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Recent studies have shown that almost all women diagnosed with breast cancer are also vitamin D deficient. In this article, we explore the science behind this link, the impact of vitamin D on breast cancer risk, and what women can do to boost their vitamin D levels and potentially reduce their risk of developing this disease.
The Recommended Dietary Allowance (RDA) of vitamin D
| Age | Female | Male |
| 0-18 years | 15 mcg (600 IU) | 15 mcg (600 IU) |
| 19-70 years | 15 mcg (600 IU) | 15 mcg (600 IU) |
| >70 years | 20 mcg (800 IU) | 20 mc (800 IU) |
| Pregnancy | 15 mcg (600 IU) | |
| Lactation | 15 mcg (600 IU) |
The body can make vitamin D from direct sunlight when outdoors.
It is also obtained through food sources like oily fish, egg yolks, red meat, mushrooms, and fortified cereals.
The link between vitamin D and breast cancer risk revolves around the VDR gene.
This gene produces a protein called the vitamin D receptor, to which the active vitamin D binds.
Mutations or changes in this gene affect vitamin D levels in the body.
According to a research review, the same changes in the VDR gene were found to increase breast cancer risk.
Many studies supporting this link have reported that many people were vitamin D deficient when diagnosed with breast cancer.
A review published in The Breast reported that up to 96% of breast cancer patients are deficient in vitamin D.
Further, some studies also suggest that low vitamin D levels are associated with a higher risk for breast cancer recurrence and metastasis.
According to a year-long study, those with the highest levels of vitamin D had the most drop in estrogen levels.
Vitamin D deficiency can lead to estrogen dominance.
This study suggests that vitamin D can be an alternative to estrogen-lowering drugs.
Low vitamin D levels are associated with a higher risk for breast cancer.
This sunshine vitamin helps regulate breast cell growth.
There’s also a direct association between vitamin D and a gene involved in tumor growth and spread called ID1.
According to a study, circulating vitamin D levels are inversely associated with ID1 protein levels.
Thus a vitamin D deficiency may favor breast cancer cell growth.
There’s no one foolproof way that guarantees breast cancer prevention.
However, by meeting your vitamin D requirements, it is possible to lower your risk for breast cancer.
According to a 2015 study, women or people assigned female at birth who are deficient in vitamin D had a 27% higher risk for breast cancer than those with adequate vitamin D levels.
Another pooled analysis reported that a serum 25(OH)D level of 47 ng/ml was associated with a 50% lower risk of breast cancer.
Thus, meeting your vitamin D needs can help significantly reduce breast cancer risk.
10-30 minutes of midday sunlight several times a week, along with a dietary intake of more than 400 IU of vitamin D/day, can help reduce breast cancer risk and recurrence.
Though sun exposure and diet are excellent sources of vitamin D, most people can’t get enough of this vitamin.
Due to various reasons like latitude, skin tone, and lifestyle, adequate sun exposure for our bodies to synthesize vitamin D doesn’t happen.
Further, not all countries have dairy products fortified with vitamin D.
In these situations, a high-quality vitamin D supplement can help you be vitamin D sufficient.
Disclaimer: Vitamin D supplements are not advised to be taken without a doctor’s advice. Consult a qualified practitioner for dosage recommendations.
Vitamin D plays a role in regulating breast cell growth.
Changes in the VDR gene that increase vitamin D deficiency risk also seem to increase breast cancer risk.
Further, lower vitamin D levels are associated with higher protein levels that play a role in cancer cell growth and spread.
Adequate sun exposure, fortified foods, and a quality D3 supplement are effective ways to meet your vitamin D needs.
Disclaimer: This blog post is for information purposes only and must not be taken as medical advice. Please consult a qualified medical practitioner for appropriate treatment.
As if menstrual cramps and bloating weren't enough, for many women, migraines can also strike during their period. But why exactly does this happen? A new study has shed light on the matter, revealing some fascinating insights into the link between hormones and headaches.
Hormonal headache is linked to hormonal fluctuations in the body.
They are most commonly associated with changes in estrogen levels, which occurs during the menstrual cycle, pregnancy, and menopause.
Hormonal headaches range from mild to severe and can often be accompanied by other symptoms such as nausea, sensitivity to light or sound, and fatigue.
