How does alcohol make you drunk ?

Ethanol: this molecule, made of little more than a few carbon atoms, is responsible for drunkenness. Often simply referred to as alcohol, ethanol is the active ingredient in alcoholic beverages. Its simplicity helps it sneak across membranes and nestle into a many different nooks, producing a wide range of effects compared to other, clunkier molecules. So how exactly does it cause drunkenness, and why does it have dramatically different effects on different people? 

To answer these questions, we’ll need to follow alcohol on its journey through the body. Alcohol lands in the stomach and is absorbed into the blood through the digestive tract, especially the small intestine. The contents of the stomach impact alcohol’s ability to get into the blood because after eating, the pyloric sphincter, which separates the stomach from the small intestine, closes. So the level of alcohol that reaches the blood after a big meal might only be a quarter that from the same drink on an empty stomach. From the blood, alcohol goes to the organs, especially those that get the most blood flow: the liver and the brain. It hits the liver first, and enzymes in the liver break down the alcohol molecule in two steps. First, an enzyme called ADH turns alcohol into acetaldehyde, which is toxic. Then, an enzyme called ALDH converts the toxic acetaldehyde to non-toxic acetate. As the blood circulates, the liver eliminates alcohol continuously— but this first pass of elimination determines how much alcohol reaches the brain and other organs. Brain sensitivity is responsible for the emotional, cognitive, and behavioural effects of alcohol— otherwise known as drunkenness. Alcohol turns up the brain’s primary brake, the neurotransmitter GABA, and turns down its primary gas, the neurotransmitter glutamate. This makes neurons much less communicative, and users feel relaxed at moderate doses, fall asleep at higher doses, and can impede the brain activity necessary for survival at toxic doses. Alcohol also stimulates a small group of neurons that extends from the midbrain to the nucleus accumbens, a region important for motivation.

Like all addictive drugs, it prompts a squirt of dopamine in the nucleus accumbens which gives users a surge of pleasure. Alcohol also causes some neurons to synthesize and release endorphins. Endorphins help us to calm down in response to stress or danger. Elevated levels of endorphins contribute to the euphoria and relaxation associated with alcohol consumption.

Finally, as the liver’s breakdown of alcohol outpaces the brain’s absorption, drunkenness fades away. Individual differences at any point in this journey can cause people to act more or less drunk. For example, a man and a woman who weigh the same and drink the same amount during an identical meal will still have different blood alcohol concentrations, or BACs. This is because women tend to have less blood— women generally have a higher percentage of fat, which requires less blood than muscle. A smaller blood volume, carrying the same amount of alcohol, means the concentration will be higher for women. Genetic differences in the liver’s alcohol processing enzymes also influence BAC. And regular drinking can increase production of these enzymes, contributing to tolerance. On the other hand, those who drink excessively for a long time may develop liver damage, which has the opposite effect. Meanwhile, genetic differences in dopamine, GABA, and endorphin transmission may contribute to risk for developing an alcohol use disorder. 

Those with naturally low endorphin or dopamine levels may self-medicate through drinking. Some people have a higher risk for excessive drinking due to a sensitive endorphin response that increases the pleasurable effects of alcohol. Others have a variation in GABA transmission that makes them especially sensitive to the sedative effects of alcohol, which decreases their risk of developing disordered drinking. Meanwhile, the brain adapts to chronic alcohol consumption by reducing GABA, dopamine, and endorphin transmission, and enhancing glutamate activity. This means regular drinkers tend to be anxious, have trouble sleeping, and experience less pleasure. These structural and functional changes can lead to disordered use when drinking feels normal, but not drinking is uncomfortable, establishing a vicious cycle.

So both genetics and previous experience impact how a person experiences alcohol— which means that some people are more prone to certain patterns of drinking than others, and a history of consumption leads to neural and behavioural changes.

 

Why is it so hard to escape poverty?

                

Imagine that you’ve been unemployed and seeking work for months. Government benefit programs have helped you cover rent, utilities, and food, but you're barely getting by. Finally, you hear back about a job application. You receive your first pay check in months, and things seem to be turning around. But there’s a catch. Your new job pays just enough to disqualify you from the benefit programs, and not enough to cover the same costs. To make things worse, you have to pay for transportation to work, and childcare while you’re at the office. Somehow, you have less money now than when you were unemployed. 

