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Health Benefits of Biotin
<p>Health Benefits of Biotin</p>
Dr. Constance Odom, MD Picture of Dr. Constance Odom, MD
Medically reviewed by
Written by our editorial team.
Last Edited 5 min read
Biotin is a B-vitamin, and is also known by the name of vitamin B7. It was once known as coenzyme R, or vitamin H. The H stood for Haar und Haut, the German words for Hair and Skin. Biotin is water soluble, which means that it dissolves in water, and has many important functions in the body.
Biotin is necessary for the functions of several enzymes that are known as carboxylases, which are biotin-containing enzymes that participate in important metabolic functions, like the production of glucose and fatty acids. Commonly recommended, the intake is about five micrograms per day in infants and thirty micrograms in adults. This can be increased to thirty five micrograms per day in breastfeeding women.
Deficiency for biotin is fairly rare, but some groups of people are more likely to experience it in mild forms, such as pregnant women. Other factors, such as consuming raw eggs, can cause a deficiency. But to do something like that, you'd have to dine on raw eggs for quite a long amount of time. Raw egg whites contain a protein called avidin, which binds to biotin and prevents it from being absorbed by the body. Thankfully, it's rendered inactive during cooking.
Biotin is a key vitamin for energy production, and several enzymes require it to properly function. These enzymes are specifically involved in fat, protein, and carb metabolizm, and initiate crucial parts of the metabolic processes of these nutrients. Biotin plays a role in fatty acid synthesis by assisting enzymes that activate reactions important to breaking down fatty acids. It's also important in gluconeogenisis, which is the metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates. Gluconeogenesis is one of the several main mechanisms used by humans and many animals to maintain blood glucose levels, avoiding hypoglycemia. It's also important in the breakdown of amino acids, as biotin-containing enzymes are involved in the metabolism of several important kinds, such as leucine.
Biotin is important for more cosmetic purposes as well, such as brittle nails for one. Brittle nails are nails that are weak can become easily chipped, cracked, or split. It's very common to have brittle nails, unfortunately, as an estimated twenty percent of people around the globe are effected. But, in one study, eight people with brittle nails were given 2.5mg of biotin, per day, for a minimum of six up to fifteen months. Thickness in the nails improved by twenty five percent in all eight participants, and nail splitting was also reduced. In yet another study, thirty five people with brittle nails found that 2.5mg of biotin a day for one and a half to seven months improved symptoms in sixty seven percent of participants. These studies were rather small, however, and more research is certainly needed.
In a similar cosmetic vain, biotin is also often associated with an increase of hair growth, and not just any kind, but healthier, and stronger hair. And while more research is certainly needed to back this claim, a deficiency in biotin may lead to hair loss, which indicated and importance in the vitamin when it comes to maintaining a lush mane of hair. Whether or not it improves hair growth in healthy people, the jury's still out on that, but people with even a slight deficiency should certainly see results from added supplementation.
Biotin may even help controlling the blood sugar levels of those who have diabetes. Type two diabetes is a metabolic disease, and is characterized by high blood sugar levels and impaired insulin function. Recently, researches have studied how biotin supplements affect blood sugar levels in type two diabetics, and some evidence shows that biotin concentrations in blood may be lower in people with diabetes, compared to healthier individuals. Studies in diabetics given biotin alone have, as of it, provided mixed results. On the other hand, several controlled studies have shown that biotin supplements, combined with the mineral chromium, may lower blood sugar levels in some people with type two diabetes.
When it comes to skin, Biotin's role in skin healthy isn't fully understood, but it is known that you may get red, scaly skin rashes if you have a biotin deficiency. Other studies have also suggested that biotin deficiency may sometimes cause a skin disorder known as seborrheic dermatits, or cradle cap, as it's more commonly known. Biotin's role in skin healthy could possibly be related to it's effect on fat metabolism, which is important for the skin and may be impaired when dealing with a deficiency.
Biotin is important when it comes to pregnancy and breastfeeding, and require an increased requirement for the vitamin. It's actually been estimated that about half of all women who get pregnant may develop a mild deficiency in the vitamin. This means that it may start to affect their well being, but not enough to cause noticeable symptoms. Deficiencies are thought to occur in pregnant women thanks to faster breakdown during pregnancy. Additional, a major cause for concern in these women is that animals studies have found that a biotin deficiency has shown to be alongside many birth defects, and may be a contributing factor. Nevertheless, remember to always consult your doctor or dietitian/nutritionist before taking supplements during pregnancy and while breastfeeding.
Biotin also may affect multiple sclerosis, which is an autoimmune disease. In MS, the protective covering of nerve fibers in the brain, spinal cord, and eyes is damaged or destroyed. This protective covering is called myelin, and biotin is known to be an important factor in producing it. In fact, a pilot study in twenty three people with progressive Multiple Sclerosis tested the use of high doses of biotin, and over ninty percent of participants had some degree of improvement. And of course, this finding needs much more study, at least two randomized controlled trials have been carried out in people with progressive MS. The final results have not been published, but the preliminary results are promising.
Biotin is found in a rather wide variety of foods, which means that deficiency while not impossible, is rare. Such foods include Wheat germ, whole-grain cereals, whole wheat bread, eggs, dairy products, peanuts, soya nuts, Swiss chard, salmon, and chicken are all sources of biotin, alongside organ meats, such as liver and kidney and mushrooms. A bit of it is even produced by the bacteria in your stomach, on it's own or as a component of mixed vitamin supplements.
To top all of these benefits off, biotin is considered extremely safe. Even massive doses of up to three hundred milligrams a day, which is what was used to test multiple sclerosis and it's effects, have not led to any adverse side effects. And because it's a water-soluble vitamin, excess of it is lead out of the body in urine. However, there have been some reports of high-dose biotin causing strange results on thyroid tests, so check with a doctor before using if you are currently taking thyroid medication.
This article is for informational purposes only and does not constitute medical advice. The information contained herein is not a substitute for and should never be relied upon for professional medical advice. Always talk to your physician about the risks and benefits of any treatment. Nu Image Medical may not offer the medications or services mentioned in this article.
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How Aromatherapy Works
Aromatherapy works by stimulating receptors in the nose responsible for smell, sending messages by olfactory cells to the part of the brain that controls the drive for survival, emotions, and instinct called the limbic system. The olfactory cells recognize scents as specific aromatic molecules that fit into receptors on these cells. Although not fully understood, scientists believe that these nerve signals’ action causes powerful mood changes in response to particular smells.
Massage Therapy in Harmony with Aromatherapy
Massage therapy, combined with essential oils, candles and incense, stimulates positive emotions and relaxation, equipping clients with coping mechanisms for many other health issues. An aromatherapy massage is a popular multi-purpose way of using supplemental care for health issues. The skin absorbs essential oils maintaining suppleness, it offers pain relief, and the aroma’s mental stimulation provides clients with the ultimate massage session.
VIP Mobile Massage offers specialist care for each client, operating 7-days a week from 9:00 AM to 11:00 PM. Call us on 305-586-1267 to book an appointment or inquire about our services.
About Author
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When it comes to maximizing your gains in strength and muscle mass, understanding the role of hormones in strength training and muscle growth is crucial. Hormones act as messengers in your body, orchestrating the complex processes that lead to muscle hypertrophy and strength enhancements. In this comprehensive guide, we'll delve into the specifics of how hormones influence your fitness journey.
The Key Hormones Involved in Muscle Growth
Several hormones play pivotal roles in muscle growth. Among the most influential are testosterone, growth hormone (GH), and insulin-like growth factor 1 (IGF-1). Each of these hormones facilitates muscle hypertrophy in distinct ways:
• Testosterone: Known as the primary male sex hormone, testosterone is critical for protein synthesis and muscle repair. It directly influences the anabolic environment in the body, promoting the growth of muscle fibers.
• Growth Hormone: Released by the pituitary gland, GH stimulates overall growth and cell reproduction. It promotes the release of IGF-1, which further enhances muscle growth.
• Insulin-like Growth Factor 1: IGF-1 works alongside GH to stimulate muscle growth and repair, thereby boosting muscle hypertrophy.
Testosterone: The Anabolic Powerhouse
Testosterone is often dubbed the king of anabolic hormones. A study published in the Journal of Applied Physiology showed that men with higher testosterone levels experienced greater muscle mass and strength gains from resistance training compared to those with lower levels (source). Here's how it works:
1. Increased Protein Synthesis: Testosterone enhances the rate at which muscle proteins are synthesized, aiding in quicker recovery and growth.
2. Reduced Muscle Breakdown: It decreases the activity of catabolic hormones that break down muscle tissue, preserving the muscle mass you work hard to build.
3. Enhanced Neural Adaptations: Higher testosterone levels can improve neuromuscular communication, leading to more effective strength training sessions.
Understanding the impact of testosterone can help you adjust your training and lifestyle to optimize its levels. Factors such as sleep, nutrition, and resistance training intensity all play roles in maintaining healthy testosterone levels.
Growth Hormone and IGF-1: The Dynamic Duo
The relationship between growth hormone and IGF-1 is akin to a duo of superheroes working together to combat muscle atrophy. Growth hormone stimulates the liver to produce IGF-1, which then circulates to the muscles and promotes growth. This relationship was highlighted in a review by the European Journal of Endocrinology (source).
Growth hormone peaks during sleep, making quality rest essential for maximizing muscle growth. Incorporating proper sleep hygiene and a balanced diet rich in protein can significantly enhance GH and IGF-1 levels, contributing to better muscle gains.
Practical Tips for Maximizing Hormonal Benefits
Here are some actionable steps to make the most of your hormonal responses for muscle growth:
• Optimize Your Sleep: Aim for 7-9 hours of quality sleep per night to support GH production.
• Focus on Compound Movements: Exercises like squats, deadlifts, and bench presses stimulate testosterone and GH release more than isolation exercises.
• Eat a Balanced Diet: Ensure you get enough protein, healthy fats, and carbs to fuel muscle growth and hormonal balance.
• Manage Stress: High stress levels can increase cortisol, a catabolic hormone. Practice stress-reducing activities like meditation or yoga.
Conclusion: Boost Your Gains by Understanding Hormones
Understanding the role of hormones in strength training and muscle growth can give you the edge you need to optimize your workouts and nutrition. By focusing on hormones like testosterone, growth hormone, and IGF-1, you can create an optimal internal environment for muscle hypertrophy. Implement the practical tips we've discussed, and you'll be on your way to maximizing your strength and muscle gains.
