A recent explanation by Howes in 2012 suggests that hiccups may have evolved along with other reflexes developed in mammals that allow them to coordinate suckling milk and breathing. Hiccups are only found in mammals, and are most common in infants, becoming rarer as mammals age. This may suggest that they evolved to allow air trapped in the stomach of suckling infants to escape, allowing more milk to be ingested.

The hypothesis suggests that the air bubble in the stomach stimulates the sensory limb of the reflex at receptors in the stomach, esophagus and along the diaphragm. This triggers the hiccup, which creates suction in the chest, pulling air from the stomach up and out through the mouth, effectively burping the animal.

This theory is supported by the strong tendency for infants to get hiccups, the component of the reflex that suppresses peristalsis in the esophagus, and the existence of hiccups only in milk-drinking mammals.

Hiccups may be triggered by a number of common human conditions. In rare cases, they can be a sign of serious medical problems.

The effects of myoclonus in an individual can vary depending on the form and the overall health of the individual. In severe cases, particularly those indicating an underlying disorder in the brain or nerves, movement can be extremely distorted and limit ability to normally function, such as in eating, talking, and walking. In these cases, treatment that is usually effective, such as clonazepam and sodium valproate, may instead cause adverse reaction to the drug, including increased tolerance and a greater need for increase in dosage. However, the prognosis for more simple forms of myoclonus in otherwise healthy individuals may be neutral, as the disease may cause few to no difficulties. Other times the disease starts simply, in one region of the body, and then spreads.

In some cases (particularly where whole litters are affected) FCKS can be due to genetic factors: certain bloodlines are known to produce a preponderance of kittens with the condition, and close matings very commonly produce it in the offspring. Isolated cases are more likely due to environmental factors or slight prematurity of the kittens concerned, and even complete litters suffering from FCKS may have no genetic component—repeat matings that have produced flat kittens in one instance have often not produced it again, and recovered FCKS that have been bred from have likewise not necessarily produced offspring that suffered from the condition.

Crucial in the decision to breed would be the primary cause of FCKS in the litter, which may or may not be genetic. Some recovered FCKS adults have produced FCKS offspring in their turn (or lines that consistently produce flat kittens), and breeding from them is therefore inadvisable. However, repeat matings in which FCKS has appeared does not always result in further FCKS kittens. Queens and studs who consistently throw complete litters of kittens with the condition are generally neutered since a genetically linked cause for the condition can be introduced into lines that do not produce it by breeding with lines in which it is common. Isolated instances of single flat kittens in an otherwise healthy litter are unlikely to have a genetic component in the condition, and neutering of parents of such kittens is not usually necessary in pedigree breeding, especially since this may have detrimental effects on the gene pool.

If the cause of flattening is colic related to over-production of milk then this would not be cause for neutering. The only way to determine if the cause is digestive would be if the condition was alleviated in all cases by pinching the phrenic nerve and/or use of liquid paraffin to relieve colic resulting in improvement in the condition.

Line-breeding or inbreeding is highly inadvisable in lines where FCKS has appeared, and the practice may cause the condition to appear in lines where it has not previously been recorded.

Research on myoclonus is supported through the National Institute of Neurological Disorders and Stroke (NINDS). The primary focus of research is on the role of neurotransmitters and receptors involved in the disease. Identifying whether or not abnormalities in these pathways cause myoclonus may help in efforts to develop drug treatments and diagnostic tests. Determining the extent that genetics play in these abnormalities may lead to potential treatments for their reversal, potentially correcting the loss of inhibition while enhancing mechanisms in the body that would compensate for their effects.

In the United States, the annual incidence is 18 cases of acute pancreatitis per 100,000 population, and it accounts for 220,000 hospitalizations in the US. In a European cross-sectional study, incidence of acute pancreatitis increased from 12.4 to 15.9 per 100,000 annually from 1985 to 1995; however, mortality remained stable as a result of better outcomes. Another study showed a lower incidence of 9.8 per 100,000 but a similar worsening trend (increasing from 4.9 in 1963-74) over time.

In Western countries, the most common cause is alcohol, accounting for 65 percent of acute pancreatitis cases in the US, 20 percent of cases in Sweden, and 5 percent of those in the United Kingdom. In Eastern countries, gallstones are the most common cause of acute pancreatitis. The causes of acute pancreatitis also varies across age groups, with trauma and systemic disease (such as infection) being more common in children. Mumps is a more common cause in adolescents and young adults than in other age groups.

Locoregional complications include pancreatic pseudocyst (Most common, occurring in up to 25% of all cases) and phlegmon / abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis, pancreatic ascites, pleural effusion, sterile/infected pancreatic necrosis.