What is meant by Remote Diuretics & Remote Vomiting?

What is meant by Remote Diuretics & Remote Vomiting?

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I have encountered the terms Remote Diuretics & Remote Vomiting separately or sometimes in association in various articles related to medicine.

But I am unable to find any reference to what they actually mean.

Can you help me understand these terms please?



Urine sodium less than 10 mmol/L indicates extrarenal loss of urine (remote diuretic use and remote vomiting).


Go to google and search for "remote diuretic" to get more references, some are:

"Remote" can mean distant/far away, often in space but also in time (as in, the "remote past"). In just the search results you included in your question it is fairly clear that these sources are using the word "remote" to mean (relatively)"far away in time" or simply "not recent."

For example:

associated with remote diuretic use, therefore, diuretic effects were already washed off

Referring to diuretic use in the past, so there is not current diuretic effect but the secondary consequences are still present.

Note that these terms are quite uncommon in the literature, I get 21 results in Google Scholar for "remote diuretic" and 16 for "remote vomiting" and nearly all seem to be related to the specific context of hypokalemia.

Monitoring (medicine)

In medicine, monitoring is the observation of a disease, condition or one or several medical parameters over time.

It can be performed by continuously measuring certain parameters by using a medical monitor (for example, by continuously measuring vital signs by a bedside monitor), and/or by repeatedly performing medical tests (such as blood glucose monitoring with a glucose meter in people with diabetes mellitus).

Transmitting data from a monitor to a distant monitoring station is known as telemetry or biotelemetry.

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Nature and Nurture

In addition to linking eating disorders to genetics, other researchers are exploring the interplay of both genetics and the environment. In the face of certain stressors, it appears that some people who are genetically predisposed to the condition may develop the disorder.

Figure 2. Lori Zeltser, a developmental neuroscientist and associate professor of pathology and cell biology at Columbia University. (Photo courtesy of Lori Zeltser.)

Lori Zeltser, a developmental neuroscientist and associate professor of pathology and cell biology at Columbia University (Figure 2), has studied the brains of developing mice, trying to identify feeding circuits that increase susceptibility to obesity in adulthood. Zeltser published a paper in a 2016 issue of Translational Psychiatry in which she reported on mice with a variant in a gene that in people is linked to anorexia. On its own, the variant didn’t seem to make much of a difference in mouse behavior. But when the mice were given diets restricting calories by 20%–30% and then subjected to stress which included isolation, they stopped eating [4].

“Some people try to draw a false dichotomy by arguing the primacy of either nature or nurture,” says Zeltser. “Our research using mouse models suggests that it is the combination of genetic and environmental risk factors that drives susceptibility to anorexia.”

Her research raises interesting questions about how environmental stressors, including stress spurned on by life lived in a social media world (or more recently, life lived in isolation during a pandemic), might lead some kids toward anorexia. Especially if those kids happened to be trying out a fad diet to lose a few pounds.

“One lesson from our studies is that both the type and timing of the stress matters,” says Zeltser. “We have used social isolation stress in mice as a surrogate for social phobias often observed in patients with anorexia. We are finding that chronic exposure to social isolation affects feeding behaviors in response to stress. Interestingly, beginning this isolation in adolescence vs. adulthood has different effects on stress responses in males and females. The social isolation experienced during this pandemic will likely impact susceptibility to disordered eating, but the direction of the effects (i.e., promoting vs. inhibiting eating) will likely depend on the age and biological sex of the individual, severity of the isolation and genetic factors.”

Research conducted by Joanna Steinglass, professor of clinical psychiatry at Columbia University (Figure 3), has revealed differences in MRI brain scans of people with eating disorders and those without. In people with anorexia, MRI scans revealed that the region of the brain associated with selecting foods was the dorsal striatum, which is a key region involved in forming habits. In people without an eating disorder, a different brain region is associated with food choices.

Figure 3. Joanna Steinglass, professor of clinical psychiatry at Columbia University. (Photo courtesy of Joanna Steinglass.)

