Allergy vs. Immunity

Allergy vs. Immunity

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What is the difference between these two phenomena in our organism: allergy and immunity? Both cause producing of antibodies which struggle against antigens. Is it true, that allergy always leads to destruction of tissues and organs? If yes, why does destruction take place in case of allergy but not within immunity?

First line of wikipedia > Immune system

The immune system is a host defense system comprising many biological structures and processes within an organism that protects against disease

First line of wikipedia > Allergy

Allergies, also known as allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment.

In other words, the immune system is here to defend the organism against diseases. However, sometimes this immune system misinterprets a harmless substance and start triggering an immune response against it. Such immune response against harmless substance is called an allergy. An allergy is hence a defect of the immune system. There are other defects of the immune system though, such as autoimmune diseases.

Lasting immunity found after recovery from COVID-19

Colorized scanning electron micrograph of a cell, isolated from a patient sample, that is heavily infected with SARS-CoV-2 virus particles (red). NIAID Integrated Research Facility, Fort Detrick, Maryland

After people recover from infection with a virus, the immune system retains a memory of it. Immune cells and proteins that circulate in the body can recognize and kill the pathogen if it’s encountered again, protecting against disease and reducing illness severity.

This long-term immune protection involves several components. Antibodies—proteins that circulate in the blood—recognize foreign substances like viruses and neutralize them. Different types of T cells help recognize and kill pathogens. B cells make new antibodies when the body needs them.

All of these immune-system components have been found in people who recover from SARS-CoV-2, the virus that causes COVID-19. But the details of this immune response and how long it lasts after infection have been unclear. Scattered reports of reinfection with SARS-CoV-2 have raised concerns that the immune response to the virus might not be durable.

To better understand immune memory of SARS-CoV-2, researchers led by Drs. Daniela Weiskopf, Alessandro Sette, and Shane Crotty from the La Jolla Institute for Immunology analyzed immune cells and antibodies from almost 200 people who had been exposed to SARS-CoV-2 and recovered.

Time since infection ranged from six days after symptom onset to eight months later. More than 40 participants had been recovered for more than six months before the study began. About 50 people provided blood samples at more than one time after infection.

The research was funded in part by NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and National Cancer Institute (NCI). Results were published on January 6, 2021, in Science.

The researchers found durable immune responses in the majority of people studied. Antibodies against the spike protein of SARS-CoV-2, which the virus uses to get inside cells, were found in 98% of participants one month after symptom onset. As seen in previous studies, the number of antibodies ranged widely between individuals. But, promisingly, their levels remained fairly stable over time, declining only modestly at 6 to 8 months after infection.

Virus-specific B cells increased over time. People had more memory B cells six months after symptom onset than at one month afterwards. Although the number of these cells appeared to reach a plateau after a few months, levels didn’t decline over the period studied.

Levels of T cells for the virus also remained high after infection. Six months after symptom onset, 92% of participants had CD4+ T cells that recognized the virus. These cells help coordinate the immune response. About half the participants had CD8+ T cells, which kill cells that are infected by the virus.

As with antibodies, the numbers of different immune cell types varied substantially between individuals. Neither gender nor differences in disease severity could account for this variability. However, 95% of the people had at least 3 out of 5 immune-system components that could recognize SARS-CoV-2 up to 8 months after infection.

“Several months ago, our studies showed that natural infection induced a strong response, and this study now shows that the responses last,” Weiskopf says. “We are hopeful that a similar pattern of responses lasting over time will also emerge for the vaccine-induced responses.”


There are continuous advances in our current understanding of the immune system and how it functions to protect the body from infection. Given the complex nature of this subject, it is beyond the scope of this article to provide an in-depth review of all aspects of immunology. Rather, the purpose of this article is to provide medical students, medical residents, primary-care practitioners and other healthcare professionals with a basic introduction to the main components and function of the immune system and its role in both health and disease. This article will also serve as a backgrounder to the immunopathological disorders discussed in the remainder of this supplement.

Neanderthal DNA Gave Humans Allergies, Immunity Boost

Interbreeding of anatomically modern Homo sapiens with Neanderthals (Homo neanderthalensis) around 40,000 years ago may have left humans with gene variants responsible for the immune response, according to two studies in the American Journal of Human Genetics. This inheritance may have also left some of us more prone to allergies.

Neanderthal. Image credit: Trustees of the Natural History Museum, London.

Earlier studies have shown that 1-6% of modern Eurasian genomes were inherited from ancient hominins, such as Neanderthal or Denisovans.

The two new studies highlight the functional importance of this inheritance on Toll-like receptor (TLR) genes – TLR1, TLR6, and TLR10, which are expressed on the cell surface, where they detect and respond to components of bacteria, fungi, and parasites. These immune receptors are essential for eliciting inflammatory and anti-microbial responses and for activating an adaptive immune response.

“We found that interbreeding with archaic humans has influenced the genetic diversity in present-day genomes at three innate immunity genes belonging to the human Toll-like-receptor family,” explained Dr Janet Kelso of the Max Planck Institute for Evolutionary Anthropology, lead author of one of the studies.

“These, and other, innate immunity genes present higher levels of Neanderthal ancestry than the remainder of the coding genome,” said Dr Lluis Quintana-Murci of the Institut Pasteur, lead author of another study. “This highlights how important introgression events may have been in the evolution of the innate immunity system in humans.”

Dr Quintana-Murci and co-author set out to explore the evolution of the innate immune system over time. They relied on data available from the 1000 Genomes Project together with the genome sequences of ancient hominins.

The scientists focused on a list of 1,500 genes known to play a role in the innate immune system. They then examined patterns of genetic variation and evolutionary change in those regions relative to the rest of the genome at an unprecedented level of detail.

Finally, they estimated the timing of the changes in innate immunity and the extent to which variation in those genes had been passed down from Neanderthals.

