Antioxidants are any compounds that help prevent cell damage in the body. One of the common reasons for cell damage is oxidation, where an atom or a molecule loses electrons.
While oxidation is useful for a few processes, excess oxidation leads to cell damage. The use of antioxidants is to regulate the level of oxidation in the body.
Depending on whether the antioxidants are soluble in water or fat (lipids), they are classified into two broad categories:
There are four basic levels of defense that all antioxidants have:
Inside the body, the following factors determine antioxidant absorption and utilization:
The effectiveness of antioxidants depends on the internal environment they survive in.
Generally, larger molecules of antioxidants are broken down by the gut bacteria to help them enter the cell membranes.
The liver produces a few very important antioxidants. The cell membranes absorb some, while a large part is excreted out through urine.
Have you heard of the famous egg or chicken question? The debate over whether the egg or the chicken came first to the world is never-ending. Until recently, scientists debated whether antioxidants were produced before or after the earth received oxygen through photosynthesis.
One may assume that microbes developed the ability to produce oxygen through photosynthesis first. This caused oxidative stress, and their bodies adapted themselves to produce antioxidants.
This is not the case, though!
According to this 2017 article, an anaerobic bacterium (oxygen-free bacterium) started producing an antioxidant called ergothioneine before it started the process of photosynthesis.
If not for neutralizing the effects of oxidation, what was the use of this antioxidant? Researchers are still trying to find out the answer to this question.
Free radicals are unstable molecules that contain an unpaired electron. Because of this, they are highly reactive. Free radicals start taking electrons from the cells in your body and damages them in this process.
Free radicals are found in the air you breathe in, in the water you drink, in the foods you eat, and even in certain medications!
Antioxidants help by sacrificing/giving up their own electrons to the free radicals, thereby neutralizing them. Instead of damaging your cells, the free radicals damage the antioxidants, keeping you safe.
When your body does not have antioxidants, your cells are damaged faster because of free radicals, and this causes a variety of physical issues, including:
Selenium is an important antioxidant that is needed for the healthy functioning of the body. Many enzymes in the body that fight free radicals are affected by how much selenium you get in your food.
Certain variations in the proteins GPX1 because of inadequate selenium intake are associated with increased cancer risk. In the rs1050450 SNP of the GPX1 gene, a minor allele ‘A’ increases your risk of developing cancer when your dietary selenium levels are low.
Lycopene is a type of carotenoid that gives the red color to fruits and vegetables. This is also a very important antioxidant.
The PON1 gene helps produce the PON1 enzyme to protect against the oxidation of Low-Density Lipoprotein (LDL). LDL oxidation results in risks of atherosclerosis, heart attacks, and strokes.
The Q192R (denoted by rs662) is a polymorphism in the PON1 gene. The presence of the TT allele can imply lower or decreased levels of PON1 enzyme activity. The higher the PON1 enzyme activity, the lower is the risk for heart disease.
Unhealthy food habits – Most of the antioxidants required by your body can be obtained by including various fruits, vegetables, and other plant-based ingredients regularly. If you depend on restaurant takeaways or packaged and frozen foods for your meals, you may be at a higher risk for developing antioxidants deficiency.
Harvesting and handling of fruits and vegetables – Certain methods of harvesting and handling fresh fruits and vegetables can cause a reduction in the antioxidant levels in these produces. Consuming these fruits and vegetables will not give you your recommended values of antioxidants.
Cooking methods – According to a study boiling and pressure cooking the vegetable bring down the antioxidant levels. Opt for gentler cooking methods like steaming and quick frying instead.
It is difficult to get an overdose of antioxidants with just food sources. However, it is possible to overdose when you are using antioxidant supplements. Here are some of the symptoms of excess antioxidant consumption:
A 2018 study analyzed the intake of 10 antioxidants. The antioxidants under consideration were beta carotene, alpha-carotene, beta-cryptoxanthin, lutein, lycopene, zeaxanthin, selenium, zinc, and vitamins C and E.
