Tuesday, July 26, 2016

Immune Cells

The role of immune networks is to defend the body against foreign invasion. Microbes such as bacteria invade the body and activate innate antibacterial systems, such as the complement cascade. Polymorphonuclear leukocytes are attracted to this activity and attempt to ingest the bacteria.

The surfaces of the body are protected by cells on duty much like a military organization defends a country. The interior body surfaces are lined with a moist mucous-secreting surface that senses and reacts to the ambient environment. Antigens are protein molecules that are recognized by immune cells. Any chemical can link to a protein and become an antigen. Immune sensors or lymphoid tissues are present in the surface linings or mucosa of the intestine and respiratory tract (MALT).

These sensors are mast cells, macrophages and mobile lymphocytes of both T and B varieties. B and T-helper lymphocytes can only see antigen presented by macrophages and other antigen-presenting cells (APC).

The purpose of the surveillance is to detect and respond to foreign antigens. In the gut, lymphocytes are also contained in follicles, the solitary lymphoid nodules (SLN), found along the length of the intestine and in much of the upper and lower respiratory tracts. SLNs sample the soluble and particulate matter from the environment. The gut-associated lymphoid tissues (GALT) and the lung or bronchus-associated lymphoid tissues (BALT) are sensing agents for the whole body, identifying antigens for later detection by internal immune defenses. Both GALT and BALT and SLNs, contain predominantly B cells in which the major immunoglobulin classes synthesized are IgM and IgA.

Antigen Presenting Cells

Immune responses often begin with macrophages, dendritic cells and other antigen-presenting cells (APC) that ingest process and then present antigens on their surface. The antigen signal attracts other immune cells who recognize it and are activated by it. Antigen is presented adjacent to the major histocompatability complex (MHC) proteins on the surface of APCs. The details of how APCs ingest, digest and then express foreign antigens are being worked out. The antigen moves through the cell membrane and is incorporated into a phagosome which interacts with acts endoplasmic reticulum, a protein transfer system that moves the antigen via a transporter to a location in the cell where the antigen binds to MHC class I molecules. The antigen-MCH complex is then moved thorough the cell membrane to appear on the outside as a receptor.

Molecules on bacterial membranes activate toll-like receptors (TLRs) on macrophages and dendritic cells. These cells respond by secreting proinflammatory cytokines as well as proteins such as CD86 and CD40 that activate other cells amplifying the original signals and exciting an inflammatory cascade. Dendritic cells (DCs) discover antigens in peripheral tissues and then migrate to the local lymph nodes, where they encounter CD4+ or CD8+ T cells, which are activated by the presentation of antigen-derived peptides in association with major histocompatibility complex (MHC).

DCs take up antigen through different receptor families, such as Fc receptors for antigen-antibody complexes, C-type lectin receptors (CLRs) for glycoproteins, and pattern recognition receptors, such as Toll-like receptors (TLRs), for microbial antigens. Geijtenbeek et al suggested that:” DCs are continuously sampling and presenting self- and harmless environmental proteins to silence immune activation. Uptake of self-components in the intestine and airways are good examples of sites where continuous presentation of self- and foreign antigens occurs without immune activation. In contrast, efficient antigen-specific immune activation occurs upon encounter of DCs with nonself-pathogens. Recognition of pathogens by DCs triggers specific receptors such as TLRs that result in DC maturation and subsequently immune activation. Here we discuss the concept that cross talk between TLRs and CLRs, differentially expressed by subsets of DCs, accounts for the different pathways to peripheral tolerance, such as deletion and suppression, and immune activation.”

Monocytes are circulating macrophages that can enter tissue spaces and promote inflammation. Macrophages are found within the endothelium generally and are concentrated in the lung, liver and spleen where they remove antigen and immune complexes from the blood.

Some tissues have resident macrophages such as the Langerhan's cells in the skin. Killer T-cells recognize antigen presented on MHC class I on all types of somatic cells. The purpose of the surveillance is to detect, and respond to foreign antigens. Since most antigens are proteins and foreign proteins arrive daily in the food ingested, I am interested in the mechanisms by which food proteins activate immune cells and cause disease.

