What is the difference between an allergy and a sensitivity
A physician will consider patient history and act out a thorough physical examination if a person reports having hay-fever-like symptoms. If necessary, the physician will do an allergy test. According to the Mayo Clinic, people can get a skin-prick test, in which doctors prick the skin on a person’s arm or upper back with diverse substances to see if any cause an allergic reaction, such as a raised bump called a hive. [7 Strange Signs You’re Having an Allergic Reaction]
Blood tests for allergies are also available. This test rates the immune system’s response to a specific allergen by measuring the quantity of allergy-causing antibodies in the bloodstream, according to the Mayo Clinic.
The symptoms of allergic rhinitis may at first feel love those of a freezing.
But unlike a freezing that may incubate before causing discomfort, symptoms of allergies generally appear almost as soon as a person encounters an allergen, such as pollen or mold.
Symptoms include itchy eyes, ears, nose or throat, sneezing, irritability, nasal congestion and hoarseness. People may also experience cough, postnasal drip, sinus pressure or headaches, decreased sense of smell, snoring, sleep apnea, fatigue and asthma, Josephson said. [Oral Allergy Syndrome: 6 Ways to Avoid an Itchy, Tingling Mouth]
Many of these symptoms are the immune system’s overreaction as it attempts to protect the vital and sensitive respiratory system from exterior invaders.
The antibodies produced by the body hold the foreign invaders out, but also cause the symptoms characteristic of allergic responses.
People can develop hay fever at any age, but most people are diagnosed with the disorder in childhood or early adulthood, according to the Mayo Clinic.
Symptoms typically become less severe as people age.
Often, children may first experience food allergies and eczema, or itchy skin, before developing hay fever, Josephson said. «This then worsens over the years, and patients then develop allergies to indoor allergens love dust and animals, or seasonal rhinitis, love ragweed, grass pollen, molds and tree pollen.»
Hay fever can also lead to other medical conditions. People who are allergic to weeds are more likely to get other allergies and develop asthma as they age, Josephson said.
But those who get immunotherapy, such as allergy shots that assist people’s bodies get used to allergens, are less likely to develop asthma, he said.
Hay fever treatments
Dr. Sarita Patil, an allergist with Massachusetts General Hospital’s Allergy Associates in Boston, talked to Live Science about strategies for outdoor lovers with seasonal allergies.
Patil suggested figuring out exactly what type of pollen you’re allergic to, and then avoiding planning outdoor activities during peak pollinating times in the months when those plants are in bloom.
Numerous grasses, for example, typically pollinate in tardy spring and early summer and release most of their spores in the afternoon and early evening.
Her other strategies: Be capable to identify the pollen perpetrator by sight; monitor pollen counts before scheduling outdoor time; go exterior at a time of day when the plants that make you go achoo are not pollinating; and wear protective gear love sunglasses, among other tips. [7 Strategies for Outdoor Lovers with Seasonal Allergies]
Allergy sufferers may also select to combat symptoms with medication designed to shut below or trick the immune sensitivity in the body.
Whether over-the-counter or prescription, most allergy pills work by releasing chemicals into the body that bind naturally to histamine — the protein that reacts to the allergen and causes an immune response — negating the protein’s effect.
Other allergy remedies attack the symptoms at the source. Nasal sprays contain athletic ingredients that decongest by soothing irritated blood vessels in the nose, while eye drops both moisturize and reduce inflammation.
Doctors may also prescribe allergy shots, Josephson said.
For kids, allergy medications are tricky. A 2017 nationally representative poll of parents with kids between ages 6 and 12 found that 21% of parents said they had trouble figuring out the correct dose of allergy meds for their child; 15% of parents gave a kid an adult form of the allergy medicine, and 33% of these parents also gave their kid the adult dose of that medicine.
Doctors may also recommend allergy shots, a neti pot that can rinse the sinuses, or a Grossan Hydropulse — an irrigating system that cleans the nose of pollens, infection and environmental irritants, Josephson said.
Alternative and holistic options, along with acupuncture, may also assist people with hay fever, Josephson said.
People can also avoid pollen by keeping their windows closed in the spring, and by using air purifiers and air conditioners at home.
Probiotics may also be helpful in stopping those itchy eyes and runny noses. A 2015 review published in the journal International Forum of Allergy and Rhinology found that people who suffer from hay fever may benefit from using probiotics, or «good bacteria,» thought to promote a healthy gut. Although the jury is still out on whether probiotics are an effective treatment for seasonal allergies, the researchers noted that these gut bacteria could hold the body’s immune system from flaring up in response to allergens — something that could reduce allergy symptoms.
