhelmed. This can be a beneficial time to check in with ourselves and identify how we’re feeling. Those experiencing high stress often put themselves last, which only leads to more stress. Yoga encourages us to to take some time for ourselves. When we look deep, breathe, and practice self-care, we can often deal with negative emotions and the situations that are causing them. Bottom Line: The regular practice of yoga can reduce stress and lessen the release of cortisol, helping to combat the symptoms of adrenal fatigue syndrome. 9. Yoga Strengthens Bones Weight-bearing activities have long been known to strengthen bones, which is why many of those who are at risk for osteoporosis are encouraged to begin a strength-training workout regimen. Yoga training, with its many positions that  put pressure on different body parts, can be considered weight-bearing and has shown the ability to build bone mass in scientific studies. In contrast to other, more intense cardio exercises like jogging or weight training, yoga does not damage cartilage or stress the joints. Instead, it lengthens and holds muscles, which creates tension on the bone. This helps to build bone strength. The release of cortisol, the hormone triggered by stress, is another factor in osteoporosis. Yoga, with its relaxing and stress-calming nature, can reduce the amount of cortisol that is released and therefore lessen the impact it has on the bones. As few as a dozen yoga poses held for 30 seconds each, if done on a daily basis, can be enough to ward off osteoporosis and strengthen bones in the spine, arms, and legs. Bottom Line: Performing weight-bearing exercises, including various yoga poses, can reduce calcium-destroying cortisol and build bone density. 10. The Healing Powers of the Breath Aid in Improved Respiration Yoga is all about harnessing the healing powers of the breath. Though all of us must breathe to live, most of us do not breathe efficiently. Experts agree that to feel your best, you should breathe approximately 5 to 6 breaths per minute. However, most of us take anywhere from 14 to 20 breaths per minute, which is three times faster than what is healthy. Breath changes depending on emotion, and vice versa. When we get panicked, upset, or angry, we tend to breath more shallowly and at a faster rate. When we get used to breathing this way because of chronic stress, our body gets used to it and we develop the habit of breathing quickly even in normal circumstances. When we breathe at a slow and relaxed pace, we are signaling to the brain that it can rest and that no dangers are present. This reduces stress hormones, turns off danger warnings, and allows our body to recover. Not only do we turn off the ‘fight or flight’ response of our nervous system when we breathe deeply, but we also increase chest wall expansion and lung volumes. This is beneficial to all who practice yoga, but can be especially important for those dealing with a respiratory illness or condition such as asthma. Everything in yoga is based on the breath. Pranayamic breathing exercises can be performed anywhere when you are in need of stress relief or relaxation. Make sure the air quality in your practice environment is good, however - consider getting an air purifier if that is not the case. All other forms of yoga, from the extremely gentle restorative yoga to the more intense vinyasa and ashtanga practices, also rely on a basis of breathing deeply and being aware of how your breathing affects every part of your body and mind. Bottom Line: All forms of yoga are based on breathing. The regular practice of yoga teaches us how to pay attention to the breath and can improve lung volume and chest capacity, helping those who deal with respiratory issues. 11. Chronic Pain Can Often Be Managed Effectively with Yoga Chronic pain, whether caused by a disease like fibromyalgia, an accident, or a side effect of treatments for other conditions, can easily impair quality of life. If bad enough, it can also trigger brain structure changes that are linked to impaired cognition, anxiety, and depression. The regular practice of yoga can help those with chronic pain manage it on a number of levels. If pain is due to muscle or joint issues, such as the case with arthritis, carpal tunnel syndrome, or back pain, the simple act of regular stretching with a yoga ball chair and range of motion exercises can be enough to significantly reduce pain. The increased flow of oxygen to brain and muscle tissues that results from the breathing and movement of yoga also help improve energy levels and general feelings of well-being, making it easier to deal with physical pain. This breathing, combined with the physical movements of yoga, can help release muscle tension held in your body. This often decreases pain or, in some cases, relieves it entirely. The benefits of yoga as it relates to pain management do not stop there, however, Yoga also appears to increase gray matter in your brain through a process called neurogenesis. There are also indications that it can strengthen white matter connectivity. Many researchers believe that reduction of gray matter and weak connectivity are the most significant factors in chronic pain. Yogis dealing with pain can also benefit from the stress reduction and decrease in cortisol release the practice brings. This not only helps with tension, but can also help them cope with the anticipation of pain. Instead of having a ‘fight or flight’ reaction to pain, those who have practiced yoga may be able to form a more gentle reaction that does not trigger additional stress. Bottom Line: The breathing and movement associated with yoga can help those suffering from muscle or joint pain. Regular yoga practice can also trigger changes in the brain that can help chronic pain sufferers deal with and lessen pain symptoms. 12. Those Who Practice Yoga See Fewer Allergy Symptoms Do you deal with the misery of itchy eyes, scratchy throat, fatigue, and congestion that comes with allergies? Millions of people suffer from allergies brought on by pollen, grass, dust, pet dander, or other substances to the point that it affects their work, their social life, and their sleep. How do allergies develop? Many scientists have studied the phenomenon and found that an allergic reaction occurs when your immune system over-responds to an otherwise harmless substance. Your body mistakenly treats this substance like a dangerous invader and releases histamines. Histamines are a faulty immune response, and they can condition the body to display symptoms that start to resemble a disease. Many argue that, to be susceptible to allergies, sufferers may have a compromised immune system, weak digestive system or be experiencing toxic overload. Yoga addresses many different levels of wellness that can lead to a reduction in allergy symptoms. Stress is a leading cause of a poor immune system and digestive problems, and can also be a toxin that makes the body weaker. As we’ve already addressed many times in this article, the regular practice of yoga is one of the best stress reducers on the planet. Of the many benefits of stress reduction, an improvement in allergies is just one. Kriyas, or cleansing practices, are another element of yoga that can help with allergies. These practices range from rapid breathing exercises to gentle cleansing of the nasal passages with salt water, which can remove viruses and pollen from the nose. Studies have also found that regular yoga practice may reduce inflammation in the body. Another harmful effect of stress, inflammation can worsen allergies and cause attacks to be more severe. Bottom Line: Those who practice traditional yoga or engage in cleansing kriyas can reduce their susceptibility to allergies and also improve the symptoms associated with them. 13. The Increased Blood Flow and Reduced Stress Associated with Yoga Can Increase Fertility Couples who have struggled with conceiving a child often turn to fertility drugs or even more intensive measures of in vitro fertilization to realize their dreams of having a baby. Before turning to costly and sometimes side-effect laden treatments, couples should first explore the more gentle treatment of practicing yoga. Yoga enhances fertility in the ways one might expect: by reducing stress that can often harm the chances of conceiving. Stress can lead to the release of an enzyme, called alpha amylase, which can impact a woman’s fertility. Many women who have problems conceiving are stressed to begin with, then become more stressed as they fail to conceive. This can lead to a vicious cycle where stress continues to increase each month, making it more and more difficult to get pregnant. In addition to stress reduction, yoga can also increase blood flow to reproductive organs, which not only improves their function but also improves hormone function. All regular yoga practices can help with fertility, but those who are actively trying to conceive may benefit from the more targeted fertility yoga practice. This is aimed specifically at nurturing, supporting, and strengthening the endocrine and reproductive system. Fertility yoga incorporates specific poses that re-balances the system and strengthens muscles and organs that are used during pregnancy and childbirth. This helps make for a healthy pregnancy once a woman conceives. Bottom Line: The stress reduction and rebalancing benefits of yoga can help women who want to conceive. Those struggling with fertility issues may want to practice targeted fertility yoga that helps with both conception and a healthy pregnancy. 14. A Consistent Yoga Practice Can Lead to a Balanced Metabolism Your metabolism is the basic biochemical process that converts the food you eat into the energy you need to live. A sluggish metabolism can mean weight gain, low energy, and problems with regularity. Though long thought to be a practice focused mostly on relaxation and stretching, yoga can actually be a moderately strenuous workout that increases muscle, increases heart rate, and revs up the fire of your metabolism. In addition to increasing heart rate to boost metabolism, the practice of yoga also affects digestion, circulation, and muscle tone, all of which have an impact on how efficiently your body creates energy. With the majority of your digestive tract located in your core, the yoga positions that engage the abdomen, especially those that involve twisting or bringing the knees to the chest, can wring out toxins and encourage waste to pass through your body. Circulation is another factor important to your metabolism. If your body has poor circulation, your organs suffer from a lack of nutrients and oxygen, which slows metabolism. The deep breathing inherent in yoga helps open up arteries and release pressure, all of which help with proper circulation. Many people make the mistake of thinking yoga is not strenuous enough to build muscle mass. However, the weight bearing features of many of the poses target large and small muscle groups, building them in size and density. When we build muscle, we not only increase strength, but we also burn more calories. Muscle burns more than fat, and the more calories we burn, the more our metabolism rate increases. Bottom Line: Yoga has an effect on digestion, circulation, and building muscle, all of which positively affect your metabolism. 15. Practicing Yoga at any Time of Day Helps You Sleep Better Sleep is crucial to our energy levels, mood, concentration, and ability to be happy and successful in our everyday lives. Those most sleep experts recommend that adults get 7 to 9 hours of quality sleep per night, most of us get far less than this. Even if you are in bed for the necessary hours, inability to get to sleep, waking up frequently, or tossing and turning can turn those hours into less-than-quality rest. Insomnia or reduced sleep quality can be the product of stress, underlying illness or disease, poor sleeping conditions, vitamin deficiency, or hundreds of other factors. This often makes it difficult to identify what issues are at play. Though every person may have a different reason for not sleeping well, yoga can have a beneficial effect on everyone’s sleep quality. Because the nervous system is responsible for a restful sleep, yoga’s calming effects are especially helpful. A calm mind leads to a calm body, both of which play a part in how easy it is to get to sleep and how restful that sleep is. Many people are bothered by a ‘busy mind’ that simply cannot shut off at the end of the day. Yoga teaches us how to breathe deeply and disconnect from our worries and from those distracting thoughts that tend to keep us up at night. By giving ourselves the tools to put thoughts aside and instead focus on our breath, we give ourselves an excellent tool for the perfect night of sleep. Although a regular yoga practice done consistently at any time of day will undoubtedly affect your sleep, those who really struggle may benefit from poses done at night that are specifically aimed at helping you sleep more soundly. These poses include uttasnasana, halasana, and savasana and should be done as close to bedtime as possible. Others benefit more from a Kundalini yoga sequence before bed that incorporates long, slow breathing and meditation. It’s best to try out both methods to see what leads to a better night of sleep for you. The Bottom Line: The stress-relieving benefits of a consistent yoga practice can help improve your sleep quality. Those with sleeping problems can also benefit from a bedtime routine that includes specific poses or deep breathing paired with meditation. 16. All Forms of Yoga Work Wonders on Your Range of Motion Range of motion is important to our overall quality of life, and it decreases as we age. Important for injury prevention as well as as our ability to do daily tasks with minimal discomfort, range of motion can be increased with regular yoga. Why does range of motion decrease as we age and how can yoga combat this? As we get older, the tissue around joints tend to thicken and cartilage decreases. The knees and hips are especially susceptible to these depletions, making them more prone to injury in older individuals. As muscle mass decreases, this also affects our range of motion as we age. Our ease of movement decreases, and general fitness levels tend to drop. When range of motion decreases, it often triggers a snowball effect. Movement becomes more difficult, so individuals tend to move less often. This, in turn, triggers more movement impairment. Yoga is based on controlled, prolonged stretching. This type of movement is still comfortable for those who are experiencing a lack of flexibility or injury that restricts range of motion. Not only is yoga a practical exercise for those in this situation, but it also tends to reverse the lack of flexibility that they experience. A daily practice of prolonged stretching that is inherent in any yoga program elongates the muscles and enables joint flexibility. The slow, deliberate process of gently stretching muscles over a long period of time is both beneficial and achievable for those of all ages. It can be done throughout the lifetime and rarely needs to be suspended due to injury or other ailments. Bottom Line: The gentle and prolonged stretching that makes up the core of yoga helps increase range of motion and preserve it throughout the lifetime. 17. Practicing Yoga Can Help Treat Arthritis Arthritis is an excruciating affliction that severely impacts quality of life. Rheumatoid arthritis, or RA, can occur at any age, and is triggered by a faulty immune system. Osteoarthritis, or OA, is a degenerative disorder that usually takes place as a person ages. It’s estimated that there are over three million cases of OA in the United States per year. While medication can greatly help both those suffering from RA and OA, exercise is always recommended as well. Because arthritis is characterized by painful swelling in the joints, many forms of traditional exercise may be unbearable. Yoga is incredibly easy on the joints and is usually a comfortable activity for even the most severe arthritis sufferers. The gentle stretching of yoga can ease joint discomfort and the focused breathing can help those in pain distance deal with the chronic distress. The muscle-building and energy-boosting effects of yoga can also help those with arthritis. OA and RA tend to zap energy, which leads to a sedentary lifestyle and muscle atrophy. Those who practice yoga tend to be more active, which lessens arthritis symptoms. The psychological benefits of yoga on those suffering from arthritis are also to be noted. Those with arthritis who regularly practice yoga suffer from less depression, improved coping abilities, stress reduction and an enhanced sense of well-being. Bottom Line: Yoga is a safe and effective form of exercise for those suffering from both osteoarthritis and rheumatoid arthritis. It helps ease joint discomfort and boosts energy and a sense of well-being. 18. Practicing Yoga Leads to a Healthy Lifestyle and Enhanced Self-Care Bad choices lead to more bad choices. A lack of exercise can easily lead into bad eating habits, which leads to weight gain, which leads to even less exercise. A sedentary and unhealthy lifestyle results in a depressed mood, low energy levels, and an overall pessimistic attitude. Sometimes, it just takes one thing to start turning it all around. Yoga can be that one thing. Because it can be practiced by individuals at any age and in any shape, yoga is a practice that can be adopted by virtually everyone. Yoga increases our awareness, which often leads practitioners to start making changes in every part of their lives. As they develop more self-awareness, they often make changes that include healthier food choices, fewer toxic relationships, and more time to take care of themselves. Over time, these choices add up to a much healthier and happier lifestyle. The increase in overall quality of life can even equal more years on your life. Bottom Line: Yoga increases self-awareness, which leads to other healthy choices and overall increase in wellness and happiness. Read the full article

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Each neuron may be connected to up to 10,000 other neurons, passing signals to each other via as many as 1,000 trillion synaptic connections, equivalent by some estimates to a computer with a 1 trillion bit per second processor. Estimates of the human brain’s memory capacity vary wildly from 1 to 1,000 terabytes (for comparison, the 19 million volumes in the US Library of Congress represents about 10 terabytes of data). Unlike other body cells, most neurons in the human brain are only able to divide to make new cells (a process called neurogenesis) during fetal development and for a few months after birth. These brain cells may increase in size until the age of about eighteen years, but they are essentially designed to last a lifetime. Interestingly, the only area of the brain where neurogenesis has been shown to continue throughout life is the hippocampus, an area essential to memory encoding and storage. Information transmission within the brain, such as takes place during the processes of memory encoding and retrieval, is achieved using a combination of chemicals and electricity. It is a very complex process involving a variety of interrelated steps, but a quick overview can be given here. A typical neuron possesses a soma (the bulbous cell body which contains the cell nucleus), dendrites (long, feathery filaments attached to the cell body in a complex branching “dendritic tree”) and a single axon (a special, extra-long, branched cellular filament, which may be thousands of times the length of the soma). Every neuron maintains a voltage gradient across its membrane, due to metabolically-driven differences in ions of sodium, potassium, chloride and calcium within the cell, each of which has a different charge. If the voltage changes significantly, an electrochemical pulse called an action potential (or nerve impulse) is generated. This electrical activity can be measured and displayed as a wave form called brain wave or brain rhythm. Synaptic transmission This pulse travels rapidly along the cell's axon, and is transferred across a specialized connection known as a synapse to a neighbouring neuron, which receives it through its feathery dendrites. A synapse is a complex membrane junction or gap (the actual gap, also known as the synaptic cleft, is of the order of 20 nanometres, or 20 millionths of a millimetre) used to transmit signals between cells, and this transfer is therefore known as a synaptic connection. Although axon-dendrite synaptic connections are the norm, other variations (e.g. dendrite-dendrite, axon-axon, dendrite-axon) are also possible. A typical neuron fires 5 - 50 times every second. Each individual neuron can form thousands of links with other neurons in this way, giving a typical brain well over 100 trillion synapses (up to 1,000 trillion, by some estimates). Functionally related neurons connect to each other to form neural networks (also known as neural nets or assemblies). The connections between neurons are not static, though, they change over time. The more signals sent between two neurons, the stronger the connection grows (technically, the amplitude of the post-synaptic neuron’s response increases), and so, with each new experience and each remembered event or fact, the brain slightly re-wires its physical structure. The interactions of neurons is not merely electrical, though, but electro-chemical. Each axon terminal contains thousands of membrane-bound sacs called vesicles, which in turn contain thousands of neurotransmitter molecules each. Neurotransmitters are chemical messengers which relay, amplify and modulate signals between neurons and other cells. The two most common neurotransmitters in the brain are the amino acids glutamate and GABA; other important neurotransmitters include acetylcholine, dopamine, adrenaline, histamine, serotonin and melatonin. ??? Did You Know ??? During childhood, and particularly during adolescence, a process known as "synaptic pruning" occurs. Although the brain continues to grow and develop, the overall number of neurons and synapses are reduced by up to 50%, removing unnecessary neuronal structures and allowing them to be replaced by more complex and efficient structures, more suited to the demands of adulthood. When stimulated by an electrical pulse, neurotransmitters of various types are released, and they cross the cell membrane into the synaptic gap between neurons. These chemicals then bind to chemical receptors in the dendrites of the receiving (post-synaptic) neuron. In the process, they cause changes in the permeability of the cell membrane to specific ions, opening up special gates or channels which let in a flood of charged particles (ions of calcium, sodium, potassium and chloride). This affects the potential charge of the receiving neuron, which then starts up a new electrical signal in the receiving neuron. The whole process takes less than one five-hundredth of a second. In this way, a message within the brain is converted, as it moves from one neuron to another, from an electrical signal to a chemical signal and back again, in an ongoing chain of events which is the basis of all brain activity. The electro-chemical signal released by a particular neurotransmitter may be such as to encourage to the receiving cell to also fire, or to inhibit or prevent it from firing. Different neurotransmitters tend to act as excitatory (e.g. acetylcholine, glutamate, aspartate, noradrenaline, histamine) or inhibitory (e.g. GABA, glycine, seratonin), while some (e.g. dopamine) may be either. Subtle variations in the mechanisms of neurotransmission allow the brain to respond to the various demands made on it, including the encoding, consolidation, storage and retrieval of memories. As has been mentioned, in addition to neurons, the brain contains about an equal mass of glial cells (neuroglia or simply glia), the most common types being oligodendrocytes, astrocytes and microglia. Because they are so much smaller than neurons, there are up to 10 times as many in number, and different areas of the brain have higher or lower concentrations of glia. It used to be thought that the role of glial cells was limited to the physical support, nutrition and repair of the neurons of the central nervous system. However, more recent research suggests that glia, particularly astrocytes, actually perform a much more active role in brain communication and neuroplasticity, although the extent and mechanics of of this role is still uncertain, and a substantial amount of contemporary brain research is now focused on glials cells.