“These investigations revealed little change over long periods of time for some innate-immunity genes, providing evidence of strong constraints,” the scientists said.

“Other genes have undergone selective sweeps in which a new variant came along and quickly rose to prominence, perhaps because of a shift in the environment or as a result of a disease epidemic. Most adaptations in protein-coding genes occurred in the last 6,000 to 13,000 years, as human populations shifted from hunting and gathering to farming.”

But the biggest surprise for the team was to find that the TLR6-TLR1-TLR10 cluster is among the genes presenting the highest Neanderthal ancestry in both Europeans and Asians.

“We show that innate immunity genes present higher Neanderthal introgression than the remainder of the coding genome. Notably, among the genes presenting the highest Neanderthal ancestry, we find the TLR6-TLR1-TLR10 cluster, which also contains functional adaptive variation in Europeans.”

Geographic distribution of the Neanderthal-like TLR haplotypes: world map showing the frequencies of Neanderthal-like core haplotypes in the 1000 Genomes dataset (upper image) and the Simons Genome Diversity Panel (lower image). On the second map, the size of each pie is proportional to the number of individuals within a population core haplotypes (III – orange IV – green non-archaic core haplotypes V, VI, VIII, IX – blue) are colored. Image credit: Michael Dannemann et al.

Dr Kelso and co-authors came to the same conclusion.

They screened present-day human genomes for evidence of extended regions with high similarity to the Neanderthal and Denisovan genomes, then examined the prevalence of those regions in people from around the world. Those analyses led them to the same TLR6-TLR1-TLR10 cluster.

“We document a cluster of three Toll-like receptors (TLR6-TLR1-TLR10) in modern humans that carries three distinct archaic haplotypes, indicating repeated introgression from archaic humans. Two of these haplotypes are most similar to the Neanderthal genome, and the third haplotype is most similar to the Denisovan genome,” they said.

Types of Immunity: Natural & Acquired | Immunology | Microbiology

Two general types of immunity are recognized – natural immunity and acquired immunity.

The word “immune” is derived from the Latin stem immuno, meaning safe, or free from. In its most general sense, the term implies a condition under which an individual is protected from disease. This does not mean, however, that one is immune to all diseases, but rather to a specific disease or group of diseases.

Immunity or disease resistance is the ability of an organism to resist the development of a disease. The study of immunity is called immunology, while the infected person with no disease is known as immune. Immune system forms the third line of defence. The most peculiar characteristic of immune system is that it can differentiate between ‘self (body’s own cells) and ‘non-self (foreign microbes).

Type # 1. Natural Immunity:

Natural immunity is an inborn capacity for resisting disease. It begins at birth and depends on genetic factors expressed as physiological, anatomical, and biochemical differences among living things. Examples of natural immunity are the lysozyme found in tears, saliva, and other body secretion, acidic pH of the gastrointestinal and vaginal tracts, and interferon produced by body cells to protect against viruses.

A race or species may inherit a resistance to a certain infectious disease. This resistance is spoken of as natural immunity.

Species Immunity:

Many of the organisms that attack humans do not attack animals. Typhoid-fever infections do not occur in animals except after massive experimental inoculations with the specific organisms. Human leprosy has never been transmitted to animals successfully. Meningitis does not occur spontaneously in animals but may be produced experimentally. Many of the animal diseases do not occur spontaneously in man.

It is not known why differences in species susceptibility exist. It may be because of differences in temperature, metabolism, diet, etc. Diseases of warm-blooded animals cannot ordinarily be transmitted to cold-blooded animals, and vice versa.

Racial Immunity:

The various races probably exhibit differences in their resistance to disease, although in many cases this may be due to differences in living conditions, to immunity acquired from mild infections in childhood, or to other causes. Negroes and American Indians are said to be more susceptible to tuberculosis than the white race. On the other hand, Negroes exhibit more immunity to yellow fever and malaria than the white race.

Individual Immunity:

Laboratory animals of the same species, kept under identical environmental conditions, exhibit only slight differences in their resistance or susceptibility to experimental disease. On the other hand, humans show wide differences in susceptibility to disease.

For example, during an epidemic of influenza there are always some individuals who do not contract the disease even though in close contact with the virus. These individuals exhibit a higher degree of resistance than do the majority of people.

Type # 2. Acquired Immunity:

Acquired immunity, by contrast, begins after birth. It depends on the presence of antibodies and other factors originating from the immune system.

Although the emphasis will be on antibodies and antibody-mediated immunity it should be remembered that cellular immunity is also an important consideration in the total spectrum of resistance. An individual of a susceptible species may acquire a resistance to an infectious disease either accidentally or artificially. This resistance is spoken of as an acquired immunity.

Many of the infectious diseases, such as typhoid fever, scarlet fever, and measles, usually occur only once in the same individual. The resistance of the host to the disease is increased so that another exposure to the same specific organism usually produces no effect. This resistance or immunity may last for a limited time or for life.

Immunity may be acquired artificially by means of vaccines or by the use of immune serums. If the immunity is acquired by means of vaccines, it is spoken of as active immunity if it is acquired by the use of immune serums, it is spoken of as passive immunity.

Four types of acquired resistance are generally recognized:

i. Naturally Acquired Active Immunity:

Active immunity develops after antigens enter the body and the individual’s immune system responds with antibodies. The exposure to antigens may be unintentional or intentional. When it is unintentional, the immunity that develops is called naturally acquired active immunity.

Naturally acquired active immunity usually follows about of illness and occurs in the “natural” scheme of events. However, this need not always be the case because subclinical diseases may also bring on the immunity. For example, many individuals have acquired immunity from subclinical cases of mumps or from subclinical fungal diseases such as cryptococcosis.