Economists call this demoralizing situation the welfare trap— one of the many different poverty traps affecting millions of people around the world. Poverty traps are economic and environmental circumstances that reinforce themselves, perpetuating poverty for generations. Some poverty traps are tied to an individual’s circumstances, like a lack of access to healthy food or education. Others can affect entire nations, such as cycles of corrupt government or climate change. But the cruel irony of welfare traps in particular is that they stem from the very policies designed to battle poverty. Most societies throughout history employed some strategies to help people in poverty meet basic needs. Before the 20th century, religious groups and private charities often led such initiatives. Today, these are called welfare programs, and they usually take the form of government-provided subsidies for housing, food, energy, and healthcare. Typically, these programs are means-tested, meaning that only people who fall below a certain income level are eligible for benefits. This policy is designed to ensure aid goes to those who need it most. But it also means people lose access as soon as they earn more than the qualification threshold, regardless of whether or not they're financially stable enough to stay there. This vicious cycle is harmful to both those in poverty and those outside of it. Mainstream economic models assume people are rational actors who weigh the cost and benefits of their options and choose the most advantageous path forward. If those in poverty know they'll gain no net benefit from working, they're incentivized to remain in government assistance. Of course, people work for many reasons, including societal norms and personal values. But income is a major incentive to pursuing employment. And when less people take on new jobs, the economy slows down, keeping people in poverty and potentially pushing people on the cusp of poverty over the edge. Some have suggested this feedback loop could be removed by eliminating government assistance programs altogether. But most agree the solution is neither realistic nor humane. So how can we redesign benefits in a way that doesn't penalize people for working? Many countries have tried different ways to circumvent this problem. Some allow people to continue receiving benefits for a given period after finding a job, while others phase out benefits gradually as income increases. These policies still remove some financial incentive to work, but the risk of a welfare trap is lower. Other governments provide benefits like education, childcare, or medical care equally across all their citizens. One proposed solution takes this idea of universal benefits even further.

A universal basic income would provide a fixed benefit to all members of society, regardless of wealth or employment status. This is the only known policy that could entirely remove welfare traps, since any earned wages would supplement the benefit rather than replace it. In fact, by creating a stable income floor below which no one can fall, basic income might prevent people from falling into poverty in the first place. Numerous economists and thinkers have championed this idea since the 18th century. But for now, universal basic income remains largely hypothetical.

Although it's been tried in some places on a limited scale, these local experiments don’t tell us much about how the policy would play out across an entire nation— or a planet. Whatever strategy governments pursue, solving the welfare trap requires respecting people’s agency and autonomy. Only by empowering individuals to create long-term change in their lives and communities can we begin to break the cycle of poverty.

You could have a secret twins !

 

While searching for a kidney donor, a Boston woman named Karen Keegan stumbled upon a mystery. When her three adult sons underwent genetic testing to determine whether they were a match for kidney donation, the test showed that two of them weren’t actually her sons. Keegan knew she was her sons’ mother— she had conceived and given birth to them. Figuring there must have been an error, her doctors pursued further testing, only to uncover something even more confusing: she was her children’s biological aunt. It turned out that Keegan had a second genome in some tissues and organs. 

In other words, some of her cells had a completely different set of genes from the others. This second set of genes belonged to her twin sister— who had never been born. This condition, where an individual has two genomes present in the tissues of their body, is called chimerism. The name comes from Greek mythology, where chimera is an amalgam of three different animals. Individuals with chimerism might have two-toned skin or hair, or two different colored eyes, but most are believed to have no visible signs of the condition. Chimerism can come from a twin in utero, from a tissue or organ transplant, or happen between a fetus and a pregnant woman. So how exactly does it happen? In one of the most common forms, a mother and fetus swap cells in the flow of nutrients across the placenta. The mother can inherit fetal stem cells, undifferentiated cells that are able to develop into any specialized cell. The fetal cells initially go undetected because the mother’s immune system is suppressed during pregnancy. But in some cases, cells with the fetus’s DNA persist in the mother’s body for years or even decades without being destroyed by her immune system. In one case, a mother's liver was failing, but suddenly started to regenerate itself. Her doctors biopsied her liver, and found DNA in the regenerated tissue from a pregnancy almost 20 years earlier. The fetal stem cells had lodged in her liver and specialized as liver cells. Karen Keegan, meanwhile, acquired her second genome before she was born. Very early in her own mother’s pregnancy with her, Keegan had a fraternal twin. Keegan’s embryo absorbed some fetal stem cells from her twin’s embryo, which did not develop to term.

By the time Keegan’s fetus developed an immune system, it had many cells with each genome, and the immune system recognized both genomes as her body’s own— so it didn’t attack or destroy the cells with the second genome. We don’t know how much of her body was composed of cells with this second genome that can vary from one organ to another, and even between tissues within an organ: some might have no cells at all with the second genome, while others might have many. At least some of the egg-producing tissue in her ovaries must have carried the second genome. Each time she conceived there would be no way to predict which genome would be involved— which is how two of her children ended up with the genes of a woman who had never been born. This can also happen to fathers. 

