Daily Recommended Intakes

Having a child with multiple food allergies is challenging in many ways. One of the large tasks of food allergy is to ensure proper nutrition while removing an entire line of food, sometimes a whole food family.   If there can be a food that replaces the allergenic food that has been removed, nutrients can be filled in.  If there is no replacement, you can risk a nutritional deficiency.   Having a Registered Dietitian help analyze the diet for nutritional adequacy is very helpful and reassuring.   But in between dietitian visits, or in the absence of one, there are online resources that can be a guidance. One useful one is this one from the USDA.

Nutrigenomics: The Scientific Link Between Genetics and Nutrition

"Nutrigenomics: The Scientific Link Between Genetics and Nutrition".   A home study course I completed, put out by the Institute for Natural Resources and I am unable to locate an online version.   But I did find this link that outlines much of the same information:  Nutrigenomics

The article begings with a great introduction essentially introducing you to the world of nutrigenomics...did you ever wonder what it would be like if we knew what we could and couldn't eat from the day we are born?....or if we knew what we were predisposed to and could alter our eating habits specifically for those diseases. (Diabetes, heart disease, Cronhs, Cancer).   We may be able to with combining the worlds of Nutrition and Genomics.  "Nutrigenomics tries to determine the influence of common dietary ingredients on the genome and relate the resulting phenotypes to differences in the cellular and/or genetic response of biologic systems.  It analyzes the response of whole systems to nutrients and studies how food or food ingredients affect the metabolic pathways and alter gene expression".  

A major project took place from 1990-2003: The Human Genome Project yielded this field of nutrigenomics.  "Information from the human genome is making it possible to identify the genetic factors that influence a person's susceptibility to disease associated with diet.....In dietary related disorders, these interventions will involve dietary changes or the inclusions of functional food components, or both."

"Genes evolve in response to many types of environmental stimuli including nutrition." (genetics loads the gun, environment pulls the trigger).   There are genetic markers for many chronic diseases, one has not been found yet for FPIES but it is clear from the research thus far that there is a genetic component.   But what component turns it on?   It is the maternal diet?   Is it the infants diet?   Is it the gut flora?  It is antibiotic use? 

The tools used in Nutrigenomics are multidisplinary: Transcriptomics, Proteomics, Metabolomics, and Bioinformatics.  
"Transcriptomics measures the level of expression of all or a selected subset of genes based on the amount of RNA in a sample, using mircoarray analysis to see how genes react to change.  Nutrients can have a direct effect and interact with transription factors to regulate gene expression."  
"Proteomics is the study of proteins that can be expressed within an organism.  Proteomics focuses on the analysis of proteins and their interactions with other biologic molecules>'
"Metabolomics is the study of the complete set of metabolites that an organism produces.  Genes are turned on and off according to metabolic signals that the nucleus receives from internal factors such as horomones and external factors such as nutrients."
"Bioinformatics handle the vast amount of data produced.  It is now possible to predict gene function and identify the regulatory regions in the genome that influence gene expression". 

Understanding nutrigenomics requires an understanding of the cell.   DNA is the genetic material of the cell, it is arranged in untis called chromosomes, of which we have 23 and genes are spread throughout these chromosomes. 

The study of nutrigenomics also requires knowledge of polymorphisms.   "A polymorphism is the quality of existing in several different forms.  These differences can result from genetic predisposition, environmental influences, or a combination of both.....Several genetic polymorphisms important to nutrition have been identified."  These can be catagorized into 2 catagories:
1). Monogenic Diseases, in which a disease arises from on abnormal gene, these can range from lactose intolerance to PKU or galactosemia.  
2). Chronic Diseases such as cardiovascular disease, diabetes, cancer, obesity, and inflammatory bowel disease. 

The course goes on to discuss effects of micro and macro nutrients at the molecular level as well as the current dietary inteventions and guidelines for disease.   This is my job description in a nutshell so I skimmed over this! But essentially, nutrients have many roles in the body from influencing metabolism and physiology at the molecular level to fuel and co-factor roles.  The role of foods from macronutrients (carbohydrates, fats, proteins) to micronutrients (vitamins, minerals) play is complex and closely intertwined.   "Eat a balanced diet" is always good advice!  It does go on to discuss Dietary Interventions and Guidelines and how with the possibilities of nutrigenomics, one could "tailor" their diet to offer precise dietary advice for specific genetic testing results.   Currently, genetic predisposition with generalized healthy recommendations are what we work with but this can be restricting if there are multiple genes interacting with each other coupled with environmental variables that contribute to the diseases.   

