Well, you’ve heard it umpteen times that you are what you eat. You are probably gearing up already to redesign your food chart to throw in a few healthy choices based on nutritionists' recommendations.
In that case, you must be familiar with the term “antioxidants” – the magical word in the lexicon of health and nutrition that has become a synonym of power-houses of nutrients.
After all, who wouldn’t want to look perennially young, be energetic, and free of ailments! Though such a proposition may sound a fantastic probability, you can turn it into a possibility by opting for a sensible diet plan that includes foods rich in antioxidants.
Antioxidants are naturally occurring chemicals in foods that help to counter the detrimental effects of oxygen free radicals, which form during normal metabolism.
External factors like pollution, ultra-violet radiation, and X-rays also produce free radicals that affect our system. Free radicals are deprived of oxygen and are responsible for the development of serious ailments, including cancer and heart disease.
Antioxidants convert the free radicals into harmless waste products that are eliminated from the body before any damage is done to the body. Thus, antioxidants act as scavengers that rid our body of free radicals that cause serious metabolic disorders by damaging the tissues and cells.
Plants are one of the primary sources of antioxidants.
Fruits, vegetables, nuts, legumes, cereals, and seeds are foods that are naturally rich in antioxidants.
The best way to ensure adequate intake of the antioxidants is to consume a variety of fruits and vegetables through a diet consisting of 5 to 8 servings of fruits and vegetables per day.
Fruits and vegetables can help guard against heart disease, cancers, and the effects of radiation, pollution, and aging.
Pomegranate, grape, orange, pineapple, plum, apple, and guava are some of the fruits that have the highest concentration of antioxidants.
In addition to being deliciously sweet, berries such as raspberries, blueberries, and strawberries are rich in antioxidants.
These berries are rich in proanthocyanidins - the antioxidants that can help prevent cancer and heart disease as well.
Broccoli, cabbage, carrots, spinach, lemon, ginger, peppers, parsley, kale, red beets, and tomato are vegetables rich in antioxidants.
Broccoli, a cruciferous vegetable, is one of the best antioxidants. It contains more vitamin C than an orange and has more calcium than a glass of milk.
In addition to minerals and vitamins, broccoli is filled with disease-fighting chemicals called phytonutrients.
Sulforaphane, a phytonutrient found in broccoli, has been shown to lower the risk of many types of cancers.
Tomato is the richest source of a powerful anticancer agent called lycopene.
Broad beans, pinto beans, soybeans are some of the best antioxidant foods.
Barley, millet, oats, corn are cereals rich in antioxidants.
Pecans, walnuts, hazelnuts, groundnut or peanut and, sunflower seeds contain a good amount of antioxidants.
Garlic, ginger, cloves, cinnamon, and oregano are antioxidant spices.
It also has been used as a natural antibiotic to kill off some strains of harmful bacteria.
Garlic is also useful for decreasing blood pressure and cholesterol, removing heavy metals from the body, preventing cancer, and acting as an antifungal and antiviral agent.
One clove of garlic contains vitamins A, B, and C, selenium, iodine, potassium, iron, calcium, zinc, and magnesium.
Green tea contains high concentrations of catechin polyphenols. It is also a powerful antioxidant and is very effective against cancer, heart disease, and high cholesterol.
Vitamin A includes carotenoids and retinol.
They are essential for healthy eyes and prevent macular degeneration or age-related blindness.
The antioxidant in vitamin A neutralizes free radicals and boosts your immunity.
Beta-carotene, which is sometimes called provitamin A, can be found in fruits and vegetables such as tomatoes, broccoli, guavas, carrots, pumpkins, apricots, and all green leafy vegetables.
All B vitamins are essential to a woman’s health.
They are essential for brain functioning, red blood cell formation, and DNA building. The important B vitamins are:
Vitamin C, also called ascorbic acid, serves as an antioxidant that facilitates wound healing.
It helps in the formation of collagen, which is essential for the wounds to heal.
It also helps in the production of new red blood cells, which deliver oxygen to your brain and to the other cells of your body.
Vitamin C is present in citrus fruits, grapefruits, strawberries, tomatoes, kiwi, oranges, and broccoli.
Also called cholecalciferol, this vitamin functions as a hormone and regulates bone homeostasis, together with calcium.
It is an important vitamin for women as it maintains strong and healthy bones.
A deficiency of this vitamin can cause you to have osteoporosis.
Exposure to sunlight helps your body produce vitamin D.
The dietary sources of vitamin D are eggs, fish, and vitamin-fortified products like milk.
Vitamin E or tocopherol acts as an antioxidant that aids in the production of red blood cells and the maintenance of the integrity of cellular membranes.
It also helps to slow age-related changes in the body.
Sources of this vitamin include nuts and nut products, wheat germ, cod liver oil, corn oil, and safflower oil.
In reality, eating healthy is never a cumbersome task. It all starts with a simple step of ringing in variety to your table.
