auto immunity

1©2008 BAUMAN COLLEGE Holistic Nutrition and Culinary Arts 800-987-7530 • www.baumancollege.org©2008 BAUMAN COLLEGE Holistic Nutrition and Culinary Arts 800-987-7530 • www.baumancollege.org

I find it mystifying that most doctors are not aware of,or even interested in learning, the causes, triggers, and natural approaches to assessing, managing,

and alleviating autoimmune conditions.

Ed Bauman, M.Ed., Ph.D.

When people are living stressful, chaotic lives, noteating well, drinking coffee in the morning, diet

soda during the day, and alcohol with dinner and intothe evening, it is no wonder that they become vulnera-ble to dis-ease. This susceptibility, coupled with an ever-increasing exposure to environmental pollutants in ourair, water, and food, creates a disturbance in one’sblood, organs, and tissues that provokes an up-regu-lated immune response.

The prevalence of this category of disease, whichcan affect more than one body site or system, is a sadcommentary on the toxic-stress culture of our so-calledcivilized society. Metabolically, an autoimmune condi-tion speaks to a defect or, in most cases, an acquireddeficiency in our natural defense systems — from the

skin on the outside to the liver, gut, and cell membraneson the inside. They become less proficient at clearingforeign molecules, called antigens, that can form com-plexes with antibodies and become part of our joints,nerves, and endocrine tissues if they are not clearedfrom the body. Immune suppression, the mainstreammedical treatment of choice for auto-immune disorders,completely overlooks the upstream cause, toxic over-load, and the downstream detoxification deficiency thatleads to the immune system’s confusion in distinguish-ing self from invader.

Let’s investigate this phenomenon and attempt tosolve the mystery of why the body sometimes eats itselfand how this tendency can be turned around.

In an intricate dance of complexity, our immune sys-tems protect us from harmful and potentially lethalorganisms and substances that enter our bodies from the

Self Destructive Tendencies: Natural Strategies for Managing Autoimmunityby Jodi Friedlander, M.S. & Ed Bauman, M.Ed., Ph.D.

Self Destructive Tendencies: Natural Strategies for Managing Autoimmunity—CONTINUED

outside world. Too little immune involvement and wewould quickly succumb to the numerous viruses, bacte-ria, fungi, and parasites that assault our bodies daily. Wewould also likely fall prey to cancerous growths. Toomuch activity and we become susceptible to autoimmu-nity, a misdirected immune reaction wherein the body’sdefense system attacks its own tissues.

Autoimmune diseases (AD), when considered as sin-gle entities, are rare, but taken as a group they are farmore prevalent, affecting 14 to 22 million people in theUnited States, five to eight percent of the population(Fasano & Shea-Donohue, 2005). AD is the third mostcommon category of disease in the U.S., after cancer and

heart disease. At least 75% of those suffering from ADare women (JHU, 2001). In fact, AD, which includes atleast 80 distinct disorders, are among the top ten lead-ing causes of death in women up to age 65 (JHU, 2001).

Among the best known and most studied AD arerheumatoid arthritis, which attacks proteins within thejoints; systemic lupus erythmatosus (SLE), which attacksDNA, RNA, nuclei, erythrocytes, and more; and Type I(juvenile) diabetes, which attacks the insulin-producingislet cells of the pancreas.

The list of autoimmune diseases and the objects oftheir antibody attacks also includes (Royston, 2003):

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CONDITION ANTIBODY ATTACKS

Addison’s disease Adrenal cells

Autoimmune hemolytic anemia Erythrocytes

Chronic active hepatitis Hepatocytes

Graves’s disease Thyroid-stimulating hormone receptor

Idiopathic hypoparathyroidism Parathyroid cells

Idiopathic thrombocytopenic purpurea Platelets

Iritis Iris of the eye

Myasthenia gravis Acetylcholine receptors

Pemphigus Intercellular substance of skin

Pernicious anemia Gastric parietal cells

Polymyalgia rheumatica Muscle cells esp. in proximal muscle groups

Primary biliary cirrhosis Mitochondria within liver

Rheumatoid arthritis Proteins within joints

Scleroderma Nuclei and centromeres of some organs

Sjogren’s syndrome Nuclei and centromeres

Systemic lupus erythematosus (SLE) Nuclei, DNA, RNA, erythrocytes, etc.

Thyroiditis (Hashimoto’s) Thyroid

Type I (Juvenile) Diabetes Pancreatic islets

Ulcerative Colitis Large bowel endothelium

Vitiligo Melanocytes (of skin)

3©2008 BAUMAN COLLEGE Holistic Nutrition and Culinary Arts 800-987-7530 • www.baumancollege.org


©2007 BAUMAN COLLEGE Holistic Nutrition and Culinary Arts 800-987-7530 • www.baumancollege.org

When Good Immune Systems Go BadThe immune system exists to keep at bay the organisms— primarily bacteria and viruses — that would otherwiseconsider us a fine dining experience. It operates at thefollowing three distinct levels, each one activated anddeactivated as necessary to handle specific conditions:

. The barrier defenses of our skin and mucusmembranes, along with their componentbiochemicals, work to prevent invaders fromentering the “restaurant” — our bodies;

. The non-specific search-and-destroy mission ofthe innate immune system provides the fastfirst line of defense against bacteria, parasites,or virus-infected cells; and

. The slower adaptive response of the humoral(antibody-related) and cell-mediated immuneprocesses, directed primarily at viruses, conferlong-term immunity from future invasions ofpathogens that have already sampled ourinternal “buffets.”

Each of these immune functions interacts with theothers and is carefully orchestrated to provide a systemthat neither over-reacts nor under-reacts, and one thatexpresses tolerance to the self. These layers of checksand balances do a very good job of weeding out self-reactive cells, but sometimes things go wrong. Whenthey do, it isn’t because the immune system itself hasmistakenly gotten off-track somehow, but that it hasreceived an assault to which it is reacting to the best ofits ability.

While an in-depth description of the workings ofthe immune system is not appropriate for the purposesof this paper, a brief consideration of one set of its cells— T cells — will be helpful in understanding some ofwhat occurs in auto-immune diseases. The body pro-duces lymphocytes — B and T cells — which are born inthe bone marrow and mature in the marrow or in thethymus gland (thus the ‘B’ and the ‘T’). B cells produceantibodies and are responsible for humoral immunity,conferring long-term protection against pathogens that

have previously invaded us. T cells are involved in boththe innate and the adaptive responses. There are differ-ent types of T cells — cytotoxic T lymphocytes (CTLs),which help virus-infected cells commit suicide; regula-tory or suppressor T cells that work to keep other T cellsunder control; and helper T cells, which secrete proteinscalled cytokines that send signals that dramaticallyaffect other immune system cells. These last appear intwo forms — Th-1 and Th-2 — and drive cell-mediatedand antibody-mediated immune reactions.