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Heart Murmurs and Other Sounds
During a regular medical checkup, your doctor will use a stethoscope to listen to your heartbeat to determine whether your heart is beating pro...
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What Are Heart Murmurs and Other Sounds?
During a regular medical checkup, your doctor will use a stethoscope to listen to your heartbeat to determine whether your heart is beating properly and has a normal rhythm. This gives the doctor information concerning the health of your heart. If your doctor hears a “murmur” or any other abnormal sounds coming from your heart, it may be an early indicator of a serious heart condition.
How Are Heart Murmurs and Other Sounds Evaluated?
A normal heartbeat has two sounds, a lub (sometimes called S1), and a dub (S2). These are caused by the closing of valves inside the heart. If there are problems in the heart, there may be additional sounds or abnormal sounds.
Your doctor will listen to your heart with a stethoscope (a medical device used for listening (auscultation) to the heart, lungs, and other organs of the human body). If problems are detected, your doctor may order an echocardiogram (a test that uses sound waves to create a moving picture of the heart) to get a better understanding of the abnormal sounds detected.
Heart Murmurs
The most common abnormal heart sound is a heart murmur. A murmur is a blowing, whooshing, or rasping sound that occurs during a heartbeat. There are two kinds of heart murmurs, innocent (also called physiological) and abnormal murmurs.
An innocent murmur is found in children, and is due to small holes between the different chambers of the heart. This usually does not cause significant problems, but may need to be monitored over time. An abnormal murmur in a child is due to congenital (present at birth) heart malformations, and may need to be corrected with surgery.
An adult abnormal murmur is usually due to problems with the valves that separate the chambers of the heart. If a valve does not close tightly and some blood leaks backward, this is called regurgitation. If a valve has become too narrow or becomes stiff, known as stenosis, it can also cause a murmur.
Murmurs are graded depending on how loud the sound is. The scale for grading is from one to six, where a one is very faint and a six is very loud—so loud it may not need a stethoscope to be heard. Murmurs are also categorized as occurring either during the first sound (S1) as systole murmurs, or during the second sound (S2) as diastole murmurs.
Galloping Rhythms
Other heart sounds include a “galloping” rhythm, with the occurrence of additional heart sounds S3 and S4. An S3 gallop or “third heart sound” is a sound that occurs after the diastole, S2 “dub” sound. In young athletes or pregnant women, it is likely to be harmless, but in older adults, it may indicate heart disease.
An S4 gallop is an extra sound before the S1 systole “lub” sound. This is always a sign of disease, likely the failure of the left ventricle of the heart. You may also have both an S3 and an S4 sound, and this is called a “summation gallop” when the heart is beating very fast. A summation gallop is very rare.
Other Sounds
Clicks or short, high-pitched sounds may also be heard during the regular heartbeat. This could indicate a mitral valve prolapse, when one or both flaps of the mitral valve are too long. This can cause some regurgitation of blood into the left atrium.
Rubbing sounds may be heard in patients with certain kinds of infections. A rubbing sound is usually caused by an infection in the pericardium due to a virus, bacteria, or fungus.
If your doctor finds any abnormal heart sounds, he or she may ask you questions about your family. If any of your family members also have abnormal heart sounds or have a history of heart problems, it is important to tell your doctor. It may make diagnosing the cause of your abnormal heart sounds easier.
You doctor will also ask if you’ve had any other symptoms, such as bluish skin, chest pain, fainting, distended neck veins, shortness of breath, swelling, or weight gain. Your doctor may also listen to your lung sounds and see if you have signs of liver enlargement. These symptoms may provide clues about what type of heart problem you are experiencing.
What Are the Causes of Heart Murmurs and Other Sounds?
The heart is made up of four chambers. The two upper chambers are called the atria and the two lower chambers are called the ventricles. Valves are located between these chambers to make sure that blood always flows in one direction.
The tricuspid valve goes from the right atrium to the right ventricle. The mitral valve leads from the left atrium to the left ventricle. The pulmonary valve goes from the right ventricle out to the pulmonary trunk, and the aortic valve goes from the left ventricle to the aorta. The pericardial sac surrounds the heart and protects it. Problems with these parts of the heart may lead to unusual sounds that can be detected by listening with a stethoscope or by performing an echocardiogram test.
Congenital Malformations
Murmurs, especially in children, may be caused by congenital (present at birth) heart malformations. These can be benign and never cause symptoms or can be severe malformations that require surgery or even a heart transplant. Innocent murmurs include pulmonary flow murmurs, Still’s murmur, and a venous hum.
One of the more serious congenital problems that is a cause of heart murmurs is called the “Tetralogy of Fallot”. This is a set of four defects in the heart that lead to episodes of cyanosis. Cyanosis is when the skin of an infant or child turns blue from lack of oxygen during activity (like crying or feeding).
Another heart problem that causes a murmur is patent ductus arteriosus, in which a connection between the aorta and the pulmonary artery fails to close correctly after birth. Other congenital problems include atrial septal defect, coarctation of the aorta, and ventricular septal defect.
Heart Valve Defects
In adults, murmurs are usually the result of problems with the heart valves. This may be caused by an infection, such as endocarditis or infectious endocarditis. Valve problems can also simply occur as a part of the aging process due to wear and tear on the heart.
Regurgitation, or backflow, is when the valves do not close properly. The aortic valve can have aortic regurgitation. The mitral valve can have regurgitation, either acute (caused by a heart attack or a sudden infection) or chronic (caused by high blood pressure, infection, mitral valve prolapse, or other causes). The tricuspid valve can also suffer from regurgitation, usually caused by the enlargement (dilatation) of the right ventricle. Pulmonary regurgitation is caused by the backflow of blood into the right ventricle when the pulmonary valve cannot close completely.
Stenosis is a narrowing or stiffening of a valve. Mitral stenosis occurs most often due to rheumatic fever (a complication of untreated strep throat or scarlet fever). Mitral stenosis can cause fluid to back up into the lungs, causing pulmonary edema. Aortic stenosis can also occur because of rheumatic fever, and it may cause heart failure. Tricuspid stenosis can occur because of rheumatic fever or heart injury. Pulmonary valve stenosis is usually a congenital problem and runs in families. Aortic and tricuspid stenosis can also be congenital.
Another cause of heart murmurs is stenosis due to hypertrophic cardiomyopathy. The muscle of the heart thickens making it harder to pump blood through the heart. This results in a heart murmur. This is a very serious disease that is often passed on through families.
Causes of Clicks
Heart clicks are caused by problems with the mitral valve. Mitral valve prolapse is the most common cause, when one or both flaps of the mitral valve are too long. This can cause some regurgitation of blood into the left atrium.
Causes of Rubs
Heart rubs are caused by friction between layers of the pericardium—a sac around the heart. This is usually caused by an infection in the pericardium due to a virus, bacteria, or fungus.
Causes of Galloping Rhythms
A galloping rhythm of the heart, with a third or fourth heart sound, is very rare. An S3 sound is likely caused by an increased amount of blood within the ventricle. This may be harmless, but could indicate heart problems, such as congestive heart failure. An S4 sound is caused by blood being forced into a stiff left ventricle. This is a sign of serious heart disease.
What Can Be Expected in the Long-term?
Abnormal heart sounds often indicate some type of heart disease. This may be treated with medication, or may require surgery. It is important to follow up with a heart specialist and learn the details of your condition.
Written by: Christine Case-Lo
Edited by:
Medically Reviewed by: [Ljava.lang.Object;@7fb372e7
Published: Aug 1, 2012
Published By: Healthline Networks, Inc.
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Nevertheless, when the MTSE string length was risen to 8 or 10 carbons, fewer proteins adducts had been noticed regardless of the duration or dosage of incubation tested
Nevertheless, when the MTSE string length was risen to 8 or 10 carbons, fewer proteins adducts had been noticed regardless of the duration or dosage of incubation tested. Ideally, these real estate agents could have low toxicity against regular cells fairly, and can inhibit the development and proliferation of tumor cells specifically. Our group while others possess previously proven that breasts cancer cells show increased MCH-1 antagonist 1 mitochondrial air consumption weighed against non-tumorigenic breasts epithelial cells. This shows that it might be possible to provide redox active substances towards the mitochondria to selectively inhibit tumor cell rate of metabolism. To show proof-of-principle, some mitochondria-targeted smooth electrophiles (MTSEs) continues to be designed which selectively accumulate inside the mitochondria of extremely energetic breasts tumor cells MCH-1 antagonist 1 and alter mitochondrial proteins. A prototype MTSE, IBTP, Mouse monoclonal to 4E-BP1 inhibits mitochondrial oxidative phosphorylation considerably, resulting in reduced breasts tumor cell proliferation, cell connection, and migration at high concentrations after short-term publicity [2, 7, 9, 10], although exact mechanisms stay defined poorly. In this scholarly study, we analyze the bioenergetic outcomes of directing electrophilic TPP bifunctional substances towards the mitochondrion. These substances, termed mitochondria-targeted smooth electrophiles, (MTSEs), MCH-1 antagonist 1 differ considerably within their reactivity from poisonous electrophilic medicines and environmental toxicants extremely, that are very difficult electrophiles [11] fairly. Hard electrophiles type adducts with hard nucleophiles such DNA bases and serine proteins residues; whereas smooth electrophiles type adducts with smooth cellular nucleophiles, cysteine thiols particularly. While hard electrophiles possess regularly been dismissed as therapeutics because of the systemic toxicity in medication studies, there is certainly accumulating proof that smooth electrophiles are much less poisonous in and natural model systems [11, 12]. Additionally it is vital that you consider how the smooth electrophile course of substances have a variety of reactivity spanning many purchases of magnitude [13]. The reactivity of the smooth electrophile can be straight proportional towards the poisonous results also, with an increase of reactive substances exhibiting higher toxicity in mobile and animal versions [14C16]. Therefore, chances are that smooth electrophiles of low reactivity fairly, including MTSEs, could be useful as restorative agents. Actually, other such smooth electrophiles possess known helpful physiological effects you need to include diet electrophiles within broccoli (sulforaphane) and curry (curcumin) [17], aswell as created anti-inflammatory prostanoids such as for example 15-deoxy prostaglandin J2 [18 endogenously, MCH-1 antagonist 1 19]. One of the most essential factors in developing book drug leads can be ensuring specific discussion of the substances with desired focus on protein(s). In the entire case of MCH-1 antagonist 1 electrophilic signaling substances, the specificity of response depends upon the chemical substance properties from the substances themselves, including hydrophobicity, reactivity, electrophile softness, and focus on softness [11]. Generally, lower reactivity from the electrophile leads to higher selectivity for particular targets. Probably the most reactive smooth nucleophiles inside the cell are selenocysteine and deprotonated (or low pKa) cysteine residues [20, 21]. While cysteine exists generally in most protein, it represents significantly less than 2% of the full total protein amino acidity composition. Furthermore, not absolutely all cysteines are vunerable to oxidative changes, since few cysteines can be found mainly in the deprotonated fairly, nucleophilic type [21, 22] which can be reactive with electrophiles. It really is therefore that specific proteins thiols are poised to mediate varied redox signaling reactions to multiple stimuli [23]. Oddly enough, accessible reactive proteins thiols can be found in the energetic sites of several mitochondrial protein. Mitochondrial protein face probably the most reducing environment inside the cell and so are susceptible to changes because of the fairly high internal mitochondrial matrix pH due to the proton pumping from the electron transportation string [24]. Mitochondrial proteins that are redox-sensitive consist of mitochondrial dehydrogenases such as for example -ketoglutarate dehydrogenase [25], isocitrate dehydrogenase [26], and mitochondrial aldehyde dehydrogenase [27], aswell as the mitochondrial complexes I, II, and V [28, 29]. To be able to determine the consequences of mitochondrial proteins changes on the rate of metabolism of tumor cells, we synthesized some MTSEs that alkylate mitochondrial protein and analyzed the differential ramifications of a prototype MTSE on oxidative phosphorylation and glycolysis in tumorigenic versus non-tumorigenic breasts cells. Furthermore, we established the resultant ramifications of MTSEs on breasts tumor cell proliferation, adhesion and migration. This scholarly study shows that MTSEs cause.
