Bioactive Food as Dietary Interventions for Liver and Gastrointestinal Disease: Bioactive Foods in Chronic Disease States

Turkey

Chapter 1

The Alkaline Way in Digestive Health

R. Jaffe

Health Studies Collegium, Ashburn, VA, USA

The biochemical consequences of diet are the greatest influence on overall metabolism for most patients. Food choices clearly affect the course of common pathophysiological errors such as insulin resistance, metabolic syndrome, and their sequella. However, these dynamics can also be considered a leverage point – an opportunity to reverse immune reactivity through practical interventions that patients can implement in their daily lives.

1 Dietary Factors in Metabolism

The intestinal tract plays a key part in nutrient absorption, immune defense against foreign invaders, physiologic repair from wear and tear, growth, neurohormone regulation and stress management. Disorders anywhere in the gastrointestinal system can affect the function of the entire body and overall health. Digestive competence tends to predict survival and the capacity to thrive years to decades later.

1.1 Profile: Metabolic Acidosis as a Major Cause of Chronic Disease

Toxin accumulation in the body can result from a diet that promotes metabolic acidosis (net acid excess after metabolism) as shown by low levels of buffering minerals such as potassium and magnesium. A number of large research studies involving thousands of participants have reported about the association between metabolic acidosis and insulin resistance (Jaffe and Mani, 2006; Souto et al., 2011), type 2 diabetes (Jaffe and Mani, 2006; Schulze et al., 2003), cardiometabolic risk (Murakami et al., 2008), coronary heart disease (Liu et al., 2000), and osteoporosis (Jaffe and Brown, 2000; Jehle et al., 2006), as well as cancer (Tavani et al., 2000). A typical American diet provides insufficient minerals and fiber to counter or buffer the buildup of metabolic acids and to help displacement of toxic wastes. As a result, alkaline cellular reserves within the body reduce and deplete as the intracellular environment becomes progressively acidic, mineral depleted and proton rich (Lim, 2007; Zeidel and Seifter, 1986).

1.1.1 Associated signs and symptoms

The symptoms associated with metabolic acidosis include malaise and fatigue, metabolic syndrome and diabetes, osteopenia and osteoporosis, and depression. Metabolic acidosis is associated with a broad range of clinical conditions in the body because of the biochemical reduction of the proton gradient, upon which cell energy depends. The ratio of ATP: ADP is a measure of cell energy. A ratio of 100:1 is healthy. A ratio less than 80 begins to shift cells from an elective protective, proactive, and prevention mode to a survival mode.

1.1.1.1 Fatigue

Low energy is the major complaint that patients report to their primary care physician. Energy production and the ability to remove toxins safely are compromised when even minor increases in acidity occur. Metabolic acidosis has also been linked to chronic fatigue immune dysfunction syndrome (Jaffe and Brown, 2000). Fibromyalgia and chronic muscle pain that is unresponsive to pain medication have been documented to produce acidic end products that directly irritate and inflame nerve muscle end plates (Deuster and Jaffe, 1998). We observe restoration of vitality and quality of life when metabolic acidosis is corrected comprehensively using predictive tests compared to best outcome reference ranges thus incorporating personalized biochemical individuality into primary care.

1.1.1.2 Osteopenia and osteoporosis

Excess acid within the cells is also a key factor in osteoporosis (Maurer et al., 2003). One of the best examples of this metabolic sensitivity is the influence of acid–alkali balance on skeletal structure, health, and integrity. Skeletal muscles are the largest storehouse of available minerals in the body and are thus exquisitely sensitive to small changes in pH. Even a 10% reduction in pH increases osteoclastic activity while inhibiting osteoblastic function, inducing amplified bone mineral loss (Jehle et al., 2006). For the past 20 years, we have consistently observed 2–10% new bone growth confirmed by DEXA scores after just 2 years.

1.1.2 Relevant evaluations

One of the most useful assessments in the management of metabolic acidosis is self-testing for pH, which can be performed simply by the patient in their home. After 6 h of rest, we find the urine pH is equilibrated with the urinary tract cells. Costing pennies per day, this is a useful self-care test that motivates better compliance with healthier choices. Another assessment involves laboratory testing for reactive food antigens. In tandem, these tests can be pivotal in correcting metabolic acidosis and repair deficits often called inflammation and their myriad sequellae.

1.1.2.1 Self-evaluation: Testing for pH

The hazard of metabolic acidosis is that it requires additional minerals to buffer and remove excess acids from the body, stripping out needed minerals with potential harm to the kidneys and urinary tract. The role of metabolic acidosis in chronic kidney disease has been extensively documented (Sahni et al., 2010).

A pH assessment of the first morning urine provides a clinically useful measure of metabolic acidosis risk. The urine pH is a predictive indicator of the body’s mineral reserves, as well as acid/alkaline status (Whiting and Bell, 2002). Typically pH balance is restored during sleep and rest when excess acids are excreted (Shafiee et al., 2002). This capacity varies widely based on the specific toxic load and the individual’s ability to make energy, deactivate toxins, and excrete those toxins as reported by Bazhin (2007) (see Figure 1.1, pH strips and Figure 1.2, reference range for urine measurement).

Figure 1.1 Picture of pH strips.

Figure 1.2 Interpretation of first, morning-urine measurements.

A value of 7.0 indicates a neutral state, a balance of acid, and alkaline elements. The first morning urine pH goal of 6.5–7.5 shows healthy mineral balance. Neutral or low-level acid excess reflected in lower pH values indicates that metabolic chemistry is appropriately alkaline and that the small amounts of metabolic acids built up from daily metabolism have been easily concentrated and excreted. Cell cytoplasm or ‘cell juice’ functions in an exquisitely narrow, slightly alkaline optimum functional pH range (De Young, 1994; Zeidel and Seifter, 1986).

