Skincare - LifeDNA

Are Varicose Veins Genetic?

Aira on August 10, 2024

What Are Varicose Veins?

Varicose veins are a common condition of the blood vessels characterized by swollen, enlarged, and twisted veins visible beneath the skin’s surface. Most frequently occurring in the legs and feet, these veins can range from dark purple to blue. Though varicose veins can be unsightly, they often pose more than just a cosmetic problem; they can lead to discomfort, pain, and sometimes severe medical issues related to the circulatory system.

A healthy vein allows blood to flow smoothly back to the heart through a series of one-way valves. In a varicose vein, these valves malfunction, allowing blood to accumulate, leading to enlargement and a twisted, rope-like appearance. While smaller veins are often red or purple, more prominent varicose veins tend to be bluish.

Are Varicose Veins Genetic?

While varicose veins can be influenced by factors like age, weight, and lifestyle, there could also be a genetic component.

Research on Genetic Markers

Studies on the genetic aspects of varicose veins have mainly focused on symptoms of specific disorders of the blood vessels (like Klippel-Trenaunay Syndrome). Previous research indicates that changes in genes like FOXC2, thrombomodulin (THBD), and desmuslin (SYNM) could contribute to varicose veins by affecting how veins function. However, these investigations have generally involved small sample sizes, ranging from 18 to 700 participants, and there needs to be more follow-up studies to confirm these findings.

A 2019 Genome-Wide Association Study (GWAS), including nearly 10,000 cases and 300,000 controls, identified 30 genetic locations strongly linked with varicose veins. The most notable associations were found in the intron region of CASZ1 (rs1112165), previously implicated in blood pressure, and in the 16q24 region, where the PIEZO1 gene is located.

CASZ1 Gene

In the past few years, multiple GWAS have been carried out, focusing specifically on varicose veins in the lower limbs. The initial study was undertaken by 23andMe and involved European subjects who self-reported having varicose veins. This was succeeded by another GWAS that used clinically verified German cohorts. More recently, a validation study on the key findings from both studies, using independent samples from Russia and the UK Biobank, was also done.

The most compelling association was with rs11121615, a variant initially identified in the 23andMe study. This single nucleotide polymorphism (SNP) is situated within an intron of the Castor Zinc CASZ1 gene, but its functional impact remains uncertain.

PIEZO1 Gene

The association of both the CASZ1 and the PIEZO1 gene was confirmed in a significant and perhaps largest GWAS to date, conducted in 2022, focusing on surgically confirmed varicose vein cases. Another study found uncommon protein-truncating variants (PTVs) in the PIEZO1 gene that were linked to the occurrence of varicose veins. The findings indicate that while rare, these PTVs in PIEZO1 could serve as potent genetic risk factors for varicose veins.

Non-Genetic Risk Factors of Varicose Veins

While genetics can play a significant role in developing varicose veins, various non-genetic factors can also contribute. Recognizing these factors can help individuals take preventive measures. Here’s a closer look at some of the most prevalent non-genetic risk factors.

Age

As people age, their risk of developing varicose veins increases. The valves in the veins weaken over time, making it more challenging to maintain proper blood flow. While you can’t stop aging, being aware of this risk can help you take preventive steps.

Pregnancy

During pregnancy, blood volume increases, but blood flow from the legs to the pelvis decreases. This circulatory change is designed to support the growing fetus but can also result in enlarged veins in the legs.

Obesity

Carrying excess weight puts additional pressure on the veins, which can lead to varicose veins. The extra weight can also exacerbate existing conditions and make it more challenging for the veins to pump blood back to the heart.

Sedentary Lifestyle

A lack of physical activity can impair blood circulation, increasing the risk of developing varicose veins. Regular exercise helps improve blood flow and can mitigate the risk.

Occupation

Jobs that require prolonged standing or sitting can inhibit proper blood circulation and contribute to the formation of varicose veins. If your job requires long periods of immobility or air travel, taking breaks to move around is essential.

Previous Medical History

If you’ve had blood clots, injuries that affect the veins, or surgery that alters the blood flow in your legs, you may be at higher risk for varicose veins.

How To Tell If You Have Varicose Veins?

Varicose veins can manifest in various symptoms, ranging from mild to severe. Recognizing these signs and symptoms early can help you take the necessary steps to manage the condition effectively.

Visual Indicators

The most evident symptom of varicose veins is their visual appearance. The veins appear enlarged, swollen, and twisted, often with a blue or dark purple color. They are usually visible under the skin and are most commonly found in the legs and feet.

Physical Discomfort

This can be especially pronounced after long periods of standing or sitting.
Burning Sensation: Some individuals experience a burning or throbbing feeling around the area where the varicose veins appear.
Muscle Cramping: Muscle cramps, particularly at night, can occur in the legs with varicose veins.

Itching: There may be an itching sensation around the vein or the surrounding skin.

Skin Changes

Over time, untreated varicose veins can lead to changes in the skin around them. This may include:

Dry or Thinning Skin: The skin over the veins may become thin, itchy, and discolored.
Inflammation: The skin can become red and inflamed, indicative of dermatitis, a common side effect of varicose veins.
Ulcers: In severe cases, prolonged venous insufficiency can lead to the formation of ulcers, mainly near the ankles.

Complications

Bleeding: The veins close to the skin may sometimes rupture and cause minor bleeding.
Thrombophlebitis: In some cases, the varicose veins can become painful and inflamed, signaling a blood clot known as thrombophlebitis.

Aggravating Factors

Certain activities or conditions can exacerbate the symptoms, such as:

Prolonged Standing or Sitting: Being in the same position for long durations can worsen the symptoms.
Heat: Hot weather or warm temperatures can dilate the veins and make the symptoms more noticeable.
Menstrual Cycle: Some women report that their symptoms worsen during their menstrual cycle due to hormonal fluctuations.

Understanding the signs and symptoms of varicose veins is crucial for early diagnosis and effective management. If you notice any of these symptoms, it is advisable to consult a healthcare provider for a comprehensive evaluation and treatment plan.

When To Worry About Varicose Veins?

Immediately consult your healthcare provider about your varicose veins if they become painful, if the skin around them changes, or if you start to develop sores or rashes near them. Another red flag is if the veins feel warm or the skin around them becomes discolored. These could be signs of a more serious issue like a blood clot or infection that needs immediate medical attention.

Further, if there is swelling in your legs or ankles, severe and unexplained pain, or if the veins start to bleed, consult a healthcare provider as soon as possible. These symptoms could indicate complications that may require prompt medical treatment.

How To Prevent Varicose Veins?

Varicose veins can cause discomfort and may even lead to more serious health complications. Prevention is always better than cure, and in the case of varicose veins, there are several steps one can take to reduce the risk or slow down their development. Below are some of the most effective prevention methods, divided into key categories for better understanding.

Lifestyle Changes

Lifestyle changes are the cornerstone of preventing varicose veins. Such changes can include:

Regular Exercises

Physical activity, especially leg exercises like walking, jogging, and swimming, can help improve blood circulation and strengthen the veins.

Consider Weight Management

Extra pressure on veins, particularly in the legs, can increase the risk of developing varicose veins. A balanced weight can help reduce this strain, although it’s important to note that weight is just one of many factors that could contribute to varicose veins. Consult your healthcare provider for a personalized plan.

Posture and Positioning

Positioning your body throughout the day can significantly affect your vein health.

Avoid Prolonged Standing or Sitting

Standing or sitting for long periods can cause blood to pool in the legs, increasing blood pressure on the veins. Make it a habit to move around every 30 minutes.

Elevate Your Legs

Elevating your legs above heart level encourages blood flow back towards the heart when resting.

Footwear Choices

The shoes you wear can have a surprisingly significant impact on your vein health.

Choose Low-Heeled Shoes

Low-heeled shoes work your calf muscles more, which is better for your veins. Avoid high heels whenever possible.

Use Compression Stockings

For those at high risk of developing varicose veins, such as people with a family history or those who stand for long periods, compression stockings can help. These stockings apply pressure to the legs and aid in blood circulation.

Dietary Changes

Your diet plays a critical role in the health of your veins.

High-Fiber and Low-Salt Diet

A diet rich in fiber can help prevent constipation, which can contribute to varicose veins. Meanwhile, a low-salt diet helps to reduce water retention, thus decreasing the pressure on your veins.

Stay Hydrated

Proper hydration can improve blood circulation, reducing the risk of blood clots and varicose veins.

Regular Health Checks

Consult Your Doctor

If you’re at higher risk for developing varicose veins due to your family history or lifestyle, it’s important to consult a healthcare provider for a personalized prevention plan. Regular check-ups can help in early detection and management.

About The LifeDNA Skincare Report

LifeDNA Skincare Report offers personalized advice on skin care routines, product recommendations, and lifestyle changes. For instance, if you are genetically prone to tanning quickly, the report might suggest a higher SPF sunscreen and additional protective measures like wearing hats and long sleeves.

The LifeDNA Skincare report covers an analysis of Varicose Veins. Get yours here.

Summary

Varicose veins are a common but often preventable circulatory issue affecting many adults.
Genetic and lifestyle factors influence the risk, but early intervention and proper management can alleviate the symptoms and complications.
Early symptoms like pain, discoloration, and inflammation can help effectively treat and prevent complications.
Several GWAS on varicose veins have established prospective genetic markers influencing varicose veins.
Non-genetic risk factors like sedentary lifestyle, type of occupation, and footwear choices can also influence predisposition to varicose veins.

*Understanding your genetics can offer valuable insights into your well-being, but it is not deterministic. Your traits can be influenced by the complex interplay involving nature, lifestyle, family history, and others.

Our reports and suggestions do not diagnose or treat any health conditions or provide any medical advice. Consult with a healthcare professional before making any major lifestyle changes or if you have any other concerns about your results.

References

Our reports have not been evaluated by the Food and Drug Administration. The contents on our website and our reports are for informational purposes only, and are not intended to diagnose any medical condition, replace the advice of a healthcare professional, or provide any medical advice, diagnosis, or treatment. Consult with a healthcare professional before making any major lifestyle changes or if you have any other concerns about your results. The testimonials featured may have used more than one LifeDNA or LifeDNA vendors’ product or reports.

Is Psoriasis Genetic?

Aira on August 9, 2024

Overview

Psoriasis is a common, chronic skin condition occurring worldwide, presenting at any age, and leading to a substantial burden for individuals and society. It is associated with several important medical conditions, including depression, psoriatic arthritis, and cardiometabolic syndrome, impacting millions of people around the world.

Understanding this skin condition is essential for its effective management.

What Causes Psoriasis?

Psoriasis has a complex origin that can be attributed to both genetic and non-genetic factors. While genetics play a significant role in predisposing individuals to psoriasis, it’s only one piece of the puzzle. Environmental triggers and lifestyle choices also contribute to the development and progression of this condition.

Understanding both genetic and environmental factors contributing to psoriasis is vital for a better grasp of the condition and for improving support and treatment options for those affected.

Genetic Factors

Researchers have found specific gene variations related to our immune system and the skin’s protective barrier that can make the skin more sensitive and vulnerable to triggers.

In a family, if one parent has psoriasis, there’s a 20% chance their child will develop it, and this risk increases to 65% if both parents are affected.

Studies involving twins have shown that if one identical twin has psoriasis, there’s a 70% chance that the other twin will also develop the condition. In non-identical twins, this likelihood is lower, at 20%.

These findings highlight the relevance of hereditary factors in psoriasis.

HLA-C w6 and SNP rs10484554

The PSORS1 locus, located on chromosome 6, is one of the key genetic areas linked to psoriasis. Recent genetic studies have highlighted the significance of HLA-C, specifically the variant HLA-Cw6 (rs1131118), in psoriasis development, but the precise role is still under study. Additionally, SNP rs10484554 in the HLA-C region has been associated with a higher risk of psoriasis in some studies. It’s worth noting that psoriasis shares genetic overlaps with other conditions, such as type 2 diabetes, indicating complex genetic interactions. The specific mechanisms through which SNP rs10484554 influences psoriasis development are an active area of research, contributing to our understanding of the genetic complexities underlying this condition.

IL36RN and CARD14

While many genes may contribute to psoriasis risk, specific gene mutations like those in IL36RN and CARD14 have been found to independently trigger psoriasis. These mutations affect both the skin and the immune system. Also, polymorphisms (SNPs) in the IL36RN gene on chromosome 2 can lead to variations in the IL-36Ra protein, which plays a role in regulating inflammation. IL36RN mutations and polymorphisms are particularly associated with pustular psoriasis.

On chromosome 17, the PSORS2 region has also been associated with psoriasis. Recent research has identified rare mutations in the CARD14 gene, contributing to overactive immune responses in familial psoriasis cases.

TRAF3IP2

A comprehensive genetic study of psoriasis and psoriatic arthritis uncovered 10 regions significantly associated with psoriatic arthritis (PsA) and 11 with cutaneous-only psoriasis (PsC), further pinpointing the genetic distinctions between these conditions. Additionally, the study identified the previously unreported genome-wide significant association of TRAF3IP2 with PsC, adding new insights into the genetic underpinnings of these related conditions.

In a broader genetic analysis of psoriasis, a meta-analysis encompassing multiple genome-wide association studies revealed 15 novel susceptibility loci, expanding the total number of psoriasis-associated loci in European populations to 36. Moreover, this study unveiled candidate genes involved in immune regulation and innate host defense, contributing to our understanding of the genetic factors influencing immune-mediated inflammatory conditions, and emphasizing the skin’s significance in host defense mechanisms.

These findings underscore the consistent role of the TRAF3IP2 gene in psoriasis and its subtypes. This genetic factor has emerged as a critical component in understanding the genetic architecture of psoriasis.

Other Single Nucleotide Polymorphisms (SNPs)

In addition to nucleotide variation in specific genes, scientists have studied SNPs in non-coding regions of the genome. These SNPs are genetic markers that may indicate potential gene regulatory regions related to psoriasis, many of which involve the immune system’s role in the condition.