[5 Myths About Probiotics]
This article was updated on April 30, 2019, by Live Science Contributor Rachel Ross.
Today we are increasingly hearing terms such as gluten intolerance, wheat allergy and coeliac disease. On top of this, the words wheat and gluten are often used interchangeably too, even though there is a extremely clear difference between the two substances. So what do they actually mean and how are they different?
Gluten is a component of wheat and is also a protein that is found in some other grains too, including spelt, barley and rye. It’s also what gives yeast-based dough its elasticity.
Because gluten is found in a variety of grains, people who react to gluten (including those with coeliac disease, which is actually an autoimmune response triggered by gluten, as we’ll see below) need to avoid not only wheat, but also other gluten-containing grains and any foods that contain them.
A reaction to wheat can be completely diverse from a reaction to gluten. In fact, those with a true allergy to wheat are often not reacting to the gluten, but to some other part of the plant.
Researchers own actually identified 27 diverse potential wheat allergens (1), of which gluten is one type. Albumin and globulin proteins may be particularly common triggers (2).
Let’s glance more closely at the difference between wheat allergy, coeliac disease and gluten intolerance.
«Gluten-Free» and «Wheat-Free» Foods
Now let’s glance at why understanding the difference between these two terms is significant, depending on which of the above conditions/symptoms you may have.
‘Wheat-free’ foods are free from any components of wheat, including other proteins that people with a wheat allergy can react to. But foods that are just labelled ‘wheat-free’ may still contain other gluten-containing grains or substances derived from them, and are not necessarily gluten-free.
‘Gluten-free’ foods own to be free of gluten from any of the gluten-containing grains (more accurately, they own to contain less than 20 parts per million of gluten – a extremely tiny amount).
Once again, these grains include rye, barley and spelt as well as wheat. Oats can also contain little amounts of gluten via contamination from other grains. Therefore oats also need to be avoided on a gluten-free diet, unless they are specifically labelled ‘gluten-free’, indicating that the oats own been processed in facilities that eliminate risk of contamination with gluten.
However, ‘gluten-free’ doesn’t necessarily mean the food is free from other wheat components.
So if you own a wheat allergy and you’re buying packaged or processed foods, it can be wise to glance specifically for ‘wheat-free’ and not just gluten-free – or thoroughly check the ingredients list to make certain the food you’re buying doesn’t contain other wheat components.
A true wheat allergy should not be confused with gluten intolerance or coeliac disease. A food allergy is caused by the immune system producing IgE antibodies to a specific food protein or proteins. Symptoms tend to happen fairly soon after eating the food, from seconds up to two hours.
When the food protein is ingested, it can trigger a range of allergy symptoms from mild (such as a rash, itching, or sneezing) to severe (trouble breathing, wheezing, anaphylaxis). Wheat allergy symptoms may also include abdominal pain, diarrhoea and other digestive disturbances. A true food allergy such as this can be potentially fatal.
Allergy to wheat is thought to be more common in children, who may ‘grow out of’ it before reaching adulthood. But it can also develop in adults.
Those with a wheat allergy may still be capable to consume other gluten-containing grains; although in some cases these will need to be avoided too.
Sotkovský P et al. A new approach to the isolation and characterization of wheat flour allergens. Clin Exp Allergy. 2011 Jul;41(7):1031-43.
2. Mittag D et al. Immunoglobulin E-reactivity of wheat-allergic subjects (baker’s asthma, food allergy, wheat-dependent, exercise-induced anaphylaxis) to wheat protein fractions with diverse solubility and digestibility. Mol Nutr Food Res. 2004 Oct;48(5):380-9.
What´s the difference between food intolerance and food allergy?
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DIFFERENCES BETWEEN FOOD INTOLERANCE AND FOOD ALLERGY
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A gluten-free diet may also be beneficial for other conditions. These include inflammatory bowel diseases such as Crohn’s disease and other digestive conditions or symptoms such as irritable bowel syndrome or excessive bloating and gas.
There’s increasing evidence that following a gluten-free diet may be beneficial for some people with other types of autoimmune disease too.
Reading The Ingredients
If a label on a packaged food doesn’t explicitly state ‘gluten-free’ or ‘wheat-free’ then you may need to glance through the ingredients to check. But it’s not enough to avoid anything that lists the expression ‘wheat’ (or when looking for gluten-free products, the words ‘wheat’, ‘barley’, ‘rye’ or ‘spelt’). Products such as gravies, soya sauce, salad dressings and casseroles can contain derivatives of wheat or other gluten grains that are harder to identify and can also be listed under diverse names.
