Milk protein (Casein)
Milk protein hypersensitivity is thought to affect well over 40% of the population. Milk protein intolerance causes a delayed response, where it can take up to 3 days to cause symptoms. These delayed reactions to milk proteins are often tested for by measuring milk-specific IgG antibodies in blood.
Milk hypersensitivity is an IgG-mediated response (often called type III hypersensitivity reactions), and is different than an allergy which is IgE-mediated. Milk hypersensitivity in early childhood is mostly an IgE-mediated response to casein, causing immediate reactions (Anthoni, Savilahti, Rautelin, & Kolho, 2009). However, IgE reactions are often rare in adulthood. Instead, a hypersensitivity in adulthood is usually Ig-G mediated.
Many symptoms resemble irritable bowel (IBS), such as bloating, constipation, migraines, headaches, runny nose, sinusitis, fatigue, skin rashes, eczema and low mood.
Egg Protein (ovalbumin)
An egg hypersensitivity typically is associated with the egg white (albumen). This differs from an egg allergy in which involves the entire egg and is characterized by immediate allergic symptoms associated with histamine (runny nose, sneezing, watery eyes, wheezing, eczema). Egg allergies are also more common among children.
An egg hypersensitivity is characterized by gastrointestinal symptoms such as excessive gas, nausea, stomach pain, and stomach cramping. Additionally, an egg hypersensitivity can reveal itself in other symptoms such as headaches, skin problems, difficulty breathing, heart burn, joint pain, irritability and nervousness. Symptoms usually come on gradually and can be dose-dependent, and is often not life threatening.
The immune response to proteins such as egg and dairy
In normal conditions, consumed proteins, including food allergens, are completely degraded in the digestive tract to oligopeptide fragments (Gocki & Bartuzi, 2016). However, 15% of protein is often found to be incompletely digested, including a proportion of food antigens. Food antigens that were not destroyed by digestive processes (such as enzymes, bile salts, gastric pH) penetrate the intestinal epithelium of the digestive tract and reach the body’s internal environment (Gocki & Bartuzi, 2016). There are four main steps involved in the immune reaction (Gocki & Bartuzi, 2016):
- Capture of antigens by Peyer’s patch M cells, which is the microfold cell. Here there are dendritic cells, macrophages, T cells and B cells.
- Capture of antigens from the digestive tract by dendritic cell processes localized by enterocytes.
- This is where it is processed to present in an MHC molecule. The dentritic cell phagocytoses the antigen and presents a peptide of the food to CD4 T cells. CD4 binds to CD28 which evokes a TH1 response. The TH1 cell produces interferon gamma, which then initiates B cell to make IgG.
- Interferon gamma will also cause CD8 T cells specific for the food to activate macrophages to produce reactive oxygen species (contributing to oxidative stress and gut inflammation). This can contribute to production of IL-1, IL-6 and even more TNF-a (Zwickey, 2018).
- Capture of antigens by enterocytes. Food antigens can also travel between enterocytes where they can damage the integrity of the cells.
- Food antigens encounter cells of the GALT (gut-associated lymphoid tissue)
- Here, food allergens will be treated by GALT either as “innocuous antigens and induce tolerance, or as pathogens and then cause either defense reactions or excessive defensive reactions, that is hypersensitivity” (Gocki & Bartuzi, 2016).
It is also important to note that TH1 also makes TNF-alpha, which is a cytokine associated with breaking down tight junctions and leaky gut. This is also contributing to many of the symptoms associated with a hypersensitivity reaction, such as GI disturbances.
Interestingly, there is a genetic component to food hypersensitivities, making some individuals more susceptible to the loss of oral tolerance; either oral tolerance is not established or it is degraded. In fact, within the first year after birth, approximately 2.5% of infants have a cow’s milk hypersensitivity, and 80% go on to outgrow it by the time they reach five years of age. On the other hand, approximately 60% of milk allergies are mediated by immunoglobulin E (IgE) rather than by immunoglobulin G (IgG)—as is seen with hypersensitivity reactions (Sampson, 2003).
Anthoni, S., Savilahti, E., Rautelin, H., & Kolho, K. L. (2009). Milk protein IgG and IgA: the association with milk-induced gastrointestinal symptoms in adults. World J Gastroenterol, 15(39), 4915-4918.