1.1.2.2 Laboratory evaluation: Reducing immune reactivity

Immune responses directly and indirectly generate substantial amounts of acidic products. For the at-risk individual with impaired dietary buffering capacity, it is especially important to avoid immune reactions due to antigen reactivity or other causes that can contribute to additional cell acidity in the system (Jaffe et al., 2006). A lymphocyte response assay (LRA) can identify delayed allergic reactivity. Substitution of immune reactive substances lowers acid loads.

1.1.3 Clinical interventions: the alkaline way

Reduction of hyperacidity in the body can be achieved through a nutrient-rich alkaline diet, targeted supplementation with alkaline nutrients, and the inclusion of buffered fats.

1.1.3.1 Alkaline diet

The Alkaline Way diet is a health-promoting, fiber-rich diet that consists primarily of whole foods based on individual food tolerances and sensitivities. Preference is given to locally, vine-ripened, organic, or biodynamic sources of foods. Mineral-rich water is the preferred beverage. Reducing the net excess cell acidity supports a range of health benefits.

1.1.3.1.1 Enhancing immune defenses

Alkalinizing foods improve immune defense and repair functions (Lee and Shen, 2008) by reducing host hospitality to chronic infections. This reduced infectious challenge results in lower levels of inflammation, more resources for anticancer surveillance, and enhanced repair capacity. Clinical strategies that accompany an alkaline diet include a rotation or a substitution diet to reduce exposure to reactive foods coupled with health-promoting food choices, fresh fruits and vegetables, pulses and grasses, whole grains, minimal animal protein, and a program of individualized nutritional supplements to fully meet biochemical needs.

1.1.3.1.2 Buffering cellular chemistry

A metabolically alkaline diet means that food has a buffering or cell acid neutralizing effect on in vivo cellular chemistry, in vivo (Budde and Crenshaw, 2003). The effects of specific food responses within the body can differ from that food’s test tube chemistry (Gonick et al., 1968). For example, citrus fruits are alkalinizing in the body because citrate, malate, succinate, and fumarate all promote the generation of more than twice as much bicarbonate as the acid contributed from the total amount of food metabolized (Brown and Trivieri, 2006). This means that citrus fruits and similar foods are acidic in a test tube environment, yet alkaline forming in the body.

Figure 1.3 reflects this real-time perspective on metabolism – assessing nutrition for in vivo efficacy rather than merely evaluating the ash residue of the food as has been historically performed in nutrient assays. The foods listed here are categorized based on an empirical formula calculated from the actual composition of the foods’ total protein, fat, carbohydrates, minerals, cofactors, and fiber contents (Jaffe, 1987).

Figure 1.3 Food and chemical effects on acidic/alkaline body chemical balance.

1.1.3.2 Alkaline nutrients

A diet high in acidic foods tends to be less-nutrient-dense and fiber-rich than an alkaline forming, whole foods, immune tolerant diet. Once mineral depletion occurs, cells become progressively more acidic and less energetic. The cell cytoplasm proton gradient is required for the cellular power centers, mitochondria, to work effectively. When the cell becomes acidic, the proton gradient is reduced and cells become dependent on anaerobic survival metabolism. This is a less efficient form of energy production. Lower energy production shifts cells into minimal function survival mode until adequate mineral buffers are restored.

1.1.3.2.1 Buffering minerals

Minerals are required to activate enzyme catalysts within cells; lack of specific minerals has been linked to numerous specific types of enzyme deficits. Supplementation at maintenance levels includes a healthy balance of calcium and magnesium, as well as copper and zinc, and all of the divalent cations that perform essential buffering minerals needed for healthy function. These minerals are required supplements for individuals suffering from metabolic acidosis (also known as net acid excess) because buffered minerals neutralize metabolic acids to maintain healthy pH homeostasis inside the cell.

1.1.3.2.2 Buffering fats

Short-chain and medium-chain fatty acids with less than 16 carbons such as octanoate and decanoate are alkalinizing. Found in palm kernel oil, coconut oil, and ghee (clarified butter), these short and medium chain fatty acids can accept acetate molecules.

1.1.4 Individual essential nutritional supplementation

Additional functional strategies in clinical management include the reduction of oxidative stress, support of detoxification processes (through healthy methylation), and reduction of risks such as homocysteine. We find a healthier, least risk goal value for homocysteine to be <6 μmol/l. With a combined 20-fold risk difference between a homocysteine of <26 versus <6 μmol/l, healthier homocysteine levels are a major clinical opportunity.

1.1.4.1 Antioxidants: Ascorbate to zinc

Ascorbates are the principal antioxidants in eukaryotic cells. As one of but three species that are unable to convert glucose to ascorbate, people are vulnerable to chronic as well as acute scurvy. Ascorbates uniquely set the cell redox electrochemical potential. Ascorbates recycle and regenerate vitamins E, taurine, glutathione, alpha lipoic acid and can even salvage mitochondrial cytochromes. Cumulative antioxidant deficits become repair deficits observed clinically as inflammation, in turn is associated with metabolic acidosis. Antioxidant supplements are provided to protect against oxidative damage, restore cell energy production, rehabilitate mitochondria, and reset homeostatic mechanisms (Jaffe and Brown, 2000). We suggest a functional personalized assessment of ascorbate need (www.PERQUE.com).

1.1.4.2 B-complex vitamins to support methylation

Impaired methylation is commonly reflected in elevations in homocysteine above the healthy value of <6 μmol l−1. Problems with cell communication, detoxification, and transport result from such impaired methylation. This reframes these common states in physiologic rather than pathologic terms, and offers integrative approaches to care as evidence-based options to be included as first-line comprehensive care.

