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Hand clasping or hand folding is the interlocking of the fingers of one hand with the fingers of another. It is commonly used to express authority above or respect for others. It is also common to clasp the hands during prayer.
When clasping the hands, a person tends to interlace the fingers in one of two ways. People who hold the fingers of the right hand above the left fingers are classified as phenotype R (right), while those who hold the fingers of the left hand above those of the right are phenotype L (left).
Although some people do not prefer one type of hand clasping, most do. Once adopted, hand clasping tends to be consistent throughout life. When an individual attempts to clasp the hands in the opposite configuration from the usual one, that person may feel a sense that something is out of the ordinary.
Lai and Walsh (1965) suspect that genetic factors are important in determining these characteristics. They looked at a sample of 18 families. [1]
Based on the comparison of a series of monozygotic and dizygotic twins, Freire-Maia (1961) concluded that the preference in the type of hand clasping was affected by certain genetic factors, and (perhaps) to a significant extent. [2]
Falk and Ayala (1971) found a significant correlation between parent-offspring and for this feature suggested model polygenic inheritance. [3]
Martin (1975) presented the results of studies of twins and found that genetic factors are still determining the phenotypic expression of this trait. [4]
Reiss (1999) found that 55% of the population belongs to the phenotype L, and 44% have a "right type" clasping; the remaining 1% did not care. [5] [6]
In support of the hypothesis about the significant influence of genetic factors on the phenotypic expression of the extreme dimorphism clearly demarcated by the data on a very wide range of variation in the frequency of phenotypes tested parts of the world's population.[ clarification needed ]
Population | N | R (%) | References |
Belgium | 644 | 48.1 | Leguebe (1967) [7] |
Bosnia and Herzegovina | 10,073 | 55.1 | Hadžiselimović et al. (1979) [8] |
Bulgaria | ? | 70.1 | Boev, Todorov (1970) [9] |
Greece | ? | 81.2 | Pelecanos (1969) [10] |
Poland | 771 | 48.0 | Wolanski et al. (1973) [11] |
Scotland | 598 | 60.0 | Lutz (1908) [12] |
Serbia: Užice | 2,217 | 54.0 | Hadžiselimović et al.(1979) [13] |
Serbia: Voivodina | 2,686 | 51.9 | Gavrilović, Božić (1972) [14] |
Spain | 486 | 52.1 | Pons (1961) [15] |
Sweden | 981 | 52.1 | Beckman, Elston (1962) [16] |
Hand wringing is a gesture characterized by repeatedly rubbing or twisting one's hands together, often as a sign of distress or nervousness, while folding or clasping. Hand wringing has been studied in psychology to understand its underlying motivations and implications for mental well-being, of which include nonverbal communication and self-soothing behavior. It is often attributed to physical, cognitive, and mental conditions.
The act of hand wringing, along other motor actions, has been observed common in people with Rett syndrome, a genetic brain disorder, for decades. [17] [18] [19] In a study investigating stereotypical hand movements in individuals with the syndrome, hand wringing was identified as one of the most prevalent stereotypies, observed in approximately 60% of subjects. [20] It found that hand wringing tended to be more prevalent in women aged 19 years or older. Additionally, associations were noted between specific mutations and hand-wringing behavior, with certain mutations being more commonly associated with this stereotypical movement. However, there were no clear relationships between hand-wringing and the severity of mutations.
Hand wringing is also common in people with autism [21] [22] and obsessive-compulsive disorder. [23] [24]
Some studies suggest that when attempting to mitigate certain behaviors through interventions like response blocking, unintended consequences may arise. [25] For instance, in the treatment of stereotypic behavior such as head and tooth tapping, blocking these behaviors may inadvertently lead to an increase in other stereotypic responses, such as hand wringing. This collateral effect, observed in individuals diagnosed with autism, indicates that the reduction in the targeted behavior may result in the emergence or exacerbation of alternative behaviors.
Hand clasping holds significance in several religious and spiritual practices around the world, often symbolizing different aspects of faith. While not explicitly addressed in religious texts or practices, individuals may engage in the behavior during moments of spiritual reflection such as prayer or meditation.
In Christianity, hand clasping can be seen during prayer or as a gesture of fellowship and unity among believers. It often symbolizes solidarity in faith and mutual support within the community. In some Christian ceremonies, such as weddings or baptisms, hand clasping may signify the joining of two individuals or families in a sacred bond.