Memory cells residing in the lymphoid tissues are responsible for the production of antibodies that yield naturally acquired active immunity. The cells remain active for many years and produce IgG immediately upon later entry of the parasite to the host. Such an antibody response is sometimes called the secondary anamnestic response, from the Greek anamnesis, for recollection.

ii. Artificially Acquired Active Immunity:

Artificially acquired active immunity develops after the immune system produces antibodies following an intentional exposure to antigens. The antigens are usually contained in an immunizing agent such as vaccine or toxoid and the exposure to antigens is “artificial”.

Viral vaccines consist of either inactivated viruses incapable of multiplying in the body or attenuated viruses, which multiply at low rates in the body but fail to cause symptoms of disease. The Salk polio vaccine typifies the former while the Sabin oral polio vaccine represents the latter.

Bacterial vaccines fall into similar categories: the older whooping cough (pertussis) vaccine consists of dead cells, while the tuberculosis vaccine is composed of attenuated bacteria. Whole microorganism viral and bacterial vaccines are commonly called first-generation vaccines.

One advantage of vaccines made with attenuated organisms is that organisms multiply for a period of time within the body, thus increasing the dose of antigen administered. This higher dose results in a higher level of immune response than that obtained with the single dose of inactivated organisms. Also, attenuated organisms can spread to other individuals and re-immunize them or immunize them for the first time.

However, attenuated organisms may be hazardous to health because of this same ability to continue multiplying. In 1984, for example, a recently immunized soldier spread vaccinia (cowpox) viruses to his daughter. She, in turn, infected seven young friends at slumber party.

With only one notable exception, there are no widely used bacterial vaccines made with whole organisms and used for long-term protection. The exception is the older pertussis vaccine, now in the process of being replaced by the acellular pertussis vaccine composed of Bordetella pertussis extracts. Other bacterial vaccines made with organisms are used for temporary protection.

For instance, when health officials suspect that water contains typhoid bacilli, they may administer a vaccine for typhoid fever. Bubonic plague or cholera vaccines are also available to limit an epidemic. In these cases, the immunity lasts only for several months because the material in the vaccine is weakly antigenic.

Weakly antigenic vaccines are also available for laboratory workers who deal with rickettsial diseases such as Rocky Mountain spotted fever, Q fever, and typhus. The danger in these vaccines is that the residual egg protein in the cultivation medium for rickettsiae may cause allergic reactions in recipients.

Immunizing agents that stimulate immunity to toxins are known as toxoids. These agents are currently available for protection against diphtheria and tetanus, two diseases whose major effects are due to toxins. The toxoids are prepared by incubating toxins with a chemical such as formaldehyde until the toxicity is lost.

To avoid multiple injections of immunizing agents, it is advantageous to combine vaccines into a single dose. Experience has shown this possible for the diphtheria-pertussis-tetanus vaccine (DPT), the newer diphtheria-tetanus-acellular pertussis vaccine (DTaP), the measles-mumps-rubella vaccine (MMR) and the trivalent oral polio vaccine (TOP).

There is even a vaccine that will immunize against four diseases simultaneously – in 1993, the FDA approved a combined vaccine which includes diphtheria and tetanus toxoids, whole-cell pertussis vaccine, and Haemophilus influenzae b (Hib) vaccine. Marketed as Tetramune, the quadruple vaccine is used in children aged 2 months to 5 years to protect against the DPT diseases as well as Haemophilus meningitis.

For other vaccines, however, a combination may not be valuable because the antibody response is lower for the combination than for each vaccine taken separately. Immunologists believe that poor phagocytosis by macrophages is one reason. Activation of suppressor T-lymphocytes may be another reason.

Modern immunologists foresee the day when preparations called subunit vaccines, or second- generation vaccines, will completely replace whole organism vaccines. For example, pili from bacteria may be extracted and purified for use in a vaccine to stimulate antipili antibodies. These would inhibit the attachment of bacteria to tissues and facilitate phagocytosis.

Another example is the vaccine for pneumococcal pneumonia, licensed for use in 1983. The vaccine contains 23 different polysaccharides from the capsules of 23 strains of Streptococcus pneumoniae. Still another example is the vaccine against Haemophilus influenzae b, the agent of Haemophilus meningitis.

Also composed of capsular polysaccharides, the so-called Hib vaccine has been available since 1988 and has been a critical factor in reducing the incidence of Haemophilus meningitis from 18,000 cases annually (1986) to a few dozen cases in current years (1995).

Another form of vaccine is the synthetic vaccine, or third-generation vaccine. This preparation represents a sophisticated and practical application of recombinant DNA technology.

To produce the vaccine, three major technical problems must be solved: the immune-stimulating antigen must be identified: living cells must be reengineered to produce the antigens and the size of the antigens must be increased to promote phagocytosis and the immune response. Thus far, the process has been successful for a vaccine for foot-and-mouth disease licensed in 1981.

The genetic engineering process has also worked for a synthetic vaccine for hepatitis B. The vaccine is marketed by different companies as Recombivax and Engerix-B. Because the vaccine is not made from blood fragments (as the previous hepatitis B vaccine was), it relieves the fear of contracting human immunodeficiency virus (HIV) from contaminated blood.

Many immunologists believe that the synthetic agents will usher in a Renaissance of vaccines. In 1993, for example, biotechnologists announced the development of a cholera vaccine containing Vibrio cholera whose genes for toxin production were experimentally removed. An AIDS vaccine also looms on the horizon.

Immunizations may be administered by injection, oral consumption, or nasal spray, as currently used for some respiratory viral diseases. Booster immunizations commonly follow as a way of raising the antibody level by stimulating the memory cells to induce the secondary anamnestic response. This is why a “tetanus booster” is given to anyone who sustains a deep puncture wound by a soil- contaminated object if they have not had a tetanus immunization in the previous ten years.

