The synthesis of melanin by melanocytes allows the DNA and other critical organelles to be protected from harsh rays of UV light. Melanin absorbs the UV light, darkening the skin, and protects folate levels within the skin.

Darwin noticed that people with darker colored skin lived much closer to the equator, andlightly pigmented people were found closer to the north and south poles. However, he rejected the idea that climate was the cause of these different pigments.

One explanation is that the selective pressure for dark skin decreases as UV intensity decreases. At the same time there is selection for lighter skin to absorb more UV radiation, which is needed for vitamin D production.

Rickets is most common in children who are between 6 and 36 months old. Children are at the highest risk of rickets because they’re still growing. Children might not get enough vitamin D if they live in a region with little sunlight, follow a vegetarian diet, or don’t drink milk products.

Rickets is a bone disease that affects infants and young children. The child’s growing bones fail to develop properly due to a lack of vitamin D. This can result in soft and weakened bones, fractures, bone and muscle pain, and bony deformities.

pain – the bones affected by rickets can be sore and painful, so the child may be reluctant to walk or may tire easily; the child’s walk may look different (waddling) skeletal deformities – thickening of the ankles, wrists and knees, bowed legs, soft skull bones and, rarely, bending of the spine.

Rickets has declined in frequency but it is still a problem. Rickets is a disease of infants and children. It disturbs normal bone formation (ossification).

Left untreated, rickets can lead to: Failure to grow. An abnormally curved spine. Bone deformities.

What are the symptoms of rickets? Young babies with rickets can be fussy and have soft skulls. Infants and toddlers may not develop, walk, or grow well. Older children may have bone pain and bowed legs, or their wrists and knees may get wider.

In rare cases, children can be born with a genetic form of rickets. It can also develop if another condition affects how vitamins and minerals are absorbed by the body. Read more about the causes of rickets.

Babies need vitamin D for healthy growth and development. It helps them build strong, healthy bones and teeth. Babies who don’t get enough vitamin D are said to have a deficiency. If the levels are low enough, they are at risk of getting rickets, a disease that affects the way bones grow and develop.

As most cases of rickets are caused by a vitamin D and calcium deficiency, it’s usually treated by increasing a child’s intake of vitamin D and calcium.

1. eating more foods that are rich in calcium and vitamin D.
2. taking daily calcium and vitamin D supplements.

Most cases of rickets can be treated with vitamin D and calcium supplements. Follow your child’s doctor’s directions as to dosage. Too much vitamin D can be harmful. Your child’s doctor will monitor your child’s progress with X-rays and blood tests.

Signs of vitamin D deficiency in babies Vitamin D deficiency isn’t easy to spot in babies, partly because they can’t tell you how they’re feeling. And fatigue and muscle pain, symptoms of vitamin D deficiency, are common symptoms of several other conditions.

The most common cause of rickets is a lack of vitamin D or calcium in a child’s diet. Both are essential for children to develop strong and healthy bones. Sources of vitamin D are: sunlight – your skin produces vitamin D when it’s exposed to the sun, and we get most of our vitamin D this way.

Listen to pronunciation. (RIH-kets) A condition in children in which bones become soft and deformed because they don’t have enough calcium and phosphorus. It is caused by not having enough vitamin D in the diet or by not getting enough sunlight.

Symptoms of hypocalcemia depend on how low the baby’s calcium is and how fast the drop happened….What Are the Signs & Symptoms of Hypocalcemia in Babies?

• be fussy.
• vomit.
• seem weak or floppy.
• twitch, shake, or seem jittery.
• not feed well.
• be sluggish.
• have seizures.

Including foods with vitamin D in your child’s diet may help prevent rickets. Foods with vitamin D include fresh fatty fish (e.g. salmon, herring, mackerel and sardines), liver, some mushrooms and egg yolks. Some foods have vitamin D added, such as margarine and some breakfast cereals or dairy products.

Good sources of vitamin D

• oily fish – such as salmon, sardines, herring and mackerel.
• red meat.
• liver.
• egg yolks.
• fortified foods – such as some fat spreads and breakfast cereals.

Vitamin D deficiency rickets can be caused by a lack of vitamin D in the diet, a lack of exposure to the sun, or malabsorption syndromes such as celiac disease, in which there is an inability of the intestines to adequately absorb nutrients from foods.

Inheritance. Hereditary hypophosphatemic rickets can have several patterns of inheritance. When the condition results from mutations in the PHEX gene, it is inherited in an X-linked dominant pattern .

The long-term outlook ( prognosis ) for people with hypophosphatemic rickets is good. With appropriate management, normal health and normal lifespan are expected. If the condition is not treated (especially while children are growing), skeletal deformities may be permanent.

Inheritance. Hypophosphatemic rickets is most often inherited in an X-linked dominant manner. This means that the gene responsible for the condition is located on the X chromosome , and having only one mutated copy of the gene is enough to cause the condition.

Vitamin D deficiency is a well-known risk factor for rickets, and some evidence suggests it may increase susceptibility to autoimmune diseases such as multiple sclerosis (MS), rheumatoid arthritis and type 1 diabetes, as well as certain cancers and even dementia.

Many retrospective studies found that a high proportion (up to 80%) of patients reported uncommon emotional stress before autoimmune disease onset. However, because of the nature of stress, proving that it actually causes autoimmune disease or describing the mechanism of causation is a challenging task.

In severe cases, untreated, long-term nutritional rickets can increase the risk of: bones that break easily. permanent bone irregularities. heart problems.

Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare bone disorder characterized by symptoms associated with hypophosphatemic rickets, including muscle weakness, short stature, skeletal deformities, and bone pain. The disorder is inherited in an autosomal recessive pattern.

Vitamin D deficiency rickets can be life threatening. Vitamin D supplementation is therefore crucial, especially in breastfed infants and some ethnic minorities (dark-skinned people, poor sun exposure), more at risk for developing severe rickets if not supplemented.

X-linked hypophosphatemia (XLH) is an inherited disorder characterized by low levels of phosphate in the blood. Phosphate levels are low because phosphate is abnormally processed in the kidneys, which causes a loss of phosphate in the urine (phosphate wasting) and leads to soft, weak bones (rickets).

X-linked dominant Hypophosphatemic Rickets (XLHR) is the most frequent form of rickets encountered (1:20,000births) in developed countries [14]. XLHR is due to inactivation mutations in PHEX (PHosphate-regulating Endopeptidase homologue, X-linked) (MIM#300550) encoding a zinc metallopeptidase expressed by bone cells.