The following should every be avoided: durum wheat, spelt, kamut, couscous, bran, wheat bran, wheat germ, farina, rusk, semolina, wheat starch, vegetable starch, vegetable gum, malt extracts, vegetable protein, cereal filler, cereal binder and cereal protein.
Alternatives To Wheat and Gluten Grains and Flours
The following are alternatives that are both wheat and gluten-free: maize (corn), corn flour, potato, potato flour, rice flour, soya beans, soya flour, buckwheat, millet, tapioca, quinoa, amaranth, sorghum, arrowroot, chickpea (gram) flour and lentil flour.
Chickpeas, beans and lentils are excellent fillers and can be added to soups and gravies, while wheat-free pasta and rice noodles are a grand alternative to standard wheat pasta.
Many people who do not own coeliac disease can still experience uncomfortable symptoms when they consume gluten.
This is known as non-coeliac gluten sensitivity or gluten intolerance.
Researchers continue to debate just how numerous people are truly sensitive to gluten, but the number has been estimated to be approximately 6% of the population.
As some of the symptoms of coeliac disease, gluten intolerance and even wheat allergy can overlap, it is significant to be tested by your doctor to determine which of these may be causing your symptoms.
According to the Coeliac Society (www.coeliac.org.uk), coeliac disease is a well-defined, serious illness where the immune system attacks the body’s own tissue, when gluten is eaten.
This causes damage to the lining of the little intestine and means that the body cannot properly absorb nutrients from ingested food. Generally diagnosed by a gastroenterologist, it is a digestive disease that can cause serious complications, including malnutrition and intestinal damage, if left untreated. Coeliac disease is not a food allergy or intolerance; it is an autoimmune disease where the sufferer must completely avoid gluten from every grains – not just wheat.
The Coeliac Society states that one in 100 people in the UK is thought to own coeliac disease, but only 24 per cent of these people are diagnosed.
This leaves almost half a million people in the UK who could own coeliac disease but aren’t yet diagnosed (www.coeliac.org.uk/coeliac-disease/myths-about-coeliac-disease).
Understanding the difference between wheat and gluten can assist avoid any unnecessary symptoms that may be brought on by ingesting the incorrect foods. Confusing wheat and gluten may own less of an impact on people with non-coeliac gluten sensitivity/intolerance, or wheat sensitivity/intolerance, but it can own more serious consequences for those with a true wheat allergy and coeliac disease.
Clearspring’s Range of Gluten-Free Products
The Clearspring promise is to provide great-tasting, yummy foods that support excellent health and provide optimum nutrition.
We desire to give our customers who need to avoid gluten or wheat the chance to own great-tasting food and to be capable to cook with confidence. This has inspired us to launch a range of gluten-free ingredients, from meal staples such as soya protein, rice and vegetable pastas to seasonings, sauces and garnishes. These are tasty, nutritious alternatives perfect for those on a gluten-free diet but equally yummy for the whole family.
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Frequently Asked Questions about Food Protein-Induced Enterocolitis Syndrome (FPIES)
What Does IgE vs Cell Mediated Mean?
IgE stands for Immunoglobulin E.
It is a type of antibody, formed to protect the body from infection, that functions in allergic reactions. IgE-mediated reactions are considered immediate hypersensitivity immune system reactions, while cell mediated reactions are considered delayed hypersensitivity. Antibodies are not involved in cell mediated reactions. For the purpose of understanding FPIES, you can disregard every you know about IgE-mediated reactions.
What is Shock and What are the Symptoms?
Shock is a life-threatening condition.
Shock may develop as the result of sudden illness, injury, or bleeding. When the body cannot get enough blood to the vital organs, it goes into shock.
Signs of shock include:
Weakness, dizziness, and fainting.
Cool, pale, clammy skin.
Weak, quick pulse.
Shallow, quick breathing.
Low blood pressure.
Extreme thirst, nausea, or vomiting.
Confusion or anxiety.
How Do You Care for a Kid With FPIES?
Treatment varies, depending on the patient and his/her specific reactions. Often, infants who own reacted to both dairy and soy formulas will be placed on hypoallergenic or elemental formula.
Some children do well breastfeeding. Other children who own fewer triggers may just strictly avoid the offending food(s).
New foods are generally introduced extremely slowly, one food at a time, for an extended period of time per food. Some doctors recommend trialing a single food for up to three weeks before introducing another.
Because it’s a rare, but serious condition, in the event of an emergency, it is vital to get the correct treatment. Some doctors provide their patients with a letter containing a brief description of FPIES and its proper treatment. In the event of a reaction, this letter can be taken to the ER with the child.
What Does FPIES Stand For?
