Genetics of Food Allergy and Intolerance

Can genetics explain if you are allergic to some pollens or foods?

White blood cell patterns determined genetically and designated as HLA DQ and DR genes have been identified with an increased risk of pollen, dust, latex, and food allergies. The intriguing part of this story is that there is an advantage to knowing your HLA DR and DQ type when evaluating your risk for pollen allergies and their associated food allergies or cross reactions.

Genetics of Food Reactions and Allergies

As I explain in more detail in my articles on the genetics of gluten sensitivity, we all have proteins on the surface of our cells that are genetically determined. These patterns are easily detectable by testing cells from blood or from the mouth obtained by a Q-tip type swab. Specific patterns have been associated with increased risk for autoimmune conditions, gluten sensitivity and celiac disease.

HLA DQ Genetics and Celiac or Gluten Sensitivity

HLA DQ2 is present in more than 90% of people who have celiac disease while HLADQ8 is present in most of the rest, though not all people with celiac have been found to have DQ2 and/or DQ8.

DQ and DR Genetic Patterns Associated with Food and Pollen Allergies or Sensitivities?

Now it appears certain DQ or DR patterns are associated with food and pollen allergies as well. As the Food Doc, I continue to search the literature for more information about genetic links to food allergy and intolerance. My search has led to me to a couple of interesting articles in the unusual area of oral allergy syndrome (OAS). The relationship between seasonal and perennial nasal allergies and food allergies is certainly well established but not generally known by most doctors or patients. It appears that some of us need to avoid eating certain foods if we have hay fever or allergies, especially during the hay fever season. This problem also appears to be inherited.

Research Documents Genetic Association With Certain Food and Pollen Allergies

Boehncke, et al. from the University of Frankfurt reported in 1998 that certain white blood cell types known HLA class II genotypes or HLA DQ and DR genetic patterns were found more frequently in people with certain pollen associated food allergies. HLA-DQB1*0301 is present in more people with grass pollen allergy. Those with HLA-DRB1*08, an inherited white blood cell protein pattern linked with a grass pollen allergy, have six times the increased risk of peanut allergy. Those who have inherited the HLA-DRB1*12 white blood cell pattern are 13 times higher at risk for carrot allergy.

Tree Pollen Allergy to Birch Tree Pollen Appears to be Worst

Birch pollen associated hazel nut allergy is linked to HLA-DRB1*01, DQA1*0101, and DQB1*0501. Hazel nut, almond, walnut and apple are the most common food allergies associated with birch tree pollen. Allergies to those foods are commonly associated with birch tree pollen in other studies.

Weed Allergies Also Associated With Food Reactions

In 2004, Wang et al. from China published that the inherited white blood cell type DQA1*0302 is found in more people with Artemisia pollen-induced allergic rhinitis, hay fever due to Mugwort or Sagebrush weeds. Mugwort allergy is associated with several food allergies including apple, celery, hazelnut, pistachio, lettuce, almond, peanut, and carrots.

Where to Get Genetic Testing

There are three commercial labs that I am aware of that offer full HLA DQ typing. They are Quest Laboratories, The Laboratory at Bonfils in Denver, and Enterolab. Bonfils runs the Enterolab genetic tests. Enterolab offers the test run on samples of cells obtained from a Q-tip swab of the mouth. The test can be obtained directly from Enterolab without a doctor's order though it is not covered by insurance. It however is very reasonable from a genetic testing standpoint at $149. Bonfils also does the DQ typing on cells obtained from blood samples sent to them from other labs.

The Future of Genetic Testing in Pollen and Food Allergies

In the future such testing should be very helpful in evaluating suspected food allergies, intolerance and pollen allergies. In the meantime those of us interested in this interesting story anxiously await more research findings in this exciting area. Dr. Fine, founder of Enterolab, has previously published the HLA DQ patterns associated with microscopic colitis. He has found that microscopic changes in the colon or large intestine are similar if not identical to what is seen in the small intestine in celiac disease. Several articles now document that a gluten free diet works in many people with microscopic, lymphocytic and collagenous colitis. It also helps many with Crohn's disease and ulcerative colitis.

A finding of intraepithelial lymphocytosis in the distal small intestine (terminal ileum) is associated with an increased incidence of celiac disease in the proximal small intestine. Now, adding to the intrigue, are these articles linking certain inherited white blood cell protein gene patterns to pollen allergy and food allergy cross reactions that are well recognized but rarely pursued clinically. Oral Allergy Syndrome (OAS), also called the "burning mouth syndrome", occurs in many people but frequently goes undiagnosed. Symptoms include burning, painful and/or itching sensation of mouth or throat with or without swelling that occurs almost immediately after eating certain foods. The foods causing these reactions are commonly associated with pollen, latex or dust allergies.