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[22/6 8:26 ಪೂರ್ವಾಹ್ನ] Babu Anjanappa: ╭───────────────────╮

🌄 *S̴h̴u̴b̴o̴u̴d̴h̴a̴y̴ : 22 Jun/जेस्ट मासा (Tuesday) ग्रीष्म ऋतू*🙏🏻

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*Today's top News* ➣➣➣➣➣➣➣➣➣➣➣➣➣➣

1. Nation celebrated the seventh International Day of Yoga virtually due to the coronavirus pandemic. The lead programme of the event, held by the Union Ministry of AYUSH, began at 6:30 am. During the programme, Union Minister of State for AYUSH Kiran Rijiju & PM Modi addressed the nation.

2. Vice President, M. Venkaiah Naidu appealed to the people to make Yoga a part of their daily lives.

3. The Record of 80 lakh COVID-19 vaccine doses administered so far on 1st day of nationwide free vaccination drive (21 June). All citizens above the age of 18 can avail free vaccination at any govt facility. The Centre will buy 75% of the total vaccine production from vaccine manufacturers & give it to the state govts free of cost.

4. J&K govt cancels annual Shri Amarnath Ji Yatra in view of COVID-19 pandemic.

5. The Govt has extended the waiver of Inter-State Transmission system (ISTS) charges on transmission of electricity generated from solar & wind sources up to 30th June 2025. Earlier, it was up to 30th June 2023.

6. Former Inspector General of Punjab Police Kunwar Vijay Pratap Singh today joined the Aam Aadmi Party at Amritsar.

7. Tripura, Chief Minister Biplab Kumar Deb on 21 June inaugurated the mega vaccination drive for the age group of 18- 44 yrs as part of the pan-India vaccination drive for June 21 and 22.

The programme was organised at IMA house Agartala.

8. Tamil Nadu Assembly session to continue till June 24. The session began yesterday with the address of Governor Banwarilal Purohit.

9. Tamil Nadu govt has released guidelines for protecting school students from sexual abuse. The regulation states that every school should have a eight member student protection counsel group consisting of the school headmaster or headmistress, teachers, members of the parent teachers association, non teaching staff, outside members and management representatives.

10. Ahead of PM Modi’s June 24 J-K outreach the Congress has demanded repeal of JK Reorganisation Act, 2019, and restoration of status quo ante in the erstwhile state.

11. From Jul 2021, a higher Tax Deducted At Source (TDS) rate would be applicable for Income Tax Return (ITR) non-filers, according to the Finance Act, 2021. If a taxpayer has not filed TDS in the last 2 years & TDS deducted each year more than ₹50,000, the tax department will charge more while filing the ITR from July 1.

12. The Centre has initiated major penalty proceedings against former West Bengal Chief Secretary Alapan Bandyopadhyay for alleged misconduct & misbehavior. The wrangle over Bandopadhyay began after the chief minister and he both skipped a meeting with Prime Minister Narendra Modi over Cyclone Yaas last month.

13. The Central Board of Secondary Education (CBSE) and Council for the Indian School Certificate Examinations (CISCE) boards have told the Supreme Court that class XII board examination results would be declared by July 31.

14. The security forces Indian Army & CRPF on Monday (21June) morning eliminated 3 top Lashkar-e-Taiba (LeT) terrorists, including Mudasir Pandit, in an encounter at Gund Brath in J&K Sopore.

15. The Indian Air Force (IAF) has raised the 2nd Rafale squadron, the ' *101 Falcons of Chhamb & Akhnoor* ' at Ambala. Ambala ahead of their formal induction at the Hasimara airbase in West Bengal.

16. Chief of Defence Staff General Bipin Rawat has called a meeting on Wednesday of the tri-services and other stake holders to understand their concerns over theatre commands and iron out differences before working towards the raising of maritime and air defence commands this year.

*✈INTERNATIONAL NEWS*

1. PM Modi announced that our country, along with UN and WHO, is launching an app called M-Yoga aiming to provide easy access to Yogic practice all over the world.

2. Pakistan Foreign Minister Shah Mahmood Qureshi has alleged that India is using Afghanistan for “carrying out terrorist activities” in Pakistan.

3. The Canadian govt has extended the suspension of direct flights from India to Canada till next month (21 July). The announcement in this regard was made on (21 June) Monday by the Public Health Agency of Canada.

4. India received USD 64 billion in Foreign Direct Investment in 2020, the 5th largest recipient of inflows in the world, according to a UN report.

5. Swami Vivekananda Cultural Centre, Embassy of India, Seoul South Korea, celebrated the 7th International Day of Yoga (IDY) celebrations in Seoul by organising yoga events at Busan University of Foreign Studies and Gandong-gu office in collaboration with Korea Yoga Association Yesterday (21 June).

*🌎WORLD NEWS🌍*

1. *International Yoga Day:* The UN has marked the day to raise awareness about the many benefits of practising Yoga for people all over the world. The date 21 June was chosen because it is the longest day in Northern Hemisphere. The word Yoga has originated from the Sanskrit word Yuja which means 'to join or to unite.

2. *US Navy tests new aircraft carriers's metal with powerful explosions* . The massive explosive was set off underwater near USS Gerald R. Ford, the first of a new class of advanced aircraft carriers, in the Atlantic Ocean.

3. The 7th International Day of Yoga was observed in Bangladesh with great enthusiasm across the country. Several events were organised in Dhaka & other parts of Bangladesh to mark the occasion.

4. Sweden's parliament ousted PM Stefan Lofven in a no-confidence vote on 21 June, giving the Social Democrat leader a week to resign & hand the speaker the job of finding a new govt, or call a snap election.

*🚣🚴🏇🏁🏊Sports:*

1. Men's Cricket WTC Final: 4th day's play between New Zealand and India washed out completely due to rain.

Uganda's Olympic squad has become the first to test positive for COVID-19 on arrival in Japan. The competition is due to start on 23rd of July.

2. Union Minister of Youth Affairs and Sports and Minister of the Ministry of Ayush Kiren Rijiju announces 25 Fit India Yoga centers across 9 states on occasion of IYD2021.

*USD 74.19 💷GBP 103.34*

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*🇮🇳Facts about India🇮🇳*

Rishikesh is a city in India’s northern state of Uttarakhand, in the Himalayan foothills beside the Ganges River. The river is considered holy, and the city is renowned as a center for studying yoga and meditation. Temples and ashrams (centers for spiritual studies) line the eastern bank around Swarg Ashram, a traffic-free, alcohol-free and vegetarian enclave upstream from Rishikesh town.

Rishikesh is primarily famous for its spiritual importance. ... Rishikesh is the beginning of the famous Char Dham Yatra (Gangotri, Yamunotri, Kedarnath, Badrinath). There are a number of Ayurveda centres also where you can experience the ancient healing methods for body and mind.

The Bharat Mandir was established on the banks of the holy Ganges in around 12th Century by Guru Shri Shankaracharya. Inside the temple, there is an idol of lord Vishnu, made out of a single Saligram. Shri Shankaracharya also placed the Shri Yantra above the Vishnu idol.

*😀Thought of the day*

Happiness is when what you think, what you say, and what you do are in harmony." — *Mahatma Gandhi*

*Joke of the day*

*पप्पू* : मां सारे खिलौने बेड के नीचे छिपा दो...

*पप्पू की मां* : क्यों..?

*पप्पू* : क्योंकि मेरा दोस्त डब्बू आ रहा है..

*पप्पू की मां* : डब्बू खिलौने चुरा लेगा क्या...?

*पप्पू* : नहीं, वह अपने खिलौने पहचान लेगा

*😳Why❓❓❓*

*Why Don't We Remember Being Babies?*

Virtually nobody has memories from very early childhood because at that age, our brains don't yet function in a way that bundles information into the complex neural patterns that we know as memories. This is called "semantic memory

Until sometime between the ages two and four, try you however, children lack "episodic memory" -- memory regarding the details of a specific event. Such memories are stored in several parts of the brain's surface, or "cortex." For example, memory of sound is processed in the auditory cortexes, on the sides of the brain, while visual memory is managed by the visual cortex, at the back. A region of the brain called the hippocampus ties all the scattered pieces together. The hippocampus, tucked very neatly in the middle of our brain, is responsible for pulling those all together and tying them. At the age of seven, children could still recall more than 60% of the recorded events, but children who were just a year older remembered only about 40 %

The reason we don’t remember being babies is because infants and toddlers don’t have a fully developed memory. But babies as young as six months can form both short-term memories that last for minutes, and long-term memories that last weeks.

*LEARN Sanskrit*🙏🏻

*आकृति* : आकार Shape

🤔 *How it works* ⁉

*How the Telephone Works.*☎️📞

When a person speaks into a telephone, the sound waves created by his voice enter the mouthpiece. An electric current carries the sound to the telephone of the person he is talking to. ... When a person talks into the telephone, the sound waves strike the diaphragm and make it vibrate.

When two telephones are connected, analog voice data is transmitted over the copper wires of the PSTN (Public Switched Telephone Network). The voice data is then converted into electrical signals which are eventually routed in the switching centers. Finally, a connection is made and communication is possible.

The number dialled on a landline is routed via the telephone wire to the Electric cross connect system at the local telephone exchange. This system has a direct mapping for the number dialled to the location of the called person. It simply switches the call to subsequent cross connects till the destination is reached.

Something that converts energy from one form to another is called a *transducer* . The loudspeaker in a phone works in the opposite way: it takes an incoming electrical current and uses magnetism to convert the electrical energy back into sound energy you can hear.

💁🏻‍♂️ *GK TODAY*

*Alexander Graham Bell* , best known for his invention of the *telephone* , revolutionized communication as we know it. His interest in sound technology was deep-rooted and personal, as both his wife and mother were deaf.

🛕 *VEDIK GNAN*

*NARASIMHA* Avatar, Lord Vishnu incarnates himself as a semi-man, semi-lion in this world. The king of demons (asuras), Hiranyakasyapa, wanted to become immortal and wanted to remain young forever. To this end, he meditated for Lord Brahma and because of his severe penance, the gods were frightened and asked Brahma to pacify the king. Brahma was impressed by his austerity and granted him a wish. HiranyaKasyapa wished that he be neither killed by a man or beast, nor in daylight or at night and neither inside or outside a building. Having obtained the wish he considered himself the supreme God and frobade all worship of gods by anyone.

But his son Prahlada, was an ardent devotee of Vishnu. This enraged Hiranyakasyapa very much. He ordered numerous ways to kill Prahlada including asking his sister Holika to sit with Prahlada in the fire. But everytime Prahlada escaped unhurt. Enraged, once he asked Prahlad to show him the Lord Vishnu. Prahlad said, "He is everywhere". Further enraged, Hiranyakasyapa knocked down a pillar, and asked if Lord was present there. Lord Vishnu then emerged as a half lion, half man from the pillar which was neither inside the house nor outside, and the time was evening, neither night nor day. He then killed Hiranyakasyapa thus saving the life of his devotee Prahlada.

🧬 *HEALTH CARE:© HOME REMEDIES*🩺

( *Note* : These home tips followed in villages/ancient traditions, it is up to you to use it or not🙏🏻)

*Health Benefits of Sweet Lime or Mosambi*

Juice helps enhance Immunity.

Vitamin C and other antioxidants present in sweet lime or its juice can help strengthen immunity. It helps stay away from colds and flu. Stimulate blood circulation and thus strengthens the immune system.

*Regards*

───────────────────╮

*🙏PLZ FOLLOW GOVT. NORMS, MAINT SOCIAL DISTANCE, KEEP YOURSELF ©YOUR FAMILY SAFE🌼*

╰───────────────────╯

[23/6 7:46 ಪೂರ್ವಾಹ್ನ] Babu Anjanappa: ╭───────────────────╮

🌄 *S̴h̴u̴b̴o̴u̴d̴h̴a̴y̴ : 23 Jun/जेस्ट मासा (Wednesday) ग्रीष्म ऋतू*🙏🏻

╰───────────────────╯

*Today's top News* ➣➣➣➣➣➣➣➣➣➣➣➣➣➣

1. A two-day monsoon session of the Maharashtra legislature will begin from July 5 to 6th July.

2. The all-party meeting convened by PM Modi in New Delhi on Thursday (24 June).

3. J &K former CM Farookh Abdullah and Mahbooba Mufti to attend all party meeting called by PM Modi on June 24.

4. Leaders of several opposition parties including the Trinamool Congress, the Samajwadi Party, the Aam Aadmi Party, the Rashtriya Lok Dal and the Left assembled at Natinoalist Congress Party chief Sharad Pawar's residence in New Delhi on 22 Jun (Tuesday) & discussed various issues facing the country, amid heightened speculation about the possibility of a third front against the ruling BJP.

5. *Gujarat CM Vijay Rupani e-launches Agricultural Diversification Scheme-2021,* benefiting vanbandhu- farmers in tribal areas. will get fertilizer-seed assistance of Rs. 31 crores in which 45 kg of urea, 50 kg of NPK and 50 kg of ammonium sulphate will be provided. Seeds of crops like maize, Bitter Melon (karela), Calabash (dudhi), tomato, millet, etc. are provided under this scheme.

6. Lok Sabha Speaker Shri Om Birla virtually inaugurated an online Indian and foreign language learning course for Members of Parliament, State / UT Legislatures, Officials and their families.

7. 22 cases of the Delta Plus variant of the coronavirus have been detected in India, with 16 from Maharashtra & the remaining from Madhya Pradesh and Kerala.

8. To check whether a taxpayer will be eligible to pay Tax Deducted at Source (TDS) at higher rates from next month, the Income Tax department has introduced a new functionality on the tax portal. The new section 206AB. If a taxpayer has not filed TDS in the last 2 years & aggregate of TDS exceeds Rs 50,000 in each year, the Income Tax department will charge more while filing the income tax returns (ITR) from July 1. The rate of TDS will be either twice the rate specified under the relevant section or provision or 5%, whichever is higher.

9. *The last date of filing Tax Deducted at Source (TDS) for the fourth quarter of financial year 2020-21 has been extended to June 30*

10. Tamil Nadu Chief Minister MK Stalin assures resolutions in Assembly against Farmer laws, the Citizenship Amendment Act. He said it would not be appropriate to adopt such resolutions.

11. The Andhra Pradesh High Court on Tuesday sentenced two IAS officials to one month’s imprisonment and a fine of Rs 1,000 each for not implementing court orders on the filling of certain vacancies in the horticulture department. panchayat raj commissioner Girija Shankar and horticulture commissioner Chiranjeevi Chowdary .

12. Supreme Court to hear plea of convict in Rajiv Gandhi assassination case after 3 weeks. A G Perarivalan, serving life sentence in the Rajiv Gandhi assassination case, seeking grant of parole. Rajiv Gandhi was assassinated on the night of May 21, 1991 at Sriperumbudur in Tamil Nadu by a woman suicide bomber.

13. Bengaluru court in Karnataka has directed former PM HD Deve Gowda to pay Rs 2 crore to Nandi Infrastructure Corridor Enterprise Ltd for allegedly defaming the company in 2011.

14. *CBSE to conduct optional exam between 15 August to 15 Sept* : The CBSE said if the candidates are not satisfied with their result, CBSE will provide online facility for registration for the examination. The facility to register for written exam will be offered online at CBSE’s official website - cbse.nic.in.

15. Raksha Mantri Rajnath Singh will visit the Cochin Shipyard Limited on June 25 (Friday) to review the progress of the Indigenous Aircraft Carrier (IAC). He is on two-day Kochi visit.

16. Lt. Gen. Ajay Kumar Suri took over as the Director General (DG) and Colonel Commandant of the Army Aviation on 21 June.

17. The Defence Ministry has signed a contract with Goa Shipyard Ltd for construction of two Pollution Control Vessels for Indian Coast Guard today. The Defence Ministry has said that it has been done at a cost of about Rs 583 crore.

18. *Born Today*🐣

Actor *Raj Babbar* (born 23 June 1952) is a Hindi and Punjabi film actor and politician belonging to Indian National Congress. 3 times member of the Lok Sabha and a 2 times member of the Upper House of the Indian Parliament. He was the President of Uttar Pradesh Congress Committee.

*✈INTERNATIONAL NEWS*

1. External Affairs Minister S Jaishankar is scheduled to address the United Nations Security Council (UNSC) debate on Afghanistan on 23 June (Wednesday).

2. UN Secretary-General on Myanmar has claimed that about 10,000 refugees have fled from Myanmar to India & Thailand as clashes in that country led to “acute” new displacements and alleged that the regional threat of the crisis is real.

3. India & China are likely to hold another round of diplomatic talks this week on eastern Ladakh with a focus on moving forward in disengagement of troops in the remaining friction points.

4. The United Kingdom posted a liaison officer at the Indian Navy's Information Fusion Centre (IFC) that has emerged as a key hub in tracking movements of ships and other developments in the Indian Ocean. Lt Commander Stephen Smith will be based full-time at the Centre.

5. US Pharma giant Pfizer is in the final stages of an agreement with India to supply anti-COVID-19 vaccines, Chief Executive Officer Dr Albert Bourla said.

*🌎WORLD NEWS🌍*

1. Pak PM Imran Khan has ruled out hosting American bases in Pakistan for military action inside war-torn Afghanistan, fearing it might lead to his country being "targeted in revenge attacks" by terrorists.

2. US President Joe Biden is looking forward to meet with his Afghan counterpart Ashraf Ghani on 25 June (Friday).

3. American Airlines will cut hundreds of flights over the next 3 weeks to avoid overloading its operation as demand for summer air travel rises faster than once expected.

4. Today 23 June - International Widow's Day is observed. To raise awareness globally about the violation of human rights that widows suffer & faces in several countries following the death of their spouses.

*🚣🚴🏇🏁🏊Sports:*

1. The ICC has announced prize money for the winner and runner-up of the World Test Championship Final. The winning team of the final between India and New Zealand will receive about 12 crore rupees along with an ICC Test Championship Mace. The losing team will receive 6 crore rupees approximately. The final match will start on June 18 at Ageas Bowl, Southampton.

2. Chinese swimmer star Sun Yang was banned for more than four years on Tuesday for breaking anti-doping rules, after a retrial at the Court of Arbitration for Sport.

