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Few people talk about the benefits of nicotine. But on the topic that nicotine is harmful to the human body, you can talk for a long time, based on scientific facts that scientists and not only scientists cite in their works. Pictures are also published on cigarette packages that warn a person about the dangers of smoking tobacco for health.

Of course, there is some truth in this, they are people who die of nicotine if they use it in excessive quantities, but we would like to talk about how nicotine is useful.

Is there a benefit in nicotine?

First, let's see why so much attention has been paid to the topic of the harmfulness of nicotine. For many years, doctors have been studying this issue and have provided a huge amount of evidence that there is no benefit in nicotine. But after all, when a person smokes a cigarette, at the same time absorbs a lot of carcinogenic smoke, and nicotine has absolutely nothing to do with it.

On the contrary, if there is very little nicotine in cigarettes, in this case they are harmful to human health, especially if the smoker is used to inhaling deeply. Scientists have known about this for a long time, but now it is not customary to talk about the beneficial properties of nicotine. What other arguments have been made about the benefits of nicotine for the human body?

Nicotine negatively affects the taste and olfactory receptors in humans. That is why those who smoke feel the taste of food in a completely different way, it seems bland to him. Due to this, appetite decreases, and, as a result, excess weight goes away. For people suffering from obesity, this fact is just a godsend. The only thing is that the appetite grows very strongly when a person tries to quit smoking. Then the kilograms come back at a fast pace.

1. Nicotine and Alzheimer's disease

In 1992, Dr. James D'Fan made a grand discovery about the benefits of nicotine. He convinced the whole world that smoking is an excellent preventive method in the fight against Alzheimer's disease. According to the scientist, those who smoke almost never suffer from dementia in old age.

By the way, it should be noted that the conclusion of the scientist is not refuted by American doctors. They found that nicotine, getting into the human body, begins to actively disintegrate in it, turning into "nornicotine" - a substance thanks to which the neurons of the brain do not die. But it should also be noted here that the resulting substance is toxic, so you should not abuse cigarettes just in order to save yourself from the fate of facing Alzheimer's disease in old age.

2. Nicotine against Parkinson's disease

American scientists have discovered one more fact, than nicotine is useful for humans. A doctor named Harvey Chekoway from Washington has proved that people who smoke are 70% less at risk of developing a disease like Parkinson's disease, which progresses very slowly and develops into a chronic pathology related to neuralogy.

As a rule, this diagnosis is made to elderly people. What is the benefit of nicotine in this case? The substance has a very beneficial effect on the genes of dopamine receptors, thanks to which old people can boast of good attention, they are always concentrated, just not for a long time. To maintain concentration, you need to constantly smoke a cigarette. But again, here we must not forget about the toxicity of nicotine, which can simply destroy human health.

It turns out that nicotine softens the symptoms of schizophrenia, because this substance has a good effect on the human thought process and inhibits the progression of the disease. If you read the composition of the numerous drugs that are prescribed for schizophrenics, you can be sure that nicotine is also included in it, because it is thanks to it that it is possible to stop the patient's hallucinations, his apathy and indifference in everything.

3. Beneficial effect of nicotine on the digestive system

Doctors in the field of gastroenterology have revealed another fact, how nicotine is useful. According to them, this substance reduces intestinal peristalsis. After a person smokes several cigarettes, gas formation in the organs of the digestive tract is noticeably reduced, because mucus in some parts of the intestine under the influence of nicotine begins to be intensively produced, and due to this, the likelihood of ulcerative colitis in humans is reduced. Moreover, those who smoke never experience diarrhea.

Only in addition to the unequivocal benefits of nicotine, it is necessary to mention its dangers - it is he who provokes the active development of oncological diseases. According to the WHO, it is smokers who most often fall victim to cancer.

4. Benefits of nicotine for women's health

American scientists believe that the female hormone estrogen depends on the level of nicotine that enters the body of a lady. According to doctors from Dortmund, if a woman smokes, then she has:

• the risk of developing malignant tumors on the endometrium of the uterus is automatically reduced (due to the effect of nicotine, cells do not divide so quickly, especially cancerous ones);
• fibromatous nodes are not formed on the uterus - that is, the connective tissue does not grow, because this process in the body is inhibited;
• endometriosis never occurs in girls who started smoking at an early age (this fact has not yet been scientifically proven, scientists are working in this direction to find a relationship);
• in pregnant women who smoke, nicotine prevents eclampsia - they do not have an increase in blood pressure, and preeclampsia - they do not develop gestosis, which can disrupt cerebral circulation in the mother and child. All these are only indirect advantages, which it is better for pregnant women to forget about, if it is important to preserve the health of their baby and protect him from the likelihood of births with numerous defects of internal organs.

It was not possible, to this day, to determine exactly why such significant things happen in the body of a woman who smokes. There is an assumption that tobacco, getting into the lungs, decomposes, the potassium salt (thiocyant) is formed, which has a very high hypotensive property, that is, the ability to lower blood pressure.

In addition, scientists from the United States have established many more facts than nicotine is useful for women's health.

These include the following items:

• Nicotine relieves dysmenorrhea, that is, a woman can survive the menstrual period without pain and other unpleasant symptoms that cause her severe discomfort. This is achieved through the effects of tobacco on prostate, which are the sources of dysmenorrhea. However, if you are looking for a way to get rid of unpleasant symptoms during your period, then it is better to just take some pain reliever than poison your body with tobacco smoke.
• In the mammary glands and on the cervix, malignant neoplasms do not form during the period when a woman reaches menopause, because nicotine inhibits uncontrolled cell division.

In addition to the benefits of nicotine, one should also mention its harm to the health of a woman, especially the one that carries a child under the heart. If a pregnant woman smokes excessively, then she is more likely to have a premature birth. In addition, a smoking mother runs the risk of giving birth to a sick baby.

5. The benefits of nicotine in a stressful situation

Continuing to argue for the benefits of nicotine, doctors say the substance helps a person cope with stressful situations in life. Every smoker knows that after you smoke one or two cigarettes, the whole world seems kinder, more pleasant and more rosy. Why is this happening? This fact can be explained by certain physiological processes occurring in the human body after the received dose of nicotine:

• breathing at the time of smoking becomes rhythmic and balanced (all this contributes to the fact that a person calms down);
• the smoke emanating from a cigarette relaxes the mind (especially if the smoker is accustomed to watching the rings of smoke that form when he exhales during the smoking process);
• at the moment of puffing a cigarette, provided there is complete silence around, the person completely relaxes;
• nicotine activates neurotransmitters responsible for the production of the "happiness hormone" (that is why all smokers, in the event of any problem or unpleasant situation, feel the urge to smoke and immediately run around the corner to smoke a few cigarettes).

Note that a noticeable improvement in the mood of a smoker at the moment of inhalation is short-term. After some time, apathy returns again, there is a desire to re-smoke a cigarette in order to fall into a state of euphoria, which a person likes so much, and helps him to cope with numerous difficulties in life.

6. Nicotine will prevent allergies

Eminent scientists of mankind give several scientifically substantiated arguments about what nicotine is still useful for. In their opinion, this substance reduces the likelihood of a person developing allergies, because at the time of smoking even one cigarette, mast cells (cells that play an important role in the adaptation of the body to the effects of a number of allergens on it) begin to grow actively.

For example, a person who smokes has a much easier course of allergic ailments such as hives or hay fever. Of course, a person who is prone to allergies cannot afford to escape from it by stocking up on thousands of cartons of cigarettes. This is too reckless and unreasonable. Also, keep in mind that tobacco smoke itself can be an allergen. It is he who provokes the development of complicated diseases of the bronchopulmonary system in humans, for example, asthma.

Nicotine: More Good or Harm?

Based on the foregoing about what nicotine is useful for, it must be said that everything is completely ambiguous in this matter. You cannot afford to trust only those doctors who are convinced that smoking can only harm a person's health, but you also should not be led by scientists who give dubious arguments about what nicotine is useful for. Just stop believing in stereotypes and understand that nicotine can also be a dangerous substance for humans, because it enters the body together with carcinogenic tobacco smoke, but in some cases it can also be beneficial, but short-term.

Still, a smoker absorbs not only nicotine and carcinogenic smoke, but also numerous hazardous substances that are included in its composition, and there are more than 400 of them. Naturally, they cause numerous factors in the human body that lead to the development of life-threatening ailments , some of them become simply incompatible with life.

Nevertheless, knowing all this, many doctors are smokers, and heavy smokers. How can this fact be explained? Here we will not talk about how stressful the work of the medical staff is. It's just that it is not a problem for doctors to find a "golden mean" in smoking, so that their bodies receive the benefits of nicotine, and not just harm. They believe that if you smoke within "reasonable limits", then you do not have to worry that your health will be spoiled.

And what does it mean, within "reasonable limits":

• you cannot smoke more than 4 cigarettes per day (this applies to men of large build);
• sick people and women, especially pregnant women, should not smoke more than 2 cigarettes per week.

We would like to urge you all the same to the fact that smoking is a vice, from which you need to get rid of urgently. There is more harm than good from it. Health will definitely suffer if you constantly smoke. It cannot be considered a miracle cure or psychotropic drug. If you want to live a long time, not get sick, do not constantly visit hospitals and other medical institutions, then you should definitely give up the habit of smoking. So you will not only save your life and protect your family from carcinogenic smoke, which they also have to breathe, but also significantly save money in order to spend them on something more useful.

