Have you ever felt like taking a random, unplanned decision or an impulsive choice because you ‘felt like’ doing it?
Buying that dress or handbag just like that?
Making that travel booking because you felt like going on a holiday? Or quitting your well-paying job because you had a tiff with your boss?
Do you know people who take such impulsive decisions?
Some instances mentioned above are examples of impulsive decisions that people take.
It is not surprising that we find impulsive people in our day to day lives.
But, how do you define impulsivity?
If you or someone you know has a tendency to act without foresight or thought about the consequences of their actions, it is termed as impulsivity.
While some people are impulsive by nature, for many others, it is a sign of an underlying disorder.
Everyone expresses a certain amount of childish impulsivity occasionally, and this is acceptable in adults.
But, being too impulsive is not considered normal.
It is, however, very common in children as they take quick decisions without much thinking.
In the later years, this slowly gives way to maturity and self-control as they grow older.
Impulsive adults are also mighty risk-takers because many a time they don’t think through their decisions or actions and end up taking a huge risk.
Impulsivity is believed to occur due to the failure of the brain’s inhibitory function to work when making decisions.
This leads to the individual making a decision without thinking it through.
Many studies exploring the causes of such behavior has more than often lead the researchers along the path of genetics.
The HTR2A gene, also known as the 'impulsivity gene' is closely associated with the condition.
Individuals carrying a certain variant of the gene are predisposed to impulsivity.
In these individuals, the brain’s inhibitory control either slows or is lost and prevents the individual from making rational decisions.
An SNP analysis showed that there existed a combined phenotype within the 5-HT2a receptor gene or the HTR2A gene attributing to the condition.
The SNPs involved in impulsivity are rs63163 and rs6311. A study found that the T allele of rs6313 was protective in opioid and alcohol dependence studies, whereas, the A allele was associated with alcohol dependence and abuse.
Also, the G allele of the rs6311 had similar effects as the T allele of rs6313.
| GENE | RS Id | RISK ALLELE |
|---|---|---|
| HTR2A | rs6313 | T |
| HTR2A | rs6311 | G |
Impulsivity is a symptom of many behavioral disorders such as
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Impulsivity is one of the three primary symptoms of ADHD or Attention Deficit Hyperactivity Disorder.
In fact, attention deficit and impulsivity are some of the characteristics of the DSM-IV criteria of ADHD.
There is evidence that links the trait with psychiatric patients who suffer from various other conditions.
A few psychological conditions implicated in impulsivity are mood disorders, borderline personality disorders, pathological gambling, and self-harming behavior.
There are several human studies that prove the link between impulsivity and alcohol abuse.
These studies show that alcohol abuse triggers impulsive behavior in an individual.
It is also not a surprise that impulsive individuals tend to lose self-control and end up in alcohol abuse.
It is not uncommon to make impulsive decisions when it comes to food.
Individuals with this trait are seen to be prone to conditions like emotional eating, frequent and intense food cravings, eating at night and addictions to certain types of foods.
However, there is a need for additional research to further correlate impulsivity with overeating.
We mentioned earlier that individuals of impulsive nature are risk-takers.
Many studies reveal that highly impulsive people take greater risks than those with less impulsive nature.
This also implies that highly impulsive adolescents are more likely to injure themselves and others.
There are two popular impulsivity questionnaires that enable individuals to self-evaluate whether or not they suffer from impulsivity.
These questionnaires are also useful to identify high-risk individuals.
The treatment is multifaceted and involves addressing various aspects of the condition.
However, proper education and psychiatric intervention, allows us to address the loss of control and impulsivity in individuals who suffer from more severe forms of the symptom.
Upload your DNA raw data to Xcode Life. Our Traits and Personality Report analyses, impulsivity, intelligence, extraversion, and 29 more such categories.
PON1 gene in humans is located on the long arm of chromosome 7.
This gene was the first discovered gene of the paraoxonase multigene family along with the PON2 and PON3 genes.