It continues to describe how bioactive food components "alter gene expression in a host of cellular events".

The paragraph within the functional food chapter was of interest to me, and I think will be to other FPIES families: "One of the targets of functional foods will be the gut, which acts as an interface between ingested food and the body.  In addition, the gut serves as the barrier to harmful substances entering the circulation.   Ingestion of functional foods will be beneficial to the microflora of the gut.   These bacteria, in addition to their protective function, generate energy by digesting fermentable carbohydrates.  The microflora of the large intestine is aquired shortly after birth, and its composition is dependent on diet.   We all have our own specific microflora.  Certain species of gut microflora can help reduce the risk of gastrointestinal infections, constipation, irritable bowel syndrome, inflammatory bowel diseases, and possibly colorectal cancer.   Therefore, intestinal microflora could be a part of a personalized nutritional program." 

It goes on to describe probiotics and prebiotics.  "Probiotics and prebiotics could be developed to alter the microflora of the gut....a prebiotic is a non-digestible food ingredient that beneficially affects the host by selectively stimulating the growth and/or modifying the metabolic activity of one or a limited number of bacterial species in the colon that have the potential to improve host health....to be classified as a prebiotic, a food must not be absorbed in the upper part of the gastrointestinal tract and must stimulate growth of the beneficial microflora that is resident in the colon.   Prebiotics also have additional benefits on the immnue system and may inhibit the formation of adenomas and carcinomas".

The conclusion is "Genes are turned on and off by what we eat".   "The interaction between nutrition and the human genome determines gene expression and the metabolic response".  

So, we really are what we eat....

Allergy Nutrition

I first published this post on my blog last September, when I began to do further research into my son's FPIES.   I started with Allergy, with one of my favorite resources at that time (remaisn a top resource):
Vickerstaff Health Services


Janice Joneja Vickerstaff, PhD, RD is an inspiration for me. I had the privilege of hearing her speak at a Nutritional Peds conference a few years ago, her discussion on allergy’s intrigued and inspired me.  I bought one of her books on “Dealing with Food Allergies in Babies and Children” right away, and hungry for more information, I also bought another one of her Allergy books. I have also since bought Digestion, Diet, and Disease to learn more about gut health from her perspective. I find her books very easy to read and follow, and full of valid medical information; so have utilized it as a resource time and again.

I’d like to explain more, from my understanding of her books. I will be using her words for much of it but not always directly quoting all of it- I merely want to provide an overview/synopsis/outline of the pertinent information to this “type” of allergy. 


“Reasons that one child’s body responds to food by developing distressing symptoms and another uses the same food for comfort and nurture may be found in several factors”.
1. Child’s inherited genetic make up.
2. Circumstances within first food encounter
3. Microorganisms that live in child’s GI tract
4. Medications take by mouth, or exposed to (such as mothers milk)
5. Other factors research is only beginning to understand.

“Food sensitivity is unlike any other disease entity….any food is capable of triggering an allergic reaction to a child who has been sensitized to it, or lacks the systems required to process it adequately when it enters the body”.

What is the mechanism for food allergy? And how could this relate to FPIES?

When an allergen enters the body of a person at risk for allergy, an extremely complex series of events “set in motion that will finally result in the release of chemical (called inflammatory mediators) that act on body tissue to cause the symptoms of allergy. All immunological processes involve the various white blood cells (leukocytes), and different type of chemicals they produce”.

First step: the body recognizes the invading antigen. “An antigen is a protein within the cells of any living material that enters the body. When an antigen causes an immune response, it is an allergen. When the antigen enters the body, the white blood cells (lymphocytes) are activated. Lymphocytes are the first cells of the immune system that recognize and respond to anything foreign entering the body (sentinels of the immune system)”. There are two types of Lymphocytes in the blood: Tcells and Bcells. Tcells are the ultimate gatekeepers and controllers of the immune system. “Th (helper T cells) are responsible for identifying foreign materials that enter the body. Th cells initiate and direct the subsequent activities of the immune system if foreign material is deemed a threat…. T Cells exert control by means of messenger chemicals, cytokines”.