Since the end of the 17th century, mankind has known what nicotine is. It belongs to alkaloids. Plants from the nightshade family contain a lot of it. The highest harmful concentration of nicotine is observed in tobacco leaves and makhorka. An alkaloid is poisonous. It contains toxic psychotropic components and is similar in action to a drug. Due to the widespread use of tobacco smoking, mortality among the entire population of the planet has increased manifold.

The use of an alkaloid provokes pathologies of the cardiovascular system. This applies not only to smoking cigarettes, hookah, but also to the use of mixtures, weed, chewing tobacco (nasvay). Nicotine is also found in e-cigarettes.

Nicotine often leads to intoxication. The main danger of the substance lies in its ability to provoke cancer in humans. The fact that smokers inhale and exhale smoke increases the effect of factors that increase the risk of developing more than 15 types of cancer. It chooses lungs, stomach, larynx as the main target organs and penetrates into their tissues. The substance reduces the process of natural death of body cells, which leads to their degeneration into a tumor.

Due to the action of nicotine on the body, blood vessels grow in cancer cells. This phenomenon is confirmed by pathophysiology. This branch of medicine established a pattern between smoking and the development of cancer in humans. The negative effects of nicotine on vision have been confirmed. It also slows down muscle growth and protein synthesis.

The alkaloid has a negative effect on the health of pregnant women. It becomes the cause of congenital abnormalities in children. A child born to a woman who smokes is more likely to develop type II diabetes. Children whose mothers smoked during pregnancy are more likely to develop respiratory disorders and neurobehavioral defects.

The fact of the negative impact of the alkaloid on the reproductive system has been proven. It impairs the quality of sperm in men, becoming a factor in the subsequent development of infertility.

The effect of nicotine on the human body causes paralysis of the nervous system. Doses of 0.5 to 1 mg / kg are sufficient to stop respiration, cardiac arrest and death. Frequent exposure to an alkaloid on the body means the formation of persistent not only physical, but also mental dependence.

The substance acts on the brain and central nervous system. The alkaloid stimulates the production of serotonin, endorphins, dopamine, norepinephrine, and aminobutyric acid. These substances contribute to the formation of pleasure, calmness and happiness in the smoker. This artificial stimulation underlies the development of depression, schizophrenia and other disorders in humans. Nicotine is similar to alcohol in terms of its influence on the human psyche.

Effects on the body

The alkaloid negatively affects all health indicators. It harms the heart and blood vessels, the gastrointestinal tract, the brain, the respiratory system, and the reproductive system. Nicotine smoke has a negative effect on the condition of the skin, accelerates the aging process. From tobacco on the dermis of the face, deep wrinkles appear faster. The alkaloid also reduces immunity in humans.

Gastrointestinal tract

All elements, from teeth to intestines, suffer from tobacco smoke. In smokers, the following phenomena are observed in the gastrointestinal tract:

• increased salivation;
• persistent irritation of the oral mucosa;
• frequent bleeding of the gums;
• yellowing of teeth, thinning of their enamel;
• the development of periodontitis;
• decreased appetite (the use of an alkaloid replaces food intake);
• excessive production of hydrochloric acid by the stomach;
• the release of the contents of the stomach into the esophagus, leading to the contraction of its muscles and the formation of erosions and ulcers in it;
• slowing down the process of digestion of food;
• deterioration of the liver;
• violation of normal weight;
• failure in the intestines in the form of loss of essential minerals and vitamins;
• the appearance of diarrhea and constipation.

Due to the intake of nicotine, stomach cramps occur. Against the background of oxygen starvation of the blood, the organ begins to contract, and severe irritation occurs in its mucous membranes. The consequence of smoking is the development of gastritis, which is one of the harbingers of stomach cancer. Due to nicotine addiction, ulcers and gastroesophageal reflux often occur.

Cardiovascular apparatus

Tobacco alkaloids provoke an increase in blood viscosity. Because of this, there is a risk of blood clots. Nicotine also affects the blood supply to tissues. Its effect contributes to the increase in pressure. Smokers often develop arterial hypertension. Arrhythmia and heart palpitations are common signs of nicotine addiction.

A side effect of tobacco use is the active formation of cholesterol plaques on the walls of blood vessels. All this leads to an increased risk of developing myocardial infarction and stroke. Nicotine also causes coronary artery disease. With a long smoking experience, heart failure begins to progress in a person. An alkaloid leads to a lack of iron in the blood, which causes anemia.

The state of the brain and central nervous system

Several options are known for how the neurotoxins present in nicotine are reflected on the central nervous system. Small doses of a substance are its stimulants, leading to the excitation of receptors. But this effect of smoking is short-term. Long-term supply of nicotine to the brain can give rise to the development of an acute lack of oxygen. Against the background of its lack, a person increases the risk of sudden death from a stroke.

Smoking harms the activity of the central nervous system, which leads to the following changes and characteristic symptoms:

• constant irritability;
• lethargy;
• headaches turning into migraines;
• drowsiness.

Due to a failure in the cerebral circulation, smokers develop atherosclerosis.

Respiratory system

In medical science, alkaloid is ranked among the most common mechanisms of lung cancer in smokers. A common consequence of tobacco use is the development of malignant neoplasms in the mouth and larynx, requiring urgent surgery.

Important! In men who smoke, the incidence of oncological diseases of the respiratory system is 17.2% higher than among those who do not have this habit. Among women, the indicator is 11.6%. Among non-smokers of both sexes, the incidence of lung cancer is 1.3%. Statistics reflect data from recent years.

The main harmfulness of nicotine is manifested in the provocation of chronic bronchitis and asthma. The reason lies in the excessive production of phlegm, which accumulates in the respiratory tract. Through coughing, they begin to clear every time a person smokes.

People who abuse tobacco are more likely to develop respiratory infections in the form of laryngitis, sore throat, and pharyngitis. In the majority of smokers, emphysema is a typical case. The most common consequence of long-term use of cigarettes is the development of chronic pulmonary obstruction.

Reproductive system

The use of smoking herb, tobacco mixtures, vaping, electronic cigarettes, marijuana leads to a distortion of spermatogenesis in men. Against this background, the quality of the semen deteriorates. This circumstance serves as an active factor in the development of impotence and infertility.

During pregnancy in women, nicotine leads to the following consequences:

• increased risk of sudden fetal death (especially at the embryonic stage);
• development of asphyxia in the womb;
• provoking premature birth at any period of gestation;
• the probable lag of adolescents in physical and intellectual development, frequent illnesses in the process of growing up.

A nursing mother who continues to smoke transfers to the newborn, along with breast milk, all the toxic components of tobacco, which can provoke severe poisoning in him. Also, the alkaloid disrupts the hormonal background in the fairer sex, which is reflected in the malfunction of the thyroid gland. Because of it, estrogen compensation decreases, which is the main factor in the development of female infertility. Nicotine also worsens heredity in subsequent generations.

The main harm of cigarettes to the human body is the formation of a drug-like addiction. At the same time, abstinence (independent refusal of the habit of their own free will) is significantly complicated due to the persistent mental and physical need for smoking. When treating addiction, it is necessary to prescribe special anti-nicotine drugs and sedatives. However, they do not guarantee a complete rejection of addiction. You can quit the habit by sewing a special capsule under the skin or fixing an anti-nicotine patch on it.

From the action of cigarette smoke, there is a disruption in the work of absolutely all structures. The most vulnerable systems are the respiratory, cardiovascular, digestive and reproductive systems. The skin and hair of the smoker suffers significantly from the effects of nicotine tar. A bad habit reduces the immune defense, it provokes cancer more often than other addictions. Also, smoking is one of the factors in the appearance of tetanus, from which it is necessary to be vaccinated.

Useful video

Nicotine addiction will be discussed below:

In contact with

Nicotine is the most famous and one of the many alkaloids found naturally in tobacco. Nicotine itself is present in many other plants of the nightshade family, such as eggplant or pepper, but in minimal amounts. The effect of pure nicotine isolated from tobacco products or cigarettes is significantly different from that of tobacco itself, and in any case should be considered as the effect of a single substance. Essentially, nicotine has several mechanisms of action. The first is that it mimics the action of the neurotransmitter acetylcholine and can directly activate acetylcholine receptors, which can then induce increases in catecholamines such as adrenaline and dopamine. This mechanism underlies both the potential for nicotine addiction and the fat burning mechanism. Nicotine can also act as an anti-estrogenic compound, directly inhibiting aromatase and one of two estrogen receptors, which may underlie some of the side effects associated with chronic nicotine use, especially in women. Finally, nicotine by its nature causes oxidative stress, but at a level that is hormesis for the cell. This refers to mimicking the action of acetylcholine mentioned earlier and anti-inflammatory action. It is very likely that, due to its mechanisms of action on the body, nicotine is a fat burner, since as a result of its action, the level of adrenaline increases, which then acts on beta-adrenergic receptors (the molecular target of ephedrine). The increase in adrenaline levels mediates a significant but short-lived increase in metabolic rate in the moderate nicotine user. It is believed that the increase in the rate of lipolysis (breakdown of fatty acids) is not associated with adrenaline, but indirectly by other, possibly causing oxidative stress, mechanisms. Increases in catecholamines also underlie many of the cognitive benefits of nicotine (mainly related to increased focus and focus), while mimicking the action of acetylcholine can promote inherently nootropic effects. With regard to addiction, we can say that its risk is determined by the ratio of how much nicotine a person took (the more the amount, the greater the risk) and the speed with which nicotine enters the brain (the faster the concentration of nicotine in the brain rises, the stronger the effects are felt and the higher risk of addiction). The development of addiction is not an inherent characteristic of nicotine, as evidenced by the results of nicotine therapy used to curb cigarette addiction. Gum and patches have less potential addiction risk than cigarettes because of the speed at which nicotine reaches the brain. In the short term, due to increased levels of catecholamines, the potential side effects of nicotine are similar to the acute side effects of other stimulants such as, or. In the long term, nicotine may rival ephedrine in terms of its side effect profile, as they both maintain catecholamine secretion over time (yohimbe and caffeine lose their effectiveness within two weeks or less).