3. Former captain Younis Khan on Tuesday (June 22) stepped down as Pakistan's batting coach. He was appointed last year in November on a two-year contract until the 2022 ICC T20 World Cup. The Pakistan team is due to start a tour of England from June 25 to July 20 for three ODIs and three T20Is. The team will next go to the West Indies from July 21 to August 24 to feature in five T20Is and two Tests.

4. *Norman Pritchard*

An Indian athlete & the first Olympic medal winner from India : Norman Gilbert Pritchard (23 June 1877 – 31 October 1929), also he was a British-Indian sportsperson and actor who became the first Asian-born athlete to win an Olympic medal when he won two silver medals in athletics at the 1900 Paris Olympics representing India.

5. International Olympics Day is observed on June 23 every year to celebrate sports and health. The occasion marks the day when International Olympic Committee was founded in 1894. ... Baron Pierre de Coubertin founded the International Olympic Committee (IOC) in 1894 and laid foundation of the Olympic Games.

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Ⓝⓐⓥⓔⓔⓝ Ⓚⓤⓜⓐⓡ

*🇮🇳Facts about India🇮🇳*

[howlongisabriefessay569]

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About me

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Buy Essay Online Cheap At Short Notice From $9 Over time, the monkey started getting higher on the recreation as a result of he needed extra scrumptious pellets. The monkey had discovered to make the neuron fire and inadvertently became the topic of the primary actual brain-machine interface. And that’s about what we’ve got, a minimum of in widespread usage. Scans additionally have the benefit of providing info about what’s going on in the entire brain at any given time, and it’s protected and totally non-invasive. He can’t be kind of electrocuted, or extra electrocuted—he’s either not electrocuted in any respect, or he’s absolutely electrocuted to the very same diploma every time. So our man’s physique stem—the neuron’s axon—has a unfavorable “resting potential,” which signifies that when it’s at rest, its electrical cost is slightly unfavorable. At all instances, a bunch of people’s toes maintain touching12 our man’s hair—the neuron’s dendrites—whether or not he likes it or not. Their ft drop chemical compounds referred to as neurotransmitters13 onto his hair—which cross through his head and, relying on the chemical, elevate or decrease the charge in his physique a little bit. That’s a pc constructed by Alan Turing in 1950 known as the Pilot ACE. Truly leading edge in its time. In 1969, a researcher named Eberhard Fetz related a single neuron in a monkey’s brain to a dial in front of the monkey’s face. When the monkey would assume in a means that fired the neuron and the dial would transfer, he’d get a banana-flavored pellet. That’s not the way it normally works—usually, the napkin is up on prime of our Madison Square Garden mind and stuffed with deep folds . In fact, lower than a third of the cortex napkin is up on the surface of the mind—most is buried contained in the folds. It’s somewhat disagreeable for our neuron man, but not an enormous deal—and nothing else happens. Now for a long time, I thought these major lobes were chunks of the mind—like, segments of the whole 3D structure. But really, the cortex is simply the outer two millimeters of the mind—the thickness of a nickel—and the meat of the house underneath is usually just wiring. Your hippocampus (Greek for “seahorse” because it looks like one) is like a scratch board for memory. When rats begin to memorize directions in a maze, the reminiscence will get encoded of their hippocampus—fairly literally. This is the state of the early BMI business, and it’s the second when Elon Musk is getting into it. For him, and for Neuralink, today’s BMI business is Point A. We’ve spent the whole publish up to now prior to now, constructing up to the present second. Now it’s time to step into the long run—to figure out what Point B is and how we’re going to get there. Many dad and mom of deaf babies at the moment are having a cochlear implant put in when the baby’s about one year old. Like this child, whose reaction to hearing for the first time is cute. We’d have a super exhausting time doing that on our 1,000X mind. Our 1,000X brain that additionally happens to be a nice flat serviette. And after all, there’s the entire neuroplasticity thing. The voltages of every neuron would be constantly altering, as many as lots of of instances per second. And the tens of millions of synapse connections in our dice could be frequently altering sizes, disappearing, and reappearing. These two things are occurring naturally in your brain all the time. Right now, your eyes are making a selected set of horizontal actions that let you learn this sentence. That’s the mind’s neurons outputting data to a machine and the machine receiving the command and responding. That image then stimulates neurons in another a part of your mind that allows you to course of the information embedded in the picture and absorb the sentence’s that means. This is why brain-machine interfaces—a subset of the broader subject of neural engineering, which itself is a subset of biotechnology—are such a tantalizing new business. We’ve conquered the world many instances over with our technology, but in terms of our brains—our most central device—the tech world has for essentially the most half been too daunted to dive in. Let’s zip again in time for a second to 50,000 BC and kidnap somebody and produce him back here to 2017. Around 15 – 20 billion of those neurons are in the cortex, and the remainder are within the animal components of your mind . This is a binary state of affairs—either nothing occurs to our man, or he’s fully electrocuted.

[kazimirov-archive]

Cor: 7, 10 (u gotta pick another name !), 18, 27, 34, 42, 44, Brose: 3, 16, 18, 20, 29, 39, 40 Orlan: 47, 39, 18, 30, 17, 11, 5. :D also i gave them all 18 lol

Cor

1. If you could be a mythical creature, which would you choose?

“Oh. Hm. I don’t know if I’d want to be any fantasy creature that I can think of? Of course, elf is always the immediate reaction, but if we mean Tolkien’s elves, and I assume we are, they’re really kind of boring aren’t they? But I guess I’m also boring also. Or actually! a Water horse or hippocampus. They’re not super smart or anything, but there’s something infinitely cool about being a sea monster of sorts, but a sea monster that looks friendly enough to not be perceived as a threat.”

10. Do you like your name? Would you ever change it?

“I mean, yes? My parents gave me this name of course I like it. But if I had to change it, probably...jeong?? it’s weird to have it as a one character name, but one of the hanja for it means quiet or calm. i believe in choosing names for their meanings so having a name that actually fits me, and doesn’t just mean war horn would be nice. though i guess you could argue war horn does fit me since i think the horn players didn’t fight. they just played music and died, which sounds about right.”

18. Tell us about an early childhood memory.

“When I was little, my mom really tried to keep her Korean heritage alive for me. She spoke Korean to me and fed me Korean food and told me stories about her side of the family and their lives. I don’t remember very many details about my childhood, but I remember on several instances  sitting on her lap in bed as she went through Korean children’s books with me. She would point to the rabbit and ask, “Mwoya?” ‘What is it?’ and I would giggle and shout, “Naya!” ‘It’s me!’. To this day I mutter “naya” to myself whenever I see wild rabbits.”

27. Do you like your cereal crunchy or soggy?

“I don’t like the use of soggy here. Soggy has bad connotations. I like my cereal soft with a little bit of a crunch, and that is definitely not soggy.”

34. Do you address older people by their first or last name?

“Usually by their last. It’s very rude in Korea to address a stranger, particularly an older or higher ranking one, by their first name, so even though I grew up speaking Korean in America and Italy, you get into the habit of using last names anyway because the language is structured around that. And also both my parents and my aunt were very strict in regards to politeness, so last name was always safest.”

42. Where do you feel the safest?

“At home, wherever that may be. There’s something comforting about being surrounded by your own stuff in your own home and knowing that you belong there. I also find safety in certain people. Marcus, for example, is a very grounding person and I always seek him out in crowds or stressful situations because he makes me feel protected. Cesaire is also a very safe person to be around, but moreso on the ‘will neutralize any threats instantly’ end of the spectrum rather than the ‘chill person’ end.”

44. If you could travel back to any era, which would you choose?

“Well, we’re living in objectively the best era to be in, right? The best healthcare, the highest life expectancy, the most equality, and all that. So permanently? I would stay right here. But if it was just a trip, probably pre-colonial Africa or Asia or South America or something. It would be fascinating to see what those cultures were like before European influence, to see what they thought of religion and time and gender and all that. I’m not sure which one I would want to visit, though, I’ll have to think on that.”

Brose

3. If you could learn a new skill, what would it be?

“oh oh oh! knitting. it’s really domestic i know but paris is SO COLD and i want to learn how to make everyone aesthetic mittens and hats and all that! alaina and i could match :D”

16. Who do you want to be closer to?

“everyone??? i want to be closer to all my friends i want to be the most important person in their lives 800000% of the time. but more seriously, probably asiel?? weirdly enough. we’re friends of course but i dunno the bond he has with alaina just seems really nice, even though i also have that bond with her i guess. i just want more bonds!!”

18. Tell us about an early childhood memory.

“when i was almost three italy made it to the final round of the world cup, literally for the first time in like 12 years. so like my family was PUMPED. and i was really little of course but i remember being forced to stay up super late and watch the game and my parents gave me espresso because italians i guess. and then we lost BUT we still got second place and it had been 12 years and ohmyGOSH the shouting and cheering was insane!! and i was the tiniest 2 1/2 year old ever so i was literally passed around like a trophy and hoisted up into the air as everyone celebrated. it was amazing. i still have a picture of me swimming in my cousin’s jersey.”

20. What can you see outside your bedroom window?

“uhhh the city? lots of cool buildings and stuff i guess? also the seine which i hate to admit it but is a much nicer river to look at than the tiber. still not as nice as my hometown, though. ((((but a million times better than new york so i’m not bitching.))))”

29. Do you like reading? What was the last thing you read?

“uhhhh i don’t?? read??? i’ve never been much of a reader- i’m dyslexic and it’s just not my thing. the last thing i read was probably actually the bible?? i joined this online bible study and it’s been very interesting to compare people’s ideas about passages. but, fun trick i use: i have an audiobook of an italian translation, so it’s reading but only sort of.”

39. What is one thing you would want to teach your children?

“only one thing?? probably acceptance. acceptance of people’s differences, acceptance of life’s hardships, acceptance of your own existence, acceptance of truth even when it hurts. fighting is good and all, but being able to sit down and say ‘i accept whoever and whatever comes my way’ is really powerful. no that doesn’t mean you never stand up for yourself, you have to also accept that certain people and things might not be right for you, but it means that you are able to be at peace with life and if they come away with any lessons, i want it to be that.”

40. If you had to have a tattoo, what would it be and where would you get it?

“i actually cracked and got one! i have my mom’s birthday on my ribs with my favorite bible passage under it. and and then alaina and i are getting ones, but the design and everything is a surprise!”

Orlan

47. How would you spend your ideal day?

“my ideal days are ones when things go right. i like being able to sit back and relax and not worry about plans or people messing up. on a day when everything is going right i would probably spend it lying around with thelry and just relaxing and watching tv and maybe cooking some real food. y’know, maximizing the relaxation.”

39. What is one thing you would want to teach your children?

“to always fight for what they believe in. that’s what my mamma taught me and it’s been my driving force my entire life. never stand down and let people walk over you or let the bad guys get away with it, because if you do you’re just as bad as them.”

18. Tell us about an early childhood memory.

“i don’t have many positive ones, especially since my mom died when i was fairly young, but we shared a bed and i remember having her arms around me and she would be right there if i had a nightmare or wanted a hug, ready to pull me closer and chase all the darkness away. i miss that.”

30. How do you show someone you love them?

“with closeness. like emotional closeness and also physical closeness. i let myself be open with them and let them be open with me and spend as much time in their presence as possible. i’m pretty obvious.”

17. Do you miss someone at the moment?

“mamma, always mamma.”

11. Who is a mentor to you?

“there’s no one in particular, but i like to study revolutionaries and rule breakers of the past. they inspire to me to stand behind my beliefs and morals, but also to be smart and not just charge ahead aimlessly. i particularly like studying insurgents of the past, it’s interesting to see how they played the game from both sides. as for mentors in my real life?? weirdly enough, probably some of the bosses i’ve come in contact with. our morals are the exact opposite,if they even have morals, but they are ruthless in their execution.”

5. What was your favourite book as a child?

“we had a copy of fiabe italiane growing up and my mother used to read to me from it and i’ve always said it was my favorite book. the problem is that she would rework the stories to make them less gory, because she thought fiction shouldn’t be violent if real life already was, so when i finally read the book on my own after she died i was shocked! so maybe not fiabe italiane, but i’m not sure what else to say.”

[health-wellbeing]

Psycho Fear or Brain Babble

Have you ever been afraid of anything? Do you realize that what is destroyed in the stomach is a bit annoying?

 Can this fear be real or just a fruit?

 Consider the possibility that you did it without knowing it to protect yourself.

 It sounds crazy, no. I mean, how on earth could we be able to scare a heavy state to stay safe.

 In truth, it is simpler and certainly more typical than anyone would have thought.

 Many people use this system as a supervised trick to deal with previous occasions, injuries or distress, usually as a teenager.

 Why is it a problem now? Because it does not help anymore.

 At the moment, I'm not talking about the fear of a man-eating hovering shark preparing to break his jaw, but even his idea can make you shiver. I'm talking about things that you know are usually not afraid, but trigger a terrible feeling that is flooding somewhere inside.

 The psychology of human needs is based on TWO things:

 1. The fear of disappointment in such a case that you bomb, you will not be enough

 2. The fear of not being appreciated

 These feelings of concern appear in various structures, such as the concern to start a business of their own, to speak openly or, in any case, to ask you about your deep desire to live in the city.

 This thing destroys life.

 So why are we afraid ... To put it simply, it's a huge area that needs to be covered in a lonely position, but these little tips could change your life now:

 Your brain is simultaneously a channel, a wipe, and the best "superior creator".

 Your encounters framed your insights and removed sincerely charged memories that you considered important, and then they give you meaning (these are stored somewhere in the hippocampus in the brain to do more) that topic in a later post because this could save a marriage, a relationship or the recovery from stress).

 Some encounters or memories break and float in your mind like a mist of thunder; Unleash the ruin if you do not dare to be under pressure. Research has shown that this is the case in post-traumatic stress disorder (PTSD) or the event of a power failure.

 Why do our minds do this and what can be done to live a creative and peaceful life?

 It's all a matter of use. For this situation, the vitality in comparison to the probability to stay safe.

 Your mind needs to spare vitality, it is someone who wants or not. It consumes about a quarter of your total vitality needs for the afternoon

 Memories and passionate connections in the enthusiastic part of our mind, where our hippocampus is located, are linked to a small collection of synapses that are in our temple (these phones allow you to increase your level of mindfulness and inspiration) as well in the context of our attention somewhere in the lower part of our brain.

 Imagine, you have a railway line from north to south with three main stations, one at the top, the middle and the base

 Let's say the temple (above) is Leeds, the hippocampus (middle) is Birmingham and the fear stove (base) in London.

 Messages come and go in these footsteps and seek in these stations at a speed so useful that even Superman would have difficulty keeping up.

 Depending on the strength of the message, they will trigger all or part of the focal lengths for recording:

 Here is the important piece now, the focus on anxiety is always on, always on the lookout for danger and watchful, even if you are deep in sleep, it is very likely that it will also check your fantasies.

 Terrible messages that have been added enliven the home of the FEAR of mastering and stopping us. They can even drive us into the deep opening that is the sadness when it is revived to new.

 Great, sincerely added messages enliven the MOTIVATION focus and open us to more attention, serenity, openness, and joy.

 Have you ever felt awkward, nervous or tense and do not usually know why?

 Your fear focus is on, this could be an external occasion that you did not intentionally see or, in all likelihood, a terrible memory or vice versa. Why is this happening?

 Since this saves the vitality of your mind, it is activity number 1. To keep you safe.

 The mind is the best derivation machine known to man. It should bounce off the gun just in case there is a real risk to your well-being.

 Also, because the rebound of the weapon kept us alive as an animal. The development keeps this in our heritage mix.

 The mind takes a kick in the new circumstance that triggers an enthusiastic reaction and memory as well, like the terrible memory ... However, this will probably not happen even if you feel anxious, ill well or anxious all the time you realize reasonably that it is not good.

 You may have an eerie feeling when your supervisor asked you to make a presentation on the board or to speak at a rally or explore new territory.

 The former affiliation or affiliations best speculation checked in our memory and case they would not be undesirable, your dreaded care causes a degree of distress or anxiety to varying depending on the power of sincere charged memory.

 Mostly, you have no idea what is going on, that is happening on the subconscious out of our attention until it manifests as an inclination or a feeling in the body.

 THE GOOD NEWS

 There are approaches to gaining strength and understanding how to perceive the vibrations that prevent us from liberating ourselves and enjoying life.

 Since your character's sound can process only 2000 bits of data per second and the other piece of your mind 4 billion a second, it's an important test to cope with such a revolutionary preparation machine that operates more quickly and is more down to earth than the healthy "me it knows "brain.

 But it is conceivable. One can consciously develop more synapses in the brain earlier, giving you more control, a full consciousness, and a versatile cerebral brain to make higher work even more beneficial.

 Focused consideration

 At any time, should you feel something that makes you panic or makes you feel anxious or upset, breathe deeply, unravel securely you are protected (better sit in your favorite home chair), look safe and relax? At this point, just look at the alarming idea of ​​how to move it with a woolly cloud in the sky, do not wear judgment, no answer (you can do as such), pay attention to your body, worry everywhere and sit down and breathe in gently.

 If you are just struggling, do it, all your thoughts are moving on the feeling of air passing through your nose as you go deep and easy. At this point, you will return to this fluffy cloud, if it is still there ...

 In the long run, anxiety and thoughts will blur.

 Do you see? Having brought your mind and now you have started to manage your fear of concentration, so you thought it would not be that.

 This fear is your observation experienced as authentic, from time to time is useful, but most of the time, it blocks your progress and even destroys life.

 That must not be.

 Cerebrum filters show that the fear is always activated a quarter of a second ahead of you. This may be why he feels so authentic and part of the mark of your identity.

 Excluding all the others you and others know, you know your 3 brains

 Neurosciences and Human Needs Brain research show that we can purposefully develop and influence our minds.

 The potential that you can unload is much greater than we thought it would be 10 years ago. The proof is clear, we have three brains, not just one, but also free, how your heart, lungs and liver work, but they are with help, you are connected. Currently, you can effectively build your 3 heads to have a higher life.

https://brainboosters.co/nootrobox-nootropic-stack/

[studyingbymylonesome]

MDMA is sometimes described as a cross between a psychostimulant and a mild hallucinogen.

The drug's influence feels highly controllable. MDMA tends to enrich the user's sense of self-identity, not diminish it. MDMA "provides a centering experience, rather than an ego diffusing experience" (Dr. Philip Wolfson), though it may also cause a "softening of the ego-boundaries". Sometimes a degree of derealisation on MDMA may occur, but rarely depersonalisation in the ordinary sense of the term. On the contrary, users feel they can introspectively "touch inside" to their ideal authentic self with total emotional self-honesty.

As well as acting as a "gateway to the soul", MDMA "opens up the heart". Taking MDMA induces an amazing feeling of closeness and connectedness to one's fellow human beings. MDMA triggers intense emotional release beyond the bounds of everyday experience. The drug also enhances the felt intensity of the senses - most exquisitely perhaps the sense of touch. The body-image looks and feels wonderful. Other people look and feel wonderful too. Minutes after dropping a pill, a lifetime of Judaeo-Christian guilt, shame or disgust at the flesh melt away to oblivion.