T cell receptors, on the surface of the cells, receivemessages from human leukocyte antigen (HLA), a classof protein designed to present possible antigens toimmune cells. HLA is encoded by the major histocom-patibility complex (MHC). Histo means tissue, and this isthe means by which our bodies recognize self proteins;HLA is able to differentiate self from invader. When a Tcell is confronted with what it considers to be a non-self molecule, it raises an alarm and notifies other cellsto mount an immune attack by emitting cytokines.

T helper cells do not secrete cytokines haphazardly,but rather in subsets of mixtures that create separateimmune effects. Th-1 cytokines instruct the innate andadaptive systems to produce cells and antibodies thatare particularly effective against invading viruses orbacteria in the blood and tissues (Sompayrac, 2003; p.61). A dominance in this subset is generally found inautoimmune individuals, its production driven byinflammation (Metagenics, n.d.). Th-2 cells producecytokines necessary to initiate an allergic reaction or todefend against a mucosal infection (Sompayrac, 2003;p. 61). Immune system dysfunctions occur when eithersubset is dominant, so a balance between the two iscritical to good health.

CausesTheories abound as to why the body begins to attack non-self proteins. Because of the complex workings of theimmune system, no single cause or pathway stands out asthe culprit, though adaptive immunity and an imbalancetowards Th-1 dominance appear to underlie the pathol-




ogy. It is likely that multiple mechanisms are responsiblefor the initiation and progression of hyperimmunity.

All humans experience a certain degree of autoim-munity, as measured by autoantibodies — antibodiesdirected at the self — and other immune markers (JHU,2001). This generally benign condition is considered anormal part of the human experience, perhaps neces-sary for good health, but if the number of markersincreases considerably, the condition can progress to apathological level.

AD are generally divided into organ-specific andmulti-system groups (Sompayrac, 2003; p. 102), but thisserves only to identify the target(s) of the disease, asthese immune reactions all reflect system-wide involve-ment and, perhaps, a shared mechanism of action.

There are two very popular, though somewhatdebunked, hypotheses surrounding the etiology of AD:

. Molecular mimicry has been a favoritehypothesis of immunologists attempting toexplain how infections might lead to abreakdown in self tolerance. The theory holdsthat when lymphocytes — usually T cells — areactivated in response to a microbial infectionand they recognize the invading antigen’s

peptides, the amino acid sequencing might besimilar enough to that of a self antigen that theimmune system launches an attack against theself, as well. But because our bodies are so goodat eliminating self-reactive lymphocytes,another factor is required to keep themactivated: ongoing inflammation in the sametissues in which the self-antigen is expressed,caused by the invading microbe or by some othercoincidental infection or trauma (Sompayrac,2003; p. 102). This would set off a new cascadeof events and chemicals destined to keep theself-reactive T cells activated. Newer evidencesuggests that in most human autoimmuneconditions molecular mimicry may play a role inthe progression of the disease, but not in itsinitiation (Fasano and Shea-Donohue, 2005).

. The hygiene hypothesis states that the immunesystem requires constant low-level stimulation,beginning early in life, to work efficiently atprotecting us from the “bad guys”. Better hygieneand protection from disease by immunization arethought to contribute to reduced immunologicalstrength later in life, in much the same way thatan unexercised muscle will atrophy. How can theimmune system learn to recognize the “badguys” if there are never any of them around? Thisview holds that the immune system requires ahardening period — time in which to mature — inorder to prevent over-activation, hyperimmunity,from overproduction of Th-1 cells later on. Thereis not much research to support this hypothesis,but some well-studied populations have co-existed with parasites and other micro-organismspicked up from the environment withoutexperiencing any of our autoimmune conditions.There is also evidence that children who growup around pet dander or in close contact withfarm animals experience a lower incidence ofasthma (Ullrich, 2004). As will be explainedfurther on, this theory, too, is now in question.

T cells, shown in yellow, have multiple functions in theimmune system — including regulating each other.Image Courtesy of Haverford University.



Triggers and Mediators No one knows with any degree of certainty what causesautoimmune diseases, but the most current and well-designed research studies point to several factors thatinitiate or exacerbate the condition. Before discussingthem, though, it is important to understand that geneticsusceptibility is almost always a requirement for thedevelopment of AD. This is not to say that geneticdefects cause autoimmunity but rather that specificgenetic polymorphisms — small changes in DNAsequencing — allow some people to more easily lose tol-erance to various self antigens. This is why generalautoimmunity and/or specific autoimmune conditionstend to cluster in families. Several genetic factors havebeen found that confer susceptibility to either a specificAD or to more than one. For example, autoimmune thy-roid diseases — both Graves disease and Hashimoto’s —are closely associated with Type I diabetes in families,and some of the genes that confer susceptibility to anyone of these are common to all (Tomer, 2004). Geneticfactors are incompletely understood, though it appearsthat multiple genes are involved in the development ofeach of the conditions.

Another important aspect of genetic susceptibilityinvolves estrogen, since such a high percentage of thosewith AD are women. It is speculated that estrogen dom-inance, a condition of hormone imbalance — either toomuch estrogen or too much in relation to other hor-mones, especially progesterone — can tip the scales infavor of hyperimmunity. But the beginning point is hav-ing considerable estrogen in the system to begin with,i.e., being female.

Given a genetic susceptibility, it is unclear whetherthe following factors actually trigger autoimmune dis-eases, exacerbate already existing conditions, or both.As with most disease processes, there is often a geneticfactor “loading the gun,” but it is environmental factorsthat “pull the trigger.”

. Chemicals in the environment have emerged asthe most-studied and most-suspected com-ponent contributing to the rise in autoimmune

conditions seen since the end of World War II.Many agricultural chemicals have been shownto have immune-modulating effects because oftheir estrogenic properties, and many othertypes of chemicals are now thought to induce,and possibly also exacerbate, autoimmunity.Oxidative stress is probably one of the maintriggering mechanisms at work here.

A former bacteriologist turned rancher andenvironmental writer, Donna Felzer (2006), hasbecome convinced that:

• ALL autoimmune disorders are variations ofthe same theme.

• They are NOT the body attacking itself.

• The body is slowly and painfully dying frompoisons exceeding its capacity to detoxify.

• The evidence abounds in the scientific liter-ature, but is being ignored and wronglyinterpreted as “the body attacking itself.”

• This is the greatest blunder of modern medicine.

Similarly, Edward Bauman, M.Ed., Ph.D. (2005)believes that autoimmunity arises from the body’sattempt to rid itself of pathogens — whether viral, bac-terial, or fungal agents, heavy metals, or other toxins —by attacking and damaging or destroying the cells thatcontain them. And Lernmark (in Powell et al., 1999) hashypothesized that autoreactivity may be the price thebody pays for the immune system’s vigilance inattempting to prevent tumor growth.

Several chemicals have notable associations withautoimmune conditions (Powell et al., 1999, unless oth-erwise noted):

. Agricultural and household chemicals:Pesticides (including insecticides, herbicides,fungicides, androdenticides) concentratedfertilizers, and probably many other types ofsynthetic chemicals, can wreak immune systemhavoc. Some pesticides are known endocrinedisruptors because of their estrogen-mimickingproperties, creating a hormone imbalance that




tips towards estrogen dominance. This is notthe body’s natural estrogen, of course, thoughthe body incorporates it into cells and attemptsto use it accordingly.