The study concluded that those deficient in these ten antioxidants had lowered anti-inflammatory activities and lowered HRQOL – Health-Related Quality Of Life. It includes factors needed for physical, mental, social, and emotional quality of life.
Oxidative stress, over time, can damage healthy cells in the body. This can result in increased risks of:
## Recommendations To Get The Right Amounts Of Antioxidants
**Include a variety of vegetables and fruits** – Vegetables and fruits are very rich sources of different antioxidants. One of the best ways to prevent antioxidant deficiency is to include colorful fruits and vegetables in your diet. Studies show that fresh fruits and vegetables bring down your risk for developing several diseases apart from keeping you fit.
**Prefer food-based antioxidants over supplements** – Unless you have been advised specifically, stay away from supplements and change your food habits to increase your antioxidant intake.
**Know how your genes affect you** – If you are genetically prone to requiring more antioxidants than normal individuals or at a higher risk for developing certain diseases because of antioxidant deficiency, plan your food choices right.
**Supplement antioxidants with caution** – While supplements can easily cause an overdose, supplements can also interact unpleasantly with certain medications you consume.
**Change your cooking methods** – Your cooking methods matter a lot. Choose healthier cooking options like broiling, steaming, and quick frying on a flat pan instead of boiling and pressure cooking.
## Summary
1. Antioxidants are compounds that help prevent cell damage. There are 1000s of individual antioxidants available in nature.
2. While most antioxidants are obtained from food sources, few very vital ones are produced in the body.
3. Antioxidants bring down the risks of several diseases and keep you younger for a longer time.
4. Antioxidant overdose is rare and occurs only upon consuming supplements. Antioxidant deficiency can lead to a lowered Health-Related Quality Of Life (HRQOL).
5. Some people can be genetically inclined to absorb lesser quantities of antioxidants than others. Such individuals may need to compensate with supplements.
6. For healthier individuals, it is recommended to get the dose of antioxidants from food rather than from supplements.
https://www.hsph.harvard.edu/nutritionsource/antioxidants/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249911/
https://www.nccih.nih.gov/health/antioxidants-in-depth
https://pubmed.ncbi.nlm.nih.gov/18630141/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3614697/
https://www.ahajournals.org/doi/10.1161/circ.136.suppl_1.12351
https://www.nccih.nih.gov/health/antioxidants-in-depth
https://pubmed.ncbi.nlm.nih.gov/24915343/
https://www.sciencedaily.com/releases/2009/04/090415163730.htm
https://www.health.harvard.edu/staying-healthy/understanding-antioxidants
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249911/
https://www.cbc.ca/news/health/antioxidant-supplement-overload-can-be-hazardous-1.1412993
Just like how water exerts pressure on the walls of the pipes when flowing, blood too exerts pressure on the surface blood vessels. The pressure exerted must be constant and of a particular value. A drop or hike in this pressure may likely be a warning of an abnormality.
When the pressure exerted by blood on the walls increases beyond a certain level, it is known as hypertension or high blood pressure. Hypertension is a pretty common health condition, with nearly half the American population expected to be diagnosed with it.
Most people don’t experience any particular symptom until the condition becomes severe. That is why hypertension is rightly known as the “silent killer.” Even when people do experience the symptoms, they are almost always associated with other issues.
Some of these warning signals for hypertension include:
– Severe headaches
– Nose bleed
– Difficulty in breathing
– Chest pain
– Extreme tiredness and fatigue
– Sweating and anxiety
The causes of hypertension or high blood pressure are still being studied. Some of the well-accepted and scientifically proven causes are smoking, obesity or being overweight, diabetes, having a sedentary lifestyle (one involving very minimal physical activities), and unhealthy eating habits.
Riboflavin, or vitamin B2, is a water-soluble vitamin. B vitamins are important for making sure the body’s cells are functioning properly.
In addition to energy production, riboflavin also acts as an antioxidant and prevents damages by particles called free-radicals. It is involved in the production of folate (vitamin B9), which is crucial for red blood cell formation.
People need to consume vitamin B2 every day because the body can only store small amounts, and supplies go down rapidly.