FPIES is Food Protein-Induced Enterocolitis Syndrome.
It is commonly pronounced «F-Pies», as in «apple pies», though some physicians may refer to it as FIES (pronounced «fees», considering food-protein as one word). Enterocolitis is inflammation involving both the little intestine and the colon (large intestine).
What is a Typical FPIES Reaction?
As with every things, each kid is diverse, and the range, severity and duration of symptoms may vary from reaction to reaction. Unlike traditional IgE-mediated allergies, FPIES reactions do not manifest with itching, hives, swelling, coughing or wheezing, etc.
Symptoms typically only involve the gastrointestinal system, and other body organs are not involved. FPIES reactions almost always start with delayed onset vomiting (usually two hours after ingestion, sometimes as tardy as eight hours after). Symptoms can range from mild (an increase in reflux and several days of runny stools) to life threatening (shock). In severe cases, after repeatedly vomiting, children often start vomiting bile. Commonly, diarrhea follows and can final up to several days. In the worst reactions (about 20% of the time), the kid has such severe vomiting and diarrhea that s/he rapidly becomes seriously dehydrated and may go into shock.
How is FPIES Diagnosed?
FPIES is hard to diagnose, unless the reaction has happened more than once, as it is diagnosed by symptom presentation.
Typically, foods that trigger FPIES reactions are negative with standard skin and blood allergy tests (SPT, RAST) because they glance for IgE-mediated responses. However, as stated before, FPIES is not IgE-mediated.
Atopy patch testing (APT) is being studied for its effectiveness in diagnosing FPIES, as well as predicting if the problem food is no longer a trigger. Thus, the outcome of APT may determine if the kid is a potential candidate for an oral food challenge (OFC).
APT involves placing the trigger food in a metal cap, which is left on the skin for 48 hours. The skin is then watched for symptoms in the following days after removal. Please consult your child’s doctor to discuss if APT is indicated in your situation.
How Do You Treat an FPIES Reaction?
Always follow your doctor’s emergency plan pertaining to your specific situation. Rapid dehydration and shock are medical emergencies. If your kid is experiencing symptoms of FPIES or shock, immediately contact your local emergency services (9-1-1).
If you are uncertain if your kid is in need of emergency services, contact 9-1-1 or your physician for guidance. The most critical treatment during an FPIES reaction is intravenous (IV) fluids, because of the risk and prevalence of dehydration. Children experiencing more severe symptoms may also need steroids and in-hospital monitoring. Mild reactions may be capable to be treated at home with oral electrolyte re-hydration (e.g., Pedialyte®).
When Do FPIES Reactions Occur?
FPIES reactions often show up in the first weeks or months of life, or at an older age for the exclusively breastfed kid. Reactions generally happen upon introducing first solid foods, such as baby cereals or formulas, which are typically made with dairy or soy.
(Infant formulas are considered solids for FPIES purposes.) While a kid may own allergies and intolerances to food proteins they are exposed to through breastmilk, FPIES reactions generally don’t happen from breastmilk, regardless of the mother’s diet. An FPIES reaction typically takes put when the kid has directly ingested the trigger food(s).
Does FPIES Require Epinephrine?
Not generally, because epinephrine reverses IgE-mediated symptoms, and FPIES is not IgE-mediated.
Based on the patient’s history, some doctors might prescribe epinephrine to reverse specific symptoms of shock (e.g., low blood pressure). However, this is only prescribed in specific cases.
How Do I know If My Kid Has Outgrown FPIES?
Together with your child’s doctor, you should determine if/when it is likely that your kid may own outgrown any triggers. Obviously, determining if a kid has outgrown a trigger is something that needs to be evaluated on a food-by-food basis.
As stated earlier, APT testing may be an option to assess oral challenge readiness. Another factor for you and your doctor to consider is if your kid would physically be capable to handle a possible failed challenge.
When the time comes to orally challenge an FPIES trigger, most doctors familiar with FPIES will desire to schedule an in-office food challenge. Some doctors (especially those not practicing in a hospital clinic setting) may select to challenge in the hospital, with an IV already in put, in case of emergency.
Each doctor may own his or her own protocol, but an FPIES trigger is something you should definitely NOT challenge without discussing thoroughly with your doctor.
Be aware that if a kid passes the in-office portion of the challenge, it does not mean this food is automatically guaranteed «safe.» If a child’s delay in reaction is fairly short, a kid may fail an FPIES food challenge while still at the office/hospital. For those with longer reaction times, it may not be until later that day that symptoms manifest.