Other known immune disruptors include dioxinand polychlorinated biphenyls (PCBs), whosecombined total number comes close to 300different substances (Shames and Shames,2001; p. 184). According to Fezler (2006),

• It has been well documented that halo-genated aromatic hydrocarbons (HAHs) suchas dioxin (TCDD), polychlorinated dibenzofu-rans (PCDFs), and PCBs, affect immuneresponse, and they appear to affect all func-tional arms of the immune system (innateimmunity and host resistance, cell-mediatedimmunity, and humoral immunity).

. Heavy Metals: Mercury, which is especiallytoxic to humans because it can cross the blood-brain barrier, has conclusively been shown tocause autoimmunity in genetically susceptiblerats and in humans (Bigazzi, 1994). A morerecently discovered autoimmune mercury-induced nephritis (kidney disease) has helpedclarify this metal’s ability to modify selfproteins, leading to molecular and antigenicalterations.

In addition to mercury, silver, gold salts (used totreat rheumatoid arthritis), and cadmium arestrongly associated with autoimmune diseases(Bigazzi, 1994). Any heavy metal body burdenfound by hair mineral analysis or other meansshould be suspect.

. Iodine: In the form of dietary iodide, iodineenhances genetic susceptibility to autoimmunethyroiditis (Hashimoto’s Disease). It appears tomodify thyroid glycoproteins — key immunesystem chemicals comprised of protein/carbohydrate chains — which leads directly to anautoimmune response. Adequate dietaryselenium may negate this effect (Xu et al., 2006).

. Vinyl chloride (VC): A petrochemical and aconstituent of polyvinyl chloride (PVC) pipesand other construction materials. It is alsofound in plastic food wrappers and containers.Exposure is via wastewater from manufacturingplants and through leaching into foods heatedin plastic (EPA, 2006). The exact mechanismthat causes autoimmune reactions is notcompletely understood, but VC inhibitssuppressor T cells and other immune cells,which likely contributes to the effect.

Many other plasticizers and plastics, such aspthalates and bisphenol-A (BPA), ubiquitous inconsumer products such as food containers andwraps, are known endocrine disruptors and aresuspected of contributing to immune dysfunction.

. Prescription drugs: These include anticon-vulsants, beta-blockers, and sulfonamides, as wellas estrogens, penicillin, and interferon. In all, over70 drugs have been associated with autoimmunity(Metagenics, n.d.).

. Canavanine: A non-essential amino acid and ananalogue to l-arginine, produced by plants toreduce their palatability. It is found in alfalfa,especially in the seeds, and many studies haveshown it to induce autoimmunity in test animals.

. Organic solvents: A group of petrochemicalsthat include aromatic hydrocarbons, aliphatichydrocarbons, and chlorinated solvents. Theyare found in such things as paints, varnishes,adhesives, and degreasing/cleaning agents.They are also used in the production of somepharmaceuticals (NIOSH, n.d.). Many are knowncarcinogens and there is a strong association ofthe entire group with autoimmune systemicsclerosis.

. Silica: Whether from natural deposits or as acomponent of manufactured goods, silica is ahealth problem when it is in particulate form.Mining and sandblasting offer the most likelyroutes of exposure. In this form, silica is



associated with specific lung diseases but hasalso been shown to increase the risk ofautoimmune conditions, including arthritis,SLE, and scleroderma (a condition that causeshardening of the connective tissue).

. L-tryptophan: An essential amino acid and aneffective sleeping aid. In 1989 it was pulled fromthe over-the-counter retail market due to whatwas considered to be a contaminated batch thatcaused eosinophilic myalgia, an acute conditionof intense muscle pain and high eosinophil count(a type of white blood cell). Unfortunately, thiseffect has since been duplicated with uncon-taminated l-tryptophan, though only in highdoses and in susceptible individuals. Kynurenineand serotonin, metabolites of tryptophan,promote fibrinogensis, a factor in scleroderma.There is a strong association between serotoninand the onset of scleroderma.

. Particulates: In the form of ultrafine micro-particles, these are an increasing component ofthe human diet and are associated with theonset of Crohn’s Disease, an autoimmunecondition that damages the small intestine. Asfood additives, naturally occurring soilcontaminants, or particles formed in theenvironment or GI tract, we consume alumino-silicates, mixed silicates, and titanium dioxide.It is in their man-made form as additives ornewly-formed molecules that they present adanger to the immune system. It is thoughtthat pathogenesis is caused by altered mucosalantigen processing.

. Mucosal immune system: This term refers to themucus linings of the parts of our bodies that arein contact with the outside world. This includesour respiratory tract, mouth, skin, nasal passages,and most especially our gastrointestinal (GI)tracts, where upwards of 70% of our immunecells reside. This intestinal barrier is home to ourgut associated lymphoid tissue (GALT), which

includes several types of immune cells thatcontinuously sample the multitude of substancesthat enter our bodies. GALT works to regulatemolecular traffic between the environment andour circulatory systems, protecting us fromantigen overload and keeping the immune systemfree of accumulated debris (Bauman, CD, 2005).This intestinal mucus defense and the perm-eability of the gut are the determining factors inthe delicate balance between tolerance andimmune reaction to potential antigens, and thisbalance is responsible in turn for healthy intes-tinal function (Fasano and Shea-Donohue, 2005).Healthy GI tracts are essential for good immunehealth, and imbalances and malfunctions canhave serious consequences. Several gastroin-testinal factors can contribute to autoimmunity:

. Intestinal Permeability: Also called leaky gutsyndrome (LGS), this condition is key to many, ifnot all, autoimmune conditions. It has long beenrecognized that untreated Celiac Disease, aprimary cause of leaky gut, can lead to insulin-dependent diabetes mellitus, Hashimoto’sThyroiditis, autoimmune hepatitis, andconnective tissue diseases (Fasano et al., 2000).



Small intestine permeability has also beenimplicated in inflammatory bowel disease (IBD)(Danese et al., 2004).

Intestinal barrier integrity fails when theregulation of a complex network of proteinsthat make up the intercellular tight junctions isimpaired (Fasano and Shea-Donohue, 2005).These junctions work to selectively permitnutrients and other substances passage to andfrom the circulatory system in a carefullycoordinated assembly and disassembly of theproteins. Inflammatory cytokines have beenshown to alter the mucosal integrity and toaffect a protein called zonulin, which opens upthese junctions to allow greater permeability(Fasano and Shea-Donohue, 2005). Fasano, aleading researcher of mucosal integrity, and hiscolleague Shea-Donohue (2006) propose that inaddition to genetic susceptibility, exposure toenvironmental triggers, and miscommunicationbetween the innate and adaptive immunesystems, impaired regulation of the permeabilityof mucosal barriers, mostly in the GI tract andlungs, is required for autoimmunity to develop.

