Drugs 2010; 70 (12): 1487-1503

THERAPY IN PRACTICE 0012-6667/10/0012-1487/$55.55/0

ª 2010 Adis Data Information BV. All rights reserved.

Laxative Abuse
Epidemiology, Diagnosis and Management
James L. Roerig,1,2 Kristine J. Steffen,2 James E. Mitchell1,2 and Christie Zunker 2
1 Department of Clinical Neuroscience, University of North Dakota School of Medicine and Health
Sciences, Fargo, North Dakota, USA
2 Neuropsychiatric Research Institute, Fargo, North Dakota, USA

Contents
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1487
1. Introduction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1488
2. Gastrointestinal Functioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1489
3. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1490
3.1 Eating Disorders. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1490
3.2 Habitual Laxative Abuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1490
4. Presentation/Diagnosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1491
5. Types of Laxatives. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1493
5.1 Stimulant Laxatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1493
5.1.1 Diphenylmethane Derivatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1493
5.1.2 Anthraquinone Derivatives. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1494
5.1.3 Castor Oil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1494
5.1.4 Colorectal Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1495
5.2 Bulk-Forming Laxatives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1495
5.3 Saline Laxatives. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1495
5.4 Osmotic Laxatives. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1495
5.5 Surfactants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1496
5.6 Lubricants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1496
6. Medical Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1496
6.1 Electrolyte Disturbances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1496
6.2 Metabolic Disturbances. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1497
6.3 Bowel Disturbances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1497
6.4 Kidney Disturbances. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1497
6.5 Miscellaneous Disturbances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1498
7. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1498
8. Summary and Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1499

Abstract Laxatives have been used for health purposes for over 2000 years, and for
much of that time abuse or misuse of laxatives has occurred. Individuals who
abuse laxatives can generally be categorized as falling into one of four groups.
By far the largest group is made up of individuals suffering from an eating
disorder such as anorexia or bulimia nervosa. The prevalence of laxative abuse
has been reported to range from approximately 10% to 60% of individuals in
this group. The second group consists of individuals who are generally middle
aged or older who begin using laxatives when constipated but continue to
overuse them. This pattern may be promulgated on certain beliefs that daily
1488 Roerig et al.

bowel movements are necessary for good health. The third group includes
individuals engaged in certain types of athletic training, including sports with
set weight limits. The fourth group contains surreptitious laxative abusers
who use the drugs to cause factitious diarrhoea and may have a factitious
disorder.
Normal bowel function consists of the absorption of nutrients, electrolytes
and water from the gut. Most nutrients are absorbed in the small intestine,
while the large bowel absorbs primarily water. There are several types of
laxatives available, including stimulant agents, saline and osmotic products,
bulking agents and surfactants. The most frequently abused group of laxa-
tives are of the stimulant class. This may be related to the quick action of
stimulants, particularly in individuals with eating disorders as they may er-
roneously believe that they can avoid the absorption of calories via the re-
sulting diarrhoea.
Medical problems associated with laxative abuse include electrolyte and
acid/base changes that can involve the renal and cardiovascular systems and
may become life threatening. The renin-aldosterone system becomes acti-
vated due to the loss of fluid, which leads to oedema and acute weight gain
when the laxative is discontinued. This can result in reinforcing further
laxative abuse when a patient feels bloated and has gained weight.
Treatment begins with a high level of suspicion, particularly when a pa-
tient presents with alternating diarrhoea and constipation as well as other
gastrointestinal complaints. Checking serum electrolytes and the acid/base
status can identify individuals who may need medical stabilization and con-
firm the severity of the abuse. The first step in treating laxative misuse once it
is identified is to determine what may be promoting the behaviour, such as an
eating disorder or use based on misinformation regarding what constitutes a
healthy bowel habit. The first intervention would be to stop the stimulant
laxatives and replace them with fibre/osmotic supplements utilized to estab-
lish normal bowel movements. Education and further treatment may be re-
quired to maintain a healthy bowel programme. In the case of an eating
disorder, referral for psychiatric treatment is essential to lessen the reliance on
laxatives as a method to alter weight and shape.

1. Introduction who are generally middle aged or older who begin

For more than 2000 years, purgative use has
been an important element in medical therapy.
However, laxatives are increasingly used as a
method of weight control.[1] Individuals who
abuse laxatives can generally be categorized as
falling into one of four groups. The first includes
those with eating disorders, a group of patients
who are well known to have a high prevalence of
laxative abuse.[2] In light of the high prevalence of
laxative abuse in this group, reported to range
from approximately 10% to 60%, we review it in
detail. The second group consists of individuals
using laxatives when constipated, but who con-
tinue to overuse them to the point that their
bowel becomes relatively refractory to the laxa-
tives.[3] Considering that normal stool frequency
on a Western diet is at least three times a week,
excessive use may begin with the belief that daily
bowel evacuation is necessary for good health.[4]
It can also be the result of increased constipation
associated with a variety of causes including poor
diet, decreased mobility or concomitant drug
therapy. As these patients become dependent on
laxatives, it becomes increasingly hard to inter-
vene. Both of these use patterns are associated