Healthy alkaline cell balance is clinically assessed through first, morning-urine pH measurements. An increase in alkali-forming foods and supplements is recommended in proportion to individual need to reach the healthy goal range of 6.5–7.5 for first, morning-urine pH. Healthy methylation and detoxification is reflected in a plasma homocysteine of less than 6 mg dl−1. Other measures of detoxification such as glucarate, mercapturate, and hippurate urine excretion are discussed elsewhere (Jaffe, 2006). A slow, steady uptake of glucose by managing glycemic load is another important aspect of this approach.

2 Glycemic Load as a Tool for Better Digestive and Cardiovascular Management

Simple carbohydrates are easily taken up and cause a rapid rise of glucose in the bloodstream, which requires the release of insulin to return blood sugar levels to a safer level. Ongoing stress on the glucose–insulin–energy regulatory system frequently leads to high insulin levels of less functional insulin. Chronically elevated insulin is associated with a series of sequella with adverse long-term health effects. It is increasingly apparent that progress in treating chronic illness requires effective management of food glucose–insulin interaction. We suggest the Alkaline Way to improve insulin sensitivity through corrected metabolic acidosis, antioxidant, and mineral deficits and enhanced toxin removal.

2.1 Associated Signs and Symptoms

The consumption of a high sugar, low fiber diet invites the continuum of weight gain, obesity, metabolic syndrome and diabetes. Associated risks include poor glucose management, with effects such as lipogenesis, loss of insulin sensitivity, development of insulin resistance, and a wide range of cardiovascular and systemic consequences.

2.2 Self-evaluation

Two tools useful in glycemic management by patients include the glycemic index and calculation of glycemic load.

2.2.1 Glycemic index: Older and less useful

The glycemic index measures the effects of carbohydrates on blood sugar levels (Atkinson et al., 2008). A measure of 100 on the index reflects the typical metabolic response to white sugar (based on research-determined norms). Foods rated 55 or below on the index are identified as healthful because they require lower levels of insulin, defined as ‘insulin-sparing’ (Foster-Powell et al., 2002). Fructose, certain processed foods as well as the size, complexity and constituents of a meal, can provide conflicting glycemic index results.

2.2.2 Glycemic load: Newer and more useful

The glycemic load is a better measure of the impact of carbohydrate consumption. It takes the glycemic index into account, but provides a fuller picture than the index alone (Murakami et al., 2007). Glycemic load indicates how rapidly a specific carbohydrate food raises blood sugar and factors in the actual amount of the particular carbohydrate being consumed (see Figure 1.4 for an ideal glycemic response to a low glycemic load meal that includes 100% whey). This is evident since the experimental meal was 2.5 times the basic carbohydrate load and still showed a small change in blood glucose. The contrast with the blood glucose change with 50g carbohydrate (bread + jam) was dramatic.

Figure 1.4 Comparison of glycemic response between 100% native whey meal and standard 50 g carbohydrate load from bread and jam.

This chapter focuses on cellular metabolic acidosis and glycemic load as key clinical aspects of the Alkaline Way. Immune tolerance and delayed allergies are also discussed.

2.3 Intervention: Low to Moderate Glycemic Diet

Glycemic management involves the reduction of refined food products in the diet – foods that trigger the release of high levels of insulin, resulting in lipogenesis and weight gain. By definition, these foods are high on the glycemic index and have a high glycemic load (Jenkins 2004; Riccardi et al., 2008). Foods containing a large proportion of simple carbohydrates include white flour and other refined grains, white rice, white potatoes, and corn, as well as cane sugar, corn syrup, fructose, honey, maple syrup, and other sweeteners. The optimal diet is high in fresh fruits and vegetables, whole grains, and protein (De Natale et al., 2009; Jenkins, 2004; Riccardi et al., 2008). Note that this is essentially a more alkaline diet, so that the two systems can be used in tandem by both clinicians and consumers. For other reasons, we suggest a minimum non-caloric sweeteners.

3 Native Whey-Based Meals and Gastrointestinal Health

Research suggests that high amounts of animal protein can cause undesirable gastrointestinal issues. Excessive amounts of protein from meat and fish have the potential to increase disease risk as high as threefold in the development of inflammatory bowel disease and ulcerative colitis (Jantchou et al., 2010). A large Italian study of more than 10 000 individuals demonstrated a significant association between meat intake and the development of cancer (Tavani et al., 2000).

In selecting optimal protein sources, a quality whey protein provides essential amino acids, such as glutamine and cysteine, and fatty acids, such as conjugated linoleic acid (Belobrajdic et al., 2003). The high cysteine content of whey has been found a superior means of supporting glutathione levels and, therefore, antioxidant function, a finding reported by Bounous (2000).

For healthy glycemic control, a balance of all food groups is essential with an emphasis on nutrients from fiber-rich whole foods that maintain stable blood glucose levels.

4 Food Allergies and Sensitivities

Immune responses to specific foods, chemicals, or contaminants can take the form of classic allergies or of delayed sensitivities. For decades, the conventional approach to allergy focused on histamine immunoglobulin E or IgE reactions, which can trigger a harmless case of hives or life-threatening anaphylactic shock. However, it is now widely recognized that reactivity can be driven by type 1 allergies (typical skin tests or radioallergosorbent (RAST) IgE reactions), or by type 2 antibody reaction (IgA, TgG, or IgM reactive antibodies), type 3 immune complexes, and type 4: T-cell mediated responses. In contrast, helpful neutralizing antibodies are often misunderstood when conventional ELISA or EIA IgG tests are done.

