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Depression is the most common psychological disorder. One out of ten adults have ever been diagnosed with depression. In general, 17% of all people, 24% of women and 12% of men. Depression in adolescence and among young adults can lead to suicide, among others. Suicide is number three of leading causes of death.
The diagnostic criteria are described in DSM-IV or DSM-V. At least five of the following symptoms must be experienced for at least two weeks:
Another form of depression is the reactive depression. This is often accompanied by a big change in someone's life. This depression is similar to a major depression, but it only disappears in a few weeks to a month, and in this type the period of depression alternates with periods of normal mood.
Deviations in serotonin and norepinephrine systems can cause depression. This is known because medications that act on these monoamines (serotonin and norepinephrine) reduce or cause the depression. Evidence for this is the drug Reserpine that was used for high blood pressure, but as a side effect it causes depression. Once the drug was stopped, the depression disappeared again. This is how the monoamine hypothesis of depression came about. In the first version of this one did not know which of the monoamines were responsible for the depression and how this was could be caused. A contradiction to the monoamine hypothesis is the lag time. This is the time between taking the medicine and when the medicine starts to work. In antidepressants, for example, two weeks may pass before changes in symptoms occur.
The current version of the monoamine hypothesis states that depression is the result of neural degeneration in the hippocampus and the frontal cortex. This is because monoamine neurons no longer produce growth factors here. An important protein in this is the Brain derived neurotropic factor BDNF . BDNF is a protein that ensures that cells survive and receptors and new neurons grow. If this does not happen, the neurons in the hippocampus and frontal cortex can no longer communicate properly. Chronic treatment with antidepressants leads to an improvement in activity. However, it takes some time before it recovers. There are genetic characteristics that cause these receptors to work worse so that someone is more susceptible to develop a depression. Chronic stress also leads to a reduction in the production of BDNF, which can lead to depression.
Various medications have been used for the treatment of depression over the years. Only the most important ones are discussed in this chapter.
These are the first medications that were used in the treatment of depression. They were discovered in the 50s of the last century. The use of these medicaments for depression has been accidentally discovered. The naming is derived from the structure. All tricyclic drugs are composed of three molecule rings that are attached together. Additions to this structure give each medicine its own characteristics. The drugs bind to the proteins that enable the reuptake of serotonin and norepinephrine. In this way they influence the time after which these neurotransmitters are taken up again. In this way, the fabrics stay active longer in the synaptic gap. The drugs work after a few weeks and provide an upregulation of the BDNF.
Unfortunately, the tricyclic antidepressants also have side effects. By blocking the histamine receptors, fatigue and drowsiness is common in patients. They can also cause dry mouth, dizziness, high blood pressure, constipation, blurred vision and concentration problems by blocking the ACH receptors. In addition, sleep problems often occur. After an overdose (about 10 times the prescribed amount), cardiac arrhythmias and very high blood pressure can occur. The medications can even lead to death. This is a very dangerous option for depressed patients.
These medications were developed at the end of the 1950s. They were first developed to treat tuberculosis, but turned out to cause a mood-induced reaction. Some time later, they were also used for the treatment of depression.
The medications are made from all monoamines. MAOIs ensure the storage and use of neurotransmitters. They can be divided into two groups.
Group 1: MAO-a, including norepinephrine, serotonin and dopamine.
Group 2: MAO-b, including dopamine and phenylamine.
MAOIs permanently deactivate the MAO until the MAO is replaced, which can take several weeks. Later, the MAOIs came up with fewer side effects. The lag time of the MAOIs is two weeks.
The side effects that the current MAOIs can have, can be very serious. The MAOIs deactivate all MAO in the body, including those in the liver. When eating dairy products, extra large amounts of tyrimine are released, which will be broken down in the liver by MAO. If the tyrimine is not broken down it can increases the norepinephrine levels in the body. An excess of norepinephrine can cause severe headaches, sweating, nausea and even hypertension. Eventually, this can lead to a stroke.