Food Intolerances. (2014, May 6). Milk Allergy or Intolerance? Retrieved 2018, May 11 from https://www.yorktest.com/milk-allergy-or-milk-intolerance/
Gocki, J., & Bartuzi, Z. (2016). Role of immunoglobulin G antibodies in diagnosis of food allergy. Postepy Dermatol Alergol, 33(4), 253-256. doi:10.5114/ada.2016.61600
Sampson, H. A. (2003). 9. Food allergy. Journal of Allergy and Clinical Immunology, 111(2), S540-S547. doi:10.1067/mai.2003.134
Zwickey, Heather. (n.d). Immune Response to Food. [presentation] Retrieved (2018, May 11) from https://learn.muih.edu/courses/6679/modules
I am very interested in alternative therapies that can be used either stand alone or in conjunction with conventional therapies like chemotherapy. I found a paper in regards to AHCC that looked promising, but unfortunately has not reached mainstream. Many immune enhancers are natural compounds that have proved to be nontoxic for humans and with great potential for anticancer activity (Yin, Fujii, & Walshe, 2010). ACHH is active hexose correlated compound (AHCC), an extract prepared from mycelia of the basidiomycete mushroom Lentinula edodes. 74% of AHCC is oligosaccharides containing about 20% of the -1, 4-glucan type. It has received special attention in the past few years by its reported benefits. AHCC is commercially used as a nutritional supplement and contains a mixture of polysaccharides, amino acids, and minerals (Yin et al., 2010). Results of this particular study suggest that AHCC can enhance CD4 and CD8 T cell immune responses in healthy persons via increasing production of cytokines IFN-gamma and TNF-alpha from T cells. It has also been found that the effects of AHCC are more evident in hosts with the impaired immune function. The study measured the frequency of IFN-gamma and TNF-a producing CD4 and CD8 T cells in adults over age 50 before and after taking AHCC. The results were pretty interesting. AHCC was provided as 500-mg capsules. Total daily dose was 3 g (3 capsules twice daily). The production of the cytokines was measured at 30 and 60 days after AHCC intake and 30 days after the last dose. Interestingly, the frequency of CD4 T cell subsets producing the cytokines was higher at 30 and 60 days. Even after 30 days of discontinuing the AHCC, the frequency of CD4 T cells producing the combination of IFN-gamma and TNF-a at visit 4 was still higher compared to baseline levels. This implies that the effect of AHCC on CD4 T cells could last for several weeks even after this compound is discontinued (Yin et al., 2010)
Two published peer-reviewed human clinical studies (on 269 and 40 subjects respectively) evaluating advanced liver cancer showed extended survival, lower recurrence and improved quality of life among patients taking AHCC. Several other studies demonstrated the ability of AHCC to significantly increase NK cell activity in immune compromised patients. “Given the abundance of preliminary positive results across different infections, AHCC supplementation demonstrates valuable and clinically-relevant potential as an immune-enhancing compound” (Pescatore, n.d.). Finally, AHCC boasts a strong safety profile supported by a Phase I study conducted at Harvard, a 20-year history of use in Japan, its adoption by over 700 clinics and use by an estimated 70,000 people worldwide (including 20,000 in the U.S.). Thus, there is a strong case to be made for adding AHCC to a daily supplement regimen to support the body’s immune system, not only during the apparent times of increased infectious threat such as the flu season, but also all year long.
How can this help the population with bladder issues?
Theoretically, AHCC should be able to boost your natural immune system to defend you against pathogens that cause UTI’s. Both human and animal studies have pointed to AHCC’s ability to enhance the activity of natural killer cells (“NK cells”). These cells provide a crucial first defense for the body, launching a rapid attack while the other cells of the immune system are still mobilizing. AHCC has been the subject of several studies, which investigated its potential as a countermeasure to various infectious diseases, methicillin-resistant Staphylococcus aureus (MRSA) and several other opportunistic infections (Klebsiella pneumoniae, Candida albicans and Pseudomonas aeruginosa.) Looking at “opportunistic” or hospital-acquired infections, the effects of AHCC supplementation on the resistance to Klebsiella pneumoniae (principally associated with bacterial pneumonia and urinary tract infections) was studied in both infected and stress induced mice. Again, the AHCC-supplemented mice demonstrated increased survival, increased mean time until death, decreased susceptibility to infection and increased bacterial clearance from the blood.
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Pescatore, F. (n.d.) AHCC a Powerful Aid in Fighting Viruses and Infections
Yin, Z., Fujii, H., & Walshe, T. (2010). Effects of active hexose correlated compound on frequency of CD4+ and CD8+ T cells producing interferon-gamma and/or tumor necrosis factor-alpha in healthy adults. Hum Immunol, 71(12), 1187-1190. doi:10.1016/j.humimm.2010.08.006