MDMA may sometimes cause "inappropriate bonding". Prudence should be exercised before taking it with ex-girlfriends, boyfriends or culturally inappropriate love-objects. 

On pure MDMA, subjects feel at peace with themselves and the world. They discover an enhanced sense of self-worth, self-forgiveness and complete self-acceptance. Cynical thoughts and negative feelings disappear. Aspects of life normally too sensitive to talk about can be explored freely. Heightened feeling allows long-forgotten and repressed emotional memories from childhood to be retrieved with unusual ease. In some settings, painful, highly-charged and even hitherto unmentionable problems may be discussed with (rose-tinted) candour. On MDMA, a lifetime of accumulated psychological barriers and defence-mechanisms go down, somehow magicked out of existence with a pill. Anger, irritability and ingrained fear dissolve; the hostile amygdala is subdued, if only for a few hours. Ecstasy users tell each other affectionately what beautiful people they are; and they do so from the depths of their hearts.

MDMA's capacity to induce empathetic bliss, heightened introspection and an increased ability and desire to communicate feelings can create a rapport with the therapist and accelerate a successful outcome. MDMA acts to boost self-esteem and self-confidence, while paradoxically diminishing egotism. The user's sense of social isolation vanishes. "I love the world and the world loves me", affirmed one beneficiary of MDMA-assisted therapy.

On a more sceptical note, it's hard scientifically to validate claims of long-lasting therapeutic success. For MDMA's stunning short-term results make double-blind, placebo-controlled trials effectively impossible. Such a problem doesn't always bedevil today's lame "antidepressants", the results of whose trials often struggle to reach statistical significance. Investigational drugs are lab-tested by Big Pharma to discover whether or not non-human animals will self-administer them. Candidate compounds are normally discarded if the animals do so, arguably a perverse route to uncovering antidepressants with good clinical efficacy and high patient compliance. By contrast, MDMA is a warm, fast-acting, non-sedating mood-enricher that banishes social anxiety and physical pain alike. Unlike opioids or the anxiolytic benzodiazepines, MDMA doesn't cloud consciousness even at relatively high doses. This doesn't stop less cerebrally-inclined ravers from getting "cabbaged" by swallowing pills all weekend.

Safe, long-acting MDMA analogues may prove therapeutic in the treatment of social phobia, eating disorders and obsessive-compulsive disorder (OCD).

Again, MDMA use increases sensitisation to the rewarding effects of euphoriant dopaminergics such as cocaine; and once more, this is not inherently a sign of "brain damage".

In the process of recovery from a prolonged MDMA-binge, the hippocampus, a brain structure critical for episodic memory formation, may actually be hyperinnervated, but reinnervation of the dorsal cortex is sparser. It has been suggested that the heavy MDMA user who discerns no long-lasting ill effects, and who displays minimal functional impairment, may still be subtly damaging his or her serotonergic "functional reserve". The disturbing parallel drawn here is with neurodegenerative disorders: clinical signs of Parkinson's disease, a progressive disorder caused by outright dopaminergic cell death and frequently prefigured by depression, only become apparent after 70-80% of dopamine cells have been lost. It is fiendishly hard to demonstrate MDMA-induced dopaminergic cell damage without virtually killing the victim; in contrived circumstances it can be done. Yet the most notorious attempt to show MDMA-induced dopaminergic neurotoxicity,

Some studies suggest that possible MDMA-induced neurotoxicity to the serotonin system can be largely prevented by taking a double dose of fluoxetine (Prozac) or another SSRI shortly after starting to "come down". Post-E Prozac in particular mitigates the oxidative stress and consequent risk of serotonergic axon damage caused by reactive products of dopamine deamination. The long-acting SSRI Prozac/fluoxetine, and its even longer-acting metabolite norfluoxetine, apparently prevents the uptake of dopamine (and any toxic metabolite(s)?) into the serotonergic nerve terminals by binding to the serotonin reuptake transporter with higher affinity than MDMA or serotonin. Unfortunately, although liquid refreshment is now freely available at most MDMA-propelled raves, most chill-out rooms don't offer Prozac. Two days and more after taking MDMA, heavy recreational users are typically more irritable, subdued, unsociable and subtly less empathetic than before their weekend binge: the "Terrible Tuesday's" syndrome of midweek blues. So with cruel irony, two or three days after communing on Ecstasy and declaring their undying love, couples are more likely to have rows and split up. Other heavy regular MDMA users, even those who aren't self-medicating for a pre-existing malaise, may experience depression, anxiety, emotional burnout, rejection-sensitivity, fatigue, insomnia, aching limbs, subtle cognitive deficits, immune system dysfunction, body temperature dysregulation, and a sense of derealisation or depersonalisation for several weeks or months afterwards. This litany of woe sounds a high price to pay even for the peak experience of a lifetime.

las, adopting a prophylactic SSRI regimen isn't a realistic long-term option for frequent MDMA users either, or at least not if they intend to continue using their hugdrug of choice. This is because a sustained regimen of SSRIs largely blunts MDMA's empathogenic and entactogenic effects. SSRIs inhibit the binding of MDMA to the serotonin transporter. Thus pre-treatment with SSRIs prevents MDMA-triggered serotonin-release; and this in turn reduces dopamine-release in the striatum.

  Tolerance to MDMA itself develops quite rapidly with steady use. If MDMA is taken several days in a row, amphetamine-like and eventually dysphoric effects start to predominate. Monoamine neurotransmitters, most drastically serotonin, are depleted from the axon terminals; serotonin synthesis is choked off following oxidative inactivation of tryptophan hydroxylase; and the nerve-cell receptors re-regulate. Thus MDMA is not addictive in the conventional sense. Taken chronically, it soon ceases to be rewarding. Even dedicated ravers typically don't binge more than once a week. Wiser heads save the drug for "special occasions". Yet MDMA's non-addictive profile is no guarantee that (as was once fondly hoped), "once you get the message you hang up the phone." The mind/brain isn't built like that. If you really like a drug-delivered message, you want to hear it again and again. But with MDMA, the message can subtly change with time; and its primal magic gets sullied or forgotten.

There are other options for neuroprotection besides taking post-Ecstasy Prozac. On one hypothesis of MDMA-induced serotonergic neurotoxicity, the extra dopamine released into the synapses is transported into the depleted serotonin axonal terminals where it is deaminated by the enzyme monoamine oxidase type-B present in the terminal. MAO has two isoforms, MAO-A and MAO-B. These differ in their substrate affinities and inhibitor sensitivities: the MAO-A isoenzyme has a greater affinity than the MAO-B isoenzyme for serotonin, but mainly MAO-B is present in the serotonergic axonal terminals, where it breaks down "foreign" neurotransmitters. However, after a subject has taken a high dose of MDMA, excess dopamine is taken up by the so-called serotonin transporters into the depleted serotonin terminals. Here its oxidation produces a glut of toxic free radicals - highly reactive chemicals with one or more unpaired electrons - such as hydrogen peroxide (H2O2). These toxic free radicals are liable to exhaust or overwhelm the free radical scavenging systems of the cell. In consequence, the serotonin fine axonal terminals are broken down by lipid peroxidation. Why exactly the serotonin reuptake transporters lose their normal selectivity for serotonin and take up dopamine isn't known for certain. Possibly it's because by this time there's far less serotonin around for the reuptake pump to use. After the directionality of the reuptake pump is reversed by MDMA, serotonin released into the synapse can't be recycled back into the cell; and so it diffuses away. In any event, the monoamine oxidase inhibitor selegiline [l-deprenyl/Eldepryl] appears to be neuroprotective at monoamine oxidase type-B-selective dosages i.e. 2 x 5mg daily or less. Selegiline also protects against MDMA-induced inhibition of tryptophan hydroxylase. Interestingly, Prozac too has MAO-B inhibiting properties; and these may contribute to its neuroprotective effect. Selegiline itself has additional free radical scavenging properties that may exert a neuroprotective action. It will be instructive to compare the neuroprotective efficacy of selegiline with rasagiline (Azilect, Agilect) for E-users. Rasagiline is a selective MAO-B inhibitor licensed from mid-2005 in the EC for the treatment of Parkinson's disease; rasagiline lacks selegiline's trace amphetamine metabolic by-products. Whatever the older compound's neuroprotective efficacy compared to rasagiline, selegiline is potentially valuable too because, unlike taking a SSRI, adopting a long-term selegiline regimen doesn't impair MDMA's subjective effects. Even so, no controlled clinical trials of their co-administration are currently planned.

 One reason for such caution beyond a reflex Just-Say-No dogmatism is that it's potentially dangerous to tamper with the MAO enzyme. Selegiline has lifespan-extending properties in "animal models", and possibly in humans too; but if used recklessly, then it could abruptly shorten life instead: selegiline is an irreversible MAO-B inhibitor. Prohibitionism and a consequent absence of quality-control means that the "Ecstasy" sold in clubs often contains liberal quantities of amphetamine. Amphetamine and MAO inhibitors should not be combined. Both enantiomers of MDMA itself have MAO-inhibiting effects, preferentially for isoenzyme type-A. Taken at dosages of above 2 x 5mg per day, selegiline loses its selectivity for MAO-B. Individual variation in MAO status makes it imprudent for the MDMA user to take selegiline even at 10mg daily; and selegiline itself, like MDMA, is a weak inhibitor of MAO-A. MAO-A deaminates serotonin; and the serotonin syndrome, characterised inter aliaby hyperthermia, autonomic instability and altered muscle tone, is potentially lethal. Serotonin 5-HT2A antagonists like ketanserin (Sulfrexal) can inhibit the syndrome; but they aren't widely available on the street or average dance-floor.

       Milder cases of the serotonin syndrome are not uncommon among the hard-rolling stackers and piggybackers dancing all night at crowded ill-ventilated raves. Dehydration and overcrowding tend to worsen drug-induced toxicity. Heat exhaustion and severe hyperthermia are probably the gravest risk to the raver's health. MDMA tends to raise body temperature by a degree or so, sometimes by quite a bit more if the user dances all night without rest ["Saturday night fever"]. MDMA also increases the body's secretion of antidiuretic hormone, arginine-vasopressin. Ravers sometimes overcompensate for the risk of dehydration by gulping down too much pure water. This can cause hyponatraemia (literally "low salt": "water intoxication"). Sipping a couple of sports-drinks every hour or so instead is a prudent way to maintain electrolyte balance. Indeed it would be safer if sports drinks were distributed with each E-tablet sold as a matter of course, perhaps accompanied with a neuroprotectant mix and a health-tips sheet thrown in for good measure.

       Unfortunately, tips found on the Net are no substitute for systematic, well-planned health-education programs. Organisations like the Berkeley-based Dancesafe, funded by Microsoft millionaire the late Bob Wallace and founded to promote safe raving, are rare; their activities are also controversial. Until psychopharmacologybecomes part of the educational core curriculum, any responsibly designed drug cocktail, and any harm-reduction program, must be formulated with the recklessness of a minority of sensation-seekers in mind, not just risk-averse research scientists. Such a revolution in mental healthcare for young people is sorely needed. An examination system akin to ritualised child-abuse wreaks terrible damage on the young minds incarcerated in our educational institutions. Critics of exam-culture claim an "education" based around competitive testing screws kids up far more than empathetic drugs. Unfortunately, what's tested in these rituals of abuse isn't our children's emotional well-being, levels of reflective self-insight, capacity for loving empathy or social intelligence. Nor do schools and colleges offer courses in effective technologies to promote them.

       A healthcare revolution of this magnitude isn't going to happen tomorrow. So more realistically for now, clubbers seeking neuroprotection against MDMA-induced toxicity may do well to use humble antioxidants such as ascorbic acid (Vitamin C), alpha-tocopheryl-acetate (Vitamin E), zinc, alpha-lipoic acid, and L-cysteine. The optimal mix and dosage before, during, and after dropping an E to maximise their respective neuroprotective action, and minimise any post-ecstatic hangover, hasn't yet been established. Even at high dosage, the neuroprotection such antioxidants offer may be inadequate for heavy MDMA users. More encouragingly, antioxidants also reduce tolerance between exposures. Clearly a lot more research is needed, hopefully without the usual animal holocaust that accompanies drug testing today.

The serotonin precursors L-tryptophan and 5-hydroxytryptophan (5-HTP) are also neuroprotective against MDMA-induced toxicity, possibly in part because of their antioxidant effect but mainly because of their precursor role. 5-HTP is the metabolite of L-tryptophan. It's the direct metabolic precursor to serotonin (5-HT). In contrast to the catecholamine neurotransmitters dopamine and noradrenaline, the synthesis of serotonin isn't subject to strong end-product inhibition. Like L-tryptophan, 5-HTP is sometimes used as an antidepressant and antianxiety agent; it seems to have a relatively narrow therapeutic window. Unlike SSRIs, L-tryptophan and 5-HTP can be taken chronically without blunting MDMA's effects. Indeed some clubbers pre-load with L-tryptophan or 5-HTP to intensify and enrich the MDMA experience and prevent serotonin depletion. Serotonin depletion increases the vulnerability of the axon terminals to damage. Though such a tactic is sensible enough in theory, excess preloading with 5-HTP may potentially precipitate or exacerbate the serotonin syndrome. So care is in order.

One novel and unlikely-sounding proposal to minimise MDMA-induced neurotoxicity is pretreatment with aspirin. Aspirin inhibits the enzyme prostaglandin H synthase (PHS). PHS catalyses the transformation of amphetamines into toxic free radical products. Therefore taking aspirin before MDMA use may also indirectly block the conversion of amphetamines into reactive oxygen species responsible for long-term neurotoxicity. As of 2014, no controlled trials of aspirin have yet been conducted with MDMA-using humans. But if aspirin pretreatment does prove an effective harm-reduction strategy, then this is potentially a godsend - not least because other candidate neuroprotectants (SSRIs, selegiline, etc) carry hazards of their own in conjunction with E-use. Aspirin itself cannot strictly be described as risk-free; but the risk/benefit ratio of its use is both favourable and well-known.

MDMA itself rapidly depletes serotonin from the axon terminals and inactivates the enzyme tryptophan hydroxylase needed for its renewed biosynthesis. By contrast, altering the density and signal-transduction efficiencies of the mission-critical receptor subtypes [5-HT1B(?), 5-HT2A(?), dopamine D2(?)], could, ideally, deliver sustained ecstasy without emotional burnout. Such receptor re-regulation might involve a time-lag of one-to-three weeks, as is normal with conventional "antidepressants". Delayed-onsetmagic, if achievable, would offer an immense social and therapeutic advantage. This is not just because the magic should be sustainable without limit, but because postponing the onset of drug-induced reward minimises a medicine's "abuse-potential" without compromising its efficacy. The practice of tobacco-smoking, for instance, is so addictive not because of the surpassing joys of inhaling a cigarette, but because a tobacco abuser need wait only seven seconds or so between taking a puff and the miniscule hit. The reward from oral MDMA takes somewhat longer; but the delight of E-like consciousness needs to be divorced from its intimate association with pill-popping.

Although there are indeed other, non-neurotoxic amphetamine derivatives that acutely induce transporter-mediated serotonin release, achieving the all-important goal of sustainability may entail the use of drug cocktails. Thus one might explore combining e.g. 1] new synthetic allosteric modulators of the serotonin 5-HT1Bautoreceptors that regulate the evoked release and synthesis of serotonin; 2] agents acting selectively on the 5-HT1B-autoreceptors and heteroreceptors; 3] the right 5-HT2C receptor antagonist or inverse agonist to make the E-like state more ecstatic; 4] the right dopaminergic(s) or, ideally, agents targeting the medium spiny GABAergic projection neurons in the rostromedial shell of the nucleus accumbens directly. This is all still very speculative and unfunded.

A brief comparison of GHB and MDMA may be instructive because one therapeutic challenge ahead will be to design agents that reverse SSRI-like flattening of affect without inducing mawkish sentimentalism (cf. ethyl alcohol). In contrast to mainstream psychiatric drug therapies, both GHB and MDMA deliver a rare emotional intensity of experience, albeit an intensity different both in texture and molecular mechanism. GHB is known by clubbers if not structural chemists as "liquid ecstasy". GHB and MDMA are indeed sometimes mixed at raves; but the two drugs are chemically unrelated. GHB is an endogenous neuromodulator derived from GABA, the main inhibitory neurotransmitter of the brain. A naturally-occurring fatty acid derivative, GHB is a metabolite of normal human metabolism. GHB has its own G protein-coupled presynaptic receptor in the brain. Sold as a medicine, GHB is licensed as an oral solution under the brand name Xyrem for the treatment of cataplexy associated with narcolepsy. Unlike MDMA, GHB stimulates tissue serotonin turnover. GHB increases both the transport of tryptophan to the brain and its uptake by serotonergic cells. Taking GHB stimulates growth hormone secretion; hence its popularity with bodybuilders. GHB offers cellular protection against cerebral hypoxia, and deep sleep without inducing a hangover. GHB also stimulates tyrosine hydroxylase. Tyrosine hydroxylase converts L-tyrosine to L-dopa, subsequently metabolised to dopamine. Unlike MDMA, the acute effects of GHB involve first inhibiting the dopamine system, followed the next day by a refreshing dopamine rebound. GHB induces mild euphoria in many users. In general, the neurotransmitter GABA acts to reduce the firing of the dopaminergic neurons in the tegmentum and substantia nigra. The sedative/hypnotic effect of GHB is mediated by its stimulation of GABA(B) receptors, though GHB also modulates the GABA(A) receptor complex too. The main effect of GABA(B) agonism is normally muscle relaxation, though interestingly, pretreatment with the GABA(B) agonist baclofen also prevents an MDMA-induced rise in core body temperature. Whatever the exact GABA(A), GABA(B), and GHB-specific mechanisms by which GHB works, when taken at optimal dosage GHB typically acts as a "sociabiliser". This is a term popularised by the late Claude Rifat (Claude de Contrecoeur), author of GHB: The First Authentic Antidepressant (1999). Rifat was GHB's most celebrated advocate and an outspoken critic of Anglo-American psychiatry. Similar therapeutic claims have been made for GHB as for MDMA, despite their pharmacological differences. GHB swiftly banishes depression and replaces low mood with an exhilarating feeling of joy; GHB has anxiolytic properties; it's useful against panic attacks; it suppresses suicidal ideation; it inhibits hostility, paranoia and aggression; it enhances the recall of long-forgotten memories and dreams; and it promotes enhanced feelings of love. Like MDMA, and on slightly firmer grounds, GHB has been touted as an aphrodisiac: GHB heightens and prolongs the experience of orgasm. GHB disinhibits the user, and deeply relaxes his or her body. Inevitably, GHB has been demonised as a date-rape drug ["I was at this party, and this guy gave me a drink. Next thing I know, it's morning and I'm in someone's bed. I've no idea what happened in between..."]. GHB has a steep dose-response curve. Higher doses will cause anterograde amnesia i.e. users forget what they did under the influence of the drug. It's dangerous to combine GHB with other depressants. So despite GHB's therapeutic and pro-social potential, GHB is probably unsafe to commend to clubbers. This is because a significant percentage of the population will combine any drug whatsoever with alcohol regardless of the consequences to health. If used wisely, sparingly, and in a different cultural milieu, then GHB could be a valuable addition to the bathroom pharmacopoeia. But even then, it's still flawed. GHB may intensify emotion and affection, but not introspective depth or intellectual acuity. Unlike taking too much MDMA, overdoing GHB makes the user fall profoundly asleep. If our consciousness is to be durably enhanced, then sedative-hypnotics have only a limited role to play in the transition ahead.