In the 1970s more research came into the differences in behavioural stimulation and mood influences caused by antidepressants. We searched for differences between serotonin and norepinephrine systems. There has been thought that behaviour was influenced by norepinephrine and mood by serotonin. Since that moment, they started to develop agents that only affected the serotonin and at the same time tried to eliminate the side effects on histamine and acetylcholine. In 1988 the first breakthrough came, this was the drug Fluoxetine (better known as Prozac). These drugs are called the second generation of antidepressants. The biggest difference with the medication of earlier days, is that this generation of medicines has been especially developed for the treatment of depression.
SSRIs only block the serotonin receptors. They do this by binding to all subtypes of serotonin transport proteins. For example, serotonin cannot be processed further and remains present in the synaptic cleft. Because they bind to all subtypes, and also to the 5-HT2a serotonin receptors, there are specific side effects of SSRIs. Examples include: sexual dysfunction, reduced appetite, insomnia and agitation. There may also be a condition called the serotonin syndrome. The serotonin syndrome is a reaction to the serotonin that is toxic for the body. This can cause serious side effects and in some cases lead to death. It often occurs in combination with the use of other medications that increase serotonin activity such as other antidepressants (other than SSRIs) or certain herbs. For a long time it has been thought that SSRIs contribute to suicide attempts, but research has shown that this contribution is minimal. SSRIs have been shown to be more effective than the use of a placebo.
These drugs focus purely on the neurotransmitters serotonin and norepinephrine. As a result, they have slightly fewer side effects than the first generation of antidepressants. New drugs such as those that are still on the market are only improvements of older ones. People who make a new drug, are always trying to reduce the side effects, reduce the lag time and treat more and more symptoms with one drug.
The SNRIs have an effect on serotonin, norepinephrine and sometimes also on dopamine. Every SNRI works differently. A number of known SNRIs are: Duloxetine, Mirtazapine and Nefazodone.
Medications for depression that do not modify the available neurotransmitters in the brain are called atypical antidepressants. Initially, the SNRIs also belong to this group, because they only affect serotonin and norepinephrine. Two known and still used atypical antidepressants are Bupropion and Trazodone.
Bupropion is just as effective as other antidepressants, only it works in a different way. Instead of focusing on serotonin and norepinephrine, the drug blocks only dopamine receptors. Because it only focuses on dopamine, the side effects that appear at the SSRIs do not occur here. Side effects that do occur with dopamine and are as follows: tremor, restlessness, weight loss, less appetite and seizures. This drug cannot be used in patients with anxiety disorders, panic disorders or manic periods. Bupropion is used in combination with SSRIs to reduce its side effect.
Trazodone belongs to the groups serotonin antagonists and reuptake inhibitors. Trazodone blocks the serotonin reuptake transporters, but it also minimizes the side effects, which you see a lot with the SSRIs.
Not all patients respond to medication. Approximately 40% of patients do not respond to any medication or therapy. Sometimes the effects of the medication may fade over time. It is difficult to say anything about the effects of antidepressants because in many studies the placebo group also made progress. Nevertheless, most studies show that medicines work better than an (active) placebo. With an active placebo, there are substances in the placebo that ensure that the patient gets the side effects of the real medicine and therefore thinks that he really has the original medicine. In contrary to the real drug, the placebo has no effective substances in it.
The question of whether herbs can also have a healing effect on depression has long been discussed. There are many studies on one herb, the St. John's wort or hypericum perforatum. This is an herb that has been used since time immemorial to heal all kinds of diseases and pain, it is even available in the form of a pill. Research has shown that it is indeed effective in the short term for mild depression, but that it does not apply to chronic or severe depression. The herb works by ensuring that the absorption of the neurotransmitters (serotonin and norepinephrine) and its storage are blocked.
