Peanuts and Tree Nut Allergies
On one hand, peanuts are the leading cause of food related anaphylaxis deaths. On the other hand children in developing nations are avoiding starvation because of life saving peanut butter mixes.
Peanuts contain "ara h" allergens which have an affinity for bacteria, cause inflammation, an IgE immune system reaction and other more mild symptoms. These allergens are resistant to heat and stomach acids.
At the same time peanuts have unsaturated oil and proteins (good for arthritis and diabetes) and resveratrol, which is an antioxidant and anti-inflammatory.
Other contradictions include advice to people who have out grown their peanut allergies to eat lots of peanuts and carry an epinephrine (EPI) pen.
Another contradiction is the fact that peanuts are full of proteins as well as protease inhibitors (enzymes that breakdown protein).
Peanuts, groundnuts and lupin flour (all related) are found in foods, of course, but they are also found in medications, costmetics, supplements, wines, and salsa.
There are allergens in peanuts but researchers are also looking at who is eating peanuts. The less adaptable and immune competent the person eating the peanuts the more likely they are to cause problems.
Peanut allergies are reported by 3 million Americans and just under 2 percent of the British population.
Currently avoidance of allergens is best. There are also promising Chinese herbal therapies.
Food Anaphylaxis
“Food anaphylaxis is the leading single cause of anaphylactic reactions treated in emergency departments in Westernized countries. In the US, it is estimated that there are 29,000 anaphylactic reactions to foods treated in emergency departments and 125-150 deaths each year.
Peanuts, tree nuts, fish and shellfish account for the vast majority of severe food anaphylactic reactions. “ (Sampson,2000).
Quality of Life
“Children with a peanut allergy (PA) are faced with food and social restrictions due to the potentially life-threatening nature of their disease. This inevitably impacts upon their quality of life (QoL). QoL of 20 children with PA and 20 children with insulin-dependent diabetes mellitus (IDDM) was measured.
PA subjects felt more threatened by potential hazards within their environment, felt more restricted by their PA regarding physical activities, and worried more about being away from home. (Avery,2003)
Peanut Anaphylaxis Increasing
“Peanut (Arachis hypogaea) allergy is a major cause of food-induced anaphylaxis, with increasing prevalence worldwide. To date, there is no cure for peanut allergy, and, unlike many other food allergies, it usually persists through to adulthood.
This article reviews current knowledge on clinically relevant peanut allergens, in particular Ara h 1, Ara h 2 and Ara h 3, together with options for T-cell-reactive but non-IgE-binding allergen variants for specific immunotherapeutic strategies.” (de Leon,2007).
Chemistry of Sensitization
“In the gastric [stomach] mucosa, peanut allergens are taken up by specialized epithelial cells called M cells and transferred to antigen-presenting cells such as dendritic cells, where they are processed into peptide fragments. Activated Th2 cells [Helper T cells or T lymphocytes that belong to the CD4+ subset] recognize peanut allergen-peptide [MHC complexes on the surface of B cells], releasing cytokines interleukin 4 (IL-4) and IL-13, which promote immunoglobulin E (IgE) antibody production by B cells. Secreted IgE antibodies bind to Fc1RI receptors on effector cells such as mast cells, which become sensitized.” (de Leon,2007).
“Studies characterizing peanut allergens have revealed Ara h 1 and Ara h 2 as the most potent allergens, but Ara h 3 may be more allergenic than previously thought. There appears to be a relationship between the diversity of IgE-binding patterns and the severity of clinical symptoms.” (Palmer,2006).
The Second Peanut Leads To Inflammation & Allergic Symptoms
“Upon secondary encounter with the same peanut allergen, the allergen crosslinks cell-bound IgE, activating mast cells to release inflammatory mediators. Additional production of IL-4 and IL-13 by mast cells and basophils results in further Th2-cell differentiation and IgE synthesis. Th2 cells and mast cells also produce TNF-a, IL-5 and chemokines which drives the recruitment of eosinophils to the site of inflammation.
This cascade of events ultimately leads to the induction of symptoms commonly associated with peanut allergy. (de Leon,2007).
“Peanut-specific IgE antibodies that cross-react with tree nut allergens can cause effector-cell activation and may contribute to the manifestation of tree nut allergy in peanut allergic subjects.”(de Leon,2005)
Eight Peanut Allergens
The three main peanut allergens – Ara h 1, Ara h 2 and Ara h 3 – are well characterized Ara h 1 and Ara h 2 are reported to be highly allergenic, with most studies showing a high frequency of peanut allergic individuals having serum-specific IgE to these allergens.
Most of the identified peanut allergens are members of seed storage protein families, with the exception of Ara h 5 and Ara h 8.
Ara h 5 belongs to the profilin family, a group of actin binding proteins responsible for cytoskeleton formation in plant cells and known to be a major cause of pollen-associated food allergy.
Ara h 8 is distinct from the other peanut allergens as it is found to be a major allergen in individuals in central Europe who exhibit co-allergy to peanut and birch pollen. Ara h 8 is a member of the pathogenesisrelated protein family PR-10, which is similarly involved in pollen-associated food allergy.” (de Leon,2007).
The Botany of Nuts Allergies
Some people are allergic to food items in the same plant family. For the person who gets a rash that looks like poison ivy if he eats cashews or mangos, it is interesting to note that Cashew Nuts, Poison Ivy, Pistachio Nuts and Mangos are all in the same plant family. That means cashews are more closely related to mangos than to other nuts like, almonds.
Almonds are in the plum family, along with peaches, apricots, cherries, wild cherries, nectarines, plums, prunes.
Chestnuts (Beechnut family), Macadamia nut (Protea Family), Filberts and Hazelnuts from the Birch family and Brazil nuts are all considered tree nuts.
Nuts from the Walnut family are also common allergens for people with tree nut sensitivity. They include black walnuts, butternuts, pecans, hickory nuts and English walnuts.
Pinion/pine nuts from the pine family, nutmeg, lychee nuts and coconut are not usually included as a tree nut for people with nut allergies. Water chestnuts are a vegetable, part of the sedge family.
Peanuts and Tree Nuts
Some people’s immune system reacts to both peanuts and to tree nuts. According to de Leon, there is "IgE cross-reactivity between the major peanut allergen Ara h 2 and tree nut allergens".
In the study de Leon, found that peanuts, almonds and Brazil nuts share a common immune system irritant called, Ara h 2 , which cause an IgE immune system reaction. This is the part of the immune system that when triggered leads to an anaphylactic shock reaction.(de Leon,2007).