Much remains to be learned about the exactmechanisms that create the inflammationleading to permeability, which leads to furtherinflammation, perpetuating a never-ending cycleuntil the gut is allowed to heal. Celiac Disease —an inherited inflammatory reaction to gluten — isthe best understood of these processes because itdirectly inflames intestinal tissues. Less is knownabout gut pathology with extraintestinal AD, butfood allergies and sensitivities are almostcertainly involved. In allergic or sensitive people,the ingestion of food antigens may cross-reactwith specific tissues, causing chronic inflamm-ation and an ensuing autoimmune reaction(Gaby, 2004). By eliminating offending foodsfrom the diet, many autoimmune conditions havebeen vastly improved.

. Microflora imbalance of the mucosa: Thiscondition — most especially in the gastro-intestinal tract — appears to play a strong role inthe etiology of several autoimmune conditions, aswell as some cancers (Tlaskalová-Hogenová et al.,2004). Commensal bacteria — friendly bacteriathat the health of the body depends on —colonize the mucosa and skin surfaces in greaternumbers than the sum of all the cells in thehuman body. Most of these bacteria are in thegut. They are able to activate both the innate andadaptive immune systems and have a specializedanti-inflammatory function for eliminating andtolerating foreign invaders, such as food, airborneantigens, and other microflora. Recent studieshave shown them to be vital to immune function(Fasano and Shea-Donohue, 2005). Tlaskalová-Hogenová et al. (2004) suggest that imbalancesin these bacteria produce an excessive immuneresponse, resulting in inflammation thatinfluences mucosal immunity, promoting theonset of autoimmune diseases.

These findings help debunk the hygienehypothesis, whose basis lies in the theory thatthe body over-produces Th-1 cells in responseto exposure to micro-organisms. It has recentlybeen suggested that our immune systems haveevolved with all types of micro-organisms thatour bodies accept as harmless, and that this Th-1 over-production does not occur. A newerhypothesis, based on further research, statesthat it is immunoregulation — maturation ofregulatory T cells by friendly gut flora — thatmore directly affects Th-1/Th-2 balance(Hanaway, 2006).

. Stress: This refers not only to the emotions butto the effects of free-radical activity andexposure to toxins and food antigens, is animportant mediator of autoimmunity. This maybe because of its effect on mucosal integrity,which is affected by both low and high




concentrations of cortisol, our main stresshormone. High levels of cortisol suppress theimmune system by reducing the amount ofsecretory IgA (sIgA), the main mucosal antibodyresponsible for eliminating pathogens from theintestinal tract and in other mucus membranes(Harding, 2002). Persistent high cortisol levelswill eventually lead to adrenal depletion andsignificantly reduced levels of the hormone.Low cortisol can lead to overly aggressive sIgAreactions and the onset of an autoimmuneattack (Harding, 2002).

Corticotropin releasing factor (CRF), a mediatorof cortisol release, is also a potent immuneregulator, reducing the production of Th-1 cells(Steinman et al., 2003). It releasescorticotrophin, which in turn stimulates therelease of cortisol. CRF increases underconditions of reduced caloric intake. Steinmanet al. (2003) have suggested that short-termstress, such as that produced under conditionsof fasting, appear to alleviate, and perhapsreverse, autoimmune reactions because of thisextra CRF release.

. Leptin: A cytokine responsible for regulatingfood intake — it induces satiety — as well ascertain metabolic and endocrine functions. Italso plays a regulatory role in inflammation,immunity, and blood cell production. It isproduced primarily in fat cells, and itsproduction is partially managed by the innateimmune system (Fantuzzi and Faggione, 2000).Obese people, who produce an overabundanceof leptin, can become resistant to it despitelarge serum concentrations, in much the samemanner as with insulin, making high levels athreat to health. Leptin is present in greaterconcentrations in women; it is also increased inthe presence of inflammatory agents and hasbeen shown to be produced at the sites ofautoimmune pathology (Steinman et al., 2003).

Leptin, as an immune modulator, has beenshown to affect the production of T cell-mediated cytokines and to increase thedominance of Th-1 (Fantuzzi and Faggione,2000; La Cava et al., 2004; Matarese et al.,2005). Lower levels of leptin, and higher levelsof CRF, work in parallel roles to suppresshyperimmunity in a finely tuned interactionthat is related to body weight and energymetabolism (Steinman et al., 2003).

The bottom line appears to be that excess serumleptin, produced from over-consumption ofcalories or resulting from cellular resistance, canlead to the “heating up” of the immune system,resulting in chronic inflammation and the onsetof autoimmunity. The key to regulation of leptinlevels is reducing the intake of food.

Dietary Factors

. Glycation and glycation end products (AGEs):Certain sugars in our bodies, called reducingsugars, can interact with and greatly alter thefunctioning of the amino groups of proteins andlipids. This process is called glycation. Accordingto Alan Gaby, M.D. (2004), glycation can changethe structure of proteins so much that theimmune system will no longer recognize themas self and will attack them as foreign antigens.A small amount of glycation is a normal process,but over-consumption of sugars, especiallyfructose, can overwhelm our metabolicmachinery and accelerate the process.

AGEs present the same problem, but instead ofbeing produced endogenously, they are formedduring the heating of many common foods,including browned meats and baked goodscontaining high fructose corn syrup. Lactose isalso a reducing sugar, making browned foodsthat contain dairy products a potential problem(Gaby, 2004).




In general, over-consumption of refinedcarbohydrates — sugars and refined flours — canlead to hyperglycemia, which contributes toglycation and leads to the over-production ofinflammatory prostaglandins (Devroey, 2004).

. Nutrient Deficiencies: We live in an overfedbut undernourished culture, and many of us areliterally eating ourselves to death. Despite thevast quantities of food available to us, we arerife with nutrient deficiencies, any one of whichcan disturb immune function.

There are a few micronutrients that areespecially critical for the regulation ofinflammatory and/or immune functions, andimbalances in any of these may speed the onsetof autoimmune conditions:

• Antioxidant vitamins A, C, E

• Vitamin D

• Vitamin B6 and folic acid

• Essential fatty acids

• Iron

• Selenium

• Copper / Zinc ratio

. Age emerges as a factor in autoimmunitybecause damage from so many of the above-mentioned factors accrues over time. Oxidativestress from poor diet and environmental toxins,nutrient deficiencies, AGEs, and other factorsall exact a greater toll with the passage of time.

TestingIn addition to whatever standard medical tests are con-sidered necessary for particular conditions, the follow-ing additional assessments can provide further in-depthinformation that may prove indispensable for designinga health-promoting autoimmune protocol.

Serum Tests

. Vitamin D: Measured inthe serum, is very criticalto immune function.

. Sedimentation rate(SED rate): by measuringthe effects of proteinssticking to red blood cellsand how quickly theysettle to the bottom, isuseful for determininglevels of inflammation. Itis used to screen for certain AD.