Bipolar disorders are distinguished from other depressions by the presence of manic episodes. A manic episode is a state of euphoria, in which someone can also suffer from delusions and hallucinations. In order to be able to diagnose this, the behavioural fluctuations between a mania and depression must be present for at least four days. Until a mania is detected, the wrong diagnosis of unipolar depression can be made. This is very difficult, given that the medication for the treatment of unipolar depression can worsen the condition of someone with bipolar depression.
Bipolar disorder often occurs late in adolescence and occurs as much in men as in women. In the DSM three types of bipolar disorders are mentioned: bipolar disorder 1, bipolar disorder 2 and cyclothymia. The differences between these can be found in the severity of the symptoms. Thus, for the diagnosis of bipolar disorder 1, one manic or mixed period is necessary. A depression does not have to occur here. In bipolar disorder 2, one depressive period is necessary and at least one manic period. Someone with bipolar disorder 1 still has problems with social intercourse between the mania, while someone with bipolar disorder 2 can function normally in between.
Cyclothymia is a type of chronic bipolar disorder, where there have to be at least two years of fluctuations between mild depression and mania.
Determining a manic episode according to the DSM:
If there is a mixed period, there must be both the manic criteria and the depression criteria and they have to change quickly during at least one week.
Little is known about the pathology of bipolar disorder. It has been known for a long time that a genetic component is present. This genetic component gives a chance of developing a bipolar disorder of 70% in identical twins and 12% in bipolar twins. The disorder often appears in families. Recent research has shown that the genes that cause serotonin transporter 5-HTT and BDNF are affected, both in bipolar and unipolar disorders. Manic periods can be linked to certain changes in the brain. For example, there are often enlarged ventricles in patients who have already had multiple manic episodes. There is also a reduction in neurons, which corresponds to the abnormalities in the BDNF.
John Cade discovered in 1948 the anti-manic effect of lithium. He believed that mania was caused by a by-product of metabolism. If this product was too much, it would lead to mania. To test this, he collected urine and injected it into guinea pigs. The urine of people with a mania was more toxic, but did not produce mania in the guinea pigs. Through much research, he discovered that lithium carbonate eased mania. It was not until 1970 that the drug was approved for use by the FDA.
The FDA is a company that investigates whether medication can be used and what it may be used for. If it has been said that it can be used since a certain year, it has been approved by the FDA in that year.
Lithium is a metal that looks like sodium. Lithium carbonate is the active substance used in the medicine. It is a natural product. The drug is easily absorbed into the blood stream and is difficult to get through the blood-brain barrier. The therapeutic index of lithium is very small and when you take too much, a dose can be fatal.
Only slightly higher doses are prescribed for the control of an acute mania. Lithium poisoning can also occur if someone loses too much salt, for example during exercise. Prolonged use can cause weight gain, thyroid disease, rash, kidney failure and a diminished immune system. That is why patients often stop using lithium. Sometimes the drug is also used in depression because it reduces suicidal tendencies. In addition, it restores the affected parts in the brain. Until now, lithium is the most commonly used drug in bipolar disorders. Because of the side effects, new drugs are being developed.
The new medicines (called anticonvulsants ) are also used in the treatment of seizures and anxiety disorders, in addition to the treatment of bipolar disorders.
Valproic acid is an anticonvulsant and comes from 1994. It stimulates the growth of BDNF and the activity of various neurotransmitters such as GABA and dopamine. Valproic acid works faster and is better responded to by patients. The most common side effects are sedation, tremor, ataxia, fainting and weight gain.
Gabapentin has not been approved by the FDA, but is used a lot outside the booklet since 1993. It works very effectively against neuropathic pain. Neuropathic pain can be caused by an autoimmune disease, cancer and the death of neurons. Gabapentin is made to mimic GABA. It reduces the influence of calcium by blocking the voltage-dependent calcium channels.
Lurasidone (Latuda) is an atypical antipsychotic. It has proven effective in fighting depression when used in combination with a mood stabilizer such as lithium. It is a powerful antagonist and works in the same way as many other atypical antipsychotics, only the side effects of this drug are less intense. It is a fairly new drug so not much is known about the long-term effect.