“Many people suffering from peanut allergy are also allergic to one or more tree nuts. Although peanut and a number of tree nuts belong to different plant families, they arise from the same class, namely Magnoliopsida, and therefore may contain homologous proteins that play a role in allergenic cross reactivity.
Tree nuts that have been shown to share IgE-binding epitopes with peanuts include almond, Brazil nut, hazelnut, macadamia and pistachio. USDA, IUIS, Allergome and (de Leon,2007).
For a Summary of Peanut Allergens and a Picture of Ara h 1 Trimer see the de Leon article. (de Leon,2007).
Anaphylaxis Signs &Symptoms
mild flushing
upper respiratory obstruction with or without vascular collapse
increased plasma histamine levels
marked vascular leakage
shortness of breath
difficulty breathing
coughing, sneezing, wheezing
burning sensation in the throat
vomiting, nausea, diarrhea
rapid swelling throughout body
edema of the lips and ears
urticaria or hives
hypothermia
watery eyes
changes in consciousness (including confusion, light-headedness, or stupor),
blue skin [lack of oxygen]
severe abdominal pain
Increasing Frequency of Anaphylaxis
“Anaphylaxis is a rarely anticipated, potentially life-threatening systemic allergic reaction.
Anaphylaxis is IgE mediated, whereas non-IgE mediated anaphylatic reactions are termed anaphylactoid. Food-induced anaphylactic reactions, particularly peanut, are being recognized with increasing frequency.” (Sheffer,2004).
“Systemic anaphylaxis is the most severe form of immediate hypersensitivity reaction. The activation of the complement system occurs during anaphylactic shock.
Peanut allergen results indicate that neither mannan-binding lectin (MBL) nor activation of the complement cascade is crucial for the induction of anaphylaxis.” (Windbichler,2006).
Mild Allergic Symptoms in More People Than Anaphylaxis
In an article entitled, "Anaphylaxis Facts and Fallacies", Paul Brand notes, "the most common causes of anaphylaxis are food allergens, such as peanut and tree nuts, insect stings, and drugs, in particular antibiotics. Many patients with peanut or tree nut allergy show only mild allergic symptoms; only a minority develop anaphylaxis upon exposure." (Brand,2007).
Early Peanut Allergies
Hourihane reports, “the first definite reference to an allergic reaction to nuts that I can find was by Blackfan in 1920. Blackfan described a 10-year-old child with eczema which was 'always intensified' by eggs, fish and nuts.” (Hourihane,1997).
Pregnancy & Infants
“We postulated that the increase of peanut allergy is due to the increased consumption of peanut by the increasingly allergic British population.
Our simple, practical advice to our local mothers is that peanut is not a staple food and few people would suffer nutritional consequences by avoiding it; atopic [allergic hypersensitivity] mothers do not need to eat peanuts and their consumption of peanut may have significant consequences for their unborn child.” (Hourihane,1997).
“In June 1998, the UK government suggested that atopic pregnant and breast-feeding mothers and their infants should avoid peanuts.
A total of 1072 mother-child pairs were studied in school. Only 36 mothers (3.8%) followed the Government's advice by stopping the consumption of peanuts while pregnant. Thirty children (2.8%; 95% CIs, 1.8% to 3.8%) had a positive peanut skin prick test result. Twenty children (1.8%; 95% CIs, 1.1% to 2.7%) were shown to have peanut allergy. This is the highest prevalence for peanut allergy recorded to date.
The prevalence of peanut sensitization in this cohort is 2.8%, and peanut allergy now affects 1.8% of British children at school entry. (Hourihane,2007).
Heat and Pepsin Resistance Peanut Allergens
“Resistance to proteolytic enzymes and heat is thought to be a prerequisite property of food allergens.. Both Ara h 2 and Ara h 6 [peanut] allergens contain cores that are highly resistant to proteolytic digestion and to temperatures of up to 100 degrees C.
The extreme immunological stability of the core structures of Ara h 2 and Ara h 6 provides an explanation for the persistence of the allergenic potency even after food processing. (Lehann,2006).
Researchers concluded, “Ara h 2 and Ara h 6 appeared to be more potent than Ara h 1 and Ara h 3. Both SPT reactivity to low concentrations of Ara h 2 and Ara h 6 and to higher concentrations of Ara h 1 and Ara h 3 were shown to be indicative of severe symptoms.” (Peeters,2007).
Prevalence
Allergy to peanuts and tree nuts (TNs) is the leading cause of fatal and near-fatal food allergic reactions. Peanut allergy appears to be increasing in prevalence. A male predominance of peanut-TN allergy was reported in children younger than 18 years, and a female predominance was reported among adults. Self-reported peanut allergy has doubled among children from 1997 to 2002, and peanut allergies, TN allergies, or both continue to be reported by more than 3 million Americans. (Sicherer,2003).
“In North America and the United Kingdom, prevalence rates among schoolchildren are now in excess of 1%, framing an increasing public health concern and raising research questions about environmental, immunologic, and genetic factors that may influence outcomes of peanut allergy.” (Sicherer,2007)
Aflatoxin
Some of the problems with peanuts is not the nut itself but the toxins / aflatoxins produced by fungal infections of the peanut plants.
In this study, “the prevalence of aflatoxin B1 (AFB1) in 186 peanut products (140 peanuts, 32 peanut butter, and 14 nut cakes) from supermarkets, road vendors, and sale outlets, and 40 feed samples from dairy farmers was determined.
Overall 2.2% of 226 peanut products and feeds positive for AFB1, and 6.1% of 212 milk samples positive for AFM1.” (Offiah,2007).
“Aflatoxins are a family of fungal toxins that are carcinogenic to man and cause immunosuppression, cancer and growth reduction in animals.
The impact of groundnut [a legume related to peanuts] consumption on aflatoxin exposure was limited in this population.
Ingestion of A. flavus and aflatoxin was high in certain agro-ecological zones (SS and SGS) and among the higher socio-economic strata due to higher frequencies of groundnut consumption.”(Egal,2005).
IgE 101
“In peanut-allergic adults, IgE [an immune system marker] is mainly directed to Ara h1 and Ara h2. More recently, a role for Ara h6 has been suggested. In contrast to adults, IgE in children can fluctuate over time. Therefore, children may have a more dynamic reactivity to peanut.” (Flinterman,2007).