Nicotine: methods of administration (recommended dosage, active amounts, other details)

Nicotine can be introduced into the body in several ways (excluding cigarettes, which are not recommended for use due to risks that significantly outweigh the benefits of this method of taking nicotine):

An inhaler that allows you to quickly feel the effects of nicotine (and which, in fact, is associated with a greater risk than other methods, due to the speed at which nicotine enters the body);

Nicotine patch, when used, absorption is delayed for about an hour after application. The patch allows you to maintain a constant level of nicotine in the blood serum, but causes a smaller cognitive leap (minimum risk potential, minimum nootropic potential);

Chewing gum, the advantages and disadvantages of which are somewhere in between compared to the methods described above.

At the moment there is data on the "optimal dose" of nicotine for a non-smoker. It would be prudent for a non-smoker to follow the same guidelines as for stimulants, that is, start with low doses and gradually increase them. This involves buying a 2mg gum or a quarter of a 24mg patch to start with and then increasing it to what appears to be the minimum effective dose. At the moment, there is no dedicated threshold level when the risk becomes too great, since this level is individual. When using nicotine in nicotine replacement therapy (to curb the urge to smoke), it is sufficient to follow the instructions for use of the product. The amounts described in these instructions may be excessive for a non-smoker.

Sources and structure

Cigarettes and other sources

Nicotine is the main tobacco alkaloid (minor alkaloids are nornicotine, anatabine, anabasine) and is present in tobacco leaves as a pesticide that kills insects that try to feed on them (phytoalexins resveratrol and caffeine have a similar origin). Nicotine accounts for up to 1.5% of the total weight of commercial cigarette tobacco and 95% of its total alkaloid content. On average, a cigarette contains 10-14 mg of nicotine, but only 1-1.5 mg reaches the bloodstream after smoking. Most of the alkaloids found in tobacco are found only in tobacco and are structurally similar to nicotine, including myosmin, N "-methylmyosmin, cotinine, nicothirine, nornicothyrine, nicotine N" -oxide, 2, 3 "-bipyridyl, and metanicotine. Miosmin is not unique tobacco alkaloid and is quite widespread in the human diet, as well as nicotine, which is present in small amounts in plants of the nightshade family (2-7 μg / kg vegetables). The average amount of nicotine that a person receives through vegetables from the nightshade family is at the level 1.4 mcg per day, 95 percent of the population gets no more than 2.25 mcg of nicotine from vegetables they eat. This is about 444 times less than the amount of nicotine in one cigarette. Nicotine is the main alkaloid in tobacco. It is also found in plants of the nightshade family such as eggplant. potatoes and tomatoes, but in such small quantities that they cannot induce the neurological effects that smoking causes.

Pharmacology of nicotine

Suction when smoking

Under normal conditions, nicotine is a weak base with pKa = 8.0 and in acidic environments, where nicotine is usually ionized, it cannot easily penetrate membranes. Smoke from warm air-dried cigarettes (pH 5.5-6.0) is in most cases acidic, so nicotine cannot easily pass through the mucous membrane of the mouth. A certain amount of nicotine can still pass through the mucous membrane, because nicotine gum droplets may have a higher pH, but most of the absorption in the case of tobacco smoking occurs in the respiratory tract. Nicotine can pass through the oral mucosa at elevated pH levels. This refers to air-cured tobacco, which is usually used in pipes and cigars (different from the already mentioned warm air-cured tobacco of North American cigarettes). Nicotine in such tobacco is usually non-ionizing and can pass through the oral mucosa. In the mouth, nicotine can pass through the oral mucosa if the medium (tobacco smoke) is alkaline. This environment is typical for pipe and cigar tobacco and nicotine gum. In the lungs, nicotine is absorbed when it comes in contact with the alveoli. The absorption rate is considered high due to the large area of ​​the alveoli and due to the fact that the pH in the lungs = 7.4, which facilitates the transport of nicotine across the membrane. Rapid absorption of nicotine is carried out in the lung tissues.

Suction (other types)

In chewing tobacco, nicotine gum and snuff, special pH-increasing substances are added to facilitate the passage of nicotine through the oral mucosa. The same substances are added to the nicotine patch to improve the absorption of nicotine by the skin. The overall bioavailability of nicotine in nicotine gum is less than when inhaled, and is approximately at the level of 50-80%. The lower bioavailability is due to the absorption of nicotine in the intestine, which enters there along with the swallowed saliva under conditions of presystemic metabolism. Nicotine patches differ in absorption, depending on the brand, although any patch usually allows the nicotine to enter the bloodstream within an hour after adhering. Remaining nicotine (10% of that contained in the patch) still enters the bloodstream after the patch is already peeled off. This nicotine enters the bloodstream from the nicotine-soaked skin.

Pharmacokinetics in the bloodstream

Some studies of cigarette smoking show that Tmax (time to reach the maximum concentration of nicotine in the blood) coincides with the end time of smoking a cigarette, while for chewing and snuff the corresponding time is slightly longer (more difficult to titrate), and when chewing nicotine gum, this the same maximum concentration of nicotine in the blood, as with an equivalent dose of nicotine obtained by smoking cigarettes or by using chewing tobacco. The first maximum effect of cigarette nicotine on the nervous system occurs within 10-20 seconds after a puff, however, the exact amount of nicotine received by a person during this time may vary, since the puffs themselves can be different (they can be large or small, their speed can be different can be influenced by how much the puff is diluted with air), although the average amount of nicotine reaching the systemic circulation for the average smoker who prefers the average North American cigarette is 1-1.5 milligrams. Smoking cigarettes leads to a very rapid increase in the concentration of nicotine in the bloodstream. Chewing gum containing 6 milligrams of nicotine is thought to increase blood nicotine levels by 15-20 nanograms / milliliter, while a smoked cigarette can increase this level by 15-30 nanograms / milliliter.

Distribution

A pH level of 7.4 in the blood indicates that nicotine is in a state where the ratio of its ionized to non-ionized portion is 69:31, and its binding to blood plasma proteins is less than 5%. The average sustained volume of distribution of nicotine is 2.6 liters / kg. Nicotine is widely distributed throughout the body. The organs such as the liver, kidneys, spleen, and lungs have the highest affinity for nicotine; the smallest is adipose tissue. This was determined by autopsy of smokers. The concentration of nicotine in skeletal muscle and in the blood is the same. In smokers, compared with nonsmokers, nicotine can bind to brain tissue with greater affinity and have an increasing ability to bind to the receptor. Nicotine accumulates in body fluids, especially saliva and gastric juice, due to ionic uptake, and can also accumulate in breast milk in a ratio of 2.9: 1 (milk: plasma). In addition, it easily crosses the placental barrier and can accumulate in the amniotic fluid at a concentration slightly higher than the serum concentration and can penetrate the fetus.

Neurokinetics

Due to the rapid passage of smoke into the lungs, as well as rapid absorption into them, nicotine can be contained in the brain tissue 10-20 seconds after a cigarette inhalation, which is faster than with an intravenous injection. The rapid delivery of nicotine to the brain, as well as the ability of nicotine to induce addiction (reward context), and, in addition, the smoker's ability to control the smoking process according to their own preferences, make cigarettes the most dangerous method of using nicotine in terms of addiction. The volume of distribution of nicotine in plasma (the volume of distribution in plasma not in the brain is taken as 100%) is at a level of about 20% for the whole brain (insignificant, as shown by a study in primates in which this value was obtained) with a predominant distribution in the preexisting field ( 29%) and amygdala (39%) and less spread in the white matter (10%). However, in the study that identified these data, an aromatase inhibitor was used for evaluation, while in primates, the distribution of aromatase competes with the distribution indicated above (although in humans, a large amount of aromatase is found in the thalamus). The use of nicotine by smoking cigarettes is, from a neurological point of view, the most effective method of introducing nicotine into the body due to its pharmacokinetics and the smoker's ability to control the nicotine entering the body according to individual needs.

Metabolism

Nicotine is extensively metabolized in a variety of ways, but the main pathway for nicotine metabolism is through cotinine (70-80%). Despite the fact that 10-15% of all nicotine metabolism products excreted in the urine is cotinine, the main metabolism occurs through cotinine, and cotinine itself undergoes further metabolization. The direct conversion of nicotine to cotinine occurs through the participation of an intermediary. This mediator is ionized nicotine-Δ1 "(5") - iminium, the conversion of nicotine into which occurs thanks to the P450 enzyme CYP2A6. Further conversion to cotinine occurs due to cytoplasmic aldehyde oxidase. Cotinine can subsequently be glucuronidated and excreted in the urine in the form of cotinine glucuronide, or it can be transformed into cotinine N-oxide or into trans 3-hydroxycotinine (which can then also be glucuronidated and excreted in the urine). It should also be noted that nicotine itself can be glucuronidated and excreted in the urine as nicotine glucuronide. This process occurs with 3-5% of the total amount of nicotine that has entered the human body. It is believed that in addition to 10-15% of nicotine metabolized through cotinine and 3-5% of nicotine metabolized by glucuronidation, other metabolic products are trans 3-hydroxycotinine (the most significant metabolite, 33-40% of metabolism), cotinine glucuronide (12-17 %) and trans 3-hydroxycotinine glucuronide (7-9%). The main route of metabolism of nicotine is metabolism via cotinine. Cotinine is then either excreted unchanged in a detectable amount, or it undergoes further metabolism. Glucuronidation (attachment of glucose to a molecule) can undergo both nicotine or cotinine and cotinine metabolites. Another phenomenon responsible for 4-7% of metabolism is nicotine N-oxide, which is the result of the reaction of nicotine with flavin-containing monoxidase 3 (FMO3) and produces mainly the trans isomer of nicotine N-oxide. It is a product of the urinary tract and can be found in urine or converted back to nicotine in the intestines. This metabolite, together with alkaline nicotine glucuronide (3-5% of all nicotine ingested), is responsible for the bulk of what remains from metabolism via cotinine.