The response to cytokines is Th1 or Th2 and this response controls the way the body reacts. “When a pathogen (disease causing microorganism- virus, bacteria, other foreign material) enters, the immune system protects the body by a Th1 response (IgG). Cytokines are produced and stimulate the formation of antibodies of the IgG class which destroy the invading microorganisms by means of the complement cascade…symptoms such as fever, aching muscles, fatigue, malaise (much like the flu) are the result of the body’s response to cytokines and other inflammatory mediators produced during this battle between the immune system and foreign invader”. “The complement cascade is a group of over 20enzymatic proteins in the blood that act together in response to antigen and antibody to destroy foreign cells by splitting them apart (lysis); this process releases various chemical byproducts that act on opsonin’s, chemotoxins, and anaphlatoxins to help destroy a threat to the body and results in inflammation in various tissues.”

So, if FPIES is an IgG response, it is the Th1 response that is activated. It sees the food as a foreign substance – in the same way it would see and attack a virus or bacteria.

Th1 response protects the body from disease, and the IgG antibodies are responsible for the ultimate destruction of the invader. The Th2 response results in allergy, IgE antibody.

So, if Th1 is the first line of defense against IgE, FPIES is an overreactive Th1 response 

Some evidence that allergy is inherited… “the characteristic inherited is the potential to respond with a Th2 response when harmless foreign materials enter the body…. Some suggest Th2 is more primitive response than Th1 and as baby matures, the potential for immune system to respond with Th2 is gradually diminished. This decline, together with the maturation of the digestive tract (that provides a barrier between food molecules and immune cells) would explain why children outgrow their allergies”.

What is Oral Tolerance? “Oral tolerance is a term to indicate that although the immune system of the digestive tract can recognize that all the material we consume as food is completely foreign to our bodies, a tolerizing event has occurred that has taught the T cells that the foreign material is harmless and can safely enter the body”.

Something is askew in the FPIES child that the T cells perceive this as a harmful substance; they are taught to remember that it was originally perceived as a harmful substance; each subsequent ingestion has more T cell memory (army) to fight this perceived invader.


All food is foreign to the body (upon first ingestions)….what is it that allows food to apparently evade the barriers of the immune system in a normal child vs. an FPIES child that food is perceived as invaders to the immune system?


Immune System and Digestive Tract
The Immune system of the GI is different than other parts of the body, it is called the GALT- Gut Associated Lymphoid Tissue. “Processing of food through this system allows the uptake of nutrients through the digestive tract walls without triggering the protective response that would otherwise form a barrier to the foreign materials in food. At the same time- any virus or bacteria taken in through the digestive tract are effectively excluded by the GALT. We have a system that can- at the same time and in the same place- recognize and differentiate foreign materials that is safe (food) and foreign material that is a threat (microorganism, toxins….).”

So, is FPIES a breakdown in the GALT? A deficiency mechanism, or an over reactive one?


“But that isn’t the whole story, the GALT must also distinguish between invading microorganisms and other permanent residents of the large intestine- gut microflora”. And many moms have suspected/known their little one’s microflora is “off”. “Microorganisms in the large intestine defend the bowel from invasion by harmful microorganisms by competing with them for space and nutrients; also keeping surrounding tissue healthy by stimulating the GALT in a positive manner”.

Process of Tolerance:
“The process of oral tolerance involves the T cells and their “messenger chemicals” cytokines. T cells that first encounter the foreign food when it enters the very first time (breast milk or solid foods) are of the Th1 type (Th3 immunological protection). Food molecules are picked up by special cells in the infants digestive tract. The antigenic parts of the food (proteins) are then “presented” to the T cells where they couple of special receptor molecules on the T cell surface”.

“T cells with attached food molecules are then transported on the lymphatic system to the thymus gland. There, the regulatory T cells (Treg) stop any further action on the part of the Th1 cells when it is discovered that the “foreign molecules” pose no threat to the body. This process of inhibiting T cell action is carried out by cytokines especially TGFβ(Transforming Growth Factor-Beta) and possibly IL-10 (Interlukein 10).”