The different neurons in our brains, and in particular the interaction between them, are responsible for human behaviour. They do this by sending and receiving neurotransmitters. Knowledge of associated processes is very important to have a good understanding of the effect of psycho pharmaceuticals.
This chapter describes the functioning and interaction of neurons to get a better picture of how the brain responds to the environment and adapts to it.
The different neurons in our brains do not all look the same. The function and location of the neuron affects the size, shape and other properties of the neuron. The three most important neuronal groups are sensory neurons, motor neurons and interneurons. The sensory neurons pick up signals, the brain interprets these signals and the motor neurons then respond to this. In the central nervous system you find the interneurons which enables the transition between the other two groups of neurons.
The cell body is also called soma and is the largest part of the neuron. Here the metabolism of the cell takes place and you can find the nucleus with DNA.
Dendrites receive signals from surrounding neurons. The more dendrites a neuron has, the more information this neuron can receive. The location of the neuron affects the number of dendrites, for example, interneurons have more dendrites than neurons in the spinal cord.
The signal from the neuron is passed through the axon, which is an extension of the cell body and can have a length of a few millimetres to tens of centimetres. The axon hillock is the place where both the axon and the electrical signal start. Some axons have a myelin layer, especially the peripheral axons. The myelin is a glial cell that isolates the axon and enables an accelerated transportation.
The end of the axon is called the terminal button. Here, neurotransmitters are stored, released and in some cases reuptake takes place. A particular protein is very important for this reuptake, which will get more attention later in this chapter, as many psychotropic drugs work on this protein.
The neural transfer is the process by which the signal from the terminal button is transported to the dendrite of the next neuron (in the central nervous system). Signals are transmitted through nerves in the peripheral nervous system.
The lipid bilayer is a double layer of lipids that form the membrane of the neuron. This membrane enables that the neuron can have its own internal environment. In the membrane there are proteins which enable that glucose and ions can enter the cell and carry waste products out of the cell. By transporting the ions, the electric potential of the neuron changes. The important ions are An - , Cl - , Na + and K + . The sodium and chloride ions only enter the cell
.....read moreDepression is the most common psychological disorder. One out of ten adults have ever been diagnosed with depression. In general, 17% of all people, 24% of women and 12% of men. Depression in adolescence and among young adults can lead to suicide, among others. Suicide is number three of leading causes of death.
The diagnostic criteria are described in DSM-IV or DSM-V. At least five of the following symptoms must be experienced for at least two weeks:
Another form of depression is the reactive depression. This is often accompanied by a big change in someone's life. This depression is similar to a major depression, but it only disappears in a few weeks to a month, and in this type the period of depression alternates with periods of normal mood.
Deviations in serotonin and norepinephrine systems can cause depression. This is known because medications that act on these monoamines (serotonin and norepinephrine) reduce or cause the depression. Evidence for this is the drug Reserpine that was used for high blood pressure, but as a side effect it causes depression. Once the drug was stopped, the depression disappeared again. This is how the monoamine hypothesis of depression came about. In the first version of this one did not know which of the monoamines were responsible for the depression and how this was could be caused. A contradiction to the monoamine hypothesis is the lag time. This is the time between taking the medicine and when the medicine starts to work. In antidepressants, for example, two weeks may pass before changes in symptoms occur.