Women are more likely than men to experience hormonal headaches and often find their headaches more frequent or severe during certain times of the month.
Menstrual migraine is a specific type of hormonal headache that occur in women in the days leading up to or during their period.
These migraines are often more severe and longer-lasting than a typical migraine.
Symptoms include nausea, vomiting, and sensitivity to light and sound.
The exact cause of menstrual migraines is not fully understood, but it is believed to be related to changes in estrogen levels.
As estrogen levels drop before and during menstruation, it can trigger the release of certain chemicals in the brain that can cause migraine.
Women who experience menstrual migraines may benefit from tracking their menstrual cycle.
A study published on February 22, 2023, in the online issue of Neurology explored the cause behind attacks experienced by cisgender women during periods.
Study Participants
Three groups of 30 (total of 90) cis-gendered women with episodic migraine was considered for this study.
They all experienced migraines for at least three days in the month before the study.
The group included those with regular menstrual cycles, those on oral contraceptive pills (OCPs), and those who had gone through menopause.
Three groups of 30 cis-gendered women, each without migraines, were considered for reference.
Study Design
The researchers measured the levels of a protein called CGRP (calcitonin gene-related peptide).
When CGRP is released, it results in the inflammation of the protective layer of the brain called the meninges.
This can result in a migraine attack in some.
To measure CGRP levels, the researchers collected blood and tear fluid samples.
The samples were collected around ovulation time (CGRP levels highest) in those with regular menstrual cycles.
For those on OCPs, sample collection was done during hormone-free and hormone-intake time.
Sample collection was at random times for those who attained menopause.
For those with migraines and regular menstrual cycles, CGRP levels were higher during menstruation than those with migraine - 5.95 pg/ml in the former group and 4.61 pg/ml in the latter group.
For those on OCPs and those who attained menopause, the CGRP levels weres similar between the migraine and non-migraine groups.
The increase in CGRP levels following estrogen fluctuations can help explain why migraines are more likely to occur during periods and why the attacks decline post-menopause.
Accurate blood measurement of CGRP levels is challenging due to its short half-life.
CGRP measures through tear fluid are non-invasive but still exploratory.
The hormone levels were considered around ovulation time; however, they may not have been taken on the exact day of ovulation.
So the full extent of estrogen level fluctuation may not have been captured.
There are several strategies that women can use to help prevent and manage period migraines.
Triptans are a type of specific painkiller for migraine. They work by calming down overactive pain nerves.
Nonsteroidal anti-inflammatory drugs, or NSAIDs, like naproxen, can also be used to get relief from pain.
NSAIDs are also used as prophylactic drugs - to prevent pain by taking the tablets at a prescribed dose for up to 5-6 days before periods.
Some research suggests that oral contraceptives may reduce the frequency of menstrual migraines.
However, this doesn’t apply to all OCPs, and not everyone may experience the benefit.
It is also essential to discuss with your doctor any personal risk factors you may have for taking OCPs, as they can affect different women with migraine differently.
Much research suggests that regular exercise, especially aerobic exercise, can help prevent migraine headaches. HIIT and yoga can help too.
However, over-exertion could also be a trigger for migraines.
A regular sleep schedule, which includes clocking in 7-9 hours of daily sleep, can have magical effects on migraine in terms of reduced frequency, intensity, and duration.
Daily oral magnesium supplement has been proven effective in preventing menstrual migraines, especially for those who experience migraine before their periods.
The mechanism behind how magnesium plays a role in preventing migraines is still hazy. Some scientists theorize that magnesium may help decrease neuronal firing.
The healthcare practitioner can decide the type and dosage of magnesium.
Please do not start any nutritional supplements without a consultation.
Techniques like guided meditation, breathing exercises, and yoga flow to relax muscles can help reduce stress, which is a common trigger for menstrual migraines.
Working with a healthcare provider to develop a personalized treatment plan for menstrual migraines is essential, as the best approach may vary depending on the individual.
Additionally, tracking menstrual cycles and migraine symptoms can help identify patterns and potential triggers, making it easier to prevent migraines before they occur.
A new study sheds light on the cause of menstrual migraines.
The study reports that levels of a protein called CGRP that plays a role in inflammation in the brain are higher in those experiencing menstrual migraines.
