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Year : 2019  |  Volume : 5  |  Issue : 1  |  Page : 2

Slipping into darkness: How starvation eats away vital organs

Editor, JRNM; Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication15-Nov-2019

Correspondence Address:
Dr. Anita Saxena
Editor, JRNM; Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jrnm.jrnm_52_19

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How to cite this article:
Saxena A. Slipping into darkness: How starvation eats away vital organs. J Renal Nutr Metab 2019;5:2

How to cite this URL:
Saxena A. Slipping into darkness: How starvation eats away vital organs. J Renal Nutr Metab [serial online] 2019 [cited 2020 Sep 23];5:2. Available from: http://www.jrnm.in/text.asp?2019/5/1/2/271047

During starvation, several changes in metabolism and hormone regulation take place in the body. Carbohydrate is stored as glycogen in the liver for readily available energy. During starvation, the body tries to compensate for the lack of energy by switching over carbohydrate metabolism to catabolism of fat and protein. The glucose and ketones become the main source for energy. The body goes into a state of catabolism. Protein catabolism ensues and results in loss of lean body mass, which affects major organs, such as the heart, lungs, intestines, liver, and kidneys. Due to atrophy of myocardium, there is poor contractility and diminished cardiac output. There is decreased protein synthesis due to liver wasting, leading to more metabolic changes. Gastrointestinal system becomes weak and degenerates causing malabsorption and dysmotility, further worsening the malnourished state, and increased risk for infection. Kidneys move into the state of diuresis as they lose their ability to concentrate urine.[1],[2],[3]

Vital organs lose their function as the cellular mass is lost. Consequently, there is intracellular loss of potassium, magnesium, and phosphate. Insulin secretion decreases and the basal metabolic rate slows down to 20%–25% to conserve energy. Consequently, the body becomes bradycardic, hypothermic, and hypotensive. The circulating levels of growth hormone and thyroid hormone decrease. Once nutrition is reintroduced to a patient who has been starved for an extended period of time, anabolism begins instantaneously. The body shifts back to carbohydrate metabolism from protein and fat catabolism, and glucose becomes the primary source of energy once again. A surge of insulin takes place because of increased glucose load, leading to cellular uptake of glucose, potassium, magnesium, and phosphate. This shift of electrolytes back into the cell causes hypokalemia, hypomagnesemia, and hypophosphatemia. This scenario results in refeeding syndrome. Symptoms of refeeding syndrome vary from mild drop in serum electrolytes to severe electrolyte disorders. Metabolic changes that occur in refeeding syndrome can be unyielding to cause cardiorespiratory failure and death. Most symptoms willfirst occur between 1 and 3 days after refeeding is initiated, although in some cases up to 5 days. Hypophosphatemia is the hallmark of refeeding syndrome, which can occur within 24–72 h of introducing nutrition.

Metabolic abnormalities accompanying hypophosphatemia, are hypokalemia and hypomagnesemia, along with sodium and fiuid retention. This syndrome emerges with unbalanced and overzealous feeding (oral, enteral, or parenteral nutrition) to patients who have not eaten for 5 days or more. In this issue, a mini review on refeeding syndrome briefiy describes preventive strategies for the development of this syndrome.

  References Top

Mehanna HM, Moledina J, Travis J. Refeeding syndrome: What it is, and how to prevent and treat it. BMJ 2008;336:1495-8.  Back to cited text no. 1
Carol Rees Parrish Refeeding the Malnourished Patient: Lessons Learned Nutrition Issues in Gastroenterology, Series #155 Practical Gastroenterology; September 2016.  Back to cited text no. 2
Judy F. Literature review in pediatric. J Clinics North America 2009;56:1201-10.  Back to cited text no. 3


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