The PON1 gene codes for the enzyme serum paraoxonase/arylesterase 1 or PON1 that has esterase and paraoxonase activity.
The PON1 enzyme is composed of 354 amino acids and is synthesized by the liver.
PON1 associates itself with High-Density Lipoprotein (HDL) in the circulation.
The PON1 gene shows many polymorphisms in the coding and promoting regions.
Polymorphisms in the PON1 gene have an association with coronary artery disease and diabetic retinopathy.
PON1 plays a major role in oxidative stress and inflammatory response by virtue of its association with HDL cholesterol in the body.
HDL facilitates the secretion of the PON1 enzyme, which in turn prevents the oxidation of HDL and stimulates cholesterol efflux from the cells.
These together offer an atheroprotective function to HDL.
As the name goes, these substances and compounds inhibit oxidation in the body.
Antioxidants are natural compounds that help neutralize free radicals in our bodies.
Free radicals are substances whose elevated levels can be harmful to the body.
The elevated levels have an association with diseases like cancer, heart disease, diabetes, and aging.
Our body cells constantly produce free radicals as a reaction to internal body and environmental pressures and stresses.
The cells in our body are responsible for the production of these free radicals.
These are unstable molecules, and thus can cause slow cell damage.
Since these free radicals are reactive oxygen species, the antioxidants naturally counter them.
Antioxidants are neutralizers of these free radicals and can be obtained by consuming foods that are rich in them.
In individuals who are healthy and disease-free, there is a balance of antioxidants that counter the effects of the reactive free radicals.
| SNP | Allele | Risk |
|---|---|---|
| rs854560 | T | Beneficial of antioxidant needs |
| rs662 | C | Risk of antioxidant needs |
SNP rs854560 is a polymorphism that is present on the PON1 gene associated with antioxidant needs.
The variants of this SNP affect levels of the PON1 enzyme and have an association with coronary diseases and diabetes. The T allele is the more favorable form of the SNP and codes for methionine, which leads too elevated levels of paraoxonase.
This is beneficial to the body.
However, the A allele codes for leucine; this leads to reduced paraoxonase activity, which is harmful to the body.
| SNP | Allele | Risk |
|---|---|---|
| rs854560 | AA | 2x Higher risk of Coronary Heart Disease and Diabetic retinopathy |
| rs854560 | AT | 2x Higher risk of Coronary Heart Disease and Diabetic retinopathy |
| rs854560 | TT | 1.8x Higher risk of Coronary Heart Disease and Diabetic retinopathy. |
SNP rs662, also called as Q192R is a polymorphism of the PON1 gene.
The C allele codes for arginine, whereas the less common T allele codes for glutamine.
The presence of the TT allele can imply lower or decreased levels of PON1 enzyme activity. Higher the PON1 enzyme activity, the lower is the risk for heart disease.
The TT allele also increases the risk of coronary heart disease by 2.3x and also increased the risk of vascular dementia, kidney disease, ischaemic heart disease, and male infertility.
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HLA or the Human Leukocyte Antigen complex is a group of proteins that are involved in the regulation of the immune system of our body.
The HLA is the human equivalent of the Major Histocompatibility Complex or MHC that is found in many other animals.
The HLA gene is involved in providing the instructions for the formation of these HLA proteins.
The MHC in humans is made up of over 200 genes that are placed closely on chromosome 6 and are broadly divided into three groups:
There are 3 classes of the MHC I gene namely, HLA- A, HLA- B, and HLA- C.
The 6 classes of the MHC II gene include HLA-DPA1, HLA-DQA1, HLA-DQB1, HLA-DRA, and HLA-DRB1.
The MHC III genes are also involved in immunity and inflammation.
The histocompatibility genes have many genetic variations involving a lot of single-nucleotide polymorphisms.
Some of these variants are known to be associated with many forms of allergies.
Gluten is a protein that is found in grains such as wheat, barley, and rye.