Enzyme interactions

The aromatase enzyme (CYP1A1 / 2) appears to be inhibited by nicotine, with an IC50 of 223 +/- 10μm, and since nicotine is twice as potent as its metabolite cotinine, both of these together can inhibit aromatase more potently. High doses of androstenedione can reverse the inhibition of aromatase by nicotine and cotinine. Other aromatase inhibitors found in tobacco include myosamine (IC50 33 +/- 2μm; 7 times more potent inhibitor than nicotine), anabazine, N-n-octanoylnornicotine (comparable to aminoglutethimide), and N- (4-hydroxyandecanoyl) anabazine. Nicotine inhibits aromatase. However, it is a relatively weak inhibitor when considering the concentrations required to inhibit 50% of the enzyme activity. Other substances found in tobacco are more potent aromatase inhibitors. In one study using intravenous nicotine injections in baboons (at levels close to the nicotine content of a cigarette; 0.015-0.3mg / kg), aromatase inhibition was observed in the brain.

Neurology

Neurophysiology

Nicotine injections (in smokers) increase neural activity in the frontal and lumbar regions of the brain, as well as in the nucleus accumbens and amygdala, areas of the brain involved in addictive processes.

Attention and reaction time

A meta-analysis of nicotine and its effects on the brain in humans has shown that there is ample evidence that nicotine enhances attention (both the ability to respond instantly and to various external stimuli). This meta-analysis focused more on nicotine per se, as previous studies focused more on smokers and looked at the effects of nicotine on the brain only after quitting. Another meta-analysis focused only on laboratory studies of healthy people and excluded smokers who quit nicotine or those who were not in the double-blind study when compared with placebo. This meta-analysis summarized data from 41 studies and analyzed the parameters of instantaneous response (accuracy and response time), as well as response to stimuli (accuracy and response time), 76% of the trials, and the meta-analysis itself was not associated with the tobacco industry (were independent ). Nine of these studies examined the accuracy of instantaneous reactions, and 8 of these studies plus 5 others looked at reaction times. Only 5 (unique) studies examined the accuracy of response to stimuli as well as response time to stimuli, in addition to the other six studies. Significant and positive was observed with respect to the accuracy of the instantaneous response (g = 0.34, z = 4.19, p less than 0.001), the time of the instantaneous response (g = 0.34, z = 3.85, p less than 0.001) and the response time to the stimulus (g = 0.30, z = 3.93, p less than 0.001). Minor improvements were seen in the accuracy of response to stimulus (g = 0.13, z = 0.47, p less than 0.6). A rigid linear dependence was observed with respect to these parameters. Relative improvements in attention scores were noted with different doses of nicotine in a dose-dependent paradigm. Improvements were observed in the direction and retention of attention to stimuli, exactly, and in switching attention between stimuli, however, the improvements in the accuracy of switching attention may not be as significant.

Anxiety and depression

In a study of patients with mild cognitive decline (non-smokers), it was shown that the use of nicotine patches at a dose of 15 mg for 6 months daily was associated with an improvement in subjective indications of anxiety, which is an indicator of the anxiolytic effect of nicotine. In the same study, there was no significant improvement in the subjective assessment of depression. One study using nicotine in non-smokers found that a 2mg dose of nicotine (nicotine gum) caused an increase in the activity of brain regions associated with negative perceptions compared to a placebo. Thus, it is suggested that nicotine may increase anxiety.

Aphrodisiac

One study comparing regular cigarettes and cigarettes without nicotine found that cigarettes containing nicotine had a negative effect on sexual effects through the bloodstream (measurements of the diameter of the penis were made). Thus, it is suggested that nicotine may act as an anaphrodisiac. Two more recent studies in nonsmoking men and women showed that nicotine can reduce sexual stimulation (induced by watching pornographic films or on its own) without significantly affecting other mood parameters; men also reported a decrease in erection after taking nicotine.

Nootropic Effects

A meta-analysis of nicotine has shown that nicotine improves memory, especially short-term memory. A 6-month study of patients with mild cognitive impairment (over 55 years of age reporting memory lapses) found that daily use of 15 mg nicotine patches (release over 16 hours) was associated with improvements in memory, attention, and psychomotor speed. reactions.

Fatigue

Nicotine has been shown to reduce brain fatigue in individuals with increased impulsivity (and decreased self-control), with little effect on those with decreased impulsivity.

Reward mechanism

In a study in non-smokers, 14mg nicotine patches (two 7mg patches) enhanced the reward response to non-drug stimuli. The study used a sophisticated computer imaging test. Users who were given nicotine responded better to incentives associated with reward, with the reward mechanism lasting longer than the control group. The same conclusion was reached by researchers who gave money to smokers after the trial. Similar results were obtained in animal trials where nicotine administration was associated with an increased response to reward in relation to non-drug stimuli. Quitting nicotine use has been associated with decreased response to reward.

Impulsiveness

In a study of gambling addicted smokers, it was noted that although ingestion of 4mg nicotine (via inhaler) suppressed cigarette cravings, there was no effect on gambling addiction relative to placebo. In the study of nicotinic acetylcholine receptors (which activates nicotine) using transdermal nicotine patches (7mg) and the assessment of impulsivity using three different tests, it was noted that nicotine improved indicators associated with impulsivity in the group with an increased baseline level of impulsivity (decreased self-control). with no significant effect on individuals with low impulsivity. At the same time, various indicators of reaction time were observed, the best indicators were recorded in the group with reduced impulsivity.

Neurology (Addiction)

Mechanisms

The currently prevailing theory of the mechanisms of the development of nicotine addiction is the activation of nicotinic acetylcholine receptors (nAChRs) on mesocorticolimbic dopaminergic neurons, which serve to enhance the response to rewards and motivation, as well as to non-pharmacological stimuli. Through these mechanisms, the nootropic effect of nicotine is also manifested. Secondary to the activation of α4ß2 and ß2 nicotinic acetylcholine receptors on dopaminergic neurons, they depolarize, causing an increase in neuronal firing. Direct activation of α4ß2 nicotinic acetylcholine receptors directly excites these dopaminergic neurons. All of these mechanisms lead to dopamine influx into the nucleus accumbens, which is also associated with the addictive mechanism underlying the action of substances such as heroin and cocaine. Inhibition of this dopaminergic process results in decreased cravings associated with nicotine. Activation of a7 nicotinic acetylcholine receptors increases excitation across the nucleus accumbens from the ventral tegmental area (VTA), as well as two other areas known as the pedunculopontine tegmental nucleus (PPT) and the laterodorsal tegmental nucleus (LDT), as binding to presynaptic a7 nicotine receptors glutaminergic activity and provides long-term potency. Unlike α4ß2 and ß2 receptors, which desensitize rather quickly after activation, a7 nicotinic acetylcholine receptors are desensitized slowly, which ensures their long-term potentiation through an increase in glutaminergic signaling. In many cases, the inhibitory potential of GABAergic neurons is reduced. GABAergic neurons, which are expressed mainly in the ventral tegmental region, and under normal conditions oppose the excitation of glutaminergic neurons, express mainly α4ß2 receptors. In cases where smokers constantly absorb nicotine and maintain elevated levels of nicotine in their bodies, these receptors are desensitized and their effect is reduced due to reduced activation of α4ß2, leading to a sharp increase in a7 nicotinic acetylcholine receptors and activation of glutaminergic neurons. The activation of dopaminergic neurons is directly related to many of the short-term effects of nicotine in this area of ​​the brain, and the activation of a7 nicotinic acetylcholine receptors on neurons other than this area of ​​the brain enhances the neuronal network and is a long-term addictive mechanism. Addicted smokers exhibited increased dopamine release that was absent in non-smokers in this study. When comparing nicotine per se and tobacco from cigarettes in addicted smokers who were previously given 4 mg nicotine lozenge versus placebo, and then comparing smoking cigarettes without nicotine in both groups, it was shown that smoking cigarettes, regardless of their nicotine content, was associated with feelings of pleasure and decreased cravings for smoking, and that pre-use of nicotine reduced the number of puffs and further reduced cravings. In other studies, these findings have also been confirmed for nicotine cigarettes.