LifeDNA’s Skincare Report can provide valuable insights to help you determine if you have a genetic predisposition (potential) for developing psoriasis and offer suggestions on managing this skin condition.

Non-Genetic or Environmental Factors

Several non-genetic elements have been associated with a predisposition to the development and exacerbation of this skin condition.

Physical Trauma

In an intriguing historical discovery, Heinrich Koebner observed that physical trauma, like cuts, burns, insect bites, and even tattoos, could trigger and worsen psoriasis. This response, known as the Koebner response, often results in new psoriatic lesions that closely mirror the type of injury sustained.

The prevalence of this response in psoriasis patients ranges from 24% to 51%. The development of psoriasis following an injury can take anywhere from 3 days to 2 years and may depend on factors like the season and the severity of the skin condition.

Drug-Induced Psoriasis

Some medications have been linked to the onset and worsening of psoriasis. Common causes include drugs such as lithium, beta-blockers, antimalarials, tetracyclines, and non-steroidal anti-inflammatory medications.

More recently, medications that include TNFα blockers, IL-6R blockers, and certain interferons, along with the TLR7 agonist imiquimod, have also been reported to induce or exacerbate psoriasis. Other medications such as ACE inhibitors, calcium channel blockers, and IL-2 in the form of cancer immunotherapy have also been associated with psoriasis worsening.

Infections

Infections, especially in children, have been identified as significant triggers for psoriasis. Guttate psoriasis, characterized by small, drop-like lesions, has been linked to Streptococcus pyogenes infections through both the throat and skin routes. Additionally, infections like Staphylococcus aureus, Malassezia, and Candida albicans in the gut or on the skin have been associated with psoriasis worsening. In some cases, Helicobacter pylori infection has been observed to correlate with psoriasis severity.

Researchers suspect that toxins from these microorganisms and bacterial components could activate T cells and lead to abnormal immune responses, thus contributing to psoriasis development.

Stress

Psychological stress is known to exacerbate psoriasis by affecting the immune system. Stress hormone levels can increase due to the activation of the hypothalamus–pituitary–adrenal axis, potentially leading to psoriasis worsening.

In particular, cutaneous CRH and CRH-receptor 1 have been shown to regulate local homeostasis in the skin, and in psoriasis, expression of CRH is significantly increased. The pro-inflammatory effects of CRH on the skin are still being studied, but it may stimulate the production of key cytokines, further exacerbating psoriasis.

Alcohol and Smoking

The relationship between alcohol and psoriasis is multifaceted and debated. Studies suggest that alcohol abuse is associated with a higher prevalence of psoriasis. Furthermore, moderate to severe psoriasis patients are at an increased risk of alcohol-related conditions and mortality.

While the exact mechanisms remain unclear, laboratory studies have shown that ethanol can stimulate T cells and induce keratinocyte hyperproliferation. Smoking is another risk factor for psoriasis, with a stronger correlation among women and former or current smokers. Recent research indicates that genetic susceptibility to psoriasis, combined with smoking and alcohol use, can significantly increase the risk.

Obesity

Obesity has been identified as a risk factor for psoriasis, and studies have also suggested a connection between obesity and psoriasis severity. The mechanism behind this link is not fully understood, but it may involve adipokines such as leptin and resistin, which are often found in higher concentrations in psoriasis patients and obese individuals.

These adipokines can stimulate the production of proinflammatory cytokines, leading to skin inflammation. However, the relationship between obesity, weight loss, and psoriasis is complex, and more research is needed to understand their interactions fully.

Curious about your genetic predisposition to psoriasis and seeking personalized skincare advice to proactively address and manage this skin condition? Unlock LifeDNA’s DNA skincare report today.

Is Psoriasis Contagious?

Psoriasis is not contagious; it doesn’t spread through air or touch. It’s rooted in immune system dysfunction, where skin cells grow at an accelerated rate, leading to the formation of dry, scaly patches. This rapid cell turnover contributes to the hallmark plaques of psoriasis.

Does Psoriasis Ever Completely Go Away?

Regrettably, psoriasis has no permanent cure. It falls under the category of chronic conditions. While symptoms can be managed, they typically persist over the long term. New treatment approaches, like biologics targeting immune responses, have revolutionized psoriasis management, enhancing patients’ quality of life.

Is Psoriasis an Autoimmune Condition?

Psoriasis is indeed an immune-mediated genetic skin condition. The interplay of the innate and adaptive immune systems, orchestrated by various cells such as T cells, dendritic cells, macrophages, and keratinocytes, play a central role. Recent years have seen the development of biologics, which are drugs created from living organisms and are designed to focus on specific molecules or pathways in the body.

These target various cytokines, such as tumor necrosis factor-α, interleukin-23, and interleukin-17, drastically altering psoriasis treatment. While genetics are involved, various environmental factors also influence psoriasis onset and exacerbation. Furthermore, psoriasis has been associated with systemic inflammation, cardiovascular comorbidities, and other autoimmune and auto-inflammatory conditions.

Psoriasis Treatment Options

Psoriasis has a history of several treatment options that have proven effective in managing this condition. These include:

Topical Therapy: Traditional treatments like corticosteroids and vitamin D3 analogs have been the cornerstone of psoriasis management, effectively controlling mild to moderate symptoms.
Phototherapy: Historic narrowband UVB therapy utilizes ultraviolet light to alleviate symptoms in moderate to severe cases.
Acitretin: A synthetic retinoid, used to treat moderate to severe psoriasis, often in combination with other therapies.
Methotrexate: A systemic treatment inhibiting folate biosynthesis, employed for moderately severe to severe psoriasis and psoriatic arthritis.
Cyclosporine: A calcineurin inhibitor known to be beneficial for rapidly improving symptoms in moderate to severe psoriasis, despite its potential side effects.

Advanced psoriasis treatments, including biologic therapies such as infliximab, ustekinumab, adalimumab, and etanercept, have transformed psoriasis management. These highly effective treatments target specific proteins or pathways in the body, providing personalized and safe care. These therapies represent promising advancements in the field of psoriasis treatment.

Summary

Psoriasis is a common and chronic skin condition with significant societal and individual burdens.
Its causes are multifaceted, involving both genetic and non-genetic factors.
Genetic factors play a role, with specific gene variations related to the immune system and skin’s protective barrier increasing the potential for developing the condition or its severity.
Environmental factors, such as physical trauma, certain medications, infections, stress, alcohol, smoking, and obesity, can trigger or exacerbate psoriasis.
While there’s no permanent cure for psoriasis, modern treatment options, including biological therapies, have significantly improved symptom management.

References

Is Male Pattern Baldness Genetic?

Aira on August 9, 2024

What is male pattern baldness?

The most typical reason for male pattern baldness, also known as androgenetic alopecia (AGA), is hair loss. A steady and regular pattern of hair loss and thinning characterizes this inherited disorder. Male pattern baldness can substantially affect a person’s self-esteem and confidence, even if it is mostly a cosmetic matter.

The main factors affecting male pattern baldness are hormones and genetics. It frequently comes from one of the two sides of the family—the mother’s or the father’s. The hormone dihydrotestosterone (DHT), which can shrink hair follicles and cause them to generate shorter and finer hair, is linked to the disorder. Affected follicles may eventually completely stop generating hair.

Male pattern baldness frequently begins with thinning hair at the top of the head and a receding hairline at the temples. These bald spots may grow larger as the condition worsens, eventually resulting in partial or total baldness on the top of the head.

At what age does male pattern baldness start?

Male pattern baldness can begin at different ages, and the elements that affect it genetically, hormonally, and personally can affect the timing of it. Although there is no specific age at which it starts, comprehension of the basic features of male pattern baldness can help in understanding how it progresses.

In their late teens or early twenties, some men may already start to detect the first indications of this condition. Early-onset male pattern baldness can be emotionally difficult as it impacts self-image during a formative stage of life. These symptoms frequently include a receding hairline, thinning at the temples, or a more pronounced “widow’s peak.”

The mid-to late-twenties are typically when male pattern baldness starts to become more obvious. At this point, the hairline may further recede and the crown of the head’s thinning hair may become more noticeable. However, each person will progress at a different rate and degree.

Male pattern baldness often advances more by the time men are in their thirties and beyond. The Norwood scale is frequently used to describe the pattern of hair loss, with variable degrees of hairline recession and crown balding. While some men may have a reasonably consistent way of hair loss throughout this time, others may undergo severe hair loss.

What are the leading causes of male pattern baldness?

When estimating the risk of developing male pattern baldness, hereditary factors are to be considered. You may be more likely to develop early-onset baldness if your family has a history of the condition. It can even be a hereditary trait that can be passed down through many generations.

A DNA test might help you know more about certain traits related to your hair health. While LifeDNA test results are not meant to diagnose any disease, your DNA analysis, however, can give you insights into your possible genetic predisposition for early on-set male pattern baldness or early AGA and what you can do to manage the risk.

Genetic Factors

One of the most significant indicators of male pattern baldness risk is the family history. Individuals with close relatives, particularly on the maternal side (mother’s father), who experienced male-pattern baldness, are more likely to inherit the genetic predisposition.

The Androgen Receptor (AR) Gene, located on the X chromosome, is a key genetic factor in this hair condition. Variations in this gene can make hair follicles more sensitive to the hormone dihydrotestosterone (DHT), which leads to the shrinking of follicles and the production of shorter, finer hair.

The Genome-Wide Association Studies (GWAS) have identified multiple other genetic markers associated with AGA as well. These studies have shed light on the complex genetic underpinnings of the condition, involving numerous genes and genetic variants. These Genes and SNPs include SNPs rs2497938 (AR), rs6047844 (PAX1, FOXA2), rs2180439 (LINC01432, RPL41P1), rs9287638 (HDAC4), rs2073963 (HDAC9), rs12565727 (TARDBP), rs12373124 (Intergenic), rs6945541(AUTS2), rs10502861 (SETBP1).

Non-Genetic (Environmental) Factors

Male pattern baldness is largely inherited, although hormonal, environmental, and lifestyle variables can also have an impact on how the illness manifests. These factors can interact with genetic predispositions, influencing the onset and severity of the condition.

In people who are genetically susceptible to hair loss, hormonal imbalances, particularly high levels of dihydrotestosterone (DHT), can hasten the process. DHT is a testosterone-derived hormone that can cause hair follicles to shrink, resulting in thinner and shorter hair. Another important non-genetic contributing element to male pattern baldness is aging. As people age, hair loss frequently becomes more obvious, and both the pace and degree of hair loss tend to accelerate.

Chronic stress can accelerate male pattern baldness in those who are vulnerable to it and also lead to hair loss in general. Hormones associated with stress can alter the natural cycle of hair development and increase shedding. Additionally, unhealthful eating habits and nutritional deficiencies, such as a lack of vitamins and minerals necessary for healthy hair (such as biotin, iron, and zinc), can accelerate hair loss.

Some drugs, such as those prescribed for depression, hypertension, and cancer, can also cause hair loss as a side effect, which could make male pattern baldness worse. It’s important to note that while these non-genetic factors can contribute to male pattern baldness, they do not cause the condition on their own. Instead, they often exacerbate hair loss in individuals who are genetically predisposed to it.

Can you reverse male pattern baldness naturally?

Although there are no 100% effective natural treatments for AGA, several strategies might be helping to reduce hair loss and support healthy hair. While these natural approaches may complement a comprehensive hair care routine, they are unlikely to fully reverse male pattern baldness, especially in advanced stages.

Healthy hair can be supported by eating a balanced diet that is high in vitamins, minerals, and proteins. Beneficial nutrients include biotin, iron, zinc, and omega-3 fatty acids. Additionally, maintaining hydration and controlling stress can lessen hair loss.

(Other) hair care regimens could be beneficial as well. Regular scalp massage may increase blood flow to the hair follicles and may encourage hair growth. Avoid using excessive heat styling equipment, harsh hair products, and tight hairstyles because these things can harm hair and make hair loss worse.

Superfoods are also said to help with hair loss. Aloe vera, onion juice, and essential oils like peppermint and rosemary have all been investigated for their potential to encourage hair growth. Their effectiveness is still being studied.

Can you prevent male pattern baldness?

To a limited extent, certain tactics and lifestyle modifications may help postpone or lessen the onset and severity of male pattern baldness. A balanced diet full of vital minerals, such as biotin, iron, and zinc, helps support healthy hair. A healthy body weight and being hydrated can both be helpful.

Hair loss can also be significantly influenced by ongoing stress. Its effects could be lessened by practicing stress-reduction exercises like yoga, meditation, or regular exercise. Avoid using harsh hair products, tight hairstyles, and excessive heat styling because they can harm hair and cause hair loss.

The FDA has approved prescription drugs including finasteride and minoxidil for the treatment of male pattern baldness. In certain people, they might help decrease hair loss and encourage regrowth. When medical therapies like minoxidil or finasteride are started as soon as hair loss symptoms are identified, hair preservation may be improved.

Is male pattern baldness genetic?

AGA is primarily inherited from one’s parents and can be passed down through generations. Genetic predisposition to male pattern baldness is influenced by a combination of multiple genes, making it a complex trait.

From which parent is it inherited?

Male pattern baldness is primarily inherited through genetic factors that can be passed down from both parents, but the inheritance pattern is more complex than a simple “from one parent” scenario. While the genes responsible for male pattern baldness can be inherited from either parent, research suggests that the condition may be influenced by multiple genetic factors from both maternal and paternal sides of the family.

The androgen receptor gene (AR) located on the X chromosome plays a significant role in male pattern baldness. Sons inherit one X chromosome from their mother and one Y chromosome from their father.

If a mother carries genetic variations associated with male pattern baldness on one of her X chromosomes, she can pass that predisposition on to her son. However, this doesn’t mean that the father’s genes are irrelevant; they also contribute to the son’s genetic makeup and can influence the likelihood and severity of male pattern baldness.