4.1 Associated Signs and Symptoms

Eighty percent of food reactions are not IgE-type reactions – rather, they are delayed types of reactions. Reactive antibodies can cause symptoms that become apparent from hours to weeks later, so that they are frequently difficult to identify. Given the range of potential antigens and the various types of responses, a comprehensive food assessment is vital. IgE tests do not measure delayed reactions.

4.1.1 The link between allergies and digestive competence

Food intolerance and allergies result from impaired digestion. All of the following issues typically develop before food allergies or intolerances occur:

• Maldigestion results in partially digested digestive remnants that are recognized as foreign antigens – thus evoking immune responses to neutralize the foreign invader.

• Infectious and noninfectious foreign antigens (partially digested food) invade the gastrointestinal mucosa/are treated equally as invasive antigens. This means that with increased presence of digestive remnants, the individual has fewer immune defense and repair resources to defend against infection or repair from daily wear and tear. This results in a loss of immune tolerance and emergence of delayed hypersensitivities with a shift from homeostasis to self-attacking immune responses. The Alkaline Way restores homeostasis and tolerance by personalized diagnostics and including therapeutic monitoring to assess how much of the healthy goal states have been achieved.

4.1.2 Lactose intolerance

With this type of functional impairment, the enzyme that digests milk sugar – lactase – is either not produced or available in such low levels that milk cannot be completely digested. This intolerance is almost always acquired as a byproduct of maldigestion and enteropathy.

4.1.3 Gluten or casein intolerance or sensitivity

Casein is one of the major proteins in milk. Gluten is a protein from grains like wheat. Both are among the most difficult foods to digest. Intolerance to casein or gluten can occur when digestive ability is impaired. Upper abdominal discomfort and alternating constipation and diarrhea sometimes accompany this condition. Functional hypochlorhydria, maldigestion, dysbiosis, and enteropathy are typically the underlying causes.

Gluten intolerance results from maldigestion, food intolerance, or delayed allergic hypersensitivity. Advanced ex vivo LRAs can be employed to measure all delayed allergy pathways.

4.2 Evaluation: LRA by ELISA/ACT Tests

Testing for delayed, acquired sensitivities focuses on the type of functional antibody and the specific reactive allergens. Sensitivities reflect the variety of immune reactions present (see Figure 1.5). Older technologies, such as IgG antibody assays, have proven at best only temporarily helpful in the treatment of chronic autoimmune conditions. The tests do not distinguish helpful from harmful antibodies. Newer functional tests such as LRAs are recommended because they detect only the reactive antibodies. These antibodies are indications of a burdened immune system. LRA lab tests can measures reactions just as they occur in the body (ex vivo). This type of functional testing targets antibodies that cannot be distinguished by standard antibody detection systems.

Figure 1.5 Wheel of immune response mechanisms.

Assessing delayed allergy or hypersensitivity to foods or other chemicals provides an ‘immunologic fingerprint’ of the foods, chemicals, and medications to which the individual is tolerant and those which their lymphocytes react against. Tests such as the LRA by ELISA/ACT™ can sensitively, specifically, and predictively identify underlying causes of immune burdens and increased hospitality to infection, as well as accelerate degenerative, chronic, and autoimmune conditions with less than 3% variance day to day (Jaffe and Kruesi, 1992). These tests have been employed to identify the epigenetic burdens on a given individual’s immune system. The causes of autoimmunity are typically provoked by exposures to specific foods or chemicals to which the person has acquired hypersensitivity. Substituting other food choices for reactive items and minimizing chemical exposure, while evoking human healing responses is part of the Alkaline Way. With over 50,000 cases in our database, we suggest this technology helpful in all conditions where immune tolerance is lost. This includes all autoimmune and most chronic, degenerative ills.

4.3 Intervention: Hypoallergenic Diet

By avoiding offending food and chemical substances, following an alkalinizing diet, and utilizing targeted supplementation, the body can stimulate healing and induce repair. This concept has been successfully tested in controlled outcome studies on diabetes (Jaffe et al., 2004, 2006), as well as fibromyalgia and chronic fatigue syndrome (Deuster and Jaffe, 1998). Clinical data indicate that other autoimmune conditions respond to this approach as well. The Akaline Way includes the identification of acute and delayed food and chemical allergies and intolerances. This allows for a diet that can be digested, assimilated, and eliminated efficiently, while enhancing the individual’s vitality and homeostatic competence. Mental and physical exercises are as important for gastrointestinal health as they are for any organ system. A high-nutrient, low-toxicity diet in the context of a lifestyle of mindfulness and gratitude rounds out the Alkaline Way to sustainable health.

5 The Role of Specific Nutrients in Digestive Health

When chronic digestive disorders are present, the use of nutritional supplementation can improve clinical outcome. Thousands of research studies evaluating nutritional supplements have shown the benefits of specific nutrients in treating a wide range of complex conditions. The following table provides a brief overview of major nutrients that have been found to play an important role in digestive disorders. Supplementation with standardized ingredients makes it possible to provide nutrients at a level that will support active metabolic function, while improving compromised digestion and assimilation based on individual requirements revealed through their functional, integrative approach (Table 1.1).

Table 1.1 Major Nutrients Noted for Beneficial Effects in Digestive Health

Source: Gaby A. Nutritional Medicine. Hendler, S.S., Rorvik, D.M., 2000. PDR for Nutritional Supplements, second ed. Thomson Reuters, New York; Jaffe, R., 2010. The Alkaline Way: Integrative management of autoimmune conditions. Townsend Letter for Doctors and Patients. November, pp. 44–51; Shils, M.E., Shils, M., Ross, A.C., Caballero, B., Cousins, R.J., 2005. Modern Nutrition in Health and Disease, tenth ed. Lippincott Williams and Wilkins, Philadelphia, PA.

