Amphetamine is a central nervous system (CNS) stimulator used to treat medical conditions like Attention Deficit Hyperactivity Disorder (ADHD) and narcolepsy.
CNS stimulators affect the chemicals in the brain and cause hyperactivity and impulse control.
ADHD is a complex psychological disorder caused by genetic and non-genetic factors.
It is the most common neurodevelopmental disorder occurring in childhood.
Children with ADHD have trouble paying attention, controlling impulsive behaviors, and being overly active.
Aside from its medical uses, Amphetamine is also a habit-forming (highly addictive) substance with a long history of abuse.
Apart from a few brands, Amphetamine is not recommended for children below the age of three years.
Today, Amphetamine is also being used for treating obesity, depression, and chronic pain, although off-label.
Amphetamine is a CNS stimulant that increases the amount of neurotransmitters (chemical messengers) like dopamine, norepinephrine, and serotonin in the synapse via different mechanisms.
A synapse is a small gap between two nerve cells where transmission of electrical impulses occurs.
Amphetamine enters the nerve cell at the synapse by diffusion and is taken up by transporter molecules at the synapse.
Once inside the nerve cell, Amphetamine disrupts the electrochemical gradients required for standard impulse transmission.
Amphetamine also inhibits the metabolism of monoamine neurotransmitters (chemical modifications that monoamine transmitters undergo) by inhibiting Monoamine Oxidase (MAO) enzymes.
MAO inhibitors are responsible for degrading neurotransmitters. So, if Amphetamine inhibits MAO, the quantity of specific neurotransmitters increases.
Though Amphetamine is safe when taken legally and in doses strictly prescribed by the doctor, some people may experience mild to severe side effects on taking it.
These side effects may be physical or psychological.
Physical side effects of Amphetamine include:
Psychological side effects of taking Amphetamine may include:
Some studies have also shown that when Amphetamine is used to treat ADHD in children, it can retard or slow down growth.
Some minor effects have also been observed in the cardiovascular system, including increased heart rate and blood pressure.
However, more research is required to confirm this.
When Amphetamine is taken at higher doses or through routes not prescribed by a doctor, the risk of adverse effects increases.
Taking excess Amphetamine increases dopamine levels in the brain.
Overuse or abuse of Amphetamine may lead to:
People who take Amphetamine for recreational purposes may also experience withdrawal symptoms like depression and sleep disturbances when they stop taking the drug.
Many drugs, nutritional supplements, and herbal supplements may interact with Amphetamine.
Therefore, you must always inform your doctor about medications or supplements you are currently taking.
Drug interactions may change how drugs work and increase the risk of adverse reactions.
Some drugs that interaction with Amphetamine are:
Monoamine Oxidase Inhibitors of MAO inhibitors are a class of drugs used to treat depression.
Taking MAO inhibitors with Amphetamine may cause serious and possibly fatal drug interactions.
Therefore, you must avoid taking Amphetamine with MAO inhibitors like isocarboxazid, linezolid, metaxalone, methylene blue, etc.
You must also avoid taking MAO inhibitors for two weeks before taking Amphetamine.
Speak to your doctor to know when you should stop taking MAO inhibitors before starting on Amphetamine.
If you are taking drugs like methadone, dextromethorphan, or methylenedioxymethamphetamine (also called ecstasy) that increase serotonin production, taking Amphetamine can lead to serotonin syndrome or toxicity.
Amphetamine is similar to dextroamphetamine or lisdexamfetamine.
To avoid adverse effects or overdose, you must not take these medications together.
Amphetamine may interfere with routine lab tests like blood, urine analysis, and brain scan for Parkinson’s disease and give false results.
So, you must inform your doctor if you are taking Amphetamine before undergoing these tests.
The CYP2D6 gene gives instructions for the production of Cytochrome P450 Family 2 Subfamily D Member 6 enzyme.
The CYP2D6 enzyme plays a vital role in the metabolism of most psychostimulants (drugs that can stimulate the central nervous system), including Amphetamines.
Over 100 forms of the CYP2D6 gene have been identified.
They are classified as normal function, decreased function, or no function.
Though most people carry two copies of the CYP2D6, a few people might have more than two copies.
Individuals who carry one decreased function allele and one no function allele of the CYP2D6 are called intermediate metabolizers of Amphetamine.
Individuals who have two no-function alleles of the gene are called poor metabolizers of the drug.
A majority of people carry two normal function alleles of the CYP2D6 and are normal metabolizers of Amphetamine.
