This is in sharp contrast to girls where virtually none are engaging in masturbation before age 13, and only around 20% by age 13–14.People in their 60s and early 70s generally retain a healthy sex drive, but this may start to decline in the early to mid-70s. Older adults generally develop a reduced libido due to declining health and environmental or social factors. In contrast to common belief, postmenopausal women often report an increase in sexual desire and an increased willingness to satisfy their partner. Women often report family responsibilities, health, relationship problems, and well-being as inhibitors to their sexual desires. Aging adults often have more positive attitudes towards sex in older age due to being more relaxed about it, freedom from other responsibilities, and increased self-confidence. Those exhibiting negative attitudes generally cite health as one of the main reasons. Stereotypes about aging adults and sexuality often regard seniors as asexual beings, doing them no favors when they try to talk about sexual interest with caregivers and medical professionals. Non-western cultures often follow a narrative of older women having a much lower libido, thus not encouraging any sort of sexual behavior for women. Residence in retirement homes has affects on residents libidos. In these homes, sex occurs, but it is not encouraged by the staff or other residents. Lack of privacy and resident gender imbalance are the main factors lowering desire. Generally, for older adults, being excited about sex, good health, sexual self-esteem and having a sexually talented partner can be factors.
Hennekam syndrome also known as intestinal lymphagiectasia–lymphedema–mental retardation syndrome, is an autosomal recessive disorder consisting  of intestinal lymphangiectasia, facial anomalies, peripheral lymphedema, and mild to moderate levels of growth and intellectual disability.It is also known as "lymphedema-lymphangiectasia-mental retardation syndrome".Hennekam Syndrome is subdivided according to the causative genetic lesion, most (or all) of which are affecting the VEGF-C/VEGFR-3 signaling pathway:

Type 1 (mutations in CCBE1) 
Type 2 (mutations in FAT4)
Type 3 (mutations in ADAMTS3)The first recognition of a genetic association was with CCBE1, published by its namesake, Raoul Hennekam. The molecular mechanism of the lymphedema phenotype in CCBE1-associated cases was identified as a diminished ability of the mutated CCBE1 to accelerate and focus the activation of the primary lymphangiogenic growth factor VEGF-C. Mutations in the FAT4 gene had previously been only associated with van Maldergem syndrome, but the pathogenetic molecular mechanism and the function of FAT4 within lymphangiogenesis are still unknown. References


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