It is the component that allows the flour to rise, holds the dough and allows absorption of liquids.
This property is also used to thicken sauces and gravies.
However, there is a small percentage of people who cannot tolerate gluten and are called gluten-intolerant or gluten-sensitive individuals.
Gluten sensitivity is genetically linked.
Two genes namely HLA DQ2 and HLA DQ8 have primarily been linked to celiac disease (the most severe form of gluten sensitivity).
Other genes such as HLA DQ1 and HLA DQ3 are also believed to predispose an individual to gluten sensitivity.
Though only 1 % of the population has celiac disease, a larger part of the population suffers from gluten sensitivity.
Every individual gets two copies of the HLA DQ gene, one from their mother and one from their father.
The 2 copies of the HLA DQ gene you get determines your sensitivity to gluten.
| rsid | gene name | risk allele | implications |
|---|---|---|---|
| rs4639334 | HLA DQ 7 | A | Increased risk for gluten sensitivity |
| rs7454108 | HLA DQ 8 | C | Increased risk of developing the celiac disease and Type-1 Diabetes |
| rs2395182 | HLA DQ2.2 (M1) | T | Increased risk for gluten sensitivity. Having the T allele of the HLA DQ2.2 gene on chromosome 6 increases the risk of gluten sensitivity and celiac disease by 71% as compared to having the G allele. |
| rs7775228 | HLA DQ2.2 (M2) | C | Increased risk for gluten sensitivity. The presence of the minor C allele increases the risk of autoimmune disorders such as celiac disease and hay fever. |
| rs4713586 | HLA DQ2.2 (M3) | G | Decreased risk for gluten sensitivity |
| rs2187668 | HLA-DQ 2.5 | A | Increased risk for gluten sensitivity For most individuals, having the G/G alleles for SNP rs2187668 of HLA-DQ 2.5 gene reduces the risk of celiac disease. However, for those having the A allele, the risk increases by 2.1 times for those with A/G alleles and by 3 times for those with A/A alleles. The A allele puts the individual at risk of not just celiac disease and gluten sensitivity but also other autoimmune diseases like Lupus. |
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Commonly found allergic conditions such as asthma, hay fever, and eczema occur due to increased levels of Immunoglobulin E(IgE) produced in the blood in response to certain allergens.
Out of the many studies that are currently underway to understand the nature and cause of this IgE allergic response, one genetic epidemiological study in atopic individuals shows strong associations between HLA class II genotypes and IgE response to antigens.
These HLA molecules are membrane-bound glycoproteins that bind processed antigen polypeptides and present them to T cells.
The HLA class I antigens are found on all nucleated cells and platelets and are cytotoxic in nature.
The HLA class II molecules are found mainly on B cells, activated T cells, and monocytes/macrophages.
There are many studies that have shown some form of a strong association between HLA genes and IgE mediated allergic responses.
There is still some uncertainty over the exact role of HLA class II genetic polymorphisms in triggering these responses.
But, there is a certainty that HLA genes have a crucial role to play in allergic reactions.
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Dust mite allergy is a type of allergy to tiny bugs that live in house dust.
The symptoms of dust mite allergy are very similar to that of hay fever and include sneezing and runny nose.
Certain genetic variants of the HLA-DRA gene have been associated with the increased risk for dust mite allergy.
| rsid | gene | risk allele | implications |
|---|---|---|---|
| rs3177928 | HLA-DRA | A | Increased risk for dust mite allergy. The A allele of SNP rs3177928 is strongly associated with allergic reactions, including those to dust mites. The same SNP is also linked with LDL increased risk of high cholesterol and total cholesterol levels. |
Pet allergy is a type of allergy that occurs in individuals due to exposure to certain proteins in the saliva, hair or skin of pet animals like cats, dogs, hamsters, etc.