6 Conclusion

The combined effects of individualized dietary programs, supplementation targeted to the specific needs of the patient, and reduction of allergenic stimulation offer the provider viable tools for conservative and effective clinical management of cardiovascular conditions. In this context, treatment strategy includes a detailed history of health, lifestyle, and diet. Laboratory assessment, development of a case-specific treatment plan that includes diet and nutritional supplements, and a long-term plan to support patient motivation and compliance, reinforced by ongoing caring and competence.

References

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Relevant Websites

1. http://www.Healthstudiescollegium.org.

2. http://www.ELISAACT.com.

3. http://www.PERQUE.com.

4. http://www.PERQUEWheyGuard.com.

5. http://www.ncbi.nlm.nih.gov/pubmed.

Chapter 2

Functional Assessment of Gastrointestinal Health

R. Jaffe

Health Studies Collegium, Ashburn, VA, USA

Digestive illness is frequently a cause of or disposition to maldigestion-induced autoimmune conditions, as well as a factor in chronic degenerative disorders such as cancer and cardiovascular diseases. Worldwide, more than 1.5 million children die each year from diarrheal diseases (UNICEF/WHO, 2009).

In the United Kingdom Department of Health, digestive disorders affect one of every three people and are associated with one of every four surgeries (DoH, 2002/2003). In the United States, digestive health issues affect 60–70 million people at a direct annual cost of $97.8 billion (Everhart, 2008). The association between digestive disorders and health issues is reflected in conditions such as acute and delayed allergies, insulin resistance, and metabolic syndrome, as well as diabetes, an avoidable, costly, too common consequence. Furthermore, gut malfunction and pathogen overgrowth are the common underlying factors in numerous other chronic conditions, as discussed below.

1 Physiology of Digestion

Digestion is a series of sophisticated metabolic processes that convert plant carbohydrates, proteins, fats, and other nutrients into building blocks that the body can utilize for nourishment, growth, and repair when toxin load and stress hormones permit. Healthy digestion produces molecular building blocks that support immune system tolerance and enable proactive repair. Multiple mechanisms exclude trap and neutralize larger molecules that can be bioactive and sometimes immunogenic. With cumulative stress, toxin exposure and nutritional deficits, maldigestion replaces eudigestion. The erosion of digestive defenses and the shift of immune responses from tolerant to hyper-reactive is a molecular expression of what people feel when they are chronically unwell although somewhat functional. In the 1960s, my gastroenterology professors were alarmed at the rapidly rising epidemic of epidemics related to the many expressions and comorbidities of maldigestion. Digestive metabolism involves chemical and mechanical functions that break down food so it can be assimilated, utilized, and eliminated efficiently, safely, and effectively. Essential nutrients released or manufactured by the body during this process must be derived in sufficient amounts to meet individual genetic, epigenetic, and sustainability needs for the body to grow, heal, and function well.

Digestion begins with the initial visual and gustatory contacts with food that tell the brain and then the body which digestive juices to secrete. The process of seeing the food to be eaten, tasting it, and smelling the aromas stimulates the release of saliva containing specific enzymes such as lipase (which begins the processing of fats) and amylase (which opens up and begins breaking down carbohydrates). This favors the locavore, ‘slow food’ approach.

The stomach exerts remarkable competence in mechanically churning diverse food mixtures. This process breaks up and acidifies the stomach contents (to create a mixture termed chyme), while adding the digestive enzyme pepsin to the stomach’s contents. This exposes food molecules to enzymes and hydrochloric acid that hydrate, cleanse, and process carbohydrates and protein-rich foods. The resulting predigested chyme, the consistency of oatmeal, is passed from the stomach to the small intestine. When sufficient hydrochloric acid is present, biosensors are triggered to empty contents into the duodenum. If the chime is sufficiently acidified, bicarbonate and pancreatic digestive enzymes are then released. Adequate stomach acid is essential for healthy digestion. Blocking stomach acid production disposes one to maldigestion and its pervasive consequences.

Digestion occupies ~60% of the body’s energy production and its consumption is devoted to digesting food. If the 20 ± 10 ft of intestines were unfolded to create a flat surface, the intestinal membrane surface covers an area the size of a tennis court, a remarkable 2500 ft² or 260 m² of surface area.

2 Clinical Issues in Digestive Health

The issues reviewed in this chapter impact or are comorbidities for numerous chronic health issues. Approximately a third of the gastrointestinal (GI) complaints seen are truly disabling, whereas 2/3rds are a part of an underlying chronic issue. We will also see how living the Alkaline Way™ restores digestive health.

2.1 Profile: Dysbiosis

Healthy flora are a major, increasingly appreciated aspect of health. The contents of the healthy human digestive tract typically contain at least 1800 different species of flora that in total number in the trillions. The presence of infection by a foreign pathogen or the overgrowth of any resident species is termed dysbiosis, which can result in poor health and a range of nondescript symptoms (Cani and Delzenne, 2010). Beneficial microflora minimize this type of imbalance. Healthy bugs in abundance crowd out bad bugs. Pathogenic organisms do not give out their toxins until crowd signaling confirms that they are present in high density.

2.1.1 Associated signs and symptoms

In a healthy human body, there are typically five to seven pounds of bacteria, of which more than 95% are anaerobes. Antibiotic therapy has been found to destroy both harmful and beneficial bacteria in the body (Charteris et al., 1998). When healthy flora is absent, food decomposition is slowed or incomplete, impairing digestion and reducing the level of nutrients available for absorption. Symptoms and diagnoses associated with compromised flora and dysbiosis include diarrhea, constipation, urinary tract infections, irritable bowel syndrome (IBS), irritable bowel disease (IBD), Crohn’s disease, and even diabetes (Vaarala et al., 2008). Digestive health protects and promotes health. Digestive ill health is a comorbidity in almost all autoimmune, chronic, and degenerative illnesses.