A study published by the American Journal of Clinical Nutrition revealed that one in ten people could significantly lower their blood pressure and, in turn, their risk of heart disease and stroke by increasing their vitamin B2 intake.
Previous studies have found an association between the 677C–>T polymorphism in MTHFR and hypertension. This transition from C to T results in increased homocysteine levels. About 30 to 40 percent of the American population may have a mutation at gene position C677T.
The relationship between riboflavin and hypertension was examined because riboflavin is known to have an important modulating effect on elevated homocysteine.
A study demonstrated that increasing riboflavin status reduced systolic blood pressure by 13 mmHg and diastolic blood pressure by almost 8 mmHg, specifically in patients with the TT genotype.
Another study showed that riboflavin (1.6 mg per day) lowers homocysteine levels in healthy adults with the TT genotype but not in those with CT or CC genotypes.
rs1801133 is an SNP in the MTHFR gene that is commonly studied. It is also known as C677T, Ala222Val, and A222V.
People with the TT type have a lower blood pressure upon riboflavin/vitamin B2 administration than those with the CT or CC type.
People whose blood pressure responds better to vitamin B2 should consider increasing their riboflavin intake. Vitamin B2 supplements can be taken after consulting with a qualified medical practitioner.
Another way to get vitamin B2 is through dietary sources.
https://www.medicalnewstoday.com/articles/219561
https://www.tandfonline.com/doi/abs/10.1081/CEH-120020391?journalCode=iceh20
https://pubmed.ncbi.nlm.nih.gov/19952781/
https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.105.580332
Copper is an essential mineral for the body. Along with iron, it plays a vital role in the formation of Red Blood Cells (RBCs). It is a cofactor for several enzymes (cofactors are substances required for enzyme activation). Copper is a trace element – which means our body requires it only in small quantities. It is also crucial for organ functioning and a healthy metabolism. Meeting your copper requirements is important for the prevention of osteoporosis and cardiovascular diseases. The body cannot synthesize copper on its own – therefore, it must be consumed through diet or supplements.
Hepatocytes – cells of the liver – are the primary sites for copper metabolism.
When copper enters the body through dietary sources, it is first absorbed by the intestines.
It is then transported to the hepatocytes by a tube-like structure called the portal vein.
The copper then enters the hepatocytes – this is mediated by a protein called copper transporter (CTR1). After it enters the hepatocytes, either of the two things happens:
1. With the help of another transporter protein ATP7B, it reaches the ‘Golgi apparatus’ (packages protein to transport it to the destination) where it binds to another protein, ‘apoceruloplasmin.’ Once copper binds to this protein, it becomes ceruloplasmin. Subsequently, this ceruloplasmin exits the hepatocytes and is transported to other organs.
Sometimes, the copper is loosely bound to another protein called albumin and is circulated in the blood. This is called free serum copper.
Free serum copper + ceruloplasmin = Total serum copper
These three parameters are very important for blood diagnostics of copper metabolism.
2. If the body doesn’t require copper, it is transported to the bile ducts. From there, it is excreted into the bile.
If the ATP7B protein doesn’t function well, the copper gets accumulated in the cells leading to Wilson’s disease.
Copper is found in the cells of almost all organs. It plays an important role in blood vessel formation, maintenance of the nervous and the immune system.
Our body needs copper for several activities. These include:
1. Formation and functioning of RBCs
2. Immune functioning – by forming white blood cells
3. Fetal and postnatal brain growth and development
4. Collagen formation
5. Turning sugar into energy
6. Protection from cell damage
7. Absorption of iron
8. Maintenance of healthy skin and connective tissue
Copper deficiency is associated with changes in lipid levels. According to animal studies, low copper levels can lead to cardiac abnormalities.
Some researchers believe that people with heart failure can benefit from copper supplementation.
Some studies have shown that copper may help delay or prevent arthritis. That’s why wearing a copper bracelet as a remedy for arthritis is popular.
For adolescents and adults, the RDA is about 900 mcg per day.
The upper limit for adults aged 19 years and above is 10,000 mcg, or 10 milligrams (mg) a day. An intake above this level could be toxic.