. Highly Sensitive C-Reactive Protein (hs-CRP):Laboratory reference ranges vary somewhat, butgenerally levels >1.3 (mg/L) are indicative of aninflammatory condition in the body, either acuteor chronic (LEF, 2003; p. 525). Levels <0.8 mg/Lare desirable.

. Homocysteine: Desirable levels are <9 µmol/L.Helps to assess the presence of inflammationand deficiencies of vitamins B6, folate, andB12, which are critical for proper estrogenmetabolism and many other processes.Measuring levels of B12 can help define whichB vitamin is missing if homocysteine is high.

Metabolic Assessments

. Health Assessment Questionnaire to helpdetermine more in-depth assessments.

. Screening for antigens, allergens, andpathogens is critical for eliminating auto-immune triggers (Bauman, 2007). Blood-spotand serum testing can screen for all antibodies— sIgA, IgE, IgG, and IgM. Stool analysis canhelp determine pathogens. Gaby (2004) findsthe use of elimination diets slower but moreaccurate for determining food sensitivities,especially beneficial for those who find thecosts of testing prohibitive.



. Hair mineral analysis to determine heavymetal toxicity and mineral imbalances.

. Comprehensive Metabolic Profile to assessnutrient deficiencies, detoxification capacity,fatty acid balance, and energy productionefficiency.

. Estrogen metabolism to determine if it is beingconverted to 2-hydroxylated estrone (OHE),instead of the 16a-OHE, which may contributeto autoimmune disease (Metagenics, n.d.).

Home Tests

. Beet Test: This test helps determine the needfor additional stomach acid (HCl), crucial forprotein digestion and absorption of criticalnutrients. Cook and eat one whole medium redbeet. Pink urine afterwards indicates HCldeficiency.

. Transit Time: If possible, after eating the beet,check feces for traces of red to determinetransit time — time from ingestion toelimination. Time should be in the range of 12-18 hours to ensure proper assimilation ofnutrients. If the beet is too difficult to see, thetest can be done with corn kernels.

. Urine and Saliva pH: Checking urine and salivapH with commercially available test papersprovides a quick assessment of overall bodyacidity, a possible indication of inflammation.

Natural InterventionsThe aim of a dietary and lifestyle protocol for managingautoimmune conditions consists of:

. Eliminating toxins and reactive foods from thediet and environment.

. Supplying a reduced-calorie, hypoallergenicdiet with optimal nutrition to provide:

• Gentle detoxification

• Anti-inflammatory support

• Protection from free-radical damage

• Lowered levels of leptin

• Nutrients to heal the GI tract if require

• Proper metabolism of hormones, especiallyestrogen

. Providing supplements and herbs to supportdetoxification and optimize digestion.

. Providing methods to reduce Th-1 expression.

. Recommending lifestyle changes to reducestress and to complement all of the above.

DietScience has recognized the profound effect of diet onthe immune system for over 50 years (Homsy et al.,1986), but research conducted within the last 20 yearshas begun to elucidate its specific effects.

In 1986, Homsy et al. published a study that con-cluded that calorie restriction extended life and pre-vented upregulation of the immune system. Reducedcaloric intake lessens the number of circulating immunecomplexes (CIC; groupings of antigens and antibodies),lowers antibody concentrations, and reduces the signsof aging that characterize autoimmunity (Muthukumaret al., 2000). These last can result from oxidative stressfrom toxins, glucose-induced surges in insulin, and liverstress brought on by overeating. Other studies have cor-roborated these findings, showing a strong reduction inpro-inflammatory markers in study subjects, mainlymice, on restricted calorie diets (La Cava et al., 2004). Itis now also well-established that restricting caloriesreduces levels of leptin and increases release of CRF(Steinman et al., 2003), both of which can slow andsometimes reverse the autoimmune process.

Calorie restriction does not imply malnutrition; infact it is sometimes referred to as Calorie Restriction/Optimum Nutrition (CRON). Benefits can be achieved byeating several small nutritious meals throughout the day,never allowing oneself to get that “stuffed” feeling.CRON depends on high nutrient density and high-quality foods and can be accomplished by following theEating for Health™ dietary model, which provides a




nutritious, anti-inflammatory protocol based on wholefoods that are organically grown to the extent possible.The nutrient density of Eating For Health™ is furtherenhanced by the use of special booster foods, therapeu-tic herbs, and nutrient supplementation when necessary.

Lowered caloric intake can also be achieved withshort fasts, preferably utilizing freshly made vegetableand fruit juices, vegetable broths, and herbal teas. Thistype of fasting provides the body with essential nutri-ents while both cleansing and rejuvenating tissues andorgans (Bauman, 2008; p. 62). When one has an alreadydiagnosed condition, fasts are best done under thesupervision of experienced professionals. More informa-tion can be obtained from Bauman College atwww.baumancollege.org/newsite/services/vitality-fasting-retreats.html

What to EatIn the Eating For Health™ diet plan, follow the cleansingdirection to gently detoxify, alternating with the build-ing direction to provide adequate protein for healing.

Emphasize:

. Lean protein such as:

• Grass-fed beef

• Wild-caught fish

. Vegetable proteins from:

• Tempeh

• Tofu

• Beans

• Legumes

. Fiber-rich whole grains and fruits and vege-tables to ensure optimal bowel transit time.

. Plenty of healthful fluids:

• Filtered water

• Herbal teas

• Mineral broths

. Omega-3 rich foods to soothe inflammation,including:

• Wild-caught (not farmed) cold water fish,such as salmon, mackerel, and herring

• Pastured beef

• Omega-3 enriched or pasteurized eggs;

• Flax seeds, pumpkin seeds, and chia seeds;

• Walnuts

. Olive oil as the main source of fat (Leopold,2006) and virgin organic coconut oil forsautéing; raw dairy products, including rawbutter from grass-fed cows, as sources of highquality saturated fat, conjugated linoleic acid,and vitamin A; health-promoting fats are alsopresent in avocados, nuts, and seeds.

. Arginine-rich foods, which can help down-regulate production of Th-1 (Royston, 2003):

• Lentils

• Hazelnuts

• Walnuts

• Peanuts



. Garlic and onions as sources of sulfur-containing compounds that can help the bodyeliminate heavy metals (Murray, 2000; p. 72).

. Cilantro with garlic to help chelate unwantedmetals.

. Foods high in antioxidants, including:

• Carotenoids

• Flavonoids

• Isoflavones

• Phyto-anti-inflammatories (Leopold, 2006)

. Carotenoid-rich foods:

• Apricot

• Limes

• Yams

• Cantaloupe

• Lemons

• Winter squash

• Oranges

• Carrots

• Sweet potato

• Tomato

• Kale

• Spinach

. Flavonoid-rich foods:

• Green tea

• Berries (dark)

• Cherries

• Citrus fruits

• Tomatoes

• Greens

• Peppers

• Oolong tea

• Red wine

. Isoflavone-rich foods:

• Edamame*

• Tofu*

• Tempeh*

• Miso*

* Isoflavones have been shown to balance Th-1 and Th-2 production (Royston, 2003).