The symptoms of pet allergies are similar to any other allergies and include incessant sneezing, runny nose, itchy and watery eyes, nasal congestion, cough, etc.
| rsid | gene | risk allele | implications |
|---|---|---|---|
| rs7775228 | HLA-DQB1 | C | Increased risk for pet allergy. The C allele of the SNP rs7775228 of HLA-DQB1 shows increased risk of allergy to allergens in dog dander. |
| rs3177928 | HLA-DRA | A | Increased risk for pet allergy. The A allele of SNP rs3177928 is strongly associated with allergic reactions, including pet allergies. |
| rs9266227 | HLA-C | C | Increased risk for pet allergy. |
Unlike many other allergies, peanut allergy can lead to a grade IV allergic reaction called anaphylaxis, which can be fatal if not treated in time.
Common symptoms of anaphylaxis include redness or swelling on the skin, runny nose, itching, tingling, and tightening around the mouth and throat.
Individuals may also experience digestive problems like diarrhea, and shortness of breath with wheezing.
| rsid | gene | risk allele | implications |
|---|---|---|---|
| rs7192 | HLA-DRA | G | Decreased risk for peanut allergy. |
| rs9275596 | HLA-DQB1 | T | Decreased risk for peanut allergy. |
The presence of the G allele on the SNP rs7192 of the HLA-DRA gene reduces the risk of developing a peanut allergy.
| rsid | risk allele | implications |
|---|---|---|
| rs7192 | G/G | Normal |
| rs7192 | G/T | 1.7x higher risk of developing peanut allergy. |
| rs7192 | T/T | 3x higher risk of developing peanut allergy |
Another SNP rs9275596 is associated with the increased susceptibility to develop peanut allergy in people of European descent.
The presence of the T allele is associated with the decreased risk of developing a peanut allergy.
| rsid | risk allele | implications |
|---|---|---|
| rs9275596 | T/T | Normal |
| rs9275596 | C/T | 1.7x higher risk of developing peanut allergy. |
| rs9275596 | C/C | 3x higher risk of developing peanut allergy. |
Pollen allergy is basically the allergy to pollen that is shed by plants during the spring or summer seasons.
The symptoms of pollen allergy are similar to other allergies.
Presence of the T allele in SNP 2155219 increases one’s risk of developing hay fever and allergy to grass pollen.
While it is possible to avoid some of our known allergens, we still tend to encounter an allergic reaction every now and then.
Even though there are anti-allergic medicines such as antihistamines that can be taken to resolve an allergic reaction, many people prefer to use some natural home remedies.
Here is a list of home remedies which have proven to be effective in treating allergic reactions:
Antibodies are substances that are produced by the human body in response to foreign substances that enter the body.
HLA antibodies are also formed in pregnant women.
During blood transfusions and organ donation, these HLA antibodies are not harmful to the person producing it.
However, when there are HLA antibodies already present in the blood or plasma products that are transfused, it can create complications to the recipient.
This HLA antibodies-containing transfusion can lead to a serious complication called Transfusion-Related Acute Lung Injury.
This is characterized by a sudden acute respiratory distress post-transfusion.
A blood test can help detect the presence of HLA antibodies in one’s blood.
If you test positive for HLA antibodies, it poses no risk to you but you will not qualify for plasma or plasma blood products donation.
However, you can still donate your red blood cells.
The ALPL gene codes for the tissue non-specific isoenzyme called Alkaline Phosphatase (TNSALP).
This enzyme is responsible for the growth and development of bones and teeth.
It is also found in other organs such as the liver and kidneys.
Over 300 mutations have been observed in this gene in people with hypophosphatasia, an inborn error of metabolism.
Such mutations lead to the formation of a defective TNSALP which prevent effective mineralization of the bones and teeth.
When these ALPL gene mutations eliminate the activity of TNSALP, it results in severe forms of hypophosphatasia.
This condition has either an autosomal recessive or autosomal dominant pattern of inheritance.
Vitamin B6 is composed of three closely related compounds – Pyridoxine, Pyridoxal, and Pyridoxamine.