The copper requirement changes with age, gender, and events like pregnancy.
The SELENBP1 is located on chromosome 1 and encodes selenium-binding protein.
Selenium is an essential mineral and is known for its anticarcinogenic properties, and a deficiency of it can result in neurologic diseases.
While selenium-binding protein has majorly been studied only for its tumor suppressant activities, a 2013 study found a significant association between this protein and erythrocyte (red blood cells) copper levels.
rs2769264 of SELENBP1 and Copper Deficiency Risk
rs2769264 is an SNP in the SELENBP1 gene. It is located on chromosome 1. This SNP has been associated with serum copper levels. According to a study, the presence of the G allele increases the copper levels by 0.25-0.38 units.
The SMIM1 gene is located on chromosome 1 and encodes Small Integral Member Protein 1. This protein plays a vital role in the formation of red blood cells.
rs1175550 of SMIM1 and Copper Deficiency Risk
rs117550 is an SNP in the SMIM1 gene. This SNP has been associated with serum copper levels. People who have an A allele in this SNP are at a greater risk for copper deficiency – the presence of A allele decreases copper levels by 0.14-0.26 units.
Breastfeeding
Infants fed on formula milk had lower copper levels than those on breast milk.
Excess zinc
Consuming excess zinc can lead to an inefficient absorption of copper.
Gastrointestinal (GI) diseases
GI conditions like celiac diseases, short-gut syndrome, and irritable bowel syndrome can impair copper absorption.
Certain health conditions
Some conditions, such as central nervous system demyelination, polyneuropathy, myelopathy, and inflammation of the optic nerve, can increase the risk of copper deficiency.
Clinical symptoms of copper deficiency include:
– Premature hair greying
– Fatigue and weakness
– Sensitivity to cold
– Easy bruising
– Weak and brittle bones
– Learning and memory problems
– Pale skin
– Unexplained muscle soreness
– Loss of vision
Copper toxicity means you have more than 140 mcg/dL of copper in your blood. It can be caused due to excess copper in drinking water, eating meals cooked in uncoated copper cookware, and IUDs (Intrauterine devices like copper-T).
Some symptoms of copper poisoning include:
– Fever
– Headaches
– Vomiting
– Diarrhea
– Yellow skin (jaundice)
– Dark stools
– Abdominals cramps
– Anxiety
– Mood changes
If left untreated, copper toxicity can lead to liver damage, heart failure, and in some cases, death.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6034109/
https://pubmed.ncbi.nlm.nih.gov/10721936/
https://academic.oup.com/eurheartj/article/27/1/117/608121
https://en.wikipedia.org/wiki/Wilson%27s_disease
https://academic.oup.com/hmg/article/22/19/3998/571929
https://www.snpedia.com/index.php/Rs2769264
https://www.snpedia.com/index.php/Rs1175550
https://bmcpediatr.biomedcentral.com/articles/10.1186/s12887-015-0474-9%20
Choline is one of the nutrients that has risen in ranks very quickly. The Institute of Medicine declares choline as an ‘essential nutrient’. There are many complex roles performed by this nutrient in the body.
While humans do produce choline in their bodies, the quantities are mostly insufficient. It is hence important to also obtain choline from the foods you eat. Choline acts like amino acids and facilitates various processes to function seamlessly.
It is not easy to decide on the global recommended values for choline intake. Certain genetic changes increase or decrease a person’s choline needs. We will discuss more of this in the genetic section.
Here are some of the important functions of choline in the body.
Helps in making fats that holds together cell membranes
Choline is useful in producing acetylcholine. This is a basic neurotransmitter (messengers that transmit signals from one cell to another)
Helps with DNA synthesis (the production/creation of DNA molecules)
In the middle of the 19th century, a large number of researchers were analyzing the chemical composition of tissues of living organisms.
During the 1850s and 1860s, several scientists were working on a new molecule at the same time in different parts of the world.
In 1850, Theodore Gobley, a pharmacist in Paris extracted this new molecule from the tissues of the brain and named it ‘Lecithin’. The word meant egg yolk in Greek.
