Most of us don't worry about getting vitamin D when the weather is warm and the sun is shining. But during the winter, it may be useful to take nutritional supplements to meet the body's need for the vitamin.
It is known that the best way to get vitamin D is by exposure to sunlight for a short time, as ultraviolet rays (especially ultraviolet B rays, which have a shorter wavelength) interact with a form of cholesterol called 7-dehydrocholesterol in the skin, which is then transformed into To vitamin D.
Since vitamin D production depends on UVB radiation, this means that our ability to produce it decreases in the winter months.
Vitamin D production also depends on where you live, as those who live near the equator produce a greater amount of the vitamin than those who live near the poles.
Given the prevalence of vitamin D deficiency in the winter (due to cloudy weather, short days, and lack of regular sun exposure), and the importance of the sunshine vitamin to our health, experts offer recommendations on how much vitamin D people should aim to get in the winter.
They recommend getting ten micrograms (or 400 IU) of vitamin D daily. This would help people avoid severe deficiency.
This can be achieved either by taking nutritional supplements, or eating certain foods rich in vitamin D, including fatty fish, such as herring, mackerel and wild salmon.
The most obvious benefit of taking vitamin D supplements is bone health. In fact, vitamin D was first discovered 100 years ago because of its ability to prevent rickets, which causes weak or curved bones.
In adults, vitamin D deficiency can cause bone pain, muscle pain and weakness, as well as an increased risk of osteomalacia, which causes bones to weaken or soften.
The reason that vitamin D deficiency can have such an impact on bone health is due to the vitamin's relationship with calcium and phosphate. Both of these minerals help keep our bones strong, but they need vitamin D to be able to strengthen bones.
Other health benefits
In addition to its effects on the skeleton, a growing body of research is beginning to suggest that vitamin D supplements may have additional benefits for our health. For example, studies show that there is a link between vitamin D deficiency and an increased risk of certain viral diseases, including the common cold, influenza, and “Covid-19.”
Likewise, several studies have shown, in cell models, that vitamin D enhances immunity against microbes, such as the bacteria that cause tuberculosis. This means that vitamin D may prevent some types of infections.
Vitamin D may also suppress inflammatory immune responses, which can protect against autoimmune diseases, such as multiple sclerosis and rheumatoid arthritis.
One 2022 trial, which looked at data from more than 25,000 people over the age of 50, found that taking 2,000 IU (50 micrograms) of vitamin D supplements daily was associated with an 18% lower risk of developing autoimmune diseases, especially arthritis. Rheumatoid.
Vitamin D supplements may also be linked to a lower risk of cardiovascular disease. A large Australian study, which examined data on more than 21,000 people aged 60 to 84, found that participants who took 2,000 IU of vitamin D daily for five years had a lower risk of major cardiovascular disease (such as stroke or heart attack).Compared to those who did not take supplements.
It is currently unknown why vitamin D has these benefits in these areas of our health, therefore, it will be important for future research to examine these reasons.
Scientists identify a new major cause of infertility in women
Infertility affects about 48 million couples worldwide and can have various causes. In about 1 to 2% of cases, the problem is caused by the failure of the ovaries to release eggs.
A new study conducted by scientists at Tsinghua University in China sheds light on a new underlying cause that may explain this condition of infertility in women.
Changes in a specific gene called Eif4enif1 have been identified as a driver of a problem in the ovaries that makes pregnancy almost impossible.
Scientists discovered that the predictive genetic change causes a problem in egg cells that prevents the ovaries from releasing eggs regularly.
Without the release of eggs (ovulation), fertilization cannot occur. Specifically, the damaging pattern of DNA affects the functioning of mitochondria (a double-membrane cellular organelle found in most eukaryotic organisms) within egg cells - the "force" Which converts fuel into energy.
Speaking about the findings, Professor Kekui Ke, from Tsinghua University in China, who helped lead the study, said the relationship between Eif4enif1 and mitochondria had not been identified before.
In medical terms, problems with the production and release of eggs are known as primary ovarian insufficiency and premature ovarian insufficiency.
These terms refer to the fact that the problem occurs before menopause, in which ovulation naturally stops.
In 2019, Chinese scientists came across a family suffering from premature ovarian insufficiency, all of whom had changes in the Eif4enif1 gene.
The team reproduced this genetic change in mice to see how it affected human fertility.
They allowed the mice to grow and compared their fertility to mice whose DNA had not been modified. They found a distinct pattern of changes in mitochondria in eggs.
The average number of total follicles, the small sacs on the surface of the ovaries that contain developing eggs, was reduced by about 40% in the older, genetically modified mice.
The average number of pups per litter also decreased by 33%, since when grown in a laboratory dish, about half of the fertilized eggs do not survive past the early stages of development.
When the scientists examined eggs from the less fertile mice under a microscope, they found that the mitochondria were not evenly spread throughout the egg, as they should be, but rather were clumped together.
Misbehaving mitochondria appeared to be contributing to the mice's infertility. Scientists believe that restoring proper mitochondrial behavior could improve fertility.
Their next steps will be to see whether mitochondrial defects also appear in the eggs of human patients.
The study was published in the journal Development.
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