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Nicotine's Effects on Meal Patterns in Rats
Scientists have conclusively proven that nicotine decreases meal size in rats. When administered intravenously, nicotine treated rats ate 20% less food overall. As a result, these rats gained less weight than the control group. There is evidence that corticotropin releasing factor agonists can alter meal structure and decrease overall food intake. During light periods, rats ate significantly less when administered nicotine, but treated rats seemed to increase frequency of taken meals during the night, suggesting compensatory behavior. Post-cessation, it was discovered that the rats that were treated with nicotine gained weight at a faster rate than the controls.

Nicotine Self Administration on Types of Foods
A study was performed to measure the effects on nicotine self administration (NSA) and its effects on the consumption of bland chow compared to sucrose chow. The study found that the decrease in food intake during nicotine treatment may be more selective in the type of foods preferred. Rats administered nicotine displayed a selective decrease in bland food consumption compared to sucrose consumption. This effect was prominent during the cessation phase, where formerly administered rats displayed significant increases in sucrose consumption especially. The implications of this study suggest that post-cessation increases in weight gain are related to dietary preferences, and that treatment in humans should focus on counteracting increases in carbohydrate consumption.

Nicotine Neuroscience in Humans
The popular believe that nicotine decreases appetite and promotes weight loss has been investigated in animals and humans. Research has concluded that nicotine effects the melanocortin system (MC) in the brain, which regulates appetite and body weight. Increased activity in MC receptors is shown to promote weight loss and decrease food intake. The activity in the MC depends on two neuron populations, POMC and AgRP. When calorie intake is decreased, these neurons POMC activity is decreased and AgRP activity is increases, which causes weight to be regained. Research concluded that nicotine activates POMC neurons and increases their communication with MC receptors, thus causing sustained appetite decrease and enabling weight loss.

Stimulants and Malnutrition
Because of their weight loss effects, and a cultural shift in favorability of productivity, many Americans have adopted regular stimulant use to increase their capacity to work and lose weight. Stimulant use appetite suppression can cause deficiencies in crucial nutrients. Two of the most popular stimulants are nicotine and caffeine. Counselors have began to focus on the symptoms of unhealthy stimulant use beyond behavior issues by investigating the physical symptoms that come with stimulant associated malnutrition. In one article, particular drugs of interest were cocaine, amphetamine, and MDMA. Cocaine and amphetamines were reported to be associated with the most significant vitamin deficiencies. Reports conclude that cocaine is commonly associated with depletions of the vitamin B complex and vitamin C. Vitamin B deficiencies can cause decreasing in total motor function, with prominent symptoms of muscle tension, spasms, anemia, cold extremities, poor coordinations, and decrease in energy associated with ATP production. Vitamin C deficiencies can cause decreased immune function, sore gums, tooth decay, poor wound healing, and dry mouth and eyes. Amphetamines are commonly linked to anemia and blood clots. Overall, all stimulants cause weight loss and decreased appetite, which can be associate with malnutrition.

The Health Consequences of Nicotine
Since nicotine and other stimulants are all psychoactive substances, there is an inherent psychological connection to this research inquiry.

The controversy surround nicotine is its typical method of administration. Nicotine is the addictive substance in tobacco products. Tobacco has been the subject of 50 years of federally funded studies. Tobacco use has been found to be the leading cause of premature death in the United States. A common form, smoking, is found to decrease relative life expectancy by at least 10 years compared to non-users. Tobacco use has been linked to cardiovascular and respiratory disease, several types of cancer, and birth defects.

Policy Targeting Tobacco Use
Because of the health risks associated with tobacco use, there have been numerous attempts to implement policy to lessen the public health burden of tobacco products. Since nicotine is the primary addictive ingredient in tobacco products, the regulation of nicotine levels in tobacco products is a common target for policy. Regulatory action on tobacco use includes the outlawing of use in public spaces, workplaces, and tax increases along with mandatory price minimums. These policies have been limitedly effective, reducing nicotine use about 1% a year at best. Manufacturers have advertised "light" products as safer, touted for filters and less nicotine induction. A new FDA policy initiative sought to evaluate the reinforcement threshold for nicotine compared to the addiction threshold. The premise of this initiative is that the addiction threshold is difficult to determine outside of a controlled environment, while determining the reinforcement threshold may be a more practical approach to determining any future nicotine-content regulations. The primary limits of this concept is that these measurements are very subject on a user basis. Users are affected by a combination of habits, mentality, administration method, as well as psychological and biological predispositions, therefore it would be difficult to speculate an effective nicotine content level that would create an effective policy.

Nicotine Cessation and Weight Gain
An important obstacle in any policy initiative is to examine the rationale behind continued use. Understood to be an anorectic, nicotine is commonly used in weight reduction. About one third of college smokers report that they use nicotine to control their weight. The anorectic properties of nicotine are commonly associated with a lack of desire to quit. This is also due to the association of smoking cessation with weight gain. Studies have examined the nicotine's effects on metabolic weight compared to effects on caloric intake. Caloric intake is found to increase by between 250-300 calories per day during the first few weeks after cessation. This is regarded as a key aspect of withdrawal. After the suspected withdrawal period, results are much less consistent. It is understood that the inability to curb appetite after cessation is a common reason for relapse. Nicotine has found to have an acute increase on metabolic rate. it has been found that both smokers and nonsmokers experience this metabolic effect, with no differences based on tolerance. Decreased caloric intake, however, has been determined to decrease with tolerance. This study encourages further investigation into the length and effects of the withdrawal period, and the effects on metabolic rate, including effects of smoking on physical activity and its associate effect on metabolism.

Nicotine Cessation and Set-Point Theory
To further evaluate nicotines psychological impact on human behavior, including the relapse related to weight gain avoidance and its use as an anorectic, researchers returned to the physiology of nicotine associated effects on weight. Researchers examined the response to sweet-stimuli on nicotine users and nonusers. The study found that oral and transdermal nicotine did not decrease the initial palatability of sweet stimuli, but accelerated the onset of displeasure by repeated ingestion. In other words, nicotine is suspected to make subjects cease eating faster. It was concluded that nicotine use acutely lowers the bodyweight set point throughout the duration of usage. Cessation related weight gain could therefore be understood as the removal of the condition that was lowering the set point induced by nicotine. Using this determination, cessation related weight gain could be combatted through the lens of creating healthier diet and exercise habits, and engineer psychological treatment to communicate to ex-users that weight gain is simply the body's recalibration following use. Emphasizing this, and de-stigmatizing the effects of cessation while empowering those seeking help would be important in preventing relapse because of a desire to avoid weight gain.