ª 2010 Adis Data Information BV. All rights reserved. Drugs 2010; 70 (12)
Laxative Abuse
with medical complications that may have a sig-
nificant impact on the health of the patient, and
highlight the need for early detection and inter-
vention. The third group includes individuals
engaged in certain types of athletic training,
including sports with set weight limits. The sub-
group here that has perhaps been best char-
acterized includes wrestlers, who take laxatives as
a way to drop weight.[5] The fourth group con-
tains surreptitious laxative abusers who use the
drugs to cause factitious diarrhoea and may have
a factitious disorder.[6,7]
Eating disorder patients constitute the largest
group of individuals who abuse laxatives and are
certainly the best characterized. These patients
may initially take laxatives in response to con-
stipation. This is particularly true of patients with
anorexia nervosa who, because of low food in-
take and dehydration, frequently have problems
with constipation. However, most eating disorder
patients take laxatives to induce diarrhoea in or-
der to feel thinner, and in an attempt to get rid of
unwanted calories and lose weight. Often, laxa-
tives are misused following eating binges, when
the individual mistakenly believes that the laxa-
tives will work to rush food and calories through
the gut before they can be absorbed and, thus,
will prevent calorie absorption and weight gain.[8]
Obviously, these individuals are very concerned
about weight and shape, and see laxative abuse as
one method of controlling their bodyweight. This
abuse sets up a vicious cycle in which they become
dehydrated because of fluid loss, retain fluid be-
cause of the renin-angiotensen response to dehy-
dration, gain fluid weight and then need to use
the laxatives again to dehydrate themselves. Also,
because their bowels become relatively refractory
to laxatives, they need to escalate the dose to get
the same effect, and eventually develop patterns
of using large amounts of laxatives.[9] The goal of
this review is to acquaint the practitioner with the
epidemiology, presentation and management of
laxative abuse.
2. Gastrointestinal Functioning
The main function of the gastrointestinal (GI)
tract is the extraction of fluid and nutrients from
ª 2010 Adis Data Information BV. All rights reserved.
1489
the contents present in the lumen. Nutrients are
absorbed mainly by the small intestine and the
right colon absorbs mainly water and electro-
lytes. As faecal matter moves into the left colon,
it becomes more formed.[10] Control of the GI
tract involves intrinsic and extrinsic innervation.
The intrinsic innervation involves the enteric
nervous system,[11-13] and comprises myenteric,
submucosal and mucosal neuronal layers. Nor-
mal functioning of these layers involves inter-
neurons and utilizes neurotransmitter amines
and/or peptides, including acetylcholine, vaso-
active intestinal peptide, opioids, noradrenaline
(norepinephrine), serotonin, adenosine triphos-
phate and nitric oxide. The myenteric plexus
regulates smooth-muscle function. The submu-
cosal plexus regulates secretion, fluid transport
and vascular flow.[14,15] The extrinsic innerva-
tion of the GI tract involves the parasympathetic
autonomic nervous system which modulates
motor and secretory functions. The excitatory
neurotransmitters controlling motor function are
acetylcholine and the tachykinins, such as sub-
stance P.
Ultimately, fluid content is important in the
determination of stool consistency and volume,
with water accounting for 70–85% of total stool
weight. A balance exists between the ingestion
and secretion of water and electrolytes into the
GI tract and the absorption over its length. Eight
to ten litres of fluid enter the small intestine daily.
Due to osmotic gradients, absorption of water in
the small intestine reduces the fluid presented to
the large bowel to only 1–5 L. The colon extracts
most of the remaining fluid, leaving about
100 mL of faecal water daily. This process can be
altered by neurohumoral mechanisms, pathogens
and drugs. The extent of water absorption is also
influenced by the GI transit time. Colon motility
is made up of two types of contractions: non-
propulsive contractions provide a mixing func-
tion and propulsive contractions move the
contents of the bowel toward the rectum. Slowed
GI motility results in a slower GI transit time,
allowing more water to be absorbed, which can
lead to constipation. Rapid transit time results in
less water absorption, with the potential for re-
sulting diarrhoea.[14,15]
Drugs 2010; 70 (12)
1490
Various drugs can affect this system. The use
of anticholinergic drugs such as benztropine or
diphenhydramine results in a slowing of the GI
tract with the potential for constipation. On the
other hand, a variety of drugs have a prokinetic
effect on the bowel. These include cholinergic
agents (bethanechol), acetylcholinesterase inhibi-
tors (neostigmine or donepezil), dopamine-receptor
antagonists (metoclopramide), serotonin enhancing
drugs such as selective serotonin reuptake inhibi-
tors, and motilin receptor agonists (erythromycin
and other macrolide antibiotics).[16-18]
3. Epidemiology
3.1 Eating Disorders
Studies investigating the prevalence of laxative
abuse are complicated. Virtually all investiga-
tions rely on self report and many have used dif-
ferent criteria to define laxative abuse. Overall,
the lifetime occurrence of laxative abuse has been
reported to be 4.18% in the general popula-
tion.[19] However, the authors reported that the
rates are substantially higher in people who suffer
from an eating disorder. The lifetime occurrence
among individuals with bulimia nervosa was
14.94%, greater than a 3-fold increase over the
prevalence in the general population. Other stud-
ies have reported that laxative abuse among
patients with bulimia nervosa range from 18% to
75%.[20-22] In a consecutive series of 100 patients
with bulimia nervosa, Mitchell et al.[23] reported
finding that 36% had abused laxatives for weight
control purposes during the month prior to eva-
luation. More recently, Steffen et al.[24] reported
that laxatives had been used at some point to
control weight or ‘‘get rid of food’’ by 67% of 39
eating disorder patients surveyed. Of these, 31%
reported abuse of laxatives during the month
prior to evaluation. Phelps et al.[1] studied the
prevalence of laxative abuse over time in adoles-
cent females. They surveyed students on three
occasions (1984, 1989 and 1992). Prevalence of
laxative use for weight control remained rela-
tively stable over the time period, ranging from
3.2% to 5.5% of those in high school and 0–1.8%
of those in middle school (ages 13–15 years).
ª 2010 Adis Data Information BV. All rights reserved.
Roerig et al.
Recently, Steffen and colleagues[25] explored the
use of herbal laxatives and found that of 100
participants with eating disorder symptoms, 26%
reported having used a herbal laxative at some
point in time.
A difference in the prevalence of laxative
abuse between eating disorder diagnoses may
exist. A study compared subjects with bulimia
nervosa – purging subtype (BN-P) and eating
disorders not otherwise specified – purging only
(EDNOS-P) with controls.[26] Laxative abuse was
utilized significantly more frequently in the
EDNOS-P group than by BN-P subjects (62% vs
27%; p < 0.04) as their purging method, while
vomiting was more frequently used in the BN-P