These compounds metabolize to form Pyridoxal phosphate that acts as a coenzyme in many important reactions in the body.
Vitamin B6 is responsible for the formation of heme (an iron-containing compound which is a part of hemoglobin molecule ), synthesis of nucleic acids, lipid, carbohydrate, and amino acids.
When the body is unable to get the required amount of vitamin B6, it leads to a deficiency of the vitamin.
We meet our daily requirements of vitamin B6 from the food we eat, and therefore, a dietary deficiency is quite rare.
But, one can be deficient in vitamin B6 due to other secondary causes.
Primary vitamin B6 deficiency is rare in the general population.
But, secondary causes such as digestive troubles, kidney or liver troubles can still lead to vitamin B6 deficiency.
The common signs and symptoms of vitamin B6 deficiency are:
This is one of the first signs that appear in an individual with vitamin B6 deficiency.
The tongue becomes sore, red, swollen, and smooth (due to loss of tongue papillae). This condition is known as glossitis.
Another characteristic feature of vitamin B6 deficiency is cracked, swollen, and red lips along with cracked corners of the mouth.
This makes it difficult to perform regular activities such as talking, eating, and yawning.
Vitamin B6 deficiency causes peripheral neuropathy, which is characterized by tingling or burning sensation in the hands and feet.
Vitamin B6 deficiency commonly causes lethargy, tiredness, and fatigue in the body.
Vitamin B6 deficiency is also associated with weakened immune function, making the individual more susceptible to infections.
This happens because vitamin B6 is involved in the production of WBCs and antibodies.
Vitamin B6 is involved in the synthesis of neurotransmitters such as serotonin. Thus its deficiency leads to irritability, anxiety, and mood swings.
Vitamin B6 deficiency can be of two types:
But, dietary vitamin B6 deficiency is very rare as many foods that we regularly eat contain adequate amounts of vitamin B6.
| rsid | gene name | risk allele |
|---|---|---|
| rs1780316 | ALPL | T |
| rs1697421 | ALPL | T |
SNP rs1780316 is located on chromosome 1 and is associated with the risk of vitamin B6 deficiency.
A trial study conducted on stroke prevention showed that rs1780316 has genetic associations with plasma B12, B6, and folate levels in people with ischemic stroke.
The T allele of the SNP rs1697421 has also been associated with vitamin B6 levels in the body.
The normal range of the biologically active form of vitamin B6 (pyridoxine) is 5-50 µg/L.
There is a lot of speculation about whether vitamin B6 causes weight gain.
But, the fact is that vitamin B6 by itself does not contain calories, and therefore, it cannot cause weight gain.
However, the foods that are rich in vitamin B6 can cause weight gain.
As mentioned earlier, many commonly consumed food items are rich in vitamin B6. These include:
The FTO gene, nicknamed as the 'fatso' gene, codes for the enzyme alpha-ketoglutarate-dependent dioxygenase.
Functionally, it is an mRNA demethylase enzyme.
Also called the fat mass and obesity-associated protein (FTO), it is found to have an association with obesity in humans.
The FTO gene is present on the 16th chromosome and is one of the most extensively researched genes for its weight gain/loss association.
The FTO protein is primarily involved in breaking DNA strands.
In technical terms, it is called a demethylase.
It is also studied to be expressed more, or upregulated, in the hypothalamus during periods of starvation, which can result in increased consumption of high-calorie foods.
Thus, this gene has been negatively associated with inducing over-eating.
A study has found an association between rs8050136 and intake of carbohydrates, where individuals with the A variant were found to have a higher risk of obesity than ones with the CC wild type.
Several other studies have also established a direct relationship between the SNP rs1558902 and an increased BMI.
| rsid | Effect Allele | Risk |
|---|---|---|
| rs8050136 | A | 2.46x increased risk of obesity |
| rs1558902 | A | Higher BMI than normal |
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A significant association has been found between rs11076023 and dietary fiber intake.
