Testing for IgG4 against foods is not recommended as a diagnostic tool.

EAACI Task Force Report

Food-specific IgG4 does not indicate (imminent) food allergy or intolerance, but rather a physiological response of the immune system after exposition to food components. Therefore, testing of IgG4 to foods is considered as

irrelevant for the laboratory work-up of food allergy or intolerance and should not be performed in case of foodrelated complaints.

Obesity and Food Intolerance

Obesity (body mass index (BMI) >30 kg/m2) represents the most common complex metabolic disorder in the industrialized world and its prevalence continues to grow. Insulin resistance is closely related to obesity, and predisposes fat subjects to certain complications, including hypertension, hyperlipidemia, cardiovascular diseases and Type 2 diabetes (Reaven 1988). There is a close correlation between degree of obesity and insulin resistance in diabetics and non-diabetics. Risk of Type 2 diabetes is 11 times greater with a BMI increase from 20 to 30 kg/m2 (Carey et al., 1997).

Since obesity represents an expansion of the fatty tissue mass, insulin resistance related to excess weight could be explained by the production by fatty tissue of factors whose systemic action renders some subjects more resistant to insulin than others. The cytokines TNFa, IL-6 and IL-1 play a major regulatory role in metabolizing fatty tissue. Their increased synthesis following an inflammatory response constitutes a basic element in obesity and related metabolic disorders.

One of the many secretions from adipocytes, TNFa plays an important role in glucose and lipid metabolism. TNFa is considered an adipostat, which protects fatty cells against lipid overload (Kern et al., 1995). TNFa produced locally by fatty tissue could regulate the size of adipocytes. An overproduction in obese subjects could limit the size of adipocytes through a combination of several catabolic channels. Increased production of TNFa is proportional to fat mass (BMI) and hyperinsulinemia (Bullo et al., 2002). This cytokine is implicated as a causal factor in adiposity associated with insulin resistance and in the pathogenesis of Type 2 diabetes. The metabolic effects of TNFa would be due to several mechanisms including (Hotamisligil, 2000; Moller, 2000):

• Reduced function of genes required to maintain insulin’s normal activity (Hotamisligil et al., 1995; 1993; Kern et al., 1995).
• Indirect action by stimulating the production of stress hormones (Grimble, 2002)
• Direct action on the insulin signaling pathway. Reduction in insulin receptor tyrosine phosphorylation in muscle and fat tissue by stimulation of the TNF p55 receptor (TNFR) and of sphingomyelinase is observed in Type 2 diabetes (Hotamisligil, 1999; Kanety et al., 1995). At the molecular level, TNFa causes phosphorylation in the serine substrate of the IRS-1 insulin receptor by induction of SOCS-3. This modified form of IRS-1 has an inhibitory action (Hotamisligil et al., 1996). TNFa also interferes with transport by decreasing synthesis of GLUT-4 carriers (Halle et al., 1998; Stephens 1998; et al., 1997). These effects involve the production of H2O2 (Hansen et al., 1999). Oxidative stress due to increased production of TNFa would also occur, inducing insulin resistance at an early stage of the disease. In addition, oxidative stress would play a major role in the development of complications related to diabetes (Wierusz-Wysocka et al., 1995).
• Inhibition of lipoprotein lipase (LPL) and stimulation of hepatic lipolysis with elevated levels of free fatty acids (Patton et al., 1986).
• Nutritional effects, including de-differentiation involving negative regulation of ‘peroxisome proliferator activated receptor g’ (PPAR-g), an important receptor for insulin sensitivity and regulating cell volume and induction of apoptosis (Coppack, 2001). PPAR-g activity is also modulated by insulin, leptin, lipids and growth factors (Mueller-Wieland et al., 2001). Reduction in the activity of transcription factors such as PPAR would play an important role in the pathogenesis of cardiovascular diseases. The PPARs modulate the recruitment of white blood cells at the endothelial level, control the inflammatory reaction and lipid homeostasis of monocytes/macrophages, and regulate the production of inflammatory cytokines by smooth muscle cells. Clinical studies have shown the anti-atherosclerotic activity of PPAR-a and PPAR-g in vivo ((Duval et al., 2002).
• Increase in type 1 inhibitors of plasminogen activator in adipocytes (PAI-1). The increased incidence of cardiovascular diseases in obese subjects is related to elevated plasma levels of hemostatic factors such as fibrinogen, factor VII and inhibitor I of PAI-1. Exaggerated PAI-1 concentrations interfere with fibrin clearance and thereby facilitate formation of thromboses, including myocardial infarctions (Samad et al., 1999).
• TNFa induces elevated plasma levels of insulin and increases the expression of TGFb in fatty tissue. Insulin and TGFb increase PAI-1 activity in plasma and in fatty tissue (Samad et al., 1998). TGFb exhibits extensive biological activity and can be implicated in atherosclerosis (Wang et al.,1997) and renal fibrosis (Border, 1994), two common complications of obesity.
• TNFa exhibits cytotoxic activity for vascular endothelium and cartilage, bone and muscle tissue (Cavaillon 1995).

