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Procrastination is the constant and unnecessary postponing of essential tasks.
It can be a simple chore like cleaning your desk or something more urgent, like sending that vital email to your boss.
Procrastination can prevent you from achieving your goals and increase stress levels due to the piling up of essential tasks until the last minute.
It can be a debilitating condition that hampers your well-being.
Research on behavioral traits in the last decade confirms that your tendency to procrastinate is partly genetic.
According to a study in Psychological Science, genetics can explain at least 46% of a person’s tendency to procrastinate.
A 2018 study reported compelling evidence connecting procrastination with a gene involved in regulating dopamine, or the happy hormone.
Our brains experience a dopamine rush when we do something we love.
That is how we are motivated to complete a task.
The TH gene produces tyrosine hydroxylase enzyme that helps regulate dopamine production.
But scientists have found that a particular protein interferes with the brain’s reward system and decreases dopamine secretion.
Mutation in this gene reduces dopamine production and hampers the reward system.
Reduced dopamine secretion in the body can make people feel unmotivated and depressed, resulting in serial procrastination.
However, the dopamine-procrastination relationship seems slightly different for women.
Females with the TH mutation were more likely to have higher dopamine levels and be procrastinators.
These researchers hypothesize the role of estrogen in this.
Some studies suggest that having a larger amygdala is related to procrastination.
Amygdala is the part of the brain that helps process emotions.
If you have a low threshold of tolerating negative emotions, then you might be more prone to procrastination.
Many people are of the opinion that procrastination is just laziness.
But modern research has revealed a lot more about procrastinators and what exactly goes on in their minds.
Procrastination can even be a symptom that points to deeper mental health issues.
Procrastination often stems from clinical depression and acute anxiety. Some people get extremely anxious about even starting a task, so they don’t do it at all.
Others fear failing at the task and then being criticized for it, so they keep avoiding it to delay the heartbreak.
There also appears to be a relationship between obsessive-compulsive disorder (OCD) and procrastination.
Attention deficit hyperactive disordered patients also procrastinate because their minds are always racing, and they have difficulty focusing on one task.
Poor physical or mental health might be another major reason for procrastination. Lack of energy or mental exhaustion can also lead to postponing important tasks.
Procrastination can point to a deeper problem, especially if it is a chronic issue that hampers daily life.
Contrary to popular belief, procrastination is not the same as laziness.
It can signify an underlying mental health condition like anxiety, depression, or OCD.
Research studies suggest that genes can explain 46% of a person’s tendency to procrastinate.
These genes may play a role in dopamine regulation, which controls the brain reward system.
Due to variations in these genes, some may not feel positive and rewarded when completing and task and, thus, may tend to postpone it.
There is no easy answer when it comes to determining whether or not genius is genetic.
However, there are a few key points that can be looked at when trying to make this determination.
First, it is important to understand what genius actually is.
A genius is often defined as someone with exceptional natural ability or talent, particularly in a specific field.
This definition leaves room for interpretation, as many people may be considered genius in one area but not another.
The average genius IQ is said to be around 140.
Some signs that may qualify a person as a “genius” include:
Sir Cyril Burt, between 1943 and 1966, conducted numerous twin studies on IQ and genetics.
He concluded that IQ has a significant genetic component.
Several other studies report that the heritability of intelligence could be as high as 0.8 (on a scale of 0.0 to 1.0).
DTNBP1 is a gene of interest associated with intelligence.
It produces a protein called the dystrobrevin-binding protein 1 and is a candidate gene for schizophrenia.
Recent studies report that DTBNP1 may play a role in cognition.
A study found that a specific type of the DTBNP1 gene was associated with higher educational achievement in those with schizophrenia.
The authors hypothesize that this genetic change modifies schizophrenia risk by enhancing cognition.
This could explain why geniuses like Vincent Van Gogh or Sir Isaac Newton had their own share of mental illnesses.
According to studies, genetics can drive anywhere between 30-75% of the variations in people’s IQ levels.
However, certain environmental factors and socioeconomic status can prevent a person from achieving their true genetic potential of IQ levels.
Having the genetic traits of a genius but not having the support or encouragement to channel these talents is futile.
Studies show that parents who nurture their children’s talent by providing the right guidance and training are making geniuses.
Let’s now have a look at some environmental factors that can shape someone to be a genius.
A lack of financial stability may hinder the resources that can be provided to a child to reach their full IQ potential.
According to a research study, children of the highest and lowest socioeconomic status, on average, differ in IQ by 6 points at the age of 2 years.
Further, by the age of 16, the IQ gap had almost tripled.
Certain nutritional components of your diet help improve cognitive functioning.
According to a study, nutritional deficiencies at the age of 1 to 5 can reduce IQ by up to 15 points!
Good parental relationships, encouraging comments, constructive criticism, and regular feedback can all help forester a child’s genius potential.
Getting information about your/your child’s cognitive abilities can help identify and use the correct tools to support these abilities.