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Open Access
Review | May 2021
Risk Stratification and Clinical Utility of Polygenic Risk Scores in Ophthalmology
Author Affiliations & Notes
• Ayub Qassim
Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia
• Emmanuelle Souzeau
Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia
• Georgie Hollitt
Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia
• Mark M. Hassall
Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia
• Owen M. Siggs
Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia
• Jamie E. Craig
Department of Ophthalmology, Flinders University, Flinders Medical Centre, Bedford Park, Australia
• Correspondence: Ayub Qassim, Department of Ophthalmology, Flinders University, Level 2 Car Park Tenancies, 1 Flinders Drive, Bedford Park, SA 5042, Australia. e-mail: [email protected]
Translational Vision Science & Technology May 2021, Vol.10, 14. doi:https://doi.org/10.1167/tvst.10.6.14
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Ayub Qassim, Emmanuelle Souzeau, Georgie Hollitt, Mark M. Hassall, Owen M. Siggs, Jamie E. Craig; Risk Stratification and Clinical Utility of Polygenic Risk Scores in Ophthalmology. Trans. Vis. Sci. Tech. 2021;10(6):14. https://doi.org/10.1167/tvst.10.6.14.
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Abstract
Combining genetic and clinical data into an informative risk prediction profile has been an important ambition of personalized medicine. Single-nucleotide polymorphisms are commonly found throughout the genome and account for the majority of interindividual genetic variation. To date, genome-wide association studies have led to the discovery of thousands of disease-associated loci, including across dozens of ophthalmic diseases and traits. However, compared with the clinical utility of identifying rare Mendelian variants, the translation of these results to clinical practice has so far been limited because such variants are found commonly in the population, and individually account for a very small risk. Recently, combining large numbers of these genetic variants into polygenic risk scores (PRS) has shown clinically meaningful risk prediction across several common diseases. PRS have the potential to translate the discovery of common risk variants into individualized disease risk prediction, prognostication, and may enable targeted treatments. In this context, we review the clinical utility of PRS in three common, genetically complex ophthalmic conditions: primary open angle glaucoma, age-related macular degeneration, and myopia.
Translational Relevance: Common genetic variants can be used to effectively stratify the risk of disease development and progression and may be used to guide screening, triaging, monitoring, or treatment thresholds.
Introduction
The rapid development of genomics in recent years has substantially accelerated our understanding of the genetic architecture of many complex diseases. The increased affordability and throughput of genomic assays, development of better tools to process genomic data, and the availability of increasingly large public datasets has allowed an unprecedented exploration of human genomic variation. Over the past decade, genome-wide association studies (GWAS) have been extensively used to find associations between a disease or trait and genetic loci, represented by single-nucleotide polymorphisms (SNPs). SNPs are variations in a single DNA building block (nucleotide) in the gene. A few million SNPs are found in each person's unique genetic sequence, bearing in mind that the majority are not thought to be associated with any disease.1 Only relatively common SNPs—with allele frequency of at least 1%—are statistically confidently discovered to be associated with a trait in GWAS, although increasing sample sizes and newer analytical approaches are continuously improving the ability to detect robust associations with rarer variants.
A better understanding of an individual's risk of disease, the severity of disease in those who develop it, and their response to therapy are cornerstones of personalized medicine—the notion that screening, management, and interventions can be tailored specifically to an individual, or at least stratified across groups of similar individuals. This review will focus on the polygenic risk model of diseases, and its application in ophthalmology with a focus on primary angle glaucoma (POAG), age-related macular degeneration (AMD), and myopia, the leading causes of blindness worldwide.2
Polygenic Model of Complex Diseases
Monogenic or Mendelian diseases are primarily driven by alterations in a single gene. These genetic variants are typically rare but have a high effect size and penetrance, meaning that they generally confer a high risk of developing the associated disease. For example, rare pathogenic variants in the OPTN (optineurin) gene and copy number variants of the TBK1 (Tank-binding kinase 1) gene lead to familial normal tension glaucoma with highly penetrant autosomal dominant inheritance.3,4 Similarly, most retinal dystrophies arise from Mendelian variants and over 330 such retinal dystrophy genes have been identified, such as mutations in RHO (rhodopsin) leading to retinitis pigmentosa.5
In contrast, complex diseases have a polygenic genetic architecture, which may involve hundreds or thousands of contributing genes.6 In these common complex diseases, each genetic variant has a relatively small effect and does not lead to the disease by itself. Therefore the discovery of these disease-associated genomic variants requires studies of large cohorts, especially for common variants with very small effect sizes. This is commonly the result of GWAS in which millions of genetic variants are studied across many thousands of individuals for association to a disease or trait. It is important to note that individual SNPs discovered by GWAS are relatively common in the normal population, often with a minor allele frequency above 1%. That is, these variants are present in at least 1% of the normal population if heterozygous, or slightly lower proportions accounting for homozygous people; thus the study of disease association of these variants requires a large and ideally well-phenotyped cohort. Disease association for rarer variants requires a different approach such as linkage mapping or whole-exome sequencing of families with the same rare disease. Many common adult-onset diseases have polygenic and environmental contributions, including POAG, AMD, type 2 diabetes, dyslipidemia, and coronary artery disease.610 For example, although there is a strong genetic contribution to AMD risk, smoking has been well established as a key modifiable environmental risk factor for the development and progression of AMD.11,12
Although each SNP explains only a small proportion of genetic risk and heritability, the additive effects of tens or hundreds, up to hundreds of thousands in some studies, of SNPs amount to a risk equivalent to a single monogenic variant.13 Furthermore, common variants of very small effect sizes are difficult to isolate statistically from noise in GWAS, yet they still contribute to disease risk and account at least partially for the missing heritability unexplained by the currently discovered variants.14 As larger studies discover additional loci,8,9,15 it is evident that SNPs with small effect sizes conjointly play a significant role in genetic risk.16 The complex interplay of these genetic networks and the effect of one locus on multiple phenotypes (termed pleiotropy), likely owing to their involvement in a shared biological pathway, as well as environmental influences are important in the development of complex traits.16,17
Development of Polygenic Risk Scores
A polygenic risk score (PRS)—also known as a genetic risk score—is a quantitative probabilistic summary of an individual's genetic susceptibility to a disease or trait (Fig.). In its simplest form, it is a sum of the number of risk alleles carried by an individual.18 More commonly, the variants are weighted by their magnitude of effect on the disease or trait—the estimated regression coefficient of the variant—based on the summary statistics of the GWAS.18 This allows the risk score to reflect the effect size of the variants in addition to their total numbers, and therefore is a more accurate risk predictor.
Figure.
Development and clinical utility of a PRS for a sample disease.
Figure.
Development and clinical utility of a PRS for a sample disease.
Disease-associated SNPs included in a PRS are discovered via GWAS, in which several million SNPs are statistically compared with a disease (case–control setting) or phenotype. To minimize false discovery from multiple testing, a stringent genome-wide P value threshold of 5 × 10−8 is used in discovery studies, and P value adjustment methods such as Bonferroni correction are used for validation studies. However, SNPs with borderline significance not meeting the genome-wide threshold may still be associated with disease,16,19 thus a PRS may improve the estimate of the “true” genetic risk and predictive power by including a larger number of SNPs using more lenient statistical thresholds.18 To account for correlated and coinherited SNPs (said to be in high linkage disequilibrium [LD]), SNPs that are in high LD to others are usually excluded via P value thresholding; alternatively, LD is modeled into the PRS mathematically using methods such as LDpred or lassosum.20,21
When applied in a clinical context, the raw number of an individual's PRS (e.g., 12.395) is not intuitive to interpret, and so is better presented as their percentile risk relative to the normal population or study cohort (e.g., 90th percentile). For instance, a person in the 90th percentile of a weighted PRS carries disease-associated alleles whose combined effect sizes—i.e., the genetic burden—exceeds that of 90% of the normal population or study cohort. A commonly used PRS stratification method is quintiles, in which the bottom 20% is considered low risk, the top 20% as high risk, and the rest as intermediate risk.9,13,22,23 Similarly, tertile or decile groups may be used. Importantly, a PRS allows disease risk stratification but is never a diagnostic tool: its clinical utility is best achieved when combined with demographic and/or clinical factors usually evaluated in routine clinical risk assessment.