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Affecting more than 415 million people globally, rosacea is a common skin condition, although a poorly understood one. The face and eyes are primarily affected, and the condition is often mistaken for being an 'adult acne'. According to a National Rosacea Society survey, close to 95% of patients know next to nothing about the signs just before being diagnosed. So, what are the types of rosacea and how different are they from acne? And, what's the role of your DNA in all of this?
Dating back to the 14th century, Rosacea was first called 'goutresse’, by a French doctor because of the facial redness it caused. The condition is now known to be chronic and inflammatory. There are different types of rosacea, most often accompanied by swollen red bumps and small visible blood vessels.
Since the condition mostly affects the face, they’re often mistaken for acne, eczema, or allergy. It predominantly known to affect females, especially when they are between 30 and 50 years of age. Those of European ancestry are also at a higher risk for the condition.
Rosacea is kind of an umbrella term that covers the four different subtypes:
| Erythematotelangiectatic rosacea (ETR) Symptoms: Facial redness, flushing, and visible blood vessels. | Papulopustular (or acne) rosacea Symptoms: Acne-like breakouts, swelling, and redness. |
| Phymatous/Rhinophyma rosacea Symptoms: Thickening and redness, mostly on the nose. Often co-exists with other types. | Ocular rosacea Symptoms: Redness in the eye, along with irritation and swollen eyelids. |
Before taking up a certain course of treatment, dermatologists often look for common triggers that cause a rosacea flare-up. The common triggers are:
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Genetic factors have been shown to play a role in increasing the risk of the condition. Since the most apparent symptoms are redness and inflammation of the skin, rosacea could be caused by genes associated with blood vessel abnormalities and immune reactions. Rosacea is caused by mutations in two gene families:
The HLA genes, primarily involved in immune function, help the body in distinguishing foreign proteins from the body’s own. Variations in these genes have also been linked to rosacea symptoms - when the immune system misdirects the response, causing inflammation of the blood vessels.
The proteins encoded by the GSL gene family help in protecting cells from oxidative damage - for example, the ones caused by exposure to sunlight and UV rays. Mutations in this gene complex could affect its efficiency in protecting skin cells, leading to rosacea.
A genome-wide study that analyzed over 20,000 individuals with European descent was able to set forth a genetic basis to Rosacea. In this preliminary study, volunteers who were in the ‘cases’ group having answered yes to rosacea symptoms, were tested for genetic variation. One variant was found to be associated with disease occurrence, and this is located between two genes - HLA-DRA and BTNL2. The variant was found to influence the inflammatory response associated with rosacea.
A coincidental finding of this study was that variations in the HLA gene were also related to symptoms of diabetes and celiac disease, giving a suggestive link that rosacea may act as a visual cue to another underlying disease.
It is easy to misdiagnose rosacea for acne, but there are several subtle differences:
| Trigger | Organs affected | Risk group | Treatment | |
| Rosacea | - Stress - Sunlight - Exercise - Spicy food - Alcohol | - Eyes - Eyelids - Cheeks - Nose - Forehead | - 30+ years - Women - Men (severe form) | - Topical solutions - Retinoids - Laser therapy - Antibiotics |
| Ance | - Hormonal imbalances - Medications - Stress - Diet | - Face - Chest - Back - Shoulders | - Teenagers - Young adults | - Topical solution - Retinoids - Chemical peels - Antibiotics |
There is no direct diagnosis for this condition. The main indicator of rosacea is that the redness is contained to the face or the presence of enlarged blood vessels on the face.
I. Preliminary diagnosis:
The preliminary diagnosis occurs with a physical examination of the face. If there is scarring elsewhere (like on the scalp), or if the doctor suspects another medical condition, like lupus, blood tests would be ordered.
II. Clinical tests:
Other clinical tests would also be performed to rule out other confounding conditions like psoriasis or eczema. If the symptoms include the eyes, consultation with an ophtlamologist may be required.
Several foods could trigger flare-ups. It is preferred that these are limited or avoided:
Foods that reduce inflammation, healthy fats, probiotics, and fiber-rich foods may be able to help or reduce the severity of some rosacea symptoms. These include:
People with rosacea may develop really sensitive skin, that could be easily irritated by the wrong choice of cleansers, creams, and makeup. Some common triggers:
Rosacea could become severe if left untreated. However, most treatment practices help in managing symptoms. The course of treatment usually differ based on the types of rosacea.
It is important to note that rosacea is a chronic condition and so these treatments only help in reducing the intensity of the symptoms.
There are a lot of DIY/home remedies to manage rosacea:
In all, the many types of rosacea are chronic and inflammatory that requires intensive care and a strict diet and skincare regime. The exact cause of this condition is unknown, and maybe there could be a link between rosacea and other underlying diseases, but that can only be determined through more studies. Currently, there is no treatment, however, symptoms can be managed.