2.1.2 Etiology

Multiple courses of antibiotics favor pathogenic bacterial overgrowth (Esposito et al., 2007; Majewski and McCallum, 2007), such as Clostridium difficile, and yeast overgrowth, such as the Candida species. In some cases, this promotes antibiotic-resistant strains of bacteria or other pathogens to which the individual is exposed and vulnerable. A diet high in sugars, milk, or meat products can also result in the overgrowth of various bacterial species with adverse effects on health (Jantchou et al., 2010). Harder to digest foods like cow dairy and grains become sources of digestive intolerance.

2.1.2.1 Sidebar: initial probiotic research

In 1908, Nobel prize-winning scientist Elie Metchnikoff of the Pasteur Institute in Paris provided the first evidence that microorganisms may be responsible for the health-promoting effects of fermented milks. After observing that Bulgarian peasants live to ripe old ages, Metchnikoff became convinced that their health and longevity were linked to the beneficial microbes in the cultured milk they drank copiously. In his book, The Prolongation of Life, Metchnikoff suggests that disease-causing bacteria were minimized or eliminated by ingesting large amounts of Bulgarian kefir or yogurt, which contained beneficial bacteria later identified as Lactobacillus bulgaricus. These organisms are members of the bacterial species Lactobacillus – bacteria that produce lactic acid. Bifidobacter and Streptococcus thermophilus are other major beneficial probiotic organisms. We recommend 40–100 billion probiotic organisms taken daily between fermented foods and bioactive supplements.

2.1.3 Intervention: probiotic supplementation

Restoration of a healthy level of gut microflora helps promote the balance toward healthy and away from harmful microorganisms.

2.1.3.1 Benefits of microflora

Beneficial microflora provide a surprisingly extensive range of protective functions in the body. Probiotic organisms decompose food in both the small and large intestines to liberate nutrients to be assimilated and utilized for energy and repair.

2.1.3.1.1 Production of digestive enzymes by microflora

Probiotic bacteria normally found in a healthy gut support the production of essential enzymes, which increases the availability of nutrients as food is more efficiently and completely broken down (Chapman et al., 2011). For example, the enzyme lactase, produced by lactic acid bacteria, improves digestion, metabolism, and absorption of milk sugar (lactose). Heyman (2000) found that these bacteria also facilitate the action of intestinal lactase, improving overall digestion by reducing symptoms such as diarrhea.

2.1.3.1.2 Reduced lipid levels

A variety of studies have shown that healthy probiotics at adequate levels can improve overall health, increasing metabolic breakdown of certain lipid or lipophilic substances and reducing toxins, binding toxins to prebiotic fiber that are contained in bile (Vaarala, 2008). This is important, for example, in fat emulsification that occurs in the upper area of the small intestine (duodenum), where fats are mixed with bile during digestion. Improved lipid metabolism also reduces the reuptake of cholesterol and fatty acid products, and this has been associated with a 5–17% reduction in serum cholesterol after just 1 month of daily consumption of viable probiotic organisms in the 10–20 billion organism/day (colony-forming units, CFU) range (Jackson et al., 1999).

2.1.3.1.3 Inhibition of pathogens

One of the major beneficial effects of probiotics is the suppression of harmful microorganisms (Fuller and Gibson, 1997). When the microflora are significantly depleted, there is heightened risk for intestinal conditions such as viral gastroenteritis (Biller et al., 1995). Research by Campieri and Gionchetti (1999) suggests that when there are sufficient numbers of healthy probiotics in the gut, the risk of inflammatory bowel disease/syndrome (IBD/IBS), is substantially reduced. Conditions such as IBD and IBS, ulcerative colitis, and regional enteritis (Campieri and Gionchetti, 1999) have been reversed in individuals who have developed these symptoms through the use of probiotics as part of comprehensive care. Recent research also reports probiotic mixtures beneficial in the treatment of diarrhea, gut microbiota modulation, and Helicobacter pylori infection, as well as atopic disease and respiratory tract infections (Chapman et al., 2011). In our experience, an ounce of prebiotic and probiotic supplementation is worth a pound of digestive diseases cures.

2.1.3.2 Probiotic dosage

When flora are killed off by taking antibiotics, or from xenotoxins or distress, beneficial bacteria levels can be restored with probiotic supplements. Current clinical recommendations suggest a maintenance intake of 10–50 billion bacteria daily from a variety of mixed cultures. We prefer multiple strains of human implantable acidophilus, bifidobacter, and healthy S. thermophilus.

2.1.3.2.1 Preventive applications

When one is traveling, under stress, or recovering from illness or disease, or post antibiotic consumption, the ideal dosage is a probiotic culture that contains 20–100 billion viable probiotic organisms consumed daily for 2–3 months to restore digestive competence. Products are currently available on the market that provide as many as 200 billion count in a single dose.

2.1.3.2.2 Therapeutic interventions

Probiotics are recommended in cases of bacterial and yeast infection or overgrowth (Gionchetta and Campieri, 2000). To address these forms of dysbiosis, many researchers now advocate antibiotic/probiotic combinations of 20–200 billion CFU mixed flora for conditions such as constipation, diarrhea, urinary tract infections, and infective endocarditis (Charteris et al., 1998).