“To understand anti-IgE therapy and its role in treating allergies and asthma, it is first important to understand the relationship between allergies and the body's immune system. IgE antibodies are key players in allergic reactions. IgE antibodies prompt other cells (mast and basophil cells, among others) to begin the complex chain reaction that culminates in allergy and asthma symptoms.
Traditionally, allergies and allergy-induced asthma are managed using medications that treat IgE-mediated symptoms once they have already begun in the body. While each treatment has its use, none of the available therapies provides a preventive measure against the binding of IgE to mast cells.
A novel, more targeted approach to the treatment of allergies and allergy-induced asthma is called anti-IgE therapy. This new class of medications holds great promise for people with moderate-to-severe allergies and asthma because it is specifically designed to block IgE from initiating the allergic response, potentially preventing the onset of symptoms before they start.
Despite its potential, it's important to note that anti-IgE therapy is not a cure for asthma or allergies. It is advised that people still continue to maintain their allergen avoidance program.” (Berger,2001).
Accidental Exposure Down
“Accidental exposure to peanut occurs at a lower frequency than previously reported, but most reactions are managed inappropriately. A further reduction and better education on allergy management are desirable.” (Yu,2006).
Therapeutic Strategies for Peanut Allergies and Asthma
“Among the therapeutic strategies reviewed are sublingual and oral immunotherapy, anti-IgE, Chinese herbal medicine, and vaccine strategies.” (Sicherer,2007)
Chinese Herbal for Peanuts Anaphylaxis
“A Chinese herbal medicine preparation, food allergy herbal formula-2 (FAHF-2), prevented peanut allergy (PNA) in mice when administered during sensitization.
All sham-treated mice challenged at weeks 14 and 18 showed anaphylactic symptoms. In contrast, FAHF-2-treated mice showed no sign of anaphylactic reactions. PN-specific IgE levels in FAHF-2-treated mice also were reduced whereas IgG2a levels were increased.
Furthermore, MLN cells from FAHF-2-treated mice produced markedly less IL-4 and IL-5, but more IFN-gamma, and contained increased numbers of IFN-gamma-producing CD8+ cells as compared with sham-treated mice.
FAHF-2 treatment established PN tolerance in this model, which persisted for at least 4-week post-treatment. This result was associated with modulation of intestinal T helper type 1 cell (Th1) and Th2 cytokine production, and with increased numbers of mesenteric IFN-gamma-producing CD8+ cells.” (Qu,2007).
“Food allergy herbal formula (FAHF)-1, blocked peanut-induced anaphylaxis in a murine model when challenged immediately posttherapy. IgE levels were significantly reduced by FAHF-2 treatment and remained significantly lower as long as 5 weeks posttherapy. Splenocytes from FAHF-2-treated mice showed significantly reduced IL-4, IL-5, and IL-13, and enhanced IFN-gamma production to recall peanut stimulation in vitro .
“FAHF-2 treatment completely eliminated anaphylaxis in mice allergic to peanut challenged as long as 5 weeks posttherapy. This result was associated with downregulation of TH2 responses. FAHF-2 may be a potentially effective and safe therapy for peanut allergy.” (Srivastava,2005).
Chinese Herbals for Asthma
A study from Mt Sinai School of Medicine in New York found, “favorable reviews in the Western medical community for the use of Chinese herbs as an effective alternative to steroid use.”
An Oct. 18, 2005 press release from Decision News Media stated, "An oral combination of three Chinese herbs could be as effective as conventional medicines at alleviating asthma symptoms but without such severe side effects, report Chinese and American researchers."
An herbal pill was administered to subjects with moderate to severe "persistent asthma" over a four-week duration. Forty-six patients were given 12 capsules of the herbal formula per day, plus a placebo similar in appearance to prednisone. A control group of 45 people were given 20 mg of Prednisone a day, plus 12 capsules of placebo herbal capsules. The researchers measured lung function as well as serum cortisol, cytokine and IgE levels before and after treatment. Subjects were also monitored for side-effects of both treatments.
Results showed a "slightly better" effect on lung function with the prednisone, but the results of the herbal formula were quite impressive. While also beneficial to lung function, the herbal formula showed no adverse effects on adrenal function, and had a more beneficial effect on TH1 and TH2 cytokine levels. Prednisone patients also experienced gastric discomfort and weight gain not seen in the herbal group.
The formula was labeled ASHMI (for Antiasthma Herbal Medicine Intervention Formula) and produced by Weifeng Pharmaceutical Factory in China. For a daily dosage, 32 grams of raw herbs were concentrated down to 3.6 grams, and given in 12 capsules. The following three herbs were used:
(1) Ling zhi (ganoderma lucidum) 20 g, has immune-enhancing effects, and at this dosage, one can accept that the cytokine levels moved towards normalization. It is also a radio-protective agent.
(2) Ku shen (radix sophorae flavascentis), 9 g, reduces heat in the lung (in addition to its strong antimicrobial effects), which could prove important in relaxing bronchial spasm. Most asthma is thought, both in TCM and Western medicine, to be the consequence of allergic inflammation, and the cooling properties of ku shen reduce that.
(3) The use of a small amount of gan cao (radix glycerrhizae), 3 g helps to harmonize ling zhi with ku shen.
The idea of "harmonization" here, in traditional herbal medicine, is to be able to take two distinctive or opposing herbal effects and allow them to present together, in this case ling zhi and ku shen. In addition, gan cao has the effect of regulating and enhancing adrenal function.
After administering the herbal formula, Dr. Xiumin Li evaluated various components of immune response and inflammatory reaction, including TH2-type cytokine release, airway inflammation, mast cell degranulation, release of histamine, tryptase, leukotrienes, and others.3 The researchers also tested the effect on the lymphocytes thought to be ultimately responsible for asthma.
Now that she has concluded her studies on ASHMI for bronchial asthma, Dr. Li's current project (with Dr. Sampson) involves applying her research skills for an herbal formula to treat food allergies, particularly the potentially fatal peanut allergy. For this, she is using the traditional formula wu mei san with the addition of ling zhi. Due to FDA concerns, she removed from the original formula aconite (fu zi) and asarum (xi xin).
The formula used is the following:
ling zhi (ganoderma lucidum), 28.17% ; wu mei (fructus pruni mume), 28.17%; huang lian (rhizoma coptidis), 8.46%; ren shen (radix ginseng), 8.45%; huang bai (cortex phellodendri), 5.63%; gan jiang (rhizoma zingiberis officinalis), 8.45%; dang gui (radix angelicae sinensis), 8.45%; gui zhi (ramulus cinnamomi cassiae), 2.81%; chuan jiao (pericarpium zanthoxyli bungeanum), 1.41% .