group than by EDNOS-P subjects (86% vs 38%;
p < 0.001). A study in adolescents diagnosed with
anorexia nervosa examined laxative use via self-
report and biochemical laboratory evaluation,
which included serum electrolytes, calcium,
magnesium and phosphate levels, and urinary
laxative screening for the stimulant laxatives
bisacodyl, phenolphthalein and rhein.[27] Cau-
tion should be utilized when monitoring laxative
use via laboratory assessment; difficulties with
assays for senna and bisacodyl have recently
been reported.[9] The frequency of laxative use
from self-report alone was 12% and when com-
bined with urine screening was 19%. With pro-
spective follow-up, the frequency of laxative
use increased to 32%. By all accounts, laxative
abuse is not uncommon in patients with eating
disorders.
3.2 Habitual Laxative Abuse
Unfortunately, the prevalence of chronic
laxative use is difficult to quantify in light of the
condition often being overlooked or the diag-
nosis being made only after extensive investiga-
tions have proven negative.[28,29] Studies suggest
that the prevalence of constipation is as high as
50% in the elderly, which increases to 74% of
nursing home residents using daily laxatives.[30-32]
However, this probably under-represents the true
impact of constipation and subsequent medical
use, as many people either do not seek medical
attention or use over-the-counter remedies (either
Drugs 2010; 70 (12)
Laxative Abuse
alone or in combination with those prescribed by
their physician).
The elderly are a group of individuals with
unique health challenges and different medical
needs than their younger counterparts. The high
frequency of laxative use in the elderly may be
caused, in part, by underestimation of stool fre-
quency.[30] This can lead them to plan their
schedules around their bowel movements. Un-
fortunately, laxative treatments in these patients
often precipitate loose stools and incontinence.
Subsequently, they may present to their health-
care provider with diarrhoea of unknown origin.
Habitually used laxatives constitute an important
cause of chronic diarrhoea in these patients.[33]
Extensive medical investigations and an increase
in the lengths of hospital stays are associated with
diarrhoea of unknown origin. However, there are
many people who are well served by chronic
laxative use, such as patients with chronic con-
stipation due to slow colonic transit or pelvic
floor dysfunction.
4. Presentation/Diagnosis
The most important factor in making the
diagnosis of laxative abuse is a high index of
suspicion on the part of the clinician. If possible,
objective evidence for laxative abuse should be
obtained. However, laxative use is often carried
out in secret and patients may be less than
forthcoming regarding self report. The only sign
that has been found to be suggestive of chronic
laxative use is melanosis coli, a non-pathological,
reversible, pigmentation of the colon associated
with anthraquinone use.[34] A pattern of diar-
rhoea alternating with constipation, as well as
other GI symptoms, may be reported. A variety
of laboratory tests are helpful in determining the
diagnosis. Serum hypokalaemia in eating dis-
order patients has been suggested to be definitive
evidence of purging, including by laxative use.[35]
In the presence of culture-negative diarrhoea,
faecal electrolytes can aid in diagnosis.[33] This
analysis includes quantification of the osmolality,
the electrolyte composition and the pH level of
stool water, with the calculation of the osmotic
gap.[36-38] Diarrhoea caused by stimulant laxa-
ª 2010 Adis Data Information BV. All rights reserved.
1491
tives (such as bisacodyl), is associated with an
osmotic gap that is small; in patients with ele-
vated magnesium levels, the gap is much greater.
Faecal magnesium concentration testing can aid
in determining the presence of abuse with a
magnesium-containing laxative. Fine and collea-
gues[39] reported that the upper limits of faecal
output of soluble magnesium and faecal magne-
sium concentration in healthy volunteers were
14.6 mmol/day and 45.2 mmol/L, respectively.
They defined a concentration of magnesium above
50 mmol as diarrhoeogenic. For pure magnesium-
induced diarrhoea (without additional laxatives
such as phenolphthalein), stool magnesium con-
centration in excess of 100 mmol indicate the use
of a magnesium-containing laxative such as milk of
magnesia. Laboratory tests for the presence of
laxatives themselves are found in table I.
Many patients report that the feeling of having
emptied themselves is associated not only with
gratification resulting from the apparent weight
loss but also with a sense of purification.[41] Eating
disorder patients also believe that laxatives can
reduce nutrient absorption. However, most nu-
trient absorption occurs in the small intestine.[42]
Nutrient absorption has been reported to be re-
duced by only 12% by laxative use.[43] The patient’s
weight may be reduced slightly by the expulsion of
water leading to a temporary mood-elevating ef-
fect further reinforcing the laxative use.[8]
Several publications have suggested that
laxative abuse may characterize a more ill sub-
group of patients with eating disorders, and a
number of investigations support this observa-
tion in patients diagnosed with anorexia nervosa.
A group of anorexia nervosa patients who abuse
Table I. Laboratory screening for laxative abuse[40]
Analyte Duration of detection
Anthraquinones – cascara, 150 mg dose: 32 hours post dose
danthron, senna (mg/mL)
Bisacodyl (mg/mL) 5 mg dose: 32 hours post dose
Oxyphenisatin (mg/mL)a 10 mg dose: 18 hours post dose
Phenolphthalein (mg/mL)a 150 mg dose: 32 hours post dose
Magnesium (mg/L) Faecal water sample
Phosphorus (g/L) Calculated normal: 0.3–1.1 g/L
a No longer on the market.
Drugs 2010; 70 (12)
1492
laxatives have been reported to have higher
scores on histrionic personality assessments.[44]
Kovacs and Palmer[41] assessed 117 patients di-
agnosed with anorexia nervosa. They found that
22 (18.8%) used laxatives for weight control.
Subjects abusing laxatives were rated higher on
the Ineffectiveness, Body Dissatisfaction and
Drive for Thinness subscales of the Eating Dis-
order Inventory, and on the depression, somati-
zation and global scores on the Symptom
Checklist-90-Revised. They also scored higher on
the Rosenberg Self-Esteem Scale (RSES),[45]
suggesting lower self-esteem. In this series of
adults, logistic regression revealed that in subjects
with anorexia nervosa, body dissatisfaction
(p < 0.002) and RSES scores (p < 0.033) were signif-
icant predictors of laxative abuse. Furthermore,
the association of lower ‘self-liking’ in subjects
suffering from anorexia nervosa and laxative
abuse and self-induced vomiting has recently
been reported.[46] A multiple regression was then
performed to determine the relative contributions
of each of these purging methods. Laxative abuse
was determined to be the sole contributor to
lower self-liking. These results suggest the possi-
bility that laxative abuse is distinct from other
types of purging by its association with self-liking
rather than self-competence. This is in line with
data indicating a significant association between
laxative abuse and lower self-esteem.[41] The di-
rection of this association has yet to be elucidated.
In patients diagnosed with bulimia nervosa,
there is ample data associating more severe
symptomology with laxative use. Bryant-Waugh