How can LifeDNA help you manage male pattern baldness?

In controlling some disorders, including AGA and hair loss, genetics is crucial. It even has an impact on how they develop in the first place. LifeDNA provides complete and detailed information about a variety of areas of your wellness, including how they relate to your genetic makeup. Want to learn more about your potential state of wellness? Try LifeDNA now.

What are the different treatment options for male pattern baldness?

Several treatments can lessen hair loss and, in certain situations, encourage hair regrowth. The efficacy and methodology of these treatments differ. Numerous drugs are either available over-the-counter or require a doctor’s prescription.

Minoxidil is an OTC topical medicine with FDA approval that comes in different formulations (liquid, foam). It has been demonstrated to encourage hair regrowth and reduce hair loss in many people when administered straight to the scalp. Oral prescription drug finasteride blocks the hormone dihydrotestosterone (DHT), which is the cause of the hair follicles shrinking in men with male pattern baldness. For many men, it works well at slowing hair loss and even encouraging regrowth.

Additional therapies for AGA include low-level lasers or light-emitting diodes that are used in Low-Level Laser Therapy (LLLT) such as laser combs and helmets to stimulate hair follicles and encourage hair growth. Even though results can vary, some people benefit from LLLT.

In a more invasive treatment regimen, a small amount of the patient’s blood is drawn, processed to concentrate the platelets, and then used to create platelet-rich plasma (PRP), which is subsequently injected into the scalp. It is assumed that it will activate hair follicles and encourage hair growth. Lastly, hair follicles from donor areas (usually the back or sides of the head) can be transplanted to balding or thinning areas during hair transplant surgery operations. This can be a durable remedy for regrowing hair in particular scalp areas.

Can male pattern baldness be cured with gene editing?

While gene editing has not been established as a cure for male pattern baldness or AGA, and its use for hair loss is still in the experimental and research phase, gene editing techniques such as CRISPR-Cas9 have shown promise in various other medical applications.

The androgen receptor gene and other genes involved in the development of the disorder, like the SRD5A2 gene, might be modified specifically using CRISPR-Cas9. These modifications could include additions, deletions, and tweaks.

With the aid of a guide RNA, the Cas9 enzyme in CRISPR-Cas9 functions as “molecular scissors” to cut DNA at a precise spot. Using standard protein-carrier methods, it is difficult to properly transport Cas9 to the dermal papilla cells in the hair follicle in cases of androgenic alopecia.

To overcome this problem, scientists have created a microbubble-based carrier system that uses ultrasound to deliver Cas9 complexed with single-carrier RNA to the hair follicle. In an animal model, topical treatment of the nanoparticle system was demonstrated to increase hair growth. As a first step toward establishing the technique as a standard, these results, which were announced in 2020, are encouraging.

The various genetic causes of male pattern baldness are still being investigated by researchers, and there is interest in creating novel therapies based on a deeper knowledge of the genes playing a role in this condition. It is to be noted that the use of gene editing for cosmetic objectives, such as hair regeneration, will be subject to ethical, safety, and regulatory concerns.

Summary

Androgenetic alopecia (AGA), another name for male pattern baldness, is a specific type of hair loss. This genetic condition is characterized by thinning and persistent hair loss.
This disease is associated with the hormone dihydrotestosterone (DHT), which can shrink hair follicles and lead them to produce shorter and finer hair.
Male pattern baldness often starts with receding hairlines at the temples and thinning hair on top of the head.
Male pattern baldness can start at various ages, and the genetic, hormonal, and individual factors that influence it can affect the timing
Family history of this condition is one of the most important predictors of male pattern baldness risk.
Although hormonal, environmental, and lifestyle factors can also affect how the condition presents itself, male pattern baldness is largely inherited.
Even though there are currently no natural AGA therapies that are 100% successful, several methods may be attempted to slow hair loss and promote healthy hair.
Researchers are still looking into the many genetic factors that contribute to male pattern baldness, and there is interest in developing new treatments based on a better understanding of these genes involved.

References

Unveiling the Genetics of Skin Dryness

Aira on March 8, 2024

What is Skin Dryness?

In a world where our skin acts as a resilient barrier against environmental stressors, the prevalence of skin dryness emerges as a common concern affecting individuals of diverse demographics.

Skin dryness, scientifically known as xerosis, results from an insufficient amount of water content in the stratum corneum, the outermost layer of the epidermis.

This condition disrupts the skin’s natural lipid barrier, leading to increased transepidermal water loss (TEWL) and compromised moisture retention. Excessive skin dryness, a more severe condition is scientifically known as ichthyosis vulgaris.

The human skin, comprising a complex matrix of cells, lipids, and proteins, requires a delicate balance to maintain optimal hydration levels. Factors such as climate, age, genetics, and lifestyle choices contribute significantly to the onset of skin dryness.

Environmental conditions, including low humidity and excessive exposure to ultraviolet (UV) radiation, can exacerbate this condition, amplifying the need for effective skincare strategies.

What Causes Skin Dryness?

Skin dryness, a pervasive dermatological concern, stems from an intricate interplay of various intrinsic and extrinsic factors.

Inadequate Moisture Retention: At the core of skin dryness lies a deficiency in the skin’s ability to retain moisture. The stratum corneum, the outermost layer of the epidermis, relies on a balanced composition of lipids and proteins to create an effective barrier against water loss. Disruption in this lipid barrier, often caused by genetic predispositions, can compromise the skin’s moisture-retaining capabilities.
Environmental Influences: External factors play a pivotal role in exacerbating skin dryness. Low humidity levels, particularly in arid climates, contribute to increased transepidermal water loss (TEWL). Additionally, prolonged exposure to harsh weather conditions, such as cold winds or excessive sunlight, can strip the skin of its natural oils, diminishing its capacity to stay adequately hydrated.
Age-Related Changes: The aging process naturally induces alterations in skin structure and function. As individuals age, there is a decline in sebum production and a reduction in the skin’s natural moisturizing factors. These age-related changes lead to a diminished ability to maintain optimal hydration levels, rendering the skin more prone to dryness and flakiness.
Harsh Cleansing Practices: Surprisingly, certain skincare habits can contribute to skin dryness. Excessive use of harsh soaps, hot water, or aggressive exfoliants can strip away the skin’s protective oils, disrupting the delicate balance required for moisture retention.
Underlying Medical Conditions: Various medical conditions, such as eczema, psoriasis, or thyroid disorders, can manifest with skin dryness as a prominent symptom. These conditions often involve disruptions in the skin barrier function, leading to increased water loss and compromised hydration.

Understanding the multifaceted nature of these factors empowers individuals to adopt targeted skincare practices and lifestyle modifications, fostering a resilient and well-hydrated skin barrier.

What Can Affect Your Skin Dryness?

Genetic Factors

Understanding your skin’s defense involves a key player – filaggrin, a vital protein in the skin barrier. In European families with ichthyosis vulgaris, mutations in the filaggrin gene (FLG) have been linked to atopic dermatitis, a skin condition. One study explored if these gene mutations also play a role in IV/AD in Japan.

European-specific mutations R501X and 2282del4 weren’t found in 253 Japanese individuals. Researchers checked the FLG gene in 4 Japanese ichthyosis vulgaris families and found 2 new mutations, 3321delA and S2554X. These mutations led to a noticeable reduction in keratohyalin granules in the skin.

Researchers then looked at 143 Japanese atopic dermatitis patients and found the FLG null mutations in 8 patients (5.6%). S2554X was in 6 patients (4.2%), and 3321delA was in 2 patients (1.4%). Importantly, these null variants were not present in 156 unrelated Japanese nonatopic and nonichthyotic controls.

These studies suggest that FLG mutations in Japan are different from those in European populations. Filaggrin null variants are significant factors for atopic dermatitis in Japan, and similar to European studies, they may indicate a more severe and persistent form of atopy.

Environmental Factors

Excessive skin dryness is often a result of a delicate balance disrupted by various environmental factors. Understanding the influence of these external elements on the skin’s moisture levels is crucial for effective skincare.

Low Humidity: Ambient humidity plays a pivotal role in skin hydration. Low humidity levels, characteristic of arid climates or heated indoor environments, can lead to increased transepidermal water loss. As the air becomes drier, the skin struggles to retain moisture, potentially resulting in dry and flaky skin.
Harsh Weather Conditions: Exposure to extreme weather conditions, such as cold winds and excessive sunlight, can adversely impact the skin’s lipid barrier. Cold weather can strip the skin of its natural oils, while prolonged sun exposure can lead to dehydration. Both scenarios compromise the skin’s ability to maintain optimal hydration, contributing to dryness.
UV Radiation: Ultraviolet (UV) radiation, a component of sunlight, poses a dual threat to the skin. Beyond its well-established role in skin aging and the development of skin cancers, UV radiation can also disrupt the skin’s barrier function. This disruption not only compromises the skin’s ability to retain moisture but also triggers inflammatory responses that may exacerbate dryness.
Air Pollution: Environmental pollutants, including particulate matter and chemicals in the air, have been linked to skin dryness. These pollutants can penetrate the skin, leading to oxidative stress and inflammation. The resulting damage impairs the skin barrier, contributing to increased water loss and decreased moisture retention.
Indoor Heating and Cooling Systems: Artificial heating and cooling systems prevalent in indoor environments can have a dehydrating effect on the skin. Both heating and air conditioning reduce indoor humidity levels, creating an environment where the skin struggles to maintain its moisture balance. Prolonged exposure to such conditions can contribute to chronic skin dryness.
Hot Water Exposure: While a hot shower may be soothing, it can strip the skin of its natural oils. Hot water can disrupt the lipid barrier, leading to increased TEWL and diminished moisture retention. Opting for lukewarm water and limiting shower durations can mitigate this risk.
Hard Water: The high mineral content of water, commonly referred to as hard water, can influence skin dryness. Hard water contains elevated levels of minerals like calcium and magnesium, which may react with skin cleansers and form deposits. These deposits can compromise the skin barrier, contributing to dryness and irritation.

Understanding the impact of these environmental factors on skin health empowers individuals to adopt protective measures. From adjusting skincare routines to mitigating exposure to harsh conditions, proactively addressing these external influences is essential in promoting and preserving skin hydration.

Is Excessive Skin Dryness Contagious?

Excessive skin dryness is not contagious; it does not spread from person to person like an infectious disease. The condition is rooted in disruptions to the skin’s natural barrier function and moisture retention mechanisms.

Internally, genetic factors play a role in determining an individual’s susceptibility to skin dryness. Mutations in genes related to skin structure and hydration, such as the filaggrin gene, can predispose individuals to dry skin conditions. However, these genetic factors are not communicable and do not transfer between people.

It’s important to recognize that skin dryness results from a complex interplay of genetic, environmental, and individual-specific factors. Unlike contagious conditions caused by pathogens like bacteria or viruses, skin dryness is a non-communicable concern.

While one person’s skin dryness does not spread to others, individuals suffering from skin dryness may share similar environmental triggers or genetic predispositions.

To manage and prevent skin dryness, adopting a tailored skincare routine that includes moisturization, protective measures against environmental factors, and a healthy lifestyle is essential.

Understanding the non-contagious nature of skin dryness underscores the importance of personalized care to address the unique factors influencing an individual’s skin health.

Can Excessive Skin Dryness Go Away Permanently?

While managing skin dryness is possible, achieving a permanent cure is challenging. Scientifically, the skin’s natural ability to retain moisture diminishes with age, making long-term management crucial.

However, adopting a consistent and effective skincare routine, including moisturization and protection against environmental stressors, can significantly improve and control dry skin. Lifestyle modifications, such as staying hydrated and avoiding harsh skincare practices, play a pivotal role.

While complete eradication may be elusive due to the multifaceted nature of skin dryness, proactive and persistent care can lead to substantial and lasting improvements. A holistic approach addressing genetic, environmental, and lifestyle aspects ensures sustained relief and enhances the overall health of the skin.

You may also be interested in: Genetics & Rosacea: What You Need To Know

Can Vitamin Deficiencies Cause Excessive Dry Skin?

Vitamin deficiencies can contribute to dry skin. Scientific evidence highlights the role of certain vitamins in maintaining skin health. Vitamin A, for instance, is crucial for skin cell development and repair. Its deficiency can lead to a skin dryness condition known as xerosis, characterized by dry, rough skin.

Vitamin E, with its antioxidant properties, helps protect the skin from oxidative stress and moisture loss. Inadequate levels may compromise the skin’s ability to retain hydration. Also, vitamin D is involved in skin barrier function, and its deficiency has been linked to various skin issues, including dryness.

B vitamins, particularly Biotin (B7) and Niacin (B3) play roles in skin metabolism and hydration regulation. Insufficient levels can contribute to dry, flaky skin. Furthermore, vitamin C is essential for collagen synthesis, promoting skin elasticity and moisture retention.

Addressing vitamin deficiencies through a balanced diet or supplements, as recommended by healthcare professionals, can positively impact skin health.

However, while vitamin deficiencies can contribute to dry skin, they are just one aspect of a comprehensive approach that includes proper skincare, hydration, and lifestyle choices for optimal skin well-being.

How to Improve and Manage Excessive Skin Dryness

Managing and improving skin dryness involves a multifaceted approach, addressing both internal and external factors that influence skin health. Scientifically-backed strategies contribute to the restoration and maintenance of optimal skin hydration.

Hydration from Within

Adequate hydration is foundational for skin health. Consuming sufficient water helps maintain the body’s overall moisture balance, reflected in the skin. Studies suggest a positive correlation between water intake and skin hydration, emphasizing the importance of internal hydration for combating dryness.

Nutrient-Rich Diet

Incorporating a diet rich in essential nutrients supports skin health. Vitamins A, C, E, and B-complex vitamins are crucial in skin function. Foods such as fruits, vegetables, whole grains, and lean proteins contribute to the maintenance of skin integrity and hydration.