The National Institutes of Health has given Dr. Li a grant to pursue this study. She has already completed her animal studies. The results are extremely promising, showing that the formula completely blocks anaphylactic reaction due to peanuts in mice.5 It remains to be seen if she will try to reduce the formula based on the research protocol she applied to MSSN-002. (Fratkin,2005), (Decision News,2005), (Wen,2005), and (Srivastava,2005).
Eat Peanuts and Carry Epinephrine??? The Resolution of Allergies Question
“Children who outgrow peanut allergy are at risk for recurrence, and this risk is significantly higher for patients who continue largely to avoid peanut after resolution of their allergy. On the basis of these findings, we now recommend that patients eat peanut frequently and carry epinephrine indefinitely until they have demonstrated ongoing peanut tolerance.” (Fleischer,2004).
Robust Adaptation = Tolerance
“Tolerance to food antigens induced via the gut ("oral tolerance") appears to be a rather robust adaptive immune mechanism. However, the neonatal period is particularly critical in terms of mucosal defense, with regard to infections and priming for allergic disease. This is so because the intestinal barrier function provided by secretory antibodies, as well as the immunoregulatory network, is poorly developed for a variable period after birth. Notably, the postnatal development of mucosal immune homeostasis depends on the establishment of a normal commensal microbial flora and also on adequate timing and dose of dietary antigens when first introduced.
In this context, breast feeding appears to exert both shielding and positive regulatory effects. Altogether, the intestinal immune system normally seems rather fit for tolerance induction against innocuous antigens because most children with food allergy "outgrow" their problems, whereas airway allergy tends to persist.” (Brandtzaeg,2002).
Allergens or The Mouth It Goes Into?
Using the same technology that can be used to “study other immune disorders such as type I diabetes mellitus and multiple sclerosis, which are characterized by abnormal antigen-specific T cell responses, “researchers feel, “lyymphocyte responses to allergenic and nonallergenic foods could reveal the differences between pathogenic and normal immune responses to foods.
Defining the cytokine-producing phenotypes of peanut-specific lymphocytes from peanut-allergic children, children who outgrew peanut allergy, and children who have always tolerated peanuts may be useful for understanding the mechanisms of food tolerance.
Peanut-allergic donors show Th2 polarization of cytokine production by peanut-specific cells (IFN-gamma (low), TNF-alpha (low), IL-4 (high), IL-5 (high), IL-13 (high)).
Conversely, nonallergic children and children who have outgrown their allergy show Th1 skewing to peanut antigens (IFN-gamma(high), TNF-alpha (high), IL-4 (low), IL-5 (low), IL-13(low)), similarly to nonallergenic food antigens (beta-lactoglobulin, OVA).
This finding suggests that peanut antigens do not intrinsically induce Th2 skewing, but that the type of response depends upon the donor's allergic status. In conclusion, food allergic status is characterized by a Th2 response whereas Th1-skewed responses underlie oral tolerance.
Furthermore, we were able to show that children with egg allergy and milk allergy similarly display Th2 skewing compared with nonallergic children. These differences in cytokine skewing are therefore not specific to peanuts, but underlie immunological responses in diverse food allergies.” (Turcanu,2003).
In addition to peanut allergies, many other things (ie) corticosteroids, (Braun,1997), cause a change in helper T cell type 1 (Th1) or type 2 (Th2) pattern of cytokine synthesis. The follwoing cause a Th2 skewing: measles vaccinations, (Dhiman,2005), Tobacco smoking, (Cozen,2004), Respiratory syncytial virus, (Becker,2006), diesel exhaust particles (DEP), (van Zijverden,2000) and tetanus. (Turcanu,2003).
“Our study of the peanut-specific cells from NA and OG donors suggest that Th1 responses underlie both nonallergic status and resolution of peanut allergy.
Our data argue against the existence of intrinsic Th2-skewing properties of food allergens. It has been suggested that certain antigens might possess intrinsic properties (physicochemical or biological) that render them allergenic. In our study, we found that the same peanut antigen extract induces a Th2-skewed response in PA donors and a Th1-skewed response in NA children. Therefore, the pattern of cytokine production seems to depend on the host immune response rather than on inherent properties of the allergen.” (Turcanu,2003).
“TH1 immunity were found in both peanut-tolerant individuals and those with peanut allergy. The continuum of responses between individuals with negative and individuals with positive skin test results, rather than TH1 versus TH2 bias, might be important in peanut allergy.” (Thottingal,2006).
Peanuts in Medications
“The increasing prevalence of food allergies has led to a discussion of how safe topical preparations containing peanut oil are with respect to allergy.
Clinical signs of peanut allergy symptoms can be observed on the skin (hives / urticaria), or in the gastrointestinal and/or respiratory tract culminating in cardiovascular symptoms and anaphylactic reactions.
There are anecdotal reports of adverse reactions after topical use of peanut oils.” (Ring,2007).
“The list of relatively commonly used topical preparations that contain arachis oil [peanuts] includes Cerumol (for removing ear wax), Siopel barrier cream, zinc and castor oil ointment, Calamine oily lotion, Dermovate (a potent topical steroid cream used for difficult eczema) and Naseptin cream.
Systemic medications containing arachis oil and likely to be prescribed by pediatricians include Abidec multivitamin drops, Isotretinoin capsules (for treating acne), Sustanon (a testosterone injection) and Calogen (a high fat calorie supplement).
Lack et al suggested the possibility that sensitization to peanut protein may occur in children through the application of ointments and creams containing arachis oil to inflamed skin.” (Dixon,2007).
Wheat and Peanuts in Cosmetics
“The risk of allergy to food proteins in cosmetics and topical medicinal agents is poorly evaluated. IgE dependent contact urticaria and contact dermatitis are observed. Wheat, egg, oats, milk, peanut proteins are incriminated by prick-tests or atopy patch-tests. Cases are related to a previous food allergy and other ones may indicate primary sensitization to topical creams mainly used for skin care of atopic dermatitis. A consecutive exercise induced anaphylaxis to wheat and a long lasting sensitization to wheat have been observed.
A clear and accurate identification of food allergens in cosmetics and topical agents is necessary. Given the hyper-permeability of infant skin, topical products containing food proteins of known allergenicity are contra-indicated for neonates, and for infants with atopic dermatitis, which may be associated with skin hyper-permeability.”(Codreanu,2006).