and colleagues[47] examined laxative use in 201
consecutive patients in an outpatient eating dis-
order population. Those who misused laxatives
were compared with those who did not. Fifty-
three (26.4%) patients had misused laxatives in
the month before assessment. Those who misused
laxatives scored higher on measures of anorectic
behaviours and cognitions, restraint, and weight
and shape concerns. A history of use was asso-
ciated with anorectic behaviours, depression and
an increase in clinical severity, regardless of
diagnosis. In a study of 23 bulimia nervosa
patients who purged with laxatives and 17 who
purged by vomiting, women who abused laxa-
ª 2010 Adis Data Information BV. All rights reserved.
Roerig et al.
tives had higher levels of state anxiety than non-
laxative-abusing women after laxative use was
discontinued.[48] This study also found that the
patients who abused laxatives were more likely to
be treated with an antianxiety medication. Fifty-
nine percent of a sample of 280 bulimia nervosa
patients were found to abuse laxatives.[44] In this
sample, patients with a laxative abuse history
were found to demonstrate greater perfectionism
and avoidant personality features. Subsequently,
40 ‘multi-impulsive’ bulimia nervosa patients
were compared with 177 non-impulsive sub-
jects.[49] A significantly greater likelihood of
laxative abuse was found in the impulsive group.
Another study evaluated the association of im-
pulsivity and compulsivity in 125 patients with
bulimia nervosa.[50] Laxative abuse was demon-
strated to be associated with the impulsive
dimension. Thus, impulsivity appears to be a per-
sonality characteristic that is frequently found in
patients who abuse laxatives.
In a large community sample of young adult
women (n = 5255), the 39 individuals who mis-
used laxatives were found to be older, perceived
themselves to be in poorer physical health and
were less likely to have sought treatment specifi-
cally for a problem with eating than those who
engaged in self-induced vomiting.[51] However,
they found little evidence that young adult women
who engage in self-induced vomiting differ from
those who misuse laxatives with respect to levels of
eating disorder psychopathology, health-related
quality of life and general psychological distress.
In contrast, recent findings suggest that mea-
sures of greater illness were associated with the
number of purging methods used and not asso-
ciated with the type of purging method.[52] In this
study, the authors reported similar levels of pa-
thology between subjects who used a single
method of purging (vomiting or laxative abuse)
and greater eating pathology in those who used
both methods. Behavioural co-morbidity found
in laxative-abusing individuals may include af-
fective disorders,[8,53,54] substance abuse,[22,55-57]
self-destructive behaviours,[54] collateral purge
methods[22] and general life impairments.[58]
A group of 43 adolescents diagnosed with an-
orexia nervosa was investigated in terms of eating
Drugs 2010; 70 (12)
Laxative Abuse
symptomology.[27] The results showed that laxa-
tive use was associated with a longer duration of
disease and with higher scores on the Eating
Concern subscale of the Eating Disorders Exam-
ination (EDE). Laxative abuse has also been
shown to predict lower quality of life in eating
disordered samples,[59] and to be associated with a
number of other variables suggestive of greater
severity, including increased rates of self-harm
and suicidal behaviours and increased rates of
borderline personality disorder (BPD).[2,60] Anal-
ysis of symptoms revealed that specific features
of BPD, including suicidality and self-harm, and
feelings of emptiness and anger, were most
strongly associated with laxative abuse.[2]
While urinary screening for laxatives may
increase the detection of laxative use, so can mon-
itoring for medical complications such as hypo-
kalaemia. Monitoring serum electrolytes as well
as faecal electrolytes, such as magnesium, may be
more cost effective.[61] Turner and colleagues[27]
reported performing 144 screens for laxatives,
which yielded only 26 positive results.
In summary, the abuse of laxatives appears to
be a marker for high rates of co-morbidity and
other problematic behaviours among individuals
with eating disorders. These patients will often
not wish to reveal their laxative abuse and it falls
on the clinician to investigate the possibility of
this condition. Serum and faecal electrolytes rep-
resent an effective screening tool in patients who
present with diarrhoea and additional GI com-
plaints. Urine analysis for individual laxatives
may be best reserved for more difficult cases. As
indicated earlier, caution should be utilized when
monitoring laxative use via laboratory assess-
ment in light of recent difficulties with assays for
senna and bisacodyl.[9]
5. Types of Laxatives
Table II lists commonly used laxatives, their
onset of effect and daily dose. Laxatives generally
act in one of the following ways: (i) enhancing
retention of fluid by hydrophilic or osmotic
mechanisms; (ii) decreasing net absorption of
fluid by effects on small and large bowel fluid and
electrolyte transport; or (iii) altering motility by
ª 2010 Adis Data Information BV. All rights reserved.
1493
either inhibiting segmenting (nonpropulsive)
contractions or stimulating propulsive contrac-
tions.[64] All of the agents, with the exception of
docusate calcium, reduce the transit time through
the small bowel. Most of the agents enhance
propulsive contractions in the large bowel and
variably increase the amount of stool water. Of
the laxative classes, stimulant types appear to be
the most commonly abused agents.[42,65] This
preference for stimulant agents may be related to
the rapid, high-volume faecal discharge asso-
ciated with these products. Of the 248 products
surveyed by Steffen et al.,[24] 89 (36%) contained a
nonprescription stimulant laxative (not including
aloe-containing compounds). In their sample of
treatment-seeking patients with bulimia nervosa,
ex-lax was the most commonly used laxative.
This agent currently contains sennosides.
5.1 Stimulant Laxatives
There are two pharmacological classes of stimu-
lant laxatives: diphenylmethane derivatives (bisaco-
dyl) and anthraquinones (senna and cascara). Some
authors also include castor oil in the stimulant class.
5.1.1 Diphenylmethane Derivatives
Previously, many of the over-the-counter
laxative preparations utilized phenolphthalein as
the active ingredient; however, concerns over
carcinogenicity led the US FDA to ban it from
laxative preparations in 1997. Ironically, two
subsequent case-controlled studies could not
identify an association of phenolphthalein and
ovarian cancer.[66,67] These discrepant findings
may be explained by the dosage (3–1000 times the
human dose) used in the animal studies upon
which the FDA based its ruling.[68,69] Currently,
the only diphenylmethane agent in use is bisaco-
dyl. This agent stimulates peristalsis by directly
irritating the smooth muscle of the intestine. It
also alters water and electrolyte secretion, produc-
ing net intestinal fluid accumulation. Bisacodyl is
well tolerated; adverse effects include mild
abdominal cramps, nausea, vomiting and rectal
burning. The tablets are manufactured with a
pH-sensitive coating so the agent will not dissolve
in the stomach or upper GI tract. If taken with
Drugs 2010; 70 (12)
1494 Roerig et al.