Curiously, the beta-ketone analogue of MDMA, methylone (3,4-methylenedioxymethcathinone, MDMCAT), is poorly researched. Only a handful of papers appear in the published scientific literature. Methylone is another creation of Dr Shulgin. The drug is sold (expensively) as a "research chemical" over the Net. Branded rather unsubtly as "Explosion", methylone is also available in several Dutch smartshops. Recently it has become very popular in the scientific counterculture. The DEA issued an emergency ban on methylone on October 21, 2011. The drug is not as potent as MDMA; and it has a higher dosage range. Methylone causes less inhibition of serotonin reuptake and triggers less serotonin release than MDMA; but its potency in promoting the synaptic accumulation of the catecholamine neurotranmitters noradrenaline and dopamine is similar. Thus methylone has activating and empathetic effects while inducing less emotional outpouring. Many subjects experience an E-like "magic", though the two drugs can readily be distinguished by experienced users. It should be stressed that the comparative safety of methylone has not yet been well established, even at relatively low dosage levels of 120-150mg. This is still a new drug. Methylone is mood-elevating; higher doses induce a clear-minded and serene euphoria. Reputedly there is less serotonergic toxicity than MDMA; but there can still be a very noticeable comedown. If methylone is taken chronically, its stimulant effects become more pronounced. Its empathogenic qualities diminish. Tolerance soon sets in: a sad and familiar story. Likewise, the empathetic euphoriant mephedrone (4-Methylmethcathinone; 2-Methylamino-1-p-tolylpropan-1-one) can be acutely rewarding; but it is a short-acting stimulant whose pharmacokinetics and toxicology are unknown. Alas our knowledge (2014) of its properties comes wholly from user reports rather than peer-reviewed scientific journals.

     First, however, MDMA's acute adverse side-effects i.e. teeth-grinding ["bruxism"], jaw-tension ["trismus"], loss of coordination ["ataxia"], eye-wiggling ["nystagmus"], profuse sweating ["diaphoresis"], nausea, appetite-suppression, tachycardia, dry mouth, hyperthermia or idiosyncratic reactions to MDMA need to be eliminated and not just minimised. The really nasty stuff - hepatotoxicity, cardiac arrhythmias, hyponatremia-induced cerebral and pulmonary edema (caused by drinking too much water), rhabdomyolysis (the breakdown of skeletal muscle), and disseminated intravascular coagulation (inappropriate blood-coagulation leading to severe bleeding) are statistically very rare. MDMA-induced incidence of these syndromes was apparently unknown in clinical practice prior to the drug's legal proscription. However, not all the problems of MDMA use can be blamed on Prohibition and the lethal mix of ignorance and criminality it spawns. Even pure, low-dose MDMA does not suit everybody. In the era of pre-genomic medicine, atypical reactions to any drug at all should be expected. Conversely, with adequate medical research the mildest bad experience on MDMA should be preventable.

        Much more speculatively, the use of personalized somatic gene-therapy may enable future scientists of the mind, or unabashed hedonists, to sustain an otherwise neurotoxic drug regimen in safety. For instance, transgenic mice carrying the sequence of the human CuZn superoxide dismutase enzyme are resistant to MDMA-induced serotonergic damage. Ideology aside, humans can benefit from genetically enhanced neuroprotection no less than intoxicated rodents. If ever we wish to adopt a potentially life-enhancing but otherwise hazardous drug-regimen indefinitely, then one option may be to protect ourselves by inserting new genes or new alleles into our legacy genome. Or we may simply induce the overexpression of endogenous antioxidant enzymes already coded for. We're already on the brink of tailoring our drugs to our genes, but in principle we can tailor our genes to our drugs. Or we may choose to design, insert, and switch on and off as desired a suite of structural and regulatory genes for whatever life-enriching chemical exotica (or old favourites) we seek to enjoy. The modes of experience they generate may thereby become available, as it were, on tap. Nature uses lateral gene transfer; and rationally, so can we. Or by contrast, it's possible some or all genetically enriched post-humans may shun adulterants of their beautiful forms of consciousness altogether. If one's soul has been purified, why defile it?

 Pre-treatment studies with receptor antagonists indicate that dopamine D2 antagonists such as haloperidol (Haldol) attenuate MDMA's positive hedonic effects; 5-HT2A antagonists like ketanserin suppress MDMA's residual psychedelic activity; and SSRIs like citalopram (Celexa / Cipramil, the most selective of the SSRIs) diminish if not abolish the full spectrum of MDMA's psychoactivity.

Drug discrimination studies performed on captive rodents may overlook certain subtleties of the MDMA experience. Intriguingly, in mice at least, the behavioural and physiological effects of MDMA are selectively antagonised by the plant alkaloid nantenine (9,10-methylenedioxy-1,2 dimethoxyaporphine). Nantenine is "antiserotonergic" and an alpha1-adrenoceptor antagonist; the effects of nantenine on ecstatic human subjects are unknown. But on present evidence, it's primarily a combination of enhanced oxytocin release and the interplay between the serotonergic and dopaminergic systems that underlies MDMA's discriminative stimulus effects/sublime magic.

The full story is complex and still poorly understood. As the user "comes up", serotonin released into the synaptic cleft activates multiple serotonin receptor subtypes (5-HT1, 5-HT2, 5-HT3, 5-HT4, 5-HT5, 5-HT6, and 5-HT7), and subpopulations (most notably, 5-HT1B, 5-HT2A and 5-HT2C). The hierarchy of their relative contributions to the subjective and behavioural effects of MDMA use may shift with increasing dosage and the course of the trip. Several of these serotonin receptor subtypes have functionally opposing roles, notably the effects of 5-HT1A and 5-HT2C receptor agonism on anxiety. As well as inducing a synaptic flood of serotonin, taking MDMA indirectly induces the release of extra dopamine in the mesolimbic reward centres. Activation of the serotonin 5-HT1B and 5-HT2A receptors leads to an increase in the vesicular release of dopamine. Dopamine levels are also increased by reuptake inhibition. In addition, dopamine synthesis is increased and turnover reduced. Increased synaptic availability of dopamine in turn inhibits glutamate-evoked firing in the nucleus accumbens. Dopamine released in the shell of the nucleus accumbens inhibits the firing of GABAergic medium spiny projection neurons. Inhibited excitability of the spiny projection neurons in the rostral shell of the nucleus accumbens - whether it's mediated by dopamine, glutamate antagonists or mu opioid agonists - is the neurological signature of euphoric bliss, whatever its guise.

       On MDMA, there's much more going on as well. MDMA induces the release of noradrenaline (norepinephrine), and inhibits its reuptake. MDMA also triggers the enhanced release of acetylcholine in the striatum and prefrontal cortex via serotonin 5-HT4 and dopamine D(1) receptor mechanisms. Taking MDMA activates the poorly understood sigma(1) receptors, contributing to its locomotor stimulant action. The role of MDMA in activation the cannabinoid CB1 receptors to modulate its rewarding action is poorly understood. MDMA exerts (weak) binding to the alpha-2 adrenergic and histamine H1 receptors; this binding contributes in unknown degree to behavioural stimulation. Activation of the noradrenaline system causes an acute elevation of blood pressure. Additionally, taking MDMA increases plasma cortisol, prolactin, and dehydroepiandrosterone (DHEA) and aldosterone secretion. MDMA use alters the expression of several proteins involved in GABA transmission. To thicken the plot further, MDMA triggers the release of hypothalamic arginine-vasopressin and oxytocin (the "cuddle hormone"). These hormonal changes may influence some of MDMA's psychological effects. But the current consensus is that enhanced serotonin and dopamine release are crucial to the magic, even though they don't explain it.

In the vertebrate CNS, serotonin-producing neurons regulate aggression, impulse-control, mood, anxiety, cognition, temperature, appetite, circadian rhythms, sexual activity, sleep, sensorimotor integration, sensitivity to pain, emotional resilience and romantic love. Serotonin entering the axonal vesicles is released over time in response to action potentials by exocytosis into the synaptic cleft, the narrow gap 10-20 nm across between pre- and post-synaptic neurons. Seven distinct families of serotonin neuronal receptors have been isolated; 14 sub-populations of G-protein-coupled receptors and one family of ligand-gated ion channels (the 5-HT3 receptor) have been cloned. Distribution, density and regulation of the serotonin receptors vary in different areas of the brain. So does both the affinity of serotonin for its different receptor subtypes and the effects of serotonin agonists on second-messenger systems. Only a few hundred thousand of the 100 billion or so neurons in the brain manufacture serotonin. The serotonergic cell bodies are confined to the raphé area in the brainstem, but their projections extend to almost all areas of the brain and spinal cord. Most notably for E-users, serotonergic projections innervate the dopaminergic nigrostriatal and mesocorticolimbic circuits. The serotonin system has co-evolved with dopaminergic projections in the course of primate evolution. Amongst many other roles, the serotonin system helps to regulate a lifetime spent in complex social hierarchies where more ancient fight-or-flight reactions have been offset by the need for an increasingly complex cognitive, emotional and behavioural response. This unique signalling complexity of the serotonin pathways and their multiple receptors ensures we can now be (un)happy in more ways than ever before.

The serotonin/5-hydroxytryptamine molecule itself is an indole amine synthesized from the essential amino acid L-tryptophan through the intermediate 5-hydroxytryptophan. Although some serotonin is present in the cytoplasm of serotonergic cell bodies and nerve terminals, most serotonin in the axonal terminals is sequestered in small membrane-bound sacs, i.e. the synaptic vesicles. This prevents the neurotransmitter from being metabolised by the enzyme MAO. Serotonin is metabolised, mainly by MAO-type A, into the inactive metabolite 5-hydroxyindoleacetic acid (5-HIAA). Numerous studies have shown self-destructive violence, aggression, poor impulse-control, reduced social status, suicide, and some types of depression are associated with low concentrations of cerebrospinal fluid 5-HIAA. Consequently, these conditions are often conceived as disorders of "low serotonin function". Firing of the serotonin neurons causes exocytosis, a rapid calcium-dependent process of neurotransmitter release. Depolarisation of the axon induces opening of voltage-sensitive calcium channels; the resultant calcium influx causes synaptic vesicles to fuse with the plasma membrane, where they empty their load of serotonin into the synaptic cleft. In the synapse, serotonin exerts an action on both pre- and post-synaptic receptor sites. Extracellular serotonin is then normally taken back up into the serotonergic neuron via the highly efficient presynaptic transport pump. The structure of the transporter protein determines how it couples ion gradients to substrate transport in ways that still need to be clarified.

Serotonin 5-HT1 agonists, sometimes termed serenics, show pronounced anti-aggressive properties. Aggressive behaviour is modulated in by the 5-HT1B receptors in particular. The presynaptic 5-HT1B terminal autoreceptors form a vital part of a feedback mechanism regulating serotonin synthesis and release. Receptor knock-out mice lacking the 5-HT1B receptor are superficially normal in appearance, feeding patterns and breeding behaviour; but they are ferocious, and highly reactive. Such knockout mice are also unusually partial to alcohol and supersensitive to the effects of cocaine, though these traits may reflect a compensatory enhancement of the dopamine system rather than offer a direct pharmacological model of 5-HT1B receptor function. By contrast, 5-HT1B receptor agonists such as the drug anpirtoline exert "serenic" effects. In "animal models", 5-HT1B receptor agonists diminish alcohol-heightened aggression. Surprisingly, perhaps, there is substantial evidence to indicate that some endogenous serotonergic pathways normally activate rather than suppress motor output. Acute activation of 5-HT1B receptors is known to play a role in MDMA-induced locomotor activity: 5-HT1B agonists and MDMA show cross-tolerance, suggestive of a common mechanism of action. 5-HT1B antagonists restrain the hyperlocomotion that rodents and clubbers typically undergo on serotonin-releasers like MDMA. Perhaps with this crude behavioural measure in mind, some "unlicensed" psychonauts try combining a supposedly 5-HT1B-selective agonist such as the piperazine derivative TFMPP [1(3-trifluoromethylphenyl)piperazine monohydrochloride] with psychostimulants like 1-benzylpiperazine (BZP, "A2", "Frenzy", "Nemesis", "Flying Angel", "Altitude", etc) to try and replicate the acute effects of taking MDMA. The effect can indeed be E-like; but results are mixed. It is now known that TFMPP binds at multiple serotonin receptors with only limited selectivity. Taken in the absence of a dopaminergic psychostimulant, TFMPP does not feel akin to MDMA. Even combined with a dopaminergic, TFMPP's activation of the 5-HT2C receptors makes some users feel anxious. The MDMA effect is hard to emulate: MDMA is "a multifaceted jewel", not a cheap-and-cheerful euphoriant.

There are further subtleties in the way of replicating MDMA's acute effects; and even more obstacles to sustaining the magic indefinitely. The serotonergic system has both 5-HT1B autoreceptors and post-synaptic 5-HT1B heteroreceptors; they play different functional roles. 5-HT1B receptors acting as autoreceptors regulate serotonin release via inhibitory feedback at the presynaptic terminals of serotonergic neurons; turnover and release of serotonin are typically increased under conditions of acute stress. 5-HT1B heteroreceptors are located on the terminals of nonserotonergic neurons. Thus 5-HT1B heteroreceptors regulate the release of other neurotransmitters. A single serotonin neuron can modulate different brain functions and multiple cellular targets in virtue of the thousands of non-synaptic varicosities on its axonal branches that project to multiple areas and neurotransmitter systems. 5-HT1B receptors within the ventral tegmental areas (VTA), for instance, function as heteroreceptors to inhibit GABA release. Since the GABA terminals in the VTA and substantia nigra exert a tonic inhibitory influence on dopamine function, inhibition of GABA by inhibitory 5-HT1B heteroreceptors leads to the disinhibition of dopamine activity. Thus agents acting directly or indirectly as 5-HT1B agonists can cause the release of dopamine in the striatum and nucleus accumbens. Indirectly again, dopamine release is also regulated by 5-HT1B heteroreceptors within the glutamatergic hippocampo-accumbens pathways. Regulation of 5-HT1B receptor function itself is under the control of 5-HT-moduline, an endogenous tetrapeptide that controls 5-HT1B receptor efficacy. 5-HT-moduline is a so-called allosteric modulator. Allosteric modulators bind to a different binding site from the natural agonist and can, potentially, circumvent the development of tolerance. 5-HT-moduline is released from adrenal medulla in response to acute stress. 5-HT-moduline plays a pivotal role in synchronising the serotonergic signalling activity of the different terminals of individual neurons, coordinating their effects on a variety of different cerebral functions. Rationally designed synthetic drugs that recognize the 5-HT-moduline binding-site on the 5-HT1B receptors, and act on the 5-HT1B receptors as allosteric modulators themselves, may potentially exert long-term serenic, anxiolytic and mood-brightening effects by increasing serotonin release.

       In general, however, care must be taken in describing serotonin 5-HT1 agonists as "serenics", even if such agents induce a syndrome outwardly suggestive of inner tranquillity. The demeanour that an animal exhibits after "serenic" administration may indeed be submissive, passive and timid - in contrast to the fierce, assertive and aggressive behaviour of 5-HT1B knockouts. Yet "serenity" tends to connote an inner E-like peace that may be lacking - and not just in the unfortunate laboratory rodent. In fact some so-called "serenics" may enhance fear/anxiety reactions: it's only their use in combination with dopamine-releasing euphoriants that makes such agents especially interesting to the psychonaut. Indeed supersensitive 5-HT1B autoreceptors are implicated in depression and obsessive compulsive disorder. By introducing extra copies of the gene for 5-HT1B receptors into serotonin neurons, researchers can breed passive and depressive rats that show signs of abject misery [i.e. "learned helplessness" and "behavioural despair"]. The syndrome of learned helplessness is associated with excess production of 5-HT1B receptors that are churned out in greater profusion by the depressive brain. This isn't to deny that 5-HT1B agonists may have therapeutic potential, whether in bipolar disorder, autism, alcoholism or disorders of impulse-control and aggression. Thus the triptans, serotonin 5-HT1B/1D receptor agonists, are clinically effective for treating migraines; they can also curb aggression. But 5-HT1B antagonists and inverse agonists such as SB-236057-A are under investigation for possible clinical use as long-term and relatively fast-acting antidepressants. Acute 5-HT1B autoreceptor blockade can increase serotonin release. Cognitive function is affected by their use too. Whereas 5-HT1B agonists may adversely affect memory via inhibition of acetylcholine release in the hippocampus, antagonists and inverse agonists of the 5-HT1B receptor can improve the consolidation of learning. This simplified outline of the neurobehavioural role of a single family of serotonin receptor subtype illustrates how inducing lifelong E-like states - as distinct from "mere" raw bliss - is going to pose a formidable technical challenge. In this case, the possible existence of multiple subpopulations of 5-HT1B autoreceptors and heteroreceptors makes inadequate selectivity of ligands even more of a problem, especially for seekers of precision-tools rather than chemical coshes.