. Phyto-anti-inflammatories:

• Olive oil (extra virgin)

• Sesame oil

• Epigallocatechin (green tea)

• Spices and herbs: ginger, curcumin (turmeric),rosemary, capsacin (hot peppers), oregano,and boswellia (frankincense)

• Quercetin: apples, green tea, onions, berries,brassica vegetables, and buckwheat

• Ursolic acid: apples, bilberries, cranberries,elder flower, peppermint, lavender, oregano,thyme, hawthorn, and prunes

What to Avoid

. Refined carbohydrates: sugars, especiallyfructose and high fructose corn syrup, as wellas refined flours and products made from them.Small amounts of whole grain flours may beOK, depending on individual metabolic needs,and small amounts of natural sweeteners —agave syrup, evaporated cane juice, maplesyrup — may be used.

Glucose overload contributes to inflammation,glycation, and immune sluggishness. Over-consumption of sugary foods may mean thatfoods with more important sugars, such asgalactose, mannose, xylose, and fucose, whichhelp cells “decorate” their membranes withidentification markers, may be missing(Devroey, 2004). These sugars are found in fruitsand vegetables.

. Arachidonic acid (AA)-producing foods shouldbe minimized. These are primarily red meat,poultry, eggs, and dairy products. AA is a fattyacid that helps promote inflammation. Smallamounts are necessary to mount attacks




against pathogens, but it is generally over-consumed in the U.S. Minimizing its intake mayhelp cool the inflammatory response in AD.

Also minimize most vegetable oils, whichcontain Omega-6 fatty acids, of which there isan overabundance in our diets. Processed oils aregenerally damaged fats and best for everyone toavoid. Trans fats, highly processed solid fatsmade from vegetable oils, are metabolic poisonand are to be strictly avoided. They are prevalentin fried foods and partially hydrogenated oils.

. Certain herbs and supplements have the abilityto upregulate immune responses, something tobe avoided with an already over-stimulatedsystem. Two in particular — echinacea andspirulina — have been studied and found to becapable of triggering the onset or flare-ups ofAD (Lee and Werth, 2004). Chlorella, though notpart of this study, acts in much the same way asspirulina. This does not mean to forego the useof these substances, especially spirulina andchlorella, which have many health-conferringbenefits. Consider using them in small amountsas part of the diet, as opposed to using largertherapeutic doses. Most herbs have not beenstudied for this effect, so a good rule of thumbmay be to abstain from very large doses of anyherb and to alternate different ones on a dailyor weekly basis. Moderation is key.

. The same is true for certain medicinalmushrooms, revered for their immune-enhancing properties. Used as foods, they arefine. Used in therapeutic, medicinal doses, theyare inappropriate for hyperimmune people. Notall mushrooms have this enhancing effect;those that do include (Stamets, n.d.):

• Agaricus brasiliensis (Himematsutake)

• Cordyceps sinensis (Cordyceps)

• Ganoderma lucidum (Reishi/Ling Chi)

• Ganoderma oregonense (Oregon Polypore)

• Grifola frondasa (Maitake/Hen of the Woods)

• Inonotus obliquus (Chaga)

• Lentinula edodes (Shiitake)

• Piptoporus betulinus (Birch Polypore)

• Pleurotus ostreatus (Hiratake/Pearl Oyster)

• Polyporus sulphureus (Chicken of the Woods)

• Polyporus umbellatus (Zhu Ling)

• Trametes versicolor (Yun Zhi/Turkey Tail)

NOTE: It is unfortunately not as simple as providingimmune suppression and avoiding immune stimulation.People with autoimmune conditions also tend to have alowered immune response to acute infections, such asbacteria and viruses, partially from increased expressionof a cytokine called transforming growth factor beta(Lowrance et al., 1994), and possibly simply because ofan exhausted state created by the immune system’sconstant vigilance. The idea is to balance the immunesystem, not to over-suppress it.

Booster Foods

. Flax seeds, for their Omega-3 fatty acids, bene-ficial fiber, and other nutrients. 1–2 Tbsp. daily.

. Sea vegetables and high-quality green powdersthat include spirulina and chlorella, powerful deto-xifiers that can help minimize heavy metal toxicity.1 serving a day, 4–5 days/week. (This low doseshould not over stimulate the immune system.)

. Low-temperature processed whey powder fromgrass-fed cows to support sIgA production andhelp heal intestinal inflammation. 1-2 Tbsp. 4-5 days/week.

. Nutritional yeast for its B vitamins andchromium; the latter helps with blood sugarbalance. Nutritional yeast and whey are goodprecursors to lactoferrin and lactoperoxidase,which are necessary to rid the gut of unfriendlybacteria (Bauman, 2005). 2 Tbsp. daily.

. Rice bran supports mucus membranes (Bauman,2005). 1-2 Tbsp. daily

SupplementsProper immune function depends on adequate intake,preferably via food, of vitamins and trace elements. Whilemany of these actually enhance Th-1 production and maynot seem appropriate for autoimmune conditions, it mustbe remembered that people with AD also experience low-ered resistance to acute diseases and infections.Micronutrient deficiencies suppress the immune responseby affecting both the T cell-mediated and the adaptiveantibody-related responses, leading to dysregulation ofthe entire system (Wintergerst et al., 2007).

In addition to a high-quality multiple vitamin andmineral supplement, the following additional supple-ments can help support an autoimmune diet protocol:

. Antioxidants: Because oxidative stress can bea triggering mechanism in AD, lessening theimpact of free radical damage is critical forsupport. Through this action, antioxidantsinfluence the production of cytokines andprostaglandins (Wintergerst et al., 2007).

• Vitamin A: Important for overall immunefunction, it promotes Th-2 production(Wintergerst et al., 2007) and can also helpheal a leaky gut (Lipski, 1996; p. 103). VitaminA is fat soluble and therefore able to build upto toxic levels. Because of this, its use duringpregnancy, especially, should be limited.

The carotenoids are vitamin A precursors andare found in red, orange, and yellow fruits andvegetables. Beta carotene supplements arewater soluble and may be safely taken inhigher doses.

• Vitamin C: Critical for a strong immune sys-tem that fights infections, detoxifies pollu-tants, and promotes production ofanti-stress hormones (Holford, 1999; p. 309).It also helps regenerate vitamin E, prolong-ing its ability to fight free radicals.

• Vitamin E: D-alpha tocopherol, one eighthof the entire vitamin E composition of fourtocopherols and four tocotrienols, is themost studied of all the components. Manyhealth experts now feel that the eight com-ponents work better as a team, and the com-bination is becoming more widely availablein supplement form. Vitamin E bolstersimmunity against infections and cancer andis a potent, fat-soluble anti-oxidant.

• Lipoic acid: Boosts all the other anti-oxi-dants, increasing levels of vitamins C, E,CoQ10, and glutathione (Packer, 1999; p. 31).It is both fat- and water-soluble, is criticalfor energy production, and can recycle itselffrom its radical form back to its anti-oxidantform (Packer, 1999; p. 32).