Table II. Selected laxatives[25,62,63]

Agent Onset of action Daily dose
Stimulant laxatives
Diphenylmethane derivatives
Bisacodyl Oral: 6–8 hours Oral: 10–15 mg daily
Rectal: 1 hour Rectal: 10 mg daily
Anthraquinone derivatives
Senna 8–12 hours Varies by product
Cascara sagrada 8–12 hours
Ricinus communis
Castor oil 2–6 hours 15–60 mL/day (90 mL for emulsion)
In fasting patient, 4 mL may be effective
Bulk-forming laxatives
Psyllium preparations Days Typically 1 tablespoon, 1–3 times daily
Methylcellulose Days 1 tablespoon, 1–3 times daily
Calcium polycarbophil 12–24 hours 1 g, 1–4 times daily
Maximum daily dose 5 g/day
Saline laxatives: watery evacuation
Sodium phosphates 1–6 hours 20–45 mL/day
Magnesium sulfate 3–6 hours 30–60 mL/day of the 400 mg/5 mL suspension
Magnesium hydroxide (milk of magnesia) 6–24 hours 30–60 mL/day of the 400 mg/5 mL suspension
Magnesium citrate 3–6 hours 150–300 mL (usually used preprocedure)

Osmotic laxatives: watery evacuation

Lactulose 6–48 hours Oral: 30–45 mL, 3–4 times daily
Polyethylene glycol <4 hours 4 L preprocedure

Surfactant laxatives: softening of faeces

Docusates 12–72 hours Docusate sodium: 50–200 mg daily
Docusate calcium: 240 mg daily
Lubricants
Glycerin 0.5–3 hours One suppository (3 g) daily
Mineral oil 6–8 hours 15–45 mL once or twice daily

dairy products or antacids, the coating will dis-
solve while the dose is in the stomach and upper
GI tract; any action of bisacodyl in these areas
will produce cramping.
5.1.2 Anthraquinone Derivatives
Anthraquinones (senna and cascara) are me-
tabolized by gut bacteria to active agents. A
distinguishing effect of these compounds is a
colouring of the bowel referred to as pseudome-
lanosis coli or melanosis coli. Its presence is
associated with 9–12 months of anthraquinone
use and can be used to identify abuse of these
agents.[70] A controversial link between pseudo-
melanosis coli and colorectal cancer has been re-
ported.[71] In fact, the anthraquinone laxative
danthron was withdrawn from the market be-
cause of tumour formation in laboratory ani-
mals. Both agents are well tolerated. Senna can
cause abdominal cramps, diarrhoea, nausea and
vomiting. Cascara has similar adverse effects and
can discolour the urine (reddish, pink or brown).
5.1.3 Castor Oil
Castor oil is derived from the bean of the cas-
tor plant, Ricinus communis. It contains two
noxious ingredients: an extremely toxic protein,
ricin, and an oil composed chiefly of the trigly-
ceride of ricinoleic acid. These agents can pro-
duce a strong laxative effect with accompanying
abdominal pain.