Kinetics

One aspect of the reward mechanism of nicotine use is the rate at which nicotine reaches the brain and is associated with perceived reward. When smoked, nicotine can reach neural tissue within 10 to 20 seconds, faster than intravenous injections, which is comparable to intranasal nicotine administration. The rapid increase in neural nicotine concentrations is one of the addictive factors. Other nicotine uses that avoid such a rapid and rapid Cmax in neural tissue (chewing gum, patches, sublingual tablets and lozenges) are associated with a lower degree of dependence, but a low dependence rate for such products is also associated with the amount of absorbed dose of nicotine. The rate at which nicotine reaches the brain and the total concentration of nicotine reaching the brain are predictors of addictive potential. High doses and rapid absorption (when smoking cigarettes) are associated with greater addiction than sustained-release forms of nicotine (gum, patches). One study of nicotine in smokers looking to quit smoking noted that in the group that used nicotine gum (2mg or 4mg; n = 127), 15mg transdermal patch (15mg; n = 124), nasal spray (n = 126 ) or nicorette inhaler (n = 127) with ad libitum products indicated that in users who had not smoked for at least 3 weeks and completed a 12-week study, all methods were equally effective in terms of the number of smokers who continued to quit smoking and average pleasure or satisfaction scores over that time period. Addiction rates during nicotine replacement therapy were assessed by how many people continued to use nicotine 3 weeks after completion of the study (37% in the spray group, 28% in the chewing gum group, 19% in the inhaler and 8% in the patch), and by subjective indications of dependence during this period of time (33% inhaler, 22% chewing gum, 20% nasal spray, 0% patch). Considering these study endpoints, nicotine gum use is associated with lower rates of subjective dependence than inhaler and nasal spray combined. The patch was associated with the lowest addiction rates. Nicotine replacement therapy itself is associated with the development of addiction, which is related to the rate and total amount of nicotine consumed. At the same time, the level of dependence is lower than when smoking cigarettes.

The effect of nicotine on men and women

Nicotine cravings are associated with sexual dimorphism, as women need less nicotine to develop addiction, and smoking cessation is more difficult for women than for men. These differences have a biological basis, as studies of laboratory animals also show such differences. Low doses of nicotine (bordering on the level at which rats may not take nicotine on their own, which is an indicator of the development of addiction) have a greater effect on females than on males. It was shown that females were willing to travel long distances to receive a dose of nicotine, compared to males. It is believed that hormones circulating in the body may play a role in these differences, since exogenous progesterone is associated with reduced cravings and the enjoyment of smoking. In addition, there has been a definite correlation between nicotine and the estrous cycle, as it is related to the development of nicotine addiction, as women report an increase in cigarette use during menstruation. This phenomenon is independent of menstrual symptoms (for example, smoking to relieve menstrual symptoms). However, some studies have failed to demonstrate this link. Particular sensitivity to smoking cessation develops during menstruation and some time after it ends. These interactions may underlie the ability of nicotine to interfere with estrogen signaling in neural tissue, directly inhibiting the beta subunit of the estrogen receptor and inhibiting aromatase.

Nicotine and the development of addiction

19.8% of the American population smoke cigarettes (not nicotine per se) (2007 data), and although 45% of smokers tried to quit smoking (2008), only 4-7% succeeded. During smoking cessation, one of the common side effects reported by respondents was difficulty concentrating. One of the most common reasons for smoking resumption was the subjective nootropic effects of nicotine. For these reasons, nicotine has been studied for a long time in relation to the development of dependence on cigarettes containing tobacco.

The cardiovascular system

Heart rate

When taking 6mg of nicotine gum in a man aged 21, an increase in heart rate is observed, as well as an increase in diastolic and systolic pressure 30 minutes after consumption. The same study in women also showed an increase in heart rate, but did not show a significant increase in blood pressure. A 6-month study using 15mg nicotine patches showed significant reductions in blood pressure, with an average increase of 9.6mmHg in the placebo group. in 6 months. In the group using nicotine patches, there was a decrease in systolic pressure by 4 mm Hg.

5interactions with glucose metabolism

Inflammation and glucose metabolism

Secondary to the anti-inflammatory effects of nicotine, nicotine can enhance insulin sensitivity if the mechanism of insulin resistance is inflammatory, and in rats, nicotine acts on insulin without affecting body weight.

Research

Smoking cigarettes per se can have a negative effect on glucose metabolism. Long-term use of nicotine gum correlates with insulin resistance. In this regard, the effects of nicotine per se are very interesting in terms of research. When looking at the effects of nicotine in isolation in healthy smokers, it was noted that the use of a 14mg nicotine transdermal patch increased insulin resistance and blood glucose levels. Nicotine infusions in nonsmokers have no effect on baseline glucose uptake levels in healthy individuals (10.9 +/- 0.3mg / kg LBM), and uptake was impaired by approximately 32 +/- 6% in type II diabetics. Thus, it has been shown that nicotine has different effects on healthy individuals and patients with diabetes. These data support earlier research that suggests that nicotine intake in diabetics worsens insulin resistance, while a study using snuff found that tobacco per se was not associated with development in healthy individuals. insulin resistance as opposed to smoking; thus, any compound found in cigarettes rather than snuff may be associated with the development of insulin resistance, and this compound is not nicotine per se. In this study, where smokers were divided into "healthy" and "diabetic" groups, the division was made on the basis of circulating levels of glucose, insulin and HbA1c (increased in diabetics); the nicotine dose was 0.3 μg / kg / min, and simulated smoking a cigarette. 6.3. Insulin sensitivity after smoking cessation It is known that after smoking cessation, weight gain is often observed, usually fat; this is due to both decreased metabolism and increased caloric intake, although this may be due in part to increased insulin sensitivity after smoking cessation. Nicotine patches have no effect on increasing insulin sensitivity after smoking cessation.

Obesity

Cigarettes are known to stimulate lipolysis (fat burning). This effect can also be replicated by intravenous administration of the same doses of nicotine; when comparing monozygotic twins, the weight of the smoking siblings was 2.5-5.0 kg less than the weight of the nonsmoking siblings. Although weight can be influenced by a variety of reasons, stimulation of lipolysis and firing of a cholinergic neuron in adipose tissue are direct fat-burning effects that are expressed through nicotinic acetylcholine receptors.

Mechanisms

Nicotine can enhance the activity of AMP-dependent kinase in adipocytes, which is associated with an increase in lipolysis, depending on the time of exposure and concentration. Since the increase in AMP-dependent kinase and lipolysis were inhibited by N-acetylcysteine, they were mediated by prooxidative effects. It is known that oxidative stress regulates AMP-dependent kinase, in particular peroxynitrate (a pro-oxidative derivative of nitric oxide), and these effects were observed at the level of circulating nicotine, which is achieved through smoking one cigarette (6nM, up to 600nM). However, activation of AMP-dependent kinase does not induce lipolysis with nicotine intake (since the inhibitor, Compound C, successfully inhibited AMP-dependent kinase but did not eliminate lipolysis). The increase in lipolysis with nicotine intake is due to the fact that nicotine inhibits fatty acid synthase (by 30% at a dose of 100 nM), which may be secondary to peroxynitrate, and a possible increase in the level of catecholamines such as adrenaline, which are released in response to stimulation with nicotine ( which has been shown after intravenous administration). The study notes that 7.2 ng / ml nicotine (levels achieved after smoking a cigarette) increased epinephrine and norepinephrine levels by 213 +/- 30% and 118 +/- 5%, respectively. The release of glycerol (144-148%) was inhibited by a cholinergic agonist (acting on the acetylcholine receptor) and decreased by 60% with propanolol (a beta-adrenergic antagonist involved in the release of catecholamines). A decrease in nicotine-induced lipolysis has also been observed in other studies, with concurrent blocking of beta-adrenergic receptors. Nicotine acts on acetylcholine receptors, releasing adrenaline and norepinephrine, which then act on beta-adrenergic receptors (the molecular target of epinephrine and ephedrine), affecting fat burning processes. This is not the only, but the most important, mechanism of action of nicotine. The activation of nicotinic acetylcholine receptors on fat cells is associated with a decrease in the secretion of proinflammatory TNF-a, and this receptor (namely, a7nAChR) is negatively correlated with body fat; people with a body mass index (BMI) of 40 or higher have up to 75% less mRNA and protein content than people of normal weight. The activation of nicotinic acetylcholine receptors on adipose cells mediates anti-inflammatory effects in the adipose cell, and decreases the secretion of pro-inflammatory cytokines.

Metabolism

In healthy people, nicotine gum containing 1-2mg of nicotine increases metabolic rate by 3.7-4.9%. These indicators increase even more with the simultaneous use of 50-100mg of caffeine in chewing gum without the dose dependence observed with addiction to caffeine. The rate of fat oxidation when taking nicotine does not change in comparison with the control group. The measurements were carried out for 180 minutes, during the first 25 the subjects chewed gum.

Research

In rodents, nicotine can reduce fat weight when fed a diet high in fat as well as a regular diet. In both cases, blocking of this effect was observed when taking the acetylcholine receptor antagonist mecamylamine; in one study, it was shown that selective inhibition of the α4ß2 receptor (using varenicline) can only partially inhibit fat burning. In experiments on rats, it was shown that the effect of fat burning is observed with controlled food intake, without reducing calorie content. These studies, however, use very high doses of nicotine (2-4mg / kg; one study used doses up to 4.5mg / kg, which is equivalent to 2.5 packs of cigarettes). These changes were observed with oral doses of 0.5 mg / kg and were dose-dependent, but their statistical significance may decrease over time (as the effectiveness decreases). In one study of male smokers (refractory to the effects of nicotine) who were given 4mg of nicotine gum or the equivalent dose in the form of a cigarette or inhaler, there was no increase in lipolysis within 180 minutes, nor was there an increase in adrenaline levels. In terms of metabolic rate, several studies have observed an increase in metabolic rate in rats with isolated nicotine supplementation. In humans, smoking cigarettes showed an increase in metabolic rate of about 210 kcal over 24 hours compared to nonsmokers. This increase in metabolic rate may be mediated simply by an increase in the amount of epinephrine and norepinephrine, with a half-life of 3.5 minutes (similar to the active half-life of adrenaline receptors). The increase in lipolysis does not show an obvious half-life. Animal studies show a significant increase in lipolysis and metabolic rate, which decreases over time (at low doses, nicotine is not very different from placebo, and only at high doses is lipolysis observed). The acceleration of metabolism may simply be due to an increase in the amount of catecholamines (adrenaline and norepinephrine). One study using nicotine patches in 55-year-old men and women showed that after 91 days of nicotine use, there was a 1.3kg weight loss (0.13kg for the placebo group). However, when re-measured after 6 months, the difference disappeared. Human studies show that nicotine use in isolation over a long period of time is not effective for weight loss.