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Being one of the top 5 abundant minerals in the human body and involved in over 600 reactions, magnesium is often the overlooked and ‘taken-for-granted’ type of mineral. The spotlight is often taken over by calcium and phosphorous. In fact, the importance of magnesium is so less known that about 48% of Americans fall deficit when it comes to daily magnesium intake. Studies have shown magnesium deficiency as a cause of several chronic conditions. So, if this mineral’s that important, what exactly does it do in the body?
The benefits magnesium offer to the body is not limited to one organ. They help in regulating diverse biochemical processes such as nerve function, blood pressure regulation. Some of the essential functions are given below:
The indispensable function of magnesium is their role in regulating signals between the brain and the rest of the body. Additionally, they take residence in the NMDA receptors of brain cells. By doing so, they prevent them from being excited unnecessarily and reduces the risk of brain damage. They can also calm down neural activity when it’s time to sleep, so you get a restful night.
When it comes to mental health, the importance of magnesium goes understated. By regulating brain signals and coordinating mood, the mineral keeps our psychological health in check. Several studies have shown the link between low levels of magnesium and increased risk for depression. In fact, restoring the magnesium levels in the body almost reversed depression, suggesting their role as an anti-depressant.
For your heart to keep beating, the muscles will need to contract and relax in a rhythmic fashion. While the contraction is taken care of by calcium, it is magnesium that relaxes the muscles after each contraction. This helps in maintaining steady heart rhythm. Magnesium also lowers blood pressure levels and reduces the risk of several heart conditions.
The main role of magnesium when it comes to blood sugar is insulin regulation. They transport sugar from the blood into the cells for storage. Low levels of this mineral, therefore, increases blood sugar levels and causes type 2 diabetes.
Magnesium is usually present in abundant quantities in the body. But, when their levels go down, and we do not get the required magnesium intake by food, it leads to hypomagnesemia.
Some of the main causes of the condition are:
The symptoms of Hypomagnesemia vary depending on the progression of the condition.
Early symptoms of magnesium deficiency include:
If not corrected in time, this leads to more severe symptoms that include:
Most commonly, oral supplements are prescribed for hypomagnesemia. Taking magnesium-rich foods are an alternative. When the deficiency is below 1.25 mg/dL, magnesium salts are given. Twice the dose of the mineral is administered to those with normal renal function, as 50% of it will be excreted in the urine. For those, who have excessive hypomagnesemia that cannot be managed with supplements alone, an IV or IM of magnesium will be given. Particularly, magnesium sulfate in 5% D/W at the rate of 1 g/hour as a slow infusion for up to 10 hours will be given.
Like other minerals and vitamins, the levels of magnesium in the body are influenced by the gene variants you carry. Several genes are involved, of which we'll discuss two:
TRPM6 gene, located on chromosome 9, is short for transient receptor potential cation channel subfamily M member 6. It regulates the entry of magnesium ions into the cell by creating a protein channel. They are primarily present in the large intestine, kidneys, and lungs. When there's requirement for magnesium, the channel promotes the entry of ions into the cell. If there's a mutation in this gene, the entry of magnesium will be affected, causing a fluctuation in their levels.
Research is presently ongoing to understand the gene variants of TRPM6. Several studies have shown few variants in the TRMP6 gene that influence the channel activity, Of particular interest is one variant, a T to C transition. This variant has been shown to enhance the function of the channel. This allows more magnesium ions into the cell.
The CASR gene, also called the calcium-sensing receptor gene, instructs the synthesis of the 'calcium sensing receptor' protein (CaSR). Located on chromosome 3, this gene is primarily concerned with maintaining calcium levels in the body. However, studies have shown that this gene also affects the levels of magnesium. Particularly, the gene influences the handling of magnesium in the kidney.
Studies are underway to understand the CaSR-mediated interactions between calcium and magnesium homeostasis. A genome-wide association study was conducted to decipher the genetic variations influencing serum calcium and magnesium levels. The study revealed that a particular variant, an A to G transition, was associated with higher serum magnesium levels in the population.
Of the total magnesium present in the body, 50-60% is found in the bones, 1% in blood, and the rest in soft tissues. The levels vary widely between individuals based on age. The following table shows the amount of magnesium required, categorized based on age group.
| Age | Male | Female |
| Birth to 6 months | 30 mg | 30 mg |
| 7 to 12 months | 75 mg | 75 mg |
| 1 to 3 years | 80 mg | 80 mg |
| 4 to 8 years | 130 mg | 130 mg |
| 9 to 13 years | 240 mg | 240 mg |
| 14 to 18 years | 410 mg | 360 mg |
| 19 to 30 years | 400 mg | 310 mg |
| 31+ years | 420 mg | 320 mg |
Magnesium is also useful to relieve certain health conditions, and the dosage of the mineral varies based on the condition.
Magnesium supplements improve a range of health markers. Since the body cannot make this mineral, it can be obtained by consuming magnesium-rich foods or taking supplements.