A research study has reported that individuals who carry the AA genotype, exhibited lower waist circumference than the T allele carriers on a high fiber diet.
| rsid | Effect allele | risk |
|---|---|---|
| rs11076023 | A | Highly likely to lose weight on a high fiber diet |
Scientists studied the effect of the A variant on two groups of people; one on a low-protein high-calorific diet and the other on a high-protein low-calorific diet.
It was found that the second group had better control over food cravings than the first, in the presence of A allele compared to TT genotypes.
| rsid | Effect allele | Risk |
|---|---|---|
| rs9939609 | A | Higher decrease in food craving when on a high protein diet |
The risk allele carriers of rs9939609 consuming a higher intake of saturated foods were found to be at an increased risk of obesity.
But similar findings were not observed for a lower intake of saturated fats.
| rsid | Effect allele | Risk |
|---|---|---|
| rs9939609 | A | Higher decrease in food craving when on a high protein diet |
The relation between the FTO gene and obesity is not direct.
Having a "faulty" FTO gene does not make one fat; it merely predisposes an individual to consume calorie-rich foods.
These individuals may have increased sugar cravings, which in turn could lead to weight gain, obesity, etc.
The conventional diet plans and workout regimes architected for weight loss need not help everyone achieve their desired goals.
There is a multitude of factors that influence weight loss, including a person's lifestyle, genetic makeup, and the environment.
Your genes can influence how you metabolize the nutrients you get from your diet. This directly has a role to play in weight gain/loss.
For instance, some people may possess a genetic variant that aids in the faster metabolization of carbohydrates, while others may carry a variant that will help in faster break-down of saturated fats.
Such genetic information can be leveraged to adopt a practical and personalized weight loss plan.
While genetic tests may not lay out the A-Z of weight loss, it certainly helps you pin the right path for your weight loss journey.
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An ideal diet should be flexible, balanced, and wholesome.
There are different diet types that an individual could opt for, but each has its shortcomings.
But we have a few FTO gene-based weight loss hacks that can save the day for you!
FTO gene variants have been linked to a lower risk of obesity and decreased food cravings when on a low-calorie diet with adequate protein intake.
Some common food sources of protein include cottage cheese, chicken, fish, and eggs.
If in case you carry a risk variant of the FTO gene, the negative effects of it can be alleviated by putting in a few hours of cardio every week.
A well-balanced diet, like the Mediterranean diet, can be very effective when it comes to weight loss. Mediterranean diet is not just well-balanced but is also a heart-healthy diet plan.
If you are an avid meat-eater, this diet may not be for you as it is a plant-based diet.
Inclusion of fruits and vegetables, some whole grains, low-fat dairy products, and kicking out the red meat is what is outlined in this diet.
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Our Gene Nutrition Report covers 33+ categories including tendency to regain weight, iron needs, tendency to overeat, etc.
MC1R or melanocortin-1 receptor gene plays an important role in the normal pigmentation process in the body.
The gene encodes the receptor for the Melanocyte Stimulating Hormone (MSH), which is one of the two hormones that regulate pigmentation.
The MC1R receptor is also known as the melanocyte-stimulating hormone receptor or the melanotropin receptor.
Polymorphisms in the MC1R gene reduce the ability of the MC1R receptor to stimulate eumelanin production. This leads to melanocytes making more pheomelanin.
The MC1R receptor is active in cells other than melanocytes as well. These include cells involved in the body’s immune and anti-inflammatory responses.
Several SNPs are associated with this MC1R gene. They are primarily linked to fair skin, red or light hair and freckles.
They also show a varying risk of melanoma and non-melanoma skin cancers.
The SNPs of the MC1R gene also influence responses to opioid analgesics that are used to treat pain.
Research shows that opioids are more effective in females with red hair, and light skin and have lesser MC1R protein activity.
Small, brown spots often present in the sun-exposed areas of the skin are called freckles.