Other factors besides TNF are involved in insulin resistance and interfere with lipid metabolism:

IL-6

IL-6 is secreted by adipocytes. The synthesis of this cytokine is increased in obese subjects. IL-6 is involved in insulin resistance (Kern et al., 2001). Like TNFa, IL-6 inhibits the expression of lipoprotein lipase (Crichton et al., 1996) but, unlike TNFa, does not stimulate lypolysis (Feingold et al., 1992).

Angiotensin II

Angiotensin II interferes with the intracellular signalling cascade for insulin analogousto that of TNFa by stimulating tyrosine phosphorylation of the insulin receptor substrates IRS-1 and IRS-2, which leads to binding of IRS to phosphatidylinositol 3-kinase (PI3K) (Folli et al., 1999). Angiotensin II may contribute to insulin resistance in hypertensive subjects exhibiting increased activity in the renin-angiotensin system. TNFa may indirectly play a role in hypertension since this cytokine stimulates the expression of angiotensin in the liver ((Brasier et al., 1996).

Leptin

Adipocytes secrete leptin, which is a hormone with a secondary cytokine structure that exercises pro-inflammatory activity, and whose concentrations are related to body fat. Leptin receptors are transmembrane proteins similar to the IL-6 receptors (Girard, 1997). Leptin constitutes a key element in long-term regulation of food intake and homeostasis of body weight. Leptin acts at the level of the central nervous system through a specific receptor and the mediation of various neuropeptides. A leptin receptor at the level of the choroid plexus is responsible for passage across the hematomeningeal (blood-brain) barrier. Interaction of leptin with the hypothalamic receptor reduces the production of orexigenic neuromediators (i.e., which stimulate food ingestion) such as NPY (neuropeptide Y), MCH (melanin-concentrating hormone), orexines and AGRP (Agouti-related peptide), and increases the expression of anorexigenic neuropeptides, including aMSH (a melanocyte stimulating hormone), which acts on MC4R (Melanocortin-4 receptor) and CART (cocaine and amphetamine-regulated transcript) and CRH (corticotropin releasing hormone) (Jequier, 2002). Elevated levels of leptin reduce the feeling of hunger, reduce body weight, increase the body’s energy output, increase activity of the sympathetic nervous system as regards the kidneys, adrenal glands and fatty tissue and thalamic thermogenesis. Leptin also has specific effects on the gastrointestinal system (Attele et al., 2002), which suggests that food intake and homeostasis are regulated by central and peripheral signals. Leptin also has multiple effects on the endocrine, cardiovascular and autonomic nervous systems and the kidneys (Haynes et al., 1998). Like TNFa, leptin is involved in insulin resistance, but the mechanism of this interaction is still unknown.

TNFa is involved in insulin resistance in muscle and fat tissues. Obese Sprague-Dawley (S-D) rats that quickly develop insulin resistance by reducing muscular transport of glucose show increased muscle concentrations of TNFa. Administration of anti-TNFa IgG to S-D rats reduces insulin resistance and causes a reduction in the muscle levels of TNFa (Borst and Bagby, 2002). The same effect was observed in the fatty tissue of fa/fa obese rats (Hotamisligil et al., 1993). In humans, elevated tissue levels of TNFa in adipocytes and muscles together with an increased release into the (blood) circulation were observed in obese cases (Hotamisligil et al., 1995; Kern et al., 1995; Nilsson et al., 1998). These TNFa plasma levels are relatively weak and the question whether this circulating TNFa exerts a systemic biological action or effect on other organs currently remains unknown. TNFa may bond to a soluble receptor that inhibits its biological activity (Engelberts et al., 1991); the systemic effects of TNFa produced by adipose and muscle tissue would therefore be limited. However, the small amount of circulating TNFa observed in insulin resistant subjects could reflect an inflammatory source (Nilsson et al., 1998), and plasma levels may also increase in the advanced stages of disease, following other metabolic changes (Zinman et al., 1999).