Authors sometimes seek to quantify the utility of a PRS using the area under the receiver operating characteristic curve (AUC). AUC is a summary statistic that indicates the discriminatory powers of a test to differentiate a binary outcome or set of categories. Mathematically, it is calculated as the area under the curve fitted to all the test sensitivities for each corresponding specificity (often one minus specificity). It can be used to set an optimal test threshold for maximized sensitivity or specificity. Although commonly reported in the PRS literature, the AUC has been justifiably criticized because of its lack of clinical interpretation—it is a metric of test performance in the study cohort and does not inform the individual about their risk, nor does it quantify the magnitude of risk.24 Furthermore, from a clinical point of view, PRS is best suited as a genetic disease risk probability index (e.g., on a continuous spectrum of risk) as opposed to the dichotomous end-point approach commonly used in AUC calculations. In the case of age-related diseases such as POAG and AMD, a limitation of any dichotomous end-point study is the uncertain likelihood of younger individuals developing the disease in question later in life, which can be mitigated to some extent by prespecified age thresholds. Instead, the utility of the PRS can be reported by how informative it is in identifying high-risk individuals compared with low-risk or average-risk individuals. This can be done by reporting the odds ratio (OR) of developing the disease between the genetic risk groups and in reference to the general population risk, or additionally, by reporting the PRS association to a disease-specific metric, such as the age of diagnosis, or other measures of severity.
Clinical Utility of the PRS in Ophthalmology
The clinical utility of PRS relies on its ability to effectively identify individuals who would benefit from modified screening approaches for disease detection (frequency or age threshold for screening tailored to risk group) or interventions for disease management or progression (e.g., prioritization of therapeutic interventions, and management of risk and benefits of interventions). In nonophthalmic diseases, the clinical utility of PRS has been mainly reported in cardiovascular diseases, diabetes, inflammatory bowel diseases, cancers, and psychiatric conditions.13,2529 For instance, disease risk stratification by PRS is effectively able to identify individuals at the highest risk of developing coronary artery disease, stroke, atrial fibrillation, and type 2 diabetes.13,28 This allows early intervention with lifestyle modification or medications, which has been shown to attenuate disease risk in high-risk individuals.28,30,31 For example, statin therapy has a greater absolute risk reduction of primary coronary heart events in high-risk PRS individuals than intermediate or low-risk groups.22 Furthermore, screening programs, particularly for breast, prostate, and colorectal cancers, can be effectively personalized to the individualized risk based on PRS and demographic stratification.26,32 An overview of personalized clinical utility of PRS has been reviewed elsewhere.33 We will review the potential clinical utility of PRS in three common, genetically complex ophthalmic conditions: POAG, AMD, and myopia.
Primary Open Angle Glaucoma
Glaucoma is the leading cause of irreversible blindness worldwide affecting over 64 million people and expected to increase in prevalence with the aging population.34 Primary open angle glaucoma is the most common subtype, in which the iridocorneal angle is open and there is no secondary cause of elevated intraocular pressure (IOP). It is one of the most heritable of all common diseases,35 and first-degree relatives of individuals with POAG are at 9.2-fold higher relative risk of developing glaucoma.36 The study of the genetic architecture of POAG has been complemented by genetic association studies of related ocular traits associated with POAG — termed endophenotypes — namely IOP and optic disc nerve head morphology such as the vertical cup-to-disc ratio (VCDR).37 POAG and its endophenotypes are highly heritable with recent association studies reporting over 100 loci associated with IOP, over 50 with VCDR, and over 100 correlated with POAG.15,38,39
The high heritability of POAG and its correlated endophenotypes, in addition to the effectiveness of early intervention (e.g., topical medications, laser, or incisional surgery) to prevent otherwise irreversible vision loss, has made POAG a focus of PRS stratification. The earliest studies have demonstrated significant but modest discriminatory powers for a glaucoma PRS.4042 In 2015, Tham et al.41 developed a glaucoma PRS combining seven IOP-associated and 18 VCDR-associated SNPs known at the time, and reported a modestly higher odds of developing POAG in the top tertile of the PRS relative to the bottom tertile in a multiethnic cohort from Singapore (IOP-PRS OR, 2.50; 95% confidence interval [CI], 1.54–4.02; VCDR-PRS OR, 2.31 [95% CI, 1.50–3.55]). Mabuchi et al.40 conducted an unweighted PRS utilizing nine IOP-associated SNPs in a Japanese cohort and reported a modest association with higher tension POAG (OR per risk allele = 1.12; 95% CI, 1.01–1.24). These early studies were limited by including only a small number of SNPs in the PRS and applying it to relatively small POAG cohorts. Mabuchi et al.40 also did not weight the loci effect size—an approach now superseded by weighted PRS.18
Backed up by larger GWAS, recent glaucoma PRS studies have utilized an increasingly larger number of variants associated with POAG and its endophenotypes. MacGregor et al.15 generated a PRS using 101 IOP-associated SNPs and two previously reported VCDR-associated SNPs, and showed that the top PRS decile of an independent Australian case–control glaucoma cohort had a significantly higher risk of POAG relative to the bottom decile (OR, 5.6 [95% CI, 4.1 – 7.6]). This magnitude of risk was previously only reported for rarer monogenic variants.43 Gao et al.44 constructed an inclusive PRS using 1691 SNPs associated with IOP using a more lenient statistical threshold (P < 5 × 10−5) and reported a six-fold higher POAG risk in the top quintile relative to the bottom quintile of an internal validation dataset (OR, 6.34 [95% CI, 4.82–8.33]). This improved risk prediction can be attributed to a more inclusive SNP selection in the PRS; however, a limitation of this approach was that the test cohort and the GWAS discovery cohort were both from the UK Biobank and thus share geographic, temporal, and methodological properties. We recently reported a PRS derived from 146 IOP-associated SNPs to be associated with higher maximal IOP, younger age of glaucoma diagnosis, more family members affected, and higher treatment intensity in an independent Australian cohort.23 These findings were also validated in an independent cohort of early glaucoma cases, further supporting the utility of IOP-derived variants in glaucoma risk stratification.23
Another PRS constructed from 68 VCDR-associated SNPs applied to a Latino population showed a relatively modest risk of POAG (OR, 1.75 [95% CI, 1.09–2.81] for the top quintile relative to the bottom quintile).45 This is likely owing to input SNPs being derived from GWAS of primarily European and Asian ancestries, which are unlikely to capture all risk variants relevant to the Latino population. Additionally, VCDR variants alone have a lower discriminatory power in identifying POAG and highlights the importance of utilizing multiple glaucoma endophenotypes at a more inclusive statistical threshold. Most recently our group reported a comprehensive POAG PRS utilizing multiple correlated traits (glaucoma diagnosis, IOP, and optic disc diameter adjusted VCDR) inclusive of 2673 uncorrelated SNPs. In an independent case–control POAG cohort, individuals in the top decile of the PRS distribution had 14.9-fold higher risk (95% CI, 10.7–20.9) of glaucoma relative to the bottom decile, along with an even greater risk in high-tension glaucoma cases only (top decile vs. bottom decile of the PRS OR, 21.5, 95% CI, 12.5–37.0).38 The addition of PRS significantly improved glaucoma risk prediction compared with a model with age and sex alone, which supports the added utility of PRS compared with demographic risk factors in risk stratification (AUC 0.76, 95% CI, 0.72–0.81 vs. 0.71, 95% CI, 0.67–0.76; P = 2.8 × 10−4).38
The transferability of glaucoma PRS—which are currently primarily derived from European ancestry individuals—have been studied in South Asian and African cohorts. Our aforementioned European ancestry–derived multitrait glaucoma PRS was predictive of glaucoma in the South Asian Ancestry individuals of the UK Biobank (AUC = 0.76 in a model with age and sex, 95% CI, 0.73–0.79).38 PRS based on glaucoma-associated loci discovered in European or Asian cohorts have shown to have transferability in risk predicting glaucoma risk in African cohorts.4648 Bonnemaijer et al.47 reported that a weighted PRS inclusive of 15 glaucoma-associated SNPs was associated with POAG in an African ancestry cohort (OR 1.59, 95% CI, 1.26–1.93), whereby the top PRS quintile had a two-fold increase in POAG risk relative to the bottom PRS quintile. Interestingly, despite the predictive ability of the weighted PRS, none of these loci were individually associated with POAG in this cohort.47 This is in keeping with the GWAS results reported by Hauser et al.,49 whereby the majority of POAG risk loci previously identified in European cohorts had a significantly smaller effect sizes and statistical significance in African ancestry individuals. Thus the predictive ability of the PRS would improve by identifying ancestry-specific variants (which may be not be the same variants identified in European ancestry only GWAS due to transethnic LD patterns) and improving fine mapping to identify causal variants.48 It is encouraging that the current PRS show some evidence of transethnic transferability despite the limitations of ethnic diversity in the discovery cohorts and the variability in effect sizes of risk loci between ancestries.49
The natural history of POAG and the benefits of early intervention make glaucoma a compelling disease for further clinical trials of PRS testing. Our study demonstrated that the glaucoma PRS was associated with a younger age of glaucoma diagnosis with individuals in the top decile being diagnosed on average 7 years earlier than the bottom decile group.38 This is in keeping with the results from another POAG PRS study that utilized 12 POAG-associated SNPs reporting younger age of POAG diagnosis (5 years younger on average in the top 5% of the PRS relative to the bottom 5%).50 Another study showed a similar trend in the age of diagnosis in a Japanese POAG cohort, using a PRS inclusive of 17 IOP-related variants.51 Furthermore, our findings showed structural progression of early glaucoma and likelihood for incisional surgery in individuals with advanced glaucoma and high PRS, even after adjustment for known risk factors of progression of age and IOP.38 We also reported that individuals with a high IOP-associated PRS had a higher early-morning and outside office hours IOP even after adjustment for a clinically measured IOP, whereby individuals in the highest quintile of the PRS were 5.4-fold more likely (95% CI, of OR 1.3–23.6) to have early-morning IOP spikes relative to the lowest quintile.52 Interestingly, this association was stronger using a PRS exclusive to IOP-associated variants than a more comprehensive glaucoma PRS, suggesting an added benefit of trait-specific PRS in predicting phenotypic variations of a disease.52 Ultimately, a comprehensive and validated glaucoma PRS may be used to personalize glaucoma monitoring and management in high-risk compared with average- or low-risk individuals.