Food Additives That May Contain Peanuts:
Calcium stearate
Calcium stearoyl lactylate
Glycerine
Lecithin
Linoleic acid
Polysorbates
Propylene glycol monostearate
Sodium stearoyl fumarate
Stearoyls
Tocopherol (alpha-Tocopherol, vitamin E)
Source: Farlow, C. Food Additives: A Shopper’s Guide to What’s Safe and What’s Not. 1993.
Agglutination
The next section talks about agglutination and receptors in human tissue that agglutinate with peanuts. With many receptors, the more of the binding substance (ie, peanuts) that is available the more the receptors proliferate.
Antibodies are protein molecules that are triggered by the presence of antigens. Antigens are molecules recognized by the immune system as foreign to the body causing an immune response.
In the blood, when many antigens bind to the antibody, the attached red blood cells clump together. This clumping of red blood cells by antibodies is known as agglutination.
Agglutination occurs when incompatible blood types are mixed, allowing a potentially fatal antibody – antigen reaction.. (Positively Aging, 2004).
Peanut Agglutinin
Peanut agglutinin (PNA) receptors occurred in a variety of normal cells and tissues, including lymphoid follicle center cells; cortical thymocytes; basal cells and the stratum spinosum of stratified squamous epithelium; columnar epithelium of the gastrointestinal tract; parietal cells and chief cells of the stomach; some endothelial cells; myelin; chondrocytes; spermatogenic cells; cells of the adrenal medulla; Bowman's capsule and the distal convoluted tubules of the kidney; prostatic, perianal and endometrial epithelium; and the extracellular matrix of connective tissues.
Neoplastic cell staining was sporadic and was most often observed in benign or well-differentiated neoplastic tissues in which the corresponding normal cells also expressed PNA binding sites.
However, PNA also bound to some tumor cells in which the analogous normal tissues were unstained, including cells of some fibrosarcomas, rhabdomyosarcomas, hemangiopericytomas and proliferating myoepithelial cells in mixed mammary tumors.
The expression of PNA receptors may be associated with neoplastic changes in some mesenchymal cell populations.” (Haines,1993).
Peanut Agglutinin Receptors in Thymus & Masked by Sialic Acid
“Haemopoietic cells from several murine organs were examined for the presence of peanut agglutinin (PNA) receptors. Foetal liver and adult bone marrow contained a number of cells, which were PNA+ but did not stain with conventional T and B markers.
Cells in the T lineage retained their PNA receptors during maturation, although these became masked by sialic acid on mature peripheral blood T cells. [Masked by sialic acid becomes relevant in the Guillian Barre section]
All organs contained cells which were capable of binding PNA, although this varied considerably from organ to organ in the total numbers of PNA+ cells as well as the staining intensity. For example, thymus possessed 86% PNA+ cells which were very bright in intensity, whereas peripheral blood although having 25% PNA+ cells were very weak in intensity. Cells from all the other organs were intermediate between these two extremes. (Newman,1980).
Neuroendocrine Tumors
Fifty-five neuroendocrine tumors and 6 adrenocortical tumors were examined immunohistochemically.
Seven carcinoid tumors were examined and found to be positive with PNA only in tubular areas and negative in solid area.” (Moorghen,1991).
Bean / Nut & Bacterial Reactivity
“The reactiveness of strains of Plesionmona shigeloides, Campylobater jejuni, Campylobacter coli and Aeromonas species with some lectins namely Soyabean agglutinin (SBA), Ricinus communis agglutinin (RCA), Peanut agllutinin (PNA), Cancanavalin-A (Con-A), Lima bean agglutinin (LMA) and Abrin were investigated.
The results obtained show that all stains of A. hydrophila, A. caviae, A. Sobria and P. shigelloides reacted very strongly with PNA and SBA.
All strains of C. jejuni studied failed to react with SBA but reacted with PNA Whereas C. coli did not show any reaction towards PNA but reacted very strongly with SBA.
All strains of the different organisms were strongly agglutinated by RCA and LMA except A. Hydrophilia and A. sobria which did not react with RCA and LMA respectively. C. jejuni was not agglutinated by Con-A unlike C. coli. Only C. jejuni, C. coli and P. shigelloides reacted with abrin.
This study suggests that the reactivities of lectins with the diarrheogenic bacteria studied may be used for their presumptive identifications and for epidemiological purposes.” (Obi,1998).
Molecular Mimicry and Guillain-Barre Syndrome Lipooligosaccharide and Sialic Acid
“Guillain-Barre syndrome (GBS) is an autoimmune neuropathy that often follows C. jejuni infection.
Sialic acid (N-acetylneuraminic acid, NANA) is a common constituent of lipooligosaccharide (LOS). The molecular mimicry between C. jejuni LOS and human peripheral nerve gangliosides is believed to play an important role in the pathogenesis of GBS.
These data suggest that the NANA residue in LOS is a crucial epitope in realization of ganglioside molecular mimicry.” (Xiang,2006).
“Ganglioside is a compound composed of a glycosphingolipid (ceramide and oligosaccharide) with one or more sialic acids (n-acetylneuraminic acid) linked on the sugar chain.
It is a component of the cell plasma membrane which modulates cell signal transduction events. It appears they concentrate in lipid rafts. They have recently been found to be highly important in immunology. Natural and semisynthetic gangliosides are considered possible therapeutics for neurodegenerative disorders. Haemagglutinin of Influenza virus exploits certain gangliosides to enter and infect the cells expressing them. (Mocchetti,2005).
“Campylobacter jejuni is recognized as the most common identifiable pathogen associated with the development of Guillain-Barre syndrome (GBS), an acute autoimmune-mediated disease affecting the peripheral nervous system.
The immune response to ganglioside-like structures in lipo-oligosaccharides (LOSs) of certain C. jejuni strains is thought to cross-react with human nerve gangliosides and induce GBS.
The results indicate that the LOS of C. jejuni HB93-13 is essential for adherence and invasion as well as for anti-ganglioside antibody induction. (Perera,2007).
Ganglioside and Guillain-Barre Syndrome
Guillain-Barré syndrome (GBS) is the most frequent cause of acute flaccid paralysis in humans, occurring with an annual incidence of 1 to 2 cases per 100,000 people.