Unusual Association of Pollen Allergies and Mouth Burning or Food Reactions

This unusual association of tree, grass, and weed pollens, latex and house dust mite allergies to food reactions, though well documented in the medical literature, is not commonly recognized by doctors or patients. The OAS literature contains numerous reports of food allergy or intolerance reactions that are associated with specific pollen, dust, mold or latex allergies. One of the best examples is ragweed pollen allergy. It is associated with a higher risk of food allergy or intolerance to only a few foods. These include foods in the gourd family (cucumbers and melons) and bananas. On other the hand, Birch tree pollen allergy is associated with sensitivity to many foods. The list includes those foods in the Rosacea family (apples, pears), tree nut family (hazelnut, almond, walnut), potatoes, and carrots. Reactions include classic allergic reactions such as skin rashes (atopic dermatitis, hives), wheezing (asthma), runny nose (allergic rhinitis), as well as the burning mouth OAS symptoms and other food intolerance symptoms.

If You Suspect Food Allergy, Intolerance or Sensitivity Get Evaluated By an Expert

Individuals who suspect food allergy or intolerance are encouraged to review the food-pollen connection and undergo appropriate evaluations for food allergy, intolerance and sensitivity. Food sensitivity includes gluten sensitivity and cow's milk (casein) protein sensitivity. Food intolerance includes lactose intolerance. Food allergies are separate and distinct from either food sensitivity or food intolerance.

Consider Getting Genetic Testing or Asking Your Doctor to Test You

This new information about the link of white blood cell protein patterns, HLA DQ types, suggests that we should consider having genetic testing done. After an adequate evaluation,

Establish a Baseline Symptom Score and Start a Food Symptom Diet Diary

I encourage everyone to establish a baseline symptom score. A detailed food symptom diary before a trial of elimination diet is also extremely helpful. An elimination diet that excludes major food lectins (dairy, grain, legumes, and nightshades) and any foods from the pollen list that one is allergic is recommended before accepting diagnoses of IBS, fibromyalgia, unexplained neuropathy or headaches, and chronic fatigue syndrome. Any symptoms not readily explained or improved with other diagnoses and treatment should be considered to be possibly due to a food reaction until proven otherwise.

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Introduction to Cancer Genetics

Cancer is a general term, describing a group of different diseases. Because these diseases are different, it is unlikely that a general cure for cancer will evolve. Each type of cancer needs its own treatment program.

There are two common properties for all types of cancer:
1. Abnormal proliferation (so called neoplasia, that results in a neoplasm structure)
2. Invasive ability. Property that separates benign tumors from cancer.

Cancer cells invade other regions by travelling through the circulatory system or lymphatic system. This process is called metastasis, in which disease is spread from one organ to another non-adjacent organ.

Cancers can be classified according to cell type.

1.Leukemia and Lymphoma
2.Carcinoma
3.Sarcoma
4.Melanoma
5.Retinoblastoma, Neuroblastoma, Glioblastoma
(1: blood-borne cancers, 2-5: solid tumors)

Cancer is a genetic disease and can also be seen as a disturbance in the cell cycle regulation system. You can inherit a predisposition for cancer, but for the disease to break out additional somatic mutations are required.

These mutations arise from:
1. Environmental mutagens (physical or chemical agents that change DNA)
2. Imperfections during DNA copying and repair (so called spontaneous mutations).

There are two ways to categorize mutated genes based on function:

1.Function in a cancer cell
- Genes that have been activated or over expressed = oncogenes (one mutated allele is enough)
- Genes that have been inactivated:

1.Tumor suppressor genes. Both alleles need to be mutated. E.g. RB1 and p53
2. DNA-mismatch repair genes
Both alleles need to be mutated.

2.Function in normal cell:
- Genes that directly control proliferation (controlling cell birth rate or death rate) = Gatekeepers
- Genes that control the rate of mutation = Caretakers

Mutation in some genes always leads to the same type of cancer, independent of what kind of mutation or where it has arisen (e.g.WT1). Mutations in other genes result in many different forms of cancer (e.g. p53)

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What is the relationship between insulin resistance and diabetes

Type 2 diabetes is the type of diabetes that occurs later in life. Insulin resistance precedes the development of type 2 diabetes, sometimes by years. In individuals who will ultimately develop type 2 diabetes, it is believed that blood glucose and insulin levels are normal for many years; then at some point in time, insulin resistance develops.

At this point, there is often an association of high insulin levels, central obesity, cholesterol abnormalities, and /or high blood pressure (hypertension). When this constellation of disease processes occur, it is know as the metabolic syndrome.

One of the actions of insulin is to cause the cells of the body, particularly the muscle and fat cells, to remove and use glucose from the blood. This is one way in which insulin controls the level of glucose in blood. Insulin has this effect on the cells by binding to insulin receptors on the surface of the cells. You can think of it as insulin "knocking" on the doors of muscle and fat cells. The cells hear the knock, open up, and let glucose in to be used by the cell. With insulin resistance, the muscles don't hear the knock as well (they are resistant), and the pancreas is notified that it needs to make more insulin, which increases the level of insulin in the blood and causes a louder knock.