Currently, genetic testing can be done in early-onset glaucoma cases to identify individuals and their relatives at a higher risk of glaucoma.53 Individuals carrying variants in genes known to cause early-onset glaucoma such as MYOC would benefit from genetic counseling and a personalized approach to screening and management. Further, common variants may influence the penetrance of incompletely penetrant “monogenic” variants. Our aforementioned PRS effectively stratifies cumulative glaucoma risk in MYOC p.Gln368Ter carriers, the most common disease-causing variant for POAG, with individuals in the highest tertile of the PRS having six-fold increase in absolute risk of glaucoma by age 60 years relative to the lowest tertile.38
The latest glaucoma PRS risk stratification is promising in identifying individuals not carrying single high-impact variants to be at a higher risk of developing advanced glaucoma and disease progression.23,38 A PRS-based risk stratification will be more effective in combination with demographic risk factors and may be best applied to older individuals (50 years or older), those with a family history of glaucoma, or those who may have optic disc features suspicious of developing glaucoma.54 In addition, PRS may aid in triaging referrals of “glaucoma suspects” to specialists by identifying high-risk individuals prior to clinical review, resource allocations in light of increasing glaucoma prevalence, and potentially a targeted screening program.54
Age-Related Macular Degeneration
AMD is known to be a highly heritable disease, and a recent large GWAS has discovered genetic variations distributed over 34 loci accounting for over half of the disease heritability.8 Although AMD is a complex disease with several common and rare genetic variants associated with the disease, variants in the genes ARMS2/HTRA1 and CFH account for a much larger risk than other genes.8 The AMD-associated variants in these genes are common in individuals of European ancestry (minor allele frequency of 20%–40%), and each account for a two- to three-fold increased risk of AMD.8,55
The discovery of relatively large-effect size genetic variants for AMD has led to a great interest in developing models of disease prediction, including those incorporating environmental and ocular risk factors.8,5557 For instance, a model with 26 AMD-associated SNPs alongside age and sex was highly predictive of late AMD (AUC, 0.82; 95% CI, 0.79–0.86), outperforming nongenetic risk models (AUC, 0.78; 95% CI, 0.74–0.82).58 After the discovery of additional AMD risk variants using a GWAS of 16,144 AMD patients, Fritsche et al.8 reported an AMD PRS including 52 AMD-associated SNPs (of which seven were rare variants with minor allele frequency <1%), in which individuals in the highest decile had a 44-fold higher risk of developing advanced AMD relative to the lowest decile. Of note, this magnitude of risk is likely an overestimate as the test dataset was a modeled general population derived from the discovery case–control dataset.
Several studies have used PRS and known ocular and environmental risk factors to stratify AMD progression risk: the majority focusing on variants strongly associated with AMD such as those in CFH and ARMS2.5963 For instance, the presence of two or more risk alleles in CFH and/or ARMS2 was associated with progression of AMD during a 10-year follow-up (OR, 2.03; 95% CI, 1.46–2.81), which appeared to be synergistic with known environmental risk factors.60 More broadly, a recent machine learning–derived model inclusive of PRS, age, diet, smoking, education, and ocular measurements was found to be highly predictive of incident advanced AMD at 5, 10, and 15 years follow-up (AUC, 0.92; 95% CI, 0.90–0.95 at 10 years).64
As observed in POAG and many other conditions, the inclusion of additional AMD risk variants in a PRS improves its predictive performance. Ding et al.57 used a PRS comprising 34 AMD-associated SNPs to stratify the risk of progression to late AMD over up to 10.3 (SD 1.7) years. There were markedly increased rates of progression to late AMD in individuals at the highest quartile of the PRS (50% progression) compared with the lowest quartile (6.9% progression) and the intermediate group (22% progression), which was further replicated in an independent cohort.57 Similarly, an AMD PRS predicted second-eye involvement in unilateral AMD cases in a Japanese cohort (51% 10-year hazard rate in the top decile vs. 2.3% in the lowest decile).65 Another PRS comprising all 52 AMD-associated variants was applied to an independent prospective German cohort of AMD patients, and was associated with drusen load in agreement with earlier reports from the AREDS cohort.66,67 Moreover, the 52-variant PRS was associated with drusen progression in individuals with low drusen load at baseline, and both drusen and AMD progression to late disease in those with intermediate drusen load during the mean 6.5 years of follow-up.66
Seddon and Rosner68 have incorporated 13 AMD-associated risk loci into a predictive model including known demographic and ocular risk factors (baseline AMD grading) in the AREDS cohort and further validated this in an independent longitudinal AMD cohort. This risk model was predictive of AMD progression to advanced disease (AUC, 0.90 over 12 years), geographic atrophy (AUC, 0.87), and neovascular disease (AUC, 0.86). Of note, both common and rare genetic variants were included in the model; these variants are only a subset of the known AMD-associated risk loci because the authors used a stepwise regression approach with P value thresholds as the inclusion criteria for genetic variants.68 This approach is useful for optimizing variable selection in the model but excludes small effect-size variants, which may additively infer additional risk. The authors further investigated the added utility of PRS in a nongenetic risk model using the Net Reclassification Improvement method, in which predicted risk stratification at baseline is compared with progression outcome between two models. The model incorporating PRS improved the classification of eyes that ultimately progressed to AMD, with progressing eyes more likely to be classified as high risk, and nonprogressing eyes as low risk, when genetic factors were considered. For instance, 63% of eyes that progressed while being classified as “medium risk of progression” (10%–30% risk over 10 years) in a nongenetic model, were more appropriately identified as “high or very high risk of progression” by the addition of genetic loci to the model.68 This highlights the improved risk stratification and added clinical utility of an AMD PRS compared with known demographic and ocular risk factors.
In summary, an AMD PRS incorporating all possible loci vastly improves on existing clinical risk stratification for both disease onset and progression. However, aside from antioxidant and mineral supplementation, there are no effective early therapies in dry AMD.69 Despite this, AMD risk factor modification such as smoke cessation and weight loss may be valuable interventions in high-risk individuals. This has previously led the American Academy of Ophthalmology to recommend against routine genetic screening for complex diseases such as AMD.70 Of note, this recommendation was published in 2012 and does not consider the evolving evidence for using the PRS in risk prediction.
Myopia
The etiology of myopia is complex, with both environmental and genetic factors, as well as the interaction between them, contributing to the clinical presentation of myopia and its progression.71 Our understanding of common genetic variants associated with myopia is largely derived from GWAS using refractive error as a continuous variable (measured as spherical equivalent) and self-reported history and age of diagnosis of myopia.72,73 A multicohort meta-analysis inclusive of individuals of both European and Asian ancestry has discovered 167 loci associated with refractive error, of which 138 loci were further replicated in the UK Biobank cohort.74
Using these results, Tedja et al.74 created a comprehensive myopia PRS from 7307 variants, which explained 7.8% of the refractive error variance of an independent Dutch cohort. Individuals in the highest PRS decile were at 40-fold greater risk of myopia relative to the lowest decile.74 Furthermore, 24% of people in the highest decile had high myopia (defined by a spherical equivalent of –6 diopters or worse) compared with 2% in the lowest decile.74 More recently, Ghorbani Mojarrad et al.75 have used a multitrait PRS combining GWAS of refractive error (spherical equivalent), age of onset of spectacle wear, and years spent in full-time education utilizing 7372 variants. This multitrait analysis approach leverages the correlated nature of these myopia-related traits despite the overlapping GWAS samples. Individuals in the highest decile of this multitrait myopia PRS had 6.1-fold (95% CI, 3.4–10.9) higher risk of developing high myopia relative to the rest, a risk that could not otherwise be inferred readily using demographic risk factors. This is of particular clinical significance, as high myopia is associated with complications that can lead to irreversible vision impairment, most commonly as a result of myopic macular degeneration.76 Finally, combining the myopia PRS with information on the number of myopic parents was more predictive (R2 = 7%) than either risk factor alone (R2 = 4.8% and 2.6% for number of myopic parents and PRS, respectively), highlighting the added predictive ability of a PRS-inclusive model.77
Despite these findings, myopia PRS have several important limitations. Environmental risk factors, such as near-work and outdoor time, have a high impact on the etiology and progression of myopia in contrast to common genetic loci with low effect-sizes.71,74 Further, gene-environment interactions significantly affect the clinical phenotype. For instance, Verhoeven et al.78 have reported lower education significantly masks the genetic penetrance of developing myopia, possibly related to lower time spent in near-work. Among individuals with a high-risk PRS group, the odds of developing a refractive error of at least –3 diopters had a stepwise decline with decreasing education level with an OR of 51, 22, and 7 among high, intermediate, and primary levels of education.78 This is in agreement with several other studies of myopia-associated variants showing differential and heterogeneous risks of myopia development depending on age and education levels.7982
Screening and diagnosis of myopia is relatively easy and affordable especially at a younger age, thereby limiting the clinical utility of genetic testing in myopia prediction. For instance, in a longitudinal study of Chinese twin children, baseline refraction, age, and sex was sufficient to predict risk of high myopia, and the addition of a myopia PRS did not improve the model (AUC 0.9569 vs. 0.9567 respectively; P = 0.7).83 A key limitation of this study, however, is that the PRS was not derived from an ancestrally matched population, likely resulting in a lower signal-to-noise ratio and incorrectly estimating the effect size of the included variants. Despite this, PRS may be useful in identifying individuals at high risk of developing pathological myopia, in which irreversible vision loss is threatened by progressive retinal atrophy, retinal detachment, or choroidal neovascularization.74,76 This subgroup may benefit from regular screening, counseling, and lifestyle modification such increased time outdoors, which may reduce progression.84
Future Directions, Advantages, and Limitations of the PRS
Complex diseases are often diagnosed late in life with a long period of preclinical or “asymptomatic” disease. A key advantage of PRS risk stratification is the ability to identify individuals before they develop symptoms or irreversible pathology, and in some cases also predict the risk of progression.15,38,57,68,74 Risk stratification is best utilized in which early low-risk intervention can alter the natural history of a disease and improve quality of life, as has been reported across a range of cardiovascular conditions.22,28,31,85 In addition, lifestyle modification (such as increasing time outdoors for myopia, or smoking cessation and dietary modification for AMD) and earlier or more frequent screening strategies can be an effective means of minimizing vision loss. POAG represents an ideal case scenario for the clinical utility of PRS: it is one of the most heritable common human diseases without any strong environmental or lifestyle risk factors35; has a prolonged asymptomatic disease phase with irreversible vision loss54; has good outcomes with early cost-effective and low-risk treatment that can effectively halt vision loss86,87; there are highly sensitive and noninvasive screening methods available using optical coherence tomography88; and the availability of highly predictive PRS of disease risk and phenotype.23,38
In health care systems with finite resources, targeting high-risk individuals with low-risk interventions, and minimizing screening and interventions in low-risk individuals, will improve the cost-benefit ratio of these strategies and optimize resource allocation. There will be a significant clinical and economic advantage to target screening strategies to individuals at high risk of developing a disease, while saving resources spent on screening low-risk individuals, as has been shown in the cancer screening setting.26,32,89 PRS can readily be generated from public GWAS summary statistics, and easily updated as newer and larger studies are completed. Because the germline genome is fixed, once generated genomic data can be queried simultaneously at any time with any number of disease-specific PRS. This is particularly beneficial in the fast-paced GWAS literature, in which new risk variants are continuously being reported and can be used to generate new and improved PRS. However, additional research is needed on how best to counsel patients on the risk of multiple diseases and the ethical challenges this imposes. One approach could be a tiered analysis during the lifetime of the individual for different diseases, based on other relevant acquired risks (notably age) and interventions and lifestyle modifications available at the time.