Magnesium supplements are available in different forms. Before deciding on a supplement, it is important to know more about its absorption rate or how well it is suitable as per your body type
Other than those suffering from hypomagnesemia, the supplements are also given to individuals with health conditions such as:
Though one can take magnesium any time during the day, some studies report that taking these supplements in the evening is beneficial as it helps in relaxing the body and improving sleep quality.
Magnesium supplements are generally considered to be safe. However, if an individual has any existing medical condition, he/she must consult with their doctor to prevent any cross reaction with other medications.
High doses can result in nausea, vomiting, dehydration, and diarrhea. Also, those with kidney diseases are more likely to suffer from the side effects.
The best way to increase magnesium levels and maintain optimum dietary intake is by eating foods that are rich in magnesium. Some of these include:
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The story of our rise, the all-too-familiar emergence of Homo sapiens, comes with a plot-twist that many are not familiar with. We owe our survival to viruses, because if not for them, we may not be here at all. Like pulling invisible strings, viruses quietly influenced our existence and shaped our evolution for hundreds of thousands of years.
For the last 500 million years, ever since they evolved, several viruses have tucked away their genes into the DNA of their hosts, humans included. However, this viral integration remained in the dark until a century ago.
It all started one night in 1910, at the Rockefeller Institute in New York. Biologist Peyton Rous, curious about the cause of tumors, transplanted a small piece of tumor from one chicken to another. Soon enough, the other chickens developed highly invasive cancer. This was most surprising to him because he had filtered out all the cancerous cells before the transplantation. So, what could possibly be causing raging cancer in the transplanted chickens if there were no cancer cells? After a relentless pursuit, the cause was found to be Rous sarcoma virus (RSV), a member of the retroviridae family. Soon enough, other retroviruses embedded in the chicken genome were identified.
This caused a wild intriguing theory among the scientists back then: Could we have parts of the viral genome in us too? With the human genome sequenced in the 1990s, we had our answer. Our genome showed countless genes of viruses embedded in our DNA. In fact, they were so common (occupying ~8% of our genome), that the scientists called these the ‘human endogenous retroviruses’ (HERVs).
Viruses are largely infectious agents. They enter the hosts, command the cell machinery to work in their favor, replicate to form new viruses and release to infect other cells. That’s just all how viruses work.
Since viruses have existed from time immemorial, our ancestors were exposed to a plethora of them. Some of the viruses are just temporary ‘visitors,’ exiting the host after establishing an infection. Others, however, are stealthier and make their way into the genome to integrate their genes into the host DNA without tipping off the immune system. Once they infiltrate, the viral genetic material can hop around, inserting chunks of their genes at random in the host genome. This causes a drastic rewiring of the human genome network and gets passed on from one generation to the next. Just like that, these viruses become one with the host.
If the viruses are long integrated with our DNA, what stops them from being infectious again? Thanks to the years of co-evolvement with the viruses, our cells have developed counter-active mechanisms to stop the infection. First, some of our genes have evolved to encode proteins that mainly work to render HERV’s proteins non-functional. Second, our DNA is twisted and tightly packed to accommodate into the nucleus. This means that proteins can be produced only if the region containing the gene to be transcribed is slightly loosened and accessible. The mechanisms tightening and loosening our DNA ensure that the viral genes remain inaccessible. Finally, over the course of evolution, much of the integrated viral genome pick up mutations that happen in human DNA. The mutations, once accumulated, may essentially inactivate the infectious components of the viral genome.
Like other cellular mechanisms, these fool-proofs to prevent the expression of the viral genome are compromised when the cell is under stress, such as during infection by another pathogen. There is mounting evidence for the role of these endogenous viruses in many illnesses (mostly neurological) such as schizophrenia, multiple sclerosis, and amyotrophic lateral sclerosis. For example, in multiple sclerosis, a protein produced by HERV, called ENV, activates microglial cells (brain’s immune cells). This leads to an attack on the neurons, causing auto-immune conditions. Several lines of research also hint at the link between HERVs and idiopathic conditions (unknown origin). However, HERVs mostly remain dormant unless there is a unique combination of cellular stress and genetic predisposition.
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HERVs are not just passive stowaways in our genome. Scientists are now unearthing clues about how they might’ve played a role in branching us off from our primate ancestors. This means our species started off with parts of the viral genome in our DNA. The viruses were believed to have influenced the expression of certain human genes, refashioning them and deciding which gene to activate when. This activated certain gene networks that gave our species the upper hand over the other primates.
One such effort to understand HERVs led to a key finding. HERVs decide which immune genes to turn ON or OFF. The first example came from studying MER41, an endogenous virus in our genome. MER41 was regulated by STAT proteins that are important for initiating the immune response. It is located right next to AIM2, a gene that issues the self-destruct code to the cell when pathogens invade. When scientists removed the MER41 sequence to test its importance, they found that the cells could no longer self-destruct in the face of threats. Soon after, many more immunity genes controlled by HERVs were identified. This provided further proof that we owe our survival to these viruses.