Despite elevated leptin concentrations in proportion to body fat in obese subjects, the expected responses (reduction of feeling of hunger and increase in energy expended) have not been observed. These subjects are resistant to endogenous leptin. This resistance is also highlighted by the absence of leptin effect on excess weight by the administration of leptin during the therapeutic trials. The many mechanisms that play a role in leptin resistance act both centrally and peripherally, and include:

• Reduction of leptin transport across the blood-brain barrier
• Inhibition of the leptin signalling pathways of hypothalamic neurons (Jecquier, 2002).
• Expression and increased secretion of the receptor antagonist for IL-1 (IL-1Ra) related to obesity. IL-1Ra opposes the action of leptin at the hypothalamic level (Meier et al., 2002).
• The increased expression of protein-tyrosine phosphatase 1B (PTP1B) which exerts a negative regulation on leptin signalling pathways (Cheng et al., 2002). The PTPs are necessary for dephosphorylation of the insulin receptor and its initial cellular substrates. The exaggerated expression of PTP1B, with its altered catalytic activity in obese subjects, also plays a part in insulin resistance (Cheung et al., 1999).

The expression of leptin may also be partially inhibited in obese subjects by:

• catecholamines via beta-adrenergic receptors and cAMP
• long-chain fatty acids via PPAR (Girard, 1997)
• TNFa and IL-1b (Bruun et al., 2002)

Fatty acids

Free fatty acids generate peripheral insulin resistance proportional to their serum level (Boden et al., 1994) with an accumulation of lipids in the muscle tissue. This interaction may be due to the accumulation of long-chain acyl CoA that changes the action of insulin by a chronic burst of isoforms of protein kinase C(Kraegen et al., 2001).

Prolonged elevation of free fatty acid levels also induces a deficit of B-cells (lipotoxicity) similar to that observed in Type 2 diabetes (Mason et al., 1999), which would be due to apoptosis via de novo formation of ceramides and an increased production of nitric oxide (Shimabukuro et al., 1998).

Food intolerance and obesity

Chronic inflammation via action of TNFa, IL-6, leptin, angiotensin II generates insulin resistance and lipid metabolism disorders predisposing to complications associated with excess weight. In fact, most obese subjects have elevated levels of inflammatory markers that correlate closely with the degree of obesity and with the degree of insulin resistance (Invitti, 2002). This phenomenon is also observed in obese children free of any other pathology. The various mediators involved in metabolic disorders related to obesity stimulate each other, creating a vicious circle. It is thus essential to thwart chronic activation of the immune system to re-establish normal metabolic activity.
Since a major part of chronic inflammation is dietary in origin, an exclusion diet based on dietary IgG antiantigen antibody titres makes it possible to cut short the vicious circle of effects of chronic and repeated activation of the immune system.

Guidelines for measuring food-related IgG antiantigens

In obese subjects: Prevention of complications related to obesity (insulin resistance, high blood pressure and cardiovascular diseases). Since the chronic inflammatory response causes an accumulation of lipids in adipose and muscle tissue, avoidance of foods in question would make weight loss possible without necessarily resorting to a hypocaloric diet. At least part of the excess weight is related to a disrupted energy balance following an inadequate immune response.
Preliminary results after a three-month follow-up in patients showed that following a diet based on the profile of food intolerance is very encouraging, since more then 90% of individuals recorded an average weight loss of 8 kg.

Dietary advice based on food specific IgG Results

Nutrition and food science Vol 37 No 1 2007 pp 16-23

Purpose – Evidence has suggested that elimination diets based on food-specific IgG measurement can lead to improvements in chronic ill health symptoms. This paper aims to review the evidence from studies on food-specific IgG measurement and dietary change.

Design/methodology/approach – A literature review of studies on the putative role for food-specific IgG-based elimination diets was undertaken.

Findings – The use of fully standardised clinically evaluated food-specific IgG tests as a basis for elimination diet could lead to a considerable improvement in many patients' quality of life.