Women can make lifestyle changes, avoid triggers, use medications, consider hormonal therapy, and try alternative therapies such as acupuncture or relaxation techniques to prevent and manage menstrual migraines.
Work with a healthcare provider to develop a personalized treatment plan and track menstrual cycles and migraine symptoms to identify patterns and potential triggers.
If you're one of the many people who struggle with getting a good night's sleep, you may have heard of various remedies to help you doze off, including taking vitamin supplements. One such supplement is vitamin B6, which is believed to have multiple health benefits, including promoting healthy sleep. But just how effective is vitamin B6 in improving sleep quality? In this article, we'll explore the scientific evidence behind this claim and provide you with a clear answer.
Vitamin B6, or pyroxidine, is an essential nutrient for the body.
It is a significant part of many bodily processes and is needed to keep the nervous system healthy.
It is also required for normal immune function.
Some people who suffer from kidney disease can have a vitamin B6 deficiency in the body.
Certain autoimmune disorders, a weakened immune system, and anemia can also cause vitamin B6 deficiency.
If you are persistently nauseous, especially in your first trimester, your doctor might prescribe vitamin B6 supplements.
It is said to improve the quality of sleep.
Dopamine, also known as the happy hormone, improves mood.
However, more evidence is needed to back this claim.
For adults aged 50 or below, the RDA of vitamin B6 is 1.3 milligrams.
After age 50, women are recommended to take 1.5 milligrams, while men must take 1.7 milligrams of vitamin B6.
It is always advisable to consult your doctor before starting any supplement.
Vitamin B6 is essential for the synthesis of the amino acid tryptophan.
Tryptophan is a precursor to serotonin, a hormone known for regulating sleep.
Vitamin B6 converts tryptophan to serotonin and niacin, or vitamin B3.
Since vitamin B6 cannot be stored in the body, getting adequate vitamin B6 from your diet is essential.
Tryptophan is also necessary for melatonin production.
Melatonin is a hormone that regulates the sleep-wake cycle, also called the diurnal rhythm.
Vitamin B6 plays a vital role in the synthesis of GABA.
GABA is an amino acid that depresses the central nervous system and produces a calming effect that reduces sleeplessness.
Pyridoxal 5’ phosphate is the active coenzyme form of vitamin B6.
Studies have shown that P5P deficiency can cause altered mental states, confusion, and depression.
The Mayo Clinic recommends 1.3 to 1.7 mg of P5P daily for adults.
The dosage increases to 1.9 to 2.0 milligrams daily during pregnancy and lactation.*
*The dosages mentioned here are for informational purposes only. Please consult a qualified medical practitioner for advice.
Clinical trials have shown that too much vitamin B6 can cause adverse side effects in the body.
This overdose is rarely due to food sources but from vitamin B6 supplementation.
More than 1000 milligrams of pyridoxine can cause sensory neuropathy, according to studies.
Perceptual and Motor Skills journal conducted a trial with 100 people in 2018.
In this trial, participants who took over 240 mg of vitamin B6 supplementation reported lowered sleep quality.
They further said that they felt more tired upon waking up.
Besides vitamin B6 or pyridoxine, vitamin B12 plays a role in regulating sleep.
It supports the production of neurotransmitters in the brain that help in sleep.
Vitamin D, also called the sunshine vitamin, helps improve sleep quality.
A study showed that vitamin D, combined with omega-3 fatty acids in fatty fish like salmon, improved sleep in subjects.
Apart from having calcium, milk is also rich in vitamin B6.
One cup of goat or cow’s milk provides 5 percent of the daily requirement of vitamin B6.
It has one of the highest concentrations of vitamin B6 among foods.
The wild varieties of salmon usually have a higher concentration of nutrients than the farmed ones.
They provide almost 10 percent of the daily recommended dose of vitamin B6.
They supply as much vitamin B6 as a glass of milk.
In addition, they are versatile vegetables that can be eaten raw or cooked.
Vitamin B6 is a nutrient that plays a vital role in metabolism.
It helps in the digestion of protein and keeps your adrenal glands healthy.
In addition, it helps protect your nervous system.
Vitamin B6 deficiency can manifest in the body as insomnia, depression, and mental confusion.