Substances called adjuvants increase the efficiency of a vaccine or toxoid by increasing the availability of the antigen in the lymphatic system. Common adjuvants include aluminum sulfate (“alum”) and aluminum hydroxide in toxoid preparations, as well as mineral oil or peanut oil in viral vaccines. The particles of adjuvant linked to antigen are taken up by macrophages and presented to lymphocytes more efficiently than dissolved antigens.

Experiments also suggest that adjuvants may stimulate the macrophage to produce a lymphocyte-activating factor and thereby reduce the necessity for helper T-lymphocyte activity. Moreover, adjuvants provide slow release of the antigen from the site of entry and provoke a more sustained immune response. A high priority in the development of synthetic vaccines is the production of suitable adjuvants.

iii. Naturally Acquired Passive Immunity:

Passive immunity develops when antibodies enter the body from an outside source (as compared to active immunity in which individuals synthesize their own antibodies). The infusion of antibodies may be unintentional or intentional, and thus, natural or artificial. When unintentional, the immunity that develops is called naturally acquired passive immunity.

Naturally acquired passive immunity, also called congenital immunity, develops when antibodies pass into the fetal circulation from the mother’s bloodstream via the placenta and umbilical cord. These antibodies, called maternal antibodies, remain with the child for approximately 3 to 6 months after birth and fade as the child’s immune system becomes fully functional. Certain antibodies, such as measles antibodies, remain for 12 to 15 months. The process occurs in the “natural” scheme of events.

Maternal antibodies play an important role during the first few months of life by providing resistance to diseases such as pertussis, staphylococcal infections, and viral respiratory diseases. Because the antibodies are of human origin and are contained in human serum, they will be accepted without problem. The only antibody in the serum is IgG.

Maternal antibodies also pass to the newborn through the first milk, or colostrum, of a nursing mother as well as during future breast feedings. In this instance, IgA is the predominant antibody, although IgG and IgM have also been found in the milk. The antibodies accumulate in the respiratory and gastrointestinal tracts of the child and apparently lend increased resistance to diseases.

iv. Artificially Acquired Passive Immunity:

Artificial acquired passive immunity arises from the intentional injection of antibody-rich serum into the circulation. The exposure to antibodies is thus “artificial.” In the decades before the development of antibiotics, such as injection was an important therapeutic device for the treatment of disease.

The practice is still used for viral diseases such as Lassa fever, hepatitis, and arthropod-borne encephalitis, and for bacterial diseases where a toxin is involved. For example, established cases of botulism, diphtheria, and tetanus are treated with serum containing the respective antitoxins.

Various terms are used for the serum that renders artificially acquired passive immunity. Antiserum is one such term. Another is hyper-immune serum, which indicates that the serum has a higher-than-normal level of a particular antibody. If the serum is used to protect against a disease such as hepatitis A, it is called prophylactic serum.

When the serum is used in the therapy of an established disease, it is called therapeutic serum. Should the serum be taken from the blood of a convalescing patient, physicians refer to it as convalescent serum. Another common term, gamma globulin, takes its name from the fraction of blood protein in which most antibodies are found. Gamma globulin usually consists of a pool of sera from different human donors, and thus it contains a mixture of antibodies including those for the disease to be treated.

Passive immunity must be used with caution because in many individuals, the immune system recognizes foreign serum proteins as antigens and forms antibodies against them in an allergic reaction. When antibodies interact with the proteins, a series of chemical molecules called immune complexes may form, and with the activation of complement, the person develops a disease called serum sickness.

This is often characterized by a hive like rash at the injection site, accompanied by laboured breathing and swollen joints. To avoid the disease, it is imperative that the patient be tested for allergy before serum therapy is instituted. If an allergy exists, minuscule doses should be given to eliminate the allergic state, and then a large therapeutic dose can be administered.

Artificially acquired passive immunity provides substantial and immediate protection to disease, but it is only a temporary measure. The immunity that develops from antibody-rich serum usually wears off within days or weeks. Among the serum preparations currently in use are those for hepatitis A and chickenpox. Both are made from the serum of blood donors routinely screened for hepatitis A and chickenpox.

Food Sensitivity, Intolerance, or Allergy: What's the Difference?

Does your autoimmune disease come with a side of food reactions that cause symptom flare-ups? You may be part of the 15-20% of people who experience food sensitivities and intolerances (20). The pain and discomfort can be invisible, and are often misdiagnosed or dismissed despite their severity.

These buzzwords can also cause a great deal of confusion. People with food sensitivities, intolerances, and even allergies and celiac disease can exhibit similar symptoms however each condition works in a different way.


Easily confused with sensitivities and intolerances, allergies are actually easy to differentiate.

Allergies are specific IgE-mediated immune responses to substances. An allergic reaction produces IgE antibodies, which attack the offending substance (like pet dander, pollen, bee venom, or peanuts). This triggers a release of histamine, causing immediate, severe, and often life-threatening reactions. The symptoms are usually experienced in the airways or on the skin in the form of anaphylaxis or hives.

In the event of exposure to an allergen, treatment must include a swift injection of epinephrine (widely known as an EpiPen) or as a second wave of defense, administration of an antihistimine.

About 35% of Americans have reported a food allergy, but it is likely that a portion of these cases are in fact non-immune-mediated food intolerances (1). While research is limited and most food allergy data relies of self-reported information, actual prevalence may be up to 10%, especially in Western countries (2).

Sensitivity v.s. Intolerance & the Microbiome

While conducting your own online research, you may notice that intolerances are sometimes called sensitivities and vice versa. The words “intolerance” or “food hypersensitivity” may also be used as an umbrella term for various non-allergic reactions to food, as is evident in some scientific studies.

For the purpose of clarity, however, we will refer to the European Society of Neurogastroenterology and Motility (ESNM) for information on the subject. ESNM is a nonprofit society uniting medical professionals all over the world. Their Gut Microbiota for Health section focuses on sharing knowledge and promoting debate regarding the microbiome.