The current version of the monoamine hypothesis states that depression is the result of neural degeneration in the hippocampus and the frontal cortex. This is because monoamine neurons no longer produce growth factors here. An important protein in this is the Brain derived neurotropic factor BDNF . BDNF is a protein that ensures that cells survive and receptors and new neurons grow. If this does not happen, the neurons in the hippocampus and frontal cortex can no longer communicate properly. Chronic treatment with antidepressants leads to an improvement in activity. However, it takes some time before it recovers. There are genetic characteristics that cause these receptors to work worse so that someone is more susceptible to develop a
.....read moreFear is a learned emotional and physiological response to events in the environment. It affects behavior, heart rate, hormone release and physical sensations. Through these experiences people learn to avoid dangerous situations. Before there is fear, signals first have to be sent to the brain. This goes with the help of the amygdala nuclei that are located in the temporal lobes. In this area, sensory information from a threat will be sent. The rest of the information from this threat, is sent via the amygdala to other parts of the brain, such as the hypothalamus, punch and medulla. The amygdala is the most important brain structure that has to do with anxiety. Without the amygdala, there are almost no emotional reactions. In addition, the hypothalamus controls the release of hormones and the punch and medulla provide responses to anxiety such as stiffening, heartbeat and facial expression.
Two other areas in the prefrontal cortex are also very important in anxiety. These are the ventromedial prefrontal cortex and the orbitofrontal cortex. These areas ensure that the context of the situation gets an emotional charge and thus lead to the behavior of the person. They receive information from the amygdala, thalamus and ventral tegmentum. Subsequently they send information back to the hypothalamus and cingulate cortex and they also send stop signals back to the amygdala. The cingulate cortex receives input about the state of the body and connects an emotion to it. An example are physiological reactions (heartbeat, breathing, facial expressions etc.) and behavior, these different stimuli are taken together under the emotion anxiety. As soon as the emotion can be ignored, stop signals are sent to the amygdala and there are no physical reactions to the emotion anymore. This is all part of a direct fear response. People can also worry for a longer time. This is another form of anxiety in which there are no emotional stimuli to cause the fear response, but where thoughts alone trigger enough. Fear because of worry can lead to various anxiety disorders that will be discussed further in this summary.
The person suffers from repeated unexpected panic attacks and is afraid of another attack or the consequences of such an attack for at least one month. Often the greatest fear is the fear of dying during an attack. During a panic attack there must be extreme anxiety and at least four of the following symptoms occur: palpitations/accelerated heartbeat, sweating, shaking or stiffening, shortness of breath, suffocation, chest pain, nausea, dizziness/fainting, depersonalization, anxiety for loss of control, fear of death, paraesthesia (numb/tingling) and shivers/heat shakes. A panic disorder can also lead to agoraphobia, in which a person no longer dares to go outside because of fear of a subsequent panic attack in a place where he/she cannot escape from the situation.
Opium has been used for thousands of years as a medicine and for religious or ritual purposes. Early medical texts already describe opiates as narcotics. The main active substance in opium is morphine. This substance became popular as an anesthetic drug since the 1850s. It has also been used against coughing, as a medicine for fever and diarrhea. Morphine is still widely used today. Since the discovery of morphine, a lot of research has been done to discover an anti-pain medication that is less addictive. This led to, among other things, heroin.
Because opium and heroin were widely available since the nineteenth century, opium addiction became popular. At the beginning of the twentieth century, a legal attempt was made to stop this addiction, unfortunately this had little effect.
In opiates, the pharmacologically active substances are morphine, codeine and thebaine alkaloids. Alkaloids are natural constituents that are available in different forms and contain nitrogen. Various attempts have been made to synthesize alkaloids. That is why the book distinguishes between opiates (natural and formed from opium) and opioids (synthetically produced anesthetics).
Morphine and heroin are injected directly into the blood stream although Codeine and opioids are often taken orally. Once opiates are in the body, they can quickly pass through the blood-brain barrier. For example, only a few seconds after administration, heroin has already reached the brain. This works differently with morphine and codeine. Because of their solubility in water, only twenty to thirty percent reach the brain, while the rest is excreted again. In the liver, morphine and heroin are both converted to morpine-6-glucuronide, which is an active metabolite. Morphine and its metabolite have a half-life of 1-3 hours, so it works relatively long as an anesthetic.
Opiates have different effects on neural activity including sedation, euphoria and respiratory depression.
