Table of Contents
Page created on March 4, 2019. Last updated on December 18, 2024 at 16:57
Introduction
Proteins are indispensable to the body as they play many roles. In their deficiency are many functions disordered.
Proteins in food can be either complete (or whole) which contain all the nine essential amino acids, or incomplete, which don’t contain these essential amino acids. Theoretically, if you just consumed incomplete protein sources would you be protein deficient. Some sources of complete proteins are meat, fish, eggs, milk, cheese, soy and quinoa.
The total mass of protein in the body is 12-14 kg (almost 20% of body weight). Every day an amount of 300-500 g of protein is metabolized, however under normal circumstances is the same amount synthesized as well, so there is no net change in protein composition. Because amino acids can be recycled can the breakdown products of the 300-500 g protein be used to synthesized new 300-500g of protein. This explains why we don’t need to consume 300-500g protein every day.
It’s important to keep in mind that digestive enzymes are also proteins and are therefore absorbed in the GI tract. In malabsorption will these proteins be lost, which contributes to a substantial protein loss.
The minimum amount of protein that should be ingested every day is 0.2-0.3 g of protein per kg of body weight. A nitrogen balance of zero is maintained only in consumption of 0.5 g/kg of body weight every day. The optimal protein intake is 1g/kg of body weight, where at least half of that should be complete protein.
Nitrogen balance
The nitrogen balance is a measure of nitrogen intake minus nitrogen loss. Nitrogen is a fundamental part of amino acids (and therefore proteins), so the nitrogen balance can be used to study protein metabolism. More specifically can it be used to determine whether the body breaks down more protein or builds up more protein.
If the nitrogen balance is positive is the intake of nitrogen higher than the loss. This means that the total amount of protein in the body increases, which is associated with periods of growth (like childhood), tissue repair or pregnancy.
If the nitrogen balance is negative is the loss of nitrogen higher than the intake. This means that the total amount of protein in the body decreases, which is associated with burns, tissue injuries, fevers, fasting and wasting. A negative nitrogen balance is always pathological and indicates a protein-deficient state.
Protein deficiency
The causes of protein deficiency can be divided into three categories:
- Insufficient protein intake
- Poverty
- Elderly
- Alcoholics
- Maldigestion/malabsorption
- Enhanced protein catabolism
- Starvation
- Diabetes
- Cushing syndrome
- Chronic inflammation
- Tumors
- Loss of protein
- Proteinuria – nephrotic syndrome
- Ascites
- Protein-losing enteropathy
Protein deficiency in children causes growth retardation. In all populations it causes decreased wound healing, decreased muscle mass and decreased cell turnover. The latter especially affects gastrointestinal epithelial cells and red blood cells. These factors lead to weakness, malabsorption and normocytic normochromic anaemia. Osteoporosis may develop. BMR may decrease as there are fewer proteins which require energy present.
Endocrine dysfunction (especially of peptide hormones) affects growth hormones and growth in children. Production of acute phase proteins decreases. The liver produces less apolipoproteins, which prevents the liver from transporting fat to the circulation, causing steatosis. Immunoglobulins are deficient. Transport proteins like haemoglobin, transferrin and albumin are deficient. Interestingly are coagulation factors not affected.
Decreased oncotic pressure in the plasma causes hypoproteinaemic oedema. Ascites may develop, especially because the liver is compromised.
If other energy-containing nutrients are deficient as well will protein breakdown be increased, which worsens the protein deficiency.
Clinical consequences
- Loss of body weight – bone mass, protein and fat stores decrease
- BMR decreases
- Hypothyroidism and hypofunction of gonads, pancreas and pituitary
- Cardiac output and blood pressure decrease
- The tendency for tachycardia increases
- Circulation time increases
- Anaemia can occur
- Leukopaenia is possible
- Malabsorption and maldigestion
- Precipitation in pancreatic ducts -> chronic pancreatitis
- Steatosis or cirrhosis
- Generalized oedema is common
- Increased risk for infections
- In children
- Disturbed brain development
- Mental retardation
Protein-calorie malnutrition
Protein synthesis requires a lot of energy. In cases of calorie malnutrition (starvation) will therefore the protein synthesis also be impaired, while at the same time is protein breakdown favoured to provide energy. Protein-calorie malnutrition or protein-energy malnutrition is a term that describes two diseases that are caused by lack of dietary protein and/or energy (calories). These diseases are marasmus and kwashiorkor.
Kwashiorkor develops on the basis of adequate carbohydrate consumption but decreased protein intake. It typically affects small children in tropical countries. These children are retarded in growth, big-bellied from ascites and have swollen legs. They don’t bear signs of malnutrition, i.e. they’re not skinny. The liver is steatotic or cirrhotic due to decreased apolipoprotein production caused by the protein deficiency. The skin is dry and dark. These children often also have mental retardation.
Marasmus develops on the basis of calorie and protein deficiency. It typically affects children. Affected persons are emaciated (very skinny). They have very little muscle mass or subcutaneous fat. Oedema is not present.
The endocrinological background of these diseases are different. The carbohydrate intake in kwashiorkor causes normal levels of insulin. Insulin prevents breakdown of proteins which would be necessary to provide amino acids for the synthesis of albumin. Hypoalbuminaemia causes ascites and oedema.
In marasmus however the low carbohydrate intake causes low insulin levels and high corticosteroid levels. The latter induces breakdown of muscle and fat, which explains the emaciated state.
if there is low insulin in marasmus, and since insuline prevent breakdown of proteins , then how come there is no edema in marasmus but we have ascites/edema in kwashiorkor(adequate CHD intake>>>insulin production)?
You have to remember that while insulin prevents protein breakdown, both disorder are protein deficient. The difference being that marasmus is also calorie deficient, while kwashiorkor isnt. The consequence of this is that insulin level in marasmus is low, the liver in patients with marasmus can produce apolipoproteins by breaking down muscle proteins, which is necessary for the production of Albumin. The liver is consequently able to produce an adequate amount of albumin to maintain the colloid osmotic pressure.
In kwashirkor, the calorie sufficient diet prevents protein breakdown through insulin, but the patient is still protein deficient, and the liver cannot produce albumin since breakdown of muscle protein is inhibited.
thanks ,G-cobra.
goodluck on monday . you,ll crush it
Thanks <3