They are almost always harmless and appear due to the overproduction of melanin in response to UV stimulation.
Freckles are essentially of two types: Ephelides and solar lentigines.
Ephelides are freckles that occur as a result of sun exposure.
Anyone who is exposed to sun rays or UV rays can develop these spots on their face, back of their hands and on their upper body.
This type of freckles is common in people with light skin and is generally seen in individuals with Caucasian and Asian descent.
The second type of freckles is called solar lentigines. It is a patch of dark skin that is harmless in nature and tend to appear in older Caucasians (above the age of 40yrs).
Freckles, as we now know, occur as a result of melanin that builds up under the skin, forming the spots.
There are two primary causes that have been cited for the development of freckles:
So, we see freckles developing after a brief exposure to the sun.
Freckles tend to become darker on increased sun exposure and can also disappear when skin cells are replaced.
The human body produces two types of melanin – eumelanin (that protects the skin from sun’s UV rays) and pheomelanin (no protective function).
But, the type of melanin an individual produces depends on the MC1R gene.
Our skin shows different types of pigmentations – moles, freckles, birthmarks, age spots, and sunspots.
But, how can we differentiate freckles from other similar looking marks?
Freckles, on exposure to the sun, appear as flat pigmented spots in clusters over a larger area of the skin.
They are irregular in shape but have clearly defined edges.
They are brown, tan or red in color and not more than 1-2 mm in size.
Individuals with lighter or fair skin are at an increased risk of developing freckles and therefore, must take extra precautions before stepping out in the sun.
These individuals are also at a higher risk of developing skin cancer.
| rsid | Risk allele | Implications |
|---|---|---|
| rs1540771 | t | 1.26X risk of freckles |
| rs1042602 | c | 1.23X risk of freckles |
| rs1805008 | t | 2.06X risk of freckles |
There are some SNPs on the MC1R gene that are associated with freckles, fair skin, and UV rays:
The T allele of SNP rs1540771 is said to be associated with 1.26x risk of freckles, and UV sensitivity and brown hair.
The rs1042602 SNP on the TYR gene is polymorphic in Europeans and the A allele derived from it is associated with light/fair skin, eye color and the absence of freckles.
rs1805008 is also known as Arg160Trp or R160W and is one of the many SNPs that is found in the MC1R gene and is associated with red hair color, especially in the Irish population.
The T allele increases the risk of melanoma in this population with individuals having CT being carriers of red hair and a higher risk of melanoma compared to those having CC alleles.
Individuals with TT alleles have 7-10 times more chance of having red hair and at a greater risk of developing melanoma.
Despite the genetic contribution to freckles, no one is actually born with it.
Freckles appear when an individual is exposed to the sun.
They tend to become darker during the summer months and fade away during the winter.
However, there are a few treatments and home remedies that one can use to get rid of these freckles.
Those who are prone to freckles must apply sunscreen every time they step out.
Using a sunscreen of SPF 30 or above can help the formation of new freckles but cannot help you get rid of the existing ones.
There are different types of lasers that target specific areas in the skin.
It can take about 2-3 weeks to recover from the treatment and more than one session is needed for achieving the desired results.
The retinoids in the cream help absorb UV B radiation and prevent the formation of new lesions.
This method can be used to treat or get rid of freckles but it can have some side effects such as hypopigmentation or blistering, but it rarely causes scarring.
The hydroquinone present in these creams suppresses the production of melanin and helps lighten the darkened areas of the skin.
When the damaged skin heals after a chemical peel, new skin appears without the freckles.
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Topical application of vitamin C is believed to reduce or lighten skin spots.
It also helps the skin heal from sun damage.
Sunspots, also called liver spots, are flat pigmented lesions that appear on the skin on exposure to the sun.
They are harmless in nature and are non-cancerous.
They appear in different shades of brown. Individuals who are over the age of 40 years are more prone to it.
Sunspots are commonly seen on the face, back of the hands, shoulders, and back.