Some may react up to three days later. Delay times may vary by food as well. If a kid has FPIES to multiple foods, one food may trigger symptoms within four hours; a diverse food may not trigger symptoms until six or eight hours after ingestion.
Is FPIES A Lifelong Condition?
Typically, no. Numerous children outgrow FPIES by about age three. Note, however, that the time varies per individual and the offending food, so statistics are a guide, but not an absolute.
In one study, 100% of children with FPIES reactions to barley had outgrown and were tolerating barley by age three. However, only 40% of those with FPIES to rice, and 60% to dairy tolerated it by the same age.
What is FPIES?
FPIES is a non-IgE mediated immune reaction in the gastrointestinal system to one or more specific foods, commonly characterized by profuse vomiting and diarrhea.
FPIES is presumed to be cell mediated. Poor growth may happen with continual ingestion. Upon removing the problem food(s), every FPIES symptoms subside. (Note: Having FPIES does not preclude one from having other allergies/intolerances with the food.) The most common FPIES triggers are cow’s milk (dairy) and soy. However, any food can cause an FPIES reaction, even those not commonly considered allergens, such as rice, oat and barley.
A kid with FPIES may experience what appears to be a severe stomach bug, but the «bug» only starts a couple hours after the offending food is given.
Numerous FPIES parents own rushed their children to the ER, limp from extreme, repeated projectile vomiting, only to be told, «It’s the stomach flu.» However, the next time they feed their children the same solids, the dramatic symptoms return.
What are Some Common FPIES Triggers?
The most common FPIES triggers are traditional first foods, such as dairy and soy. Other common triggers are rice, oat, barley, green beans, peas, sweet potatoes, squash, chicken and turkey. A reaction to one common food does not mean that every of the common foods will be an issue, but patients are often advised to proceed with caution with those foods.
Note that while the above foods are the most prevalent, they are not exclusive triggers. Any food has the potential to trigger an FPIES reaction. Even trace amounts can cause a reaction.
How is FPIES Diverse From MSPI, MSPIES, MPIES, Etc.?
MPIES (milk-protein induced enterocolitis syndrome) is FPIES to cow’s milk only. MSPIES (milk- and soy-protein induced enterocolitis syndrome) is FPIES to milk and soy. Some doctors do create these subdivisions, while others declare that milk and soy are simply the two most common FPIES triggers and give the diagnosis of «FPIES to milk and/or soy.»
MSPI is milk and soy protein intolerance.
Symptoms are those of allergic colitis and can include colic, vomiting, diarrhea and blood in stools. These reactions are not as severe or immediate as an FPIES reaction.
Fogg MI, Brown-Whitehorn TA, Pawlowski NA, Spergel JM. (2006). Atopy Patch Test for the Diagnosis of Food Protein-Induced Enterocolitis Syndrome. Pediatric Allergy and Immunology 17: 351–355. Retrieved on December 31, 2007 from http://pediatrics.aappublications.org/cgi/content/abstract/120/Supplement_3/S116.
Burks, AW. (2006). Don’t Feed Her That! Diagnosing and Managing Pediatric Food Allergy. Pediatric Basics. Gerber Products Company: 115. Retrieved on December 31, 2007 from http://www.gerber.com/content/usa/html/pages/pediatricbasics/articles/115_01-dontfeed.html.
Food Protein-Induced Enterocolitis Syndrome. (2007, April 11). Retrieved on December 31, 2007 from http://allergies.about.com/od/foodallergies/a/fpies.htm.
Sicherer, SH. (2005). Food Protein-Induced Enterocolitis Syndrome: Case Presentations and Management Lessons. Journal of Allergy and Clinical Immunology Vol. 115, 1:149-156. Retrieved on December 31, 2007 from http://www.jacionline.org/article/PIIS0091674904024881/fulltext.
Nowak-Wegrzyn, A., Sampson, HA, Wood, RA, Sicherer, SH.
MD, Robert A. Wood, MD and Scott H. Sicherer, MD. (2003). Food Protein-Induced Enterocolitis Syndrome Caused by Solid Food Proteins. Pediatrics. Vol. 111. 4: 829-835. Retrieved on December 31, 2007 from http://pediatrics.aappublications.org/cgi/content/full/111/4/829#T1.
Nocerino, A., Guandalini, S. (2006, April 11). Protein Intolerance. Retrieved on December 31, 2007 from http://www.emedicine.com/ped/topic1908.htm. WebMD Medical Reference from Healthwise. (2006, May 31). Shock, Topic Overview. Retrieved on December 31, 2007 from http://www.webmd.com/a-to-z-guides/shock-topic-overview.
American Academy of Allergy, Asthma and Immunology.