The DRD2 gene gives instructions for producing the Dopamine Receptor D2 subtype.
A particular mutation or abnormal change in this gene may cause myoclonus dystonia whereas other mutations may cause schizophrenia.
The DRD2 is also called the ‘pleasure-seeking gene due to its association with addictions.
People with the A1 type of the DRD2 gene are more prone to addictions of various kinds, including Amphetamine drug addiciton.
Some medical conditions can make it unsafe to take Amphetamine. Inform your doctor about any medical conditions that you may have, particularly:
If you have a history of sensitivity or allergy to Amphetamine, you must avoid taking the drug.
If you have a history of drug abuse or addictions, you must not take Amphetamine and inform your doctor about the same.
Inform your doctor if you are pregnant or are planning a pregnancy. Taking Amphetamine during pregnancy may cause premature birth, low birth weight of the baby, or withdrawal symptoms in the newborn.
Since Amphetamine can pass into breast milk and harm your baby, you must inform your doctor if you are breastfeeding before taking the drug.
Genetic testing helps your doctor understand how a particular drug may affect you. It can also help them determine the appropriate dosage for you based on your medical history, medications you are taking, and history of addictions.
Before taking Amphetamine, genetic testing for the CYP2D6 and DRD2 genes may be helpful to determine how you will metabolize the drug without causing side effects.
Analyze Your Genetic Response to Amphetamine
References:
Despite washing your face twice a day, using plenty of sunscreen, and following a perfect skincare routine, do you find yourself popping a pimple every now and then? What should you be doing differently? Turns out, there are good chances you aren’t doing anything wrong. Studies have shown that acne is far more genetic than environmental.
Researchers have identified a number of genes associated with acne.
In the sample report below, we've attempted to analyze some important genes that increase the risk for acne.
You can identify your genetic risk of EDS by using your 23andMe DNA data and placing an order for the Gene Skin Report.
Acne is a common and chronic skin condition affecting millions worldwide.
It is most commonly seen in adolescents but can affect people of all ages.
The most common skin condition in the U.S. is acne, which affects almost 50 million Americans yearly, as reported by the American Academy of Dermatology.
Acne is caused by a combination of factors, including hormones, bacteria, and sebum production.
There are many types of acne, ranging from blackheads and whiteheads to cysts and nodules.
Acne is not a life-threatening condition.
However, it can be extremely painful, depending on how severe the condition is.
Pimples can leave scars on the skin over time.
Acne on your face can cause emotional distress if persistent for a long time.
Acne treatment often includes a combination of medication and lifestyle changes.
To date, there’s no one “acne gene” that results in acne.
However, a combination of genes affecting various factors contributing to acne development can increase your risk for this condition.
If either (or both) of your parents are acne-prone, you may be as well.
According to a study, a mother’s acne history is one of the most important prognostic factors for acne development.
This suggests that the risk for acne may be passed down through generations via the X chromosome.
Genes that influence acne risk play various roles in the body.
For example, genes that regulate the immune system can impact how our body responds to the bacteria P.acnes, one of the major causes of acne.
Genetics can also play a role in how your skin grows and heals by regulating the production of keratinocytes, a type of skin cell.
The FST gene contains instructions for the production of a protein called follistatin.
This protein inhibits the release of follicle-stimulating hormones.
Follistatin also inhibits a protein called TGFB2, which is involved in controlling acne.
If more follistatin is produced, TGFB2 activity will be inhibited, and this, in turn, increases the development of acne and acne-causing bacteria.
rs38055
rs38055 is a variation or a single nucleotide polymorphism (SNP) found in the FST gene.
The A allele of this SNP can increase your risk of developing acne.
The TGFB2 gene contains instructions for the production of a protein called transforming growth factor beta-2.
This protein is important in all stages of life, from early development throughout life.
It is involved in various cellular mechanisms for the proper growth and development of cells.
TGFB2 also regulates the growth and healing of skin by slowing down the production of keratinocytes, a type of skin cells.
rs1159268
rs1159268 is an SNP found in the TGFB2 gene.
The A allele causes a decrease in the production of TGFB2 protein, which increases the risk of acne.
These changes are common during puberty and pregnancy and lead to breakouts.
Androgen, a hormone produced by the adrenal glands in boys and girls, triggers the sebaceous (oil) glands to secrete more oil-containing fluid called sebum.
This usually happens at puberty.
Acne is most common in teenagers but occurs in people of all ages.
Certain foods like chips, carbohydrate-rich foods, and refined sugars are found to worsen acne.