“This is meaningful on its own because it serves to underscore that there are neurobiological differences associated with this illness,” says Steinglass. “We cannot emphasize enough how important it is to remember that the symptoms of eating disorders have a neurobiological basis.”

Steinglass’ research supports the notion that persistent food restriction can become a “habit” that is initially learned through reward processes mediated by the brain’s ventral striatum but that over time switch to the dorsal striatum. There, food choices become less sensitive to an outcome and more closely tied to a trigger, like an urge to smoke a cigarette after a meal.

“By understanding the neurobiological vulnerability of some individuals, we may begin to understand why restricting food intake becomes so entrenched and so difficult to change for individuals with anorexia nervosa,” she says. “During adolescence, a lot is happening in the brain, and there may be aspects of this that create a particular period of vulnerability to the development of anorexia nervosa.”

Steinglass and her colleagues are now conducting a large NIMH-funded study examining how the brain changes during adolescence. By following teens with anorexia nervosa and their healthy peers for two years, they hope to understand whether neural systems guiding eating behavior differ between kids who respond well to initial treatment for anorexia nervosa and those who don’t. Specifically, she says, her group will test whether the neural systems associated with habit formation are contributing to illness.

Other researchers have noted other ways in which the brains of those with eating disorders differ from those without them. Walter Kaye, a psychiatrist who directs the eating disorders program at the University of California, San Diego, led a study looking at how the brains of people with anorexia behave after fasting compared to those without the disorder. In normal people, the reward and motivation brain circuits light up when receiving sugar water after a 16-hour fast. In subjects with anorexia, they don’t, or at least not to the same degree. This leads Kaye to conclude that patients can’t convert their hunger into a desire to eat. And with a diminished reward signal, they may actually interpret food as something risky, rather than rewarding.

“The distortion of signals in the brain in both depression and anorexia impact the awareness of hunger, the motivation to eat and food avoidance,” Kaye said upon the publication of the study.


Osmotic diuresis is the increase of urination rate caused by the presence of certain substances in the small tubes of the kidneys. [2] The excretion occurs when substances such as glucose enter the kidney tubules and cannot be reabsorbed (due to a pathological state or the normal nature of the substance). The substances cause an increase in the osmotic pressure within the tubule, causing retention of water within the lumen, and thus reduces the reabsorption of water, increasing urine output (i.e. diuresis). The same effect can be seen in therapeutics such as mannitol, which is used to increase urine output and decrease extracellular fluid volume. [ citation needed ]

Substances in the circulation can also increase the amount of circulating fluid by increasing the osmolarity of the blood. This has the effect of pulling water from the interstitial space, making more water available in the blood, and causing the kidney to compensate by removing it as urine. In hypotension, often colloids are used intravenously to increase circulating volume in themselves, but as they exert a certain amount of osmotic pressure, water is therefore also moved, further increasing circulating volume. As blood pressure increases, the kidney removes the excess fluid as urine. Sodium, chloride and potassium are excreted in osmotic diuresis, originating from diabetes mellitus (DM). Osmotic diuresis results in dehydration from polyuria and the classic polydipsia (excessive thirst) associated with DM. [ citation needed ]

Forced diuresis (increased urine formation by diuretics and fluid) may enhance the excretion of certain drugs in urine and is used to treat drug overdose or poisoning of these drugs and hemorrhagic cystitis. [3]

Diuretics Edit

Most diuretic drugs are either weak acids or weak bases. When urine is made alkaline, elimination of acidic drugs in the urine is increased. The converse applies for alkaline drugs. This method is only of therapeutic significance where the drug is excreted in active form in urine and where the pH of urine can be adjusted to levels above or below the pK value of the active form of drug. For acidic drugs, urine pH should be above the pK value of that drug, and converse for the basic drugs. It is because the ionization of acidic drug is increased in alkaline urine and ionized drugs cannot easily cross a plasma membrane so cannot re-enter blood from kidney tubules. This method is ineffective for drugs that are strongly protein bound (e.g. tricyclic antidepressants) or which have a large apparent volume of distribution (e.g. paracetamol, tricyclic antidepressants). [4]