(2007). Tips to Remember: What is an Allergic Reaction? Retrieved on December 31, 2007 from http://www.aaaai.org/patients/publicedmat/tips/whatisallergicreaction.stm.
Sicherer, SH. (2006). Understanding and Managing Your Child’s Food Allergies. A Johns Hopkins Press Health Book. 336.
Medical Review February 2008.
What’s really behind ‘gluten sensitivity’?
By Kelly Servick
The patients weren’t crazy—Knut Lundin was certain of that. But their ailment was a mystery. They were convinced gluten was making them ill. Yet they didn’t own celiac disease, an autoimmune reaction to that often-villainized tangle of proteins in wheat, barley, and rye.
And they tested negative for a wheat allergy. They occupied a medical no man’s land.
About a decade ago, gastroenterologists love Lundin, based at the University of Oslo, came across more and more of those enigmatic cases. «I worked with celiac disease and gluten for so numerous years,» he says, «and then came this wave.» Gluten-free choices began appearing on restaurant menus and creeping onto grocery store shelves. By 2014, in the United States alone, an estimated 3 million people without celiac disease had sworn off gluten.
It was simple to assume that people claiming to be «gluten sensitive» had just been roped into a food fad.
«Generally, the reaction of the gastroenterologist [was] to tell, ‘You don’t own celiac disease or wheat allergy. Goodbye,’» says Armin Alaedini, an immunologist at Columbia University. «A lot of people thought this is perhaps due to some other [food] sensitivity, or it’s in people’s heads.»
But a little community of researchers started searching for a link between wheat components and patients’ symptoms—commonly abdominal pain, bloating, and diarrhea, and sometimes headaches, fatigue, rashes, and joint pain.
That wheat really can make nonceliac patients ill is now widely accepted. But that’s about as far as the agreement goes.
As data trickle in, entrenched camps own emerged. Some researchers are convinced that numerous patients own an immune reaction to gluten or another substance in wheat—a nebulous illness sometimes called nonceliac gluten sensitivity (NCGS).
Others believe most patients are actually reacting to an excess of poorly absorbed carbohydrates present in wheat and numerous other foods. Those carbohydrates—called FODMAPs, for fermentable oligosaccharides, disaccharides, monosaccharides, and polyols—can cause bloating when they ferment in the gut.
If FODMAPs are the primary culprit, thousands of people may be on gluten-free diets with the support of their doctors and dietitians but without excellent reason.
Those competing theories were on display in a session on wheat sensitivity at a celiac disease symposium held at Columbia in March. In back-to-back talks, Lundin made the case for FODMAPs, and Alaedini for an immune reaction. But in an irony that underscores how muddled the field has become, both researchers started their quests believing something completely different.
Known wheat-related illnesses own clear mechanisms and markers. People with celiac disease are genetically predisposed to launch a self-destructive immune response when a component of gluten called gliadin penetrates their intestinal lining and sets off inflammatory cells in the tissue under.
People with a wheat allergy reply to wheat proteins by churning out a class of antibodies called immunoglobulin E that can set off vomiting, itching, and shortness of breath. The puzzle, for both doctors and researchers, is patients who lack both the telltale antibodies and the visible damage to their intestines but who feel genuine relief when they cut out gluten-containing food.
Some doctors own begun to approve and even recommend a gluten-free diet.
«Ultimately, we’re here not to do science, but to improve quality of life,» says Alessio Fasano, a pediatric gastroenterologist at Massachusetts General Hospital in Boston who has studied NCGS and written a book on living gluten-free. «If I own to throw bones on the ground and glance at the moon to make somebody better, even if I don’t understand what that means, I’ll do it.»
Like numerous doctors, Lundin believed that (fad dieters and superstitious eaters aside) some patients own a genuine wheat-related ailment. His group helped dispel the notion that NCGS was purely psychosomatic.
They surveyed patients for unusual levels of psychological distress that might express itself as physical symptoms. But the surveys showed no differences between those patients and people with celiac disease, the team reported in 2012. As Lundin bluntly puts it: «We know they are not crazy.»
Still, skeptics worried that the field had seized on gluten with shaky evidence that it was the culprit. After every, nobody eats gluten in isolation. «If we did not know about the specific role of gluten in celiac disease, we would never own thought gluten was responsible for [NCGS],» says Stefano Guandalini, a pediatric gastroenterologist at the University of Chicago Medical Middle in Illinois.
«Why blame gluten?»
