question: Why does caffeine increase urges to use the bathroom?
comment: Caffeine causes kidneys to filter more body fluids than usual, which increases urine production, hence increasing the frequency of bathroom use
passages: In many cases, these symptoms may be exacerbated by the consumption of certain foods or beverages, such as caffeine, particularly coffee, regular tea, green tea, soda, diet soda and fruit juice. Cranberry juice, for example, may cause extreme urgency in those experiencing such urgency.
  
  Section::::Causes.:Non-medical causes.
   Doses of caffeine equivalent to the amount normally found in standard servings of tea, coffee and carbonated soft drinks appear to have no diuretic action. However, acute ingestion of caffeine in large doses (at least 250–300 mg, equivalent to the amount found in 2–3 cups of coffee or 5–8 cups of tea) results in a short-term stimulation of urine output in individuals who have been deprived of caffeine for a period of days or weeks. This increase is due to both a diuresis (increase in water excretion) and a natriuresis (increase in saline excretion); it is mediated via proximal tubular adenosine receptor blockade. The acute increase in urinary output may increase the risk of dehydration. However, chronic users of caffeine develop a tolerance to this effect and experience no increase in urinary output.
   Because caffeine is both water- and lipid-soluble, it readily crosses the blood–brain barrier that separates the bloodstream from the interior of the brain. Once in the brain, the principal mode of action is as a nonselective antagonist of adenosine receptors (in other words, an agent that reduces the effects of adenosine). The caffeine molecule is structurally similar to adenosine, and is capable of binding to adenosine receptors on the surface of cells without activating them, thereby acting as a competitive antagonist.
   Caffeine can be quantified in blood, plasma, or serum to monitor therapy in neonates, confirm a diagnosis of poisoning, or facilitate a medicolegal death investigation. Plasma caffeine levels are usually in the range of 2–10 mg/L in coffee drinkers, 12–36 mg/L in neonates receiving treatment for apnea, and 40–400 mg/L in victims of acute overdosage. Urinary caffeine concentration is frequently measured in competitive sports programs, for which a level in excess of 15 mg/L is usually considered to represent abuse.
  
  Section::::Chemistry.:Analogs.
   Caffeine acts in multiple ways within the brain and the rest of the body. However, due to the concentration of caffeine required, antagonism of adenosine receptors is the primary mode of action. The following mechanisms are ways in which caffeine may act within the body, but depending on necessary caffeine concentration and other factors may not be responsible for the clinical effects of the substance.
  
  Section::::Mechanism of caffeine action.:Mobilization of intracellular calcium.
   In the absence of caffeine and when a person is awake and alert, little adenosine is present in (CNS) neurons. With a continued wakeful state, over time adenosine accumulates in the neuronal synapse, in turn binding to and activating adenosine receptors found on certain CNS neurons; when activated, these receptors produce a cellular response that ultimately increases drowsiness. When caffeine is consumed, it antagonizes adenosine receptors; in other words, caffeine prevents adenosine from activating the receptor by blocking the location on the receptor where adenosine binds to it. As a result, caffeine temporarily prevents or relieves drowsiness, and thus maintains or restores alertness.
   Caffeine is capable of increasing work capacity while individuals perform strenuous tasks. In one study, caffeine provoked a greater maximum heart rate while a strenuous task was being performed compared to a placebo. This tendency is likely due to caffeine's ability to increase sympathetic nerve outflow. Furthermore, this study found that recovery after intense exercise was slower when caffeine was consumed prior to exercise. This finding is indicative of caffeine's tendency to inhibit parasympathetic activity in non-habitual consumers. The caffeine-stimulated increase in nerve activity is likely to evoke other physiological effects as the body attempts to maintain homeostasis.
   Thus, by disrupting this process with acetazolamide, urinary Na and bicarbonate (HCO) are increased, and urinary H and Cl are decreased. Inversely, serum Na and bicarbonate (HCO) are decreased, and serum H and Cl are increased. HO generally follows sodium, and so this is how the clinical diuretic effect is achieved, which reduces blood volume and thus preload on the heart to improve contractility and reduce blood pressure, or achieve other desired clinical effects of reduced blood volume such as reducing edema or intracranial pressure.
  
  Section::::History.
   Section::::Mechanism of caffeine action.:Antagonism of adenosine receptors.
   Urininary urgency may be as a result of anxiety or in some cases extended sexual arousal. When a human male is attracted to a mate, there is an autonomic nervous system response, and the body is therefore not entirely under conscious control, with many hormones including norepinephrine being released in the parasympathetic system in a cascade of ways designed by genetics to make the male more likely to breed. Specifically, the release of norepinephrine will lead to sweaty palms, inability to find words, rough and lowered voice, increased need to blink and urinary urgency. 
   Section::::Causes.
  