Originality/value – This unique review captures evidence for a viable alternative to the time consuming and expensive elimination diet/food challenge approach.

Food elimination based on IgG antibodies in irritable bowel syndrome

Food elimination based on IgG antibodies in irritable bowel syndrome: a randomised controlled trial.
W Atkinson, T A Sheldon, N Shaath, PJ Whorwell Gut 2004:53 1459-1464 doi: 10.1136

BACKGROUND: Patients with irritable bowel syndrome (IBS) often feel they have some form of dietary intolerance and frequently try exclusion diets. Tests attempting to predict food sensitivity in IBS have been disappointing but none has utilised IgG antibodies. AIMS: To assess the therapeutic potential of dietary elimination based on the presence of IgG antibodies to food.

PATIENTS: A total of 150 outpatients with IBS were randomised to receive, for three months, either a diet excluding all foods to which they had raised IgG antibodies (enzyme linked immunosorbant assay test) or a sham diet excluding the same number of foods but not those to which they had antibodies.

METHODS: Primary outcome measures were change in IBS symptom severity and global rating scores. Non-colonic symptomatology, quality of life, and anxiety/depression were secondary outcomes. Intention to treat analysis was undertaken using a generalised linear model.

RESULTS: After 12 weeks, the true diet resulted in a 10% greater reduction in symptom score than the sham diet (mean difference 39 (95% confidence intervals (CI) 5-72); p = 0.024) with this value increasing to 26% in fully compliant patients (difference 98 (95% CI 52-144); p<0.001). Global rating also significantly improved in the true diet group as a whole (p = 0.048, NNT = 9) and even more in compliant patients (p = 0.006, NNT = 2.5). All other outcomes showed trends favouring the true diet. Relaxing the diet led to a 24% greater deterioration in symptoms in those on the true diet (difference 52 (95% CI 18-88); p = 0.003).

CONCLUSION: Food elimination based on IgG antibodies may be effective in reducing IBS symptoms and is worthy of further biomedical research.

Food allergy in irritable bowel syndrome: new facts and old fallacies.

Food allergy in irritable bowel syndrome: new facts and old fallacies.
E Isolauri, S.Rautava, M.Kalliomaki Gut 2004; 53 1391-1393 10.1136

The notion of food allergy in irritable bowel syndrome (IBS) is not new. However, recent evidence suggests significant reduction in IBS symptom severity in patients on elimination diets, provided that dietary elimination is based on foods against which the individual had raised IgG antibodies. These findings should

encourage studies dissecting the mechanisms responsible for IgG production against dietary antigens and their putative role in IBS

A prospective audit of Food Intolerance among Migraine patients

Headache care Vol.2 No 2 2005 105-110

Summary. This prospective audit was set up to investigate whether migraine sufferers have evidence of IgG based food intolerances and whether their condition can be improved by the withdrawal from the diet of specific foods identified by intolerance testing. Conclusion. This pilot study audit demonstrated that migraine attacks may be related to food intolerances mediated via IgG and that changing the diet to eradicate specific foods may be potentially effective treatment for migraine.

Celiac Disease

The New England Journal of Medicine 2007; 357:1731-43

Celiac disease is a unique autoimmune disorder, unique because the environmental precipitant is known. The disorder was previously called celiac sprue, based on the Dutch word sprue, which was used to describe a disease similar to tropical sprue that is characterized by diarrhea, emaciation, aphthous stomatitis, and malabsorption.1,2 Celiac disease is precipitated, in genetically predisposed persons, by the ingestion of gluten, the major storage protein of wheat and similar grains.3 Originally considered a rare malabsorption syndrome of childhood, celiac disease is now recognized as a common condition that may be diagnosed at any age and that affects many organ systems.

Alterations of food antigen-specific serum immunoglobulins G and E ...

Alterations of food antigen-specific serum immunoglobulins G and E in patients with irritable bowel syndrome and functional dyspepsia.
Clinical and Experimental Allergy, 37, 823-830

BACKGROUND: Post-prandial worsening of symptoms as well as adverse reactions to one or more foods are common in the patients with functional gastrointestinal diseases, such as irritable bowel syndrome (IBS) and functional dyspepsia (FD). However, the role played by true food allergy in the pathogenesis of these diseases is still controversial and there are no well-established tests to identify food allergy in this condition.