Studies are being done to find the impact of particular diets on acne.
Stress doesn’t directly cause acne.
However, if you already have acne, stress can make it worse.
Studies reveal that wound healing, including healing from acne, is much slower when a person is under stress.
Friction or pressure on the skin can also cause acne.
Tight collars, helmets, and backpacks can exert more pressure on your skin.
Drugs that contain testosterone, lithium, or corticosteroids can cause acne.
While there isn’t anything you can do about your genes, acne is a manageable condition with lifestyle interventions.
Even if acne runs in your family, it doesn’t necessarily mean you’ll have it all your life.
However, it can be a bit difficult to control.
Here are some science-backed effective tips to keep the breakouts at bay.
With the skincare market taking the world by storm, choosing the right product can feel like a mammoth task.
Go for “non-comedogenic” products that do not have any pore-clogging ingredients.
You can also consult a dermatologist for a suitable cleanser for your skin.
Some good skin habits that can reduce acne include:
Processed foods and refined sugar can cause and worsen acne.
Swapping them with fresh fruits, vegetables, and other healthy foods can improve skin health.
Managing stress levels is good for your skin, as well as your overall health.
Stress stimulates cortisol production, causing the oil glands to produce more oil.
This can lead to clogged pores and the development of acne.
Meditation, exercise, yoga, and therapy are effective ways to manage stress.
If none of the home remedies and skincare routine work, a dermatologist can help identify the root cause of your acne and suggest a suitable treatment option.
https://www.healthline.com/health/skin/acne
https://www.aad.org/public/diseases/acne/skin-care/tips
https://www.medicalnewstoday.com/articles/107146
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080563/
https://www.nature.com/articles/ncomms5020
https://pubmed.ncbi.nlm.nih.gov/16484821/
https://pubmed.ncbi.nlm.nih.gov/16484821/
Vitamin B2, also called riboflavin, is an essential nutrient needed for human health. It is one of the eight B vitamins. All the B vitamins are important for maintaining healthy skin. Vitamin B2 is a water-soluble vitamin. Being a water-soluble vitamin, it can be excreted out of the body easily. Your body only stores a small amount of riboflavin, and hence, you need to include riboflavin in your diet every day.
Vitamin B2 plays a role in
- Maintaining tissues
- Energy metabolism
- Secretion of mucus that prevents dryness induced oil secretion that leads to acne
- Absorption of zinc, which is essential for the skin
- Maintaining the structural integrity of the skin
- Protects cells from oxidative damage
- Maintenance of red blood cells
- Keeping the skin healthy
The recommended daily intake of vitamin B2 is as follows:
For adults
1.3 mg for healthy men
1.1 mg for healthy women
1.4 mg for pregnant women
1.6 mg for lactating women
For children
0.3 mg for infants up to 6 months
0.4 mg for infants between 6-12 months
0.5 mg for 1-3-year-old children
0.6 mg for 4-8-year-old children
0.9 mg for 9-13-year-old children
1.3 mg for 14-18-year-old males
1.0 mg for 14-18-year-old females
Vitamin B2 deficiency is not very common in the US as most of the food items like milk and whole-grain cereals, which are widely consumed, contain good levels of vitamin B2.
People with certain genetic types may need more vitamin B2 due to the inefficient transport in their bodies. Certain genes can help determine your risk for vitamin deficiency.
The MTHFR gene produces an enzyme called methylenetetrahydrofolate reductase. This enzyme is involved in the methylation cycle. MTHFR activates 5, 10-methylene TetraHydroFolate(THF) to 5-methyl THF, and this is needed for the conversion of homocysteine to methionine.
This protein is also involved in the conversion of folate to SAMe, which is involved in the methylation of DNA as it is the universal methylation donor. The methylation cycle is essential for various functions in the body.
Vitamin B2 is involved in the metabolism of homocysteine along with Vitamin B1. Vitamin B2 deficiency can lead to high levels of homocysteine, which is a harmful amino acid.
rs1801133
rs1801133 is an SNP found in the MTFHR gene.It is also referred to as C677T. The T allele decreases enzyme activity, with only a 10-20% efficiency in folate processing and leads to high levels of 0f homocysteine in the body.