Weight gain

Quitting the habit of smoking cigarettes is often accompanied by weight gain, mainly fat mass, which is associated with a slowdown in metabolism and an increase in food intake. Nicotine alone (to a small extent) may help reduce weight gain after quitting smoking, but the results are mixed and cannot be said for certain. Nicotine gum, for example, cannot withstand weight gain after quitting smoking (2mg gum; no dose limitation). One study has shown benefits with 2-4mg chewing gum in a specific regimen. A dose-dependent effect is possible (which was not confirmed later in experiments with nicotine patches). Compounds that may help prevent weight gain after smoking cessation are naltrexone, dexfenfluramine and phenylpropanolamide, and fluoxetine.

Skeletal muscle

Mechanisms

Nicotine has been shown to be able to activate mTOR when incubated in skeletal muscle culture, possibly mediating smoking-related decrease in insulin sensitivity (since mTOR activation induces IRS-1 and suppresses insulin signals).

Effects of nicotine on inflammation

Mechanisms

Nicotine exhibits anti-inflammatory properties by acting as a cholinergic agonist, activating the a7 nicotinic acetylcholine receptor (a7nAChR) on immune cells, in particular dendrin cells and macrophages. This pathway is naturally regulated by the neurotransmitter acetylcholine, released from the vagus nerve, which inhibits the ability of immune cells to respond to TNF-a and reduces its release from immune cells. More recently, it has also been demonstrated that nicotine can inhibit NF-kB activation in LPS-activated macrophages and also affect splenocytes. Obviously, activation of the nicotinic receptor by either nicotine itself or the neurotransmitter acetylcholine can suppress inflammatory responses on immune cells and reduce the secretion of pro-inflammatory cytokines. Nicotine activation of a7nAChR increases the release of JAK2 and STAT3, which in turn induces the release of tristetraproline (TTP), which destabilizes TNF-a and interferes with its action. TTP is a poorly effective cytoplasmic regulator of inflammation, and its absence causes arthritis in rats. Another possible mechanism of action of nicotine is the suppression of proteins of the high mobility group 1, which may be a possible mechanism for reducing the clinical signs of sepsis.

Ulcerative colitis

Epidemiological studies have shown that smokers have a reduced risk of developing ulcerative colitis. The relative risk is 0.6 (0.4-1.0) when compared to non-smokers. People who quit smoking have a two-fold increased risk of developing UC compared with smokers (1.1-3.7). Similar findings have been obtained in other studies, however, these rates do not apply to other diseases of the gastrointestinal tract, such as Crohn's disease (sometimes associated with an increased risk) and inflammatory bowel disease. It has been noted that ulcerative colitis is more likely to develop in quitters than in current smokers. These paradoxical effects are secondary to the fact that nicotine acts as an anti-inflammatory alkaloid. Even with the use of nicotine with the help of cigarettes, there is an inverse relationship with the development of ulcerative colitis.

Nicotine and cancer

Metabolites

N'-nitrosonornicotine (NNN), a nitrosamine found in tobacco, a metabolite of nornicotine, may have carcinogenic potential. NNN has been found in the urine of people who quit smoking and used nicotine patches or gum. It is speculated that some people may produce NNN ecdogenically from nicotine. One study using 21mg nicotine patches for 24 weeks after quitting smoking noted that urinary NNN levels dropped to near the detection limit (0.005 pmol / ml-0.021 pmol / ml). The study also noted that 40% of passive smokers (out of 10) had urine NNN levels of 0.002 pmol / ml, and although these two studies (the last of which were well-structured) noted significant increases in urinary NNN levels, at least One study showed no increase with nicotine replacement therapy (using patches).

Lungs

Activation of the α7 acetylcholine receptor promotes anabolic effects such as Akt phosphorylation and Src activation. Nicotinic receptor activation increases cytoplasmic markers of pro-inflammation (5-LOX, COX-2 and NF-kB translocations). Nicotine at a concentration of 100nM cannot induce proliferation, but may exhibit anti-apoptotic effects. Cholinergic receptors act as a signaling pathway for cell survival in lung cancer, which also applies to acetylcholine.

6interactions with hormones

Testosterone

Nicotine and its metabolite cotinine adversely affect testicular structure and circulating testosterone levels, and may reduce the number of expressed androgen receptors (rat study, prostate measurement). In part, these mechanisms are secondary to testes oxidation (including damage and depletion of enzymes), but some suppression may be secondary to testicular cholinergic agonism. Similar mechanisms work for nicotine and cotinine. In one study using doses of 0.5 mg / kg and 1 mg / kg by tube (into the stomach) for 30 days, there was a decrease in testicular weight associated with the use of nicotine. There was no clear effect on prostatic hypertrophy. The decrease in the level of circulating testosterone was observed in a dose-dependent paradigm, but returned to normal after 30 days of nicotine withdrawal. In a study using a lower dose, 0.6mg / 100g, for 12 weeks, there was also a decrease in testicular weight and suppression of circulating testosterone levels and testosterone levels in the testes. The amino acid taurine was able to halve the decrease in testosterone levels at a dose of 50mg / kg body weight. A greater effect was observed with the use of human chorionic gonadotropin. Nikitin can reduce the release of 17ß-HSD and 3ß-HSD and the expression of StAR up to 60% of the control group. These effects can be reduced with taurine and normalized with human chorionic gonadotropin. Finally, another study using mice at 20 weeks of age (average age), when given low doses of nicotine (0.0625mg / kg bw) after a short initial phase, noted that after 90 days, suppression of testosterone levels from 898.4ng was observed. / ml in the control group to 364 ng / ml (a decrease of 59.5%) in the nicotine group, which was associated with abnormal cell organization in the prostate. Similar results have already been obtained earlier. It is speculated that the cause of this is a decrease in androgen levels, although the exact cause is still unknown. In a rat study, nicotine supplementation showed suppression of testosterone levels at psychologically relevant doses, due in part to receptor activation (muscarinic cholinergic) and, in chronic situations, to testicular damage from oxidation; damage was partially reduced with the use of antioxidants. One study in men who were considered nicotine-dependent for smoking 15. 48mg nicotine (equivalent to serum levels of 20ng / ml or higher) showed no change in circulating testosterone levels when measured over two hours, although there was a downward trend. Another study in Medline is a cohort study of men aged 35-59 years (n = 221) who smoked daily prior to the study. Circulating testosterone levels were assessed in these men after a year of withdrawal. The measurements of baseline testosterone levels one year after smoking cessation were shown to be the same. A larger study in older men (n = 375, age 59.9 +/- 9.2 years) shows that smoking is associated with increased testosterone levels. Other studies show no significant difference between groups, or even a trend towards higher testosterone levels in smokers (4.33 +/- 0.53 ng / ml in nonsmokers, 4.84 +/- 0.37 ng / ml in smokers).

Estrogen

In experiments with baboons, it was shown that nicotine is an aromatase inhibitor in vivo after injections of nicotine in baboons at concentrations of 0.015-0.03 mg / kg (plasma levels reached 15.6-65 ng / ml), as after smoking a cigarette. These data contradict previous studies showing that nicotine is an active inhibitor of aromatase in vitro. This may explain why women who smoke a lot are often prone to estrogen deficiency disorders (osteoporosis, menstrual disorders, early menopause) and explain the increased levels of circulating testosterone in smokers of both sexes (which has not been demonstrated in short-term studies). The ability of nicotine (and associated nicotine alkaloids) to inhibit the aromatase enzyme may cause a shift towards androgens over estrogens over time. The degree of change observed in these studies may be higher than when nicotine is taken in isolation, due to the presence of other alkaloids in tobacco. In a study of serum estrogen levels in rats, it was shown that circulating estradiol levels decreased on average over 4 estrous cycles compared to the control group 4 days later. Some differences were observed in the degree of decline. Estrogen protects in part against damage from ischemia (lack of oxygen) and reperfusion (reintroduction of oxygen), and this protection is suppressed by prolonged use of nicotine. A later study identifying the mechanisms behind this noted that rats given 4.5mg / kg nicotine hydrogen tartrate (to exhibit effects identical to continuous cigarette smoking) for 16 days before cerebral ischemia experienced an increase in damage. caused by ischemia with the use of nicotine (oral contraceptives, innocuous in isolation, acted in synergy with nicotine, increasing the damage). These effects were thought to be mediated by estrogenic inhibition of intracellular estrogen signaling, and since these effects were also manifested with the use of 1 μM ICI 182780, it was argued that nicotine inhibits estrogen receptors and CREB phosphorylation, which mediates the neuroprotective effects of estrogen (inhibiting NADPH oxidase and reducing pro-oxidase cage); nicotine reduces the amount of ER-ß protein, not ER-a, and this inhibition of ER-ß has also been implicated in reducing neuronal plasticity and mitochondrial loss in neurons.