The infographic below explains the differences between a sensitivity and an intolerance, and their relationship to the gut microbiota.


The ESNM Gut Microbiota for Health section defines an intolerance as an abnormal, non-immune mediated, functional response to a food. This could result from an enzyme deficiency, malabsorption, or other issues.

Individuals with food intolerance are unable to properly process certain foods in the digestive tract – think lactose in cow’s milk or histamine in fermented foods. Intolerances trigger symptoms such as abdominal pain, bloating, gas, nausea, and diarrhea.

In the case of milk, intolerant individuals do not produce any or enough lactase to fully break down the lactose (milk sugars) and enable absorption by the body. The dosage tends to have an effect on the severity of the reaction, which also varies depending on the individual.

Lactose intolerance is common after infancy, and affects roughly 65% of the world’s population. It is extremely prevalent in African Americans, Hispanics, and Asians (3).

People with histamine intolerance may lack the enzyme called diamine oxidase (a.k.a. DAO), that is primarily responsible for breaking down ingested histamine and preventing build-up and absorption by the bloodstream.

As histamine intolerance is less studied and often misdiagnosed, the true prevalence is unknown, however it is estimated that it affects roughly 1% of the population (4).

Common food intolerances:

  • Lactose (dairy products)
  • Histamine (fermented foods, alcohol, shellfish, smoked meats, legumes, chocolate, certain fruits and vegetables) (Fermentable Oligosaccharides, Disaccharides, Monosaccharides, And Polyls, including fructose, lactose, mannitol, sorbitol, GOS, and fructan)
  • Caffeine (coffee, chocolate)

Lactose and histamine intolerances are functional and primarily involve the digestive system.

Other adverse food reactions – like sensitivities – may involve the immune system, but in a different way than allergies.


Food sensitivities are still a debated issue, as this term is not an official medical diagnosis and the scientific world has not yet come to a consensus on its precise meaning.

The ESNM Gut Microbiota for Health section offers some clarity, reporting that sensitivities result from an inappropriate activation of the immune system upon exposure to a particular food. This is an IgG-mediated immune response, as opposed to the IgE-mediated response involved in allergic reactions (9) or an autoimmune response as in celiac disease. Some sensitivities, like wheat or gluten, may be associated with autoimmune markers, however the mechanisms remain largely unknown (26).

Food sensitivities can cause a wide range of painful or uncomfortable reactions that may be felt immediately, or even days later. Potential symptoms include abdominal pain, anxiety, bloating, brain fog, diarrhea, fatigue, headaches, heartburn, joint pain, nausea, and rashes, which closely mirror many autoimmune disease symptoms.

Most food sensitivities are self-reported and many are discovered through elimination diets, as testing is plagued with controversy. Most experts agree that IgG testing is inaccurate and not a viable method for identifying trigger foods, as high antibody levels may actually indicate tolerance to a particular food rather than intolerance (10, 11).

A contributing factor in food sensitivities seems to be increased intestinal permeability, otherwise known as leaky gut. This condition is often seen in people with autoimmune disease, including celiac (12, 28). When the intestinal lining becomes too permeable, unwelcome molecules can cross the gut barrier and enter the bloodstream. The immune system sees these molecules – even partially digested food proteins or gut microbes – as foreign bodies and therefore prepares to attack them (13).

This imbalanced immune response may also involve the gut microbiome. Researchers suspect that “a disruption in an individual’s gut microbiota may lead to a change in how the immune system recognizes and reacts to certain foods” (1).

Eating trigger foods can result in inflammation and further disruptions in the gut microbiota.

Thus, it is no surprise that many people with autoimmune disease – who so often exhibit intestinal impermeability, chronic inflammation, and compromised gut health – may experience food sensitivities (14, 17, 8).

Common food sensitivities: *

  • Gluten (wheat, barely, rye) a.k.a. Non-Celiac Gluten Sensitivity (NCGS) or Non-Celiac Wheat Sensitivity (NCWS) (15)
  • Casein (dairy products)
  • Eggs
  • Corn
  • Soy
  • Yeast
  • Citrus
  • Nightshades (tomatoes, eggplants, peppers, goji berries)
  • Legumes (peanuts, lentils, chickpeas, beans)
  • Nuts (walnuts, cashews, hazelnuts, almonds)
  • Food additives (sulfites, artificial colors, preservatives)

*NOTE: depending on the individual, adverse reactions to foods on this list may not result from IgG-mediated immune responses, as research on food sensitivities is very limited. In addition, not enough about NCGS/NCWS is known to determine whether it is immune-mediated or not.

Celiac Disease

Unlike allergies, intolerances, and senstivities, celiac disease is a lifelong, genetic autoimmune disorder in which the body mistakenly attacks itself.

When a person with celiac disease ingests gluten (a protein found in wheat, barley, and rye) the immune system reacts by mounting an attack against the body’s own healthy cells, damaging the villi lining the small intestine. If this continues overtime, many celiacs experience the effects of malabsorption as the villi are unable to send nutrients into the bloodstream.

There are over 200 symptoms of celiac disease. The most widely experienced include fatigue, cognitive problems like brain fog, neurological problems like severe headaches, and digestive issues such as bloating, diarrhea, constipation, gas, abdominal pain, and nausea and vomiting (31). Many people with celiac disease experience kaleidoscope of symptoms, including anxiety, depression, mouth ulcers, skin rashes, joint pain, numbness and tingling, that result in misdiagnoses and a challenging path to relief.

Celiac disease can be life-threatening if left untreated, and include intestinal, neurological, and cognitive damage and the development of additional autoimmune conditions. Currently, around 1.4% of the global population lives with celiac disease (32).

For more information and resources on celiac disease, check out our Celiac Education page.