For forced alkaline diuresis, sodium bicarbonate is added to the infusion fluid to make blood and, in turn, urine alkaline. Potassium replacement becomes of utmost importance in this setting because potassium is usually lost in urine. If blood levels of potassium are depleted below normal levels, then hypokalemia occurs, which promotes bicarbonate ion retention and prevents bicarbonate excretion, thus interfering with alkalinization of the urine. Forced alkaline diuresis has been used to increase the excretion of acidic drugs like salicylates and phenobarbitone, and is recommended for rhabdomyolysis. [ medical citation needed ]

For forced acid diuresis, ascorbic acid (vitamin C) is sometimes used. Ammonium chloride has also been used for forced acid diuresis but it is a toxic compound. [ medical citation needed ] Usually however, this technique only produces a slight increase in the renal clearance of the drug. Forced acid diuresis is rarely done in practice, [5] but can be used to enhance the elimination of cocaine, amphetamine, quinine, quinidine, atropine and strychnine when poisoning by these drugs has occurred.

Rebound diuresis refers to the sudden resurgence of urine flow that occurs during convalescence from acute kidney injury. [6] In acute kidney injury, particularly acute tubular necrosis, the tubules become blocked with cellular matter, particularly necrotic sloughing of dead cells. This debris obstructs the flow of filtrate, which results in reduced output of urine. The arterial supply of the nephron is linked to the filtration apparatus (glomerulus), and reduced perfusion leads to reduced blood flow usually this is the result of pre-renal pathology. [7]

The kidney's resorptive mechanisms are particularly energetic, using nearly 100% of the O2 supplied. Thus, the kidney is particularly sensitive to reduction in blood supply. This phenomenon occurs because renal flow is restored prior to the normal resorption function of the renal tubule. As you can see in the graph, urine flow recovers rapidly and subsequently overshoots the typical daily output (between 800 mL and 2L in most people). Since the kidney's resorption capacity takes longer to re-establish, there is a minor lag in function that follows recovery of flow. A good reference range for plasma creatinine is between 0.07 - 0.12 mmol/L. [8]

Immersion diuresis is caused by immersion of the body in water (or equivalent liquid). It is mainly caused by lower temperature and by pressure. [9]

The temperature component is caused by water drawing heat away from the body and causing vasoconstriction of the cutaneous blood vessels within the body to conserve heat. [10] [11] [12] The body detects an increase in the blood pressure and inhibits the release of vasopressin (also known as antidiuretic hormone (ADH)), causing an increase in the production of urine. The pressure component is caused by the hydrostatic pressure of the water directly increasing blood pressure. Its significance is indicated by the fact that the temperature of the water does not substantially affect the rate of diuresis. [13] Partial immersion of only the limbs does not cause increased urination. Thus, the hand in warm water trick (immersing the hand of a sleeping person in water to make him/her urinate) has no support from the mechanism of immersion diuresis. On the other hand, sitting up to the neck in a pool for a few hours clearly increases the excretion of water, salts, and urea. [13]

Cold-induced diuresis, or cold diuresis, is a phenomenon that occurs in humans after exposure to a hypothermic environment, usually during mild to moderate hypothermia. [14] It is currently thought to be caused by the redirection of blood from the extremities to the core due to peripheral vasoconstriction, which increases the fluid volume in the core. Overall, acute exposure to cold is thought to induce a diuretic response due to an increase mean arterial pressure. [15] The arterial cells of the kidneys sense the increase in blood pressure and signal the kidneys to excrete superfluous fluid in an attempt to stabilize the pressure. The kidneys increase urine production and fill the bladder when the bladder fills, the individual may then feel the urge to urinate. This phenomenon usually occurs after mental function has decreased to a level significantly below normal. Cold diuresis has been observed in cases of accidental hypothermia as well as a side effect of therapeutic hypothermia, specifically during the induction phase. [16] [17]



Patients with recurring heart failure (HF) following cardiac resynchronization therapy fare poorly. Their management is undecided. We tested remote hemodynamic‐guided pharmacotherapy.