ª 2010 Adis Data Information BV. All rights reserved. Drugs 2010; 70 (12)
Laxative Abuse
5.1.4 Colorectal Cancer
Concerns have been voiced regarding the as-
sociation of long-term use of stimulant laxatives
and the development of colorectal cancer. Long-
term administration of bisacodyl has been re-
ported to be toxic to the GI tract. Disturbed
cytoplasmic and nuclear structure have been dem-
onstrated in rat small-intestinal enterocytes.[72] A
meta-analysis did find an association between
colorectal cancer and constipation and cathartic
use.[73] However, it appears that these data were
confounded by the underlying dietary habits of
the subjects. A case-controlled study involving
middle-aged adults[74] found an association be-
tween constipation and laxative use and an in-
creased risk of colorectal cancer. However, the
association with laxatives disappeared when the
data were adjusted for constipation. The asso-
ciation remained for constipation when adjusted
for laxative use. Thus, it appears that the factor
increasing the risk of colorectal cancer is con-
stipation and not the laxative abuse. Additional
studies question the colorectal cancer associa-
tion. An investigation by Nusko and collea-
gues[75] found no association between colorectal
cancer and melanosis coli or laxative use. The
results of a 26-week study in the transgenic mice
strain p53+/- revealed neither drug-related neo-
plasm nor micronuclei in polychromatic ery-
throcytes, and did not induce transformations in
the in vitro Syrian hamster embryo assay.[76]
Subsequent studies have also not found an asso-
ciation;[73,74,77-81] hence, the FDA has categorized
bisacodyl as category I (safe and effective). The
human evidence appears not to support an asso-
ciation between stimulant cathartics and colo-
rectal cancer. Various authors also question the
toxic potential of stimulant laxatives,[82,83]
particularly neuronal toxicity leading to cathartic
colon.
5.2 Bulk-Forming Laxatives
Bulk, softness and hydration of faeces depend
on the fibre content of the diet. Fibre is the part of
food that does not undergo enzymatic digestion.
It reaches the colon largely unchanged. Colonic
bacteria ferment fibre to varying degrees, depen-
ª 2010 Adis Data Information BV. All rights reserved.
1495
ding on its chemistry and water solubility. Most
of the bulk laxative formulations include a deri-
vative of semi-synthetic fibre (methylcellulose),
psyllium or polycarbophil (a hydrophilic resin).
Others contain fibre or bran products. These
agents are usually manufactured as a powder to
be mixed with fluids (water or juice). They absorb
water in the intestine to form a viscous liquid that
promotes peristalsis and reduces transit time.
Insoluble, poorly fermentable fibres have the
greatest effect on increasing bulk.
Bulk-forming laxatives soften the faeces.[15,84]
Bile acid binding such as with psyllium may reduce
the production of low-density lipoprotein.[85-87]
Bulk-forming laxatives have a slow onset of ac-
tion (between 12 and 72 hours) and substantial
relief from constipation may take several months
of continued use. Due to the longer onset of ac-
tion, eating disorder patients find these agents
inadequate to control weight. Adverse effects
with these agents are generally mild and include
bloating, allergic reactions and flatulence.[71]
Specific contraindications exist, including use in
patients with obstructive symptoms and in those
with megacolon or megarectum.[15]
5.3 Saline Laxatives
Many saline laxatives contain magnesium
salts. Their use results in an increase in osmotic
pressure in the bowel, which aids in water reten-
tion. In addition, magnesium salts may stimulate
the secretion of cholecystokinin, which increases
intestinal secretion and motility.[15] The onset of
action is dose dependent, with lower doses having
an onset of effect in 6–8 hours. The onset of effect
for higher doses can be less than 3 hours, such as
with the use of magnesium citrate to evacuate the
bowel prior to surgical and diagnostic proce-
dures.[15] Adverse effects of these agents include
hypotension, hypermagnesaemia, abdominal
cramps, diarrhoea, gas formation and respiratory
depression (see section 6).
5.4 Osmotic Laxatives
An increase in osmotic pressure in the gut lu-
men is also caused by osmotic laxatives. They
remain unabsorbed and are not digested in the
Drugs 2010; 70 (12)
1496
small intestine. Lactulose is metabolized to form
fructose and galactose then converted to lactate,
acetate and formate. Lactulose helps to reduce
the intestinal absorption of ammonia. It has fre-
quently been used to manage hepatic encephalo-
pathy associated with hepatic failure, although its
efficacy for this purpose is controversial.[88] This
agent is generally well tolerated, and adverse ef-
fects including flatulence, cramping, abdominal
discomfort, nausea and vomiting. Larger doses
can cause diarrhoea, fluid loss, hypokalaemia
and hypernatraemia.
Polyethylene glycol (PEG) is an osmotic laxa-
tive supported by good-quality evidence that has
demonstrated efficacy and safety in the treatment
of patients with chronic constipation. While lac-
tulose is more effective in relieving constipation
than placebo, it is less effective than PEG. PEG is
used prior to procedures such as a colonoscopy.
Patients are instructed to drink 4 L of a PEG so-
lution, which results in a watery bowel evacua-
tion. Fluid and electrolyte status is not altered.
Adverse effects include urticaria, abdominal
bloating, cramping, diarrhoea, flatulence and
nausea.[89]
5.5 Surfactants
The docusate compounds are often used as
stool-softening agents. They may be combined
with other laxatives such as the stimulant com-
pounds. Docusate calcium reduces the surface
tension of the oil-water interface of the stool. This
results in the incorporation of water and fat, with
resultant stool softening. These agents have lim-
ited, if any, efficacy in most cases of constipa-
tion.[15] Adverse effects of these compounds are
mild and include abdominal cramps, rashes and
nausea.
5.6 Lubricants
Mineral oil acts as a laxative by decreasing
water absorption in the colon, as well as lubricat-
ing the intestine. Onset of action is approximately
6–8 hours if administered orally and 2–5 minutes
with rectal administration. This agent is not re-
commended for use in the elderly as aspiration
may occur with resulting lipid pneumonitis.
ª 2010 Adis Data Information BV. All rights reserved.
Roerig et al.
Glycerin is a trihydroxy alcohol that acts as a
hygroscopic agent and lubricant when given re-
ctally as a suppository, and results in defecation
in about 30 minutes. Adverse reactions associated
with glycerin suppositories include local discom-
fort, burning or hyperaemia, and (minimal) bleed-
ing. Some glycerin suppositories contain sodium
stearate, which also can cause local irritation.
6. Medical Complications
Medical complications stemming from laxa-
tive ingestion depend on the severity of abuse, as
well as the frequency, duration and type of agent
used. Problems may be confined to the GI tract
or involve systemic features. The most frequent
complication of laxative abuse is obviously diar-
rhoea. GI cramping and pain may present with
the diarrhoea due to stool volume and a direct
effect of the laxative on intestinal motility. Fre-
quency of stools may reach 15–20 per day.[3]
Medical complications can be divided into dis-
turbances involving electrolytes, metabolic is-
sues, bowel, kidney and miscellaneous effects.
6.1 Electrolyte Disturbances