OBJECTIVE: To investigate serum food antigen-specific IgG, IgE antibody and total IgE antibody titres in controls and patients with IBS and FD, and to correlate symptoms with the food antigen-specific IgG titres in IBS and FD patients.

METHODS: Thirty-seven IBS patients, 28 FD patients and 20 healthy controls participated in this study. Serum IgG and IgE antibody titres to 14 common foods including beef, chicken, codfish, corn, crab, eggs, mushroom, milk, pork, rice, shrimp, soybean, tomatoes and wheat were analysed by ELISA. Serum total IgE titres were also measured. Last, symptomatology was assessed in the study. Results IBS patients had significantly higher titres of IgG antibody to crab (P=0.000), egg (P=0.000), shrimp (P=0.000), soybean (P=0.017) and wheat (P=0.004) than controls. FD patients had significantly higher titres of IgG antibody to egg (P=0.000) and soybean (P=0.017) than controls. The percentage of individuals with detectable positive food antigen-specific IgE antibodies of the three groups did not show any significant differences (P=0.971). There were no significant differences between IBS patients, FD patients and controls in the serum total IgE antibody titres (P=0.978). Lastly, no significant correlation was seen between symptom severity and serum food antigen-specific IgG antibody titres both in IBS and FD patients.

CONCLUSION: Serum IgG antibody titres to some common foods increased in IBS and FD patients compared to controls. But there is no significant correlation between symptom severity and elevated serum food antigen-specific IgG antibodies in these patients.

IgG Antibodies against Food Antigens are Correlated with Inflammation

IgG Antibodies against Food Antigens are Correlated with Inflammation and Intima Media Thickness in Obese Juveniles
Exp Clin Endocrinol Diabetes 2008; 116:241-245

OBJECTIVE: Systemic low grade inflammation may contribute to the development of obesity, insulin resistance, diabetes mellitus and atherosclerotic vascular disease. Food intolerance reflected by immunoglobulin G (IgG) antibodies may predispose to low grade inflammation and atherogenesis. We examined the relationship between IgG antibodies specific for food components, low grade inflammation and early atherosclerotic lesions in obese and normal weight juveniles.

RESEARCH METHODS AND PROCEDURES: We determined IgG antibodies directed against food antigens, C-reactive protein (CRP) and the thickness of the intima media layer (IMT) of the carotid arteries in 30 obese children and in 30 normal weight children.

RESULTS: Obese juveniles showed a highly significant increase in IMT (p=0.0001), elevated CRP values (p=0.0001) and anti-food IgG antibody concentrations (p=0.0001) compared to normal weight juveniles. Anti-food IgG showed tight correlations with CRP (p=0.001/r=0.546) and IMT (p=0.0001/r=0.513) and sustained highly significant in a multiple regression model.

DISCUSSION: We show here, that obese children have significantly higher IgG antibody values directed against food antigens than normal weight children. Anti- food IgG antibodies are tightly associated with low grade systemic inflammation and with the IMT of the common carotid arteries. These findings raise the possibility, that anti-food IgG is pathogenetically involved in the development of obesity and atherosclerosis.

A Vegan diet free of gluten improves the signs and symptoms ...

A Vegan diet free of gluten improves the signs and symptoms of Rheumatoid Arthritis..
British Society of Rheumatology, 2001 pp 1175-1179

OBJECTIVE: Whether food intake can modify the course of rheumatoid arthritis (RA) is an issue of continued scientific and public interest. However, data from controlled clinical trials are sparse. We thus decided to study the clinical effects of a vegan diet free of gluten in RA and to quantify the levels of antibodies to key food antigens not present in the vegan diet.

METHODS: Sixty-six patients with active RA were randomized to either a vegan diet free of gluten (38 patients) or a well-balanced non-vegan diet (28 patients) for 1 yr. All patients were instructed and followed-up in the same manner. They were analysed at baseline and after 3, 6 and 12 months, according to the response criteria of the American College of Rheumatology (ACR). Furthermore, levels of antibodies against gliadin and beta-lactoglobulin were assessed and radiographs of the hands and feet were performed.