Treatments for food sensitivities and intolerances may involve:

  • correcting imbalances, deficiencies, and gut health issues
  • incorporating new lifestyle practices
  • taking prescribed supplements and probiotics
  • working with a dietitian to:
    • pinpoint trigger foods and address inflammation through a healing protocol or elimination diet (like AIP, GAPS, low FODMAP, or SCD)
    • properly reintroduce foods
    • adjust eating habits

    Remember to always discuss your symptoms and concerns with your practitioners, and avoid self-diagnosing.


    GMFH Editing Team. (2018, November 21). Food Sensitivity vs Food Intolerance. Gut Microbiota for Health, European Society of Neurogastroenterology and Motility.

    Loh, W., Tang, M. (2018, September 18). The Epidemiology of Food Allergy in the Global Context. International Journal of Environmental Research and Public Health, 15(9): 2043.

    Malik, T., Panuganti, K. (2019). Lactose Intolerance. StatPearls Publishing.

    Maintz, L., Novak, Natalija. (2007, May 1). Histamine and histamine intolerance. The American Journal of Clinical Nutrition, 85(5): 1185-1196.

    The Food List. Histamine Intolerance Awareness.

    Shakoor, Z., Faifi, A., Amro, B., Tawil, L., Ohaly, R. (2016). Prevalence of IgG-mediated food intolerance among patients with allergic symptoms. Annals of Saudi Medicine, 36(6): 386-390. doi: 10.5144/0256-4947.2016.386

    Tomicic, S., Norrman, G., Falth-Magnusson, K. Jenmalm, M., Devenney, I., Bottcher, M. (2009). High Levels of IgG4 Antibodies to Foods During Infancy Are Associated With Tolerance to Corresponding Foods Later in Life. Pediactric Allergy and Immunology, 20(1): 35-41.

    Duan, L., Rao, X., Sigdel, K. (2019, Febraury 28). Regulation of Inflammation in Autoimmune Disease. Journal of Immunology Research.

    Barbaro, M., Cremon, C., Stanghellini, V., Barbara, G. (2018, October 11). Recent advances in understanding non-celiac gluten sensitivity. F1000Research.

    How to deal with food sensitivity. (2019). Harvard Men’s Health Watch, Harvard Health Publishing of Harvard Medical School.

    Hardy, A. (2018, December 5). How the gut microbiota plays a role in food sensitivities. Gut Microbiota for Health, European Society of Neurogastroenterology and Motility.

    Food Allergy vs Intolerance. GI Society, Canadian Society of Intestinal Research.

    Campos, M. (2017). Leaky gut: What is it, and what does it mean for you? Harvard Health Publishing of Harvard Medical School.

    Bischoff, S. Barbara, G., Buurman, W., Ockhuizen, T., Schulzke J., Serino, M. Tilg, H., Watson, A., Wells, J. (2014). Intestinal permeability – a new target for disease prevention and therapy. BMC Gastroenterology.

    Tuck, C., Biesiekierski, J., Schmid-Grendelmeier, P., Pohl, D. (2019). Food Intolerances. Nutrients.

    Gocki, J., Bartuzi, Z. (2016). Role of immunoglobulin G antibodies in diagnosis of food allergy. Advances in Dermatolgy Allergology, 33(4): 253-256.

    Denham, J., Hill, I. (2013). Celiac Disease and Autoimmunity: Review and Controversies. Current Allergy and Asthma Reports, 13(4): 347–353.

    Celiac disease. (2017). Food Allergy Research and Resource Program, University of Nebraska-Lincoln Institute of Agriculture and Natural Resources.

    Allergy, immunity and heredity

    The tendency to develop allergic reactions has a strong hereditary factor. This tendency is termed atopy. Atopy is diagnosed in individuals who develop an allergic reaction to an allergen in a skin prick test (when the skin is pricked and exposed to the allergen). But not all individuals who develop allergic reactions to skin prick are affected by allergy to particles in the environment. Approximately 20–30% of the population is atopic, and two-thirds of atopic individuals have allergic disease.
    It is still unknown why some people have this abnormal reaction to harmless substances in the environment, or why certain substances are more likely to cause allergies than others.

    Hypersensitivity (also known as &ldquoallergies&rdquo)

    Here, the body troops (leucocytes) respond extensively to a particular foreign substance leading to damage and excessive inflammation in various parts of the body. This is what primarily causes rashes, swelling and itching, the main symptoms of an allergy.

    For example, let&rsquos say, the troops, here leucocytes, are perfectly normal when the person has fruits like banana or strawberries. But, the moment he has a mango slice, the troops declare a high alert and rush to the spot with all their weapons. Thus, the person experiences itching sensation in his throat and even gets rashes all over his body.

    An excessive and inappropriate immune response to a specific foreign substance is known as an allergy. It is also defined as an acquired abnormal hyper immune response to a foreign substance during first and subsequent occasions.

    Prerequisites for body to trigger an allergic reaction are:

    1. The body must come into contact with the allergen
    2. Sensitization of the body must occur for the allergy to take place.

    How does sensitization of the body occur?

    Suppose there is a guy named Bob. Once upon a time in Bob&rsquos childhood, he experienced mild food poisoning due to arsenic in his food. Thus, the body had come in contact and successfully encountered foreign substance (arsenic in this case) and retained this memory. So, the body, from now on, views arsenic as a major threat.

    Now after ten years, Bob tries clams for the first time. And, immediately after a few bites, he starts feeling queasy. Why so? Because majority of edible Crustaceans contain small amounts of arsenic which is safe for human consumption. However, when Bob ate the clams, his body immediately declared high alert and activated a full- blown immune response.

    Thus, here, Bob discovered upon going to the doctor that he indeed is allergic to clams. His body has already fulfilled the two pre-requisites for an allergy to occur and that&rsquos precisely what happened when he had clams. Bob, therefore, has officially developed an allergy.