Pain can occur in many different ways. The pain receptors are called nociceptors. The pain signals are transmitted via fast myelinated fiber webs and via slow unmyelinated fiber webs. The myelinated fiber webs cause a sharp, rapid pain, while the unmyelinated fiber webs cause dull and slow pain. This pain often comes after the short, sharp pain in tissue damage. The perception of pain differs per person. Depression makes people more prone to pain.
The excitatory neurotransmitter substance P is released upon activation of the nociceptors. Opiates in the spinal cord can modulate pain. They do this by modulating the activity of serotonin and noradrenergic neurogen in the medulla. The release of substance P is inhibited.
There are different areas of the brain that play a role in the perception of pain. The cingulate cortex plays a role in feeling pain or the sensation of pain. Damage to this area does not stop make you feel pain, but that you do
.....read moreIn the United States, the lifetime prevalence of substance abuse and dependence is about 15% of the population. When tobacco is included in this estimate, it comes down to 45%. This prevalence has remained relatively stable over the past ten to twenty years.
Addiction is not always the same as dependence. An addiction is the result of specific neural changes that result from the use of drugs. These are drugs that affect dopamine activity in mesolimbic and mesocortical systems. Not all drugs that provide a dependency produce these neural changes. Alcohol, cocaine, amphetamine, opiates and tobacco do produce this, among other things.
Addiction can occur suddenly or it can develop over the years. The common threat in addiction is the pattern of destruction in the personal and family life of the addict. People with an addiction deny the pain they do to others as well as the negative financial and physical consequences that the addiction has. Alcohol addiction includes comorbid depression, bipolar disorder and anxiety disorders. Treatment of substance abuse is not often successful and is rarely completed on a first attempt.
The DSM-IV-tr makes no distinction between drug dependence and drug addiction. Drug addiction disorders are classified by the degree of deterioration and by the presence of tolerance and/or withdrawal symptoms. An individual can thus be dependent of a substance, without having a disorder. The diagnosis of a substance dependency disorder replaces a substance abuse disorder, where it is a requirement that the additional symptoms be present for a longer period of time. If this is not (yet) the case, then there is a substance dependency disorder.
Not all behavioural and neurobiological characteristics of addiction are present in all cases of dependence. An important characteristic is the intense desire or the strong motivation to take drugs, despite the serious adverse consequences. This desire is often even present after years of abstinence. The critical difference between drug dependence and drug addiction is caused by neural changes that result from the use of certain drugs. The reaction of the brain, produced by addictive substances, is due to the effect of the drugs on the reward (reward pathway) of the brain. This system is an evolutionary change that helps to allocate hedonistic values to stimuli. It also provides motivation for seeking sexual partners and for reproduction. The changes because of addictive drugs, benefit the reward system, which keeps the motivation going to search for drugs and to take them.
The critical neural structures where the path consists of: the nucleus accumbens and the ventral tegmental area (ventral tegmental area, VTA). Research on this system originated by James Olds and his student Peter Milner in 1954. They experimented with electrical stimulation in the septum of rats.
The reward system consists of:
The mesolimbic dopamine system: VTA,
.....read moreIn this chapter and the next, we will look at all different kinds of drugs ranging from caffeine to crack and cocaine. Most drugs that will be discussed in this chapter exists for hundreds or even thousands of years. The use of drugs became alarming up till 2000. Since that year, the use of drugs by teenagers is stable. There is even a little decline and the decline of alcohol and tobacco use is bigger. Only the trend of marijuana use is an increasing one.
Drug schedule refers to the potential for abuse of a drug and this has been described by the Controlled Substance Act in 1970. Schedule I drugs do have less potential for abuse than schedules II to V.
Cocaine is extracted from the coca plant, which grows in the mountains of South America. People used to chew on the leaves of this plant, because it produced feelings of confidence. Nowadays, cocaine is most exported as cocaine sulphate or cocaine hydrochloride.
Cocaine compounds are extracted by crushing the leaves in a solution (such as kerosene, gasoline or alcohol). The liquid mixture that remains is processed under heat with sulfuric acid to isolate the cocaine alkaloids and to remove the waxy residues. The cocaine sulphate paste that remains contains about 60% cocaine and is then further processed into a water-soluble crystal composition called cocaine hydrochloride.