Omega-3 Fatty Acids

Omega-3 fatty acids, found in fish oil and certain plant sources, have anti-inflammatory properties and contribute to skin barrier function. Research indicates that supplementing with omega-3 fatty acids can enhance skin hydration and mitigate symptoms of dryness.

Moisturization

External moisturization is pivotal for managing skin dryness. Applying emollients and humectants helps create a protective barrier, preventing water loss. Look for moisturizers containing ingredients like hyaluronic acid, glycerin, and ceramides, which are supported by scientific evidence for their efficacy in maintaining skin hydration.

Avoiding Harsh Cleansers

Harsh soaps and cleansers can strip the skin of its natural oils, exacerbating dryness. Opt for gentle, fragrance-free cleansers to maintain the skin barrier’s integrity. Scientifically formulated cleansers with a balanced pH are recommended for those prone to dry skin.

Limiting Hot Water Exposure

Prolonged exposure to hot water can deplete the skin’s natural oils. Opt for lukewarm water during showers or baths to prevent excessive drying. Additionally, reducing the duration of showers helps minimize the impact on skin hydration.

Humidification

Increasing indoor humidity levels can benefit skin hydration, especially in dry climates or during winter. Using humidifiers helps counteract the drying effects of artificial heating or cooling systems, maintaining a more favorable environment for the skin.

Protecting from Environmental Stressors

Shielding the skin from harsh weather conditions, UV radiation, and pollutants is crucial. Wearing protective clothing and using sunscreen with a high SPF helps minimize environmental damage, preserving the skin’s moisture balance.

Identifying and Managing Allergens

Allergens can exacerbate skin dryness, particularly in conditions like atopic dermatitis. Identifying and avoiding potential allergens, with the guidance of a healthcare professional, contributes to effective dry skin management.

Consulting a Dermatologist

Consulting a dermatologist is advisable in cases of persistent or severe skin dryness. Dermatologists can provide personalized insights, prescribe medicated creams, and conduct thorough assessments to address underlying causes.

Incorporating these evidence-based strategies into a comprehensive skincare routine empowers individuals to proactively manage and improve skin dryness, fostering a healthy and hydrated skin barrier.

LifeDNA’s Skin Dryness Trait Report

Unlock the secrets to radiant, well-nourished skin with LifeDNA’s Excessive Skin Dryness Trait Report. Our scientifically-backed Skincare Report delves into your unique genetic profile, revealing insights that empower you to take charge of your skin health.

Understanding the genetic factors contributing to excessive skin dryness allows for personalized skincare strategies, ensuring you provide your skin with precisely what it needs.

Your wellness journey starts with knowledge. LifeDNA’s comprehensive Skincare Report extends beyond excessive dryness, offering in-depth insights into other dermatological concerns like eczema, increased nasolabial folds, and psoriasis.

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Summary

Skin dryness, or xerosis, is a common concern influenced by a complex interplay of genetic, environmental, and lifestyle factors.
Genetic factors, such as mutations in the filaggrin gene (FLG), can contribute to skin conditions like atopic dermatitis, with variations observed across populations.
Environmental influences, including low humidity, harsh weather conditions, UV radiation, air pollution, and hot water exposure, play pivotal roles in exacerbating skin dryness.
Excessive skin dryness is not contagious; it is rooted in disruptions to the skin’s natural barrier function and moisture retention mechanisms.
Achieving a permanent cure for skin dryness is challenging, but proactive skincare, hydration, and lifestyle modifications can lead to substantial and lasting improvements.
Vitamin deficiencies, particularly A, E, D, B-complex, and C, can contribute to dry skin, emphasizing the importance of a balanced diet and supplementation.
Managing skin dryness involves a holistic approach, addressing both internal and external factors, with hydration, nutrition, omega-3 fatty acids, and proper moisturization playing key roles.
Avoiding harsh cleansers, limiting hot water exposure, taking care of humidification, protecting your skin from environmental stressors, identifying allergens, and consulting a dermatologist are essential strategies for managing and improving skin dryness.

References

Are Nasolabial Folds Genetic?

Aira on February 2, 2024

What are Nasolabial Folds?

The nasolabial fold, often called the “smile line” or “laugh line,” is a common feature in human faces. It is present in nearly everyone except newborns and those with facial paralysis. These lines run from the sides of the nose to the corners of the mouth and become more visible when smiling or laughing, fading away when the face is relaxed.

Unlike a medical condition or a clear sign of aging, nasolabial folds go through a change in visibility over time. Initially more noticeable during expressions, these lines deepen with age, transforming from temporary creases to lasting wrinkles that stick around even when the face is at rest.

This transformation is a result of the natural aging process, involving reduced skin elasticity, less collagen and fat volume, and repeated muscle movements tied to facial expressions.

Genetics of Nasolabial Folds

Understanding the genetic factors influencing nasolabial folds is important for advancing both medical and cosmetic fields. This knowledge allows for personalized skin care strategies, addressing individual genetic predispositions and improving overall skin wellness.

MYH11 Gene and SNP rs76053540

Homo sapiens myosin heavy chain 11 (MYH11) functions as a major contractile protein, converting chemical energy into mechanical energy through the hydrolysis of ATP.

Situated in the 16p13.11 region, the genetic variant rs76053540 has emerged as a significant factor influencing the development of nasolabial folds in Han Chinese females. The genome-wide association study (GWAS) on skin aging revealed a robust association (P = 5.0 × 10−9, dominant model) between this variant and the visibility of nasolabial folds, showcasing its specific impact on facial aging dynamics.

This genetic locus stands out for its unique influence on nasolabial folds, suggesting a dose-dependent effect where the presence of one or more copies of rs76053540-G amplifies the likelihood of nasolabial fold development.

The significance of this association is further underscored by its successful cross-ethnic replication in a meta-analysis involving independent Caucasian cohorts (P = 8.6 × 10−10), emphasizing the universal relevance of this genetic marker in influencing facial aging patterns.

Understanding the role of this MYH11 gene variant opens avenues for targeted treatments and interventions, holding promise for a more personalized approach to addressing nasolabial fold concerns in diverse populations.

SLC30A8 and RAD21 Genes

Two significant single nucleotide polymorphisms (SNPs), namely rs6980503 and rs4876369 in the SLC30A8 gene, have been pinpointed as influential markers for nasolabial folds in Japanese women. These SNPs exhibit pronounced associations with the expression of the nearby RAD21 gene, which codes for a Cohesin subunit. Cohesin mediates cohesion between replicated sister chromatids and is therefore essential for chromosome segregation in dividing cells, forming a vital link to the development of nasolabial folds.

Decoding the genetic aspects of nasolabial folds contributes to advancements in medical and cosmetic practices, offering tailored solutions for healthier skin and more effective anti-aging approaches.

Non-Genetic Factors Influencing Nasolabial Folds

The formation of nasolabial folds involves a complex interplay of anatomical components, ranging from skin thickness to muscular activity. Recognizing these factors is crucial for tailored aesthetic treatments. Below are some of the factors outside genetics that may influence the appearance of nasolabial folds:

Skin Characteristics

The nasolabial fold is more than a simple crease; it represents a three-dimensional curvature influenced by factors such as the loss of skin thickness over the sulcus and the presence of redundant skin drooping. Successful treatment necessitates a comprehensive assessment of skin characteristics and an understanding of the biomechanical support required for facial harmony.

Fat Distribution

Excessive fat deposits laterally to the sulcus, a groove from the nose to the mouth corner, contribute to nasolabial folds prominence. Understanding the role of fat-pad distribution and its impact on nasolabial folds is essential for developing targeted treatments, particularly in cases where subcutaneous fullness and fat play a critical role.

Muscular Activity

Muscular hyperactivity is a significant factor in nasolabial fold formation. Contractions of facial muscles, particularly during smiling or asymmetric movements, create dynamic wrinkles that may evolve into permanent static rhytides (fine lines or wrinkles). Selective approaches targeting specific facial muscles using treatments like BoNT-A and surgery aim to mitigate nasolabial folds associated with muscular hypercontraction.

Bone Structure

Bone retrusion, or posterior movement or positioning of a bone, can contribute to specific types of nasolabial folds. Understanding the influence of bone structure on nasolabial fold development is crucial for comprehensive assessments and tailored treatments, ensuring that interventions address the unique characteristics of each individual’s facial anatomy.

Decoding the intricacies of various factors influencing nasolabial folds is pivotal for advancing aesthetic treatments. As we navigate the aesthetic landscape, acknowledging the multifaceted nature of nasolabial folds allows for more precise, personalized, and effective approaches to facial rejuvenation and reconstruction.

How To Improve The Appearance of Nasolabial Folds

While some may find visible nasolabial folds attractive, appreciating how they accentuate cheekbones and facial features, it’s crucial to consider factors that could exacerbate the formation of permanent deep folds, potentially making you appear older than your actual age.

Here are some suggestions to minimize the likelihood of early development of pronounced nasolabial folds:

Avoid or quit smoking

Smoking is a significant contributor to premature aging. The toxins in nicotine degrade collagen and elastin in the skin, narrow blood vessels, limit oxygen supply and increase free radical production.

Limit sun exposure

Harmful UV rays can cause photo damage and premature aging. Use sunscreen with SPF 50 or higher and wear protective accessories such as sunglasses and brim hats.

Maintain optimal weight

Keeping a stable weight can prevent skin stretching and subsequent sagging due to weight fluctuations.

Follow a balanced diet

A well-rounded diet is crucial for overall well-being. Include antioxidant-rich foods like fruits and vegetables to counteract damage caused by pollutants. Supplements such as Vitamins C, A, and E, collagen, astaxanthin, and glutathione can be beneficial.

Stay hydrated

Proper hydration supports skin moisturization and strengthens the skin’s protective barrier, helping maintain elasticity and plumpness.

Adopt a skincare routine

Consistent skincare habits involving gentle cleansing, moisturizing, and regular exfoliation can improve skin wellness, texture, and elasticity. Look for products containing ingredients such as retinol, hyaluronic acid, peptides, and antioxidants known for stimulating collagen production and rejuvenating the skin.

Sleep on your back

This position can counteract the effects of gravity on laugh lines. If you prefer sleeping on your side, try alternating sides regularly.

Practice facial workout

Facial exercises or facial yoga may potentially strengthen facial muscles, boost circulation, and improve skin tone. However, individual results may vary. Some dermatological clinics offer facial exercise treatments via machines.

As individuals age, it’s common for deeper nasolabial folds to develop. If you’re concerned about your smile lines or laugh lines, discussing treatment options with a dermatologist or cosmetic surgeon could be beneficial. Numerous non-invasive and surgical treatments are available, offering solutions that suit individual needs.

About The LifeDNA Skincare Report

Experience skincare on a whole new level with the LifeDNA Skincare Report. Delving into your genetic code, this report reveals insights into your skin, offering a personalized roadmap for addressing various skincare concerns.

Empower your skincare routine with precision by unlocking genetic secrets for radiant, tailored results. Invest in the future of your skin today.

Summary

Nasolabial folds evolve naturally with age and via external factors, influenced by genetics and lifestyle choices from an early age.
Understanding genetic factors, such as the MYH11 rs76053540 variant found in Han Chinese females, holds promise for targeted treatments and personalized interventions.
Key SNPs, rs6980503, and rs4876369, linked to the RAD21 gene expression, were found to impact nasolabial folds in Japanese women and can contribute to advancements in anti-aging practices.
Factors such as skin characteristics, fat distribution, muscular activity, and bone structure play vital roles in nasolabial folds, necessitating nuanced approaches for effective treatments.
Minimizing early nasolabial fold development involves lifestyle choices, including avoiding smoking, sun protection, maintaining weight, a balanced diet, hydration status, skin care, sleep habits, and facial workouts, with personalized treatments from experts.

References

Is Acne Genetic?

Aira on October 16, 2023

What is Acne?

Acne vulgaris, commonly known as acne, is a prevalent skin disorder characterized by lesions including pimples, whiteheads, blackheads, and inflamed red skin areas like cysts. These blemishes arise due to the clogging of pores from excessive oil, dead skin cells, and bacteria, primarily affecting hair follicles and oil (sebaceous) glands.

Acne predominantly appears on the face, forehead, chest, shoulders, and upper back. While it can develop in individuals of any age, it is frequent among adolescents and young adults, with about 80% of individuals aged 12 to 30 encountering it. Various genetic and environmental factors, such as hormonal changes, stress, and humidity, contribute to its onset.

Is Acne Genetic?

Acne is a multifactorial skin condition influenced by genetic and environmental factors. Acne has a substantial heritability component. Past twin studies have estimated the acne heritability at 80%, suggesting that shared genetic variants play a significant role in acne. Scientists have identified several genes that show a potential association with acne development. Here are some of the main genetic components linked to acne:

TGFB2 Gene

The Transforming growth factor-beta 2 (TGFB-2) gene is pivotal in skin cell differentiation and function. Research has illuminated its involvement in the mechanisms underlying acne development. Over-proliferation of skin cells can obstruct normal hair growth, resulting in comedones, Cutibacterium acnes (bacteria) infection, and accumulation of dead skin cells.

Furthermore, TGFB-2 modulates sebum production by the sebaceous glands. A malfunctioning TGFB2 gene may culminate in excessive sebum production, a trait observed in acne patients. This gene also orchestrates the body’s immune response to acne. A compromised TGFB-2 function can lead to a diminished or impaired immune response, thereby exacerbating acne proliferation. Notably, research has demonstrated that individuals with acne typically exhibit reduced expression of the active TGFB2 gene compared to individuals with clear skin.

A 2014 GWAS showed that imbalances in TGFβ-driven signaling play a significant role in acne vulnerability. Another study published in August this year implicated the influence of TGFB2 variant rs1256580 in acne.