2.1.3.2.3 Medical probiotics

Probiotics harvested in the log phase for optimum growth and viability of CFU are recommended. Multiple strains, typically containing nine to ten different strains, are more effective in repopulating the gut. The level of supplementation is based on the severity of the patient condition, their response, and other factors determined by the physician. Typical replenishment needs are intakes of 20–100 billion organisms/day for 2–3 months; 5–10 billion per day for maintenance.

2.2 Profile: Hyperpermiability (Leaky Gut Syndrome)

A condition described as intestinal permeability or ‘leaky gut’ results whenever the lining of the small intestine leaks its contents into the intestinal lymphatics and then the bloodstream (Solly et al., 2001). When the body is under stress or in shock or nutritional deficit, pores that line the GI tract open wide and release metabolic and microbial toxins from the gut. These toxins are then passed on to the liver (Cariello et al., 2010), the lymphatic system, the bloodstream, and the immune system and distributed throughout the body and vasculatures. Leakage from the gut can also occur in conditions such as Crohn’s disease, with the deterioration of tissue in the intestinal wall. Intestinal surfaces are also susceptible to erosion from mechanical action, toxins, and the products of pathogenic bacteria.

2.2.1 Associated signs and symptoms

Leaky gut is implicated in chronic conditions with a broad range of clinical symptoms (Liu et al., 2005); many include a direct inflammatory component such as IBS, or toxic reactions, such as certain types of migraines. Leaky gut has also been implicated in both Type 1 and Type 2 diabetes (Secondulfo et al., 1999; Visser et al., 2009). Hyperpermeability is also implicated in skin conditions due to inflammation (recognized as repair deficit) and may reflect the intake of foods that induce delayed allergic reactions presenting as eczema, psoriasis or any other autoimmune condition. When digestion is incomplete, digestive remnants accumulate in the GI tract and increase inflammation (repair deficit). This cause atrophy and subsequently enteropathy.

Leaky gut also occurs whenever the body goes into shock in response to injury, surgery, or severe illness.

Hyperpermeability can result from any number of insults to the body:

• Alcohol abuse

• Food poisoning, parasitic infections, bacterial overgrowth

• Full range of GI conditions, including gastritis, colitis, and Crohn’s disease

• Eating disorders (particularly anorexia)

• Shock, trauma, burns, or surgery

• Cancer and chemotherapy

• Chronic hepatitis, pancreatitis

• NSAIDS and certain other medications

• Rheumatoid arthritis

• Xenotoxins (toxic metals, persistent organic pollutants, solvents, endocrine disruptors)

• Distress

When the immune system detects oversized food molecules in the bloodstream, these molecules are targeted as foreign ‘invaders’. This results in one or more delayed immune reaction that release powerful and potentially damaging cytokines and other amplifiers.

2.2.2 Intervention: recycled glutamine supplementation

Leaky gut syndrome and damaged mucosa are usually associated with glutamine deficiency. These conditions have been reversed through glutamine supplementation (Byrne et al., 1995). Glutamine and butyrate are the principal fuels that energize the intestinal lining cells. Generally speaking, digestion and normal metabolic function of the intestines are dependent on adequate amounts of glutamine, abundant in health and conditionally essential with respect to stress. The effects of glutamine have also shown to maintain the integrity of the gut barrier structure and decrease intestinal cell wall damage (Wu et al., 2006).

Through the action of glutamine on the kidneys, the body controls pH balance and eliminates acids. Research indicates that glutamine can effectively enhance bowel function in people with short bowel syndrome and other GI conditions involving extensive intestinal surgery, including transplantation (Byrne et al., 1995). Providing

L

-glutamine and pyridoxal-alpha-ketoglutarate in combination provides clinically an enhancement of glutamine uptake presumably through recycling. This approach allows full glutamine dosing without the risk of glutamate buildup.

2.3 Profile: Allergic Reactions as a Cause and Effect of Leaky Gut

Research and clinical experience indicate that allergies and intestinal hyperpermeability are linked (Yamaguchi et al., 2006). In an age of increasingly personalized medicine, LRA by ELISA/ACT tests provide insight into individual acquired delayed or late phase allergies. Comprehensive programs have been tested and found to significantly improve outcomes (Jaffe, 1998, 2006). Either of these conditions can serve as a cause or an effect. While it may be useful to identify the initial cause, such as gluten sensitivity, in practical clinical terms, it is not always possible to determine which factor is the cause and which is the effect. Consequently, it is generally advisable to treat both conditions at the same time.

2.3.1 Hyperpermeability as a cause of reactivity

The likelihood of developing antigen reactivity and food sensitivities is exceptionally high in anyone already experiencing leaky gut from any cause. In the case of food reactions, 80% of food reactions are not IgE-type reactions. Rather, they are delayed reactions caused by IgA, IgG, or IgM. Consequently, a comprehensive food assessment is vital, given the frequency of delayed reaction. An IgE screen alone will not usually pick up delayed reactions (Figure 2.1).

Figure 2.1 Lymphocyte response assays.

2.3.2 Allergies as a cause of hyperpermeability

Consumption of antigenically reactive foods can trigger hyperpermeability, often within a matter of minutes. In addition, it is common for patients to consume more than one reactive foods in their daily diet. This causes a constant state of antigenic stimulation and burdens immune responses. Chronic inflammation and immune reactivity occurs when immune tolerance is lost. Leaky gut has been associated with a wide range of chronic disorders, e.g., arthritis (joint and connective tissue disorders), asthma, eczema, psoriasis, vascular diseases and diabetes, as well as anxiety, depression, learning disabilities, and some dementias. To manage these conditions effectively, it is essential to address the relationship between delayed food allergies, nutritional distress, and leaky gut.

2.4 Profile: Maldigestion and Enteropathy

Maldigestion is one of the underappreciated causes of illness that is increasingly common in industrial society. The causes are elusive because of the long lag from antigen exposure to symptomatic expression.