    Immune Tolerance

    Tolerance is the prevention of an immune response against a particular antigen. For instance, the immune system is generally tolerant of self-antigens, so it does not usually attack the body's own cells, tissues, and organs. However, when tolerance is lost, disorders like autoimmune disease or food allergy may occur. Tolerance is maintained in a number of ways:

    Inhibitory NK cell receptor (purple and light blue) binds to MHC-I (blue and red), an interaction that prevents immune responses against self.

    • When adaptive immune cells mature, there are several checkpoints in place to eliminate autoreactive cells. If a B cell produces antibodies that strongly recognize host cells, or if a T cell strongly recognizes self-antigen, they are deleted.
    • Nevertheless, there are autoreactive immune cells present in healthy individuals. Autoreactive immune cells are kept in a non-reactive, or anergic, state. Even though they recognize the body's own cells, they do not have the ability to react and cannot cause host damage.
    • Regulatory immune cells circulate throughout the body to maintain tolerance. Besides limiting autoreactive cells, regulatory cells are important for turning an immune response off after the problem is resolved. They can act as drains, depleting areas of essential nutrients that surrounding immune cells need for activation or survival.
    • Some locations in the body are called immunologically privileged sites. These areas, like the eye and brain, do not typically elicit strong immune responses. Part of this is because of physical barriers, like the blood-brain barrier, that limit the degree to which immune cells may enter. These areas also may express higher levels of suppressive cytokines to prevent a robust immune response.

    Fetomaternal tolerance is the prevention of a maternal immune response against a developing fetus. Major histocompatibility complex (MHC) proteins help the immune system distinguish between host and foreign cells. MHC also is called human leukocyte antigen (HLA). By expressing paternal MHC or HLA proteins and paternal antigens, a fetus can potentially trigger the mother's immune system. However, there are several barriers that may prevent this from occurring: The placenta reduces the exposure of the fetus to maternal immune cells, the proteins expressed on the outer layer of the placenta may limit immune recognition, and regulatory cells and suppressive signals may play a role.

    Read more about MHC proteins in Communication.

    Transplantation of a donor tissue or organ requires appropriate MHC or HLA matching to limit the risk of rejection. Because MHC or HLA matching is rarely complete, transplant recipients must continuously take immunosuppressive drugs, which can cause complications like higher susceptibility to infection and some cancers. Researchers are developing more targeted ways to induce tolerance to transplanted tissues and organs while leaving protective immune responses intact.

    Why Isn&rsquot Everyone Sensitive to the Same Foods?

    If so many food compounds are so destructive, how come everyone doesn&rsquot have symptoms of food sensitivity all the time? How come different people have different sensitivities? Why is one person sensitive to wheat and another person sensitive to dairy?

    Most of it has to do with how someone&rsquos immune system is built. Certain people&rsquos immune systems may be better at defending against infections, but also more likely to get stimulated by the diet.

    Your innate tendencies are not fixed. Lifestyle also plays a large role. Stress, exercise and sun exposure can all change how the immune system responds to potential food triggers.

    Numerous factors impact the resilience of the gut barrier. Genetics and stress are believed to play prominent roles in strengthening or weakening the barrier, affecting whether toxins will cross over and cause inflammation [27, 28].


    By the luck of the draw, some people may always be more susceptible than others to developing food sensitivities. Certain genes, such as the cannabinoid receptor gene (CNR1), play a surprising role in protecting the gut barrier. Some versions of this gene have been associated with a weaker gut barrier that allows more inflammatory compounds to pass through [29, 30, 31].

    Celiac disease is an inherited food intolerance. Human leukocyte antigen (HLA) is a group of genes that accounts for 30-50% of the genetic component of celiac disease. The most important protein for food sensitivity is called MHC-DQ (encoded in HLA-DQB1 and HLA-DQA1 genes) the HLA-DQ2 and HLA-DQ8 forms of this protein appear to be the most problematic: nine out of ten Europeans with celiac disease have the HLA-DQ2 haplotype [32].

    Through genome-wide association studies (GWAS), HLA and dozens of other genes and gene families have been linked to autoimmune diseases like celiac disease, Crohn&rsquos disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, and more [33, 34].

    All of these autoimmune diseases have also been linked to food triggers and may be controlled through special diets [35, 36, 37, 11, 38].

    Genetic enzyme disorders can also cause food intolerance. For example, lactose and histamine intolerances are both inherited [19].

    Unfortunately, the genetics of food sensitivity have not been well researched. We have only just begun to understand the complex links between our DNA and an ideal diet.


    When we are stressed, our brains produce a signal called corticotropin-releasing hormone, or CRH. When this signal reaches the gut, it causes increased mucus production. Over time, however, the mucus &ldquoruns out,&rdquo and the protective barrier that it forms is reduced. Thus, chronic stress eventually depletes the mucus layer of the intestine [28, 39].

    CRH also increases gut permeability independent of the mucus barrier. The increased permeability allows LPS to cross tight junctions and trigger inflammation [39].

    The gut and the brain are closely linked some researchers have suggested that when the gut barrier fails, so does the blood-brain barrier. &ldquoLeaky brain&rdquo is linked to neurological problems, from dementia to depression. This conversation, therefore, goes both ways: poor mental health can lead to &ldquoleaky gut,&rdquo and &ldquoleaky gut&rdquo can worsen mental health [40].

    Gut Bacteria

    The bacteria that live in our intestines communicate with the immune system. A healthy gut flora helps maintain the balance between Th1 and Th2 immunity. It also promotes Treg cells, which suppress the immune response and prevent intestinal inflammation, autoimmunity, and allergic reactions [41, 42, 43].

    Unbalanced gut flora can even trigger autoimmunity in the eyes, a condition called uveitis. The eyes, like the brain, are normally protected by a special barrier that shields them from most compounds and immune cells in the blood. In uveitis, the gut flora causes T cells to cross this barrier and attack the eyes [44].