Medical complications of laxative abuse are
often a result of chronic diarrhoea and the asso-
ciated severe electrolyte disturbances. Potassium
is the primary electrolyte in stool water
(70–90 mmol/L), with lower concentrations of so-
dium and chloride (30–40 and 15 mmol/L, respec-
tively). With the development of hypokalaemia,
the patient may present with generalized muscle
weakness and lassitude.[90] Additionally, the pre-
sentation may include skeletal muscle paralysis,
or rhabdomyolysis with renal impairment, and
nerve palsies. More severe hypokalaemia can re-
sult in cardiac arrhythmias with an increased risk
of sudden death.[3,91] Severe hypokalaemia has
been associated with distal renal tubular acidosis
in laxative abuse.[92,93] With the expulsion of an
added volume of stool water, dehydration, hypo-
tension, tachycardia, postural dizziness and syn-
cope may occur. Renin secretion with secondary
hyperaldosteronism can develop with chronic
dehydration. Hypermagnesaemia associated with
Drugs 2010; 70 (12)
Laxative Abuse
large doses of magnesium-containing laxatives has
presented with quadriparesis and neuromuscular
junction defects.[94] Recently, it has been reported
that patients with congestive heart failure (CHF)
but normal renal function who presented with
hypermagnesaemia had a lower rate of 3-year sur-
vival than patients with normal magnesium levels.
These subjects also had a greater antacid/laxative
use profile: 82.7% versus 24.8% (p < 0.0001).[95]
Patients with pre-existing renal dysfunction are at
an increased risk of adverse effects with saline
laxatives. However, acute phosphate nephro-
pathy is an accepted complication of the use of
phosphate preparations in patients about to un-
dergo to colonoscopy. Patients’ CHF may be
exacerbated due to the sodium content.
6.2 Metabolic Disturbances
Acid-base disturbances are possible with
laxative use. Metabolic alkalosis is the most
common acid-base disturbance associated with
laxative use, and is related to hypokalaemia,
volume contraction and secondary hyper-
aldosteronism. Concomitant purging by vomit-
ing may increase the risk of developing metabolic
alkalosis. Additional acid-base disturbances in-
clude hypochloraemic metabolic alkalosis and
secondary complications such as increased renal
ammoniagenesis,[96] which promotes bicarbonate
reabsorption in the renal tubule. Laxative abuse
has also been reported to cause GI dysfunction,
particularly pancreatic damage.[97] In a small
study, Brown et al.[98] compared 18 recovered
anorexia nervosa patients with age- and weight-
matched controls. Ten of the 18 anorexia nervosa
patients had a history of laxative abuse; these
subjects showed a more gradual increase and de-
crease in insulin secretion in response to a
standard meal, but no differences in glucose res-
ponse or hunger ratings. The authors concluded
that the difference in insulin response is due to
changes in the enteroinsular axis induced by
chronic laxative abuse.
6.3 Bowel Disturbances
Bowel dysfunctions including colonic mucosa
inflammation and ulceration, ileocaecal sphincter
ª 2010 Adis Data Information BV. All rights reserved.
1497
dilation, colonic neuropathy, steatorrhoea and
protein-losing gastroenteropathy have been re-
ported with laxative abuse.[99-106] Other presen-
tations include GI bleeding[107] and dehydration
with various electrolyte abnormalities.[108] Diar-
rhoea may alternate with periods of constipation,
which causes the patient to enter a vicious cycle
alternating between the two.
Direct toxicity to the small intestinal mucosa
may be a GI complication of laxative use that
leads to steatorrhoea. Rarely, fat-soluble vitamin
malabsorption leads to osteomalacia and pseu-
dofractures.[3] Progressive laxative dosing ob-
served in some laxative users may be attributed to
hypofunctioning in bowel processes, loss of in-
trinsic innervation action and laxative tolerance
effects.[100] However, controversy exists regard-
ing the effect of senna laxatives on bowel in-
nervation and function. The adverse effects and
toxicity of stimulant-type laxatives often include
constipation[102] and cathartic colon, which is
defined as a loss of colonic myenteric neurons,
atrophy of smooth muscle, loss of haustral
markings, increased submucosal fat, fibrosis and
hypertrophy of the muscularis mucosae.[3,103,109]
Barium enema procedures have shown the term-
inal ileum to be smooth, without a normal mu-
cosal pattern.[8] However, contrary to the widely
held belief, stimulant laxatives, which promote
intestinal motility, do not seem to lead to bowel
injury.[83,109] Recently, Morales and collea-
gues[110] concluded that there is no convincing
evidence that the long-term use of senna causes a
structural and/or functional alteration of the en-
teric nerves or the intestinal smooth muscle.
Supporting these findings is the absence of
reports of cathartic colon since the removal of
phenolpthalein from clinical use. They also re-
port that current evidence does not show that
there is a genotoxic risk for patients who take
laxatives containing senna extracts or sennosides.
6.4 Kidney Disturbances
Prolonged laxative abuse is also associated
with chronic kidney disease and can lead to
renal failure.[111] Renal function is reduced by a
combination of several factors, including severe
Drugs 2010; 70 (12)
1498
hypokalaemia, volume depletion, rhabdomyolysis
and hyperuricaemia. In addition, some laxatives
are nephrotoxic and cause renal tubular damage.[3]
Urolithiasis has also been reported in conjunction
with laxative abuse.[112] Wright and DuVal[92] re-
ported five cases of laxative-associated renal da-
mage with electrolyte abnormalities.
6.5 Miscellaneous Disturbances
Recently, laxative use has been reported as a
complication in four of seven patients with rectal
prolapse and the diagnosis of bulimia nervo-
sa.[113] Causality in these cases was uncertain.
A patient intermittently abusing cascara over
2 years was reported to have developed gastric
melanosis.[114] Recently, paraesthesias and fasci-
cular and ventricular tachycardia were reported
to be associated with an Ayurveda bowel regi-
men.[115] The preparation included substrates
from the Aconitum species, Aconitum hetero-
phyllum (atvish), Aegle marmelos (bilwa), Pavo-
nia adorata (suganda bala), Cyperus rotundus
(musta), Picrorrhiza kurrooa (kutki) and Holar-
rhena antidysenterica (vatsaka). A. heterophyllum
(atvish), also known as aconite, monkshood or
wolfsbane, was thought to be the most likely of-
fending agent in this combination. Aconite roots
contain aconitine, mesaconitine, hypaconitine
and other aconitum alkaloids, which are known
cardiotoxins and neurotoxins.[115,116]
7. Treatment
The best technique for withdrawing individuals
from laxatives has not been systematically ascer-
tained. Whether a patient is habitually abusing
laxatives or using them surreptitiously, the main
goals of treatment are to stop the laxative use and
maintain healthy GI function. However, as a first
step, the patient’s beliefs regarding the laxative
use have to be determined. If the patient is ex-
pressing erroneous beliefs regarding the normal
number and frequency of bowel movements,
education is essential. If the person is suffering
from an eating disorder, an appropriate treat-
ment plan for the particular eating disorder
should be enacted. In addition, eating disorder
ª 2010 Adis Data Information BV. All rights reserved.
Roerig et al.
patients have been reported to have difficulties