PRS are an increasingly effective and accurate measure of the genetic component of disease risk, which typically outperforms self-reported family history.38,77,90,91 Although family history can capture some of the genetic risk of a disease, it is often incomplete, imprecise, and strongly confounded by shared environmental risk factors.90 Additionally, sporadic cases with no known family history of a disease would also benefit from genetic risk prediction. Nonetheless, PRS is not aimed at replacing clinical history or screening programs as it is not a diagnostic test; rather PRS can serve to improve risk stratification, screening, and clinical decision-making. There is still a need for prospective studies to test the clinical validity and utility of PRS in routine clinical practice. The design of such studies could involve stratification of disease risk based on PRS, potentially followed by randomization of high-risk patients into treatment and control (standard of care) arms. The implementation of PRS in ophthalmic practice can be done at the general practitioner level (primary prevention), optometrists (screening), and specialists (phenotypic and prognostic); however, further research is needed in this area.
There are some challenges to the implementation of PRS in clinical practice. To date, a disproportionate majority of the large-scale GWAS—and thus the PRS derived from them—were performed in populations of European ancestry.92 There is evidence that there is a disparity in LD patterns and risk allele frequencies between African and non-African populations, which impairs the translation of a majority of the current PRSs to African populations.93 Therefore the predictive power of a PRS derived from a majority European ancestry cohort can be lower when applied to other ethnicities.92 For example, although a glaucoma PRS derived from a cohort of European ancestry was predictive of glaucoma risk in South Asian individuals, it had a slightly better predictive power in an independent cohort of European ancestry (AUC of 0.76, 95% CI, 0.73–0.79 vs. AUC of 0.79, 95% CI, 0.75–0.84, respectively).38 Validation studies and mixed-ancestry GWAS are essential for the effective translation of PRS to clinical practice. Furthermore, there is little consensus on the methodology to calculate PRS, or the analysis methods used to report findings. For instance, reports of top to bottom decile comparisons exaggerate the performance of PRS for clinical settings, in which a relative risk comparison to the general population risk is more clinically relevant. This limits ease of comparison, replication, and validation of the published scores. An evidence-based and consistent analysis approach, as well as detailed reporting of the variants and methods used to generate each score, will address these issues. This is currently being addressed by the active development of The Polygenic Score Catalog, an online repository of published PRS with full annotation of variants, weights, and reported performance metrics.94 Finally, PRS research should aim to address clinical questions on the utility of the score in a disease-specific manner, rather than focusing solely on statistical prediction accuracies. For instance, a younger age of disease diagnosis (and thus a higher morbidity) or risk of disease progression or vision loss in the affected or contralateral eye would be more relevant as a translational clinical outcome. Clinicians and genetic counselors are then needed to communicate genetic risk to patients in a personalized manner with actionable monitoring frequencies and lifestyle or pharmacologic intervention suggestions. This implementation, however, will require additional clinician education, updated guidelines, and end-user engagement.
For the adaptation of PRS into clinical practice to be successful, comprehensive understanding of population attitudes toward such testing is critical. It is known that in general, genetic susceptibility testing is well received and supported. Preliminary studies have shown positive interest in genetic testing for Mendelian variants for glaucoma, particularly when applied in appropriate circumstances, such as in families with a strong family history.95 However, little is known about factors associated with uptake of PRS. A pilot study on using genetic testing to guide behavioral modification for AMD risk reduction reported that about one-third of the participants implemented specific personal protective behaviors following optometrist-guided genetic counseling.96 Another pilot study assessing uptake of polygenic risk information for breast cancer in women identified that a family history of disease, higher levels of education, and perceived benefit of testing were factors associated with improved uptake.97 However, more research is needed to better understand barriers to implementation and factors, which may influence patient decision-making.
Conclusions
PRS is a powerful tool in disease risk stratification, and prognostication in common complex diseases. The ideal clinical use scenario is in conditions in which early intervention will alter the natural history of the disease and reduce morbidity or mortality. We have summarized the existing literature supporting the utility of PRS risk stratification in three major ophthalmic conditions: POAG, AMD, and myopia. In these heritable diseases, PRS is highly informative of disease risk and may offer additional information about disease progression. A major advantage of PRS is the ability to calculate the risk of multiple diseases and phenotypes at any point in life using data from a single genotyping array. Importantly, it is not intended to be a diagnostic test, but rather a risk stratifying tool. Future research should focus on the clinical implementation of the PRS to inform personalized and targeted clinical decision-making.
Acknowledgments
Supported by the National Health and Medical Research Council (NHMRC Program Grant APP1150144 and Project Grant APP1157571). AQ was funded by a full-time Avant Doctor in Training scholarship. JEC was an NHMRC Practitioner Fellow.
Disclosure: A. Qassim, None; E. Souzeau, None; G. Hollitt, None; M.M. Hassall, None; O.M. Siggs, None; J.E. Craig, None
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Figure.
Development and clinical utility of a PRS for a sample disease.
Figure.
Development and clinical utility of a PRS for a sample disease.
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✓ Evidence Based
Heron Pose Yoga: Benefits, How To Do And Precautions
Listen to this article
🎯 Key Points
• Strengthens the legs and core muscles.
•
• Improves balance and posture.
•
• Stretches the hip flexors and opens the chest.
•
• Increases focus and mental clarity.
•
• Can help alleviate lower back pain and sciatica.
Heron Pose, also known as Krounchasana in Sanskrit, is a popular yoga pose that offers a wide range of benefits for both the body and mind. This pose is named after the heron, a beautiful bird known for its grace and elegance. In Heron Pose, practitioners mimic the bird’s posture, creating a sense of strength, stability, and poise. This article will explore the various benefits of Heron Pose, provide a step-by-step guide on how to do it correctly, and highlight some precautions to keep in mind while practicing this pose. Whether you are a beginner or an experienced yogi, incorporating Heron Pose into your yoga routine can offer numerous advantages for your overall well-being.
Benefits of Heron Pose Yoga.
Heron Pose Yoga, also known as Krounchasana, is a powerful yoga pose that offers numerous physical, mental, and emotional benefits. Here are some of the key advantages of practicing Heron Pose Yoga:
1. Increased flexibility.
Heron Pose Yoga involves deep stretching of the hamstrings, calves, and lower back. Regular practice helps to improve flexibility in these areas, allowing for better mobility and reducing the risk of injuries.
2. Strengthened leg muscles.
Holding the Heron Pose requires engaging the muscles in the legs, including the quadriceps and hamstrings. This helps to build strength and endurance in the lower body, leading to improved balance and stability.
3. Improved digestion.
The compression of the abdomen during Heron Pose stimulates the digestive organs, enhancing their function and promoting better digestion. This can alleviate issues like bloating, constipation, and indigestion.
4. Toned core muscles.
As you balance in Heron Pose, your core muscles are activated to maintain stability. This not only helps to tone and strengthen the abdominal muscles but also supports a healthy posture and spinal alignment.
5. Enhanced concentration and focus.
The combination of balance, deep breathing, and concentration required in Heron Pose Yoga helps to calm the mind and improve mental focus. Regular practice can sharpen cognitive abilities and enhance overall concentration.
6. Stress relief and relaxation.
Engaging in Heron Pose Yoga encourages deep breathing and relaxation, activating the parasympathetic nervous system. This promotes a state of calmness and reduces stress and anxiety, leading to improved mental well-being.
fiqo desk
7. Improved posture and spinal health.
Heron Pose Yoga involves sitting with an elongated spine, which helps to improve posture and strengthen the back muscles. This can alleviate back pain, correct postural imbalances, and promote a healthy spine.
8. Increased hip mobility.
The hip joint is a common area of tightness for many individuals. Heron Pose Yoga involves opening and stretching the hips, increasing their range of motion and relieving tension in the hip flexors.
9. Boosted circulation.
The various movements and stretches in Heron Pose Yoga help to improve blood circulation throughout the body. This increased circulation delivers more oxygen and nutrients to the cells, promoting overall health and vitality.
10. Mind-body connection.
Heron Pose Yoga encourages a deep connection between the mind and body through conscious breathing, focus, and awareness. This helps to cultivate mindfulness and self-awareness, fostering a greater sense of well-being and self-acceptance.
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Incorporating Heron Pose Yoga into your regular practice can provide a multitude of physical, mental, and emotional benefits, contributing to a healthier and more balanced lifestyle.
How To Do Heron Pose Yoga?
If you are interested in practicing Heron Pose, here is a step-by-step guide on how to do it correctly:
1. Begin by sitting on the floor with your legs extended straight in front of you. Keep your spine elongated and your shoulders relaxed.
2. Bend your right knee and draw it towards your torso, ensuring that your foot remains grounded on the floor.
3. Take hold of your right foot with both hands, clasping your fingers around the sole or ankle, depending on your comfort level.
4. Inhale deeply, lengthening your spine even further, and exhale as you gently lift your right leg off the floor. As you do this, try to keep your back straight and maintain balance.
5. Straighten your right leg as much as possible without forcing it. This may take some time and practice, so be patient with yourself.
6. Once your leg is fully extended, flex your right foot, pointing your toes towards the ceiling. This will help deepen the stretch and engage the muscles in your leg.
7. Keep your left leg firmly grounded on the floor, maintaining stability and balance throughout the pose.
8. Slowly and mindfully, tilt your upper body forward from the hips, hinging at the waist. Reach towards your right foot with your hands, trying to bring your torso closer to your leg. Remember to keep your spine long and avoid rounding your back.
9. Find a comfortable position for your hands – you can either hold onto your foot, ankle, or shin, depending on your flexibility. The key is to avoid straining or overstretching.
10. Stay in this pose for several breaths, focusing on your breath and allowing your body to relax and surrender into the stretch. With each exhale, you can try to deepen the stretch gently, but always listen to your body’s limits.
11. When you are ready to release the pose, slowly and with control, bring your torso upright, releasing your foot and placing it back on the floor.
12. Take a moment to observe any sensations or changes in your body, and then repeat the same steps on the other side, bending your left knee and extending your left leg.
