Chronic fatigue
Orange discoloration of the skin, particularly the feet (Carotenosis)
Infertility
Halitosis (from vomiting or starvation-induced ketosis)
Hypotension or orthostatic hypotension
Having severe muscle tension, aches and pains
Insomnia
Abdominal distension

Cognitive symptoms
An obsession with counting calories and monitoring fat contents of food. Preoccupation with food, recipes, or cooking; may cook elaborate dinners for others, but not eat the food themselves or consume a very small portion. Admiration of thinner people. Thoughts of being fat or not thin enough
An altered mental representation of ones body
Impaired theory of mind, exacerbated by lower BMI and depression
Difficulty in abstract thinking and problem solving
Rigid and inflexible thinking
Poor self-esteem
Hypercriticism and perfectionism

Affective symptoms
Depression
Ashamed of oneself or ones body
Anxiety disorders
Rapid mood swings
Emotional dysregulation
Alexithymia

Behavioral symptoms
Food restrictions despite being underweight or at a healthy weight. Food rituals, such as cutting food into tiny pieces, refusing to eat around others, and hiding or discarding of food. Purging (only in the anorexia purging subtype) with laxatives, diet pills, ipecac syrup, or diuretics to flush food out of their system after eating or engage in self-induced vomiting. Excessive exercise, including micro-exercising, for example making small persistent movements of fingers or toes. Self harming or self-loathing. Solitude: may avoid friends and family and become more withdrawn and secretive. Perceptual symptoms
Perception of self as overweight, in contradiction to an underweight reality (namely "body image disturbance")
Intolerance to cold and frequent complaints of being cold; body temperature may lower (hypothermia) in an effort to conserve energy due to malnutrition. Altered body schema (i.e.
Symptoms of OAT deficiency are progressive, and between the ages of 45 and 65, most affected individuals are almost completely blind.In some cases, affected individuals will present in the neonatal period with disease that closely mimics a classic urea cycle defect, such as ornithine transcarbamylase deficiency, as the block in ornithine metabolism leads to secondary dysfunction of the urea cycle. These individuals present with hyperammonemia, poor feeding, failure to thrive and increased excretion of orotic acid. Genetics
OAT deficiency is inherited in an autosomal recessive manner, meaning an affected individual must inherit a mutated allele from both parents. The enzyme, ornithine aminotransferase is coded for by the gene OAT, located at 10q26. OAT deficiency has an increased incidence in Finland, and this population has a common mutation accounting for more than 85% of mutant alleles in this population. It has not been described in any other populations. Diagnosis
Upon clinical suspicion, diagnostic testing will often consist of measurement of amino acid concentrations in plasma, in search of a significantly elevated ornithine concentration. Measurement of urine amino acid concentrations is sometimes necessary, particularly in neonatal onset cases to identify the presence or absence of homocitrulline for ruling out ornithine translocase deficiency (hyperornithinemia, hyperammonemia, homocitrullinuria syndrome, HHH syndrome). Ornithine concentrations can be an unreliable indicator in the newborn period, thus newborn screening may not detect this condition, even if ornithine is included in the screening panel.