APCs can ingest foreign protein and process them into peptides in proteasomes. Peptides are then transported into the endoplasmic reticulum to MHC class I molecules for presentation. Houde et al, for example, showed that latex beads labelled with fluorescent ovalbumin (egg white protein) were ingested and fluorescence could be detected in the cytoplasm, indicating that proteins are moved from outside into the cyoplasm for degradation by proteasomes. They showed that phagosomes are a site of loading onto MHC class I molecules on the cell surface, leading to T-cell stimulation.


Two major groups of lymphocytes are recognized as Thymus dependent or T-lymphocytes; and Bursa dependent or B-lymphocytes. Adaptive immune responses require B cells to provide antibody and T cells to provide cell-mediated immunity. Cell surface receptors recognize antigens. B-lymphocytes learn make antibodies to specific antigens. Although T and B cells share a common progenitor, their development occurs in different locations in the body. B cells develop in the bone marrow and mature in lymphoid tissue. T lymphocyte progenitors leave the bone narrow and travel to the thymus where they mature.
The identity of a foreign molecule, microorganism or cell, is recognized by an antigenic determinant, an amino acid sequence, usually contained in an intact protein. Once an antigenic determinant is recognized, its sequence is remembered by clones of antigen-specific B and T-memory cells which can activate other B lymphocytes that make antibodies against the antigen. T memory cells are also referred to a as helper T cells which are activated by the binding of a specific antigen encountered in the past, a signal that initiates defense against familiar pathogens.

One of the growing complexities in immunology is the description of cell surface receptors for a growing list of cytokines. Research reports are dense with acronyms, abbreviations and codes that may deter even an experienced reader. Some of these markers are described as CD followed by a number; CD122, for example is a receptor for interleukin 2- . In addition some descriptions emphasize the presence or absence of a well-studied receptor; CD122 + or -. CD receptors may be associated with other surface molecules in complexes. For example, natural killer T lymphocytes (NKT) have CD94-NKG2 complexes that bind to major histocompatibility complex (MHC) class Ib, aka Qa-1, on the surface of antigen presenting cells. CD8+ suppressor T cells regulate peripheral immune responses.
The frequencies of blood lymphocyte subsets are monitored by flow cytometry using monoclonal antibodies to identify subtypes: for example, OKT4 identifies CD4+, T-helper cells and OKT8 identifies CD8+, T-suppressor cells.

Virus-specific CD8 and CD4 T lymphocytes play an important role in controlling HIV replication; however CD4 and CD8 lymphocytes are infected by HIV virus. Identifying and counting CD4 cells is a major tool in following patients with AIDs taking antiretroviral medications.

See Immunology Notes at Alpha Online

Thursday, July 21, 2016

Food Allergy

The problem is not that 25% of people recognize symptoms from food ingestion, but that many more people do not recognize that food is making them ill. We hope the reader will take the time to find out why we think food allergy is such an important mechanism of disease and how to resolve common food-related health problems by diet revision. Food allergy, as a topic in medicine, has been suppressed for many years and is not taught in medical schools. Too many vested interests have much to lose if more people discovered that popular foods were making them ill. Commonly quoted "expert" opinions tend to minimize the incidence and importance of food allergy. While the dogma is misleading, it represents vested interests and is remarkably persistent.

The conviction that food allergy is a ubiquitous cause of disease comes from knowing the benefits of careful diet revision in medical practice. In response to allergy lobby groups in the USA, the US Congress passed a bill that requires notice on the labels of foodstuffs that contain eight of the most common food allergens. The Food Allergen Labeling and Consumer Protection Act, will require plain English labeling beginning in 2006 of products containing wheat, milk, soy, peanuts, tree nuts, fish, shellfish, or eggs. The bill also requires the Food and Drug Administration to develop a definition of the term "gluten-free" to help those with celiac disease and who require a gluten free diet for other reasons.