Methods and Results

We evaluated cardiac resynchronization therapy subjects included in the CHAMPION (CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in New York Heart Association Class III Heart Failure Patients) trial, which randomized patients with persistent New York Heart Association Class III symptoms and ≥1 HF hospitalization in the previous 12 months to remotely managed pulmonary artery (PA) pressure‐guided management (treatment) or usual HF care (control). Diuretics and/or vasodilators were adjusted conventionally in control and included remote PA pressure information in treatment. Annualized HF hospitalization rates, changes in PA pressures over time (analyzed by area under the curve), changes in medications, and quality of life (Minnesota Living with Heart Failure Questionnaire scores) were assessed. Patients who had cardiac resynchronization therapy (n=190, median implant duration 755 days) at enrollment had poor hemodynamic function (cardiac index 2.00±0.59 L/min per m 2 ), high comorbidity burden (67% had secondary pulmonary hypertension, 61% had estimated glomerular filtration rate <60 mL/min per 1.73 m 2 ), and poor Minnesota Living with Heart Failure Questionnaire scores (57±24). During 18 months randomized follow‐up, HF hospitalizations were 30% lower in treatment (n=91, 62 events, 0.46 events/patient‐year) versus control patients (n=99, 93 events, 0.68 events/patient‐year) (hazard ratio, 0.70 95% CI, 0.51–0.96 P=0.028). Treatment patients had more medication up‐/down‐titrations (847 versus 346 in control, P<0.001), mean PA pressure reduction (area under the curve −413.2±123.5 versus 60.1±88.0 in control, P=0.002), and quality of life improvement (Minnesota Living with Heart Failure Questionnaire decreased −13.5±23 versus −4.9±24.8 in control, P=0.006).


Remote hemodynamic‐guided adjustment of medical therapies decreased PA pressures and the burden of HF symptoms and hospitalizations in patients with recurring Class III HF and hospitalizations, beyond the effect of cardiac resynchronization therapy.


Race-Based Medicine Arrives

In November, a tiny company called NitroMed unveiled results showing that its drug combo, BiDil, reduced deaths due to heart failure by half.

The results were astounding, but there was a catch. The drug was only tested on African-Americans and had previously failed to show a benefit in a broader population. An editorial in The New England Journal of Medicine by M. Gregg Bloche, a Georgetown University medical ethicist, warned of the need to manage the downside of "race-based therapeutics"--and predicted that it was only a matter of time before race was linked to the effects of other drugs.

Only six months later, Bloche seems prescient. A flood of studies has emerged showing racial differences in how patients suffer from disease--or benefit from drugs--in ailments ranging from osteoporosis to cancer. And several more have looked at the effects of drugs on particular racial groups. Many of the doctors conducting the studies are African-American.

Click here for a slide show of race- and gender-based medical differences.

There is even evidence that some drugs work differently in women than in men. For instance, aspirin seems to prevent heart attacks and cause strokes in low-risk medicine, but a controversial study showed it did the opposite in women. "There is nothing in evolutionary biology more based on genetics than whether the embryo develops into a man or into woman. But people generally haven't studied drugs this way," says Harvard researcher Paul Ridker.

Part of the problem is that clinical trials have too often focused on white men. Over the years African-Americans, in particular, have been absent from many trials.

"Much of the data we have on medicines in general have been in white populations," says Keith C. Ferdinand, a pharmacology professor at Xavier University. "How do we know that any of this is true across the board?" asks Gary Butts, an associate dean at Mount Sinai School of Medicine.

For many drugs, just doing a study looking at the effects of medicines on African-Americans might be useful. Ferdinand conducted such a trial with Crestor, a cholesterol drug from AstraZeneca . Patrick Griffith, a neurologist at the Morehose School of Medicine, conducted a trial of Aricept, the Pfizer and Eisai Alzheimer's medicine, in African-Americans. Both studies, funded by the manufacturers, found the drugs to be effective in those populations.