       Whereas serotonin 5-HT1B receptor knockout animals are aggressive by nature, 5-HT1A knockouts are timid, anxiety-ridden creatures. Whereas serotonin 5-HT1B receptors are found mainly on terminal processes, 5-HT1A receptors are located solely on serotonergic nerve cell bodies within the dorsal raphé nucleus. Intriguingly, 5-HT1A receptor density is reported to be inversely correlated with susceptibility to spiritual experience, opening up the possibility of genetically amplifying our capacity for spirituality beyond anything humanly accessible today: it may be premature to assume that our descendants will be secular rationalists. Density of the 5-HT1A autoreceptors is also inversely correlated with the reactivity of the amygdala to threatening stimuli. However, the role of the 5-HT1A receptors in MDMA's acute subjective effects still isn't clear. Pretreatment with a serotonin (5-HT1A) receptor antagonist apparently reduces MDMA's pro-social effect, in rats at least. Taken over a prolonged period, selective 5-HT1A receptor agonists typically exert a delayed-onset anxiolytic as well as (sometimes) a mood-brightening activity. Their (modest) therapeutic efficacy relies on an adaptive neuronal response. Acute activation of the presynaptic 5-HT1A receptor on the raphé nuclei tends to reduce both the rate of firing of serotonin neurons and the corresponding release of serotonin from the nerve terminals; chronic activation causes the receptors to desensitise, leading serotonergic neuronal activity to rebound. Clinically, buspirone (Buspar), a 5-HT1A partial agonist, is licensed for generalised anxiety disorder. Similar agents like gepirone (Ariza), flesinoxan, tandospirone and ipsapirone are under investigation. Alas taking them doesn't remotely engender the extraordinary sense of inner peace induced by MDMA. In rats at least, 5-HT1A agonists facilitate male sexual behaviour, hypotension, increased food intake and produce hypothermia, none of which are prominent sequelae of MDMA use. In general, 5-HT1A agonists are well tolerated. But they may also on occasion induce dizziness, nausea, and headaches, probably linked to their postsynaptic receptor action rather than presynaptic anxiolytic effect. Buspirone itself is also a dopamine D2 antagonist, albeit a weak one. This may explain why it's never been wildly popular with patients. It's also very slow to work. Gepirone, on the other hand, allegedly lacks significant activity at the dopamine D2 receptors. Gepirone acts as an agonist at the presynaptic 5-HT1A receptors and a partial agonist at the post-synaptic 5-HT1A receptors. Hopefully, gepirone will prove a clinically useful anxiolytic and antidepressant. However, though 5-HT1A antagonists reduce discrimination of MDMA in animal models, the role of 5-HT1A receptor activation in MDMA's effects needs elucidation via more first-person experimental studies.

       Recent research from Sydney University neuropharmacologist Iain McGregor suggests that post-synaptic serotonin 5-HT1A receptors contribute to MDMA's acute pro-social action via the enhanced release of oxytocin. Oxytocin in turn reduces activity and weakens connections in the fear-processing circuitry of the amygdala. MDMA activates post-synaptic 5-HT1A receptors of the paraventricular nucleus and supraoptic nucleus of the hypothalamus. The paraventricular nucleus and supraoptic nucleus contain oxytocin neurons. Oxytocin is a nine amino-acid peptide hormone and neurotransmitter that promotes pair-bonding, trust and social recognition. Commercially, oxytocin is marketed by Verolabs as a spray: so-called trust-in-a-bottle: "Liquid Trust Spray - the first Oxytocin product, formulated to enhance people's trust in you!"[sic]. In future, MDMA analogues may conceivably be marketed with similar restraint. MDMA typically causes its users to trust each other to an exceptional degree, confiding intimate personal feelings and secrets they would never otherwise share. Such drug-induced intimacy may partly be mediated by an increased release of oxytocin via MDMA-activated 5-HT1A receptors. Co-administration of MDMA and an oxytocin antagonist would test this hypothesis in humans. There are methodological problems with the use of rats as test subjects in this context; but the evidence is suggestive.

       The MDMA molecule, especially the dextrorotatory "+" isomer, has only a low affinity for the serotonin 5-HT2 receptor. This is why taking the drug within the normal dose-range typically induces only minor perceptual changes. If prompted, many Ecstasy users report altered time perception, but any visual distortions are usually mild: the N-methyl group of the MDMA molecule prevents it from fitting as comfortably into the 5-HT2A receptor as does the trippier (-)-MDA enantiomer of its structural parent. Experiments with human as well as non-human animals show a correlation between a drug's psychedelic potency and 5-HT2A receptor binding affinity. Activation of the 5-HT2A receptors is a prerequisite of the "classic" hallucinogenic effects exerted by tryptamine psychedelics such as LSD and phenethylamine psychedelics like DOM. Conversely, 5-HT2A receptor inverse agonists act as antipsychotics. Despite the low affinity of MDMA for the 5-HT2 receptor, pharmacological blockade or genetic knock-out of the 5-HT2B receptor abolishes MDMA-induced hyperlocomotion and serotonin release in the nucleus accumbens and ventral tegmental area of the brain.

None of this neurobabble should disguise the fact that psychedelia is still scientifically uncharted. It's often too weirdly exotic for words. Materialistic neurosciencehas failed to close the ontological gulf between neural porridge and consciousness - whether "ordinary" or "altered" states. Some psychonauts, understandably enough, feel the neurobabblers have lost the plot. Most of today's storytelling about altered states and the chemistry of mind will doubtless seem no less archaic to our descendants than the Greek humoral psychology of classical antiquity strikes the contemporary molecular biologist. Yet fortunately for the engineering purposes of inducing sustainable E-like bliss, we need manufacture only the sufficient neural conditions for beautiful states of consciousness. We don't need a deep understanding of how and why consciousness is generated (or alternatively, some philosophers allege, its fundamental immanence in the world). We can guess even less about the possible altered states of consciousness of our redesigned successors. We don't know whether the "explanatory gap" between the physical facts and phenomenal mind can ever be closed. But either way, our emotionally invincible descendants should be able to explore entheogens, and map out even the most outlandish reaches of psychedelia, in safety. Unlike us, our genetically enriched descendants may revel in the assurance that bad trips are inconceivable, and psychological damage is impossible. This is because their obnoxious molecular substrates will have been edited out.

       Alas our own less robust minds are psychologically vulnerable to even "physically" harmless psychedelics that aren't also euphoriants. Dual-action dopamine- and serotonin-releasers like MDMA are the latter, though they aren't always harmless. With MDMA, as with so many psychoactive drugs, very often "less is more". This piety is easy to intone but hard to practise, especially when taking fast-onset euphoriants. The lucidity of the entactogenic effect of MDMA may be especially pronounced at low-to-moderate dosages. "Optimal" dosage of psychotropic agents taken for "non-approved" purposes is most often empirically determined by the user investigating what level induces maximal enjoyment. Yet the effects of lower, "sub-optimal" dosages that more subtly modulate consciousness may be of greater value for facilitating personal growth. Low-to-moderate dosage E-experience may be easier to integrate into the rest of one's E-less life. Nonetheless at higher, quite possibly neurotoxic doses of 200mg or so, MDMA can itself sometimes deliver psychedelic euphoria, entheogenic rapture, and some very interesting exotica indeed. Alas the unique effects of such doses [and likewise higher doses of other stellar phenethylamines] cannot safely be investigated in depth until the neurotoxicity of MDMA's metabolites and/or toxic free radicals can be prevented.

       In the meantime, if the user desires a completely clear sensorium, then perceptual alterations might seem eliminable altogether, in principle, by taking only the (+)-MDMA enantiomer rather than the standard racemate. Sadly, pure (+)-MDMA is scarce; it's also hard to prepare at home. Thus one unintended consequence of scheduling MDMA has been to widen youthful exposure to psychedelia, albeit psychedelia in its warmest and most gentle introductory guise. (-)-MDMA at normal doses is only minimally active at the "psychedelic" 5-HT2A receptor owing to its (comparatively) bulky methyl group. By contrast, MDA (which lacks it) is an all-in-one cocktail that can be hallucinogenic as well as empathetic and slightly speedy.

       Alternatively, if uncomplicated perceptual clarity is sought then a 5-HT2 antagonist such as ketanserin or the 5-HT2A selective MDL-11939 might help preserve total lucidity. 5-HT2A antagonists have the additional advantage of preventing MDMA-induced hyperthermia that exacerbates toxicity. Neurotoxic hydroxyl radical formation is temperature-mediated; conversely, hypothermia-inducing agents enhance neuroprotection.

       However, there are complications. Stimulation of the serotonin 5-HT2A receptors contributes to the rewarding effects of MDMA, or at least plays a permissive role in dopamine release. So trying to eliminate perceptual alterations completely while retaining the full-blooded E-magic may be difficult. MDMA is often reckoned a "serotonergic" drug. Compared to amphetamine this is true: MDMA's affinity for the serotonin transporter is greater, and its ratio of serotonin to dopamine release is higher, than amphetamine. Even MDMA's extra release of dopamine partly depends on its activation of the 5-HT2A receptors. But serotonin-releasing agents [e.g. the halogenated amphetamine appetite-suppressant fenfluramine (Pondimin)], taken on their own, aren't notably rewarding or entactogenic/empathetic, at least at ordinary dosages. The enhanced release and reuptake inhibition of dopamine is essential to MDMA's tendency to promote blissful well-being and to colour its entactogenic-empathetic effect.

       Convergent strands of evidence indicate that dopamine release is critical to the MDMA magic. Dopaminergic activity in the brain and motor behaviour may be crudely interpreted as under the inhibitory control of the serotonin system. Yet the multiple serotonin pathways play functionally different roles. According to one hypothesis, the extra serotonin released by MDMA stimulates 5-HT2A receptors located on inhibitory gamma-aminobutyric acid (GABA) striatonigral neurons. VTA dopaminergic neurons in the brain's reward centres are under continuous inhibition by GABA. Stimulation of the 5-HT2A receptors inhibits these GABA neurons, thereby allowing the disinhibition of dopamine biosynthesis. Post-E levels of dopamine in the mesolimbic reward circuitry are far higher than would be explained by MDMA's relatively weak additional release of dopamine via the uptake carrier.

       Animal drug discrimination studies, and the human behavioural evidence, tend to support this dopaminergic account. Although some MDMA users prefer reflective tranquillity and intimate group hug-ins, many loved-up clubbers opt to dance for hours at raves - a form of hyperlocomotion one would expect from Peruvian marching-powder rather than a serotonergic agent.

       However, this account is still simplistic. The release of serotonin following an MDMA-induced reversal of the reuptake pump results in a stimulation of the 5-HT1B receptors and, at higher doses, increasingly of the 5-HT2A receptors as well. Such receptor stimulation can trigger marked hyperactivity, especially in young MDMA users who rave. At lower doses, MDMA-induced locomotor activity is caused mainly by the released serotonin's preferential activation of the 5-HT1B receptor. This is because serotonin has a somewhat higher affinity for the 5-HT1 receptors than the 5-HT2 receptors. The greater flood of serotonin in the synapses triggered by higher doses of MDMA promotes locomotor activity via 5-HT2A receptor-mediated dopamine stimulation as well. To complicate matters, MDMA may itself bind, albeit weakly, to the 5-HT2A receptor. A further complicating factor is that MDMA-induced release of serotonin stimulates the 5-HT2C receptors. Activation of the 5-HT2C receptors serves to mask expression of MDMA-induced hyperactivity, sometimes evidently more effectively than others. The various subpopulations of 5-HT2C receptor located on GABAergic neurons in the ventral tegmental area and the substantia nigra tend to exert a tonic inhibitory influence over the mesolimbic dopamine system. Thus 5-HT2C receptors tonically inhibit dopamine release in the nucleus accumbens, mostly it seems in virtue of their constitutive activity i.e. entering the activated receptor state in the absence of an agonist. Other things being equal, activation of 5-HT2C receptors is anxiogenic, demotivating and generally unpleasant. Certainly the stimulant effects of MDMA are greatly enhanced following treatment with a 5-HT2C antagonist. Sustained antagonism of the 5-HT2C receptors might well we harnessed to intensify the hedonic properties of long-lasting E-like consciousness. Less speculatively, 5-HT2C antagonists such as agomelatine (Valdoxan) are under investigation as potential clinical antidepressants.

As usual, there are complications: all 5-HT2C receptors are not the same. Numerous 5-HT2C receptor isoforms are produced as a result of RNA editing, and their individual roles in modulating the MDMA effect aren't properly understood. In general, the receptor story illustrates at the molecular level that being blissful isn't the same as being blissed out. To sustain empathetic love, simply banishing all capacity for social anxiety isn't going to work. Specific and selective 5-HT2C receptor antagonism may well prove a worthwhile goal; but it's too early to say what the MDMA experience may gain or lose in consequence, whether socially or subjectively. Empathy entails caring about others, not lacking a care in the world. Thus the MDMA-induced disinhibition from social anxiety, and the lowering of psychological defensive barriers, is radically distinct from the sort of anxiolysis induced by SSRIs or the benzodiazepines - or indeed by alcohol or opiates. With none of these drugs or drug categories is a reduction in the user's social anxiety matched by an E-like upwelling of empathy or sensitivity to the feelings of others - in fact quite the reverse. There are subtleties of the MDMA experience that haven't yet been explored.

       If acute serotonin-mediated enhanced dopamine-release is indeed essential to the magic of MDMA, then a wide range of safe long-acting dopaminergics are already on offer to augment any hypothetical subtype-selective "serotonergic" therapies. Compared to our descendants, we're probably all anhedonic. So some form of dopaminergic augmentation is a therapeutic step in the right direction. "Dual-deficit" models of everyday E-less malaise are plausible; and they naturally invite dual-action remedies. Clearly, inhibition of glutamate-evoked firing in the nucleus accumbens is an ingredient of the E-magic: it is known that firing-inhibition depends on both dopamine and serotonin release; and this process is mediated by both dopamine and serotonin receptors. But beyond these superficial generalities, working out how to replicate sustainably at the molecular level the precise neurochemical signature of peak experiences will be hard. Until the dawning of the era of wholesale genomic rewrites and true designer babies, using a cocktail of subtype selective serotonin agonists and gentle dopaminergic psychostimulants still looks like the easiest way to mimic and enhance the entactogenic-empathogenic effect induced by MDMA-like compounds. However, there are many pitfalls in choosing the right dopaminergic for the job.

       In contrast with intracranial electrical stimulation, a direct chemical assault on the hedonic treadmill rarely works. This failure is witnessed by the unsatisfying and usually counterproductive effects of using catecholamine-depleting psychostimulants. Darwinian-era mood and motivation is regulated via a multitude of indirect mechanisms of feedback-inhibition. So it's worth reviewing how and why the substrates of human well-being are held in check; and what can be done about it. First, an unavoidably fast-and-furious tour of the dopamine system is in order. The CNS has three main dopaminergic pathways. They regulate movement, hormonal secretion, and emotion. Each projects from dopaminergic cell groups in the midbrain. 1) The nigrostriatal pathways extend from the substantia nigra pars compacta to the striatum. This pathway is critical to the control of involuntary motor movement; its dysfunction is implicated in the tremor, rigidity and akinesia of the "dopamine deficiency disorder" Parkinson's disease, and several other neuropsychiatric disorders such as Tourette's Syndrome. 2) The tuberoinfundibular system extends from the hypothalamus to the pituitary gland. It's involved in prolactin- and growth hormone-secretion, and the regulation of lactation and fertility. 3) The mesocorticolimbic pathway extends from the ventral tegmental area to the nucleus accumbens and the medial prefrontal cortex. The mesocorticolimbic system is central to emotion, motivation, willed action and, more subtly, the modulation of thought-processes. In crude terms again, dopamine is critical to sensorimotor integration; appetitive behaviour of all kinds; the capacity to switch from one course of behaviour to another; and the orchestration and activation of the motor output system. Dopamine has also traditionally been described as the brain's "pleasure chemical", cueing potentially (Darwinian) fitness-enhancing stimuli so they can acquire control over an organism's behaviour. Certainly, consistent with the dopamine theory of reward, electrically or pharmacologically stimulating microcircuits in the rostromedial shell of the nucleus accumbens produces intense pleasure in the absence of any goal-seeking behaviour. But this formulation can be misleading. The mesolimbic dopamine system mediates "wanting" more than "liking"; and its drug-induced or electrical stimulation may increase incentive-salience rather than the raw intensity of pleasure itself. Dopaminergic neurotransmission is critical to incentive-motivation and all forms of purposeful behaviour. Dopamine levels tend to rise if one is anticipating a rewarding event; and levels then tend to fall if the anticipated reward fails to materialise. Couched in the language of psychology rather than neuroscience, enhanced dopamine release in the pleasure centres imparts a sense of urgency, significance and a feeling of things-to-be-done. The molecular substrates of pure pleasure are still elusive.

        At the cellular level, the dopamine system doesn't quite rival the molecular, pharmacological and functional diversity of the serotonin system; but the two "classic" types of dopamine receptor (D1-like and D2-like receptors) have several subtypes and alternate splice-forms. Further, the number of different messenger RNA and dopamine binding sites substantially exceeds the five dopamine receptor genes of the human genome, a diversity that reflects the genetic polymorphism and alternative splicing events in normal dopamine gene-expression. However, each type of dopamine receptor belongs to the superfamily of G-protein-coupled receptors that activates or inhibits different forms of adenylyl cyclase inside the cell. Intriguingly, the presence or absence of variant alleles of dopamine receptor subtypes and their signal-transduction mechanisms is correlated with variants of human behaviour and personality. For example, individuals with genotypes containing the seven-repeat allele of the dopamine D4 16-amino acid repeat polymorphism tend to exhibit the personality trait of "novelty-seeking". This trait is characterised by a tendency to impulsiveness, risk-taking, exploration, excitability, and an optimistic mood, though alas not a loving, E-like temperament. For better or worse, within a few decades prospective parents will be able to select such alleles and their rationally redesigned enhancements when choosing the parameters of their future offspring. Such naturally loved-up kids may prove more easily adorable than today's Darwinian default-models.

       Like the other catecholamine neurotransmitters, dopamine itself is synthesised from the non-essential amino acid L-tyrosine. L-tyrosine is transported across the blood-brain barrier into the dopaminergic nerve cell. L-tyrosine is converted to L-dopa by the enzyme tyrosine hydroxylase. L-dopa is then rapidly converted to dopamine by L-amino acid decarboxylase. Next dopamine is sequestered in synaptic vesicles by a dopamine transporter. At the synapse, the dopamine nerve terminal displays high-affinity uptake sites. They rapidly terminate the action of the neurotransmitter on the receptors if it isn't metabolised by the MAO or COMT enzymes. Depending on concentration gradient, the dopamine carrier can transport dopamine back into the nerve cell, recycling it as normal, or alternatively, after a user has taken a classic amphetamine, the carrier can transport dopamine from the cell terminals into the synaptic cleft. In common with amphetamine, MDMA inhibits the neuronal reuptake of dopamine, albeit more weakly than MDA. Further, increased post-E administration activity of the serotonin 5-HT1B and 5-HT2A receptors causes the dopaminergic neurons themselves to fire more rapidly. This higher impulse-frequency causes increased dopamine-release via exocytosis of the dopamine-containing vesicles in the normal manner.