Defenders of NCGS generally acknowledge that other components of wheat might contribute to symptoms. In 2012, a group of proteins in wheat, rye, and barley called amylase trypsin inhibitors emerged as a potential offender, for example, after a team led by biochemist Detlef Schuppan of Johannes Gutenberg University Mainz in Germany (then at Harvard Medical School in Boston) reported that those proteins can provoke immune cells.
But without biological markers to identify people with NCGS, researchers own relied on self-reported symptoms measured through a «gluten challenge»: Patients rate how they feel before and after cutting out gluten.
Then doctors reintroduce gluten or a placebo—ideally disguised in indistinguishable pills or snacks—to see whether the symptoms tick back up.
Alaedini has recently hit on a more objective set of possible biological markers—much to his own surprise. «I entered this completely as a skeptic,» he says. Over his career, he has gravitated toward studying spectrum disorders, in which diverse symptoms own yet to be united under a clear biological cause—and where public misinformation abounds. His team published a study in 2013, for example, that debunked the favorite suggestion that children with autism had high rates of Lyme disease.
«I do studies [where] there is a void,» he says.
In NCGS, Alaedini saw another poorly defined spectrum disorder. He did accept that patients without celiac disease might somehow be sensitive to wheat, on the basis of several trials that measured symptoms after a blinded challenge. But he was not convinced by previous studies claiming that NCGS patients were more likely than other people to own certain antibodies to gliadin.
Numerous of those studies lacked a healthy control group, he says, and relied on commercial antibody kits that gave murky and inconsistent readings.
In 2012, he contacted researchers at the University of Bologna in Italy to obtain blood samples from 80 patients their team had identified as gluten sensitive on the basis of a gluten challenge. He wanted to test the samples for signs of a unique immune response—a set of signaling molecules diverse from those in the blood of healthy volunteers and celiac patients.
He wasn’t optimistic. «I thought if we were going to see something, love with a lot of spectrum conditions that I own looked at, we would see little differences.»
The results shocked him. Compared with both healthy people and those with celiac, these patients had significantly higher levels of a certain class of antibodies against gluten that propose a short-lived, systemic immune response. That didn’t mean gluten itself was causing disease, but the finding hinted that the barrier of those patients’ intestines might be faulty, allowing partially digested gluten to get out of the gut and interact with immune cells in the blood.
Other elements—such as immune response–provoking bacteria—also might be escaping. Certain enough, the team found elevated levels of two proteins that indicate an inflammatory response to bacteria. And when 20 of the same patients spent 6 months on a gluten-free diet, their blood levels of those markers declined.
For Alaedini, the beginnings of a mechanism emerged: Some still-unidentified wheat component prompts the intestinal lining to become more permeable.
(An imbalance in gut microbes might be a predisposing factor.) Components of bacteria then seem to sneak past immune cells in the underlying intestinal tissue and make their way to the bloodstream and liver, prompting inflammation.
«This is a genuine condition, and there can be objective, biological markers for it,» Alaedini says. «That study changed a lot of minds, including my own.»
The study also impressed Guandalini, a longtime skeptic about the role of gluten.
It «opens the way to finally reach an identifiable marker for this condition,» he says.
But others see the immune-response explanation as a red herring. To them, the primary villain is FODMAPs. The term, coined by gastroenterologist Peter Gibson at Monash University in Melbourne, Australia, and his team, encompasses a smorgasbord of common foods. Onions and garlic; legumes; milk and yogurt; and fruits including apples, cherries, and mangoes are every high in FODMAPs. So is wheat: Carbs in wheat called fructans can account for as much as half of a person’s FODMAP intake, dietitians in Gibson’s group own estimated. The team found that those compounds ferment in the gut to cause symptoms of irritable bowel syndrome, such as abdominal pain, bloating, and gas.
Gibson has endless been skeptical of studies implicating gluten in such symptoms, arguing that those findings are hopelessly clouded by the nocebo effect, in which the mere expectation of swallowing the dreaded ingredient worsens symptoms.
His team found that most patients couldn’t reliably distinguish pure gluten from a placebo in a blinded test. He believes that numerous people feel better after eliminating wheat not because they own calmed some intricate immune reaction, but because they’ve reduced their intake of FODMAPs.
Lundin, who was firmly in the immune-reaction camp, didn’t believe that FODMAPs could explain away every his patients. «I wanted to show that Peter was wrong,» he says. During a 2-week sabbatical in the Monash lab, he found some quinoa-based snack bars designed to disguise the taste and texture of ingredients. «I said, ‘We’re going to take those muesli bars and we’re going to do the perfect study.’»
His team recruited 59 people on self-instituted gluten-free diets and randomized them to get one of three indistinguishable snack bars, containing isolated gluten, isolated FODMAP (fructan), or neither.
