Polyphagia
| Polyphagia | |
|---|---|
| Other names | Hyperphagia |
| Specialty | Endocrinology, Psychiatry |
Polyphagia or hyperphagia is an abnormally strong, incessant sensation of hunger or desire to eat often leading to overeating.[1] In contrast to an increase in appetite following exercise, polyphagia does not subside after eating and often leads to rapid intake of excessive quantities of food. Polyphagia is not a disorder by itself; rather, it is a symptom indicating an underlying medical condition. It is frequently a result of abnormal blood glucose levels (both hyperglycemia and hypoglycemia), and, along with polydipsia and polyuria, it is one of the "3 Ps" commonly associated with uncontrolled diabetes mellitus.[2][3]
Etymology and pronunciation
The word polyphagia (/ˌpɒliˈfeɪdʒiə/) uses combining forms of poly- + -phagia, from the Greek words πολύς (polys), "very much" or "many", and φαγῶ (phago), "eating" or "devouring".
Underlying conditions and possible causes
Polyphagia is one of the most common symptoms of diabetes mellitus. It is associated with hyperthyroidism and endocrine diseases, e.g., Graves' disease, and it has also been noted in Prader-Willi syndrome and other genetic conditions caused by chromosomal anomalies. It is only one of several diagnostic criteria for bulimia and is not by itself classified as an eating disorder. As a symptom of Kleine–Levin syndrome, it is sometimes termed megaphagia.[4]
Knocking out vagal nerve receptors has been shown to cause hyperphagia.[5]
Changes in hormones associated with the female menstrual cycle can lead to extreme hunger right before the period. Spikes in estrogen and progesterone and decreased serotonin can lead to cravings for carbohydrates and fats. These can be all part of premenstrual syndrome (PMS).[6]
According to the National Center for Biomedical Information, polyphagia is found in the following conditions:[7]
- Chromosome 22q13 duplication syndrome
- Chromosome 2p25.3 deletion (MYT1L Syndrome)
- Chromosome Xq26.3 duplication syndrome
- Congenital generalized lipodystrophy type 1
- Congenital generalized lipodystrophy type 2
- Diabetes mellitus type 1
- Familial renal glucosuria
- Frontotemporal dementia
- Frontotemporal dementia, ubiquitin-positive
- Graves' disease
- Hypotonia-cystinuria syndrome
- Kleine-Levin syndrome
- Leptin deficiency or dysfunction
- Leptin receptor deficiency
- Luscan-lumish syndrome
- Macrosomia adiposa congenita
- Mental retardation, autosomal dominant 1
- Obesity, hyperphagia, and developmental delay (OBHD)
- Pick's disease
- Prader-Willi syndrome
- Proopiomelanocortin deficiency
- Schaaf-yang syndrome
Polyphagia in diabetes
Diabetes mellitus causes a disruption in the body's ability to transfer glucose from food into energy. Intake of food causes glucose levels to rise without a corresponding increase in energy, which leads to a persistent sensation of hunger. Polyphagia usually occurs early in the course of diabetic ketoacidosis.[8] However, once insulin deficiency becomes more severe and ketoacidosis develops, appetite is suppressed.[9]
See also
References
- ^ "Polyphagia". Human Phenotype Ontology. Archived from the original on 2 May 2022. Retrieved 6 October 2022.
{{cite web}}:|archive-date=/|archive-url=timestamp mismatch; 2 March 2022 suggested (help) - ^ Diabetes.co.uk
- ^ Healthline.com article "What are the 3 Ps of Diabetes?"
- ^ MACDONALD CRITCHLEY, PERIODIC HYPERSOMNIA AND MEGAPHAGIA IN ADOLESCENT MALES, Brain, Volume 85, Issue 4, December 1962, Pages 627–656, https://doi.org/10.1093/brain/85.4.627
- ^ de Lartigue G, Ronveaux CC, Raybould HE (2014). "Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity". Molecular Metabolism. 3 (6): 595–607. doi:10.1016/j.molmet.2014.06.003. PMC 4142400. PMID 25161883.
- ^ "Polyphagia: Symptoms, Causes and Treatment". Healthline. 2017-08-02. Retrieved 2022-09-28.
- ^ "Polyphagia (Concept Id: C0020505) - MedGen - NCBI".
- ^ Elliott RE, Jane JA, Wisoff JH (2011). "Surgical management of craniopharyngiomas in children: meta-analysis and comparison of transcranial and transsphenoidal approaches". Neurosurgery. 69 (3): 630–43, discussion 643. doi:10.1227/NEU.0b013e31821a872d. PMID 21499159. S2CID 12501723.
- ^ Masuzaki H, Tanaka T, Ebihara K, Hosoda K, Nakao K (2009). "Hypothalamic melanocortin signaling and leptin resistance--perspective of therapeutic application for obesity-diabetes syndrome". Peptides. 30 (7): 1383–6. doi:10.1016/j.peptides.2009.04.008. PMID 19394382. S2CID 30309208.