Vitamin B2 deficiency can lead to
- Cracked lips
- Itching of skin
- Scrotal Dermatitis
- Inflammation of mouth lining
- Inflammation of the tongue
- Scaly skin
Certain food items contain vitamin B2. These include:
- Eggs
- Kidney and liver meat, lean meats
- Green vegetables like broccoli and spinach
- Cereals, grains, and bread
- Milk and yogurt
- Lima beans and peas
- Avocados
- Artichokes
- Nuts
Riboflavin is water-soluble. While cooking food, especially boiling, vitamin content may reduce. Make sure to include a daily supply of vitamin B2-rich foods to keep your skin healthy. A balanced diet is always important to keep your skin and other parts of the body healthy.
Your doctor may prescribe certain vitamin B2 supplements to overcome your deficiency apart from your diet.
https://www.medicalnewstoday.com/articles/219561
https://www.ncbi.nlm.nih.gov/books/NBK470460/
https://www.ncbi.nlm.nih.gov/pubmed/25322900
https://www.healthline.com/health/symptoms-of-vitamin-b-deficiency
https://www.bebeautiful.in/all-things-skin/everyday/benefits-of-vitamin-b-complex
https://ods.od.nih.gov/factsheets/Riboflavin-HealthProfessional/
The skin is the largest visible organ of the body affected by internal changes (genetics and metabolism) and external factors (UV radiation, pollution).
Collagen is a protein that is a part of all the connective tissues in the human body. Collagen is found in the skin, muscles, ligaments, and even bones.
About 35% of the entire protein content in an adult’s body is made up of collagen.
The three main functions of collagen include:
- Giving structure to tissues
- Repairing damaged tissues (skin renewal)
- Keeping skin supple and strong
Collagen degradation or collagen loss is a condition where a person loses essential collagen components in the body. There can be many reasons for collagen degradation. Some of them include:
When the collagen in the body decreases, it results in the skin losing its elasticity and suppleness. The thickness of the epidermis (the outermost layer of the skin) reduces too. The skin sags and gets easily damaged. One of the major signs of collagen degradation is the formation of wrinkles.
Wrinkles are creases, folds, and lines that form on the skin, making smooth skin look saggy and wrinkled. Wrinkles are also called rhytide. Wrinkles are very common in the elderly. Thanks to unhealthy lifestyles and environmental factors like UV exposure and pollution, people lose the collagen content in their skin early on and develop wrinkles.
With the right amount of collagen in the skin, broken or injured collagen and elastic fibers are regenerated quickly, and the skin maintains the same smooth and supple texture. Because of collagen degradation, such broken and injured fibers are replaced by altered fibers that are not the right fit. This is termed misrepair.
Generally, the original fiber gets regenerated in its place. For people with collagen degradation, a long collagen fiber is replaced in that position. Long fibers do not shrink back into their original state, and hence your skin loses its ability to stretch and shrink smoothly and forms wrinkles.
The STXBP5L gene helps produce the binding protein called Syntaxin-binding protein 5. This is also called Tomosyn, which is the Japanese word for ‘friend.’ This protein plays an important role in photoaging.
A genome-wide study that analyzed the signs of skin aging in 502 caucasian women identified that the severity of wrinkles and other signs of aging increase as the women grow older.
The study also concluded that the T allele of the rs322458 SNP in the STXBP5L gene is beneficial in bringing down the risks of aging signs, including collagen degeneration and formation of wrinkles
The MMP1 gene produces a protein that helps in breaking down collagen for everyday development. The 2G/2G genotype of the rs1799750 SNP of this gene results in a higher breakdown of collagen, leading to collagen degradation. This results in the formation of wrinkles and other signs of aging
UV rays are of three types - UV-A, UV-B, and UV-C rays. The UV-C rays have short wavelengths and do not reach the skin’s surface. Both UV-A and UV-B rays can reach all the layers of the skin.
UV exposure is the cause of 80% of aging signs.
UV rays promote the development of free radicals in the skin. These free radicals can damage collagen and elastin fibers. Continuous damage to the collagen fibers results in the skin becoming loose, saggy, and wrinkled.
People with fair skin are more affected by UV rays than those with darker skin. This also increases the risk of collagen degradation and the formation of wrinkles.
As you age, your body produces lesser amounts of collagen and elastin fibers. This naturally leads to collagen degradation and wrinkles.
A study analyzed the effects of smoking on the formation of wrinkles. 160 smokers, 67 individuals who had smoked in the past, and 123 non-smokers were chosen for the study. The study showed that people who smoked had a higher degree of facial wrinkling than those who did not smoke. Nicotine in cigarettes damage collagen and elastin and leads to the formation of wrinkles.
The accumulation of Advanced Glycation End Products (AGEs) in the skin results from excess sugar consumption, natural aging, and diabetes. More AGEs in the skin increase the chances of degradation of collagen.