But issues emerged from cases where racial groups are compared, and differences are found. The labeling for AstraZeneca's cholesterol drug Crestor suggests starting the drug at a lower dose in Asians. Another AstraZeneca drug, the lung cancer pill Iressa, failed to extend life in a clinical trial but seems to have worked in Asians.

Perhaps the best-studied example is African-Americans with heart disease. Just as BiDil may have been more effective in African-Americans than others, a widely-used class of heart medicines does not work as well in black patients.

Medicines called ACE inhibitors are cornerstones of cardiology. But for reasons that are still unclear, they seem not to work as well in African-Americans. This outcome was confirmed in a recent analysis of a government-funded 33,000-patient study of blood pressure medicines. For all patients, old-fashioned diuretics, or water pills, are the preferred first treatment. But blacks do less well with ACE inhibitors.

Jackson T. Wright, a cardiologist at Case Western Reserve University who co-authored the study, says that as firms like Novartis and Merck develop new blood pressure medicines, they should be careful to look at racial subgroups.

"I have yet to see a downside to doing studies that might point out differences in populations," Wright says. "One could always envision potential harm, but thus far that has not been a major concern."

Many hope that this brief fling with differences that correlate to race and gender is just a short step on the path to using genetic tests to match a drug to a patient. Race and ethnicity may act as surrogates, either for slight genetic differences based on ancestry, or physical differences based on upbringing or environment. In the U.S., it may be a marker not only for differences in ancestry but also for differences in environment, diet, exposure to pollution and other factors.

Mount Sinai's Butts says he worries that using race to match medicine to patient is too crude a measure. Genetically speaking, race is actually a rather bad marker for genetic difference, he says. "Proceed cautiously," he warns. "It may not be race--it may be something else."

But until those tests emerge, doctors and drug companies may be eager to find something to fall back on--especially if it means they can save lives. "All I want is to pick the right drug for the right patient," says Susan Desmond-Hellmann, head of product development at Genentech . "If that's a PET scan, or if that's gender. I would caution all of us not to get too focused on a genetic test."

Robotic-Assisted Pyeloplasty for UPJO

Pyeloplasty can be curative for UPJOs. Once an obstruction is identified, Dr. Jacobs and his colleagues educate families about their options.

The Children’s Health team generally avoids pyeloplasties for newborns and often follows these younger patients for months or years without surgery, as some of these obstructions will resolve on their own. Some extenuating circumstances such, as a previous infection in the affected kidney, prompt earlier intervention.

When surgery is appropriate, Dr. Jacobs and his colleagues advise families about the differences between open and robotic surgery.

“Some families prefer open surgery and we’re happy to accommodate that, but most families opt for robotic surgery,” Dr. Jacobs says.

All of the urologic surgeons practicing at Children’s Health are certified in the Da Vinci Surgical System, which enables the team to perform pyeloplasty via 8mm incisions. The team uses the HIDES technique.

“That keeps the incisions below the bikini line and ensures that scars are not generally visible, which helps children avoid feeling self-conscious in the future,” Dr. Jacobs says.

Your Complete Guide to the Science of Hangovers

New Year's Eve is around the corner. For many of us, that means staying out late, dancing and drinking.

Thus, for some of us, the night of carousing also means a morning of hangovers.

Just in the nick of time, here's our complete guide to the science of hangovers—what we know, what we don't know, and how you can use this information to minimize your suffering.

Why Do Hangovers Happen?

Given that they're such a widespread health phenomenon, it's perhaps a bit surprising that scientists still don't fully understand the causes of a hangover. (They do, however, have a scientific name for them: veisalgia.) It's far from clear why, after all traces of alcohol have been fully expelled from your body, you can still experience a load of awful symptoms, including headache, dizziness, fatigue, nausea, stomach problems, drowsiness, sweating, excessive thirst and cognitive fuzziness.