The concept of immune responses to food antigens is useful in understanding many diseases. Many of the major unsolved disease of our civilization are either degenerative and/or inflammatory and many are recognized to be inflammatory, immune-mediated, hypersensitivity diseases. In this book, a general theory of hypersensitivity disease as a continuum of disease-causing mechanisms is presented. The term "hypersensitivity" refers to immune-mediated processes that lead to disease. As we consider the possible role of food antigens in causing or contributing to immune-mediated diseases, we look for opportunities to help patients with simple and safe therapeutic strategies such as diet revision. The basic phenomena that concern us are:
  • Food antigens activate immune networks.
  • Activated immune networks produce symptoms
  • Long-term activation of immune networks causes chronic disease, with inflammation in target organs.
  • The food supply is the most abundant and continuous source of antigenic material.

Different types of food allergy

1. The immediate or type 1 food allergy pattern is easily recognized because it involves quick and dramatic symptoms. Hay fever is the most common type 1 allergy and can be diagnosed by allergy skin tests. Some food allergy is also type 1 and shows up on skin tests.

2. Delayed patterns of food allergy are not so obvious and generally go unrecognized. Allergy skin tests do not show this problem nor do IgE antibody tests. Symptom onset is delayed many hours after eating foods and chronic disease is often the result. Rheumatic diseases, autoimmune diseases, multiple sclerosis, insulin-dependent diabetes, thyroiditis, psoriasis are examples of hypersensitivity diseases that involve humoral and cell-mediated immunity. The common specific problems that are related to food allergy include asthma, rhinitis, atopic dermatitis, urticaria, anaphylaxis, angioedema, allergic gastroenteropathy, and allergic arthritis.

Many patients will express several of these hypersensitivity phenomena over a lifetime and demonstrate an underlying tendency to be hypersensitive. An important concern is the possibility that the chemical soup created by our civilization drives increasing numbers of individuals into hypersensitivity illness. The advocates of a broad definition of food allergy run the risk of being evangelical.

At Alpha Nutrition, a major commitment is to educate people about delayed patterns of food allergy and to point to opportunities people have to resolve serious illness on their own. Our strategies of self-management are simple and straight forward, but require knowledge, perspective and self control. We are the first to acknowledge that some people lack these prerequisites and our information will not help them.

Dr. Gislason stated: "I began to learn about food allergy in 1981 when I first developed inflammatory arthritis. I discovered a simple truth that eating a few safe foods resolved my illness and returning to my previously normal diet recreated the illness that was so severe, I could not work or enjoy life. I thought that my medical colleagues would be as excited as I was to discover that such a serious illness could be cured with diet revision. I did encounter the occasional MD who shared my enthusiasm for further research but most MDs were hostile to the science of food allergy, even when the therapies they offered patients were ineffective and even harmful. I have learned a lot about the politics of medicine and the strategies used by corporations to control the market place. Corporate control has advanced remarkably since I began my quest to understand the mechanisms of food allergy and to teach self-management solutions. Drug companies own medical practice and compete for their market share with skill, determination and huge promotional budgets. They do not want people to solve health problems on their own. They want people to depend on MDs and buy dru
gs "

Learn More About Food Allergy at Alpha Online

Inflammation in Vascular Disease

The mechanisms of arterial disease appear to be multiple. Hollander of Boston University suggested that atherosclerosis was an autoimmune disorder with immune complexes injuring blood vessel walls. We think that circulating immune complexes often contain food proteins as antigens and this mechanism is important in causing a wide spectrum of food allergic disease. Since proteins derived from meat, milk, eggs and wheat have the highest risk of appearing in the blood as immune complexes, these foods are reduced or eliminated in the Alpha Nutrition Program.
We ask a simple question - If there is any possibility that chronic symptoms such as attacks of migraine, heart rhythm abnormalities, digestive disturbances, breathing difficulties or brain dysfunction are linked to food ingestion, would it not be prudent to investigate and remove food -causes using diet revision as an inexpensive, safe, effective strategy?