Sunspots occur due to:
Yes. Sunspots can be lightened or even removed completely using various home remedies and cosmetic procedures.
The cosmetic procedures need to be performed by a trained professional only and include procedures such as cryotherapy, microabrasion, chemical peels, laser treatment, or use of intense pulse light.
The antioxidants and active compounds in the tea are believed to bring about this effect.
The acetic acid present in vinegar is believed to help lighten skin pigmentations.
Lactic acid present in these substances is believed to bring about the required change.
| rsid | Risk Allele | Implications |
|---|---|---|
| rs885479 | a | 1.5X risk of sunspots |
| rs2228479 | a | 2X risk of sunspots |
Individuals with the rs885479 SNP of the MC1R gene having A allele had an increased risk for developing sunspots.
This is an SNP of the MC1R gene and is also called as Val92Met or V92M.
It is associated with light and deep red hair and skin that is prone to sunburn.
The presence of the A allele increases the risk of an individual to developing sunspots.
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Tanning is a phenomenon wherein your skin darkens on exposure to the UV rays of the sun.
When exposed to the sun, your body produces melanin as a protective mechanism to absorb the harmful UV rays and protect the skin cells.
This excess melanin production leads to darkening of the skin.
Excessive absorption of UV radiation can cause sunburns.
It is quite common to see people getting a tan for the recreational purpose either by sunbathing (lying in the sun) or by using a tanning lamp found in indoor tanning beds.
One can also get a tan by using chemicals, an activity is known as sunless tanning.
When we walk out into the sun without sunscreen or have some parts of our body exposed, we are putting our skin cells at great risk of sun damage.
We often notice that when a dark-skinned individual is exposed to the sun, they tend to get darker, whereas light-skinned individuals turn red.
These changes in body color are due to the melanocytes producing melanin, resulting in tanning or sunburn.
Production of melanin in response to sun exposure is a protective function of the melanocytes.
Melanin absorbs the harmful UV radiations and protects the other skin cells.
So, the next time you sunbathe to get a tan or inadvertently get one while walking in the sun without sunscreen or adequately cover your body, you know why your body is getting tanned.
A tan may be a fashion statement, but just like sunburn, it is a form of skin damage and can put one at risk of developing cancer in the future.
Melanoma is the term given to cancer that develops from skin cells called melanocytes.
It is also known as malignant melanoma and is a leading cause of death globally.
There has been a rise in melanoma cases primarily due to increased exposure to sun while sunbathing and indoor tanning devices.
The increase melanocyte in response to the UV rays is a grave risk factor for melanoma.
There are many useful home remedies we can try to get rid of tan or at least lighten the color.
These include vitamin C, vitamin E, glycolic acid, retinoids, etc.
It contains antioxidants that help lighten the skin and also heal and soothe the damaged skin.
Care should be taken to avoid any harsh chemical lighteners, peels, bleaches, etc., on tanned or sunburnt skin as they can aggravate the damage already done to the skin.
You might also want to read: Get flawless skin in 7 days
| rsid | Risk allele | Implications |
|---|---|---|
| rs1805009 | c | Associated with poor tanning |
| rs2228479 | a | Associated with poor tanning |
rs1805009 is an SNP that is known as Asp294His and is located on the MC1R gene. It is a variant that is linked with red hair and a low tendency to tan.
| Risk Allele | Risk |
|---|---|
| G/G | No risk of melanoma |
| C/G | 2.5X risk of developing melanoma |
| C/C | 3X risk of developing melanoma |
rs2228479 is an SNP that is present on the MC1R gene and is associated with skin pigmentation. The A/A allele increases the individual’s susceptibility to melanoma whereas the G/G allele shows a lower risk.
https://www.snpedia.com/index.php/MC1R
https://ghr.nlm.nih.gov/gene/MC1R#synonyms
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3977302/
https://www.snpedia.com/index.php/Rs2228479