Studies found that adequate amounts of vitamin B6 are necessary for good sleep, as too much or too little can disrupt it.
Chicken, fish, milk, and vegetables like carrots and spinach are all rich in vitamin B6.
Did you know that sudden weight loss can affect vitamin absorption in your blood?
Vitamin K is a fat-soluble vitamin that is essential for many bodily functions.
It requires body fat to be adequately absorbed in the blood.
So before you jump into another fad diet, read on to find out just how essential Vitamin K is for the body.
Vitamin K is a fat-soluble vitamin that naturally occurs in two forms.
Phyloquinone, or Vitamin K1, is the primary type found in green leafy vegetables like kale and spinach.
Menaquinone (MK), also called Vitamin K2, is located in fermented foods.
Vitamin K2 can have various subtypes.
MK-5 and MK-15 are in fermented foods, while MK-4 is in chicken, butter, and egg yolks.
Vitamin K is necessary for healthy bone-building in the body.
In addition, Prothrombin, an essential protein for blood clotting, is dependent on Vitamin K.
Blood clotting is a naturally occurring process that helps prevent excessive blood loss in an injury.
It involves a cascade of coordinated reactions that plugs the injury site with a clot.
Prothrombin, a protein essential for blood clotting, needs Vitamin K for proper functioning.
Thus Vitamin K is necessary to heal wounds.
An enzyme called gamma-glutamyl carboxylase is necessary for adequately functioning osteocalcin, a protein in bone.
This enzyme depends on Vitamin K.
Thus, you lose bone mass and density when your body is low on Vitamin K.
It can cause bone thinning, called osteoporosis, and frequent fractures.
Some studies show that adequate Vitamin K can prevent hypertension.
Vitamin K interacts with and regulates your blood calcium levels.
As a result, it keeps your blood pressure in check.
Calcium can get mineralized and deposited on the walls of our blood vessels as we age.
Adequate amounts of Vitamin K can help remineralize the calcium and prevent heart ailments.
Sphingolipids are found in brain cell membranes.
These lipids are involved in cellular metabolism.
Changes in their functioning can cause neurodegenerative disorders like Alzheimer’s disease.
Higher levels of phylloquinone can improve memory and prevent age-related cognitive decline.
The average amount of Vitamin K is 120 micrograms for adult men and 90 micrograms for adult women.
Vitamin K deficiency is rare in adults but not impossible.
Some medications can cause a decreased absorption of Vitamin K in the blood.
Infants are prone to Vitamin K deficiency as mother’s milk has a low concentration, and this vitamin cannot cross the placenta.
As a result, you might suffer from excessive bleeding, even from a minor injury.
You might break or fracture bones even from minor falls if deficient in Vitamin K.
Infants who do not receive a Vitamin K injection at birth are at increased risk of developing a deficiency.
Certain diseases affect Vitamin K absorption in the blood.
People with celiac disease, ulcerative colitis, and cystic fibrosis are more prone to a deficiency.
People who have undergone bariatric or weight loss surgery might also develop a deficiency of Vitamin K in the body.
Vitamin K deficiency in the body can make you suffer from many other diseases:
Vitamin K is essential for healthy bone development.
If you suffer from a deficiency of it, you may develop osteoporosis.
This disease brittle your bones, and you can easily break a bone even from a minor injury.
Some studies have shown that Vitamin K can prevent heart disease.
A deficiency of this vitamin can cause the narrowing of blood vessels in the heart and can cause coronary heart disease.
Vitamin K can have severe and harmful interactions with some other drugs.
It can interact with warfarin (Coumadin), a blood thinner or anticoagulant.
If you are on warfarin, limit the intake of Vitamin K from food and dietary supplements.
Consuming less Vitamin K might cause bleeding, while consuming more may cause blood clots.
Some food sources of Vitamin K are:
They are rich in phylloquinone.
Soybeans and Natto, a traditional fermented Japanese dish, are rich in Vitamin K.
Vitamin K is a fat-soluble vitamin found in leafy green vegetables.
It is essential for bone health and blood clotting.
Vitamin K can also prevent cardiovascular diseases and Alzheimer’s disease.
A deficiency of Vitamin K can make one prone to osteoporosis and elevated blood pressure.
