Trastornos bioquimicos y metabolicos de la bulimia nervosa y la alimentacion compulsiva

Red de Revistas Científicas de América Latina, el Caribe, España y Portugal

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Víctor Hernández Escalante, Manuel Trava García, Raúl Bastarrachea Sosa, Hugo Laviada Molina
Trastornos bioquímicos y metabólicos de la bulimia nervosa y la alimentación compulsiva
Salud Mental, vol. 26, núm. 3, junio, 2003, pp. 9-15,
Instituto Nacional de Psiquiatría Ramón de laFuente Muñiz
México
Disponible en: http://www.redalyc.org/articulo.oa?id=58232602

Salud Mental,
ISSN (Versión impresa): 0185-3325
perezrh@imp.edu.mx
Instituto Nacional de Psiquiatría Ramón de la
Fuente Muñiz
México

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TRASTORNOS BIOQUÍMICOS Y METABÓLICOS DE LA
BULIMIA NERVOSA Y LA ALIMENTACIÓN COMPULSIVA

Víctor Hernández-Escalante*, Manuel Trava-García**, Raúl Bastarrachea-Sosa***, Hugo Laviada-Molina****

SUMMARY
Binge eating disorder (BED) patients are generally obese, whereas
obesity is infrequent in bulimia nervosa (BN) patients, who tend
to have a Body Mass Index(BMI) within normal ranges. Metabolic
disorders are common in these patients. For example, BED
patients tend towards obesity because their repeated efforts at
weight-loss produce cyclical changes in weight, which can increase
metabolic efficiency. As a result, an energy conservation state that
promotes weight gain can be induced, leading to even greater
efforts at weight-loss.Psychopathologies such as depression are
also extremely frequent in both these patient types. Both the
hypothalamus-hypophysis-adrenal (HHA) axis and serotonin
alterations may be related to decreases in leptin, which may
contribute to the genesis of eating binges in BN. Diurnal leptin
secretion patterns are altered in patients with compulsive eating
episodes, who experience cessation of normal leptinlevels two
hours after the mid-day meal. As is to be expected, obese BED
patients have a higher frequency of elevated leptin levels, which is
positively correlated to BMI. High levels of neuropeptide Y (NPY),
a strong appetite potentiator, have been reported in normal-weight
BN patients, independently of BMI. Low gastrin stimulating
neuropeptide (GRP) levels have been found in BN patients, whichact as a central level anorexigenic. Paradoxically, it is also common
to find elevated levels of an appetite inhibitor, such as
cholecystokonin-pancreomycine (CCK-PM), positively correlated
to the increase in ingested portions. Elevated beta-endorphin serum
levels have been reported, which suggest elevated opioid tone in
BN patients. A possible decrease in dipeptilpeptidase IV (DPP
IV)enzyme activity is still controversial. This decrease inactivates
glucagon, which can have a determinant impact in satiety control
and can even affect the immune system. Noradrenalin (NA) and
serotonin (5-HT) serum levels are lower in BN patients in
comparison to healthy individuals, whereas their dopamine levels
are similar or lower than control subjects. These levels are strongly

related topsychopathologies such as depression. Diminished basal
tryptophan serum levels (the main precursor of serotonin) have
been found in BN patients, but with no differences in the
tryptophan/long-chain neutral amino acids (LNAA) ratio, even
after glucose ingestion. Clinical trials have shown female BN
patients to be more vulnerable to mood changes induced by a
tryptophan-deficient diet,suggesting altered modulation of the
serotonin central neuronal systems. An exaggerated insulin response
has been reported in patients with relatively infrequent vomiting
and binges, and stable weight. In contrast, no insulin response
peaks occur in patients with more frequent vomiting and binges,
unstable weight, and no basal eating pattern associated with high
plasmatic cortisol levels. Insulin...