       So what leaves so many "normal" Darwinian people - who are neither clinically depressed nor loved-up on MDMA - comparatively anhedonic and hypodopaminergic? The dopamine neurotransmitter is under powerful homeostatic control. So is the density and signal-transduction efficiency of the receptors to which it binds. Feedback-inhibition of dopamine synthesis, dopamine release and spontaneous action-potential generation in dopamine-producing cells is modulated by a variety of functionally distinct dopamine autoreceptors that regulate membrane excitability. The dopamine neurotransmitter itself functions as an end-product inhibitor of tyrosine hydroxylase, the rate-limiting step in dopamine production. Dopamine plays this role by competing with a tetrahydrobiopterin co-factor for a binding site on the enzyme. Dopamine synthesis is also modulated by the rate of impulse-flow from the nigrostriatal pathway. In addition, presynaptic dopamine receptors modulate the rate of tyrosine hydroxylation; and most mesolimbic dopamine neurons possess cholecystokinin-autoreceptors and neurotensin-autoreceptors that regulate dopamine function as well. Indeed activity of the mesocorticolimbic dopamine system is regulated by multiple neuronal pathways containing different neurotransmitters, notably serotonin, opioids, GABA and glutamate. Precisely what dopamine actually does in the all-important dopamine-sensitive shell of the nucleus accumbens is unclear. The main effect of its release seems to be the inhibition of the GABAergic medium spiny projection neurons (MSNs). These neurons come in two types. One subtype expresses dopamine D2 receptors and enkephalin. This sort of GABAergic medium spiny cell projects from the nucleus accumbens to the ventral pallidum. It is activated by "reward stimulation" of the ventral tegmental area. The other subtype of GABAergic medium spiny projection neuron co-expresses substance P, dynorphin and dopamine D1 receptors. This subtype projects directly back to the ventral tegmental area. It regulates motivation and pleasure, or our deficit thereof.

So how can this cruel and complex web of inhibitory feedback mechanisms best be modified? If our aim were pure-and-simple cloud nine euphoria, then better drugs to decrease glutamate and GABA currents in the critical medium spiny neurons of the nucleus accumbens might be adequate - at least until new genes and gene networks can be more readily inserted in the genome, and the regulation of old ones improved. But well-controlled, high-functioning euphoria is more elusive than mind-blowing rapture. Crude "natural" interventions to enrich dopamine function aren't effective. For instance, some psychonauts, clubbers and alternative therapists alike have explored taking free-form amino acid supplements of L-tyrosine and L-phenylalanine in a bid to boost native dopamine levels or reanimate a drug-frazzled brain. But tyrosine hydroxylase is normally saturated. So unlike tryptophan-loading and/or 5-HTP-loading to increase neural levels of serotonin production, this "dopaminergic" precursor strategy typically doesn't work. On the other hand, taking L-dopa does increase synaptic dopamine levels. This is especially so when L-dopa is combined (as in Sinemet for Parkinsonians) with a peripheral decarboxylase inhibitor such as carbidopa to prevent its metabolism outside the brain, At least for a minority of "normal" subjects, taking L-dopa can be an effective motivator, libido-enhancer and mood-brightener. In a more controlled setting, rodents engineered so they can't synthesize dopamine initially develop quite normally, only to die miserably a few weeks after birth following a failure to eat, drink or do very much in this world at all. Yet when such dopamine knock-out mice are abundantly maintained on L-dopa, they can flourish. Indeed L-dopa-maintained dopamine knock-out mice become hyperactive and sexually vigorous. This manipulation has not yet been attempted in dopamine knock-out humans. Augmentation should in any case be tried only cautiously and in controlled-release preparations (e.g. Sinemet SR) since high levels of L-dopa may increase oxidative stress. Whatever the mechanism, simply increasing raw dopamine levels per se is not enough. For instance, an agent such as alpha-methylparatyrosine that inhibits tyrosine hydroxylase, the rate-limiting enzyme in catecholamine synthesis, might be expected to produce a state of melancholic depression; but in non-depressives it doesn't reliably do so. This complicates any simplistic catecholamine-depletion theory of retarded depression. Nevertheless, dopamine-releasing agents demonstrably tend to induce euphoria. By contrast, dopamine receptor antagonists like haloperidol are dulling and dysphoric. All the classical dopamine D2-blocking neuroleptics blunt will-power and flatten emotion. Administering dopamine D2-blockers tends to induce apathy and anhedonia, and ruins the MDMA magic. Nasty but instructive, such magic-prevention experiments are an important pointer to what's needed to sustain the MDMA spectrum of consciousness. It's known that stimulation of the dopamine D2-like receptor causes an increase in phosphatidylinositol hydrolysis by activating enzyme phospholipase C. Enhanced phosphatidylinositol hydrolysis is implicated in euphoric mania. Conversely, the lithium used to treat "uncontrolled" euphoria inhibits the phosphatidylinositol second messenger system and darkens mood in nondepressed "euthymic" people. Understanding the principles behind the pharmacological induction of controllable non-stop euphoria will be a first step on the route to designing lifelong variations of the subtler forms of magic.

        In the meantime, dopamine antagonists like amisulpride (Solian) can be used at low doses preferentially to antagonise the synthesis-, release- and impulse-modulating presynaptic dopamine D2/D3 autoreceptors. Thus a regimen of low-dose amisulpride may potentially enhance dopamine release and boost mood and motivation, whereas many dopamine reuptake inhibitors [e.g. vanoxerine, bupropion, nomifensine] "adaptively" diminish the neuronal release of dopamine over time, even though their action on reuptake inhibition increases the neurotransmitter's synaptic availability. Unfortunately, pre-treatment with high doses of dopamine reuptake inhibitors blunts MDMA-induced release of dopamine, though not to the same degree as SSRIs blunt MDMA-induced release of serotonin. Other crude strategies to augment dopamine function involve taking dopaminergic agents such as the dopamine agonists pergolide (Permax) and bromocriptine (Parlodel); the potent, pro-sexual, long-acting D2 agonist cabergoline (Dostinex); selective D2/D3 agonists such as pramipexole (Mirapex) or ropinirole (Requip); catechol-o-methyltransferase (COMT) inhibitors such as tolcapone (Tasmar); selective MAO-B inhibitors such as selegiline (Eldepryl) or rasagiline (Azilect); adenosine 2A receptor antagonists; and centrally active nicotinic receptor agonists. Oral, centrally-active dopaminergic "pro-drugs" with higher bioavailability and fewer adverse side-effects are also under investigation. But there are obvious problems. For instance, dopamine-release promoting agents, if fast-acting and taken in the absence of anything subtype selectively "serotonergic", may not induce serenely motivated well-being as distinct from compulsive pleasure-seeking, thought disturbances or manic excitement. Any tendency to cause uncontrolled dose-escalation is likely to cause toxicity, florid psychoses and abuse. Regrettably, these worries about the "abuse-potential" of psychostimulants frequently generalise in mainstream wisdom to an unwarranted fear of all "dopaminergic" antidepressants/mood-brighteners.

Clinically-licensed SSRIs [fluoxetine/Prozac; sertraline/Zoloft; fluvoxamine/Luvox; paroxetine/Paxil; and citalopram/Celexa] may make a small minority of people feel durably "better than well". More typically, SSRIs are mood-blunters and even, for some people, psychic anaesthetisers. SSRIs commonly make those who take them more resilient and less anxious. But they don't promote depth of feeling, intellectual dynamism or clarity of thought. SSRIs can also diminish the intensity of love. MDMA, by contrast, is a veritable love-potion, what Claudio Naranjo aptly christened a "feeling intensifier". On MDMA, emotions are heightened as well as enriched. Compared to loved-up ecstatics on MDMA, the rest of us have the emotional intensity of zombies; and zombies have no real insight into what they're lacking, even if some of us can talk as though we do. Ironically, at a time when the loss of personal liberty entailed by prohibitionist drug laws is justified by the societal costs of illicit drug-taking, "psychiatric" drugs are clinically prescribed by physicians regardless of the likely effect of a medication on the personal relationships of the patient. SSRIs, by enhancing the user's emotional self-sufficiency, can either save marital relationships or wreck them. By reducing "neediness", SSRIs also diminish what today passes for love. SSRIs are prone to impair romantic ardour as well as libido. One technical (and ideological) challenge of the pharmacogenomic revolution in prospect at the interface between genetics and drug-design will be to investigate how the emotional honesty and extraordinary depth of feeling induced by MDMA can be sustained over a period of months, years and decades rather than for two-hour bursts.

       There are further complications to overcome if any bid to replicate and sustain full-spectrum E-like consciousness is to succeed. MDMA triggers the release of the neurotransmitter acetylcholine via a histaminergic H1 mechanism. MDMA is also a weak agonist of the acetylcholine muscarinic M1 receptors. MDMA's modest cholinergic activity may contribute to the exquisite lucidity of consciousness characteristic of pure MDMA taken in a therapeutic setting. For the cholinergic system is vital to memory, higher thought-processes and verbal fluency. Cholinergics such as piracetam (Nootropil) are used as nootropics or "smart drugs"; and acetylcholinesterase inhibitors like galantamine (Reminyl), rivastigmine (Exelon), tacrine (Cognex) and donepezil (Aricept) are used as palliative treatments of Alzheimer's disease. Acetylcholine-release and muscarinic receptor activation probably play no direct role in the rewarding hedonic effects of MDMA. Yet their subtle contribution to the texture of the magic can't be discounted. "Dumb-drug" antimuscarinic agents commonly induce mild euphoria via their indirect enhancement of dopamine function. Their mood-brightening effect stands in contrast to many cholinergic (e.g. muscarinic M4 receptor) agonists and cholinesterase inhibitors which have a tendency to subdue mood. A wide range of cholinergics is now under development for the palliative treatment of Alzheimer's disease, a progressive neurodegenerative disorder characterised by profound cholinergic deficits. Some depressives, however, may actually benefit from the antimuscarinic anticholinergic effects that more intellectually fastidious clinicians would call an adverse side-effect of the older tricyclics. While a great many depressed people report intellectual sluggishness and poverty of thought, other melancholic and introspective depressives endure "hypercholinergic frenzy", possibly owing to dysregulation of the cholinergic-adrenergic axis. Sadly, innumerable depressives among life's walking wounded today find the examined life scarcely worth living: they cope with life only by "just getting on with it". By contrast, MDMA allows introspection to become insightful and enjoyable even to the naturally angst-ridden. On MDMA, both philosophising and emotional self-honesty can be illuminating and fun. It's a shame that such self-insight can't more readily be prolonged.

       Another enigma is the role of DHEA. MDMA causes a rise in the adrenal corticosteroid dehydroepiandrosterone (DHEA). DHEA is the precursor to testosterone,progesterone, estradiol and other steroids. The rise and peak physiological values of DHEA between around 1 to 2½ hours post-MDMA administration is correlated with user-reported euphoria, though DHEA's precise contribution to the mood-elevation is unclear. In general, levels of DHEA decline with age after early adulthood. Long-term supplementation with DHEA seems to have beneficial effect on libido, immune function and some forms of cognition. However, in spite of a wealth of research, no firm conclusions have yet been reached on the advisability of taking DHEA supplements, or an optimal dosage if taken. Nor is it known what role enhanced DHEA might play in sustaining enriched quality of life over the longer term. Taken on its own, DHEA may brighten mood; but it's scarcely an E-like effect.

       One unwanted effect of MDMA, especially when taken at higher doses, is its tendency inhibit to tryptophan hydroxylase by triggering a rapid oxidation of the enzyme's sulphydryl sites. Tryptophan hydroxylase is the rate-limiting enzyme in serotonin synthesis. Even though the acute functional loss of tryptophan hydroxylase in the cell terminal is reversible, the axon's vulnerability to oxidative stress is increased. In order sustainably to enhance our capacity for empathetic bliss, and certainly to prevent any functional serotonergic deficit, tryptophan hydroxylase function must be enhanced, not inhibited. However, to date no stimulator (or inhibitor) of the biosynthesis of serotonin has been commercially marketed. Interestingly, the use of interventions to increase the biosynthesis of serotonin prior to MDMA use tends to trigger an increased synaptic release of dopamine, thereby enhancing the user's euphoria. Unfortunately, increased serotonin synthesis also aggravates post-E neurotoxicity. The two mechanisms are separable in principle. In the meantime, restraint is prudent.

       Ultimately, we may be able to generate sublime MDMA-like states - at will, to order, and indefinitely - only when the intracellular signal-transduction mechanisms, and regulation of genetic switching beyond the post-synaptic cascade, are better understood. The orchestrated "overexpression" of some genes and the receptor proteins they code, the redesigned "under-expression" of others, and perhaps the selective silencing of gene expression via RNA-mediated interference of anything really nasty, can amplify desirable facets of our consciousness and suppress its darker and more poisonous variants. Thus at one terrible extreme, suicide victims, for instance, tend to show heightened levels of serotonin 5-HT2A receptors. Before death, they show a greater activity in the genetic machinery churning out the 5-HT2A receptor itself. So as well as developing gene-therapy to prevent suicidality - and forestall the whole spectrum of deeply unpleasant para-suicidal and self-destructivestates - it should be possible, conversely, to engineer an unimaginably richer love of life, of ourselves and each other by genetically enhancing our own minds. Freedom to optimise (or at least improve) one's genome should prove at least as personally liberating as the freedom to optimise one's drug-regimen. Doubtless a regulatory minefield lies ahead.

        One momentous development is perhaps only a decade or so away. In the imminent era of genomic healthcare, we may each enjoy access to a read-out of our own individual genotype i.e. the set of particular forms of genes - alleles - peculiar to each individual who isn't a monozygotic twin [triplet etc]. Harnessed to pharmacogenetics, the study of how an individual's distinctive genetic inheritance affects the body's response to drugs, such intimate genetic self-knowledge should allow the design and prescription of a drug-regimen tailored to each unique person, whether for medical, social, research or "recreational" purposes. At first, only the crudest stratification of patient populations by genotype may be the medical norm. This is because commercial drug companies prefer large markets. Yet eventually we should all have optional access to the gene-expression profile of each neurotransmitter-specific neuronal subtype in the mind-brain. Such access offers scope for fine-grained manipulations of the chemistry of our souls inconceivable in the Dark Ages of pre-genomic medicine.

        Genetically personalised medicine offers another bonus. It should eliminate the possibility of idiosyncratic drug reactions caused by genetic abnormalities - for example rare polymorphisms of the cytochrome P450-2D6 system critical to drug metabolism. Owing to genetic polymorphisms in drug-metabolising enzymes, receptors and transporters, a range of drugs beneficial to c.99% of the population can't get regulatory approval. In some cases, valuable licensed medicines are pulled after post-marketing surveillance. This therapeutic opportunity is wasted because, say, 1%, 0.1%, or even 0.01% of people who take such agents suffer severe adverse reactions. The advent of genetically personalised medicine should mean that these atypical cases can be excluded; and given other medication instead. Useful older drugs can be dusted off the shelves and re-licensed. New agents can be developed and given faster regulatory approval.

       Psychoactive drug users in particular should benefit from the prospect of genetic self-knowledge. Cytochrome P450 forms a superfamily of hepatic enzymes with hundreds of different isoforms that catalyse the oxidative metabolism of a huge diversity of substrates, including MDMA. The duration of action and/or intensity of the effect of numerous drugs are determined by their rate of metabolism by cytochrome P450. Whereas some "housekeeping" enzymes are expressed constitutively i.e. they are perennially active, other enzymes are expressed essentially only when triggered by the presence of the exogenous chemical. Inducible enzyme isoforms increase both in amount and activity in response to drugs.

       The precise role of CYP2D6 in MDMA pharmacology is still unclear. MDMA is not merely a substrate for CYP2D6; it also binds to the enzyme, forming an inhibitory complex. The CYP2D6 enzyme is soon saturated even in efficient metabolisers. Other human cytochromes P450 such as CYP-1A2, CYP-3A4 and CYP-2bB are critically involved in the oxidative metabolism of MDMA. It is possible these other metabolic pathways play an important role in everything from idiosyncratic responses to MDMA to the notorious "loss of magic". If enzyme induction accounts wholly or in part for the loss, then the roots of disenchantment can be investigated and prevented, whether for MDMA or perhaps its still imperfect successors. If, however, central processes of neuroadaptation are at work, either instead or as well, then longitudinal neuroimaging studies comparing the brain-scans of, say, drug-virgins ninety minutes or so after dropping their first magical E (or perhaps its safer successor(s)) with brain-scans taken during their hundredth-odd trip should allow the neurochemical basis of any loss of magic to be pinpointed and reversed. Indeed the magic itself can presumably be amplified, probably more delightfully than an unenchanted Darwinian mind can grasp.

        More broadly, genomic medicine will deliver the freedom to choose who or what we want be, both as individuals and collectively as a species. In the long run, a spectrum of mental superhealth that is orders of magnitude richer than anything accessible today can be genetically pre-programmed. "Phenotypic plasticity" (the nearest analogue to free will a molecular geneticist will recognise) can be both vastly extended to enhance personal autonomy and, no less importantly, constrained where it's cruel and unwanted. Thus better designed gene-and-drug combinations can perpetuate truly sublime modes of consciousness whereas, conversely, a predisposition to such ancient Darwinian horrors as sociopathy or suicidality can be genetically cured. A rewritten genome can potentially liberate us from all trace of psychopathy and depression - the enemy from without and, all too often, the enemy within. When taken today, MDMA rapidly banishes the horrors of both. Alas they soon return; the acute effects of MDMA are mostly all too reversible. Prediction is always a hazardous business, but to our descendants, breeding kids with anything like our own corrupt code may seem like wanton child abuse.

[psychotherapyconsultants]

How Stress Affects Your Memory

The relationship between stress and memory is complex. A little bit of stress can enhance your ability to encode, store, and retrieve factual information. Too much stress, however, can shut the system down. You may have had this experience studying for a test. A moderate amount of anxiety is motivating and will help you perform better. Too much on the other hand, especially while taking the actual test, can prevent you from recalling what you know.

The experience of trauma and chronic stress over time can actually change the brain structures involved in memory. To understand how this happens, we need to consider one of the ways memories are formed and recalled.

When we have a sensory experience, the amygdala (associated with processing emotion) influences the hippocampus (associated with processing memory) to encode and store the information. Emotionally charged events (both positive and negative) form stronger memories. Later, when it comes time to retrieve a memory, the prefrontal cortex gives the command.

All three of these brain structures are also involved in traumatic stress.

Chronic Stress and Memory

When we experience a threat, the amygdala sets off an alarm which puts the nervous system and body into fight or flight mode. This system exposes the brain and body to high levels of circulating stress hormones. Research has shown that high levels of stress hormones over time can damage the hippocampus (it actually shrinks). This reduces its ability to encode and form memories.

Additionally, during times of stress, the amygdala will inhibit the activity of the prefrontal cortex. From a biological perspective, this is useful in keeping us alive. Energy and resources are pulled away from higher thought and reasoning (the prefrontal cortex) and re-directed to bodily systems needed to preserve our physical safety. For example, our sensory abilities are heightened. Our muscles receive oxygen and glucose so we can fight or run.   

For most if us, the fight or flight response is usually not needed to keep us alive in today’s society. It is not useful during an interview for a job you really want or while out on a date. A chronically activated nervous system actually reduces our ability to function and, over time, damages certain structures in our brain.