After eating one type of bar daily for a week, they reported any symptoms. Then they waited for symptoms to resolve and started on a diverse bar until they had tested every three.
Before analyzing patient responses, Lundin was confident that gluten would cause the worst symptoms. But when the study’s blind was lifted, only the FODMAP symptoms even cleared the bar for statistical significance. Twenty-four of the 59 patients had their highest symptom scores after a week of the fructan-laced bars. Twenty-two responded most to the placebo, and just 13 to gluten, Lundin and his collaborators—who included Gibson—reported final November in the journal Gastroenterology. Lundin now believes FODMAPs explain the symptoms in most wheat-avoiding patients.
«My main reason for doing that study was to discover out a excellent method of finding gluten-sensitive individuals,» he says. «And there were none. And that was fairly amazing.»
At the Columbia meeting, Alaedini and Lundin went head to head in consecutive talks titled «It’s the Wheat» and «It’s FODMAPS.» Each has a list of criticisms of the other’s study. Alaedini contends that by recruiting broadly from the gluten-free population, instead of finding patients who reacted to wheat in a challenge, Lundin likely failed to include people with a true wheat sensitivity.
Extremely few of Lundin’s subjects reported symptoms exterior the intestines, such as rash or fatigue, that might point to a widespread immune condition, Alaedini says. And he notes that the increase in patients’ symptoms in response to the FODMAP snacks was just barely statistically significant.
Lundin, meanwhile, points out that the patients in Alaedini’s study didn’t go through a blinded challenge to check whether the immune markers he identified really spiked in response to wheat or gluten. The markers may not be specific to people with a wheat sensitivity, Lundin says.
Despite the adversarial titles of their talks, the two researchers discover a lot of common ground.
Alaedini agrees that FODMAPs explain some of the wheat-avoidance phenomenon. And Lundin acknowledges that some little population may really own an immune reaction to gluten or another component of wheat, though he sees no excellent way to discover them.
After the meeting, Elena Verdù, a gastroenterologist at McMaster University in Hamilton, Canada, puzzled over the polarization of the field. «I don’t understand why there is this need to be so dogmatic about ‘it is this, it is not that,’» she says.
She worries that the scientific confusion breeds skepticism toward people who avoid gluten for medical reasons.
When she dines with celiac patients, she says, waiters sometimes meet requests for gluten-free food with smirks and questions. Meanwhile, the conflicting messages may send nonceliac patients below a food-avoidance rabbit hole. «Patients are withdrawing gluten first, then lactose, and then FODMAPs—and then they are on a really, really poor diet,» she says.
But Verdù believes careful research will ultimately break through the superstitions.
She is president of the North American Society for the Study of Celiac Disease, which this year awarded its first grant to study nonceliac wheat sensitivity. She’s hopeful that the search for biomarkers love those Alaedini has proposed will show that inside the monolith of gluten avoidance lurk multiple, nuanced conditions. «It will be difficult,» she says, «but we are getting closer.»
The most common allergen is pollen, a powder released by trees, grasses and weeds that fertilize the seeds of neighboring plants. As plants rely on the wind to do the work for them, the pollination season sees billions of microscopic particles fill the air, and some of them finish up in people’s noses and mouths.
Spring bloomers include ash, birch, cedar, elm and maple trees, plus numerous species of grass.
Weeds pollinate in the tardy summer and drop, with ragweed being the most volatile.
The pollen that sits on brightly colored flowers is rarely responsible for hay fever because it is heavier and falls to the ground rather than becoming airborne. Bees and other insects carry flower pollen from one flower to the next without ever bothering human noses.
Mold allergies are diverse. Mold is a spore that grows on rotting logs, dead leaves and grasses. While dry-weather mold species exist, numerous types of mold thrive in moist, rainy conditions, and release their spores overnight. During both the spring and drop allergy seasons, pollen is released mainly in the morning hours and travels best on dry, warm and breezy days.
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How do scientists know how much pollen is in the air?
They set a trap. The trap — generally a glass plate or rod coated with adhesive — is analyzed every few hours, and the number of particles collected is then averaged to reflect the particles that would pass through the area in any 24-hour period. That measurement is converted to pollen per cubic meter. Mold counts work much the same way.
A pollen count is an imprecise measurement, scientists confess, and an arduous one — at the analysis stage, pollen grains are counted one by one under a microscope. It is also highly time-consuming to discern between types of pollen, so they are generally bundled into one variable. Given the imprecise nature of the measurement, entire daily pollen counts are often reported simply as low, moderate or high.
The American Academy of Allergy, Asthma & Immunology provides up-to-date pollen counts for U.S.