Vitamin K can also react adversely with certain medications.
It can have an antagonistic effect on common anticoagulants like warfarin.
So, it is always advisable to consult your doctor before starting any supplements.
Vitamin K is naturally found in green leafy vegetables like spinach and kale.
Are you at risk of developing glaucoma?
While many factors can contribute to this debilitating eye condition, genetics play a crucial role.
Understanding the genetic components of glaucoma can help you take the necessary steps to protect your vision and prevent vision loss.
This article will share five key facts about glaucoma that you might find interesting and useful.
We may be “secret carriers” of certain conditions. This means that we may not have the condition but possess the ability to pass it to the next generation.
Glaucoma is a disorder where the optic nerves are damaged.
The optic nerves connect your eye with the brain.
Optic nerve damage happens when there is a build-up of pressure within the eye, called intraocular pressure.
This optic nerve damage can eventually lead to peripheral vision loss and eventual blindness.
Other common symptoms of glaucoma are bulging eyes and sensitivity to light, also called photophobia.
Glaucoma usually affects older adults.
Some health conditions that increase the risk for glaucoma include diabetes mellitus and hypertension.
A family history of glaucoma is another risk factor.
Early onset glaucoma affects individuals below 40 years of age.
It is a congenital type of glaucoma that runs in the family.
If glaucoma appears before age 3, it is called primary congenital glaucoma.
Our eyes have two primary fluid types: aqueous humor and vitreous humor.
These fluids provide nutrition to the eye and help maintain pressure inside the eye.
These circulating fluids also require proper drainage.
Intraocular pressure builds up when there are problems with a fluid drainage system.
As a result, the optic nerves are damaged.
Eventually, this might lead to blindness.
The most common form of glaucoma is primary open-angle glaucoma.
Primary open-angle glaucoma is hereditary.
If any of your immediate family members have this condition, you are at risk for developing glaucoma.
Make sure that you consult your eye doctor regularly.
When fluid cannot drain from your eyes, it causes open-angle glaucoma.
It, in due time, builds up pressure in the eyes, which damages the optic nerve.
It is the most common type of glaucoma.
There may be no apparent symptoms.
However, you might experience blind spots or tunnel vision.
Genes like CDKN2B-AS, SIX1/SIX6, TMCO1, and CAV1/CAV2 pose the risk of developing open-angle glaucoma.
Mutations in the WDR36 gene on chromosome 5q22 are responsible for 17% of primary open-angle glaucoma.
This condition develops when your iris is not wide open, which leads to improper fluid drainage.
This condition can have symptoms like eye pain, redness, blurred vision, and vomiting.
It may cause blindness.
Mutations in the COL18A1 can cause this condition.
The inheritance pattern of the COL18A1 gene is autosomal dominant - one copy of the faulty gene is enough to cause the condition. 50% risk for glaucoma if either parent has it.
Studies have shown that mutations in this gene can cause angle-closure glaucoma in the fourth decade of life or later.
This type of glaucoma is different from the other types because your eye pressure does not change in this condition.
Your eye doctor can still detect this condition and recommend treatment options.
Variants in a gene containing two proteins, myocilin, and optineurin, can cause this condition.
The TBK1 gene on chromosome 12q14 accounts for 1% of normal-tension glaucoma.
Glaucoma can have different inheritance patterns.
Primary congenital glaucoma is inherited in an autosomal recessive pattern.
It means that both gene copies in each cell should have the variant.
Some studies have suggested that more than 50% of glaucoma is hereditary.
In addition, the risk is ten times higher when a sibling has glaucoma.
Glaucoma is an autosomal recessive condition (except for some types).
Both parents can be carriers of the disease but not have the condition themselves.
When a child inherits these mutations from both parents, they risk developing this condition.
Glaucoma is a disorder that can affect any individual.
However, scientists have found that some groups and races are more likely to develop glaucoma.
African Americans have the highest risk of developing glaucoma.
Cataracts it is the leading cause of blindness among this group.
Aged people of Hispanic descent also show an increased risk of developing glaucoma.
Among Asians, Japanese people have the highest risk of developing normal tension glaucoma.