Is there a deficiency in the cytokines (such as tumor necrosis factor, transforming growth factor, or IL-10) that inhibits this regulation to happen in the FPIES child?

“The ‘educated’ T cells are then transported in the blood circulatory system and back into the digestive tract GALT as “memory cells”. Is this where the reactions become full body? Eczema, itching, thrombocytosis, angioedema, etc. leading up to a trigger reaction, as the T cells make their way through the body and back to the GALT and now have memory cells to attack with future ingestion's (the delayed-“build” response some of us see)?

FPIES is a Th1 response- the body sees food proteins the same as disease causing microorganisms ; there is a skew in FPIES kids bodies T cell response- Th1 is OVER REACTIVE!

IgE allergy = B cell lymphocytes= Th2 response =produce IgE antibodies


Non IgE = T cell= over reactive and does not proceed to Th2 response (thus preventing IgE food allergy- actually protecting the body- as it does for viruses/bacteria).

FPIES is a skew/”mis-fire” of the Tcell action….the food proteins should be going through the Th1 as “foreign but safe” and to the Th2 responses and either producing antibodies (IgE) or continue on as safe (already passing Th1 gate keepers). But with FPIES, the food proteins go through the Th1 response and get picked up there as foreign and perceived threats; the immune response is not initiated because it is begun in the non-immune Th1 response- it is attacked before it gets to the Th2!


-White blood cells aid the immune system in recognizing foreign proteins.
-T helper cells produce characteristic cytokines.
-Specific cytokines determine response – Th1 protection vs. Th2 Allergy vs. Th3 Oral tolerance
Food = white blood cells recognition =Lymphocyte = T cells= Th cells= cytokines= protection vs. allergy. FPIES is a disruption in the Th1/Th2 response.

Antibodies in food allergy
IgE= recognized typical food allergy response, but there are other antibodies in food sensitivity. IgG is being recognized in Celiac gluten sensitive individuals. IgG is also thought to be what FPIES response is related to, although isolating the specific levels with other factors has not been achieved for FPIES. IgG is not yet a reliable test for food allergy.
“IgG antibody can be found circulating in the blood of people who have no signs or history of adverse reaction to foods. In fact, some think that an increase in anti-food IgG in some cases may be indicative of successful resolution of IgE mediated allergy. IgG mediated allergy remains complicated because of the nature of the antibody and the immunological reactions associated with it”.

Present knowledge (IgG):
-4 classes: IgG1, IgG2, IgG3, IgG4
-IgG4 subclass high affinity for food antigens
-IgG4 may be associated with milk allergy, in particular milk protein B-lactoglobin in atopic dermatitis (eczema) in children.
-Some evidence that total (all 4 classes measured together) might represent some protection from IgE
(again showing that a good IgG response is actually protective for IgE allergy)
-Food allergy in infants frequently associated with increased gut permeability “leaky gut”

Leaky Gut
"Antigenic food molecules passing into circulation trigger production of anti-food IgG. Thus, in cases of IgE-mediated food allergy that results in inflammatory reactions within the GI tract causing non-intact digestive epithelium, it is logical to expect to find higher than normal levels of anti-food IgG. Some think that these anti-food IgG antibodies represent a protective mechanism, rather than a source of allergic pathway”.


Conditions that predispose to allergy:
1. Immaturity of Infants Immune System – Immune system elements are in place at birth but do not function at levels to provide adequate protection against all infection. Antibodies are a fraction of an adults and secretory IgA (sIgA) the first line of defense of mucous membranes is absent at birth. Babies can have impaired or delayed maturing of various functions including cytokine production.

2. Permeability of digestive tract “leaky gut” – Infants intestines are highly permeable particularly 6-12mo.(become mature by 3yrs) and can absorb large molecules of foods that trigger the Th2 response.

3. Breast feeding – “breast milk provides the ideal nutritional, immunological, and physiologic nourishment for all newborns. Components of human milk enhance the baby’s natural defense and promote maturation of the immune system”. There is data that indicates the breast milk of atopic (allergic)mothers differs immunologically from that of non-allergic mothers. Atopic mothers tend to have higher levels of the cytokines and chemokines associated with allergy in their breastmilk. In addition, they tend to have a lower level of cytokines known as transforming growth factor (TGF-B) that promotes tolerances of food components in the intestinal immune response.