ILA1 Gene

IL-1α is a cytokine, a type of immune system messenger, consistently produced in minimal amounts by keratinocytes (a type of skin cell) and immune cells when activated. Research indicates that IL-1α plays a role in the initial phases of acne development. In particular, IL-1α might elevate the generation of keratinocytes and enhance the propensity of dead keratinocytes to adhere together, leading to blocked skin pores. These clogged pores can become a breeding ground for bacteria, including Cutibacterium acnes. This bacterium potentially contributes to the onset of acne by prompting the release of inflammatory proteins from immune cells.

Moreover, researchers believe IL-1α induces the secretion of other inflammatory cytokines from various skin cells. As a result, variations in the IL1A gene might contribute to acne development by elevating IL-1α production and encouraging inflammation. For example, this 2010 study found a positive association between the minor “T” allele of the IL1A +4845(G>T) SNP and acne. Another 2014 case-controlled study conducted in the Pakistani population revealed a significant association between the variant genotypes of IL-6-572 and IL-1A-889 and the development of acne. The study’s conclusions propose that the IL-6-572 “C” and IL-1A-889 “T” alleles might play a role in acne pathogenesis within the Pakistani demographic.

TNF Gene

The TNF gene, Tumor Necrosis Factor, plays a critical role in the body’s immune response. It provides instructions for producing a protein called tumor necrosis factor-alpha (TNFα), which is involved in systemic inflammation and is a member of a group of cytokines that stimulate the acute phase reaction.

Inflammation is a fundamental factor in acne progression. Individuals with acne exhibit elevated expression of the TNF gene in their skin, which activates other cytokines, intensifying the inflammatory response. A 2014 meta-analysis showed that -308 G/A polymorphism in the TNF gene contributes to acne vulgaris risk, especially in Caucasian populations.

Other Candidate Genes

A two-stage GWAS in 2014 that investigated the Han Chinese population, involving 2,916 severe acne cases and 4,716 controls, pinpointed two novel potential SNPs: rs747650 and rs1060573. A subsequent 2021 meta-analysis confirmed that the “G” allele of rs747650 of the DDB2 gene increased the risk for severe acne.

A systematic review and meta-analysis published in 2021 showed that the FST rs629725 “A” allele poses a modest but significantly increased risk for acne.

Other single nucleotide polymorphisms (SNPs) that showed significant associations included:

Acne presentation

ACE (angiotensin-converting enzyme) I/D VNTR and
MMP2 (Matrix metalloprotease 2) rs2285053

Severe acne (2018 genome-wide meta-analysis)

MAPK11 (mitogen-activated protein kinase 1) rs144991069,
SEMA4B (semaphorin 4B) rs34560261,
SELL (selectin L) rs7531806
TGFB2 (transforming growth factor beta 2) rs1256580
TNFRSF1B rs1061622
TRAF3IP2 (TRAF3 Interacting Protein 2) rs33980500

Epidemiology

Acne is one of the most widespread dermatological conditions globally. Its epidemiology is extensive, spanning various ages, genders, and regions. Here’s an overview of the epidemiology of acne:

Prevalence

Acne is most prevalent during adolescence, affecting nearly 85% of teenagers to some extent.

While it’s primarily associated with puberty, about 50% of individuals in their 20s and 30s also experience acne. It can persist into one’s 40s and beyond for some people.

Demographic Variations

Both males and females are affected, but the age of onset, severity, and persistence might differ.

Adolescent boys are more likely to have severe acne than girls, and adult women are more likely to have persistent acne than men.

Acne prevalence can vary by region and ethnicity. However, it’s widespread across all racial and ethnic groups. Some studies have shown that certain ethnic groups might experience more acne-related post-inflammatory hyperpigmentation.

Environmental Factors

Diet, stress, urban living, and exposure to environmental pollutants have all been proposed as factors that might increase acne prevalence or severity, but direct correlations are still under study.

Contrary to popular belief, hygiene is not a direct cause of acne, though proper skin care can help manage and reduce its severity.

Comorbidities

Individuals with acne may experience other skin conditions or health issues. Additionally, the psychosocial impact of acne is notable, with some individuals developing depression, anxiety, or reduced self-esteem.

Global Impact

Acne ranks as the 8th most common disease globally. The global prevalence significantly impacts the quality of life and is a notable economic burden due to treatment costs and lost productivity.

Trends Over Time

The overall prevalence of acne seems stable over time. However, the awareness, diagnosis, and treatment options have evolved in the recent times.

Causes of Acne

Acne is a complex condition that arises due to the interplay of various biological factors:

Sebaceous Glands and Sebum Production

The skin contains sebaceous glands that produce an oily substance called sebum. Sebum’s primary function is to lubricate the skin and hair. However, excessive sebum production can clog hair follicles.

Keratinization

Human skin continuously renews itself. As new cells are produced, old cells die and are shed. In people with acne, this process of shedding dead skin cells is altered, leading to a buildup of dead skin cells in the hair follicle.

Clogged Follicles

The combination of excess sebum and buildup of dead skin cells can block the hair follicles, forming a comedo – the earliest acne lesion. Closed comedones are called whiteheads; they become blackheads if they open up to the skin surface.

Bacterial Growth

The sebaceous gland is conducive to the bacteria Propionibacterium acnes (P. acnes) to thrive. In certain conditions, these bacteria multiply rapidly in the blocked follicle. They digest the sebum and produce waste products and fatty acids, causing irritation and inflammation in the surrounding tissue.

Inflammation

The body’s immune response to the rapid multiplication of P. acnes and the waste products they produce leads to inflammation. This results in the redness, swelling, and pus characteristic of acne pimples or pustules.

Hormonal Fluctuations

Hormonal changes, particularly the increase in androgens during puberty, can enlarge the sebaceous glands, prompting them to produce more sebum. Hormonal changes during menstrual cycles and due to conditions like polycystic ovary syndrome (PCOS) can also cause acne outbreaks.

Genetic Predisposition

As discussed earlier, genetics plays a significant role in acne. If your parents had acne, you’re more likely to develop it.

Understanding the biology of acne is crucial for its effective treatment, which can range from topical treatments to address bacterial growth and reduce oil to oral medications that manage hormonal fluctuations or reduce inflammation.

Treatment Options for Acne

Treatment depends on the severity and type of acne. Here are some general treatment options for acne:

Topical Treatments

Benzoyl Peroxide: Reduces acne-causing bacteria and inflammation.
Topical Retinoids: (e.g., tretinoin, adapalene) Unclog pores and prevent new breakouts.
Topical Antibiotics: (e.g., clindamycin) Reduce acne-causing bacteria and inflammation.
Salicylic Acid: Helps unclog pores.
Azelaic Acid: Reduces inflammation and bacteria.
Alpha Hydroxy Acids (AHAs): Help to unclog pores and improve the texture of the skin.
Dapsone: Mainly used for inflammatory acne.

Oral Medications

Oral Antibiotics: (e.g., doxycycline, minocycline, tetracycline) Reduce bacteria and fight inflammation.
Oral Contraceptives: For women with acne related to hormonal fluctuations.
Spironolactone: Helps in reducing excess androgen (hormone) production in females.
Isotretinoin (Accutane): A potent medication for severe cystic or nodular acne.

Procedures

Light and Laser Therapy: Targets the deeper layers of the skin without harming the surface.
Chemical Peels: Removes the outermost layers of the skin, promoting new skin growth.
Drainage and Extraction: A dermatologist can manually remove large cysts.
Microdermabrasion: Uses tiny exfoliating crystals to treat superficial acne.
Hormonal Therapy: Beneficial for women with acne that occurs or worsens as per their menstrual cycle.
Corticosteroid Injections: An injection with a dilute corticosteroid can reduce inflammation and speed up recovery for large, painful cystic acne lesions.
Alternative Therapies: Some people find tea tree oil, green tea extract, or alpha-lipoic acid helpful, though the evidence is less robust than for other treatments.

Skincare Routine

Gentle cleansing, moisturizing, and sun protection are key. Non-comedogenic and oil-free products can reduce pore-clogging.

Dietary Changes

Though the connection between diet and acne isn’t definitive, some people find that certain foods exacerbate their acne. Reducing dairy or high glycemic index foods might be beneficial for some.

It’s essential to consult a dermatologist to determine the most appropriate treatment for individual cases. Some treatments, like isotretinoin, have significant side effects and require monitoring. Moreover, what works for one person might not work for another, and treatment can sometimes take weeks or even months to show significant results.

About the LifeDNA Skincare Report

The LifeDNA skincare report takes a deep dive into your genetic makeup that helps you to understand your skin-related characteristics such as hydration level, collagen quality, and sensitivity to environmental factors like UV rays. Utilizing your DNA data, the report offers personalized skincare ingredient suggestions and lifestyle advice to help you maintain glowing skin.

The LifeDNA Skincare report covers an analysis of the Potential for Severe Acne. Get yours here.

Summary

Acne vulgaris is a common skin disorder causing pimples, blackheads, and inflamed areas.
Acne results from clogged pores due to oil, dead skin cells, and bacteria.
Acne affects primarily the face, chest, and back and is most common among adolescents.
Genetic and environmental factors, such as hormonal changes and stress, influence acne.
The TGFB2 gene plays a role in skin cell differentiation and sebum production, affecting acne development.
The TNF gene, involved in inflammation, can exacerbate acne progression when overexpressed.
The ILA1 gene influences the initial phases of acne development, especially regarding pore blockage and bacterial growth.
Other genes like DDB2, FST, and SELL also have associations with acne risk
Treatment options range from topical treatments and oral medications to procedures such as light therapy and chemical peels.

References

Genetics & Rosacea: What You Need To Know

Aira on September 29, 2023

Overview

What is Rosacea?

Around the world, millions of individuals suffer from a variety of skin disorders. Some of them are more severe than others, altering the way of life and quality of life for those who are affected. Among these common skin conditions is a chronic skin problem called rosacea.

Rosacea is a common and persistent skin condition that mostly affects the skin of the face. Rosacea is frequently characterized by redness, visible blood vessels, and occasionally, tiny, pus-filled pimples that resemble acne. This illness commonly strikes adults in their 30s or 40s, and it can last for years. Although the precise etiology of rosacea is still unknown, it is thought to be a result of a mix of vascular, environmental, and genetic factors.

Facial redness, which can come and go but usually gets worse over time if ignored, is the primary symptom of rosacea. Usually, this redness affects the cheeks, nose, forehead, and chin as well as the middle of the face. Other typical signs and symptoms of rosacea include telangiectasia, visible blood vessels, blushing or flushing readily, and a burning or stinging feeling on the skin, in addition to redness. Some people also get papules and pustules, which are similar to acne and irritate the skin even more.

Rosacea comes in a range of degrees of severity, from mild cases with infrequent flushing to more serious kinds that have a considerable negative influence on a person’s quality of life. Ocular rosacea is a disorder that can cause symptoms like dryness, redness, and irritation in the eyes.

What Causes Rosacea?

Although the exact cause of rosacea is still unknown, scientists believe that a complex interaction of genetic, environmental, and vascular factors is to blame. Although the precise causes and mechanisms are not fully known, a number of influencing factors have been noted.

The likelihood of developing rosacea is increased in people with a family history of the ailment, therefore genetics do play a part. It is also believed that abnormalities in the facial blood vessels, persistent inflammation, and the presence of specific microorganisms on the skin are to blame. Additionally, persons who are prone to rosacea may experience worsening symptoms from environmental variables like stress, alcohol, spicy foods, and sun exposure.

Genetic Factors

Like many other complicated skin illnesses, the genetic causes of rosacea are not entirely known, but research has shed light on the role of certain genes in predisposing people to the condition. Note that while genetics contribute to the onset of rosacea, they also interact with a variety of environmental and lifestyle variables, making Rosacea a complex skin condition.

HLA (Human Leukocyte Antigen)

An increased risk of rosacea has been associated with variations in several HLA genes. The immune system uses HLA genes to help the body distinguish between its own cells and invaders. Changes in these genes can affect inflammatory processes and immunological reactions, which raises the possibility that immune dysregulation plays a role in the emergence of rosacea.

IL (Interleukin) Family

Signaling molecules called interleukins control inflammatory and immunological reactions. Variations in the IL family of genes have been the subject of some investigations on rosacea. Genetic variables that influence Interleukin expression or activity have been linked to the inflammation found in rosacea, and these factors may be responsible for the disorder.

Family History

A family history of the ailment is one of the most important signs of a genetic predisposition to rosacea. People who have rosacea in their immediate family are more likely to get it themselves. This confirms that there likely is a genetic element that is passed down through the generations.

Skin Barrier Function

The stratum corneum, the top layer of skin, serves as the skin’s barrier, which is essential for defending against outside influences and preserving skin health. The development of rosacea may be influenced by genetic changes that alter the skin’s barrier function, such as the filaggrin (FLG) gene mutations observed in diseases like eczema.

Genetic Variations for Severe Rosacea

Recent genetic research has pinpointed particular gene variants linked to rosacea susceptibility. For instance, severe rosacea risk has been linked to polymorphisms in the HLA-DRA gene, which is associated with the human leukocyte antigen D. Since HLA genes are involved in the immunological response, the development of the condition may have an immune system component. Other genetic variations that have been studied in relation to possibly developing severe rosacea are rs12203592 (IRF4), rs1129038 (HERC2), rs16891982 (SLC45A2), rs847 (IL13), rs77779142 (SNX32), rs149851565 (NRXN3/DIO2), and rs3132451 (NCR3/AIF1).

Rosacea is a complicated condition that is influenced by both genetic predisposition and environmental variables. Genetic and environmental triggers interact to cause this complex illness. More investigation is required to improve our comprehension of the particular genetic pathways driving rosacea and to create more specialized treatments.

Non-Genetic or Environmental Causes

Environmental factors such as sun exposure, extreme temperature fluctuations, spicy foods, alcohol consumption, stress, and particular skincare products can either induce or aggravate rosacea symptoms in persons who are genetically predisposed to the condition. Finding out about the genetic markers associated with rosacea and other elements that might have an impact on the genesis and progression of this ailment can help you understand it better.