Keaney et al reported that:” background Inflammation within vulnerable coronary plaques may cause unstable angina by promoting rupture and erosion. In unstable angina, activated leukocytes may be found in peripheral and coronary-sinus blood. “

A non-specific indicator of inflammation is the C-reactive protein levels in the blood. Elevated levels are associated with increased risk of heart attacks and strokes. For example, Ridker et al studied 27,939 apparently healthy American women, who were followed for eight years for the occurrence of myocardial infarction, ischemic stroke, coronary revascularization, or death from cardiovascular causes. Elevated C-reactive protein levels were a better predictor of vascular events than low LDL cholesterol levels. The researchers reported that: ” 77 percent of all events occurred among women with LDL cholesterol levels below 160 mg per deciliter (4.14 mmol per liter), and 46 percent occurred among those with LDL cholesterol levels below 130 mg per deciliter (3.36 mmol per liter)… C-reactive protein and LDL cholesterol measurements tended to identify different high-risk groups, screening for both biologic markers provided better prognostic information than screening for either alone.”

Myeloperoxidase is another serum marker of inflammation that may be informative.  Myeloperoxidase is an enzyme that generates reactive oxygen species, is released from white blood cells. In one study, plasma myeloperoxidase levels were predictive of subsequent coronary events in patients with chest pain. Myeloperoxidase levels, in contrast to troponin T, creatine kinase MB isoform, and C-reactive protein levels, identified patients at risk for cardiac events in the absence of myocardial necrosis.“

Inflammation can be treated by removing the causes of inflammation, treating infection and using anti-inflammatory medication such as ASA and  Statins. The role of food proteins and immune complexes as agents of inflammation is rarely investigated and may turn out to be the hidden agent behind many heart attacks and strokes. Several studies are investigating a variety of immune-modulating therapies to prevent heart attacks and strokes.

See Arterial Disease at Alpha Online


Obscurity to Big Pharma

Fibromyalgia and the chronic fatigue syndrome have evolved from relative obscurity to become a brand name for a bizarre assortment of products and services. Drugs are prescribed by physicians in a haphazard manner as if they were browsing through the pharmacy shelf picking out drugs at random. A variety of pain relief clinics offer another random assortment of services. A variety of imaginative explanations is offered with little evidence. Sick lifestyles and environment problems are generally ignored. Drug prescriptions include pain relievers, muscle relaxants, antidepressants, anti-anxiety drugs, sleeping pills and anticonvulsants.

WebMD in 2016 offered this  perspective:” Your fibromyalgia specialist may prescribe pain medication or antidepressants to help treat the pain, fatigue, depression, and anxiety that comes with the disease. In addition, your doctor may recommend physical therapy, moist heat, regular aerobic exercise, relaxation, and stress reduction to help you self-manage your symptoms. There is no one "pill" that treats or cures fibromyalgia. A multidisciplinary approach that uses both medication and alternative or lifestyle strategies seems to work best to treat fibromyalgia symptoms.”

Lyrica and Other Useless Drugs

Big Pharma has moved the marketing of Fibromyalgia into big-money TV advertising. The US FDA approved the drug, Lyrica (Pregabalin), for fibromyalgia and TV ads show happy patients enjoying a pain-free life.  This is  a serious anticonvulsant drug with alarming negative effects including suicide. Lyrica can cause life-threatening, allergic reactions.  Symptoms of an allergic reaction include swelling of the face, mouth, lips, gums, tongue, throat or neck. Lyrica may cause depression, anxiety, restlessness, trouble sleeping, panic attacks, anger, irritability, agitation, aggression, dangerous impulses or violence, or extreme increases in activity or talking.  

Our questions are why would any physician prescribe and why would any patient take this potentially dangerous drug?? 

Our view is that the Chronic Fatigue Syndrome (CFS) , Fibromyalgia and related disorders are not discrete diseases in the usual sense, but patterns of maladaptive responses to food and the environment. We believe that chronic fatigue syndrome is an expression of non-specific hypersensitivity disease and should be treated with diet revision as the first and most essential form of therapy. 

The Alpha Nutrition Program is designed to improve fibromyalgia, chronic fatigue and related disorders. The most definitive clearing program is a food holiday, using an elemental nutrient formula (Alpha ENF), composed of nutrients in their pure form with no other food intake. Alpha ENF allows a sick person to return to a baseline of normal functioning, without the intake of numerous adverse substances that may have been present in their food supply.

See www.nutramed.com/fibromyalgia/