Buddhism employs hand gestures, or mudras, as part of spiritual practice. Some of which include clasped hands, such as ushas mudra, symbolizing reverence, gratitude, and mindfulness. Hand clasping may also be used in meditation as a means of focusing on one's intention and connecting with inner peace.
In Mandaeism, the Mandaic term kushta (which also means 'truth') refers to a sacred handclasp that is used during Mandaean rituals such as the masbuta, masiqta, and priestly initiation ceremonies. [26] [27]
Rett syndrome (RTT) is a genetic disorder that typically becomes apparent after 6–18 months of age and almost exclusively in females. Symptoms include impairments in language and coordination, and repetitive movements. Those affected often have slower growth, difficulty walking, and a smaller head size. Complications of Rett syndrome can include seizures, scoliosis, and sleeping problems. The severity of the condition is variable.
Wolf–Hirschhorn syndrome (WHS) is a chromosomal deletion syndrome resulting from a partial deletion on the short arm of chromosome 4 [del(4)(p16.3)]. Features include a distinct craniofacial phenotype and intellectual disability.
Smith–Magenis syndrome (SMS), also known as 17p- syndrome, is a microdeletion syndrome characterized by an abnormality in the short (p) arm of chromosome 17. It has features including intellectual disability, facial abnormalities, difficulty sleeping, and numerous behavioral problems such as self-harm. Smith–Magenis syndrome affects an estimated between 1 in 15,000 to 1 in 25,000 individuals.
MECP2 is a gene that encodes the protein MECP2. MECP2 appears to be essential for the normal function of nerve cells. The protein seems to be particularly important for mature nerve cells, where it is present in high levels. The MECP2 protein is likely to be involved in turning off several other genes. This prevents the genes from making proteins when they are not needed. Recent work has shown that MECP2 can also activate other genes. The MECP2 gene is located on the long (q) arm of the X chromosome in band 28 ("Xq28"), from base pair 152,808,110 to base pair 152,878,611.
CDKL5 is a gene that provides instructions for making a protein called cyclin-dependent kinase-like 5 also known as serine/threonine kinase 9 (STK9) that is essential for normal brain development. Mutations in the gene can cause deficiencies in the protein. The gene regulates neuronal morphology through cytoplasmic signaling and controlling gene expression. The CDKL5 protein acts as a kinase, which is an enzyme that changes the activity of other proteins by adding a cluster of oxygen and phosphorus atoms at specific positions. Researchers are currently working to determine which proteins are targeted by the CDKL5 protein.
FYVE, RhoGEF and PH domain-containing protein 1 (FGD1) also known as faciogenital dysplasia 1 protein (FGDY), zinc finger FYVE domain-containing protein 3 (ZFYVE3), or Rho/Rac guanine nucleotide exchange factor FGD1 is a protein that in humans is encoded by the FGD1 gene that lies on the X chromosome. Orthologs of the FGD1 gene are found in dog, cow, mouse, rat, and zebrafish, and also budding yeast and C. elegans. It is a member of the FYVE, RhoGEF and PH domain containing family.
Jagged1 (JAG1) is one of five cell surface proteins (ligands) that interact with four receptors in the mammalian Notch signaling pathway. The Notch signaling pathway is a highly conserved pathway that functions to establish and regulate cell fate decisions in many organ systems. Once the JAG1-NOTCH (receptor-ligand) interactions take place, a cascade of proteolytic cleavages is triggered resulting in activation of the transcription for downstream target genes. Located on human chromosome 20, the JAG1 gene is expressed in multiple organ systems in the body and causes the autosomal dominant disorder Alagille syndrome (ALGS) resulting from loss of function mutations within the gene. JAG1 has also been designated as CD339.
Brunner syndrome is a rare genetic disorder associated with a mutation in the MAOA gene. It is characterized by lower than average IQ, problematic impulsive behavior, sleep disorders and mood swings. It was identified in fourteen males from one family in 1993. It has since been discovered in additional families.
Peroxisome assembly protein 12 is a protein that in humans is encoded by the PEX12 gene.
Forkhead box protein G1 is a protein that in humans is encoded by the FOXG1 gene.