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Remember, as with any yoga posture, it is crucial to listen to your body and respect its limitations. If you have any pre-existing injuries or medical conditions, it is advisable to consult with a qualified yoga instructor before attempting Heron Pose. Regular practice of this pose can help improve flexibility, strengthen the muscles, and cultivate a sense of calm and focus. Enjoy the journey of exploring Heron Pose and the transformative benefits it can bring to your yoga practice.
Who Can Do Heron Pose Yoga?
Anyone who is looking to improve their balance, flexibility, and core strength can benefit from practicing Heron Pose yoga. This pose, also known as Krounchasana, can be modified to accommodate different skill levels, making it accessible to a wide range of yoga practitioners.
Beginners can start by sitting on a blanket or block to reduce the intensity of the stretch, while more advanced practitioners can deepen the pose by straightening their lifted leg and reaching for their extended foot. However, individuals with knee or ankle injuries should exercise caution and consult with a healthcare professional before attempting this pose. With regular practice and proper alignment, Heron Pose can help individuals develop a sense of groundedness, enhance focus, and promote overall well-being.
Who Should Avoid Heron Pose Yoga?
While Heron Pose offers numerous benefits like stretching the hamstrings and improving digestion, there are certain individuals who should avoid attempting this pose. Individuals with knee injuries, particularly those with ligament tears or severe arthritis, should avoid Heron Pose as it places a significant amount of strain on the knees.
Pregnant women should also avoid this pose, especially during the later stages of pregnancy, due to the pressure it exerts on the abdomen. Additionally, individuals with chronic back pain or spinal issues should exercise caution or seek guidance from a qualified yoga instructor before attempting this pose. It is crucial to prioritize safety and listen to one’s body when deciding whether or not to practice Heron Pose.
Precautions To Take While Doing Heron Pose Yoga.
– Warm up your body properly before attempting the Heron Pose to prevent any strains or injuries.
– Practice on a non-slip surface or use a yoga mat to ensure stability and avoid slipping.
– Start with the basic version of the pose and gradually progress to more advanced variations as your flexibility and strength improve.
– Engage your core muscles to maintain balance and stability throughout the pose.
– Avoid forcing your body into the pose; instead, listen to your body and only go as far as you feel comfortable.
– If you have any knee or hip injuries, use props like blankets or blocks to support your knees and hips.
– Focus on your breath and maintain a relaxed state of mind while performing the pose to enhance the benefits and avoid unnecessary strain.
– If you have any pre-existing medical conditions, such as high blood pressure or glaucoma, consult with a healthcare professional before attempting the Heron Pose.
– If you experience any pain or discomfort during the pose, slowly release and come out of the pose.
Bottom Line.
Heron Pose Yoga offers numerous benefits for both the mind and body. By practicing this pose regularly, individuals can improve their balance, strengthen their leg muscles, and increase their flexibility. Additionally, Heron Pose Yoga helps to calm the mind, reduce stress, and enhance concentration. Whether you are a beginner or an experienced yogi, incorporating Heron Pose into your practice can greatly contribute to your overall well-being. So, why not give it a try and experience the transformative effects of Heron Pose Yoga for yourself?
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Secret Curves
/ Health / Not Losing Weight From Intermittent Fasting
Not Losing Weight From Intermittent Fasting
Celebrities like Terry Crews have popularized intermittent fasting—not eating for lengths at a time—as a weight loss tool.
The practice doesn’t guarantee you’ll drop pounds, but it can help you consume fewer calories—which aides in weight loss.
As a refresher, there are different ways to fast, but people generally follow three common schedules: alternate-day fasting, whole-day fasting, or time-restricted fasting. Melanie Boehmer, R.D. at Lenox Hill Hospital, recommends starting with time-restricted fasting. The 16:8 format, meaning you only eat for eight hours in a day, is popular for this method.
It’s always frustrating when the scale is stuck on the same number—despite your best efforts. If you’ve been fasting and haven’t seen results, it’s a good time to analyze your strategy.
Here are some common reasons that explain why you’re not losing weight from intermittent fasting.
You’re eating too many calories
You want to start a food journal before embarking on any kind of diet, says Melanie Boehmer, R.D. at Lenox Hill Hospital.
“It is helpful to monitor your intake to at least understand what your baseline is,” Boehmer tells Men’s Health.
Track everything you eat in a given week using FitDay.com, Lose It!, or MyFitnessPal.
Then, determine how many calories your body needs to maintain its current weight. This can be done using a formula or the body weight planner by the National Institute of Health.
From there, it’s just a matter of comparing your actual intake to what you need. It goes without saying that you won’t lose weight—regardless of fasting—if you consume too many calories
You underestimate portions
If you’re not losing weight—despite staying within your calorie needs—then it’s time to look at serving sizes. It’s common to miscalculate how much you’re actually eating, which leads to consuming more calories than you think. This is particularly true with calorie-dense foods such as cheese.
For example, a one-ounce serving of full fat cheese equals about four dice. Use a food scale—or eyeball portions with this tutorial—to more accurately calculate food intake.
You’re not eating enough
If you’ve hit a weight loss plateau after losing a few pounds, Boehmer says you may be eating too few calories.
That’s because our bodies adjust to whatever we throw at them, she says.
“If on average you’re only taking in 1200 calories, which is something none of us should be doing on a regular basis, your body is going to learn to function on 1200 calories.”
Reduce calories slowly and aim for more moderate weight loss, says Boehmer. She advises cutting enough calories to lose about a pound a week.
“When we talk about losing weight, the goal is always to lose as much weight eating thee most that you can so you don’t create that metabolic inhibitor,” she says.
Melissa Matthews Health Writer Melissa Matthews is the Health Writer at Men’s Health, covering the latest in food, nutrition, and health.
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1b12e5f89ebc6a1a4f0280c20029c85e
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-4,485,250,004,467,683,000
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Flossing Matters. Here’s Why!
Flossing Matters. Here’s Why!
The holiday season is officially here, and we all know what that means–delicious food and sweets galore! While heading straight to the couch after your holiday meal to digest while watching TV may be your first instinct, we are here with 3 reasons why you should consider taking a quick detour to floss first.
1. Flossing prevents cavities.
Forgetting to floss after a long day may seem harmless at the time, but the more you do it, the more damage you’re causing to your body. Plaque and bacteria feed on the sugar and food particles that remain in your mouth after eating. This build-up of bacteria and plaque can eat away at the enamel on your teeth, causing cavities and tooth decay.
2. Flossing keeps your gums healthy.
Some people may not like flossing because their gums get red or tend to bleed easily. However, if your gums bleed when you floss, that is your body’s response to trying to fight off the bacteria and plaque in your mouth. Flossing is a physical way of helping your gums do so. While the bleeding may be heavier at first, it should decrease the more you floss–and the healthier your gums get. Flossing can prevent gingivitis and gum disease, which occur when plaque and bacteria build-up.
3. Flossing helps your overall health.
Studies have shown that an unhealthy, bacteria-filled mouth can lead to serious health issues such as heart disease, stroke, and even bacterial pneumonia. Keeping your teeth and gums healthy now will cause your body to thank you later. The more you floss, the better off you are!
Perhaps one of the best things about flossing is how easy it is to take proper care of your body. Aside from keeping healthy teeth, gums, and overall health, a clean mouth equals a clean and bright smile. So, this holiday season, after you finish a delicious meal with your loved ones, take an extra 2 minutes to floss. Your smile will thank you!
Contact Crabtree Valley Dental to schedule your next appointment today.
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Min menu
Pages
Main natural nutrients for men's health
Main natural nutrients for men's health
The state of health :
physical and mental health has a significant impact on all spheres of
men's life and social activity. To preserve them
a healthy lifestyle must be followed.
Dr. Irina Popkova
• a dietitian, notes in a recent Gazeta.Ru that
• a healthy lifestyle involves regular physical activity
• a balanced diet and good sleep.
She says:
"A man needs a balanced and varied diet.
It should include high protein foods (poultry and meat)
"slow"
carbohydrates (grain and whole grain bread)
fresh vegetables and leafy vegetables
(parsley, dill, cabbage, etc.)
In addition :
it needs to normalize and wake up its sleep system, so that at least 8 hours of
continuous sleep per day. It will not harm the addition of regular physical activity.
It also has to reduce stress factors as much as possible.
Problems with the partner, struggles at work
increased anxiety - all of this can cause reduced libido. "
The expert explains that
1. the most important nutrients are zinc
2. magnesium
3. Arginine and carnitine.
It says:
• "Zinc is necessary to raise the level of testosterone
• the main male sex hormone. It is found in pumpkin seeds
• seafood and nuts.
Magnesium also stimulates the production of testosterone.
In addition :
it is considered the "main anti-stress element."
Magnesium also reduces the excitement of the nervous system
reduces anxiety :
enhances energy. So taking it is important in case of intense physical activity
as it increases the body's stamina. Magnesium
is found in dark chocolate, mackerel and salmon ".
According to nutritionists, the amino acid L-arginine directly affects the process of
erection, as it improves the circulation of the male organ. Pumpkin seeds
are rich in it. Peanuts, walnuts and poultry meat should also be added to the diet.
It says:
"L-carnitine is really strong for energy.
This substance is found in beef and lamb.
If the diet is not diversified and there is a lack of vitamins, mineral elements
and amino acids, nutrients can be taken to improve the state of health. "
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86366b9a982bc93a1cb873a2507519a5
|
3,795,296,201,230,627,000
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Quantitative computerized western blotting.
Dalit Talmi-Frank*, Charles L. Jaffe, Gad Baneth
*Corresponding author for this work
Research output: Contribution to journalArticlepeer-review
3 Scopus citations
Abstract
Western blotting allows analysis of antibody reactivity against multiple antigens separated according to their molecular weights. The distinction between immune dominant and recessive antigens is often difficult and carried out by qualitative or empirical means. Quantitative computerized western blotting (QCWB) addresses this difficulty by analyzing reactivity to specific antigens and providing a statistically measurable value for each band. This allows differentiation between immunodominant and immunorecessive determinants. QCWB is appropriate for either single time point analysis or longitudinal studies where multiple time points are evaluated and the reactivities against individual bands compared. This technique can be used to study humoral responses to complex antigenic mixtures such as allergens and infectious agents, or to identify serologic markers for early diagnosis of cancer, autoimmune, or infectious diseases, or to monitor patient's clinical status.
