Applied BiochemistryName: Moya McLeodDate: September 13, 2013.

Deficiency in amino acids will cause many different symptoms because each amino acid has different uses and functions. For example, cysteine is used to reduce the amount of free radicals in the body. These free radicals accelerate the signs of aging. Deficiency of this may lead to loss of youth health and quality of life. Lysine, on the other hand, produces carritine that gives energy and helps lower cholesterol (University of Maryland Medical Centre, 2013). It also forms collagen and helps the body absorb calcium ions. Tryptophan makes niacin and serotonin. This deficiency therefore causes mood problems and poor sleep. Serotonin is thought to boost the quality of life (American Journal of Nutrition, 2013). We will explore other deficiency diseases in this document.

Alkaptonuria is the first disorder that a genetic link was made. In this disorder there is a defect in the HGD gene. The gene defect disallows the break down of tyrosine and phenylalanine. The acid build up in the body is excreted through urine, which upon exposure turns brownish black (University of Maryland Medical Centre, 2013).

A next disorder is Maple Syrup Diseases or Branched chain ketoaciduria. This is a hereditary disorder where the body cannot break down leucine, isoleucine and valine in blood. This disorder is characterized by maple- syrup smelling urine, vomiting, feeding difficulties, lethargy and seizures among other things.

There is also a disorder called glycine encephalopathy. This disorder appears classically in infants where a lack of glycine cleavage activity causes lethargy, feeding difficulties, weak muscle tone and breathing problems. The genes that have defects are the AMT, GCSH and GISC. Glycine then builds up in cerebrospinal fluid.

A more common disorder is Phenylketonuria (PKU). It is also a hereditary disease where the enzyme phenylalanine hydroxylase cannot be synthesized hence phenylalanine cannot be broken down. This will build up and become harmful to the central nervous system showing mental retardation, seizures and tremors (British Journal of Nutrition).

The next disorder is Citrullinemia. This disorder is hereditary where the enzyme arginiosuccinate synthase cannot be synthesized. Hence, arginine cannot be broken down. This leads to a build up of ammonia and other urea cycle byproducts in the body. This build up of ammonia and other urea byproducts is harmful to the central nervous system of that body (National Urea Cycle Disorders Foundation, 2013). There is type 1 and type 2. Type one occurs in infants while type 2 occurs in adults causing confusion, abnormal behaviours, seizures and coma (Droge, 2005).

Carbamoyl Phosphate synthetase I deficiency, according to the US National Library of Medicine, 2013, is an inherited disorder that causes ammonia to accumulate in the blood. As seen in previous disorders this affects the central nervous system. It is caused by a defect in the CPSI gene that stops asparagine from being substituted for the threonine at position 1405 (T1405N). It occurs in children and usually causes unusual sleepiness, poorly regulated breathing rate or body temperature and an unwillingness to feed.Tyrosinemia is the next disorder to be discussed. In this disorder chemicals in the pathway of tyrosine cannot be metabolized. There are three types: I, II, and III. This affects the construction of brain chemicals. This therefore causes decreased alertness, depression, memory problems, lack of energy and confusion (Medscape, 2001).

Hypermethionemia is a deficiency in the amino acid methionine. It causes learning disabilities, mental retardation, neurological problems and delays in motor skills (Medscape, 2003).

Homocystinuria is a hereditary disease. It is characterized by a defect in metabolism of methionine. It is a disease of the connective tissue, muscles, central nervous system and cardiovascular system. It causes mental retardation, seizures, psychiatric disease, myopia and glaucoma upon other things (American Journal of Nutrition, 2005).

Finally, Hartnup disease affects the absorption of tryptophan that makes niacin, melatonin and serotonin. The gene defect associated with this is SLC6A19. This is characterized by photosensitivity, ataxia, nystagmus, tremor, pellagralike skin eruptions, and gross amino aciduria (Lidija Kandolf Sekulovid, 2003).