RESULTS: Twenty-two patients in the vegan group and 25 patients in the non-vegan diet group completed 9 months or more on the diet regimens. Of these diet completers, 40.5% (nine patients) in the vegan group fulfilled the ACR20 improvement criteria compared with 4% (one patient) in the non-vegan group. Corresponding figures for the intention to treat populations were 34.3 and 3.8%, respectively. The immunoglobulin G (IgG) antibody levels against gliadin and beta-lactoglobulin decreased in the responder subgroup in the vegan diet-treated patients, but not in the other analysed groups. No retardation of radiological destruction was apparent in any of the groups.

CONCLUSION: The data provide evidence that dietary modification may be of clinical benefit for certain RA patients, and that this benefit may be related to a reduction in immunoreactivity to food antigens eliminated by the change in diet.

The gut-joint axis: cross reactive food antibodies in rheumatoid arthritis

Gut 2006:55 1240-1247 originally published online 16 feb 2006

BACKGROUND AND AIMS: Patients with rheumatoid arthritis (RA) often feel there is an association between food intake and rheumatoid disease severity. To investigate a putative immunological link between gut immunity and RA, food antibodies were measured in serum and perfusion fluid from the jejunum of RA patients and healthy controls to determine the systemic and mucosal immune response.

METHODS: IgG, IgA, and IgM antibodies to dietary antigens were measured in serum and jejunal perfusion fluid from 14 RA patients and 20 healthy subjects. The antigens originated from cow's milk (alpha-lactalbumin, beta-lactoglobulin, casein), cereals, hen's egg (ovalbumin), cod fish, and pork meat.

RESULTS: In intestinal fluid of many RA patients, all three immunoglobulin classes showed increased food specific activities. Except for IgM activity against beta-lactoglobulin, all other IgM activities were significantly increased irrespective of the total IgM level. The RA associated serum IgM antibody responses were relatively much less pronounced. Compared with IgM, the intestinal IgA activities were less consistently raised, with no significant increase against gliadin and casein. Considerable cross reactivity of IgM and IgA antibodies was documented by absorption tests. Although intestinal IgG activity to food was quite low, it was nevertheless significantly increased against many antigens in RA patients. Three of the five RA patients treated with sulfasalazine for 16 weeks had initially raised levels of intestinal food antibodies; these became normalised after treatment, but clinical improvement was better reflected in a reduced erythrocyte sedimentation rate.

CONCLUSIONS: The production of cross reactive antibodies is strikingly increased in the gut of many RA patients. Their food related problems might reflect an adverse additive effect of multiple modest hypersensitivity reactions mediated, for instance, by immune complexes promoting autoimmune reactions in the joints.

Toward an understanding of Allergy and In-Vitro Testing

By Mary James N.D Great Smokies Diagnostic Laboratory

Food represents the largest antigenic challenge facing the immune system. Assuming complete digestion, an intact intestine, a sturdy constitution, and minimal antigenic exposure such that the immune system is not over whelmed, all goes well. Weaknesses in one or more of these areas, however, can result in immune attacks upon foods as if they were foreign invaders. A long list of conditions have been associated with food reactions including fatigue, migraine, irritable bowel disease, gallbladder disease, arthritis, asthma, rhinitis, ADHD, enuresis, epilepsy ,eczema, psoriasis, apthous ulcers and recurrent sinusitis, otitis media and other infections.

The therapeutic effects of eliminating allergic foods ...

The therapeutic effects of eliminating allergic foods according to food-specific IgG antibodies in irritable bowel syndrome
Yang CM, Li YQ. Zhonghua Nei Ke Za Zhi. 2007 Aug; 46(8):641-3

OBJECTIVE: To explore the therapeutic effects on irritable bowel syndrome (IBS) by eliminating the allergic foods according to food-specific IgG antibodies and to clarify the etiopathological role and mechanism of food allergy.

METHODS: The food-specific IgG antibodies to a panel of 14 different food antigens in serum were detected with ELISA in fifty five cases with diarrhea-dominant IBS, thirty two with constipation-dominant IBS and eighteen normal controls. The frequency and severity index of symptoms and scores of Irritable Bowel Syndrome Quality of Life (IBS-QOL) in thirty five cases with positive food-specific IgG were observed before and after elimination of allergic foods for two months.