The most recent infiltrations into our DNA by the HERVK virus happened tens of thousands of years ago. They’re still found to be active, particularly in human embryos. Researchers at Stanford University made a startling discovery when analyzing gene expression in an embryo that was three days old. They found gene sequences from HERVK that produced viral proteins in the 8-cell embryo. When studying them further, the researchers were astounded to see that the main role of these viral proteins was to prevent the entry and infection of other viruses. They were safeguarding the embryo, practically acting as an immune system substitute.
Another example that viruses play a role in our existence comes from studying the syncytin-1 protein (encoded by the ERVW1 gene). This protein, originating from HERVs, plays a crucial role in the formation of the placenta. However, humans are not the only species that have this protein. Other primates have them as well, most likely integrated close to 10 million years ago.
Over tens of thousands of viruses were identified to be integrated into our genomes. Scientists have just started on what appears to be a long journey to discover the roles these viruses might have played in shaping our evolution. Research on identifying the potential effects of viral integration on the genome is currently in its infancy, and we’re not sure what it may reveal. One thing’s for certain: our genome appears to be way more complicated than we’d ever imagined.
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Imagine being told when you were a child that you’ll lapse in and out of a comatose state accompanied by hallucinations for the rest of your life that will take approximately 30 years from you. What would your reaction be? Would you be shocked, or would you give a knowing smile? After all, it’s characteristic of sleep, isn’t it?
Sleep is such a puzzling behavior that provides a constellation of benefits for our well-being, coming back for us every 24 hours.
Without exception, sleep occurs incessantly all across the animal kingdom.
Even bacteria are known to have active and passive states that correspond to the light and dark phases of our planet.
Major discoveries over the last couple of decades proved that sleep comes with a host of health benefits.
It gives an opportunity to reset our body, disguised as a complex amalgam of physiological and behavioral processes.
Therefore, the saying ‘I’ll sleep when I’m dead’ is inappropriate and more than unfortunate.
Sleep has quite a magnificent cyclical architecture.
The two main stages dominating sleep, NREM and REM, occur in a recurring fashion every 90 minutes.
These two states are as different from each other as each is from wakefulness.
Pronounced as non-REM, the normal onset of sleep occurs in adults through this stage.
A quick definition of NREM is ‘a relatively inactive, yet an actively regulating brain’.
There four stages (1-4) classified under NREM. The 1, 2, 3, and 4 stages roughly indicate the depth of the sleep.
Waking a person who’s entered stage 1 is way easier than waking those in stage 4 (trust me, you don’t want to wake someone when they’re in stage 4!).
Stage 1: A wake-to-sleep transition period where the person falling asleep can be easily woken up by softly calling their name.
Stage 2: A characteristic of this stage is specific bursts of electrical activity called sleep spindles. This help in the transfer of information from the short term to long term memory. A more intense stimulus can wake the person in this stage.
Stage 3: Progressing further, slow-wave activity marks stage 3, a period of deep sleep. The body begins its restorative process and sleep slowly transitions into stage 4
Stage 4: Called ‘the deepest stage’, the body’s reset process occurs now in full-swing - the rebuilding of cells, high frequency of protein synthesis, reset of the immune system among other benefits.
Sleep then slowly ascends to the lighter stages of NREM (stages 1 and 2) which then transitions to REM.
Marked by a highly active, chaotic, and random brain in a paralyzed body is the Rapid Eye Movement (REM) stage.
Although not strictly classified into stages, REM is occasionally divided into two - the phase of bursts of eye movements, followed by the phase of relative quiescence.
The mental activity in this stage is usually associated with dreaming. People when woken up during REM, typically recall a vivid dream.
During REM, the information learned during the day is typically bounced around information boxes to relate this new piece to the existing ones.
Therefore, this stage is playfully called ‘a google search gone wrong’.
A series of studies conducted that led many to an ethically uncomfortable place identified the importance of both NREM and REM sleep.
Rats deprived of REM died 40% sooner, by day 14, while rats deprived solely of NREM died in 45 days (60% longer).
We know that sleep is important to save information we learn that day. Sleeping after we learn something will help 'hit the save button' by transferring information from the short term to long term memory.
To make matters more interesting, a new finding has shown that sleeping before learning is also crucial as it preps the brain to soak up new information.
Some sleep scientists give the metaphor of a sponge - an already filled sponge can only take so much information before it is squeezed and then it’s ready to take in more.
Now that’s settled, let’s focus on a conjecture that’s been keeping scientists engaged in the past.
We learn stuff when we are sleeping. Now that would be cool, wouldn’t it?
Thanks to the relentless research, we now have an answer and it looks like it is both a yes and a no.
A big NO to learning a new language from scratch and it’s a YES to absorbing information and forming new memories.
Although these were implicit memories, it could alter the individual’s waking behavior.
For example, in a study conducted on sleeping individuals, researches played a sound and followed it with a rotten-fish smell.
When these individuals were tested on awakening, they held their breath once the sound was played, as if anticipating a rotten smell.