It can also help highlight the areas which require further time and attention.
Geniuses are both born and made. While genetics can explain up to 75% of variations in IQ levels, factors like socioeconomic status and home environment decide whether a person achieves their full genetic IQ potential.
Glucagon-like peptide-1 agonist (GLP-1 agonist) is a class of drugs used in treating type II diabetes and helping with weight loss.
According to the American Diabetes Association, metformin remains the most preferred drug to treat type II diabetes.
However, in the case of metformin intolerance or if diabetes is combined with obesity, GLP-1 agonist drugs may help.
There are two categories of GLP-1 agonist drugs available in the market.
Drugs in this category include:
Drugs in this category include:
People with type 2 diabetes have lower levels of insulin secreted in the body.
As a result, glucose from the food is not broken down.
This leads to higher blood glucose levels.
GLP-1 agonist drugs imitate a naturally produced hormone in the body called glucagon-like peptide 1 (GLP-1).
This hormone may help improve insulin secretion in the pancreas.
Therefore, this drug can reduce blood sugar levels and control type 2 diabetes.
Recently, researchers have identified an added benefit of using GLP-1 agonist drugs - weight loss.
The GLP-1 hormone may help regulate hunger and appetite.
It helps in the following ways.
Studies show that this drug class helped people lose an average of 2.9 kg compared to people who did not take it.
According to experts, GLP-1 agonist drugs also help decrease the overall mortality rate in people with type 2 diabetes.
Post Food and Drug Administration’s (FDA) approval, the drug is prescribed for people with BMI > 30 or those with type 2 diabetes and BMI > 27.
Please note: GLP-1 agonists can only be used under the supervision of a qualified medical practitioner. Xcode Life doesn’t promote using GLP-1 or any other medication for weight loss.
Some of the common side effects of GLP-1 agonists are:
In rare cases, the patient’s body can form antibodies against GLP-1 analogs, leading to reduced efficacy.
Long-term use of these drugs may increase the risk of gastrointestinal issues.
Other rarer side effects of the drug include the following.
Doctors may prescribe GLP-1 agonist drugs for people with a BMI of more than 30 who can’t lose weight with lifestyle changes.
The drugs may also benefit those over a BMI of 27 and with type 2 diabetes.
The first oral GLP-1 agonist drug approved by the FDA for type 2 diabetes and weight loss is oral semaglutide. The drug was approved in 2019.
The following people are not recommended to take GLP-1 agonist drugs.
GLP-1 agonist drugs help suppress hunger and help people feel fuller for longer after a meal.
However, the drug needs to be backed by moderate exercise and dietary changes for it to work.
A molecule that binds to an enzyme and inhibits its activity is called an enzyme inhibitor.
Enzyme inhibitors have a vital role in all cells because of their target action.
COMT inhibitors are one of the most prominent enzyme inhibitors in Parkinson’s treatment.
Catechol-O-methyltransferase (COMT) inhibitors are a group of medications in the therapeutic approach to Parkinson’s treatment.
It inhibits the enzyme COMT, which methylates catecholamines such as epinephrine, dopamine, and norepinephrine.
Catecholamines are hormones responsible for modulating our stress responses.
COMT also methylates levodopa and carbidopa (a class of medications in Parkinson’s treatment) before entering the target site.
COMT inhibitors prevent this methylation and offer complete therapeutic benefits in treating Parkinson’s disease.
The depletion of the neurotransmitter dopamine in the brain is the major cause of Parkinson's disease.
The precursor to dopamine is provided by levodopa medication.
When the COMT enzyme degrades dopamine, COMT inhibitors prevent its action by working against the process.
It works by blocking the peripheral degradation of levodopa, enabling the drug to cross the blood-brain barrier.
This increases its effects by allowing more of it to enter the brain. Thereby increasing the bioavailability and half-life of levodopa.
The purpose of antiparkinson drugs is to extend the brain's absorption of dopamine through:
COMT inhibitors work best in combination with levodopa by blocking the drug's breakdown and prolonging its efficacy.
This saves people with Parkinson’s disease during the phase of motor fluctuations.
Motor fluctuations are caused when dopamine levels decrease in the brain. That’s when levodopa is taken, and the person functions well.
When the drug effect wears off, the person finds it difficult to move.
COMT inhibitors delay the body's ability to break down levodopa and maintain dopamine concentration even when the effect wears off.
A study reported that COMT inhibitors have potential antidepressant properties on chronic mild stress (CMS)-induced anhedonia in rats.
The findings indicate that selective, reversible COMT inhibitors have been used therapeutically to treat depression in addition to Parkinson's disease.
The most typical adverse effects of COMT inhibitors are as follows:
Humans have 23 pairs of chromosomes. Of these, 22 are called autosomes, and one pair in each cell is called the sex chromosome.
There are two sex chromosomes - the X and the Y.
People assigned females at birth (FAB) have two X chromosomes, whereas those assigned males at birth (MAB) have one X and one Y chromosome.