Luteinizing hormone

In rats, when receiving nicotine at a dose of 0.6 mg / 100 g of body weight for 12 weeks, the levels of luteinizing hormone and follicle-stimulating hormone are reduced by 40% and 28%, respectively. In one human study, when assessing LH levels within two hours of 15.48mg nicotine supplementation (via smoking in addicted smokers), it was noted that LH levels increased within 14 minutes of smoking a cigarette and was highly correlated (r = 0.642) with serum levels. nicotine.

Prolactin

Cigarette smoking in addicted smokers is associated with an increase in prolactin levels within 6 minutes of cigarette smoking. Levels remain elevated for another 42 minutes and then return to normal within 120 minutes.

Interaction with other substances

Nicotine and caffeine

The combined use of caffeine and nicotine (coffee and cigarettes) is very popular; smokers, moreover, are much more coffee lovers than non-smokers. When used together in large doses, nicotine and caffeine exhibit thermogenic effects (440mg caffeine and 18.6-19.6 cigarettes per day). This thermogenic effect is further enhanced with exercise, however, as indicated in one study, this phenomenon is only observed in men. One study found that 50-100mg of caffeine and 1-2mg of nicotine gum had more appetite suppression than nicotine alone. The use of this combination in high doses (100mg caffeine and 2mg nicotine) may be associated with nausea. One study showed that caffeine intake (at a dose of 250 gm) in smokers who had not previously consumed caffeine for 4 weeks, when used together with nicotine infusions, caused a decrease in the subjectively perceived stimulatory effect of nicotine, compared with placebo. In people who do not smoke but consume caffeine, there is no significant interaction between the use of caffeine and nicotine. One study (self-rated by respondents) found that caffeine did not enhance nicotine addiction potential when used in adequate doses of both. These results, however, contradict another study in which participants were asked to decide how much money they were willing to spend on injections of caffeine or nicotine. This study showed that caffeine's ability to reduce the "negative" effects of nicotine stimulated addiction. Nicotine replacement therapy (in order to reduce cravings for nicotine) does not in any way affect caffeine withdrawal and caffeine dependence.

Nicotine and alcohol

Alcohol (ethanol) is a popular drink in society. Alcohol is popular among smokers and vice versa. In addition, the use of nicotine stimulates alcohol consumption, especially in men. In a study evaluating the combined use of alcohol and nicotine, it was noted that nicotine (10 μg / kg) significantly suppresses the subjective perception of alcohol intoxication (the level of alcohol in the exhaled air is 40-80 mg%), but increases alcohol-related memory deficit. The sedative effect of alcohol can be diminished by the use of nicotine. Nicotine can increase the euphoria of alcohol consumption. This decrease in short-term memory has been reported previously, in the group taking the alcohol + nicotine combination, performance is worse than in the placebo group and in the group taking alcohol alone. Alcohol, nicotine, or a combination of these substances do not significantly affect attention indicators.

Nicotine and N-acetylcysteine

N-acetylcysteine ​​(NAC) is a bioactive form of the amino acid cysteine ​​(found in high amounts in whey protein) that has been researched as a substance that may reduce nicotine addiction. The theory about the role of NAC in the development of addiction is based on the transmission of glutamate. The breakdown on withdrawal of addictive drugs is associated with a decrease in baseline concentrations of extracellular glutamate. This leads to a decrease in the activation of presynaptic mGluR2 / 3 receptors, which usually suppress glutamate signaling, and to an increase in glutamate signaling; although most of the research has been done in cocaine models, these receptors are also activated in nicotine addiction. Stimulating these receptors reduces the "positive" effect of nicotine. Increasing extracellular glutamate levels reduces withdrawal symptoms. NAC can reduce withdrawal symptoms, increase extracellular levels of schutamate, and to some extent suppress cocaine and heroin addiction in rats. One double-blind study of smokers (15 or more cigarettes per day) who quit smoking abruptly and then took either placebo or NAC twice daily at a total dose of 3,600 mg did not show any reduction in nicotine cravings with NAC. The reduction in side effects was small and did not reach statistical significance. However, when subjects were invited back to the lab and asked to smoke (signaling the end of the trial), subjects who were given NAC reported a significant decrease in the pleasure of smoking compared to the control group. On a scale of 1 to 100, the placebo group rated the pleasure of smoking a cigarette at 65.58 +/- 24.7 and the NAC at 42.6 +/- 29.02 (35.1% less). This decrease in positive effects may be more relevant to people who smoke than to those who quit smoking. One study (double-blind) noted that 2,400mg per day of NAC for 4 weeks in smokers did not reduce the number of cigarettes smoked per week per se, however, in social situations (smoking and drinking) there was a significant reduction in the number of cigarettes smoked. ; these effects were more pronounced when NAC was used for 4 weeks or more.

Nicotine and St. John's wort

St. John's wort is a dopamine antidepressant investigated as a compound that affects nicotine addiction due to positive effects in mice and mechanically reduces addiction through the modulation of catecholamines (dopamine, norepinephrine, adrenaline). Buproprion (an antidepressant) is effective in smoking cessation. The first open-label (non-blind) trials of St. John's wort in nicotine addiction showed that St. John's wort at a dose of 900 mg daily for three months was associated with 24% withdrawal symptoms at the end of the study. This was followed by another double-blind study of St. John's wort at a dose of 300 mg and 600 mg three times a day (total dose 900 mg or 1800 mg; 0.3% hypericin) for 12 weeks against placebo, in which St. John's wort showed no significant difference from placebo.

Nicotine and Modafinil

Modafinil is a prescription drug for narcolepsy with nootropic effects and is being investigated as a means to reduce nicotine addiction. In one blind study, modafinil not only did not reduce withdrawal symptoms, but, on the contrary, increased the negative symptoms of nicotine withdrawal. When modafinil was taken for 8 weeks at a dose of 200mg in the morning, the dropout rate was 44.2% in the placebo group and 32% in the modafinil group (minor difference). Taking modafinil is also associated with a significant increase in depressive symptoms and bad mood, without affecting positive mood and desire to smoke.

Nicotine and Taurine

Taurine is a nonessential amino acid that contains a sulfur group. Taurine reduces (but not completely) the decrease in testosterone and other hormones (luteinizing hormone, follicle-stimulating hormone) observed with nicotine use in rats. Taurine has been investigated for this purpose because it is the most abundant free ß-amino acid in the male reproductive system and is protective against the effects of nicotine on the heart tissue as well as the bladder and urinary tract due to its antioxidant properties.

Nicotine and ephedrine

In one study using nicotine (0.2mg / kg) in rats, where there was no negative effect on cardiac tissue when nicotine was taken in isolation, slight toxicity was found when taking a combination of caffeine and ephedrine in the presence of nicotine; this study used fairly high doses of ephedrine (30mg / kg), but adequate doses of caffeine (24mg / kg) and nicotine. A dose of 0.2 mg / kg in mice is approximately equivalent to a dose of 3 mg in a 90 kg human.

Safety and toxicity

A study using nicotine patches at a dose of 15 mg for 6 months in otherwise healthy people aged 55 years with slight with slight memory impairment showed that the total number of negative effects was significantly increased with nicotine supplementation (82) than with placebo (52), however none of these effects were characterized as “serious”. The study also reported a decrease in blood pressure and an increase in cognition when taking nicotinef.

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List of used literature:

Benowitz NL, Jacob P 3rd. Daily intake of nicotine during cigarette smoking. Clin Pharmacol Ther. (1984)

Siegmund B, Leitner E, Pfannhauser W. Determination of the nicotine content of various edible nightshades (Solanaceae) and their products and estimation of the associated dietary nicotine intake. J Agric Food Chem. (1999)

Benowitz NL, et al. Nicotine absorption and cardiovascular effects with smokeless tobacco use: comparison with cigarettes and nicotine gum. Clin Pharmacol Ther. (1988)

Benowitz NL, Jacob P 3rd, Savanapridi C. Determinants of nicotine intake while chewing nicotine polacrilex gum. Clin Pharmacol Ther. (1987)

Benowitz NL, et al. Interindividual variability in the metabolism and cardiovascular effects of nicotine in man. J Pharmacol Exp Ther. (1982)

Lindell G, Lunell E, Graffner H. Transdermally administered nicotine accumulates in gastric juice. Eur J Clin Pharmacol. (1996)

Benowitz NL, Jacob P 3rd. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Clin Pharmacol Ther. (1994)

Barbieri RL, Gochberg J, Ryan KJ. Nicotine, cotinine, and anabasine inhibit aromatase in human trophoblast in vitro. J Clin Invest. (1986)

Kadohama N, Shintani K, Osawa Y. Tobacco alkaloid derivatives as inhibitors of breast cancer aromatase. Cancer Lett. (1993)

Stein EA, et al. Nicotine-induced limbic cortical activation in the human brain: a functional MRI study. Am J Psychiatry. (1998)

Heishman SJ, Kleykamp BA, Singleton EG. Meta-analysis of the acute effects of nicotine and smoking on human performance. Psychopharmacology (Berl). (2010)

Poltavski DV, Petros T. Effects of transdermal nicotine on attention in adult non-smokers with and without attentional deficits. Physiol Behav. (2006)

Rusted JM, Alvares T. Nicotine effects on retrieval-induced forgetting are not attributable to changes in arousal. Psychopharmacology (Berl). (2008)

Vossel S, Thiel CM, Fink GR. Behavioral and neural effects of nicotine on visuospatial attentional reorienting in non-smoking subjects. Neuropsychopharmacology. (2008)