with increasing anxiety with laxative discontinua-
tion.[48] This may be related to the retention of
fluid with a subsequent increase in weight. The
patient may also experience further constipation,
which may result in a strong drive to continue to
take laxatives. Close supervision is required
during this time to ensure that the laxative with-
drawal is successful.
Another risk that needs to be appreciated in
laxative withdrawal is the development of CHF.
This problem is illustrated by the case of a
60-year-old woman who presented with hypoka-
laemia and weakness.[117] She was consuming a
laxative combination of phenolphthalein and
rhubarb in doses above the package recom-
mendation. On presentation her potassium was
2.6 mmol/L. She had no signs of CHF at that
time. The laxatives were withdrawn and oral po-
tassium supplements started. Over the next
10 days she began to experience oedema, a weight
gain of 15 kg and breathlessness. By day 10, her
chest radiograph showed cardiomegaly and bi-
lateral pleural effusions. Furosimide and capto-
pril were initiated. She recovered over the next
2 weeks. The depletion of sodium and water
through diarrhoea leads to an increase in renin
secretion with secondary hyperaldosteronism.
Water retention develops with oedema and, in
this case, the development of CHF. Oedema fol-
lowing laxative withdrawal is not uncommon,
but usually subsides over a period of weeks as
sodium balance becomes re-established.
Several protocols have been published regard-
ing the intervention methods designed to reduce and
eliminate the use of laxatives. Harper et al.[118]
reported a 6-month prospective trial evaluating
a pharmacist-supervised, blinded withdrawal pro-
tocol. Ten eating disorder patients were enrolled
in the trial and seven completed the study. Five of
the seven reduced their laxative intake by at least
50%. Three of the seven withdrew completely
from laxative use. Their protocol called for dis-
continuation of all stimulant laxatives with the
substitution of docusate calcium, psyllium and
fruit lax, a mixture of natural ingredients (senna
leaves, pitted prunes, figs, pitted dates, dark rai-
sins), as tolerated. In addition, a combination of
Drugs 2010; 70 (12)
Laxative Abuse
30 mL of Magnolax (formula per mL: magne-
sium hydroxide 60 mg and mineral oil 0.25 mL)
and 30 mL of cascara was initiated in a dose that
was based on the patient’s previous dose of bisa-
codyl or an equivalent. The liquid was reduced by
5 mL every 3–7 days until no longer needed (see
table III). The withdrawal protocol included
patient education concerning normal eating and
bowel habits.
Colton et al.[119] reported on the results of their
laxative withdrawal protocol at 3 and 20 months’
follow-up. Subjects included all patients admitted
for laxative withdrawal in their eating disorders
programme between 1993 and 1995. They were
assessed with a shortened version of the EDE.[120]
Their programme consists of the following com-
ponents: initial contact, which includes abrupt
discontinuation of the laxative; an immediate
withdrawal stage (before the first normal bowel
movement), involving the provision of non-laxa-
tive aids to normal bowel function and psycho-
education; and, lastly, the desensitization stage
(after the first normal bowel movement). The fi-
nal stage initially includes visiting a pharmacy
with a staff member and no money with which to
buy laxatives, and progresses through to visiting
the pharmacy alone with money and not pur-
chasing laxatives. Aids to normal bowel function
progress over the month and initially include
bulk-forming agents with fluids, stool softeners
and glycerin suppositories. In the second half of
the month, if need be, they progress to a small
clear-water enema and, ultimately, the addition
of an irrigation agent. This programme resulted
in 57% of patients being abstinent from laxatives
at follow-up and significant reductions in laxative-
related symptom variables.
Table III. Laxative taper used in a pharmacist supervised blinded
withdrawal protocol (reproduced from Harper et al.,[118] with per-
mission)
Magnolax/cascara Previous laxative dose
Magnolax 30 mL/cascara 30 mL <20 bisacodyl 5 mg tablets/day
Magnolax 45 mL/cascara 45 mL 20–40 bisacodyl 5 mg tablets/day
Magnolax 60 mL/cascara 60 mL 40–60 bisacodyl 5 mg tablets/day
Magnolax 90 mL/cascara 90 mL >60 bisacodyl 5 mg tablets/day
ª 2010 Adis Data Information BV. All rights reserved.
1499
8. Summary and Conclusion
Abuse of laxatives is not an uncommon oc-
currence in the general population and is quite
frequent among certain groups, such as in those
with eating disorders. Both patients with anor-
exia nervosa and bulimia nervosa utilize laxatives
in an attempt to reduce weight and remove un-
wanted calories, neither of which is possible with
laxatives. Other groups that may utilize laxatives
in an unhealthy way include athletes, middle-
aged adults and the elderly. The motivation in the
elderly group is often based on rigid and some-
times false conceptions about the need for daily
bowel movements. This type of use can be diffi-
cult to identify as the individual may start out with
legitimate constipation related to other disease
states or concomitant medication use. However,
when the frequency and duration of use exceeds
the need, medical complications may occur.
Stimulant laxatives are the more frequent type
of laxative used in the eating disorder population.
Also, the presence of laxative abuse has been re-
ported to be associated with greater psycho-
pathology by some, but not all, investigators.
Certainly, the use of such a drastic purging
method places these patients at greater risk than a
person who does not purge.
In severe cases, the individual may present
with electrolyte and acid/base changes that can
involve the renal and cardiovascular systems and
may become life threatening. Due to the loss of
fluid, the renin-aldosterone system becomes ac-
tivated, which leads to oedema and acute weight
gain when the laxative is discontinued.
Treatment begins with a high level of suspi-
cion, particularly when a patient presents with
alternating diarrhoea and constipation as well as
other GI complaints. Checking serum electrolytes
and the acid/base status can identify individuals
who may need medical stabilization. At times, it
may also be helpful to check the stool water for
electrolytes, particularly magnesium, which may
be associated with abuse of magnesium-contain-
ing laxatives. Once stable, any stimulant laxatives
should be discontinued and a fibre/osmotic supple-
ment utilized to establish normal bowel movements.
Health education is of paramount importance in
Drugs 2010; 70 (12)
1500
order to enable patients to alter their diet and
bowel habits so as to avoid the need for future
laxative use. In the case of a suspected or con-
firmed eating disorder, the patient should be
referred for psychiatric treatment to lessen the
reliance on laxatives as a method to alter weight
and shape.
Acknowledgements
No sources of funding were used to assist in the prepara-
tion of this review. James Mitchell has received a research
grant from GlaxoSmithKline to study orlistat (Alli). The
other authors have no conflicts of interest that are directly
relevant to the content of this review.
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Correspondence: Professor James E. Mitchell, President,
Neuropsychiatric Research Institute, 120 8th St South,
Fargo, ND 58102, USA.
E-mail: jmitchell@nrifargo.com
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