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Perhaps you’ve heard of this - The Guinness Book of World Records removed the category of sleep deprivation.
This is from the world’s authority on record-breaking achievements that still permits free-falling down towards earth from outer space in a spacesuit.
Know why? Because the effects of sleep deprivation are considered ‘extreme’ and ‘dangerous’.
So, what happens when you’re completely deprived of sleep? What goes wrong? Let’s take a look at some of the deadly consequences.
These are some of the effects that sleep restriction exerts on your body.
The most harmful of all is that the individual fails to see how sleep-deprived they are when they’re sleep-deprived, and they tend to underestimate their performance disability.
The consequence of sleep loss is so deadly, that the World Health Organisation (WHO) has classified night-shift working as a carcinogen.
Sleep is a universal component of life, and it is not surprising that recent research has shown that genetics plays a pivotal role in its regulation.
Substantial evidence suggests that sleep is a complex trait with a strong genetic component.
Restricting the amount of sleep we receive each night voluntarily or completely depriving a night’s sleep alters the expression of a number of genes radically.
This consequently tampers with daily health and the quality of life.
Several genes are involved in sleep regulation in humans. Some of the candidate sleep genes are CLOCK, PER2, PER3, DEC2, and GRIA3.
The appropriately named CLOCK gene, short for clock circadian regulator, was one of the first genes to be identified as a regulator of sleep.
This gene is a transcription activator that forms the central component of the 24-hour circadian clock. Variations in this gene cause behavioral sleep changes.
For example, one particular variation, from A to G, can affect the way CLOCK activates other genes (ARNTL, PER2, PER3) in the circadian regulatory complex and influence the onset of sleep.
This determines the chronotype of an individual. CLOCK gene variations have also been shown to influence the habitual duration - to be either a long sleeper (>8.5 hours) or a short sleeper (<7 hours).
| Genotype | Implication |
|---|---|
| GG | Likely to have a higher sleep duration |
| AA | Likely to have a normal sleep duration |
Did you know that every living species on the planet with a lifespan of more than a few days has a 24-hour rhythm?
This ‘circadian rhythm’ helps you determine when you should be awake and when you should be sleeping.
Although everyone succumbs to its unyielding power, the pattern between individuals has striking differences.
There are the morning types, you know, the early birds and then there are the evening types, the night owls.
There is yet another less commonly known type, called the ‘afternoon types’ who don’t fit in with the other two categories.
These 'types' are called the chronotypes of an individual.
It defines whether they are most alert in the morning, during the day, or at night.
Larks: These are the morning types, who rise and shine early. They follow the principle ‘early to bed, early to rise’ strictly.
Nappers: These are the afternoon types, who wake up the sleepiest. They are most active between mid-morning and late evening, after which they’re tired again.
Owls: Favoring night time, the owls stay awake through most of the night and go to sleep well past midnight, and they don’t wake up earlier than 10 am.
The chronotype of an individual has a strong genetic component. If a person manages to sleep in synchrony with their chronotype, the night of sleep will be restful.
The repeating signal of day and night is communicated by a ‘vampire hormone’ called Melatonin.
This hormone makes the timing of sleep official.
After the sleep-onset, the levels of melatonin gradually decline through the night and well into the morning.
When the brain detects light in the morning, the release of melatonin is shut off, hinting at the end of the sleeping-process.
Right this moment, as you’re reading this line, there’s a chemical called adenosine that’s building up in your brain.
The longer you’re awake, the more concentrated their accumulation will be.
This is the chemical that’ll increase your desire to sleep at night.
Adenosine cleverly turns on the sleep-inducing regions of the brain and lowers the noise from the wake-promoting regions.
As you’re sleeping, the chemical is slowly cleared off. The total clearance of adenosine marks the onset of wakefulness.
Naps clear adenosine, therefore, many people who take naps are stay awake at night due to decreased sleep pressure.
These individuals can, therefore, take a nap early in the afternoon, to enable sufficient accumulation of adenosine again before bedtime.
For sleep-deprived individuals, naps can at least momentarily improve brain functionality.
Technology: Gadgets emit blue light that slashes melatonin by 50% and delays its further release by 3 hours. Additionally, it also reduces the duration of REM, a stage that is essential for emotional healing.
Alcohol: Alcohol is a sedative and it knocks out the cortex. Furthermore, it fragments sleep, causing many more awakenings throughout the night. These individuals don’t remember it and they wake up unrefreshed the next day and reach for caffeine.
Caffeine: It is a widely used psychoactive drug that not only delays the onset, but also reduces the amount of deep sleep. What’s scarier is, caffeine is particularly good at blocking REM. If this happens routinely, it increases the mortality rate by 60%.
Unfamiliar Location: We don’t get a restful night when in an unfamiliar location, right? This is because sleep happens in kind of a ‘lite’ version. One half of the brain doesn’t rest as well as the other, as we try to instinctively maintain vigilance in the new location from potential threats.