Original languageAmerican English
Pages (from-to)103-113
Number of pages11
JournalMethods in Molecular Biology
Volume536
DOIs
StatePublished - 2009
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Add to MyChemicals Print Friendly Page
Chemical Datasheet
FURFURYL ALCOHOL
6.1 - Poison
Chemical Identifiers | Hazards | Response Recommendations | Physical Properties | Regulatory Information | Alternate Chemical Names
Chemical Identifiers
The Chemical Identifier fields include common identification numbers, the NFPA diamond U.S. Department of Transportation hazard labels, and a general description of the chemical. The information in CAMEO Chemicals comes from a variety of data sources.
CAS Number UN/NA Number DOT Hazard Label USCG CHRIS Code
• 98-00-0 (FURFURYL ALCOHOL)
• Poison
NIOSH Pocket Guide International Chem Safety Card
Furfuryl alcoholexternal link
NFPA 704
Diamond Hazard Value Description
2
3 1
Blue Health 3 Can cause serious or permanent injury.
Red Flammability 2 Must be moderately heated or exposed to relatively high ambient temperatures before ignition can occur.
Yellow Instability 1 Normally stable but can become unstable at elevated temperatures and pressures.
White Special
(NFPA, 2010)
General Description
A clear colorless liquid. Flash point 167°F. Boiling point 171°F. Denser than water. Contact may irritate skin, eyes and mucous membranes. May be toxic by ingestion and skin contact and moderately toxic by inhalation.
Hazards
The Hazard fields include special hazard alerts air and water reactions, fire hazards, health hazards, a reactivity profile, and details about reactive groups assignments and potentially incompatible absorbents. The information in CAMEO Chemicals comes from a variety of data sources.
Reactivity Alerts
none
Air & Water Reactions
Slightly soluble in water.
Fire Hazard
Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:
Combustible material: may burn but does not ignite readily. When heated, vapors may form explosive mixtures with air: indoors, outdoors and sewers explosion hazards. Those substances designated with a (P) may polymerize explosively when heated or involved in a fire. Contact with metals may evolve flammable hydrogen gas. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form. (ERG, 2020)
Health Hazard
Inhalation causes headache, nausea, and irritation of nose and throat. Vapor irritates eyes; liquid causes inflammation and corneal opacity. Contact of skin with liquid causes dryness and irritation. Ingestion causes headache, nausea, and irritation of mouth and stomach. (USCG, 1999)
Reactivity Profile
Acetyl bromide reacts violently with alcohols or water, [Merck 11th ed., 1989]. Mixtures of alcohols with concentrated sulfuric acid and strong hydrogen peroxide can cause explosions. Example: An explosion will occur if dimethylbenzylcarbinol is added to 90% hydrogen peroxide then acidified with concentrated sulfuric acid. Mixtures of ethyl alcohol with concentrated hydrogen peroxide form powerful explosives. Mixtures of hydrogen peroxide and 1-phenyl-2-methyl propyl alcohol tend to explode if acidified with 70% sulfuric acid, [Chem. Eng. News 45(43):73(1967); J, Org. Chem. 28:1893(1963)].
FURFURYL ALCOHOL will polymerize rapidly and at times with explosive force in the presence of strong mineral acids, [NFPA 491M, 1991]. Alkyl hypochlorites are violently explosive. They are readily obtained by reacting hypochlorous acid and alcohols either in aqueous solution or mixed aqueous-carbon tetrachloride solutions. Chlorine plus alcohols would similarly yield alkyl hypochlorites. They decompose in the cold and explode on exposure to sunlight or heat. Tertiary hypochlorites are less unstable than secondary or primary hypochlorites, [NFPA 491 M, 1991]. Base-catalysed reactions of isocyanates with alcohols should be carried out in inert solvents. Such reactions in the absence of solvents often occur with explosive violence, [Wischmeyer(1969)]. An explosion occurred in a laboratory when cyanoacetic acid was reacted with furfuryl alcohol in an attempt to form the ester, furfuryl cyanoacetate. The explosion occurred a few minutes after the agitator was turned on and heat applied, [MCA Case History 858(1963)]. In the attempt to prepare furfuryl formate from furfuryl alcohol and concentrated formic acid an explosion occurred, [Chem. Eng. News 18:72(1940)].
Belongs to the Following Reactive Group(s)
Potentially Incompatible Absorbents
Use caution: Liquids with this reactive group classification have been known to react with the absorbents listed below. More info about absorbents, including situations to watch out for...
Response Recommendations
The Response Recommendation fields include isolation and evacuation distances, as well as recommendations for firefighting, non-fire response, protective clothing, and first aid. The information in CAMEO Chemicals comes from a variety of data sources.
Isolation and Evacuation
Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:
IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.
SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.
FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2020)
Firefighting
Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:
SMALL FIRE: Dry chemical, CO2 or water spray.
LARGE FIRE: Dry chemical, CO2, alcohol-resistant foam or water spray. If it can be done safely, move undamaged containers away from the area around the fire. Dike runoff from fire control for later disposal.
FIRE INVOLVING TANKS OR CAR/TRAILER LOADS: Fight fire from maximum distance or use unmanned master stream devices or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. (ERG, 2020)
Non-Fire Response
Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:
ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2020)
Protective Clothing
Excerpt from NIOSH Pocket Guide for Furfuryl alcoholexternal link:
Skin: PREVENT SKIN CONTACT - Wear appropriate personal protective clothing to prevent skin contact.
Eyes: PREVENT EYE CONTACT - Wear appropriate eye protection to prevent eye contact.
Wash skin: WHEN CONTAMINATED - The worker should immediately wash the skin when it becomes contaminated.
Remove: WHEN WET OR CONTAMINATED - Work clothing that becomes wet or significantly contaminated should be removed and replaced.
Change: No recommendation is made specifying the need for the worker to change clothing after the workshift.
Provide: QUICK DRENCH - Facilities for quickly drenching the body should be provided within the immediate work area for emergency use where there is a possibility of exposure. [Note: It is intended that these facilities provide a sufficient quantity or flow of water to quickly remove the substance from any body areas likely to be exposed. The actual determination of what constitutes an adequate quick drench facility depends on the specific circumstances. In certain instances, a deluge shower should be readily available, whereas in others, the availability of water from a sink or hose could be considered adequate.] (NIOSH, 2022)
DuPont Tychem® Suit Fabrics
No information available.
First Aid
EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.
SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas.
INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.
INGESTION: If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Generally, the induction of vomiting is NOT recommended outside of a physician's care due to the risk of aspirating the chemical into the victim's lungs. However, if the victim is conscious and not convulsing and if medical help is not readily available, consider the risk of inducing vomiting because of the high toxicity of the chemical ingested. Ipecac syrup or salt water may be used in such an emergency. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)
Physical Properties
The Physical Property fields include properties such as vapor pressure and boiling point, as well as explosive limits and toxic exposure thresholds The information in CAMEO Chemicals comes from a variety of data sources.
Chemical Formula:
• C5H6O2
Flash Point: 167°F (NTP, 1992)
Lower Explosive Limit (LEL): 1.8 % (NTP, 1992)
Upper Explosive Limit (UEL): 16.3 % (NTP, 1992)
Autoignition Temperature: 736°F (USCG, 1999)
Melting Point: -24°F (NTP, 1992)
Vapor Pressure: 0.4 mmHg at 68°F ; 1 mmHg at 89.2°F (NTP, 1992)
Vapor Density (Relative to Air): 3.4 (NTP, 1992)
Specific Gravity: 1.13 at 68°F (USCG, 1999)
Boiling Point: 338°F at 760 mmHg (NTP, 1992)
Molecular Weight: 98.1 (NTP, 1992)
Water Solubility: greater than or equal to 100 mg/mL at 73°F (NTP, 1992)
Ionization Energy/Potential: data unavailable
IDLH: 75 ppm (NIOSH, 2022)
AEGLs (Acute Exposure Guideline Levels)
No AEGL information available.
ERPGs (Emergency Response Planning Guidelines)
No ERPG information available.
PACs (Protective Action Criteria)
Chemical PAC-1 PAC-2 PAC-3
Furfuryl alcohol (98-00-0) 15 ppm 42 ppm 250 ppm LEL = 18000 ppm
(DOE, 2018)
Regulatory Information
The Regulatory Information fields include information from the U.S. Environmental Protection Agency's Title III Consolidated List of Lists, the U.S. Cybersecurity and Infrastructure Security Agency's Chemical Facility Anti-Terrorism Standards, and the U.S. Occupational Safety and Health Administration's Process Safety Management of Highly Hazardous Chemicals Standard List (see more about these data sources).
EPA Consolidated List of Lists
No regulatory information available.
CISA Chemical Facility Anti-Terrorism Standards (CFATS)
No regulatory information available.
OSHA Process Safety Management (PSM) Standard List
No regulatory information available.
Alternate Chemical Names
This section provides a listing of alternate names for this chemical, including trade names and synonyms.
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"rps_doc_frac_chars_dupe_5grams": 0.11992379277944565,
"rps_doc_frac_chars_dupe_6grams": 0.11591296643018723,
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"rps_doc_books_importance": -900.5332641601562,
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"rps_doc_openwebtext_importance": -529.7098999023438,
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"rps_doc_wikipedia_importance": -433.5013427734375,
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"fasttext": {
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}
|
{
"free_decimal_correspondence": {
"primary": {
"code": "547.8",
"labels": {
"level_1": "Science and Natural history",
"level_2": "Chemistry",
"level_3": "Chemistry, Organic"
}
},
"secondary": {
"code": "614.2",
"labels": {
"level_1": "Industrial arts, Technology, and Engineering",
"level_2": "Medicine",
"level_3": "Public health"
}
}
},
"bloom_cognitive_process": {
"primary": {
"code": "2",
"label": "Understand"
},
"secondary": {
"code": "3",
"label": "Apply"
}
},
"bloom_knowledge_domain": {
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"label": "Factual"
},
"secondary": {
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},
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},
"extraction_artifacts": {
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},
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"code": "3",
"label": "Irrelevant Content"
}
},
"missing_content": {
"primary": {
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"label": "No missing content"
},
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},
"document_type_v2": {
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"label": "Documentation"
},
"secondary": {
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}
},
"reasoning_depth": {
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"label": "Basic Reasoning"
},
"secondary": {
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"label": "Intermediate Reasoning"
}
},
"technical_correctness": {
"primary": {
"code": "4",
"label": "Highly Correct"
},
"secondary": {
"code": "3",
"label": "Mostly Correct"
}
},
"education_level": {
"primary": {
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"label": "Graduate/Expert Level"
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}
}
}
|
e5c75945c3bd979b2d86e7e39a4af05f
|
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