In 1862, Adolph Strecker, a German scientist extracted lecithin from bile and then heated it. The result was a new chemical named Choline.
In 1865, another expert named Oscar Liebreich identified a new chemical found in the brain and named it neurine.
It was later proven that choline and neurine were the same substances.
It was only in the 1930s that scientists proved fatty liver could be cured with choline supplemented food.
In 1998, choline was added to the list of essential nutrients needed for human survival.
De Novo Synthesis – De Novo synthesis of choline is the production of choline inside the body. The phosphatidylethanolamine N-methyltransferase (PEMT) is an enzyme that helps convert certain kinds of lipids called phospholipids into phosphatidylcholine.
An enzyme called Phospholipase D converts phosphatidylcholine into phosphatidic acid. In this process, choline is released, which then enters circulation.
Absorption from food – Once you eat choline-rich foods, different forms of choline enter the small intestine and then choline gets stored in the liver. The liver then passes on the choline to the bloodstream and this reaches all the cell membranes.
While this would be enough to match bare requirements, you will need to match up with the right foods to get your complete recommended levels of choline.
The PEMT gene is responsible for making phosphatidylcholine in the body. Phosphatidylcholine is eventually converted into choline. Extreme cases of choline deficiency can lead to liver damage. For some individuals, variations in the PEMT gene can result in an increased risk of liver damage, obesity, and abdominal fat build-up.
rs12325817
The C allele of the rs12325817 SNP causes increased risk of liver problems when you consume inadequate amounts of choline.
The MTHFD1 gene helps in activating folic acid into forms usable by the body. Certain variations in the MTHFD1 gene affects the choline levels in the body too.
rs2236225
The A allele of the rs2236335 SNP causes folate deficiencies. When your choline intake is also low, you can develop serious signs of choline deficiency like fatty liver. The G allele however does not cause folate deficiencies. The body is able to handle a low-choline diet better without resulting in extreme symptoms.
Pregnancy and lactation – About 95% of pregnant and lactating women consume less choline than what’s needed. Women who do not consume folic acid supplements during pregnancy are at a greater risk for choline deficiency. Talk to your gynecologist to know if you should change your diet pattern during pregnancy.
Menopause – Estrogen is an important hormone that helps produce choline internally in the body. During menopause, estrogen levels come down and so do choline levels.
Alcoholics – Alcoholics have higher needs for choline. When they do not have a healthy diet regime, the chances of them developing choline deficiency is very high.
Athletes and high endurance trainers – If you are physically very active, regular workouts and training sessions can cause a fall in the choline levels. Supplements can help stabilize the levels
Since choline is also produced internally in the body, choline deficiency is rare. However, it does happen in the below categories of individuals.
– Pregnant women
– People with genetic polymorphisms that prevent absorption of choline
– Individuals who are intravenously fed
People with choline deficiency develop Nonalcoholic Fatty Liver Disease (NAFLD). This condition usually resolves when the person is supplemented with choline. Here are some of the conditions associated with NAFLD.
– Obesity
– Hypertension
– Insulin resistance
– Increased risks of liver damage, liver cancer and liver cirrhosis
https://www.hsph.harvard.edu/nutritionsource/choline/
https://ods.od.nih.gov/factsheets/Choline-HealthProfessional/
https://lpi.oregonstate.edu/mic/other-nutrients/choline
https://www.researchgate.net/publication/233773350_A_Brief_History_of_Choline
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4422379/
https://www.foodnavigator-usa.com/Article/2014/10/17/Time-for-the-DGAC-to-look-again-at-choline#
https://ods.od.nih.gov/factsheets/Choline-HealthProfessional/
https://lpi.oregonstate.edu/mic/other-nutrients/choline#deficiency-symptoms
Calcium is the most abundant material in the body. The body stores over 99% of the calcium in bones and teeth. The rest is found in nerve cells, body tissues, blood, and other body fluids. The body uses bones as a reservoir for (and sometimes source of) calcium. A proper level of calcium in the body over a lifetime can help prevent osteoporosis.