In South America, many of the waste products that originate during the extraction process of cocaine are dumped in the river. This has very harmful ecological consequences.
Cocaine alkaloid was first isolated in 1855 by Friedrich Gaedcke, he called it erythroxyline . Albert Niemann then called it cocaine. It was used as a local anesthetic, especially in eye and nose operations. It was also added to many drinks, given the stimulating effects and you could buy cocaine in local drugstores. Freud was enthusiastic about the substance and recommended it to other people. It was only in 1914 that the use of cocaine in all forms was banned by the Harrison Narcotic Tax Act and was described as a dangerous narcotic.
Cocaine hydrochloride is a water soluble substance that divides itself into cocaine-H + and Cl - ions after its administration. The positively charged cocaine ions are able to quickly pass cell membranes and enter the brain. Snorted and orally administered cocaine goes slower and will be absorbed less complete than intravenously administered, inhaled or vaporized cocaine.
Methylbenzoulecgonine is a composition that is the result of dissolving cocaine hydrochloride in a mild ammonia solution. This composition can be vaporized for inhalation and is called crack because of the cracking sound in this process. Crack can also be manufactured by heating cocaine hydrochloride in water and sodium
.....read moreAlcohol is the most abused drug in the world. Given the availability and the large percentage of the population that uses it, it is not surprising that alcohol leads to the most common substance abuse disorder.
Distillation is a process in which alcohol is separated from other fermentation products by heating it. Although distillation can result in pure ethyl alcohol (ethanol), most spirits contain 40-50 percent alcohol.
Alcohol or ethanol is both soluble in water and fat and can easily spread through all cell membranes. Higher alcohol concentrations (stronger drinks) spread faster than lower ones. Ethanol passes the blood-brain barrier quickly, and peaks in plasma concentrations are reached between 30 to 60 minutes. The presence of food in the stomach and intestines slows the distribution of alcohol. The wall of the small intestine absorbs approximately eighty percent and the remainder will be absorbed by the stomach or is almost immediately excreted by perspiration, breathing or urine. Because all tissues, including the placenta, absorb alcohol so easily, a pregnant woman exposes her fetus to blood levels similar to their own.
The blood alcohol concentration (BAC) is expressed in the number of grams of alcohol per hundred milliliters of blood. A breath test can immediately determine the BAC by analyzing the breath of an individual. The breath contains alcohol that got into the lungs through the bloodstream. With a BAC of 0.06-0.1 you already have a much higher reaction time, problems with attention, reduced control over movements and significant limitations in cognitive functioning. With a BAC of 0.3-0.39 it becomes already very dangerous and you can get fatal symptoms. Above 0.4 it can be fatal.
Alcohol metabolism starts immediately after consumption. Approximately 90-95 percent of the alcohol is metabolized by the enzyme group alcohol dehydrogenase. The remaining five to ten percent is excreted by perspiration and breathing or is metabolized by another liver enzyme. This enzyme is called P450 and is essential for oxygen reactions that are involved in metabolism. Only a small fraction of alcohol is excreted via the urine.
Small amounts of alcohol dehydrogenase immediately begins to metabolize alcohol in the stomach. When alcohol enters the small intestine, it is quickly absorbed into the blood supply. This way it ends up in the liver, where the remaining part (80-85 percent) is metabolized. First-pass metabolism is alcohol that is metabolized by stomach and liver enzymes before it can reach the tissues. About 25-30 percent of the ingested alcohol falls below. The amount of metabolized alcohol depends on the availability of alcohol dehydrogenase and the coenzyme nicotinamide adenine dinucleotide (NAD). This coenzyme can be seen as a rate-limiting enzyme, because availability determines the rate of alcohol metabolism. Because men and women have different levels of alcohol dehydrogenase, they metabolize alcohol in different speeds.
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