GBS is considered an autoimmune disease, with the immune system mistakenly attacking myelin or axons, the nerve conduits for signals to and from the brain (32). This "mistaken immune attack" may arise because the surface of C. jejuni contains polysaccharides that resemble glycoconjugates of the human nerve tissues. This resemblance has been termed "molecular mimicry," which is defined as the dual recognition, by a single B- or T-cell receptor, of a microbe's structure and an antigen of the host, and is the mechanism by which infections trigger cross-reactive antibodies or T cells that can lead to autoimmune diseases (6).
In addition to the above, molecular mimicry between microbial antigens and host tissues forms an attractive hypothetical mechanism for the triggering of autoimmune diseases. (Yu,2006)and (Kielczynski,1991).
Campylobacter coli and Guillain-Barre Syndrome
Campylobacter coli was isolated from a patient with severe, axonal type Guillain-Barre syndrome (GBS). The patient's serum was tested by ELISA for glycolipid antibodies and showed a high titer of IgG antibodies to asialo-GM1 (GA1) and GD3.
Campylobacter coli lipopolysaccharide (LPS) was extracted and analyzed by ELISA, immunoblot binding and blocking studies, and found to avidly bind cholera toxin and peanut agglutinin.
These findings suggest that the LPS from this bacterial isolate contains a ganglioside-like epitope, which most likely resembles GA1. Thus, it appears that ganglioside cross-reactivity is not unique to Campylobacter jejuni and seems to occur in all bacterial isolates from GBS cases so far analyzed. (Bersudsky,2000).
Peanuts and the Eyes
Peanut agglutinins affect the eyes, specifically the cones or the part of the eyes affected in loss of color vision, macular degeneration and other central vision disorders.
“Peanut agglutinin (PNA), a lectin that binds D-galactose-beta (1----3) N-acetyl-D-galactosamine disaccharide linkages, selectively labels cone photoreceptors in the retinae of a variety of species. PNA binds consistently to domains of the interphotoreceptor matrix associated with cone, but not rod, inner and outer segments, to cone cell body and axonal membranes, to cone synaptic pedicles, and to portions of the inner plexiform layer.”
Trypsin [a protease or enzyme that breaks down proteins] treatment, which results in the loss of cone-associated PNA binding in the interphotoreceptor matrix, causes a visually detectable reduction in three of the six groups of PNA-binding glycoproteins in porcine retinal extracts” (Hageman,1986).
Nuts and Fatty Acids
Nuts are high in fat but have a fatty acid profile that may be beneficial in relation to risk of coronary heart disease. Nuts also contain other potentially cardioprotective constituents including phytosterols, tocopherols and squalene. In the present study, the total oil content, peroxide value, composition of fatty acids, tocopherols, phytosterols and squalene content were determined in the oil extracted from freshly ground walnuts, almonds, peanuts, hazelnuts and the macadamia nut.
Our data indicate that all five nuts are a good source of monounsaturated fatty acid, tocopherols, squalene and phytosterols. (Maguire,2004).
Arthritis: A Good Side of Peanuts
Arthritis, an inflammation of the joints, is usually a chronic disease that results from dysregulation of pro-inflammatory cytokines (e.g. tumour necrosis factor and interleukin-1beta) and pro-inflammatory enzymes that mediate the production of prostaglandins (e.g. cyclooxygenase-2) and leukotrienes (e.g. lipooxygenase), together with the expression of adhesion molecules and matrix metalloproteinases, and hyperproliferation of synovial fibroblasts.
All of these factors are regulated by the activation of the transcription factor nuclear factor-kappaB. Thus, agents that suppress the expression of tumour necrosis factor-alpha, interleukin-1beta, cyclooxygenase-2, lipooxygenase, matrix metalloproteinases or adhesion molecules, or suppress the activation of NF-kappaB, all have potential for the treatment of arthritis.
Numerous agents derived from plants can suppress these cell signaling intermediates, including curcumin (from turmeric), resveratrol (red grapes, cranberries and peanuts), tea polyphenols, genistein (soy), quercetin (onions), silymarin (artichoke), guggulsterone (guggul), boswellic acid (salai guggul) and withanolides (ashwagandha). Indeed, several preclinical and clinical studies suggest that these agents have potential for arthritis treatment. (Khanna,2007).
Resveratrol and Osteoarthritis
“Resveratrol is a polyphenolic phytoalexin that is present in various fruits, in the skin of red grapes and peanuts. Recent studies have shown resveratrol exhibits potent antioxidant properties and is able to exert anti-inflammatory and anti-catabolic properties in several cell types.
In summary, our results confirm that resveratrol is an effective inhibitor of chondrocyte apoptosis in vitro. These findings suggest that this dietary polyphenolic compound may have future applications in the nutraceutical-based therapy of human and animal OA.” (Shakibaei,2007).
Non-Toxic Resveratrol for Breast Cancer Apoptosis
“Resveratrol (RES), a natural plant polyphenol, has gained interest as a non-toxic chemopreventive agent capable of inducing tumor cell death in a variety of cancer types.
Mitochondrial permeability transition pore antagonists also blocked calpain activation. In vivo mouse xenograft studies demonstrate that RES treatment inhibits breast cancer growth with no systemic toxicities. Collectively, these results suggest a critical role for mitochondria not only in the intrinsic apoptotic pathway but also in the Ca(2+) and calpain-dependent cell death initiated by RES. Thus, RES may prove useful as a non-toxic alternative for breast cancer treatment.”(Sareen,2007).
IgG Food Allergies in Peanuts and Eggs
“OVA-specific IgG levels of egg-allergic, egg-resolved or control groups are not distinguishable. Higher peanut-specific IgG levels are associated with clinical allergy, but the range of IgG titres of the allergic and control groups overlapped.
Strong IgG responses to OVA may be a normal physiological response to a protein frequently ingested from infancy, whereas up-regulated IgG responses in peanut allergy may be indicative of a dysregulated immune response to peanut allergens.” (Tay,2007).
Genetic Engineering
Current proposed solutions to peanut allergies focus primarily on ways to alter the immune system of patients allergic to peanut. However, with the advent of genetic engineering novel strategies can be proposed to solve the problem of peanut allergy from the source. The objectives of this study were to eliminate the immunodominant Ara h 2 protein from transgenic peanut using RNA interference (RNAi), and to evaluate the allergenicity of resulting transgenic peanut seeds.” (Dodo,2007).
Lupine Allergy
Lupine allergy is caused by ingestion of the flour of a plant called Lupinus albus, a member of the Leguminosae family. Lupine allergy has been described in adult patients previously known to have peanut allergy (cross-reactivity).