These sex chromosomes play many roles in the body, though they are primarily responsible for the development and functioning of the reproductive system in men and women.
Loss of the Y chromosome (LOY) is a genetic condition detected in blood samples of people assigned MAB.
LOY has been associated with several diseases, like cancer.
Though the primary function of the Y chromosome is the normal development of males, it has several roles beyond this.
A few decades ago, doctors began noticing that blood cells in older men were missing the Y chromosome.
The exact cause for this disappearing chromosome is unclear even today.
However, researchers suspect that men allow genetic mutations (abnormal changes in the genes) to accumulate, eventually leading to diseases like cancer and heart disease.
Loss of the Y chromosome is now believed to be a part of the normal aging process.
It is called a ‘mosaic’ LOY because the loss is observed only in a fraction of the cells.
Research states that LOY is part of the normal aging process in healthy men, and the number of cells affected increases with time.
A 2014 study reported that LOY caused an average 5.5 years decrease in the lifespan of men affected with the condition.
For this reason, LOY can be used as a biological marker and helps predict the development of male age-related diseases.
LOY has been associated with the development of cardiovascular diseases.
A study on male mice found that those who lost their Y chromosome had weaker hearts.
Researchers also noticed a build-up of fibrous connective tissues in the heart of mice with a missing Y chromosome.
This stiffening of heart muscles makes it difficult for the organ to pump blood effectively.
A similar study was conducted in humans, and it was found that men who had lost the Y chromosome from at least 40% of their white blood cells were 31% more likely to die from circulatory system disease than those with abundant Y chromosomes.
Apart from cardiovascular disease risk, loss of the Y chromosome also has other health implications, which include:
The medical and research community do not yet have a complete understanding of what exactly causes migraine. Certain activities, environmental exposure, and emotion can trigger a severe migraine attack. Having to deal with pain is not just debilitating but also leads to a loss of productivity. This begs the question - why migraine happens? Are migraines hereditary? Do certain genes cause migraine?
Researchers have identified several genes associated with migraine.
In the sample report below, we've attempted to analyze some important genes that increase the risk of migraine.
You can identify your genetic risk of migraine by using your 23andMe DNA data and placing an order for the Gene Health Report.
Genetics play a big role in migraine.
Certain genes associated with migraine explain up to 60% of the reason people get migraine headaches.
While they may not directly “cause” migraine, they make the person more sensitive to environmental and lifestyle triggers that can cause migraine.
There’s no single “migraine gene.”
Studies suggest that mutations in a group of genes can contribute to migraine headaches.
A study examining 8,319 individuals across 1,589 migraine families found more than 40 genetic regions associated with migraine.
The researchers found that these families had more genetic changes associated with migraine than the general population.
Certain characteristics may indicate a strong family history of migraines.
Some important genes studied in association with migraine include:
It has long been established that migraine has a significant genetic component.
Migraines do not have a clear inheritance pattern; however, more than half the people with migraine have at least one family member with the same condition.
Further, if one or both of your parents have migraines, you have a 50-75% chance of having them.
According to family and twin studies, a first-degree relative of a person with migraine without aura (MO) has a 2x increased risk of having MO and 1.4x increased risk of having migraine with aura (MA).
A first-degree relative of a person with MA has a 4x increased risk for the same condition but no increased risk for MO.
Familial hemiplegic migraine (FHM) is a type of migraine that runs in families.
FHM can result in severe migraine episodes, which can include fever, seizure, prolonged weakness, and, rarely, coma, and death.
20% of people with FHM may develop permanent difficulty coordinating movements, a condition called ataxia.
Some genes implicated in FHM are
The first three genes regulate the movement of ions across cells, which is important for signaling in the brain.
FHM is inherited in an autosomal dominant pattern.
What does this mean?
A biological parent with FHM has a 50% chance of passing it on to their child.
So, in most cases, an affected individual has at least one affected parent.
Except in rare cases, inheriting a single specific mutation does not result in migraine.
Most migraine headaches are caused due to a combination of genetic and environmental factors.
Knowing your genetic risk for migraine in advance can help manage triggers and plan effective management strategies.
Identifying specific gene variants helps in knowing the possible cause of migraine.
This, in turn, helps plan treatments that focus on that particular pathway.
Further, it can also give guidance to testing other family members.
Genes can explain 60% of the reasons behind migraine.
KCN18 and CKIdelta are two important genes associated with migraines. The former produces a protein that regulates ion transport in cells, and the latter influences circadian rhythms.
Mutations in these genes can increase the risk of migraine with aura.
Biological parents with migraines have a 50-75% chance of having a child with migraine in each pregnancy.
Familial hemiplegic migraine is a specific type of migraine that runs in the family and is inherited in an autosomal dominant pattern.
Genetic testing can help you understand your risk for migraine, avoid the triggers, plan effective management strategies, and opt for effective treatment.