When you don’t get enough calcium, you also increase your risk of developing other conditions like:
– Osteopenia
– Calcium deficiency disease (hypocalcemia)
Other than its vital role in the formation and strengthening of bones and teeth, calcium also helps with the following:
– Muscle contractions
– Normal enzyme functioning
– Clotting blood
– Sending and receiving nerve signals
– Squeezing and relaxing muscles
– Releasing hormones and other chemicals
– Maintaining a normal heart rhythm
The present nutritional requirements of calcium is a result of a 200 million year evolution. The evidence indicates that this evolution occurred in a high-calcium nutritional environment.
Humans who lived during the Stone Age period consumed a lot more calcium (1500mg/day or even more) than we do today. The higher calcium consumption can be attributed to the requirement for higher physical exertion. Examination of bony remains from that period revealed a higher bone mass and lesser age-related bone loss.
While the Americans today get the majority of calcium through dairy foods, the stone age people had to rely on plant sources as domestication hadn’t begun by then. Their diet was also high in protein, fiber, and other micronutrients, and at the same time, low in sodium and fats. Archaeological evidence suggests that the Stone Age diet helped prevent diseases like heart disease, stroke, osteoporosis, and other chronic diseases.
Evolution has programmed our genes to adapt to a certain kind of nutritional pattern- which has many positive implications on our health. Changing our diet to match this ‘designated’ nutritional pattern can be a big challenge but can help achieve major improvements in our health.
The RDA of calcium for adults 19-50 years of age is 1000 mg for both men and women. Women who are 51 and older (post-menopausal) and men who are 71 and older require about 1200 mg of calcium.
However, the WHO states that adults require only 500 mg of calcium per day.
The Calcium sensing receptor (CASR) gene encodes a calcium-sensing receptor, which binds to calcium present in the blood. The [CASR protein}(https://medlineplus.gov/genetics/gene/casr/) is present on the cells of the parathyroid glands and is associated with the secretion of the parathyroid hormone. This hormone transfers calcium from the bone into the blood, with bones acting as storage centers for calcium.
When calcium levels are high, the levels of parathyroid hormone are low. This facilitates increased binding of calcium to CASR receptors in the kidney. This ultimately leads to more removal of calcium via kidneys.
rs1801725 of CASR Gene And Calcium Deficiency Risk
rs1801725 is an SNP in the CASR gene associated with serum calcium levels. This SNP is also called A986S. It contributes to 1.26% of the variance in serum calcium levels. The T allele of rs1801725 was associated with higher serum calcium.
rs17251221 of CASR Gene And Calcium Deficiency Risk
Previous studies have indicated that rs17251221 in the CASR gene is associated with total serum calcium levels. People with the GG + GA genotypes have higher calcium levels than those with the AA genotype.
GATA3, or GATA binding protein 3, is a gene that is located on chromosome 10 and belongs to the GATA family of transcription factors.
Defects in this gene have been associated with hypoparathyroidism.
Hypothyroidism causes a reduction in the calcium levels in the blood, i.e., hypocalcemia.
rs10491003 of GATA3 Gene And Calcium Deficiency Risk
rs10491003 is an SNP in the GATA3 gene. It is implicated in disorders of calcium imbalance. The T allele has been associated with a 0.027 unit increase in calcium levels.
The CYP24A1 gene is located on chromosome 20 and encodes the enzyme 24-hydroxylase.
This enzyme is responsible for controlling the amount of active vitamin D available in the body.
Vitamin D is absolutely essential for the proper absorption of calcium from the intestines and is also involved in various processes required for bone and tooth formation.
Many mutations in this gene are found to be associated with idiopathic infantile hypercalcemia 1.
rs1570669 of CYP24A1 Gene And Calcium Deficiency Risk
rs1570669 is an SNP in the CYP24A1 gene. The A allele in this SNP is associated with a 0.012-0.024 decrease in the serum calcium levels. People with the AA genotype are at a higher risk for calcium deficiency.
Other genes like CARS, DGKD, DGKH, GGCKR, TTC39B, and WDR81 also influence calcium levels in the body.