“To our knowledge, we describe the first case of an anaphylactic reaction after ingestion of lupine flour in a child without known allergy. In the case of peanut allergy or any anaphylactic reaction without evident cause, especially after industrially prepared food ingestion, lupine should be considered in the list of allergens tested. Lupine is increasingly used in industrially prepared food but is not regularly declared in the composition, leading to difficulties in allergen avoidance.” (Wassenberg,2007).
Another study documented, “Lupin sensitization in a population of 1,160 Spanish subjects.
Lupin is part of the Mediterranean diet and is also used as a thickener of food products. It has been recognized as a cause of serious allergic reactions. This Spanish study aimed at determining the prevalence of lupin sensitization in 1.160 subjects consulting allergologists, using SPT. A 4,1 % sensitization rate was found with a 75% co-sensitization between lupin and legumes, a 82.1% co-sensitization between lupin and pollen and a 28,5% co-sensitization between lupin and latex. This study documents a high lupin sensitization in a selected population, thus stressing the importance of lupin as a food allergen. (Reis,2007).
Lupine flour is allergenic and potentially cross-reactive with peanut allergen, thus posing some risk if used as a replacement for soy flour.” (Peeters,2007).
Peanuts and Cashews
Recently, an increasing number of patients with an anaphylactic reaction after eating small amounts of cashew nuts have been reported. Case histories involving allergic upper airway and conjunctival symptoms and constitutional eczema, allergy for cashew nuts was diagnosed in the first two and allergy for peanuts in the third. So far, three major allergens from the cashew nut (Anacardium occidentale) have been identified and purified. (de Groot,2007)
Of course another consideration is to look at whether the cashews have been cooked in peanut oil or contaminated, which is common.
In another study, “children whose worst ever reaction was to cashew nut (cashew group), were matched with two children each whose worst ever reaction was to peanut (peanut group) for sex, age of reaction and presentation, amount ingested, and asthma.
A total of 47 children in the cashew group were matched to 94 in the peanut group. There were no differences in clinical features between groups for matching criteria, except asthma (more prevalent in the peanut group). Wheezing and cardiovascular symptoms were reported more frequently during reactions in the cashew compared with the peanut group.. (Clark,2007).
Wine and Tree Nuts
Recent Australian and international legislation requires labeling of wines made by using the potentially allergenic food proteins casein, milk, egg white, or isinglass (fish-derived) where "there is a detectable residual processing aid."
We investigated whether wines fined using these proteins or non-grape-derived tannins (tree-nut derived) can provoke significant clinical allergic reactions (anaphylaxis) in patients with confirmed immunoglobulin E-mediated relevant food allergy.
No anaphylaxis was induced by wine consumption. Three mild clinical reactions to protein-fined wine and two mild reactions to unfined wine occurred. Wines fined with egg white, isinglass, or non-grape-derived tannins present an extremely low risk of anaphylaxis to fish-, egg-, or peanut-allergic consumers.” (Rolland,2006).
Soy, Peanuts and Birch Allergies
We recently described patients with soybean allergy mainly mediated by cross-reactivity to birch pollen allergens. A majority of those patients were reported to have peanut allergy.
During a double-blind, placebo-controlled food challenge, all patients experienced symptoms in the oral cavity, progressing to more severe symptoms in 40% of patients.
Peanut allergy might be mediated in a subgroup of our patients by means of cross-reaction of Bet v 1 with the homologous peanut allergen Ara h 8.” (Mittag,2004).
Citrus Seeds and Peanuts
Many individuals allergic to peanuts have multiple allergen sensitivity. To report the first case, to our knowledge, of a peanut allergic patient who exhibited cosensitivity to citrus seeds and who had experienced anaphylaxis to lemon soap.
Researchers concluded, “Citrus seeds contain numerous IgE reactive proteins that are completely cross-reactive among orange, lemon, and mandarin. When peanut allergy coexists with citrus seed allergy, IgE cross-reactivity between peanut and citrus seed proteins can be demonstrated, suggesting a basis to this cosensitivity.” (Glaspole,2007).
Menopause and Resveratrol
The lack of estrogen during menopause is associated with various symptoms including osteoporosis, cardiovascular diseases, and menopausal symptoms.
“Resveratrol (RES) is present in red wine, grapes and peanuts and has been implicated in cardioprotection and prevention of adverse side effects observed after regular HRT.” (Bottner,2006).
Unsaturated Fat Improve Diabetes
Nuts are high in unsaturated (polyunsaturated and monounsaturated) fat and other nutrients that may improve glucose and insulin homeostasis.
Our findings suggest potential benefits of higher nut and peanut butter consumption in lowering risk of type 2 diabetes in women. To avoid increasing caloric intake, regular nut consumption can be recommended as a replacement for consumption of refined grain products or red or processed meats.
Nuts contain 70% to 80% fat, and most fatty acids in nuts are unsaturated (polyunsaturated and monounsaturated), which may be beneficial for glucose and insulin homeostasis. (Jiang,2002).
Sesame
“Recently, we found sesame to be a major cause of severe IgE-mediated food allergic reactions among infants and young children in Israel.
Although sesame products have become fashionable in westernized countries, early exposure may cause sesame to share eventually the same 'noteriety and fate' as peanut - a major cause of severe food allergic reactions. (Dalal,2003).
“Tree nut and sesame allergies have been reported to occur at increased incidence in patients with peanut allergy. (Beausoleil,2006).
Edible Seeds
“With regard to the allergenicity of edible seeds and nuts, certain proteins may not be immediately accessible to digestion in the stomach and the upper small intestine because of the nature of the organization of such proteins into protein body organelles. Protein body hydration status, interactions between proteins, phytochemicals, protease inhibitors, and other matrix effects may contribute to the ability of a protein or package of proteins to reach the sites of active immune sampling in the gastrointestinal mucosa and thus be an influence on the potential allergenicity of a protein.” (Teuber,2002).
Watch Out for “May Contain”
“Foods with advisory labeling (eg, "may contain") are increasingly prevalent. Consumers with food allergies might ignore advisory labeling advice.
Consumers were less likely to heed advisory labeling in 2006 (75%) compared with in 2003 (85%); behavior varied significantly according to the form of the statement. Peanut protein was detected in 10% (20/200) of total food products bearing advisory statements, although clinically significant levels of peanut (>1 mg of peanut or >0.25 mg of peanut protein) were detected in only 13 of 200 such products.” (Hefle,2007).