The simplest and most familiar explanation is that drinking alcohol causes dehydration, both because it acts as a diuretic, increasing urine production, and because people who are drinking heavily for multiple hours probably aren't drinking much water during that time period. But studies examining the link between dehydration and hangovers have turned up some surprising data. One, for instance, found no correlation between high levels of the hormones associated with dehydration and the severity of a hangover. It's most likely that dehydration accounts for some of the symptoms of a hangover (dizziness, lightheadedness and thirst) but that there are other factors at work as well.

Most scientists believe that a hangover is driven by alcohol interfering with your body's natural balance of chemicals in a more complex way. One hypothesis is that in order to process alcohol, your body must convert the enzyme NAD+ into an alternate form, NADH. With an excess buildup of NADH and insufficient quantities of NAD+, the thinking goes, your cells are no longer capable of efficiently performing a number of metabolic activities—everything from absorbing glucose from the blood to regulating electrolyte levels. But this hypothesis, too, has been contradicted by data: In studies, people with severe hangovers weren't found to have lower levels of electrolytes or glucose in their blood.

The most compelling theory, at the moment, is that hangovers result from a buildup of acetaldehyde, a toxic compound, in the body. As the body processes alcohol, acetaldehyde is the very first byproduct, and it's estimated to be between 10 and 30 times as toxic as alcohol itself. In controlled studies, it's been found to cause symptoms such as sweating, skin flushing, nausea and vomiting.

Hangovers could also be driven by the way alcohol messes with your immune system. Studies have found strong correlations between high levels of cytokines—molecules that the immune system uses for signaling—and hangover symptoms. Normally, the body might use cytokines to trigger a fever of inflammatory response to battle an infection, but it seems that excessive alcohol consumption can also provoke cytokine release, leading to symptoms like muscle aches, fatigue, headache or nausea, as well as cognitive effects like memory loss or irritation.

Why Do Some People Get Hangovers More Easily?

Life, alas, isn't fair. Some people are extremely prone to hangovers, and some can drink with impunity.

It seems that genetics are partly to blame. Some people (disproportionately those of East Asian descent) have a mutation in their gene for the enzyme alcohol dehydrogenase that makes it much more effective in converting alcohol into the toxic acetaldehyde. Unfortunately, a significant part of this group also has a mutation in the gene for the enzyme that performs the next metabolic step, leading to a much slower conversion of acetaldehyde into acetic acid. As a result, excess buildup of acetaldehyde can happen quite rapidly. This is known to cause an immediate alcohol flush reaction (colloquially known as "Asian glow"), but might also play a role in hangovers the day after drinking.

There are other factors that affect who experiences hangovers most readily. After having the same number of drinks, women are more likely to experience hangovers than men, though this simply seems to be a result of the fact that women generally have a lower body weight as well: If you control for body weight and compare a man and woman with the same blood alcohol content, their chances of a hangover are similar.

There's conflicting evidence over whether hangovers become more frequent with age. Some studies have suggested [PDF] that adolescents are less likely to experience hangovers, but a recent large-scale survey showed the opposite—that, even controlling for total alcohol consumption, drinkers over the age of 40 experienced fewer and less severe symptoms. The authors noted that it's possible, though, that they consume the same amount of alcohol but with less intensity, spreading their drinks out instead of binging.

Why Do Some Drinks Cause Hangovers More Easily Than Others?

Because the ultimate cause of a hangover is, after all, alcohol, drinks that pack more alcohol into a smaller volume are naturally more likely to give you a hangover. Shots of liquor, in other words, are more dangerous than mixed drinks, beer or wine.

(Image via Verster et al.)

Beyond that, though, some drinks happen to have higher levels of congeners—traces chemicals produced during fermentation—that contribute to hangovers. Studies have shown that high-congener, darker-colored liquors like bourbon and whiskey lead to more severe hangovers than lighter-colored or clear liquors like vodka, which has none. A Dutch study systematically looked at the congener content and hangover risk of a variety of types of alcohol, producing the ranking above. One particular congener called methanol—found in highest levels in whiskey and red wine—has received a large amount of the blame, due to studies showing that it can linger in the body after all alcohol has been eliminated, perhaps accounting for the enduring effects of a hangover.