Overactivation of parathyroid hormone: Also called hyperparathyroidism, this condition results in excess parathyroid hormone. This results in a calcium imbalance.
Medications: Diuretics release a lot of water from the body, which results in the underexcretion of calcium. Lithium causes excess secretion of the parathyroid hormone.
Lung diseases: Certain lung diseases like sarcoidosis result in high vitamin levels, which increases the level of calcium.
Cancer: Some cancers, especially lung, blood, and breast, increases your risk for calcium buildup.
Dehydration: This, coupled with poor kidney function, can increase your calcium levels.
Also called hypocalcemia, calcium deficiency is a condition where there are low calcium levels in the body. Women are more prone to calcium deficiency, especially those who are going through menopause. This is because of the decrease in the female hormone estrogen, which plays a vital role in calcium metabolism.
Some symptoms of hypocalcemia include:
-Muscle problems such as aches, spasms, cramps
-Increased numbness and tingling in the arms, legs, hands, and feet
-Severe fatigue, lack of energy
-Dry skin
-Weak and brittle nails
-Osteoporosis, that increases the chances of breaking or brittle bones
-Dental problems like poor oral health, week roots of teeth, brittle teeth, gum irritation, increased cavities
-Depression
-Hallucinations
Hypercalcemia/excess calcium describes a condition where there are high concentrations of calcium in the blood. This can be harmful to your bones and organs, especially to your kidneys.
The parathyroid hormone controls the levels of calcium in the body. Hypercalcemia is usually the effect of overactive parathyroid glands that result in an increase in the blood calcium levels.
Hypercalcemia affects different organs differently:
Kidneys: Kidneys need to overwork to filter all the extra calcium. This causes increased thirst and frequent urination
Bones: The calcium in the bone is leached out into the blood – thus, it gets weakened, which results in bone pain
Abdomen: Symptoms related to the abdomen include nausea, constipation, vomiting, and abdominal pain
Heart: High calcium levels can result in abnormal heart rhythms
Muscles: Hypercalcaemia can cause muscle weakness and spasms
Brain: Symptoms like lethargy, confusion, fatigue, and even depression
One of the best ways to ensure healthy and optimum calcium levels is by sufficient dietary intake of the mineral.
https://www.health.harvard.edu/staying-healthy/how-much-calcium-do-you-really-need
https://medlineplus.gov/genetics/gene/casr/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908705/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3778004/
https://medlineplus.gov/genetics/gene/cyp24a1/#conditions
https://en.wikipedia.org/wiki/Parathyroid_hormone
Iron is an essential mineral that is a major component of hemoglobin – a protein in blood that transports oxygen in the body. It also binds to myoglobin, a protein present in muscle tissues, and provides oxygen.
This mineral is naturally present in many foods as well as added to some food products – iron-fortified foods. It is also available as a dietary supplement.
Dietary iron has two main forms: heme and nonheme. Heme iron (present as hemoglobin/myoglobin) is found only in animal flesh like meat, poultry, and seafood. Non-heme iron is found in plant foods like whole grains, nuts, seeds, legumes, and leafy greens. Heme iron is more well-absorbed than non-heme iron.
Studies suggest that an estimated 2 billion in the population suffer from the most common outcome of iron deficiency – Iron Deficiency Anemia (IDA).
Human skeletal remains from prehistoric times show small holes in the outer layers of the skull. This condition, called Porotic Hyperostosis (PH), was put forth by Stuart-MacAdam in 1992, who said that these findings in the remains of prehistoric times became more evident as mankind moved from being hunters to an agricultural society. One of the prominent crops that he holds responsible for iron deficiency in prehistoric humans is maize, as it is a poor source of absorbable iron. It has also been suggested that iron-deficiency causing PH usually occurs in infancy.
Chalybeate waters
Early in the 17th century, Chalybeate water (named after the Chalybes, skilled ironworkers in Roman Asia Minor) was identified. These waters were found to be rich in salts of iron. It has been suggested that the chalybeate waters have contributed to the healing properties since prehistoric times and were considered to be beneficial to cure conditions like anemia. Many British spa towns are famous for their chalybeate springs. Despite the importance of chalybeate waters for healing, the role of iron in hemoglobin formation and red cell function took centuries to be recognized.