• N-acetyl-cysteine: Used supplementally toboost levels of glutathione, the body’s mostpotent antioxidant and a powerful detoxify-ing agent. Glutathione tends to be low inpeople with damaged colons, such as fromthe autoimmune inflammatory bowel dis-eases (Lipski, 1996; p. 264). Supplementationmay best be achieved by providing these pre-cursors, as glutathione itself may not absorbwell into tissues.

• CoQ10: Helps promote energy productionand is a potent antioxidant and immune reg-ulator. It also helps regenerate vitamin E(Packer, 1999; p. 92).






. Vitamin D: Has been shown in a variety of studiesto directly prevent several autoimmune diseasesby maintaining self immunologic tolerance(Cantorna and Mahon, 2005; Ginanjar et al., 2007;Holick, 2004). Most cells in our bodies containVitamin D Receptors (VDRs), including ourimmune cells. Vitamin D modulates the immuneresponse through its activity on the VDRs ofactivated T and B cells, where it both directly andindirectly influences T cell differentiation andproduction, increases T suppressor cell activity, ora combination of both (Cantorna, 2006; Ginanjaret al., 2007). Wintergerst et al. (2007) report thatvitamin D supports Th-2 anti-inflammatorycytokine production.

Vitamin D is best obtained from exposure to thesun, but when adequate exposure is impossible,such as in the winter or in higher latitudes,supplementation becomes necessary. Optimalserum levels are 40–65 ng/ml (Cannell, 2004).

. Essential fatty acids: La Cava et al. (2004)concluded that long-chain polyunsaturated fattyacids (PUFAs) from cold water fish could preventprogression of autoimmune diseases in studymice, significantly improving production of anti-inflammatory prostaglandins. Many other studieshave shown the anti-inflammatory effects ofOmega-3s benefit many other diseases.

The Omega-6 fatty acid, gamma-linolenic acid(GLA), also helps reduce inflammation. It can befound in evening primrose and borage seed oils.

. B-complex vitamins: Vital co-enzymesimportant in multiple processes throughout thebody. They are easily depleted under conditionsof stress, and so are needed in increasedquantities in these stressful times. Because theyall function together and a deficiency in one canlead to imbalances in all, it is recommended thatthey be taken together when supplementing.Specific B deficiencies can be assessed throughtesting and addressed as needed.

. Copper: Functions as a component of the free-radical scavenger superoxide dismutase. It alsohelps the body utilize iron. Copper and zincmust be in the proper balance in body tissues,as elevated copper levels, in combination withlow zinc, can be toxic. Copper and zinc competefor absorption, so high doses of one can lead toa deficiency of the other (WHFoods, n.d.).

. Zinc: This potent antioxidant is important forimmune function, as well as for over 300enzyme reactions throughout the body. It isalso an important component of maturing T-cells (LaValle, 2004; p. 422) and, as such,increases the immune response. Studies haveshown that deficiencies of zinc can improveautoimmunity (La Cava et al., 2004). However,since many autoimmune individuals also sufferfrom low resistance to bacterial and viralinfections, perhaps striking a balance betweenlow and high dosages provides the best solutionto this dilemma.

. Iron: Often deficient in autoimmune conditions,iron is critical for oxygen transportation andenergy production.

. Selenium: Functions as an important antioxidantunto itself and helps in the production ofglutathione. It is also a powerful infection fighter.

. Probiotics: Aside from replenishing thebacteria that are necessary for intestinal healthand gut integrity, also help balance Th-1 andTh-2 production (Royston, 2003).



Nutrient Food Sources (Holford, 1999; pp. 304-322, unless otherwise noted):

NUTRIENT GOOD FOOD SOURCES

Vitamin A and carotenoids Beef liver; see chart in “What to Eat” section for carotenoid-rich foods

Vitamin C Peppers, broccoli and cauliflower, kiwi fruit, citrus, tomatoes, strawberries

Vitamin E Raw vegetable oils; nuts and nut butters; rice bran oil (Packer, 1999; p. 55)

Lipoic acid Synthesized by the body; present in small amounts in potatoes, spinach, red meat(Packer, 1999; p. 32)

N-acetyl-cysteine Cysteine is an amino acid synthesized in the body (n-acetyl form available only asa supplement)

CoQ10 Sardines, mackerel, pork, peanuts, sesame seeds, walnuts, spinach

Vitamin D Herring, mackerel, salmon, oysters, cottage cheese, eggs

Omega-3 fatty acids See “What to Eat” section

B-complex A wide range of foods, including meats, fish, poultry, dairy, whole grains, and vegeta-bles, as well as nutritional yeast. B12 is most bioavailable from animal-derived foods.

Copper Calf’s liver, crimini mushrooms, turnip greens, molasses (WHFoods, n.d.)

Zinc Oysters, pecans, Brazil nuts, peanuts, almonds, lamb, ginger, whole wheat, rye, oats

Iron Pumpkin seeds, almonds, cashews, Brazil nuts, pecans, walnuts, raisins, pork,cooked dried beans

Selenium Brazil nuts, garlic, whole grains, sunflower seeds, other nuts, seafood (oysters, tuna,swordfish) (Moss, 2001)

Probiotics Organic yogurt; naturally fermented raw vegetables, such as sauerkraut; kombuchatea (AUTHOR’S NOTE)

Supplement Recommendations (Murray, 2000; p. 157, unless otherwise noted):

SUPPLEMENT DOSAGE

Antioxidants, including:Vitamin A Maintenance: 20,000 IU/day; during infection, 50,000 IU/day for no more than

1 month

Beta carotene Maintenance: 25,000 IU/day; during infection, up to 180,000 IU/day

Vitamin C Maintenance: 500–1000 mg/day; during infection, up to 5000 mg/day, divideddoses

Vitamin E Maintenance: 200–400 IU/day; during infection, 200 IU/day (more can impairimmune function.)