Approximately 1 in every 50 Americans is a carrier for a rare genetic disorder that can cause spinal muscular atrophy (SMA).
If you are thinking of starting a family or are already pregnant, understanding your carrier status is crucial for the health of your child.
That's why carrier screening for SMA has become increasingly important in recent years.
We may be “secret carriers” of certain conditions. That is, not have the condition but possess the ability to pass it to the next generation. Learn more:
SMA is a group of hereditary diseases that damage and kill nerve cells in the brain and spinal cord.
The condition affects specialized motor neurons (nerve cells).
Motor neurons control the voluntary movement of arms, legs, face, throat, and tongue.
They also help bring about skeletal muscle activity required for actions like speaking, walking, swallowing, and breathing.
The most common form of SMA develops due to an abnormal change (mutation) or a missing part in the survival motor neuron gene 1 (SMN1).
This gene is responsible for producing a protein essential for the functioning of motor neurons.
Due to its effect on the motor neurons, SMA causes muscles supplied by these neurons to become smaller and weak (atrophy).
There are four types of SMA:
This type of SMA, also called Werdnig-Hoffman disease or infantile-onset SMA, is usually evident before six months of age.
Children with type I SMA show reduced movements and shortening of muscles or tendons.
They may also show symptoms like
Treatment is critical for children with type 1 SMA, without which they may die before age two.
This SMA type is usually noticed between six and 18 months of age.
Children with type II SMA can sit without support but cannot stand or walk without assistance.
Some children may also show respiratory difficulties.
Though the life expectancy of these children is reduced, most of them live till they reach adolescence and young adulthood.
Type III SMA is also called Kugelberg-Welander disease and is evident after 18 months of age.
Children with this type of SMA can walk independently but find it difficult to run, rise from a chair or climb stairs like their peers.
A few children with type III SMA may also develop complications like
When treated appropriately, children with type III SMA have average lifespans.
This type of SMA develops after 21 years of age, and individuals usually develop mild to moderate weakness in the leg muscles, along with other symptoms.
The SMN protein produced by the SMN1 gene is found throughout the body, with the highest concentration in the spinal cord.
It maintains specialized nerve cells called motor neurons in the brain and the spinal cord.
Motor neurons receive brain and spinal cord instructions, passing them on to skeletal muscles to cause body movements.
Mutations in the SMN1 gene can result in the loss of motor neurons, which leads to weakness and wastage (muscle death/atrophy) in the muscles responsible for movement.
95% of the individuals with SMA have a missing piece in both copies of the SMN1 gene.
In the other 5%, 1 copy of the gene has a missing piece, and the other copy has a mutation that interferes with the production and functioning of the protein.
SMA is an autosomal recessive neuromuscular disease - when both parents are carriers of the condition, and the child needs to receive two defective copies to be affected.
For a child to develop SMA, both parents must be carriers of the SMN1 gene.
Carriers have at least one copy of the affected gene but are unaffected by the condition.
It is rare that an individual inherits one recessive gene from a parent and acquires a new mutation in the other copy of the gene.
If both parents are carriers of SMA, there is a 25% chance of having a child with SMA in every pregnancy.
At the same time, there is a 50% chance of having a child unaffected by the condition and a 25% chance of having a child who is just a carrier.
Two prenatal tests can be used to detect if the growing fetus has an SMN1 gene mutation:
If both partners are SMA gene carriers, they must meet a genetic counselor before planning a pregnancy.
Carrier screening for SMA is recommended for couples at risk of having a child with the condition.
SMA carrier testing is recommended under the following conditions:
If you suspect you may be a carrier of SMA based on your family history, you must undergo a genetic test to determine your carrier status.
A genetic test can help determine if you are a carrier of SMA.
If you are a carrier for SMA, you have one healthy copy and one faulty or mutated copy of the SMN1 gene.
Around one in 40 to one in 60 people are carriers of this gene.
If you are a carrier for the SMA gene, it is recommended that your partner undergo a genetic test for their carrier status.
Prenatal testing is available for SMA.
It is recommended when both partners are carriers of the SMA gene.
Prenatal testing can be done using chorionic villus sampling (CVS) or amniocentesis.
Carrier testing for SMA costs less than $500, depending upon insurance coverage, the number of conditions tested, and the laboratory used.