  Common causes include, but not limited to:
  
  BULLET::::- Incomplete emptying of the bladder
  
  BULLET::::- Irritable bladder
  
  BULLET::::- Constipation
  
  BULLET::::- Stress
  
  BULLET::::- Urinary tract infection
  
  BULLET::::- Urgency (not “making it” to the bathroom in time)
  
  BULLET::::- Anatomic abnormality
  
  BULLET::::- Poor toileting habits
  
  BULLET::::- Small bladder capacity
  
  BULLET::::- Medical conditions like overactive bladder disorder
  
  Section::::Management.
   Section::::Results.:Alcohol and caffeine.
   Caffeine is a bio-active ingredient found in commonly consumed beverages such as coffee, tea, and sodas. Short-term physiological effects of caffeine include increased blood pressure and sympathetic nerve outflow. Habitual consumption of caffeine may inhibit physiological short-term effects. Consumption of caffeinated espresso increases parasympathetic activity in habitual caffeine consumers; however, decaffeinated espresso inhibits parasympathetic activity in habitual caffeine consumers. It is possible that other bio-active ingredients in decaffeinated espresso may also contribute to the inhibition of parasympathetic activity in habitual caffeine consumers.
   The structure of caffeine allows the molecule to pass freely through biological membranes including the blood-brain barrier. Absorption in the gastrointestinal tract reaches near completion at about 99% after only 45 minutes. Half-life of caffeine for most adults is between 2.5 and 4.5 hours when consumption is limited to less than 10 mg/kg. However, during neonatal development, half-life for the fetus is significantly longer and decreases exponentially after birth to reach a normal rate at about 6 months.
   A secondary effect of loop diuretics is to increase the production of prostaglandins, which results in vasodilation and increased blood supply to the kidney.
  
  The collective effects of decreased blood volume and vasodilation decrease blood pressure and ameliorate edema.
  
  Section::::Pharmacokinetics.
   Section::::Interactions.:Tobacco.
  
  Smoking tobacco increases caffeine clearance by 56%.
  
  Section::::Interactions.:Birth control.
  
  Birth control pills can extend the half-life of caffeine, requiring greater attention to caffeine consumption.
  
  Section::::Interactions.:Medications.
  
  Caffeine sometimes increases the effectiveness of some medications, such as those for headaches. Caffeine was determined to increase the potency of some over-the-counter analgesic medications by 40%.
  
  The pharmacological effects of adenosine may be blunted in individuals taking large quantities of methylxanthines like caffeine.
  
  Section::::Pharmacology.
  
  Section::::Pharmacology.:Pharmacodynamics.
   A 2011 review found that increased caffeine intake was associated with a variation in two genes that increase the rate of caffeine catabolism. Subjects who had this mutation on both chromosomes consumed 40 mg more caffeine per day than others. This is presumably due to the need for a higher intake to achieve a comparable desired effect, not that the gene led to a disposition for greater incentive of habituation.
  
  Section::::Chemistry.
   BULLET::::- Attention deficit hyperactivity disorder (ADHD) Children with ADHD are 2.7 times more likely to have bedwetting issues.
  
  BULLET::::- Caffeine Caffeine increases urine production.
  
  BULLET::::- Constipation Chronic constipation can cause bed wetting. When the bowels are full, it can put pressure on the bladder. Often such children defecate normally, yet they retain a significant mass of material in the bowel which causes bed wetting.
   Symptomatic treatment usually involves analgesics for both cranial and spinal CSF leaks. Caffeine and short-term bed rest can alleviate symptoms of low CSF pressure, while elevated rest and acetazolamide can alleviate symptoms of high CSF pressure.
   BULLET::::- Aldosterone release: This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.
   An influx of Ca produces increased intracellular cAMP levels and thus, an increase in motility. Hyperactivation coincides with the onset of capacitation and is the result of the increased Ca levels. It has a synergistic stimulatory effect with adenosine that increases adenylyl cyclase activity in the sperm.
   Section::::Short-term memory.:Time-of-day effects.
   The consumption of caffeinated drinks is often intended entirely or partly for the physical and mental effects of caffeine. Examples include the consumption of tea or coffee with breakfast in many westernized societies, in order to 'wake oneself up', or the deliberate consumption of energy drinks by students wishing to study through the night, or revellers seeking to maintain an alert attitude during social recreation. Caffeine can cause a physical dependence, if consumed in excessive amounts. The need for caffeine can be identified when individuals feel headaches, fatigue and muscle pain 24 hours after their last energy drink.
   In more physiologically based studies, scientists have found that while the reticular formation controls alertness, wakefulness, and arousal in the brain, many mental responses to internal and external stimuli are dictated through signals relayed to and from the thalamus. Propofol and other consciousness-altering drugs are therefore antagonists of thalamus activity, possibly leading to a drug-induced comatose state.
  
  Section::::Theories.:Modern-day perspectives.
   Section::::Long-term memory.
  
  Caffeine has been shown to have positive, negative, and no effects on long-term memory. When studying the effects of this and any drug, potential ethical restraints on human study procedures may lead researchers to conduct studies involving animal subjects in addition to human subjects.
  