Lipoic acid 100 mg/day, divided doses for maintenance; add 100 mg/day for infection (Packer,1999; pp. 32, 191)

N-acetyl-cysteine (NAC) 8–20 gm/daily for a trial of 4 weeks (Lipski, 1996; p. 264)

CoQ10 30 mg/day maintenance; another 50 mg/day therapeutic (Packer, 1999; p. 92)

Vitamin D 5–10 minutes sun exposure, 2–3 times/week (Holick, 2004); 1000–2000 IU/dailycombined sunshine and supplement, if not under professional care; professionalguidance recommended if larger doses are required; levels must be regularlymonitored (Cannell, 2004)

Omega-3’s Fish oil: 1 gm/day with 2:1 EPA/DHA for anti-inflammatory effect (may interferewith anti-coagulant medications)

Gamma linolenic acid (GLA) 3–6 gm/day (Lipski, 1996; p. 359)

B-Complex 50mg of each (more may be necessary if homocysteine or stress are particularlyhigh)

Copper No more than 2 mg/day

Zinc Maintenance: 25 mg/day; during infection, 75–150 mg/day for no more than 1week

Iron 15–25 mg/day is the therapeutic range, to be used when anemia is present

Selenium Maintenance: 200 mcg/day; during infection, 400 mcg/day

Probiotics Combination of acidophilus and bifidus strains is generally recommended, withthe addition of sacchromyces boulardii when leaky gut is involved; 1-2 capsules,or 1/4 - 1/2 tsp./day (Lipski, 1996; pp. 265, 367)






. Supplements to support thehealing of intestinal perm-eability (Lipski, 1996; pp.102–103; Bauman, 2005):

• Sacchromyces boulardii

• L-Glutamine (1-30gm/daily, as needed)

• Vitamins A, B5, and Folicacid

• Zinc

• Deglycyrrhized licorice

• All antioxidants mentioned above

• Whey powder

• Colostrum

. Supplements to specifically target the auto-immune process:

• Proteolytic enzymes — trypsin, papain, chy-motrypsin, bromelain — can be potentimmunoregulators. In pharmacologic dosesthey have been shown to selectively inhibitthe production of inflammatory Th-1, butnot Th-2, cytokines (Roep et al., 2002). Byworking to reduce circulating immune com-plexes, proteolytic enzymes are potentiallyimportant modulators of chronic inflamma-tory conditions. Cichoke (1994; p. 159) notesseveral autoimmune conditions in which theremoval of CIC and the halting of the forma-tion of immune proteins, called complement,have played an important role in theirimprovement. He advocates the use of com-binations of proteolytic, lipolytic, and amy-lolytic enzymes. He also cites studies thatshow that enzymes have a beneficial overalleffect on the immune system by reducingthe effects of stress (p. 161).

HerbsAny of the herbs known for their anti-inflammatory andantioxidant properties may be useful adjuncts for an

autoimmune protocol. There are some herbs, though,that can specifically downregulate an over-stimulatedimmune system:

. Polyphenols from green tea extract (EGCG):These have been shown to reduce totalautoantibody levels and autoimmune-inducedlymphocytic invasion of organs in experimentalmice, finally proving what had previously beendemonstrated in vitro (Hsu et al., 2007).

. Curcumin and resveratrol: Both are known fortheir anti-inflammatory properties, as well astheir beneficial effect on cancer, diabetes, andother diseases. They have recently been studiedtogether for their effects on the immunesystem. Testing done on mice has shown themto work together to suppress both Th-1 and Th-2 production, indicating a strong immunosup-pressant effect (Sharma et al., 2007).

. Calaguala (also seen as kalawala): An extractfrom the fern polypodium leucotomos, has beenshown to be an effective treatment for psoriasisand vitiligo, both of which are consideredautoimmune skin disorders. Tuominen et al.(1991) showed this compound to exert animmunosuppressive effect sufficiently strong toretard rejection of skin grafts.

. Ginger: Also well-known for its anti-inflammatory action and has most recentlybeen studied for immune effects stemmingfrom this. Tripathi et al. (2008) found that byinhibiting the actions of macrophages anddownregulating the expression of specificinflammatory cytokines, ginger exerts aninhibiting effect on T cell activation, which inturn reduces the expression of otherinflammatory cytokines. Ginger also increasesbowel motility (Bauman, 2008; p. 96), abeneficial effect for autoimmune conditionswhen bowels are moving too slowly.




Other Herbal Helpers

. Adaptogens: Help the body deal with stressand provide a balancing action on the immunesystem. Because in AD the immune system isboth hyper-stimulated and under-functioning,these may provide the best choices for herbalsupport. In particular, consider (MacDonald,2000):

• Siberian ginseng (Eleutherococcus senti-coses)

• Borage (Borago officinalis)

• Gotu cola (Hydrocotyle asiatica)

• Licorice (Glycyrrhiza glabra) (contraindicatedwith high blood pressure

• Sarsaparilla (Smilax officinalis)

. Liver support:• Silymarin, an extract of milk thistle

(Silybum marianum): A potent detoxifyingagent, rich in flavonoids and antioxidantsand an excellent herb for the liver.Recommended dosage for a standardizedextract of 70% silymarin is 420 mg/day(Tierra, 2005).

• Bupleurum (Bupleurum chinense; B. falca-tum): Works as an anti-inflammatory, aswell as a stimulator of the production andrelease of bile, which facilitates the detoxifi-cation process (Tierra, 2005).

• Schizandra (Schizandra chinensis):Considered an adaptogen but has strongliver-supporting properties as evidenced bystudies showing normalizing of liver enzymelevels. (Tierra, 2005).

Lifestyle

. Weight loss is recommended, if necessary, toreduce leptin production and inflammationcreated by elevated insulin levels.

. Exercise is an important component of thehealing regimen, to help the body detoxify, keeplymph flowing efficiently through the system,reduce stress, keep the bowels movingefficiently. The most beneficial types of exercisefor those with AD are gentler styles that includestrengthening, flexibility, and easycardiovascular conditioning. The right exerciseis one that is enjoyable and non-injurious. Thefollowing can be used solely or in combination:

• Yoga

• Tai chi

• Brisk walking/hiking

• Pilates

• Bicycling

. Stress reduction of any type can help balanceand strengthen the immune system. Consider:

• Listening to soothing music

• Meditation

• Reading inspirational works

• Laughter

. Biofeedback

. Massage or other bodywork

. Spending time with friends



CONCLUSIONIt will take the work of a patient and skillful nutritionprofessional to help a person with AD understand itsetiology, progression, and therapeutic steps that can betaken. A great number of options have been presentedin this paper. We don’t want to overload an already vul-nerable mind and body with too much good informationand too aggressive a protocol. In my experience, whenclients clean up their diets and environments, theylower the total load, which reduces the triggers that setoff the immune system.

Autoimmune diseases, though consisting of a vari-ety of seemingly unrelated conditions, have more thanone mechanism of action in common. There is almostalways a genetic predisposition at work, as well as oneor more environmental or lifestyle factors. Adopting thenutritious, hypo-allergenic, anti-inflammatory, andmostly organic Eating For Health™ dietary model as analternative to the nutrient-poor, chemically enhancedStandard American Diet, is the starting point for sup-porting a compromised immune system. Reducing expo-sure to toxins, healing digestive impairment, promotingdetoxification, and easing the effects of stress in all itsforms, are manageable steps to rebalancing one’simmune function. If AD is correctly identified and caregoes into supporting systematic detoxification, ratherthan simply suppressing symptoms, an outcome ofhealthy living and a slowing or reversing of the body’sself destructive tendencies is quite likely.

How often do people with MS, RA, or SLE hear thattheir prognosis for healing is promising and that thepower to manage and improve these conditions iswithin their control? Hope is a great healer. Instilling itin our clients soothes fear, frustration, and despair,transforming the information the mind is sending to thecells. Then instead of fighting within ourselves, we canfind ways to negotiate inner harmony and peace.

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