Peroxisome biogenesis factor 10 is a protein that in humans is encoded by the PEX10 gene. Alternative splicing results in two transcript variants encoding different isoforms.
Pitt–Hopkins syndrome (PTHS) is a rare genetic disorder characterized by developmental delay, moderate to severe intellectual disability, distinctive facial features, and possible intermittent hyperventilation followed by apnea. Epilepsy often occurs in Pitt-Hopkins. It is part of the clinical spectrum of Rett-like syndromes. Pitt-hopkins syndrome is clinically similar to Angelman syndrome, Rett-syndrome, Mowat Wilson syndrome, and ATR-X syndrome.
3q29 microdeletion syndrome is a rare genetic disorder resulting from the deletion of a segment of chromosome 3. This syndrome was first described in 2005.
1q21.1 deletion syndrome is a rare aberration of chromosome 1. A human cell has one pair of identical chromosomes on chromosome 1. With the 1q21.1 deletion syndrome, one chromosome of the pair is not complete, because a part of the sequence of the chromosome is missing. One chromosome has the normal length and the other is too short.
Michele Zappella is an Italian psychiatrist and scholar of Child Neuropsychiatry. He is a native of Viareggio, Italy.
Distal 18q- is a genetic condition caused by a deletion of genetic material within one of the two copies of chromosome 18. The deletion involves the distal section of 18q and typically extends to the tip of the long arm of chromosome 18.
Cognitive genomics is the sub-field of genomics pertaining to cognitive function in which the genes and non-coding sequences of an organism's genome related to the health and activity of the brain are studied. By applying comparative genomics, the genomes of multiple species are compared in order to identify genetic and phenotypical differences between species. Observed phenotypical characteristics related to the neurological function include behavior, personality, neuroanatomy, and neuropathology. The theory behind cognitive genomics is based on elements of genetics, evolutionary biology, molecular biology, cognitive psychology, behavioral psychology, and neurophysiology.
Autism spectrum disorder (ASD) refers to a variety of conditions typically identified by challenges with social skills, communication, speech, and repetitive sensory-motor behaviors. The 11th International Classification of Diseases (ICD-11), released in January 2021, characterizes ASD by the associated deficits in the ability to initiate and sustain two-way social communication and restricted or repetitive behavior unusual for the individual's age or situation. Although linked with early childhood, the symptoms can appear later as well. Symptoms can be detected before the age of two and experienced practitioners can give a reliable diagnosis by that age. However, official diagnosis may not occur until much older, even well into adulthood. There is a large degree of variation in how much support a person with ASD needs in day-to-day life. This can be classified by a further diagnosis of ASD level 1, level 2, or level 3. Of these, ASD level 3 describes people requiring very substantial support and who experience more severe symptoms. ASD-related deficits in nonverbal and verbal social skills can result in impediments in personal, family, social, educational, and occupational situations. This disorder tends to have a strong correlation with genetics along with other factors. More research is identifying ways in which epigenetics is linked to autism. Epigenetics generally refers to the ways in which chromatin structure is altered to affect gene expression. Mechanisms such as cytosine regulation and post-translational modifications of histones. Of the 215 genes contributing, to some extent in ASD, 42 have been found to be involved in epigenetic modification of gene expression. Some examples of ASD signs are specific or repeated behaviors, enhanced sensitivity to materials, being upset by changes in routine, appearing to show reduced interest in others, avoiding eye contact and limitations in social situations, as well as verbal communication. When social interaction becomes more important, some whose condition might have been overlooked suffer social and other exclusion and are more likely to have coexisting mental and physical conditions. Long-term problems include difficulties in daily living such as managing schedules, hypersensitivities, initiating and sustaining relationships, and maintaining jobs.
The manner in which a person folds arms is one of the clearest dynamic morphological characteristics by which each person can be assigned to one of two alternative phenotypes. Once adopted, manner of arms folding across the chest does not change throughout the lifetime and persons easily give up the unusual folding position, most commonly at the first attempt. It has been shown that the phenotypes of these properties are distributed independently with left-handed and right-handed people.
There is no cure for Rett syndrome. Treatment is directed towards improving function and addressing symptoms throughout life. A multi-disciplinary team approach is typically used to treat the person throughout life. This team may include primary care physician, physical therapist, occupational therapist, speech-language pathologist, nutritionist, and support services in academic and occupational settings.