Sun Exposure

Overexposure to the sun is a recognized rosacea trigger. Ultraviolet (UV) rays have the ability to widen cutaneous blood vessels and exacerbate inflammation. This trigger can be reduced by using sunscreen, wearing protective gear, and donning hats and clothing.

Extreme Temperatures and Climates

Flushing and the symptoms of rosacea can be made worse by exposure to extremely hot or cold weather. For those with rosacea, saunas, hot baths, and extended exposure to cold weather can all be troublesome.

Alcohol Consumption

Alcohol is a well-known rosacea trigger, especially red wine, and hard liquor. It may widen blood vessels, resulting in more flushing and greater redness. It might be wise to limit alcohol consumption or select beverages that are less likely to provoke.

Certain Foods and Beverages

Besides spicy foods and alcohol, other dietary triggers can vary from person to person. Hot liquids like coffee and tea, as well as meals high in histamines like aged cheeses and fermented goods, are also common triggers of rosacea.

Stress and Hormonal Changes

Rosacea flare-ups can be triggered by emotional stress and worry. Techniques for managing stress, such as mindfulness and relaxation exercises, may help lessen symptoms. Some people’s rosacea symptoms may also be affected by hormonal changes brought on by menopause, pregnancy, or the use of oral contraceptives.

Skin Irritants

Astringents, abrasive scrubs, and harsh skincare products can aggravate the skin and make rosacea worse. Use moderate, non-irritating skin care products and stay away from alcoholic and scented items.

Medications

Long-term use of some drugs, such as topical steroids, might worsen rosacea. It’s crucial to talk with a healthcare professional about pharmaceutical options and any potential effects they may have on rosacea.

Environmental or non-genetic factors must be managed and controlled as part of rosacea management. The frequency and severity of rosacea flare-ups can be greatly decreased by identifying individual triggers and making lifestyle changes, such as avoiding known triggers and implementing a moderate skincare routine.

When environmental triggers are difficult to avoid, healthcare professionals may occasionally advise prescription drugs or laser therapy to manage symptoms.

Is Rosacea Contagious?

Rosacea is a skin disorder that is neither contagious nor infectious. Genetic predisposition, numerous environmental variables, anomalies in the blood vessels, and the immune system all play a role in this skin disorder. Rosacea cannot be spread from one person to another through direct touch, respiratory droplets, or any other means because it is not brought on by bacteria, viruses, or fungi. Rosacea is not a skin ailment that you may “catch” from someone else.

It’s important to see a dermatologist or other healthcare professional for an accurate diagnosis and advice on managing the illness if you have rosacea symptoms including persistent facial redness, flushing, or eye irritation. Proper diagnosis and treatment can successfully assist people affected by this condition or at the very least lessen their symptoms.

What are the Types of Rosacea?

Based on the unique symptoms and clinical presentation of rosacea, distinct forms or subtypes of the disease are identified. Dermatologists and other healthcare professionals can diagnose and efficiently treat rosacea thanks to the classification of the condition’s forms.

Erythematotelangiectatic Rosacea (ETR)

Symptoms

Erythema (permanent facial redness) and telangiectasia (visible blood vessels) on the cheeks, nose, forehead, and chin are features of ETR. Skin could look burnt or flushed.

Additional Features: Patients who have ETR may occasionally blush or flush easily. A scorching or stinging sensation on the skin is frequent with this subtype.

Papulopustular Rosacea (PPR)

Symptoms

PPR, also known as inflammatory rosacea, manifests as facial skin that is red, and swollen, and develops papules (little red lumps) and pustules (bumps filled with pus). These signs might resemble acne.

Additional Features: PPR may also be characterized by prolonged facial flushing and redness as well as warmth and soreness in the affected areas.

Phymatous Rosacea

Symptoms

Skin that is thickened and bumpy is a characteristic of phymatous rosacea, which primarily affects the nose (rhinophyma), but can also affect the chin, forehead, cheeks, and ears. The skin may look uneven and bulging.

Additional Features: This subtype may cause increased sebaceous glands, which can give skin an oily look and increase pore size.

Ocular Rosacea

Symptoms

Ocular rosacea primarily affects the eyes. This subtype is characterized by a number of eye-related symptoms. Dryness, redness, itching, burning, light sensitivity (photophobia), and the perception of a foreign body in the eye are a few of these symptoms.

Additional Features: If neglected, some people with ocular rosacea may develop styes (hordeolum), blurred vision, and possibly corneal damage. Other rosacea subtypes frequently interact with ocular symptoms.

The severity of rosacea can differ greatly from person to person, and many people who have the disorder have a combination of these categories. Furthermore, effective rosacea management and halting the progression of symptoms depend on early diagnosis and therapy.

A subtype of rosacea may occasionally develop into another subtype, especially if neglected. For instance, papulopustular rosacea (PPR) characteristics may develop when erythematotelangiectatic rosacea (ETR) progresses. This underlines the significance of personalized treatment programs created to address each patient’s unique symptoms and requirements.

Treatment Options for Rosacea

Rosacea treatment primarily aims to manage and alleviate the symptoms associated with each subtype. Usually, personal symptoms and demands are taken into consideration while creating a treatment plan. Dermatologists and other medical professionals collaborate extensively with patients to identify the proper rosacea subtype and provide individualized treatment plans.

Topical and oral drugs, dietary adjustments, skincare regimens, and, in certain cases, laser therapy or surgical interventions to address phymatous alterations are among the possible treatments. Rosacea patients can manage their symptoms, and keep healthy, clear skin by seeking early assistance and careful treatment.

Topical Medications

Topical Antibiotics: Topical antibiotics available only by prescription, such as metronidazole, azelaic acid, and clindamycin, can help lessen rosacea-related inflammation and pustules. They’re frequently employed in mild to moderate situations.

Topical Anti-Inflammatories: For short-term use, doctors may prescribe topical corticosteroids to relieve inflammation and redness right away. However, due to potential side effects, prolonged use of corticosteroids is not advised.

Topical Calcineurin Inhibitors: In some situations, especially when other treatments are not well tolerated, medications like tacrolimus and pimecrolimus may be utilized to reduce inflammation.

Oral Medications

Oral Antibiotics: Antibiotics including tetracycline, doxycycline, and minocycline are frequently used for mild to severe rosacea. They aid in reducing swelling and pustules. Sometimes maintenance involves the use of low-dose, long-term antibiotics.

Oral Isotretinoin: Isotretinoin (Accutane) may be considered in extreme situations. It is a potent drug used to treat acne and has shown promise in treating some types of rosacea, particularly those with phymatous alterations.

Laser and Light Therapies

Intense Pulsed Light (IPL) Therapy: IPL can effectively target redness and visible blood vessels associated with erythematotelangiectatic rosacea (ETR).

Pulsed Dye Laser (PDL): PDL therapy is used to treat redness, visible blood vessels, and overall skin discoloration.

CO2 and Erbium YAG Lasers: These lasers may be used to address thickened and irregular skin in cases of phymatous rosacea.

Oral Steroids

Oral corticosteroids may be used for a brief period of time to control symptoms in severe cases with rapid disease development or significant inflammation. However, due to probable side effects, prolonged use of oral steroids is not advised.

Eye Drops and Ointments

Artificial tears, lubricating eye drops, and prescription drugs may be suggested for those with ocular rosacea to relieve eye-related discomfort.

Skin Care and Lifestyle Modifications

Gentle Skin Care: Using mild, non-irritating skincare products and a gentle cleansing routine can help reduce skin hypersensitivity.

Sun Protection: Wearing broad-spectrum sunscreen daily and protecting the face from excessive sun exposure is crucial to prevent flare-ups.

Avoiding Triggers: Identifying and avoiding personal triggers like spicy foods, alcohol, and extreme temperatures can help manage symptoms.

Stress Management: Stress-reduction techniques such as relaxation exercises, yoga, and mindfulness can help minimize stress-related flare-ups.

Due to the chronic nature of the disorder and the possibility of recurrence even under successful control, rosacea treatment is often a lengthy commitment. To track development and make any modifications to the treatment plan, it is crucial to schedule routine follow-up sessions with a dermatologist or other healthcare professional.

It is highly recommended that you speak with a healthcare provider to ascertain the best course of action for your particular subtype of rosacea and the severity of your condition. Most rosacea sufferers can get significant symptom alleviation and retain healthier, brighter skin with the right management and therapy.

LifeDNA’s Severe Rosacea Report

DNA analysis can be used to link familial causes to severe rosacea. Based on your individual genetic makeup, DNA testing can determine your hereditary risk of getting severe rosacea. Consider a skin DNA test to find out whether you may be predisposed genetically to certain skin traits and issues.

The LifeDNA Skincare Report provides customized guidance on skincare regimens, product suggestions, and lifestyle adjustments. For instance, you can get tailored suggestions for lifestyle adjustments and potential acceptable therapies if you are genetically predisposed to having severe rosacea. Order your copy of the LifeDNA Skincare Report right now to learn more about your tendency for severe rosacea.

Summary

Numerous skin conditions, including the rosacea skin ailment, affect millions of people.
Redness, clearly visible blood vessels, and sporadic microscopic pus-filled pimples that resemble acne are frequent signs of rosacea.
The redness typically affects the cheeks, nose, forehead, chin, and center of the face.
Genetics do play a role in rosacea and those with a family history of the condition are more likely to develop it themselves.
Rosacea is a complex disorder that is affected by both hereditary tendencies and environmental factors. This complex condition is brought on by an interaction of genetic and environmental causes.
Different forms or subtypes of rosacea are recognized based on their distinctive symptoms and clinical appearance.
Patients with rosacea can control their symptoms and maintain healthy, clear skin by getting help as soon as possible and receiving thorough care.

References

Freckles & Genetics: Are Freckles the Same as Melasma?

Aira on September 29, 2023

Overview

Freckles are small, brownish, or reddish spots that grace the skin, particularly in individuals with fair complexions. The combination of genetic susceptibility and solar exposure leads to these pigmented spots. Freckles have a distinct and persistent attraction that is sometimes connected to a youthful, sun-kissed appearance.

Melanin, a pigment, is mainly responsible for these characteristic spots which some people consider as skin imperfections. Skin tone, hair color, and eye color are all influenced by melanin. However, freckles appear when melanin production is increased locally as a result of exposure to ultraviolet (UV) light from the sun or artificial sources like tanning beds. While UV exposure continues to be the main cause of freckles, genetics do play a considerable part in who gets them.

While moles and other skin diseases can occasionally be precursors to skin cancer, freckles are mostly benign and safe to have. It is crucial, however, to keep an eye on any alterations in the size, form, or color of skin lesions and to seek medical advice if concerns develop.

Freckles are frequently viewed as a cute and lovable characteristic by people who embrace them, signifying a connection to the sun and a carefree, youthful spirit. However, a number of cosmetic procedures, including laser therapy or topical lotions, can help fade freckles for people who want to minimize their appearance.

What Causes Freckles?

Freckles have a large genetic component that greatly influences their development. Understanding the genetic causes of freckles can help explain why some people are more likely than others to develop these marks.

Genetic Causes

Understanding these genetic factors explains why some people are more prone to freckles than others. and highlights the significance of sun protection for people with a genetic predisposition to freckles

Gene Variations in MC1R

Variations in the MC1R gene (melanocortin-1 receptor) are one of the main genetic variables linked to freckles. The melanin pigment, which determines the color of the skin, hair, and eyes, is controlled by this gene. In reaction to the sun’s ultraviolet (UV) light, certain MC1R gene variations can boost melanin formation. Freckles develop as a result of this increased melanin synthesis. According to research, people with specific MC1R gene variations are more likely to be freckled. People with fair skin, especially those with European ancestry, are more likely to have these variations.

Hereditary Influence

Because freckles frequently run in families, they may be inherited. The descendants are more likely to get freckles if their parents or grandparents do. The concept that hereditary factors play a significant role in the development of freckles is supported by the clustering of freckles within families.

Skin Type and Ancestry

The development of freckles is also influenced by genetic variables related to basic skin tone and ethnicity. Freckles are more common among fair-skinned people whose skin contains less pigment. Due to a genetic propensity, people of European heritage are more likely to get freckles. Darker skin tones, on the other hand, contain more melanin, which acts as a natural defense against the growth of freckles.

Polygenic Heritability

As a polygenic trait, freckles are actually influenced by a number of genes, each of which has a tiny impact on the development of freckles. While MC1R is a key participant, other genes are involved as well. The combination of these genes increases a person’s propensity for freckles. The complexity of freckles’ genetic foundation has been highlighted by the discovery of numerous genetic loci linked to them.

Some SNPs and genes that have been linked to the genetics of freckles include rs1805007 (MC1R), rs1805008 (MC1R), rs12203592 (IRF4), rs8049897 (DEF8), rs11648785 (MC1R), rs4911414 (ASIP), rs1540771 (IRF4/EXOC2), rs872071 (IRF4), rs9328192 (IRF4), rs1042602 (TYR), rs1805009 (MC1R), rs11547464 (MC1R), rs7204478 (MC1R), rs7195066 (MC1R), rs619865 (ASIP), rs291671 (CDK5RAP1), rs154659 (MC1R), rs4911442 (ASIP), rs6088316 (ASIP), rs17305657 (ASIP), rs4812405 (ASIP), rs1474976 (ASIP) rs2153271 (BNC2), rs10810635 (BNC2), rs251468 (PPARGC1B), rs10444039 (RAB11FIP2), rs12259842 (HSPA12A), rs10886142 (RAB11FIP2), rs4752116 (RAB11FIP2), and rs17833789 (AKAP1, MSI2).

Non-Genetic or Environmental Causes

Despite the fact that polymorphisms in the MC1R gene and polygenic inheritance are the main genetic causes of freckles, the interaction between genetics and environmental variables, such as sun exposure, is critical to the formation of freckles.