Identifying iron deficiency
It was only in 1902 Bunge, a professor of physiology in Basle, identified the possibility of iron-deficiency and admitted that ‘the habitual consumption of foods poor in iron may lead to anemia.’ However, he contradicted this by stating that ‘it is difficult to imagine a diet that would not contain the small amounts of the metal required daily.’
He also conducted studies to show that human breast milk was very low on iron but recognized that foods like spinach, egg yolk, lentils, beef, and apples were iron-rich. He said that newborn infants had much higher concentrations of iron in their liver and kidneys compared to older infants, children, or adults.
Bunge considered iron deficiency ‘unimaginable’; despite that, he also stated that iron supply through just food sources is not sufficient to treat iron deficiency.
The recommended amount of dietary iron intake is slightly higher for adult women than men. For men over 18 years, the RDA is 8.7mg a day, while it is 14.8mg a day for women aged 19 to 50. Women need more iron than men to make up for the amount of iron they lose in their menstrual period.
The RDA for vegetarians is 1.8 times higher than for people who eat meat – this is because the iron from animal sources is more easily absorbed than iron from plant sources.
TMPRSS6 gene is associated with the synthesis of a protein TransMembrane PRotease Serine 6 (also known as matriptase-2). This protein regulates the levels of another protein, hepcidin, which controls the iron balance in the body.
Whenever there are low iron levels in the body, hepcidin production is reduced, allowing more amounts of iron to be absorbed from the diet.
There are two Single Nucleotide Polymorphisms (SNPs) in this gene, rs855791 and rs4820268 that influence the serum iron levels.
In a study conducted on children aged 6-17 months, G allele in rs4820268 was identified as the “Iron-Lowering Allele” (ILA) – it led to the overexpression of hepcidin, thereby reducing the serum iron levels.
In a study conducted on 2100 elderly women, people with the T allele in rs855791 had lower serum iron and hemoglobin levels.
Another study on 14,100 Danish men also revealed the T allele to be associated with lower iron levels in the body.
Some other genes that play a role in iron levels in the body are TF (transferrin) and TFR2 (transferrin receptor 2).
Some groups of people are at an increased risk for iron deficiency:
1. Pregnant women: Iron needs increase during pregnancy to meet the needs of the growing fetus and placenta.
2. People with cancer: Many cancers like colon cancer are associated with chronic blood loss – so they may require more iron. Sometimes the requirements may increase due to the risk of chemotherapy-induced anemia.
3. People who donate blood frequently: According to a study, 25-35% of frequent blood donors develop iron deficiency.
4. People with heart failure: Poor nutrition, absorption, and use of aspirin or oral anticoagulants are the common causes of iron deficiency in people with heart failure.
5. Infants and children: Iron deficiency is more commonly seen in preterm births or infants with low birth weight.
Even full-term infants can develop an iron deficiency if they do not obtain enough iron from solid foods.
The Tolerable Upper Limit – TUL (highest level of daily intake that is likely to pose no adverse health effects) for iron in healthy adults over 19 years of age is 45 mg.
Acute intakes of more than 20 mg/kg iron from supplements can lead to iron toxicity. It can also reduce zinc absorption and plasma zinc concentrations.
Some signs of excess iron consumption include:
– Nausea
– Constipation
– Gastric upset
– Abdominal pain
– Vomiting
Iron is an essential nutrient, which means that you need to get your iron from food sources/supplements.
https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2141.2003.04529.x
https://en.wikipedia.org/wiki/TMPRSS6
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6521251/
https://www.ncbi.nlm.nih.gov/pubmed/22323359
https://www.ncbi.nlm.nih.gov/pubmed/26597663
https://en.wikipedia.org/wiki/Transferrin
https://en.wikipedia.org/wiki/Transferrin_receptor
https://pubmed.ncbi.nlm.nih.gov/25668261/