Legumes
“Leguminous are a cheap source of protein that are cultivated practically throughout the world. They are the main source of food in developing countries. In the Mediterranean area and Middle East, the most commonly consumed legumes are lentils and chickpea.
In the US, UK and south-east Asia, the major legumes involved in food allergy are considered to be peanut and soy bean, respectively. The clinical manifestations of the allergy to legumes are similar for all legumes and range from oral allergy syndrome, urticaria, angioedema, rhinitis and asthmatic crises to anaphylaxis and even death. Legumes have a high degree of immunological cross-reactivity.
The allergenicity of legumes is mainly is mainly related to allergens from the storage proteins of seeds. Vicilins from this group of proteins could be an important common allergen in clinical allergy to legumes.
Profilins are considered to be a cause of cross-reactivity among fruits, vegetables and some pollens and are believed to be a panallergen. Other panallergens of increasing importance are lipid transfer proteins. (Pereira,2002).
Antimalarial Drugs and Brainstem Damage Worse in Peanut Oil
“Intramuscular injections of high doses of the oil-soluble antimalarial artemisinin derivatives artemether and arteether produce an unusual pattern of selective damage to brain stem centers (red nucleus and nuclei caudal to that nucleus) in experimental mammals, predominantly those involved in auditory processing and vestibular reflexes.
When oral artemether was given in peanut oil there was an increase in neurotoxicity and mortality compared with the aqueous suspension.
Intramuscular artemether dissolved in peanut oil is considerably more neurotoxic than the same drug given orally or as a water-soluble analogue given parenterally. However, when
oral artemether was given in peanut oil, there was significantly greater neurotoxicity. This suggests that the oral absorption, and perhaps disposition, of artemether is different when presented in oil.” (Nontprasert,2000).
Adrenals
Pure pheochromocytoma was immunopositive to peanut agglutinin 17/18. Pure neuroblastoma reacted positively to peanut agglutinin 6/6. Each component of both composite tumors reacted similarly to the pure neoplasms.
These immunohistochemical distinctions can assist the clinically important recognition of neuroblastomatous foci in composite adrenal pheochromocytoma-neuroblastoma. (Franquemont,1994).
AIDS
“Along with elevated enzyme activity, AIDS patients had small yet significant increases in the percentages of HLA-DR, terminal deoxynucleotidyl transferase, and peanut agglutinin receptor positive lymphocytes in the null fraction compared with controls.
The data imply that the cellular immune deficiency in AIDS is not a result of deficiencies in lymphocyte ADA or PNP activity, but is more likely associated with an increase in an immature and/or activated lymphocyte subset. (Murray,1985).
Protease Inhibitors
Five protease inhibitors were isolated from peanut seeds and named A-I, A-II, B-I, B-II, and B-III. These inhibitors seemed to be Bowman-Birk type inhibitors judging from their low molecular weights and high cystine contents. All the inhibitors inhibited both bovine trypsin and chymotrypsin at ratios of 1:2 and 1:1, respectively, but not simultaneously. (Norioka,1982).
“The half-site reactivity of trypsin and chymotrypsin binding to two double-headed black-eyed pea protease inhibitors a trypsin-chymotrypsin inhibitor (BEPCI) had a trypsin inhibitor (BEPTI), is explained in terms of the energetics of these inhibitor-protease interactions.
The experiment observation of the predominance of liganded monomer complexes for the lima bean inhibitor and the Bowman-Birk soybean inhibitor and the predominance of half-site-liganded complexes for BEPCI and BEPTI is the direct result of the magnitudes and signs of the coupling free energies which result from these protease-inhibitor interactions.” (Gennis,1976).
Bowman-Birk Inhibitor, Peanuts and Radiation / Chemotherapy
“The BBI family consists of many forms and isoforms of natural polypeptide serine PIs and is found in the seeds of legumes (e.g., Soybean, chickpea, and peanut) and other plants (e.g., barley). Plant serine PIs function as natural insecticides. BBIs are one of the two main families of serine plant PIs (the other is the Kunitz-type PIs). BBIs come from dicotyledonous or monocotyledonous seeds and beans, and the amino acid sequences of about 100 BBIs have been worked out, as have the three-dimensional structures of a few.”(Parakash,1996) and (Lippman,2000).
“Phenotypic mechanisms that enhance bacterial Ultraviolet Radiation (UVR) survival typically include pigmentation and DNA repair mechanisms which provide protection from UVA and UVB wavelengths, respectively.
Two Clavibacter michiganensis pigment-deficient mutants were significantly reduced in UVA radiation survival in vitro; one of these mutants also exhibited reduced field populations on peanut when compared to the wild-type strain over the course of replicate 25-day experiments.
An examination of several bacterial species from the peanut phyllosphere and a collection of environmental Pseudomonas spp. revealed that sensitivity to UVA and UVC radiation was correlated in some but not all of these bacteria. These results underscore a need to further understand the biological effects of different solar wavelength groups on microbial ecology.” (Jacobs,2005).
“The effects of Bowman-Birk inhibitor (BBI), BBI concentrate and a combination of ascorbic acid, co-enzyme Q10, L-selenomethionine (SeM) and vitamin E succinate on proton and HZE-particle [high-energy (high E) nuclei of heavier (high atomic number, Z) elements] radiation-induced cytotoxicity in MCF10 human breast epithelial cells and a phenotypic change associated with transformation in HTori-3 human thyroid epithelial cells
The results demonstrate that BBIC and antioxidants are effective in protecting against space radiation-induced cytotoxicity in MCF10 cells and BBI, BBIC and antioxidants are effective in protecting against a space radiation-induced phenotypic change associated with transformation of HTori-3 cells. (Kennedy,2006).
Summarizing The Components of Peanuts
Peanuts have 5 identified Bowman-Birk type protease inhibitors. Bowman-Birk Inhibitors (BBI) are natural insecticides. Used therapeutically they are also radio-protective (protective against radiation) of normal fibroblasts by improving nucleotide excision repair mechanisms and at the same time being used as sensitizing agents for cancer related radiation and chemotherapy.
Peanuts have 8 Ara h allergens, which cause agglutination with a number of different tumor tissues as well as normal tissues. These are IgE allergens, which activate the T-Helper cells (Th2) and T-Lymphocytes (CD4 subset). These contribute to an inflammatory effect and anaphylaxis. These allergens are also resistant to proteolytic enzymes (protease inhibitors) and heat resistant.
Resveratrol is another component of peanuts. It is an antioxidant which is anti-inflammatory and cardio-protective.