Colzato LS, et al. Caffeine, but not nicotine, enhances visual feature binding. Eur J Neurosci. (2005)

Kobiella A, et al. Nicotine increases neural response to unpleasant stimuli and anxiety in non-smokers. Addict Biol. (2011)

Gilbert DG, Hagen RL, D "Agostino JA. The effects of cigarette smoking on human sexual potency. Addict Behav. (1986)

Harte CB, Meston CM. Acute effects of nicotine on physiological and subjective sexual arousal in nonsmoking men: a randomized, double-blind, placebo-controlled trial. J Sex Med. (2008)

Harte CB, Meston CM. The inhibitory effects of nicotine on physiological sexual arousal in nonsmoking women: results from a randomized, double-blind, placebo-controlled, cross-over trial. J Sex Med. (2008)

Newhouse P, et al. Nicotine treatment of mild cognitive impairment: a 6-month double-blind pilot clinical trial. Neurology. (2012)

Potter AS, Bucci DJ, Newhouse PA. Manipulation of nicotinic acetylcholine receptors differentially affects behavioral inhibition in human subjects with and without disordered baseline impulsivity. Psychopharmacology (Berl). (2012)

Dawkins L, et al. A double-blind placebo controlled experimental study of nicotine: I – effects on incentive motivation. Psychopharmacology (Berl). (2006)

Nicotine is one of the most famous alkaloids. It is he who is mentioned when they talk about the dangers of smoking, saying that just one drop of the substance will easily kill a large horse. But is it?

What is nicotine and how toxic is it? Is it possible to get poisoned with this alkaloid in everyday life and how to help the victim if poisoning has occurred?

Chemists classify nicotine as alkaloids - nitrogen-containing substances of plant origin. This group also includes caffeine, quinine, strychnine, cocaine and some other organic compounds.

Many of them have a common feature - the ability to influence the processes taking place in the body. Some alkaloids are considered poisons and medicines at the same time, it all depends on the amount of the substance. Nicotine can also be a medicine, but it is much more commonly referred to as a dangerous toxin.

The chemical formula of this substance is C 10 H 14 N 2. It looks like a clear oily liquid, which darkens and turns yellowish brown during storage. The smell of the substance is pungent, the taste is burning. The density of nicotine practically does not differ from that of water, therefore it mixes well with it. With acids it forms salts, which also dissolve well in water.

Nicotine is a poison that is extremely dangerous to insects and cold-blooded animals. Therefore, a century ago it was used as an insecticide. Later it was proved that this substance is also dangerous to humans and other warm-blooded creatures. Therefore, it was replaced by more harmless artificial derivatives such as imidacloprid or acetamiprid.

Where can you find nicotine

Everyone knows that nicotine is in tobacco, but it is also found in other plants of the nightshade family, for example, in all the familiar tomatoes and peppers, but there its concentration is low, so it does not threaten a person. There are traces of nicotine in other plants, for example, in horsetail, baloon, or sedum.

Nicotine alkaloids can also be found in coca leaves. More than in tobacco this substance can be found only in a plant very close to it - makhorka.

But in the human body, there is normally no nicotine. He does not take part in normal metabolic processes. Theoretically, under the influence of certain enzymes, this substance can turn into nicotinic acid. It is known as vitamin PP, deficiency of which causes pellagra. But in the human body there are no enzymes capable of assimilating this toxin and converting it into a vitamin.

Although nicotine is a completely foreign substance to the human body, it is very easily absorbed through the lungs from tobacco smoke, from the digestive tract when swallowed, and even through the skin when in contact with a sufficiently concentrated solution. Once in the blood, this alkaloid quickly spreads throughout the body.

It easily penetrates the blood-brain barrier, through the placenta and other obstacles. Therefore, smoking during pregnancy is strictly contraindicated, the toxin enters the baby's blood.

After inhaling cigarette smoke, after 4-7 seconds, nicotine enters the brain. Its maximum concentration is observed approximately 10 minutes after smoking. Reducing it by half occurs only after half an hour. At the same time, the alkaloid leaves the brain.

Nicotine is excreted very slowly by the body. It disappears from the blood in about 2-3 hours. But it is possible to detect the products of its decay in the body for another one and a half to two days. The fact is that in the liver, nicotine is split into cotinine and nicotine-N-oxide. These substances are excreted by the kidneys, and it is possible to detect cotinine in urine using a test even two days after smoking a cigarette.

After entering the bloodstream, this alkaloid acts on the nerve endings, which determines its effect. In low concentrations, it acts on acetylcholine receptors, causing the following effects:

• Strengthening the production of adrenaline;
• Increase in blood pressure and vasoconstriction;
• Increased heart rate;
• The entry into the blood of glucose stored in the liver in the form of glycogen;
• Release in the brain of substances that form a psychostimulating effect.

After that, a slight dizziness appears, which in someone is accompanied by an almost imperceptible derealization, to someone it resembles a flight. For many, a cigarette helps to concentrate and collect. But this is not always the case. The first cigarette you smoke often causes nausea, headache, and disgust.

If you increase the dose of nicotine, the nerve synapses will begin to be depressed, which can provoke the appearance of unpleasant symptoms. Although it is this effect that makes cigarettes the main sedative for many people.

Nicotine is believed to be a drug. Indeed, if you smoke a lot and for a long time, psychological and physical dependence develops. But it has not yet been established whether it is caused by nicotine or other substances in the composition of cigarette smoke. In many people, addiction forms only psychological or does not appear at all.

The toxic effect of nicotine

Pure nicotine is a strong poison. Only 0.5-1 mg / kg of this substance is enough to kill a person. To assess its toxicity, it is worth saying that the lethal dose of the well-known potassium cyanide is much less and amounts to 1.7 mg / kg. But during smoking, most of the toxin contained in tobacco flies away with the smoke, and only about 20-30% enters the lungs.

Considering that cigarettes rarely contain more than 0.8 mg of nicotine, it is difficult to get serious poisoning when smoking.

In medicine, cases of fatal poisoning from smoking have been recorded. But these were competitions or bets between smokers and they "smoked" cigarettes or pipes.

To significantly worsen the state of health, sometimes it is enough to smoke several cigarettes in a row. But do not blame all the unpleasant symptoms on the effect of nicotine. There are other harmful substances in tobacco that can negatively affect human health. Typically, symptoms of nicotine poisoning include:

• Pallor and dizziness;
• Heart rhythm disorder;
• Excessive agitation or apathy;
• Chills and cold sweats;
• Blurred vision and ringing in the ears;
• Nausea, drooling, and vomiting;
• Diarrhea;
• Weakness.

In the most dangerous situations, convulsions can begin.

It should be noted that, although the likelihood of nicotine poisoning when smoking is minimal, this habit cannot be considered not harmful. Long-term exposure to small doses of the toxin leads to damage to almost all body systems - respiratory, cardiovascular, digestive, etc. Smokers may eventually develop gastritis, atherosclerosis, arrhythmias and coronary heart disease, lung cancer and many other diseases.

Nicotine alkaloid intoxication can be acute or chronic. The first type is found in those who have never smoked (or almost never smoked) and have suddenly received a large dose of the substance. All of the symptoms described above usually show up in them. Chronic poisoning occurs in experienced smokers.

Smokers rarely suffer from nicotine intoxication. This can happen if you smoke for a very long time and a lot. In such a situation, the toxin is deposited on the mucous membranes of the respiratory tract and is heated there. Having reached a critical amount, it causes poisoning. Usually, smokers with experience do not immediately notice unpleasant symptoms and therefore delay the visit to the hospital, aggravating the situation.

Nicotine can be severely poisoned by swallowing it. Adult chewing tobacco users usually control the amount. But a child, finding a cigarette or tobacco, can taste it and get serious intoxication. Sometimes the symptoms of poisoning appear very quickly in an acute form, so the child has to be rescued in a hospital setting.

You can get severe poisoning with nicotine, even with a fatal outcome, by drinking an insecticide containing it. But it is unlikely that you will be able to find a suitable composition, since they have long been considered obsolete.

Secondhand smoke can also cause poisoning if you have to spend a lot of time in a smoky room. Previously, workers in tobacco factories often suffered from this. But modern precautions have ruled out this possibility.

How to help a person with nicotine poisoning

It is not easy to independently determine that a person has been poisoned by nicotine. Therefore, it is better to call the doctors right away.

While waiting for an ambulance, you can try to flush the stomach if the substance has been swallowed and then drink enterosorbent. If the toxin got in another way, it is enough to provide the victim with a comfortable position and rest. With severe tremors or seizures, care must be taken so that the patient does not harm himself.

You should not give the victim any medication, except for enterosorbents. It is difficult for a layperson to predict how this or that drug will affect a person's condition; it is better to just stay with him and try to support him until the doctors arrive.

Poisoning treatment

In most cases, no treatment is required for the poisoned. Gradually, all unpleasant symptoms go away, leaving only an aversion to tobacco.

If poisoning occurs with concentrated nicotine, for example, in an insecticide, such intoxication is treated in a hospital setting. Supportive therapy and cleansing of the body are usually required.

The benefits of nicotine

The toxicity of many substances depends on their concentration and method of application. This also applies to nicotine. Tablets, gum, and patches containing this substance can help you quit smoking.

Research is also underway in which nicotine acts as a treatment for ADHD, Alzheimer's and Parkinson's disease, shingles, and many others. Perhaps, over time, nicotine will become the basis for new drugs and begin to benefit humanity.