Vitamin C deficiency is known to bring down collagen production in the body.
Make sure you include fresh vegetables, fruits, and greens in plenty in your diet. All these are antioxidant-rich and prevent free radicals from affecting collagen fibers. Fruits and vegetables that are rich in vitamin C also help fight collagen degradation.
Below is a list of antioxidant-rich fruits and vegetables.
- Onions, garlic, leeks
- Berries
- Grapes
- Pumpkin
- Mangoes
- Apricots
- Spinach
- Parsley
- Eggplants
Some vitamin C-rich foods include:
- Red pepper
- Oranges
- Lemon
- Lime
- Grapefruit
- Kiwi
- Brussels sprouts
- Broccoli
- Cantaloupe
Stay away from both active and passive smoking to make sure your skin stays taut and smooth for a longer time.
Use a broad-spectrum sunscreen that has a Sun Protection Factor (SPF) of 30 or higher. If you are staying out in the sun, reapply every 3-4 hours. Use protective gear like hats, gloves, and umbrellas to keep away harmful UV rays from falling directly on your skin.
If your skin has already started showing signs of wrinkles and collagen loss, consider collagen supplements. Collagen supplements can be had orally or applied on the skin as topical solutions.
Retinol is also called Vitamin A. Retinol Over-the-Counter skincare products can be used to boost collagen production in the skin. Retinols, along with vitamin C, are very effective in preventing wrinkles and collagen degradation.
Dermatological treatments like micro-needling, laser therapy, chemical peels, and radiofrequency are all created to improve collagen production in the skin. Each of these treatments comes with its own benefits and side effects. It’s important to be wary of the side effects and costs of the treatment before opting for it.
https://www.sciencedirect.com/topics/medicine-and-dentistry/collagen-degradation
https://www.intechopen.com/books/molecular-mechanisms-of-the-aging-process-and-rejuvenation/molecular-mechanisms-of-skin-aging-and-rejuvenation
https://www.healthline.com/health/beauty-skin-care/skin-elasticity#takeaway
https://www.news-medical.net/life-sciences/Collagen-Degradation-Pathways-in-Humans.aspx
https://link.springer.com/article/10.1007/s11340-007-9105-1
ACTN3, popularly called the Speed Gene, is responsible for the production of α-actinin-3, a protein expressed in fast-firing skeletal muscle fibers. This protein is deficient in approximately 1.5 billion people worldwide.
Previous studies indicate that α-actinin-3 is associated with muscle function, and an α-actinin-3 deficiency adversely affects performance in speed and power activities. Recent research suggests that α-actinin-3 deficiency generates heat in the body (thermogenesis), and as a result, α-actinin-3 deficient humans adapt better to lower temperatures.
The α-actinin-3 protein was first identified during research into muscular dystrophy defects. Further studies showed that a deficiency of α-actinin-3 was common- roughly 18% of the world population has an ACTN3 deficiency mutation. This deficiency correlates with the following factors:
A previous study exploring the evolutionary implications of α-actinin-3 deficiency indicated that a version of the ACTN3 gene became more abundant as humans migrated out of Africa into the colder climates of Northern and Central Europe.
Studies also suggest that an X derivative of the ACTN3 gene is overexpressed among marathoners and endurance athletes but underexpressed in sprinters. The X derivative indicates an incomplete ACTN3 gene and is thereby associated with α-actinin-3 deficiency.
In general, an α-actinin-3 deficiency is detrimental for sprint and power activities. Evolutionary evidence also indicates a strong positive selection of the X derivative of the ACTN3 gene in European and East Asian populations. Positive selection is the process by which the "advantageous" changes or gene variants are passed on consistently in a population.
A study conducted by a team of researchers examined the mechanism responsible for the positive selection of the X derivative of the ACTN3 gene. It aimed to understand the thermogenic role of skeletal muscle during cold exposure in humans.
The study was conducted on the following two groups: Healthy males aged 18 to 40 years, residing in Kaunas, Lithuania. They followed moderate physical activity and had no exposure to an extreme temperature for at least three months prior to the study. Thirteen age-matched 3-month-old wild-type mice and mice with inactivated ACTN3 genes, housed in a specific-pathogen-free environment. They were maintained at a constant ambient temperature of 22°C and 50% humidity on a 12 h light-dark cycle, with limited access to food and water.
The following parameters were measured in humans:
Based on the above parameters, the following were calculated:
Coldwater exposure was conducted as follows:
The following parameters were examined in both humans and mice:
Apart from these, protein analyses in humans and RNA sequencing in mice were performed, and the data obtained were statistically analyzed.