    In some circumstances, our own gut flora can cause inflammation by producing lipopolysaccharides (LPS), sometimes called endotoxins. These inflammatory compounds disrupt tight junctions and cross the weakened gut barrier [45].

    Once they have crossed the gut barrier, LPS bind to toll-like receptor 4 (TLR4), which in turn activates NF-&kappaB. NF-&kappaB is one of the most important inflammatory signals: it increases the production of inflammatory cytokines, directly triggering inflammation throughout the body [45, 46].

    Certain species of gut bacteria produce large quantities of LPS, while others don&rsquot. Some of the species that produce the most LPS include Akkermansia muciniphila and Bacteroides fragilis [45, 47].

    LPS from B. fragilis may accelerate Alzheimer&rsquos disease. A. muciniphila is a more complex case: in multiple studies, increased A. muciniphila in the gut is associated with decreased inflammation [45, 47, 48].

    Akkermansia muciniphila

    One of the most common bacteria in the human gut, A. muciniphila produces chemical signals that communicate with our bodies. These signals activate AMPK, an energy-sensing enzyme that speeds up metabolism. In the intestine, AMPK strengthens the tight junctions and decreases intestinal permeability. Thus, A. muciniphila is believed to protect the gut barrier and prevent &ldquoleaky gut&rdquo [49, 50, 51].

    One study found that people with constipation-predominant irritable bowel syndrome (C-IBS) have significantly more A. muciniphila than the healthy average. This result suggests that the presence of A. muciniphila doesn&rsquot universally prevent food sensitivity or disease however, the same study notes that this bacterium is anti-inflammatory, even in C-IBS patients [52].

    Overall, Akkermansia muciniphila is considered a beneficial and protective species.

    Bacteroides fragilis

    One of the more important species for Th1/Th2 balance is Bacteroides fragilis. In mouse studies, B. fragilis produced a polysaccharide that corrected imbalances between the different types of T cells [42, 53].


    Small intestinal bacterial overgrowth, or SIBO, is a condition in which the gut bacteria grow out of control. It often includes both an imbalance in the species of bacteria and an increase in the total number of bacteria in the gut [54].

    SIBO can cause bloating, diarrhea, poor absorption of nutrients, malnutrition, and unhealthy weight loss. SIBO and IBS have overlapping symptoms, and the interaction between them is not well understood. Up to a quarter of the people with Crohn&rsquos and up to half of the people with celiac disease also have SIBO, suggesting a relationship between SIBO and food reactions [54].


    Bacterial infection can send destructive signals to the immune system and trigger food sensitivities and autoimmunity. Some bacteria in the gut may increase zonulin, which lowers resistance in the tight junctions and increases intestinal permeability. Thus, bacterial infection may contribute to &ldquoleaky gut&rdquo [23, 55, 56].

    Chemical Exposure

    Chronic exposure to toxic chemicals in the environment may set the stage for sensitivity to completely unrelated triggers. For example, the buildup of mercury or lead in the tissues may predict &ldquosensitivity-related illness&rdquo associated with food or animal dander [57].

    These secondary sensitivities can have symptoms ranging from migraines to wheezing to unexplained panic attacks [57].

    In multiple case studies, removing the triggers (certain foods, cats, etc.) and treating the accumulated toxic metals resolved all symptoms. In these cases, after treatment, people were able to reintroduce the triggers without symptoms [57].

    Age & Sex

    Women appear to be more likely to develop food sensitivities than men. Female sex steroids, like estrogen, are pro-inflammatory and may be linked to allergies as well [58, 59, 60, 61].

    Importantly, there does not appear to be a difference in the rates of food intolerance among boys and girls before puberty. The greater danger appears and develops in adulthood, which further supports the role of estrogens [62, 59].

    Children, adults, and the elderly may also have different degrees of susceptibility to food intolerance. Younger people may be more susceptible to ovalbumin (eggs) and gliadin (wheat) sensitivities. According to one study, people under the age of 40 were significantly more likely to have sensitivities to gliadin, egg white, and barley than people over 40 [58].

    Some food sensitivities look different in children and adults as well. Children with celiac disease are much more likely to have typical gastrointestinal symptoms adults are more likely to have atypical symptoms like anemia and hypertransaminasemia (high levels of some liver enzymes) [63].

    These poorly understood differences across age and sex can make it very difficult to diagnose food intolerance.

    Now What?

    This article is the first of a three-part series. In the second part, we&rsquoll go over:

    • Our bodies&rsquo natural defenses against these foods,
    • Some of the compounds most likely to cause inflammation, and
    • Symptoms to watch out for.

    Finally, our third post will explain:

    • How &ldquofood sensitivity tests&rdquo are supposed to work,
    • Why they don&rsquot work, and
    • How to actually find and address food sensitivity.


    Food sensitivity, or food intolerance, isn&rsquot quite the same as food allergy, though they can be similar. When the immune system overreacts to a food antigen and there aren&rsquot enough regulatory T cells to suppress it, food sensitivities or food allergies can result.

    Food allergies cause quick, serious, often life-threatening inflammatory reactions based on IgE and mast cells. Food sensitivities are less obvious and more complex. They tend to produce autoimmune reactions: for example, if a food protein and a brain protein are similar enough, the body may produce antibodies that attack both.

    Not everyone is sensitive to the same foods. Genetics, stress, gut bacteria, chemical exposure, age, and sex are all believed to affect whether we have food sensitivities and how severe they might be.

    Experts are saying to avoid anything that causes inflammation during this Coronavirus pandemic, but some people have genes that make them more likely to experience inflammation. Check out SelfDecode’s Inflammation DNA Wellness Report for genetic-based diet, lifestyle and supplement tips that can help reduce inflammation levels. The recommendations are personalized based on YOUR DNA.

    About the Author

    Jasmine Foster


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