RESULTS: The positive rate of serum food-specific IgG antibodies was 63.6 percent in patients with diarrhea-dominant IBS and 43.8 percent in constipation-dominant IBS. Both were higher than that in normal controls. After eliminating allergic foods for four weeks according to the levels of serum food-specific IgG antibodies, the frequency of symptoms decreased from (3.79 +/- 1.58) to (1.67 +/- 0.70) per week and the severity from 3.18 +/- 1.46 to 1.52 +/- 0.67 with significant differences. After eight weeks, the frequency of symptoms decreased from (3.79 +/- 1.58) to (1.53 +/- 0.69) per week and the severity from 3.18 +/- 1.46 to 1.45 +/- 0.66, also with significant differences. After eliminating allergic foods, the overall health score and the eight dimensionality integrals of QOL except avoiding food in patients with IBS increased significantly than those before treatment. At the end of eight weeks, the symptoms relieved completely in 31.4 percent of the cases and remarkably in 34.3 percent.

CONCLUSIONS: Abnormal immune reactions mediated by IgG antibodies coexisted in patients with IBS. It is of great significance in treating IBS by eliminating the allergic foods according to the serum level of food-specific IgG antibodies.

Circulating immune complexes induced by food proteins ...

Circulating immune complexes induced by food proteins implicated in precocious myocardial infarction
Mustafa A, Hamsten A, Holm G, Lefvert AK. Panminerva Med. 1995 Sep; 37(3):137-41.

BACKGROUND: Circulating immune complexes (CIC) are frequently found in postinfarction patients. The constituents of these CIC are mostly unknown. AIM: The objective of the current study was to assess whether CIC containing alimentary proteins and antibodies against these proteins are implicated in precocious myocardial infarction (MI).

METHODS: Seventy-six survivors (67 men and 9 women, mean age 39 years) of a first MI before the age of 45 years were enrolled in this study. Two control groups were included. One group consisted of age-matched, randomly selected, population-based healthy individuals, 79 men and 11 women, without features of coronary heart disease. An additional control group was used only for the determination of serum antibodies against some of the alimentary proteins and consisted of 139 healthy blood donors, 95 men and 44 women, with a mean age of 42 years. Sucrose density gradient centrifugation, gel filtration and precipitation by polyethylene glycol were used for the isolation of CIC, and enzyme-linked immunosorbent assay (ELISA) was used to measure the immunoglobulin levels and specific antibodies against alimentary proteins in both sera and isolated CIC. Sodium dodecylsulfate (SDS) polyacrylamide gel electrophoresis and Western blotting were used to determine alimentary proteins in the CIC.

RESULTS: Alimentary antigens/antibodies were present in immune complex form in seven out of 14 (50%) postinfarction patients who had persistent high concentrations of CIC, the latter constituting 18% of the entire group. Antibodies of the IgG isotype predominated. A rise in CIC, signs of activation of the classical complement pathway, and a rise in plasma concentrations of von Willebrand factor antigen (vWFAg) were evident within 1 week in four patients subjected to a 2-week elimination diet followed by a single challenge with cow's milk.

CONCLUSION: This study suggests that dietary proteins occasionally give rise to persistent CIC, which may predispose to MI at a young age.

Food Allergy and Infantile Autism

Lucarelli S, Frediani T, Zingoni AM, Ferruzzi F, Giardini O, Quintieri F, Barbato M, D'Eufemia P, Cardi E. PMID: 8869369

The etiopathogenesis of infantile autism is still unknown. Recently some authors have suggested that food peptides might be able to determine toxic effects at the level of the central nervous system by interacting with neurotransmitters. In fact a worsening of neurological symptoms has been reported in autistic patients after the consumption of milk and wheat. The aim of the present study has been to verify the efficacy of a cow's milk free diet (or other foods which gave a positive result after a skin test) in 36 autistic patients. We also looked for immunological signs of food allergy in autistic patients on a free choice diet. We noticed a marked improvement in the behavioural symptoms of patients after a period of 8 weeks on an elimination diet and we found high levels of IgA antigen specific antibodies for casein, lactalbumin and beta-lactoglobulin and IgG and IgM for casein. The levels of these antibodies were significantly higher than those of a control group which consisted of 20 healthy children. Our results lead us to hypothesise a relationship between food allergy and infantile autism as has already been suggested for other disturbances of the central nervous system.

Food Intolerance and its impact on chronic disease

Dr Mike C Matthews MB BSc
Dr Mathews is a Graduate of the University College of London. And has been a General Practitioner for 26 years.