This, incidentally, could explain widely-held belief that mixing different sorts of liquor can cause a hangover—a greater variety of congeners could well lead to a wider variety of effects. It can't, however, explain any beliefs about the order of these drinks—despite the age-old adage "liquor-then-beer-you're-in-the-clear, beer-then-liquor-you've-never-been-sicker."

How Can You Prevent Hangovers?

The most effective solution is also the most obvious: Don't drink alcohol. Or, at the very least, don't drink to excess.

If you're set on drinking a fair amount, though, there are certain things you can do to minimize your change of a hangover and the severity of its symptoms, and they're all pretty intuitive. Don't drink quickly, on an empty stomach drink slowly, either on a full stomach or while eating. Food doesn't literally absorb the alcohol, but having a full digestive tract slows down the rate at which your body absorbs the drug. Additionally, even though dehydration is only partly to blame, it still plays a role, so staying hydrated while drinking alcohol can help.

How Can You Quickly Cure a Hangover?

Eggs Benedict: not a real hangover cure. (Photo via Wikimedia Commons/Amadscientist)

Is there a super food/drink/ritual that can magically removes the after-effects of a night spent binge drinking? Well, according to various local legends, you can cure a hangover by eating shrimp (Mexico), pickled herring (Germany), pickled plums (Japan) or drinking coffee (U.S.), strong green tea (China) or tripe soup (Romania). A number of popular foods and beverages—like the Bloody Mary, Eggs Benedict and even Coca-Cola—were even developed specifically to "cure" hangovers.

Unfortunately, there's no evidence that any of these homespun remedies do anything to help. There's also no evidence that the so-called "hair of the dog" technique (that is, drinking the morning after) has any effectiveness whatsoever. It might temporarily dull your senses, making you less aware of the hangover symptoms, but it does nothing to resolve the underlying physiological problems—and, of course, it can just lead to another hangover.

Other drinkers vouch for a variety of seemingly scientific cures—Vitamin B or caffeine, for instance—but studies have also failed to show that these provide any relief either.

So what can you actually do? You can lessen some of the symptoms with well-known over-the-counter drugs: non-steroidal anti-inflammatories, such as aspirin or ibuprofen (Advil), can treat headaches and other pain, while you can take stomach relief medicines (say, Tums or Pepto-Bismol) to reduce nausea.

You should NOT take acetaminophen (Tylenol) because when the liver is processing alcohol, it's especially susceptible to acetaminophen's toxic effects. You can eat food, drink water, and rest. It's boring, but at the moment, time is the only sure cure.

Is A Real Scientific Cure Around the Corner?

This past fall, the Web came alive with articles claiming that scientists are on the verge of developing a hangover-free beer. Unfortunately, a lot of the coverage overstated the science: So far, researchers have merely mixed electrolytes into light beer and showed that this caused less dehydration than normal beer. Because hangovers are the result of a bunch of other factors beyond dehydration, the new-fangled beer's no more of a hangover "cure" than drinking water along with your alcohol.

Other researchers, at Imperial College London, are working on synthetic blend of chemicals that produce the pleasant effects of alcohol with much lower levels of toxicity—which, in theory, could reduce the chance of a hangover. But the research is in very early stages, and given the rigorous approval process for drugs that actually treat diseases, it's easy to imagine that synthetic alcohol would take a while to get approval.

About Joseph Stromberg

Joseph Stromberg was previously a digital reporter for Smithsonian.


Department of Pediatrics, University of California San Diego, La Jolla, CA, USA

Sanjay K. Nigam & Kevin T. Bush

Department of Medicine, University of California San Diego, La Jolla, CA, USA

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Both authors researched data for the article, contributed substantially to discussions of the article content, wrote the manuscript and participated in the review or editing of the manuscript before submission.

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