Depending on sex, genetic and environmental factors, shrinkage of stature may begin in middle age in some individuals but tends to be universal in the extremely aged. This decrease in height is due to such factors as decreased height of inter-vertebral discs because of desiccation, atrophy of soft tissues, and postural changes secondary to degenerative disease. Working on data of Indonesia, the study by Baten, Stegl and van der Eng suggests a positive relationship of economic development and average height. In Indonesia, human height has decreased coincidentally with natural or political shocks. Average height around the world
As with any statistical data, the accuracy of such data may be questionable for various reasons:

Some studies may allow subjects to self-report values. Generally speaking, self-reported height tends to be taller than its measured height, although the overestimation of height depends on the reporting subjects height, age, gender and region. Test subjects may have been invited instead of chosen randomly, resulting in sampling bias. Some countries may have significant height gaps between different regions. For instance, one survey shows there is 10.8 cm (4+1⁄2 in) gap between the tallest state and the shortest state in Germany. Under such circumstances, the mean height may not represent the total population unless sample subjects are appropriately taken from all regions with using weighted average of the different regional groups. Different social groups can show different mean height.
Hence, there is no response to treatment with phenobarbital, which causes CYP450 enzyme induction. Most patients (type IA) have a mutation in one of the common exons (2 to 5), and have difficulties conjugating several additional substrates (several drugs and xenobiotics). A smaller percentage of patients (type IB) have mutations limited to the bilirubin-specific A1 exon; their conjugation defect is mostly restricted to bilirubin itself. Before the availability of phototherapy, these children died of kernicterus (bilirubin encephalopathy) or survived until early adulthood with clear neurological impairment. Today, therapy includes

exchange transfusions in the immediate neonatal period
12 hours/day phototherapy
heme oxygenase inhibitors to reduce transient worsening of hyperbilirubinemia (although the effect of the drug decreases over time)
oral calcium phosphate and carbonate to form complexes with bilirubin in the gut
liver transplantation before the onset of brain damage and before phototherapy becomes ineffective at later age

Type II
The inheritance patterns of both Crigler–Najjar syndrome types I and II are autosomal recessive.However, type II differs from type I in a number of different aspects:

Bilirubin levels are generally below 345 μmol/L [20 mg/dL] (range 100–430 μmol/L [6–24 mg/dL]; thus, overlap may sometimes occur), and some cases are only detected later in life. Because of lower serum bilirubin, kernicterus is rare in type II. Bile is pigmented, instead of pale in type I or dark as normal, and monoconjugates constitute the largest fraction of bile conjugates. UGT1A1 is present at reduced but detectable levels (typically <10% of normal), because of single base pair mutations.