SUMMARY
The first course of action for most people is to go to their GP to find solutions to their problems. Some patients are fortunate to get relief from symptoms without recourse to drugs but large numbers are prescribed antibiotics, painkillers, anti-depressants, anti-inflammatory drugs or ointments which are in the main providing only short term solutions and may even be damaging in the long term. The conventional approach works well for most but not everyone gets better!

It is becoming increasingly evident that there is a great deal of positive benefit to growing numbers of patients who are reporting often quite outstanding improvements to their health by the simple elimination of certain foods from their normal eating pattern. Indeed many patients reported having had their illnesses all their lives - and then went on to find relief within weeks!

Using the Genesis Diagnostics 93 Food IgG kit, YNL undertook a study of 2567 patients with long-term illnesses to investigate the impact of food intolerance on the chronically unwell. It was conducted with the assistance of the University of York. The results show that a relationship may exist between chronic illnesses and commonly eaten foods.

More than seven out of ten patients reported distinct relief from their symptoms, which had troubled them for an average of over twelve years. Most patients reported apparently intractable illnesses within six main disease conditions - gastrointestinal (mainly IBS), neurological (mainly migraines and headaches), dermatological (mainly eczema and psoriasis), musculo-skeletal (mainly arthritis), respiratory (mainly asthma, rhinitis and sinusitis) and psychological (nausea, ADHD, panic attacks and depression).

Over 97% of respondents reported that they were able to make changes to their eating habits, and the findings were that nearly two thirds were able to alter their diet rigorously. 79.2% of these reported significant benefit and 77% at the same time found relief within 60 days.

Where dietary change was reported to be moderate, a creditable 66.9% reported useful improvement.

It is reported widely that patient compliance with elimination diets is a key problem for success. In this study greater than 95% compliance was reported with more than 84% giving the highest score possible for ease of use. 87.1% of respondents recommended the test to others.

IgG vermittelte Nahrungsmittelallergie ... Dissertation

Einleitung

Funktionelle und psychovegetative Beschwerden von Fibromyalgiepatienten (z.B. polytope Schmerzen, Stressintoleranz, Abgeschlagenheit, Migräne, Depressionen, Schlafstörungen, schnelle Ermüdbarkeit u.a.) und insbesondere das Colon irritabile ähneln den Beschwerden von Patienten mit Nahrungsmittelallergien bzw. Nahrungsmittelunverträglichkeiten. Spezifische histologische Veränderungen fehlen bislang, zelluläre Entzündungszeichen lassen sich nicht nachweisen. Häufi g fi ndet sich eine Verschlechterung der Symptomatik bei intermittierenden entzündlichen Erkrankungen. Es sind spontane Remissionen beschrieben, häufi g handelt es sich jedoch um ein chronisches Krankheitsbild. Zur Therapie werden üblicherweise Physiotherapieverfahren, Wärmeanwendungen, Antidepressiva, NSAR oder Corticoide eingesetzt.

Anlass zur Initiierung dieses Projektes waren unaufgeforderte Rückmeldungen von Fibromyalgie-Patienten, die über eine deutliche Besserung Ihrer Symptome auf Grund einer Ernährungsumstellung berichten und Studien, die einen positiven Einfluss einer Ernährungsumstellung bei Patienten mit rheumatoider Arthritis zeigten 15,25,27,43,48. Der Untersucher wurde motiviert durch Untersuchungen zum Chronic fatigue syndrome (CFS) und Nahrungsmittelunverträglichkeiten 9,33,54 und die Arbeiten von Enestrom, der eine vermehrte IgG Ablagerung in der Haut von Fibromyalgie-Patienten nachweisen konnte 19,20.

Die größte Herausforderung in der Handhabung von Nahrungsmittelallergien und Nahrungsmittelintoleranzen ist die Identifizierung der verantwortlichen Nahrungsmittel. Die Unterscheidung von allergischen Reaktionen und Unverträglichkeiten ist schwierig. Eine Abklärung mit RAST und Prick-Test ist in der Regel nicht ausreichend 7,21,23,34,47,50. Das Ziel war es, durch differenzierte Untersuchungsverfahren neue therapeutische Ansätze in der Behandlung der Fibromyalgie zu finden.

Originaldissertation auf Verlangen