The study observed that the percentage of individuals able to maintain their body temperature above 35.5°C during the cold-water exposure was higher in the ACTN3 deficient (XX) group than the ACTN3 efficient (RR) group. However, there was a significant overall increase in energy consumption induced by the cold irrespective of the ACTN3 gene status. This implies that α-actinin-3-deficient individuals exhibit superior protection of core body temperature during cold exposure without a corresponding increase in energy consumption.
Researchers suggest a physiological mechanism underlying the energy-efficient cold protection in XX individuals. Mammals regulate their body temperature when exposed to acute cold temperatures through involuntary muscle contraction. This is colloquially referred to as shivering - this activity was twice as high in RR individuals as in XX individuals. In individuals with the X derivative, these contractions most likely happen in slow twitch-type muscles with a heat-generating increase in muscle tone. This conserves more energy when compared to shivering.
The X derivative of the ACTN3 gene occurs more commonly in people living in colder climates, indicating an evolutionary survival advantage of α-actinin-3 deficiency as humans migrated to colder places.
In conclusion, α-actinin-3-deficient humans use a more energy-efficient mechanism of generating body heat, thereby exhibiting improved cold tolerance.
Atopic Dermatitis (AD) is a chronic inflammatory condition that makes skin itchy, swollen, and red. In the US, about 16.5 million adults and 9.6 million children have AD.
AD is also called atopic eczema. In children, it usually first appears between ages 3 to 6 months. About 90% of people with AD start showing the symptoms before five years of age.
In people with AD, the immune system starts attacking the healthy skin cells, causing excessive dryness and itching. There are many contributors to AD - genetic, environmental, and stress-related.
For infants and young children, the whole body gets affected by AD. As children get older, dryness and itch are noticed on the elbows and the insides of the knees. For adults, the signs are mostly seen in the hands and feet.
AD is not a contagious disease, and thus it does not spread on contact. Doctors believe that there are more numbers of inflammatory cells in the skin of people with AD. AD individuals have a weaker skin barrier than normal people, and this makes their skin very sensitive.
Excessive dryness in the skin allows the entry of allergens and irritants into the skin’s surface, and this can also cause AD.
Here are some of the common triggers that make atopic dermatitis worse in those already living with the condition.
- Hot showers
- Long showers
- Living in dry and cold climates
- Using harsh chemical products on the skin
- Exposure to fabrics like wool and cheap synthetics
- Excessive workouts
- Stress
Filaggrin is important for the structure of the skin’s outermost layer, the epidermis. It also helps improve the skin’s barrier. Filaggrin is important in locking moisture in the skin and keeping it hydrated.
About 30% of people with atopic dermatitis have a lowered production of filaggrin.
The FLG gene produces profilaggrin, which in turn produces filaggrin. Changes in the FLG gene can cause lowered filaggrin production, which increases the risk of AD.
Abnormal changes or mutations in the FLG gene cause an increased risk for AD.
The A allele of the rs61816761 SNP and the C allele rs12144049 SNP of the FLG gene cause an increased risk of developing Ichthyosis Vulgaris. This condition causes dry and scaly skin and is associated with AD too.
The CARD11 gene helps make proteins involved in the healthy functioning of the immune system, especially in the functioning of the T and B cells. The G allele of rs4722404 increases the chances of developing atopic dermatitis.
Moderate cases of AD may not lead to any obvious effects on health. Severe cases may result in the following:
- Extreme itching leading to skin breakouts that lead to sores and cracks
- Pus formation on the skin’s surface
- Increased risk of skin infections
- Inability to sleep because of constant itching
- Development of skin cysts/knots
- Liquid oozing from the skin’s surface
- Psychological issues including depression, anxiety, and feeling of isolation.
https://www.aad.org/public/diseases/eczema/types/atopic-dermatitis/symptoms
https://pubmed.ncbi.nlm.nih.gov/34785669/
https://www.aad.org/public/diseases/eczema/types/atopic-dermatitis/self-care
https://www.mayoclinic.org/diseases-conditions/atopic-dermatitis-eczema/symptoms-causes/syc-20353273
https://onlinelibrary.wiley.com/doi/full/10.1111/all.12270
https://nationaleczema.org/eczema/types-of-eczema/atopic-dermatitis/
https://www.healthline.com/health/atopic-dermatitis/what-is-atopic-dermatitis#Outlook
https://medlineplus.gov/genetics/gene/flg/#conditions