The resistance of the cells continues to increase over time. As long as the pancreas is able to produce enough insulin to overcome this resistance, blood glucose levels remain normal. When the pancreas can no longer produce enough insulin, the blood glucose levels begin to rise, initially after meals when glucose levels are at their highest and more insulin is needed, but eventually in the fasting state too. At this point, type 2 diabetes is present.

The Genetics Of Asthma

With the decrease in air quality, asthma has become a very prevalent condition, especially in Western societies. An asthma allergy is often seen in children and adolescents, with it being less common in adults. Even though it is less common in adults, it is still possible for many adults to be diagnosed and suffer from asthma.

An asthma allergy is a condition in which targets the respiratory system. An irritant is breathed into the lungs, and this goes on to cause inflammation of the tubes of the lungs called the bronchi and bronchioles. This inflammation initiates release of chemicals that causes the entrances to the lung tissue to constrict. The result of this is the coughing sound produced along with any wheezing.

Even though there has not been a gene located that shows if someone will be diagnosed with asthma or not, asthma allergy does have a tendency to run in families. Therefore, scientist believe that if you have a parent with asthma, and depending on you genetic makeup, you run the risk of being predisposed to a diagnosis of asthma. Your risk of been diagnosed with an asthma allergy increases if you also have a sibling who has also been diagnosed with asthma.

However, even though asthma allergy might have a genetic tendency, the environment still plays a factor in the flare up of an attack. For example, being around pets, cigarette smoke, and dust mites can lead to an asthma attack for some people. Anyone with should try to avoid conditions that might triggers there asthma.

Genetics of Obesity

It seems that some people are destined to be skinny. They have never known being fat, and they make being thin look easy. Others of us are in the opposite situation. It is a struggle to lose weight, and being thin seems impossible. Could it be that our genes have something to do with it? As it turns out, there are several genes that play a role in obesity. Defects in some of these genes cause certain syndromes to develop. Not everything is known about the genetics of obesity, but our knowledge is expanding.

A part of the brain called the hypothalamus controls several functions of the body. One of these is the regulation of the sense of hunger. There is an interplay between various chemical messengers and the hypothalamus. This interplay is called the hypothalamic leptin-melanocortin system. Our fat cells make a signal called leptin. The more fat we have, the more leptin is produced. It binds to the leptin receptor in the hypothalamus. The hypothalamus senses a minimal amount of leptin which tells the brain that the body has at least the required amount of fat to function. Once the receptor is activated, a protein called proopiomelanocortin (POMC) is made. POMC is then cut into smaller parts by enzymes. One of these enzymes is proenzyme convertase 1 (PC-1). One of the smaller proteins produced by PC-1 is called alpha-MSH which binds another receptor in the hypothalamus called MC4R. Once MC4R is turned on, it triggers some intracellular signals that end up telling your brain that you are not as hungry. Got all that?! Check out the link at the end of this article and go to the "Genetics" tab. On the "leptin" page, there is a diagram that explains it.

A defect in the genes for any of the signals, enzymes, and receptors mentioned above can lead to an increased appetite. The most common of these mutations is a defect in MC4R. However, it is not the most severe, and some people with a defective MC4R gene are still thin. Mutations in other genes cause a voracious appetite in very young children, and they are nearly destined to eat far more than their bodies will ever need. In addition to becoming very obese, associated problems can include: small ovaries and testicles, thyroid dysfunction, decreased immunity, and low functioning adrenal glands. Fortunately, these more severe conditions are rare with only a handful of known cases. There are treatments for a few, like replacing leptin with shots. For others, like MC4R, there are to treatments.

A few genes that aid in the development of the hypothalamus are also associated with obesity. The SIM1 gene encodes signals that come from the MC4R receptor. One case of a young girl with a SIM1 mutation was obese and also tall. In addition to development of the hypothalamus, the tropomysin-related kinase B (TrkB) receptor and the chemical signal called brain-derived neutrotrophic factor (BDNF) play roles in memory, behavior, and intellect. Defects in either of these two can cause obesity and memory problems.

In the reward center of the brain, dopamine is released when we eat food. People who have mutations in a stretch of DNA called TaqIA have fewer dopamine receptors and thus need to eat more to feel the same sense of reward. This lends weight to the fact that some people may literally be addicted to food, and the sweeter the food, the stronger the addiction.

There are also several genetic syndromes associated with obesity that involve more than one gene. They are too complex for this article, but here is a list of some of them: Prader-Willi, Bardet-Biedl, Ahlstrom, Cohen, and Carpenter syndromes.

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