Of the 24 hours, humans have a recycling rate of 16 hours. That means, after every 16 hours, we need an indispensable 8 hours of shut-eye.
Sleep is, after all, what makes us fit to be awake. And so, why we fail to keep it up is a mystery.
Many physiological processes in the body have safety nets.
For example, when you’re feasting, the adipose cells store fat.
This is to use it in the unfortunate scenario of starvation.
Tragically, sleep has no such safety measures.
We are the only species on the planet that voluntarily pulls an ‘all-nighter’.
Many scientists confirm there is a global sleep epidemic underway.
This is a huge challenge to evolution.
Considering the harmful effects of deprivation - ‘the sickening health and the premature death’, it is time for our species to take a serious appreciation for sleep.
It is, ultimately, the kind nurse that nature has given us.
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Less than a month ago, the novel coronavirus disease (COVID-19) was declared a pandemic by the World Health Organisation (WHO) when it affected more than 100,000 people in 114 countries. As of today, April 7, there are over 1,000,000 cases in close to 200 countries. An unprecedented explosion in the number of cases in as little as 20 days is nothing short of terrifying.
Ever since its outbreak in December 2019, scientists have been racing to understand the novel coronavirus (SARS-CoV-2, also called nCoV19). While we know this is the deadliest pandemic the world has seen since the Spanish influenza of 1918, what we don’t really know is just how dangerous this virus is. It appears there are more questions than there are answers. For example: How did the virus make the jump from animals to humans? How does it spread undetected without causing any symptoms right away? Why does it prematurely end the lives of some, but not the others? These are some of the questions keeping virologists occupied presently.
As a string of RNA molecules packed tightly in a protein coat, all viruses function the same. Enter a host cell, hijack its internal machinery, repurpose it to produce viral components, replicate, and once new viruses are made with the host’s help, release to infect other cells. Most viruses work as simple as that.
Coronaviruses, belonging to the complex ‘coronaviridae’ family, are known for their proteins that stick out from the outer lipid layer. These ‘spike’ proteins are considered critical as they help the virus anchor to the host’s cell. Particularly, the spikes interact with angiotensin-converting enzyme 2 (ACE2) of the host to gain access to the cell, and for this, it gets the help of a host cell protein, the transmembrane serine protease 2 (TMPRSS2). On entering the cell, nCoV19 works like other viruses to produce new infectious particles.
Infections that affect animals are generally harmless to humans. However, some viruses do cross the species barrier and cause ‘zoonotic diseases’. COVID-19 is one perfect example. Such zoonotic infections are deadly because we lack pre-existing immunity to them and are unable to fight it off as efficiently. Most such infections that come from animals rarely spread from one person to the next. However, nCoV19 seems to be better evolved and adapted at this and spread between individuals.
As the cases started growing rapidly, researchers in China sequenced the genome of nCoV19 and labs around the world got to work. The genome of the virus, made of RNA and not DNA, carries 15 genes in 30,000 bases. It was found to be similar (~80%) to its sister virus that caused the SARS outbreak in 2003. Both viruses seemed to have jumped from bats (96% similarity to bat coronavirus). Genome analysis suggests that this is a one-time jump, as the genome appears stable and not mutating further. The nCoV19 poses a huge problem because it reproduces so quickly without evoking an immune response from the host. This makes containing the spread of the virus unimaginably difficult.
Thanks to advancements in genomics, we now know a lot about nCoV19 in a short span of a few weeks. For example, genome comparison studies suggest that the novel coronavirus is a chimera of two pre-existing viruses. Such recombination is not unheard of. But it would occur only if the two different viruses affect a host simultaneously under a set of unique conditions. Owing to the rare occurrence, labs are now trying to confirm the preliminary findings.
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The majority of COVID-19 cases develop flu-like symptoms and a little over 70% of the people recover on their own. However, 1 in 6 people develop shortness of breath and difficulty breathing. In yet some cases, healthy people with no symptoms are diagnosed with COVID-19. This selective nature of nCoV19 has left virologists perplexed and they are turning to genetics for an answer.
As of today, theories favor the differences in the genetic makeup of individuals that make them more or less susceptible to being infected by nCoV19. For instance, certain variants of the ACE2 gene may alter the receptor to which the spike proteins bind. This may render it difficult for the virus to gain entry into the host cells. This theory is plausible because an example of such effects could be seen in the case of HIV. A variation in the CCR5 gene profoundly affected the entry of HIV and made the individuals carrying the variation resilient to infection. Another example stems from variations in the HBB gene. This gene encodes a subunit of a protein that’ll be a part of hemoglobin (the oxygen carrying component of our red blood cells). Particular variants of HBB make individuals carrying them less susceptible to infection by malaria-causing parasites.
Considering these examples, scientists are also wondering if variations in genes that influence immune responses might have a part to play in the difference.
Presently, all of this remains a conjecture. Efforts are now underway to pool genetic data from across the globe, ranging from DNA of individuals in severely hit places to those with mild infections of COVID-19 to better understand the role of genetics in the uncharacteristic behavior of coronavirus.