Trauma and the Hippocampus

To investigate the effects of trauma on the hippocampus researchers looked at the brains of coal miners who had developed posttraumatic stress disorder (PTSD) after being involved in an explosion (2). The researchers found that the coal miners with PTSD had significantly reduced volume of the amygdala and hippocampus in comparison to non-traumatized coal miners.

These findings hold important implications when it comes to memory. Reduced volume in the hippocampus and amygdala due to chronic stress reduces the ability to form and recall memories.

What We Can Do

The brain retains its ability to change throughout the entire lifespan. Studies have already shown that the damaging effects of chronic stress and trauma on the hippocampus can be reversed. For example, the use of antidepressant medication that increases serotonin levels has been shown to counteract the effects of stress on the hippocampus. With antidepressant use, the hippocampal volume in the chronically stressed brain increased.

While the mechanism for the changes in the hippocampus is not fully understood, we can assume that in addition to the increase in serotonin, the reduction in stress that caused the damage in the first place, also plays a role in the reversal of damage to the hippocampus.

Take the steps necessary to reduce chronic stress. Not only will lower stress have a positive effect on your overall quality of life, but it may also begin the process of healing the damage to the brain structures involved in memory. Exercise, therapy, and medication are all options for reversing damages of trauma and chronic stress.

References

Bremner, J. D. (2006). Traumatic stress: effects on the brain. Dialogues in clinical neuroscience, 8(4), 445.

Zhang, Q., Zhuo, C., Lang, X., Li, H., Qin, W., & Yu, C. (2014). Structural impairments of hippocampus in coal mine gas explosion-related posttraumatic stress disorder. PloS one, 9(7), e102042.

Malberg, J. E., Eisch, A. J., Nestler, E. J., & Duman, R. S. (2000). Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus. Journal of Neuroscience, 20(24), 9104-9110.

Power, J. D., & Schlaggar, B. L. (2017). Neural plasticity across the lifespan. Wiley Interdisciplinary Reviews: Developmental Biology, 6(1), e216.

from World of Psychology https://psychcentral.com/blog/how-stress-affects-your-memory/

[marcusssanderson]

7 Ways to Boost the Happy Hormones in Your Brain

Did you know that happiness creates success, and NOT the other way around?

Mental health is a key player when it comes to accomplishment and contentedness in all areas of life. Luckily for us, our brain is on our side when we aim to succeed. If we have basic knowledge of a few key areas and chemicals in our brain, we’ll know how to trigger them in order to fulfill our goals with greater ease.

They’re not nearly as complicated to understand as you may think. In fact, they all create logical connections that can be supported just by making a few simple tweaks in your daily habits and routine.

Here, we introduce those happy hormones in the brain that keep you feeling good.

Happy Hormones In The Brain and How To Boost Them

1. Dopamine for Pleasure and Motivation

Dopamine allows us to feel bliss, pleasure, euphoria and motivation.

Dopamine is a chemical (neurotransmitter) that is used by the nerves to send messages. When a nerve releases dopamine, it crosses a very small gap in the brain called a synapse and then attaches to a dopamine receptor on the next nerve.

Basically, when dopamine levels are depleted in our brain, our message can’t be transmitted properly. This, in turn, can have an impact on our behaviour, mood, cognition, attention, learning, movement, and sleep.

When we procrastinate, have feelings of self-doubt, or lack enthusiasm, these are strong clues from the brain that we are low on dopamine.

It’s super easy to increase dopamine levels: eight hours sleep per day and regular exercise help to keep dopamine in balance. It’s also important to remember that the brain releases a little bit of these happy hormones when you achieve or succeed.

One way to get a ‘hit’ of dopamine regularly is to break down big goals into smaller goals, more easily achievable chunks, so that you can keep getting ‘runs on the board’ and feel good about the process.

Of course, you should always celebrate all those ‘little’ wins. They’re helping you, step by step, to achieve the bigger goal. Any accomplishments, no matter how small they may seem, are definitely worth recognition – and you’ll boost your dopamine.

2. Endorphins Make You Happy

Endorphins are released into your bloodstream once you have exercised, leaving you feeling more energized and in a better mood for the rest of your day. Endorphins are the counter balance to stress. So the more endorphins you release, the less stress and anxiety you will experience.

Along with regular exercise, laughter is one of the easiest ways to induce endorphin release. This tells us one BIG thing: we need to have more fun! So, always keep your sense of humor handy.

There are some studies that attest how dark chocolate and spicy foods can help release happy hormones. Therefore, consider keeping a stash of dark chocolate OR treat yourself to delicious curry every now and then for a quick endorphin boost.

  This is How You Find Your Superpower | Jim Kwik | Goalcast

Credit: GoalCast

3. Love is Blind with Oxytocin

Oxytocin –the love hormone–creates intimacy, trust and builds strong, healthy relationships.

Often referred to as the cuddle hormone, oxytocin is essential for creating powerful bonds and improving social interactions.

As the name suggests, ONE very simple way to keep oxytocin flowing is to give someone a hug – not a handshake. There is research now to explain that a hug for up to 20 seconds a day releases oxytocin, which is a natural anti-depressant and anti-anxiety agent.

Oxytocin is the hormone that allows us to feel love and connection. In fact, when we experience an increase of oxytocin, it makes us more intuitive to others’ needs. Even when someone receives a gift, his or her oxytocin levels can rise.

You can strengthen work and personal relationships through the simple gift of a massive hug.

4. Serotonin Controls Our Moods

Serotonin flows when you feel satisfied, accomplished, and important. However, a lack of serotonin can make you feel lonely, bleak and unhappy. Unhealthy attention-seeking behavior can also be a cry for serotonin.

Our brain can’t tell the difference between what’s real and imagined, so it produces serotonin in both cases. This is why gratitude practices are popular; they remind us that we are valued and have much to value in life.

If you need a serotonin boost during a stressful day, take a few moments to reflect on past achievements and victories. Alternatively, engage in a random act of kindness, or write a text or email telling one of your friends or partner how much you appreciate them.

You can also spend a minute or two ‘reliving’ a cherished moment in your head. These are simple mood boosters, just because they increase happy hormones. We also know that vitamin D (from the sun) helps to expand our brain’s serotonin production.

5. No Amygdala. No Fear.

The amygdala, known as the ‘fright, freeze and flight centre’, manages connections and is directly involved with emotional well-being. Activating the amygdala in a positive way stimulates higher cognitive processes that improve creativity and intelligence, while elevating positive emotions.

The amygdala processes positive and negative feedback depending on how we perceive an outcome. As a result, it makes us feel strong emotional responses that often lead to impulsive reactions. Keep an eye out for your emotional response as feedback because it has an essential role to play in determining whether we are consciously creating a desired outcome, or just reacting.

Being the observer of your thought process can influence your amygdala. When the amygdala is stimulated in a positive manner, it sends signals to the frontal lobe or your brain. When the amygdala signals go backwards, they generate a fear response. It is, in turn, handled by the lower level of your brain, also known as the reptilian brain.

Needless to say, thinking motivated by this part of the brain is NOT well suited for modern society. Stimulating the amygdala with regular practice can help you enter a state of flow that results in losing yourself in total bliss, joy, and creativity.

Just do the things that you love and that make you happy. 

6. Hippocampus: The Seahorse

The hippocampus is viewed as an associative memory system supporting the formation, storage, and retrieval of memories. Emotion and memory are very closely related, and you know how this plays out.

Imagine you go to a work function: what are you going to recall or remember? The individual that made you laugh the hardest, the individual who pushed you aside at the bar as if you were invisible, or the person that embarrassed you on your first day at work?

The next morning, what memory will your hippocampus recall? I’m guessing it will be the one that had the highest emotional impact.

So it would make complete sense that the limbic, emotional part of your brain is in-charge of transferring information into memory. Your hippocampus is the part of the brain that appears to be absolutely necessary for making new memories.

If we didn’t have it, we could NOT possibly experience being stuck in the past or the present. Keep in mind – as you change your mind, you can change your brain. This is known as neuroplasticity.

7. Willpower at the Pre-frontal Cortex

Your pre-fontal cortex is that part of the brain that is right behind your forehead. Its function is decision-making and regulating our behavior, self-control, and willpower. Looking after this section of our brain involves exercising will power.

Yep – the more we use our self-control, the stronger it becomes (like any muscle). If you want to lose weight, begin saving money, start exercising – it’s all actioned here in this part of the brain.

Try this: choose your new action and do it repeatedly for 21 days. If you miss a day, then you need to start again. Record your progress; you’ll see a remarkable difference from start to finish.

Astoundingly, we only use around 10 percent of our brains, yet we seldom think to invest in a little training every now and then. A new theory, neuroplasticity, has proven that we can change our brain.

Boost Happy Hormones – Do Something New Today

Your brain is a muscle. You need to exercise it regularly.

Do something different. Do something new. Stay curious.

When you experience something ‘new’, it actually stimulates and transforms your brain.

Don’t get stuck in a rut doing the same old things. The only way to change the structure of your brain is to explore, experiment, and try something new to maximise how you use your

The post 7 Ways to Boost the Happy Hormones in Your Brain appeared first on Everyday Power Blog.

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This Is Your Brain on Exercise

News flash: Exercise isn’t all about your body. In fact, building muscles and conditioning your heart and circulatory system are side effects. Exercise is really about your brain.

Humans evolved to move, and that movement — hunting, foraging, running, climbing — spurred brain growth, especially in the prefrontal cortex, which differentiates us from other animals. “Thinking is the evolutionary internalization of movement,” explains New York University neuroscience professor Rodolfo Llinás, MD, PhD, author of I of the Vortex: From Neurons to Self.

When you’re exercising, your brain is usually not what’s on your mind. But that activity is building your gray matter in myriad ways, making you more alert, creative, motivated, and perceptive, says John Ratey, MD, associate clinical professor of psychiatry at Harvard Medical School. It’s helping you learn better, remember more, and combat stress. It’s boosting your mood while helping you overcome anxiety and depression.

In sum, exercise keeps your brain healthy.

“The real reason we feel so good when we get our blood pumping is that it makes the brain function at its best,” says Ratey, author of Spark: The Revolutionary New Science of Exercise and the Brain. “The point of exercise is to build and condition the brain.”

The reverse is also true, however: “What virtually no one recognizes,” he warns, “is that inactivity is killing our brains.”

Build a Better Brain

Scientists long believed that we’re born with all the neurons we’re ever going to get, and that our brains are hardwired once we pass adolescence. In the last few decades, research has challenged those views.

“We now know that the brain is flexible, or plastic, in the parlance of neuroscientists — more Play-Doh than porcelain,” Ratey explains. Our brains are constantly growing; they can even be rewired. And exercise is the key.

Scientists understand that physical activity stresses our brains similarly to how it works our muscles. Neurons break down, then recover and become stronger and more resilient. “Aerobic exercise can change the brain’s anatomy, physiology — and function,” says New York University neural science professor Wendy Suzuki, PhD, author of Healthy Brain, Happy Life.

Numerous recent studies have revealed just how those changes occur. What’s becoming clear are the many neurological factors that activity positively influences, including the following.

Alertness and Perception

The brain is all about communication. It’s composed of 100 billion neurons that confer with each other, governing every thought and action. Synapses are the connections between neurons; they fire electrical signals that neurotransmitters carry to the next neuron’s dendrite branch. Neurotransmitters are thus key to brain function — and they’re strengthened by exercise.

“Exercise is potent,” Ratey says. “More nerve cells fire when we’re exercising than when we’re doing anything else. This activates the brain as a whole. It turns on arousal, attention, the frontal cortex, the executive functioning area — so we’re all set to participate in the world.”

Among these neurotransmitters are norepinephrine, which sparks attention, perception, motivation, and arousal; serotonin, which directs “traffic,” influencing mood, impulsivity, anger, and aggression; and dopamine, which governs attention and learning, plus our sense of contentment and reward.

Movement and Coordination

As we move, our brains learn how to move better the next time. Exercise stimulates the cerebellum, which coordinates all the body’s motor movements, like standing upright, hitting a hockey puck, and performing a plié.

The prefrontal cortex is the brain’s CEO, explains Ratey; it’s in charge of executive functions, controlling physical actions, receiving input, and issuing instructions to the body. Managing short-term working memory, judging, and planning are also its responsibility.

“When we exercise, particularly if the exercise requires complex motor movement, we’re also exercising the area of the brain involved in the full suite of cognitive functions,” he explains. “We’re causing the brain to fire signals along the same network of cells, which solidifies their connections.”

Attention and Concentration

Our brains become more active when we are active; this causes neurons to fire in unison, creating brain waves. When we’re on autopilot — sleeping, brushing our teeth, watching TV — low-frequency waves prevail. High-frequency waves called beta waves dominate when we’re focused and processing information.

Using electroencephalogram (EEG) monitoring to track electrical pulses, researchers discovered that exercise intensifies brain-wave amplitude and frequency, and more beta waves propel you into a more alert state. “The most common finding in studies on exercise is that increased aerobic exercise will improve your ability to focus attention and your ability to shift your attention,” Suzuki explains.

Experts believe this enhanced focus comes from the bump in dopamine, which calms the mind. Ratey, for example, is convinced physical activity can ease attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) in kids and adults alike.

Learning

The functions of learning and memory are concentrated in the hippocampus, a small region tucked in the brain’s center. But we wouldn’t be able to learn without aid from the prefrontal cortex — part of the reason communication within the brain is so vital.

Neurotrophins build and maintain the brain’s basic cell circuitry. Key among these in the hippocampus is the recently discovered brain-derived neurotrophic factor (BDNF), a protein that incites neuron growth.

“BDNF works in many ways,” Ratey explains. “It makes brain cells work better; it grows them; it prevents them from eroding; it helps deal with stresses; it provides the right environment for brain cells to prosper.” BDNF is released when neurons fire, causing the brain to produce more BDNF. When we exercise, those neurons fire like crazy, elevating BDNF levels.

Physical activity also prompts other hormone factors into action: Insulin-like growth factor (IGF-1), vascular endothelial growth factor, and fibroblast growth factor all push through the blood–brain barrier and work with BDNF to enhance the molecular machinery of learning. In addition, the hormone IGF-1 delivers the brain’s primary fuel — glucose — to neurons to spur learning.

So, while going for a run won’t transform us into geniuses, Ratey says exercise certainly boosts our potential for learning and increases our rate of learning. Both Ratey and Suzuki believe that kids need physical education integrated into classrooms to optimize how they learn.

And for adults? “We don’t have to be looking for that magic pill to make us smarter,” says Suzuki. “We really should be looking for that magic exercise regimen that will optimize all these different brain areas.”

Memory

Using magnetic resonance imaging (MRI), Columbia University researchers discovered that BDNF helps the brain create new neurons (a process called neurogenesis) in just two regions: the hippocampus, which is crucial for long-term memory, and the olfactory bulb, the area responsible for smell and taste. This process affects our perception of the world.

In tests on rodents, exercise doubled the rate of neurogenesis in the hippocampus, Suzuki reports. Plus, it increased the number of dendritic spines on the neurons as well as their length — all of which improve neuronal communication.

These physiological changes are called long-term potentiation (LTP), and in further rodent studies, researchers found that exercise-induced LTP improved hippocampal function as measured by a broad range of memory tests.

Other studies have shown similar memory gains for people. In a 2016 report published in Frontiers in Human Neuroscience, researchers conducted MRI scans of cross-country runners and identified “significantly greater connectivity” between parts of their brains associated with attention, decision-making, multitasking, processing sensory input, and memory, compared with a control group of nonrunners.

Creativity and Imagination

The hippocampus — which lights up with electrical activity during exercise — also fuels imagination, or thinking about the future and other possibilities. A 2014 study published in the Journal of Experimental Psychology divided 176 college students and adults into two groups, one of which walked while taking a creativity test; the other was sedentary during the test. The walkers scored 81 percent higher.

“We’re not saying walking can turn you into Michelangelo,” says study coauthor Marily Oppezzo, PhD, a Stanford University psychologist. “But it could help you at the beginning stages of creativity.”

Suzuki believes that such a boost in creativity and imagination could help build a better world. “This also raises the possibility that increased exercise might enhance our ability to imagine the future in a new way,” she says.

Exercise and Mental Health

Beyond our cognitive abilities, exercise plays a profound role in our mental health. Some theorize that depression is caused at least in part by depleted levels of a category of neurotransmitters called monoamines, which include serotonin, norepinephrine, and dopamine — all of which are magnified by exercise.

“Going for a run is like taking a little bit of Prozac and a little bit of Ritalin because, like the drugs, exercise elevates these neurotransmitters,” says Ratey.

In the process, exercise helps our brains balance hormones. Ratey believes that, along with alleviating depression, this harmonizing of our hormones also inoculates us against toxic stress and eases anxiety. “Keeping your brain in balance can change your life,” he says.

Exercise has other effects on mood, as well. Just as our muscles demand more energy during exercise, our brains gobble up glucose. In a 2016 study published in the Journal of Neuroscience, University of California, Davis, researchers discovered what the brain was doing with all that fuel: making more neurotransmitters.

MRI scans found that levels of glutamate and gamma-aminobutyric acid (GABA) swelled in participants after a stationary-bike session. This may aid in tempering depression, according to lead researcher Richard Maddock, MD, MS, because the stores of glutamate were centered in regions of the brain where the neurotransmitter had been depleted in depressed individuals.

Keeping the Brain Young

All the processes that physical activity induces in the brain add up to one sum: Exercise keeps our brains young. “Everything we’ve learned continues to confirm that exercise helps prevent cognitive decline as we age,” Ratey says. “All the antiaging protocols include exercise in a big way — it’s often the No. 1 lifestyle change to help people prevent aging and cognitive decline.”

Exercise not only makes our brains stronger; it also protects them. Physical activity induces the brain to create enzymes that chew up the amyloid beta-protein plaque that triggers Alzheimer’s by strangling neurons, explains Harvard neurology professor Rudolph Tanzi, PhD, coauthor of Super Brain, a New York Times bestseller.

A new study by Tanzi’s research team suggests exercise also battles inflammation in the brain. A basic immune-system response to injury, inflammation can become chronic as we age, and studies have identified it as a primary agent in Alzheimer’s. Exercise — along with lifestyle changes such as solid nutrition and good sleep — may actually help reverse Alzheimer’s and cognitive decline, Tanzi says.

Finally, among the flurry of research over the past decade is a 2009 study from the University of North Carolina at Chapel Hill, published in the American Journal of Neuroradiology, that used magnetic resonance angiography on 14 participants between the ages of 60 and 74. Those who exercised weekly significantly increased the number of capillaries in their brains compared with a control group. This contributes to optimum brain function — similar to the effects of exercise on healthy muscles.

Lead study author Elizabeth Bullitt, MD, writes, “Our findings suggest that aerobic activity appears to be associated with a ‘younger-appearing brain.’”

This originally appeared as “Your Brain on Exercise” in the May 2018 issue of Experience Life.

Get the full story at https://experiencelife.com/article/this-is-your-brain-on-exercise/