Question

Explain the difference between Marasmus and Kwashiorkor from a biochemical standpoint/detailed mechanism of what is occurring in the body during both metabolically.

Answer 1

Marasmus is a form of severe malnutrition characterized by energy deficiency. It can occur in anyone with severe malnutrition but usually occurs in children.Body weight is reduced to less than 62% of the normal (expected) body weight for the age.Marasmus occurrence increases prior to age 1, whereas kwashiorkor occurrence increases after 18 months. It can be distinguished from kwashiorkor in that kwashiorkor is protein deficiency with adequate energy intake whereas marasmus is inadequate energy intake in all forms, including protein
Protein wasting in kwashiorkor generally leads to edema and ascites, while muscular wasting and loss of subcutaneous fat are the main clinical signs of marasmus.
The overall metabolic adaptations that occur during marasmus are similar to those in starvation, which have been more extensively investigated. The primary goal is to preserve adequate energy to the brain and other vital organs in the face of a compromised supply. Early on, a rise in gluconeogenesis leads to a perceived increased metabolic rate. As fasting progresses, gluconeogenesis is suppressed to minimize muscle protein breakdown, and ketones derived from fat become the main fuel for the brain.

With chronic underfeeding, the basal metabolic rate decreases. One of the main adaptations to long-standing energy deficiency is a decreased rate of linear growth, yielding permanent stunting. The energy saving is partially attenuated by the diversion of energy from muscle to the more metabolically active organs. Further adaptations to crisis situations, such as significant infections, may have some parallels to those that are observed in a stressed, malnourished animal model. [13] The rise in energy expenditure and urinary nitrogen excretion following surgery were significantly less in malnourished rats. This suggests that malnutrition can impair the ability of the organism to mobilize substrates to respond to stress. However, the healing process in these animals remained normal, indicating the ability to prioritize this biological activity.

Energy metabolism

With reduced energy intake, a decrease in physical activity occurs followed by a progressively slower rate of growth. Weight loss initially occurs due to a decrease in fat mass, and afterwards by a decrease in muscle mass, as clinically measured by changes in arm circumference (see image in Body Composition section above).

Muscle mass loss results in a decrease of energy expenditure. Reduced energy metabolism can impair the response of patients with marasmus to changes in environmental temperature, resulting in an increased risk of hypothermia. Furthermore, during infection, fever is reduced compared to a well-nourished patient. In case of nutrient deficiency, the metabolism is redirected to vital function (requiring 80-100 kcal/kg/d). During recovery, the energy cost of catch-up growth has to be added (up to 100 kcal/kg/d). At this stage, energy needs can be massive.

Protein metabolism: Intestinal absorption of amino acids is maintained, despite the atrophy of the intestinal mucosa. Protein turnover is decreased (as much as 40% in severe forms), and protein-sparing mechanisms regulated by complex hormonal controls redirect amino acids to vital organs. Amino acids liberated from catabolism of muscle are recycled by the liver for the synthesis of essential proteins. Total plasma proteins, including albumin, are decreased, whereas gamma globulins are often increased by the associated infections.

Albumin: An albumin concentration lower than 30 g/L is often considered as the threshold below which edema develops from decreased oncotic pressure. However, in marasmus, albumin concentration can occasionally be below this value without edema. Prealbumin concentration is a sensitive index of protein synthesis. It decreases with decreased protein intake and rapidly increases in a few days with appropriate nutritional rehabilitation. Insulinlike growth factor 1 (IGF-1) is another sensitive marker of nutritional status.

Carbohydrate metabolism: This has mainly been studied in order to explain the serious and often fatal hypoglycemia that occurs in the initial renutrition phase of children with marasmus. The glucose level is often initially low, and the glycogen stores are depleted. Also, a certain degree of glucose intolerance of unclear etiology is observed, possibly associated with a peripheral resistance to insulin or with hypokalemia. One 2012 study, showed reactive hyperglycemia with reintroduction of carbohydrate indicating insulin impairment. Impaired glucose clearance in both kwashiorkor and marasmus may be related to dysfunctional pancreatic beta cell function without evidence of hepatic or peripheral insulin resistance. The reputed mechanism in kwashiorkor, and possibly marasmus, is related to pancreatic atrophy, fatty infiltration, and increased oxidative stress in beta cells. [14] In the initiation of renutrition or in association with diarrhea or infection, a significant risk of profound and even fatal hypoglycemia occurs. Small and frequent meals are recommended, including during the night, to avoid death in the early morning. Furthermore, the digestion of starch is impaired by the decreased production of pancreatic amylase. Lactose malabsorption is frequent but is generally without clinical consequences. In most cases, renutrition using milk is possible.

Fat metabolism: Dietary fats are often malabsorbed in the initial phase of marasmus renutrition. The mobilization of fat stores for energy metabolism takes place under hormonal control by adrenaline and growth hormone. Blood lipid levels are usually low, and serious dysregulation of lipid metabolism can occur, mainly during kwashiorkor and rarely during marasmus.