To understand if the severity of the disease reflects variations in the genome, 23andMe is actively recruiting hundreds of thousands of its customers across the United States. The researchers at 23andMe are planning an online survey followed by a GWAS. This will help analyze the key genetic variants associated with the differences in the severity of the symptoms. While they are optimistic, they forewarn that identifying the role of genetics in symptom-severity is not assured.
Other researchers support the concept of ‘viral load’ i.e. the dose of the virus at the time of exposure. A higher viral load would translate to a severe case, while a lower dose can be easily fought off by the immune system and does not cause severe symptoms. However, emerging evidence suggests that the relationship between the infection and severity may not be so simple either. This makes COVID-19 stand out from other such viruses. Minimizing exposure to the virus still helps as our immune system is efficient to take down lower loads of nCoV19.
Despite performing reams of research and analyzing a spell of data from different countries, we still don’t have an answer. The estimates are wide, with mortality ranging from as low as 1 in 1000 to as threatening as 1 in 30. There appears to be no defined answer, with the fatality rate different in each country. Italy has a death rate of 12% while in Germany, it’s 1%. The difference in the rate could be attributed to the age group of the population affected. The first few cases affected in Italy were the older people, while in Germany most cases affected were under the age of 40.
However, the statistics don’t give us a general estimate of how many infected people will lose their lives to the infection. One important question to ask in this scenario is - how many people are left undiagnosed because they show no, or if at all, mild symptoms? When antibody tests are approved, we may be able to estimate the missed cases. But for now, we don’t know just how fatal COVID-19 is.
Thousands of people have recovered from coronavirus. Does that mean they are immune for life? Or can they catch the disease again? Several reports in China and Japan have identified second positives for nCoV19. This caused panic among people, as it meant that unless a vaccine is in place, we may all be subjected to nCoV19 multiple times. To study this, a group of scientists tried to reinfect four rhesus macaque after their first infection. Surprisingly, they were immune the second time around. This gave hope as immunity could be established against nCoV19. However, there’s not been enough time to analyze the immunity to nCoV19. Scientists are not certain for how long the immune responses clad us with protection against COVID-19.
Ever since COVID-19 was declared a pandemic, the sale of alcohol has been on the constant rise. As the stressful time has made most people fragile, many psychologists are worried about the overuse of alcohol and the toll it could take on the immune system. Along with the risk of mental health issues, alcohol would also make people more susceptible to infection by nCoV19, by compromising their immunity. In fact, it has become so much of a concern that WHO has issued a warning against the excessive use of alcohol, especially during the pandemic.
Winters generally see the peak in flu cases for a few reasons. First, viruses love the cold, dry weather. Second, the immune system is not at it’s best due to minimal sunlight exposure. Could this be the case with COVID-19? The evidence is conflicting but the WHO warns that the virus is capable of spreading in hot and humid weather. A study conducted in China which agrees with WHO identified that nCoV19 is suited to spread in warm temperatures. However, a large-scale study of cases till February 29 found a lower incidence of disease onset in regions that have a higher temperature. Scientists believe that an accurate prediction of seasonality is possible only by keeping track of the number of cases as the season changes.
Like all viruses, nCoV19 requires hosts’ living cells to survive. The main strategy with the vaccines is to nudge the body and alert the presence of a pathogen and letting our immune system take care of the rest. Alternatively, interfering with any step of the viral replication will be helpful too. So then, if we know how a virus can be stopped, why is it taking so long? It is because there is so much more that we’re not sure of. More importantly, we have to keep the safety and efficacy of the vaccine in mind. In the words of a scientist at Mayo Clinic, ‘We’re building the plane as we’re flying’.
Usually, developing a vaccine takes years. Thanks to the scientists working at breakneck speed in the labs around the world, we may be able to get a vaccine in as short as 12-18 months.
We now have several vaccine candidates, all of which are currently under trial. To date, there is no one vaccine to treat/stop the spread of the virus. Therefore, it has become all the more important to have good immunity to be able to fight off the incoming pathogen. Taking care of your immune system, the resilient force of your body is the way to go especially in the face of threats like the COVID-19.
https://www.who.int/dg/speeches/detail/who-director-general-s-opening-remarks-at-the-media-briefing-on-covid-19---11-march-2020
https://www.contagionlive.com/news/zoonotic-threats-as-unpredictable-as-they-are-dangerous
https://www.who.int/blueprint/priority-diseases/key-action/novel-coronavirus-landscape-ncov.pdf?ua=1
https://www.nature.com/articles/s41586-020-2012-7
https://www.medrxiv.org/content/10.1101/2020.02.13.20022715v1
https://www.medrxiv.org/content/10.1101/2020.03.18.20036731v1
https://www.biorxiv.org/content/10.1101/2020.03.13.990226v1
https://www.japantimes.co.jp/news/2020/02/28/national/coronavirus-reinfection/#.Xo1eZ8gvOLR
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