In 2014, when ancestry testing determined that a father was actually his baby’s biological uncle, researchers discovered that 10% of the father’s sperm carried a second genome from an embryonic twin. Cases like this challenge our perception of genetics. Though there are very few documented cases of chimerism from an embryonic twin, we’re all amalgams to some extent, carrying around the different genetic codes of our gut bacteria and even our mitochondria. And given that 1 in 8 individual births started out as twin pregnancies, there could be many more people with two genomes— and many more lessons to learn about the genes that make us who we are. 

 

Why do we dream ?

      

In the third millennium BCE, Mesopotamian kings recorded and interpreted their dreams on wax tablets. A thousand years later, Ancient Egyptians wrote a dream book listing over a hundred common dreams and their meanings. And in the years since, we haven't paused in our quest to understand why we dream. So, after a great deal of scientific research, technological advancement, and persistence,  we still don't have any definite answers, but we have some interesting theories. We dream to fulfil our wishes.

In the early 1900s, Sigmund Freud proposed that while all of our dreams, including our nightmares, are a collection of images from our daily conscious lives, they also have symbolic meanings, which relate to the fulfilment of our subconscious wishes. Freud theorized that everything we remember when we wake up from a dream is a symbolic representation of our unconscious primitive thoughts, urges, and desires. Freud believed that by analysing those remembered elements, the unconscious content would be revealed to our conscious mind, and psychological issues stemming from its repression could be addressed and resolved. We dream to remember. To increase performance on certain mental tasks, sleep is good but dreaming while sleeping is better.

In 2010, researchers found that subjects were much better at getting through a complex 3-D maze if they had napped and dreamed of the maze before their second attempt. They were up to ten times better at it then those who only thought of the maze while awake between attempts, and those who napped but did not dream about the maze.

Researchers theorize that certain memory processes can happen only when we are asleep, and our dreams are a signal that these processes are taking place. We dream to forget. There are about 10,000 trillion neural connections within the architecture of your brain. They are created by everything you think and everything you do. 

A 1983 neurobiological theory of dreaming, called reverse learning, holds that while sleeping, and mainly during REM sleep cycles, your neocortex reviews these neural connections and dumps the unnecessary ones. Without this unlearning process, which results in your dreams, your brain could be overrun by useless connections, and parasitic thoughts could disrupt the necessary thinking you need to do while you're awake.

We dream to keep our brains working. The continual activation theory proposes that your dreams result from your brain's need to constantly consolidate and create long-term memories to function properly. So when external input falls below a certain level, like when you're asleep, your brain automatically triggers the generation of data from its memory storages, which appear to you in the form of the thoughts and feelings you experience in your dreams. In other words, your dreams might be a random screen saver your brain turns on so it doesn't completely shut down. We dream to rehearse. 

Dreams involving dangerous and threatening situations are very common, and the primitive instinct rehearsal theory holds that the content of a dream is significant to its purpose. Whether it's an anxiety-filled night of being chased through the woods by a bear or fighting off a ninja in a dark alley, these dreams allow you to practice your fight or flight instincts and keep them sharp and dependable in case you'll need them in real life. But it doesn't always have to be unpleasant.

For instance, dreams about your attractive neighbour could give your reproductive instinct some practice, too. We dream to heal. Stress neurotransmitters in the brain are much less active during the REM stage of sleep, even during dreams of traumatic experiences, leading some researchers to theorize that one purpose of dreaming is to take the edge off painful experiences to allow for psychological healing.

Reviewing traumatic events in your dreams with less mental stress may grant you a clearer perspective and enhanced ability to process them in psychologically healthy ways. People with certain mood disorders and PTSD often have difficulty sleeping, leading some scientists to believe that lack of dreaming may be a contributing factor to their illnesses.

We dream to solve problems. Unconstrained by reality and the rules of conventional logic, in your dreams, your mind can create limitless scenarios to help you grasp problems and formulate solutions that you may not consider while awake. John Steinbeck called it the committee of sleep, and research has demonstrated the effectiveness of dreaming on problem-solving. It's also how renowned chemist August Kekule discovered the structure of the benzene molecule, and it's the reason that sometimes the best solution for a problem is to sleep on it. And those are just a few of the more prominent theories. 

As technology increases our capability for understanding the brain, it's possible that one day we will discover the definitive reason for them. But until that time arrives, we'll just have to keep on dreaming.