UV Radiation Exposure

Exposure to ultraviolet (UV) radiation from the sun is conceivably the most important environmental element influencing the development of freckles. UV radiation in sunlight encourages the synthesis of melanin, the pigment that gives skin its color. Skin reacts to UV exposure by creating more melanin in an effort to shield itself from the harmful effects of UV rays.

This increased melanin production can cause freckles to appear in people who are genetically predisposed to them. During the summer when it is sunny, freckles often appear or become more noticeable, and during the winter when UV exposure is lower, they may disappear entirely.

Sun Exposure Duration and Intensity

Freckle development depends heavily on sun exposure duration and intensity. Freckle production is more likely with prolonged or severe sun exposure, especially without proper sun protection. Freckles are more likely to appear on parts of the body that are frequently exposed to the sun, such as the face, neck, and arms.

Sunbeds and Synthetic UV Sources

Freckle production can also be influenced by artificial UV radiation sources like sunlamps and tanning beds. These gadgets release UV rays that might increase the skin’s melanin synthesis and cause freckles to emerge. In this aspect, prolonged or excessive use of tanning beds poses a concern.

Altitude and Climate

Freckle development may be influenced by environmental factors such as your location’s altitude and climate. Due to increased UV exposure, people who live in sunny climates or at higher altitudes may have a higher risk of developing freckles.

Medications and Hormonal Changes

The skin may become more vulnerable to UV radiation due to certain drugs and hormonal changes. For instance, when paired with sun exposure, certain birth control drugs and hormone replacement therapy can raise the incidence of freckles. These elements must be taken into account while thinking about sun protection strategies.

Understanding these environmental factors emphasizes the significance of sun protection measures, such as using sunscreen, wearing protective clothes, and finding shade, in order to avoid or reduce the development of freckles and maintain overall skin health.

Types of Freckles and Other Skin Spots

Freckles, those endearing pigmented spots on the skin, as well as sun spots, come in various types, each with its own characteristics and underlying causes. Understanding these different types of “freckles” can provide insights into their development and appearance.

Ephelides (Common Freckles)

The most prevalent and well-known type of freckles are ephelides. They often have a flat, round, or oval shape and are tiny in size. Common freckles can range in color from pale to dark brown to reddish or slightly pink.

They may fade or become less obvious over the winter when there is less sun exposure. They tend to be more noticeable during the brighter months. Most frequently, a combination of genetic predispositions and sun exposure results in common freckles. Ephelides are more likely to form in those with pale skin.

Solar Lentigines (Sun Spots or Age Spots)

Solar lentigines are darker and larger than typical freckles, sometimes known as sun spots or age spots. These patches are often circular or asymmetrical in shape and can range in color from light tan to dark brown.

Solar lentigines, in contrast to ephelides, typically last all year long and do not drastically deteriorate in the winter. The main cause of solar lentigines is long-term cumulative sun exposure, and older people are more likely to develop them. They are frequently connected to photoaging and other skin changes brought on by the sun and are not directly tied to heredity.

Lentigines Simplex (Flat Moles)

Lentigines simplex, also known as flat moles, are sometimes mistaken for freckles due to their resemblance in appearance. These marks can be circular or oval in shape and range in color from light brown to almost black.

In contrast to typical freckles, they typically have a more stable color and structure. Lentigines simplex are not typically linked to sun exposure and are brought on by an excess of melanin. They may be present from birth or start to manifest during childhood, and they are mostly influenced by hereditary factors. Normally, these patches don’t deteriorate or change much over time.

While these are the most common types of skin spots, it’s crucial to remember that a person’s skin may also have variants and mixtures of different types of spots. In addition, although they may resemble freckles, various skin disorders, and lesions can have different underlying origins and traits. If you are worried about any pigmented patches on your skin, it is best to see a dermatologist to ensure proper identification and therapy.

Can Freckles Go Away Completely?

Freckles can lighten or fade with time but typically do not go away completely. The extent to which freckles diminish or persist varies from person to person and depends on various factors.

Seasonal Changes

Many people observe that during the winter when there is less sun exposure, their freckles become less prominent or lighter. When freckles are exposed to the ultraviolet (UV) rays of the sun, they frequently darken or become more noticeable. Therefore, taking precautions to protect your skin from the sun, such as donning sunscreen and wearing clothes that provide coverage, might lessen how prominent your freckles are.

Age

With time, some freckles, especially ephelides (common freckles), may fade from prominence. As people age, changes in their skin may occur that make freckles appear lighter or less prominent. Individual differences exist, therefore not all freckles will noticeably lighten with age.

Genetic Factors

The degree to which a person’s freckles disappear or remain can depend on their genetic makeup. It’s possible that some people are genetically predisposed to having freckles that don’t fade as easily, while other people may discover that their freckles gradually disappear over time.

Are Freckles the Same as Melasma?

Freckles and melasma are two distinct pigmentation issues of the skin, each with its own causes, characteristics, and treatment considerations. While they may share some similarities in appearance, they are not the same condition.

Causes

Genetic predispositions and sun exposure’s ultraviolet (UV) radiation are the main causes of freckles. They develop as a result of the skin’s pigment, melanin, overproducing as a reaction to UV exposure. Fair-skinned people are more prone to getting freckles.

Contrarily, hormonal changes, notably those that occur during pregnancy, the use of birth control pills, or hormonal treatments are predominantly responsible for melasma. Although it is not the main cause of melasma, UV exposure can make symptoms worse.

Characteristics

Small, flat, round, or oval dots that are often light to dark brown, but can also have a reddish or faintly pink hue, are the most common kind of freckles. In the summer, they are typically more conspicuous, and in the winter, they may disappear or become less obvious.

Melasma manifests as bigger, irregularly distributed patches of hyperpigmentation on the skin that are frequently brownish or gray in color. Melasma patches are often larger than freckles and lack a distinguishing round or oval shape.

Location

Freckles are usually seen on skin that is frequently exposed to the sun, such as the face, neck, arms, and shoulders.

Melasma frequently affects the cheeks, forehead, upper lip, and chin on the face. Although it can also appear in other sun-exposed places, it is usually less noticeable than freckles.

Treatment

Although freckles are usually not harmful, many people choose to control or lessen their appearance by strategies like sun protection (such as sunscreen and protective clothing), and cosmetic procedures like laser therapy or topical lightening agents.

Because melasma has a hormonal component, treating it can be more difficult than treating freckles. Topical creams, chemical peels, and laser treatments are frequent treatment choices, although results might vary and recurrence is frequent, especially if hormonal triggers continue.

When to Consult a Physician

In certain circumstances, speaking with a doctor about freckles or any skin spots is imperative to confirm that these pigmented spots are not a sign of a more serious skin problem, or to go over treatment options for controlling their appearance.

Change in Appearance

It’s important to see a doctor right away if you observe any noticeable changes in the size, shape, color, or texture of a skin spot. Such alterations may be a sign of skin disorders such as the skin malignancy melanoma. For excellent outcomes, skin cancer therapy and early detection are essential.

Family History of Skin Cancer

Even though freckles look harmless, people with a family history of skin cancer may be at a higher risk. You may need regular skin examinations with a doctor or dermatologist to ensure that any skin problems are addressed immediately.

Continual or Obtrusive Freckles

While freckles are often not harmful, a dermatologist can offer advice on treatment alternatives to lessen their appearance, in case you find their appearance annoying or if they are harming your self-esteem.

Hyperpigmentation or Melasma

Consulting a doctor or dermatologist can assist in confirming the diagnosis and deciding on the best course of action if you have any reason to believe that what you initially believed to be just freckles may actually be melasma or another type of hyperpigmentation.

While freckles are frequently safe and benign, there are some situations where it’s essential to see a doctor or dermatologist. In particular, if you observe changes in your freckles or have a family history of skin cancer, regular self-examinations, and expert skin checks can aid in the early detection of any possible abnormalities.

LifeDNA’s Skincare Report

Freckle formation can be traced back to hereditary factors using DNA analysis. DNA testing can identify your hereditary likelihood of having freckles based on your unique genetic makeup. To determine your potential inherited predisposition to particular skin features and problems, consider a skin DNA test.

Individualized advice on skincare routines, product recommendations, and lifestyle changes are offered through the LifeDNA Skincare Report. For instance, if you are genetically susceptible to getting freckles, you can receive individualized recommendations for lifestyle changes and possible reasonable treatments. The LifeDNA Skincare Report examines your propensity for freckles; order your copy today.

Summary

Small, brownish, or reddish skin patches called freckles are common, especially among those with fair skin.
The main cause of these recognizable skin flaws is the pigment melanin. Melanin has an impact on the color of the skin, hair, and eyes.
When melanin production is elevated locally due to exposure to ultraviolet (UV) light from the sun or artificial sources like tanning beds, freckles develop.
Freckles are mostly caused by UV exposure, but genetics still play a significant role in who develops them.
While freckles are generally harmless and safe, there are some circumstances wherein you may need to contact a dermatologist or physician.

References

Nature or Nurture: Is Eczema Genetic?

Aira on September 22, 2023

Overview

Eczema, another name for atopic dermatitis, is a widespread skin condition that affects millions of people worldwide. Understanding what eczema is will help you manage and cope with its challenges. Although this chronic condition can be uncomfortable and frustrating, it is not contagious.

Eczema is a persistent skin condition marked by irritation and inflammation. It frequently manifests as rashes on the skin’s surface that are red, itchy, and even painful. Even though eczema can affect people of any age, it is more prevalent in infants and young children, with some people growing out of it as they age. This skin condition, however, can also last a lifetime.

What are the Main Causes of Eczema?

Eczema is generally thought to be caused by a confluence of genetic and environmental factors. Several genes, particularly those linked to skin barrier function, immunological response, and inflammation, have been recognized as potential eczema contributors. Genetic variations in these genes can lead to the weakening of the skin’s barrier defenses and increasing sensitivity to irritants, allergens, and infections.

The role of the immune system is crucial in eczema. When the skin is exposed to eczema triggers such as allergens or irritants, the immune response is frequently hypersensitive in eczema patients, which causes excessive inflammation. Redness, itching, and the distinctive skin lesions associated with eczema can all be symptoms of this heightened immune response.

LifeDNA offers full and comprehensive information about many aspects of your skin health and its relationship with your genetic variation.

Genetic Causes

Eczema frequently runs in families, which suggests a close genetic connection. Children are more likely to get eczema if either one or both parents have it. Several specific genes, including the filaggrin gene, have been linked to eczema susceptibility.

Our skin serves as a barrier, shielding the body from the harm outside. The integrity of the skin barrier may be jeopardized by genetic abnormalities in the genes necessary for maintaining it. One such protein necessary for the operation of the epidermal barrier is filaggrin. The skin’s natural barrier function can be disrupted by genetic polymorphisms (SNPs) in the filaggrin gene (FLG), leaving the skin more susceptible to allergens and irritants from the environment. Therefore, those who carry certain FLG SNPs are more prone to experience eczema, and genetic abnormalities that affect the production of filaggrin can result in dry, cracked skin that is more prone to the onset of eczema.

Eczema can also be caused by genetic differences in immune system-related genes. When the skin comes into contact with triggers like allergens or irritants, there is frequently an excessive immune reaction. Genetic factors may have an impact on these immune system abnormalities, rendering certain people more susceptible to eczema.

Personalized therapy modalities may be possible with an understanding of the genetic causes of eczema. Individuals may have particular genetic abnormalities and immune system anomalies that can be identified through genetic testing, allowing for individualized treatment plans. This could involve specific treatments meant to repair the skin barrier or control the immune system.

Non-Genetic (Environmental) Causes

Even though genetics are important, eczema is a result of a complicated interaction between genes and the environment. Environmental variables can interact with genetic predispositions to cause eczema flare-ups or exacerbate current symptoms. These factors include exposure to allergens, pollution, and dietary choices.

Allergens

An important environmental cause of eczema is exposure to allergens. Mold, pet dander, dust mites, and pollen are examples of typical allergens. These allergens may cause an immune system overreaction in people with eczema, resulting in inflammation and irritated skin.

Diet

Despite being less well known, some people’s eczema may also be affected by specific dietary decisions. Food sensitivities or allergies may indeed be a factor in eczema flare-ups. This external component of eczema can be managed by recognizing and avoiding particular trigger foods.

Harsh Chemicals

Abrasive substances such as soaps, detergents, and scents can irritate the skin and damage its barrier of defense. When this barrier is breached, allergens and irritants can enter more easily, which can cause flare-ups of eczema. Utilizing hypoallergenic products and avoiding certain irritants can help reduce this environmental cause.

Weather

Eczema can also be greatly affected by changes in the environment and weather. The skin can lose moisture in dry and low-humidity environments, increasing dryness and irritation. On the other hand, extreme heat and humidity can cause perspiration, which can make eczema symptoms worse. The effects of these environmental factors can be reduced by maintaining a steady and comfortable environment.

Stress

Another well-known environmental element that can cause or exacerbate eczema symptoms is emotional stress. Stress can impair the skin’s natural defenses and weaken the immune system, increasing the likelihood of flare-ups. People with eczema may find it easier to deal with this environmental factor by using stress management approaches including mindfulness, relaxation exercises, and counseling.

Want to know more about your genetic likelihood of developing eczema and get personalized skincare suggestions to help prevent and manage this condition? Unlock LifeDNA’s DNA skincare report today.

Is Eczema Contagious?

Despite its prevalence as a visible skin condition, atopic dermatitis or eczema is not contagious. Understanding that eczema is not contagious is crucial for dispelling misconceptions and reducing the stigma associated with the condition.

The etiology of eczema, a non-infectious skin illness, is complex and mostly involves genetic and environmental factors. It is not brought on by microorganisms like bacteria, viruses, or fungi that can spread from one person to another by touch or exposure, although people with eczema may be more prone to infections due to the weakened skin barrier function. Eczema is brought on instead by the intricate interplay between the immune system, genes, and environmental factors.

Even though eczema is not contagious, it can run in families. Since eczema frequently has a genetic component, those who have had the ailment in their families are more likely to experience it themselves. This genetic propensity does not, however, indicate that eczema can be transmitted directly from one person to another by touch.

A compromised skin barrier and an overactive immune response are linked to this skin disease. These immune system abnormalities can render the skin more susceptible to environmental and infectious triggers. Different environmental factors, such as allergens, irritants, stress, and weather conditions, can cause or aggravate eczema symptoms.

Chronic eczema is a disease that can be controlled but not cured. Topical treatments, moisturizers, dietary changes, and avoidance of environmental irritants are frequently used in treatment. Instead of preventing transmission to others, these therapies concentrate on symptom relief and preventing flare-ups.

While eczema itself is not communicable, it should be noted that some skin illnesses may exhibit symptoms that are similar to eczema and may be mistaken for it. A medical expert can offer an accurate diagnosis and the best course of treatment in such circumstances.

Does Eczema Ever Completely Go Away?

Eczema seldom totally disappears, even though it occasionally becomes much better or even seems to be gone for a while. As they get older, some people may notice a progressive improvement in their symptoms, with the illness either getting milder or going away altogether. This occurs frequently in cases of infantile eczema.

The sensitive skin that many eczema sufferers have, however, makes them more susceptible to flare-ups brought on by allergens, irritants, stress, or environmental causes. With the right skincare regimens, lifestyle changes, and medical care, these flare-ups can be effectively treated.

Instead of hoping for a permanent cure, eczema management aims to achieve long-term control and reduce symptoms. Even though eczema never totally goes away, people with it can live healthy, pleasant lives by adhering to recommended treatments, avoiding irritants, and maintaining good skincare habits.

Is Eczema an Autoimmune Condition?

Eczema is not considered to be an autoimmune disease. Instead, a chronic inflammatory skin condition is the primary classification. Autoimmune illnesses, including rheumatoid arthritis, lupus, and multiple sclerosis, are brought on when the immune system erroneously targets and destroys healthy tissues and cells within the body.

Instead of a systemic autoimmune reaction affecting many organs, eczema predominantly involves an aberrant immune response within the skin itself. In eczema, the immune system is frequently susceptible to environmental factors such as allergens or irritants, which results in inflammation and malfunction of the skin barrier. The outermost layer of the skin is predominantly affected by this heightened immune response, which can also result in lesions or blisters in addition to dryness, redness, and itching.

Although eczema is not an autoimmune disease, it does have certain immune system abnormalities in common with autoimmune illnesses. Both entail aberrations of the immune system, but there are substantial differences in the processes and targets of these immunological responses.

Is Eczema Genetic?

Molecular Basis

Atopic dermatitis etiology is still being researched. Epithelial barrier failure, immunological response, and interactions between neurons and the immune system all seem to be crucial factors.

As for the role of genetics, a meta-analysis study of 26 genome-wide association studies (GWAS) containing about 21,000 patients and 95,000 controls identified 31 loci related to atopic dermatitis. One of the genes identified in several studies is the FLG gene which produces filaggrin, a protein that is found in the epidermal differentiation complex (precursor profilaggrin) on chromosome 1q21.

Filaggrin is important for the skin barrier function and it is a component of natural moisturizing factors (NMF). FLG loss-of-function mutations are the key genetic risk factors for developing atopic dermatitis. In meta-analyses, FLG loss-of-function mutations have been associated with a three- to fourfold increased risk of developing atopic dermatitis

Natural moisturizing factors, or NMF, maintain skin hydration and water retention in the stratum corneum in low-humidity situations. The stratum corneum controls water homeostasis and acts as the first line of defense against environmental allergens and infections, and is composed of vertical layers of keratin filament-filled anucleate corneocytes.

Increased transepidermal water loss in the altered stratum corneum leads to increased permeability, decreased water retention, and changed lipid composition.

Eczema has a long history of being a difficult skin condition to treat. Options for traditional or historical eczema treatment have developed over time, incorporating many cultures and cures. Even though modern medicine has greatly improved our understanding of how to control eczema, some old methods are still useful and may provide relief to people looking for alternative or complementary options. Both traditional and modern treatment options are still used today.

Non-Genetic (Traditional or Historic) Treatment Options

Some traditional or historic treatment options include oats, herbal medicines, different types of natural oils, herbal plants, and superfoods like honey and milk.

Oatmeal

For a very long time, oatmeal has been valued for its calming qualities. Warm baths with colloidal oatmeal added can help reduce eczema-related itching and irritation. On the skin, the oatmeal creates a layer of protection that keeps moisture in and calms inflammation.

Herbs

The symptoms of eczema have been treated with numerous natural treatments. Herbs with calming and anti-inflammatory effects include calendula, chamomile, and witch hazel. Skin with eczema has been treated topically using remedies including herbal teas, poultices, or infused oils.

Virgin Coconut Oil

As a natural moisturizer for skin prone to eczema, coconut oil has grown in popularity. Its fatty acids aid in retaining moisture and minimizing dryness. Virgin coconut oil can offer comfort and enhance the skin’s barrier performance when applied to the affected regions.

Aloe Vera

Aloe vera, known for its cooling and anti-inflammatory properties, has been used to soothe eczema symptoms. Fresh aloe vera gel or commercially available preparations can be applied to affected skin to reduce itching and redness.

Honey

Honey has natural antibacterial properties and can help with wound healing. Some individuals with eczema have found relief by applying raw honey to their skin and covering it with a clean bandage or cloth.

Milk

Milk baths, often attributed to the ancient Egyptian queen Cleopatra, involve adding milk to a warm bath. The lactic acid in milk can help exfoliate the skin gently and provide relief from itching and inflammation.

Traditional Chinese Medicine

Practitioners of traditional Chinese medicine have treated eczema with acupuncture and a variety of herbal preparations. These therapies work to correct underlying imbalances that are thought to contribute to eczema while also balancing the body’s energy.

Genetic or Modern Treatment Options

At the cutting edge of dermatological research, genetic eczema therapies provide exciting new directions for the individualized and efficient therapy of this challenging skin condition. Individuals who have battled eczema for years now have hope thanks to the development of novel medicines that target particular genetic variables as a result of our growing understanding of the genetic foundation of eczema.

Biologic Therapy

A modern method of treating eczema is biologic therapy. Biologics can target particular immune system chemicals that are known to contribute to the onset of eczema, such as interleukin-4 (IL-4) and interleukin-13 (IL-13). Biologics successfully lessen eczema-related inflammation and irritation by blocking these molecules. The first biologic treatment for eczema to receive FDA approval, Dupilumab, has demonstrated excellent results in clinical studies and has provided relief to numerous sufferers.

Topical Janus Kinase (JAK) Inhibitors

Topical Janus Kinase (JAK) Inhibitors are a novel class of medications designed to disrupt the inflammatory signals involved in eczema. These treatments target specific enzymes that play a role in the immune response. Tofacitinib, a JAK inhibitor, has demonstrated effectiveness in reducing eczema symptoms and improving the skin’s appearance.

Gene Therapy

Gene therapy is another contemporary eczema treatment that shows promise for people with severe genetic abnormalities that cause eczema even if it is still in the experimental stage. To provide a long-term cure, researchers are looking into ways to repair or correct the defective genes that cause immunological dysregulation or reduced skin barrier function.

When to Consult a Physician?

To pinpoint precise genetic factors causing an individual’s eczema, genetic testing and profiling are becoming more widely available. By choosing medications and therapies that address the particular genetic components of the disorder, healthcare professionals can customize treatment strategies. Personalized strategies can improve treatment results and reduce negative effects.

While these modern genetic treatment options for eczema hold significant promise, it’s important to note that they may not be suitable for everyone. Each individual’s eczema experience, and likely the etiology as well, is unique, and treatment should be tailored to their specific needs and genetic profile.

It is best to speak with a healthcare provider, such as a dermatologist, before attempting any traditional or old-fashioned treatments to be used along with modern treatments. This is to make sure they are secure and suitable for your particular situation. Additionally, as part of a holistic approach to eczema management, these ancient therapies can supplement modern therapeutic procedures and prescribed pharmaceuticals rather than replace them.

Summary

Atopic dermatitis, often known as eczema, is a common skin illness that impacts millions of people worldwide.
Eczema is a chronic skin disorder characterized by itching and swelling. It frequently appears as red, itchy, and sometimes painful rashes on the skin’s surface.
The prevailing consensus is that a combination of hereditary and environmental factors contribute to eczema.
Eczema typically runs in families, which raises the possibility of a strong genetic link. If one or both parents have eczema, a child is more likely to have it.
Even though modern medicine has made significant advancements in our understanding of how to control eczema, some traditional remedies are still effective and may offer relief to those seeking an alternative or supplementary course of treatment.

References

Your Skin Tanning or Sunburning Based on DNA

Aira on July 3, 2023

While getting a bit of sun every day is never a bad thing, there are negative effects to sun exposure that can be harmful to your skin and even your overall well-being. Getting a tan might be the norm when going to the beach for a vacation, but this does not necessarily mean it is healthy or good for your skin. Skin tanning and sunburning are two different things. They are both reactions of the skin to too much sun exposure but one can be more painful than the other.

Skin color is a big factor to consider in how your skin will respond to prolonged sun exposure. However, there are other factors as well such as genetics, skin type, and underlying medical conditions. Genetics plays a role in how your skin will respond to the sun’s rays and knowing more about it via genetic skin testing can help you plan your next day out better.

Understanding Skin Tanning vs. Sunburning

By definition, skin tanning happens when the UV rays of the sun hit the skin and leave behind mutations that activate melanocytes to combat them by releasing extra melanin. This extra melanin causes the skin to darken. Sunburn, on the other hand, is a type of inflammation. When the skin is exposed to too much sun, it can blister, swell, and develop a rash due to the damage ultraviolet (UV) rays have caused. The skin can also become red and hot to the touch when it is sunburnt.

Skin tanning gives your skin that glowy, healthy appearance while sunburning can be scratchy and painful. However, experts say that both are types of damage to the skin and can equally lead to premature skin aging and even skin cancer if you’re not careful enough.

Fairer skin types have lesser melanin which means they produce fewer melanocytes that can combat the sun’s rays. Instead of tanning, people with fairer skin types tend to burn, the degree of which varies on the amount of time they have had sun exposure, their genetics, and their skin type. Whether you are aiming to have a nice tan or just want to be outdoors when the weather is nice, good quality sunscreen, adequate protective clothing, and avoiding the midday sun can protect your skin from sun damage.

How long does sunburn last?

It typically takes two to six hours after sun exposure for sunburn to show itself. Depending on the severity of the sunburn, it can be at its “peak” of redness and swelling 24 hours after being under the sun. It can fade in as little as 48 hours or last up to a week. There are a few factors that might affect how long a sunburn will last including skin fairness, length of sun exposure, certain medication and conditions, environmental climate or weather, and genetics. Some people are genetically predisposed to heal from skin damage at a much faster rate than others.

What is the best thing for sunburn?

The tired, old saying that prevention is better than a cure might be more true than you think. Preventing sunburn is much more effective (and efficient) than treating it. The number one thing many experts agree on? Wear sunscreen often, reapply when necessary, and do your research on how much SPF you will need to protect your skin.

If you’re already sunburnt, don’t sweat it too much. If it is mild to moderate and the symptoms are tolerable, it should go away in a day or two without much help on your part. Try to keep the area clean and moisturized, avoid rubbing it with your hands or abrasive clothing, and try to stay hydrated to help your skin bounce back. If the pain is too much, try to see if you can get prescriptions for pain relief from your primary care physician in topical or medication form.

Does sunburn turn into tan?

There are certain situations where sunburn may somewhat turn into tan. Most individuals with fair skin, for example, just get sunburnt after heavy sun exposure. Due to less melanin production, even after a few hours under the sun’s rays, fairer skin will turn red, swell, and often be painful. After the sunburn has completely healed, the skin may look tanner or darker in color but this usually will fade as well and at a quicker rate, depending on a few factors.

Can you sunburn your eyes?

Your skin is not the only one at risk when exposed to the sun’s UV rays. Your eyes are also vulnerable to the sun and can get sunburnt. This condition is called photokeratitis or ultraviolet keratitis. It is an inflammation of the cornea, the clear covering of your front eyes. Some symptoms of photokeratitis include eye pain, headache, swelling, redness, blurry vision, and a gritty sensation as if sand has entered your eyes. Just like protecting your skin, the best deterrent for sunburnt eyes is protection in the form of proper eyewear like sunglasses.

How long does it take to get sunburn?

It depends on several factors including the amount of melanin in your skin, your genetics, and the amount of sun exposure you were subjected to. Some people get sunburnt in as little as half an hour under the scorching sun while others take a little longer to get baked under the sun. At its peak, the sun is at its hottest at around 10 A.M. until 3 P.M. Getting sun exposure during this window increases your likelihood of getting sunburnt.

Genetic Factors and Skin Tanning or Sunburning

Many skin conditions have been found to be directly linked to genetics such as acne, psoriasis, rosacea, and eczema. While skin tanning and sunburning are acquired skin conditions rather than directly genetic skin conditions, your genetic variation can still affect how your skin responds to what causes skin tanning and sunburning.

You may have genetic variations that let your skin tan rather than burn even with hours of sun exposure. You may also be genetically predisposed to get sunburnt despite being out for only a short period. Either way, your genes play a role in how your skin responds to the sun’s ultraviolet rays. Moreover, your skin’s reaction to UV rays is also its mechanism to protect what is under your skin, that is, your DNA.

Knowing more about your DNA and how it relates to your skin can help you protect your skin and overall well-being better. Genetics plays an important role in learning about your genetic predispositions certain skin conditions like sunburns and even influences their development in the first place. A skin DNA test can help you figure out what you need. Curious to know more if you are more likely to tan or burn under the sun? Try LifeDNA today.