2.4.1 Comorbidities

Prevalent symptoms of impaired or incomplete digestion include weight management issues, adult failure to thrive, lack of restorative sleep, skin disorders, and allergies. Impaired digestive function can result from any number of functional disorders, including low levels of essential stomach acid (hypochlorhydria), insufficient pancreatic digestive enzymes, and bile salt deficiency. Disorders of the liver, kidneys, and pancreas can all result from, or contribute to, maldigestion.

2.4.2 Cause and Consequences

2.4.2.1 Low enzyme levels

When pancreatic enzyme levels decrease, the cause is usually functional hypochlorhydria. Symptoms such as bloating, heartburn, constipation, diarrhea, insomnia, muscle aches, pain, and skin conditions that occur when the skin is used as an accessory ouster of excretes. Causal factors include an abundance of processed food in the diet and overuse of medications such as antibiotics and painkillers.

Enzyme insufficiencies can be caused by genetic conditions or low levels of probiotics, which result in a lack of the enzymes needed for digestion. Two potential solutions include the supplementation of probiotics (described in the section ‘Profile: Maldigestion and Enteropathy’) and enzymes (Domínguez-Muñoz et al., 2005). We find implantable probiotics, unprocessed dietary fiber a whole food-based immunocompatible diet to restore digestive and detox competence that in turn restores neuro-hormonal balance of the immune system.

2.4.2.2 Poorly timed gastric emptying

Early or delayed gastric emptying are additional signs of incomplete digestion. These disturbances in the naturally orchestrated processes of digestion compromise the nutrition available to the body (see the Section ‘Profile: Maldigestion and Enteropathy’ for a discussion of interventions).

2.4.2.3 Surgical restructuring of the GI tract

Surgery can induce maldigestion if portions of the large or small bowel are removed or if the stomach is reconstructed. In some cases, these structural changes are deliberate, for example, in cases of bariatric weight loss in which surgery is intended to limit digestion. All metabolic management approaches should be performed before surgery is evaluated.

2.4.2.4 Malabsorption

Chronically poor digestion can lead to malabsorption. The individual does not obtain sufficient nutrients from the diet and therefore experiences health problems as a result. Increase in intake of prebiotics (40–100 g/day) and replenishment of probiotics (40–100 billion/day) and essential nutrients for healthy digestion, such as recycled glutamine, is recommended.

2.4.2.5 Enteropathy

Loss of digestive competence can occur as a result of atrophy, a lack of essential nutrients, or excess toxins such as heavy metals, biocides, and hormone disrupters. Repair nutrients described above are recommended for a year or two it typically takes to restore and rebuild digestive competence after enteropathy.

2.5 Transit Time

The speed at which digested food moves through the GI tract is described as the transit time. This time is the interval between food consumption and the elimination of digested waste.

2.5.1 Associated signs and symptoms

A number of factors affect transit time, including diarrhea, constipation, and metabolic toxicity. Even with different sections of the GI tract, the time required for food to move through the digestive process is significantly affected by the composition of the meal passing through. Fats, for example, speed up muscle contraction and peristalsis. Transit time is also influenced by factors such as psychological stress, gender, and reproductive status (Riccardi and Rivellese, 1991).

2.5.1.1 Delayed transit time

The longer the transit time, the greater the potential for putrefaction and the development of dysbiosis. When this occurs, unhealthy waste products are frequently reabsorbed and interfere with proper metabolism or with the overgrowth of specific types of bacteria such as Helicobacter pylori, Clostridium or species of Escherichia coli (associated with high concentrations of meat products in the bowel). The result is predisposition toward intestinal or systemic illnesses or their exacerbation.

2.5.1.2 Rapid transit time

Very short transit times may not provide adequate opportunity to digest and assimilate the food consumed. Symptoms and response are always individual and appropriate for discussion with a health professional. It is recommended that transit time be rechecked twice a month until healthy bowel movements and normalized transit time are achieved.

2.5.2 Evaluation: self-test for transit time

Although various methods have been suggested to track transit time, a simple protocol can be used using charcoal capsules. (Charcoal is also sometimes utilized for symptomatic relief of intestinal gas.) This protocol involves taking 1.5–6 g of charcoal with 8 oz. of water on a specific occasion and recording the time of consumption. Choose a high-quality brand of activated charcoal capsules. For the most accurate results, the capsules are ingested just after a bowel movement. The ideal dosage is based on body weight (see Table 2.1).

Table 2.1 Transit Time Evaluation: Charcoal Dosages

2.5.2.1 Observations

The first step is to note and record the time at which the charcoal is taken. This marks the beginning of the transit-time test. Patients are encouraged to observe the consistency of their stool and note anything unusual or different about the quality, texture, color, or composition of bowel movements.

2.5.2.2 Transit time test interpretation

Twelve to eighteen hours is considered a healthy transit time. Unfortunately, many Americans have a 36–144 h transit time or longer. Slow transit time allows the production and absorption of various toxins produced within the body – xenotoxins that are absorbed from the chyme and stool directly into the bloodstream.

The longer the transit time, the greater the possibility that putrefaction can occur (with the overgrowth of either commensal bacteria or pathogenic species), leading to unhealthy waste products that are too often reabsorbed and interfere with proper metabolism. The result is predisposition toward chronic intestinal or systemic illness, or the amplification of existing conditions.

On the other hand, very short transit times may not provide adequate time to digest and assimilate the food consumed. It is recommended that the transit time be rechecked twice a month until a healthy transit time is achieved.

2.5.3 Interventions

Initial interventions for maladapted transit time are relatively basic and can be implemented by patients through simple changes in lifestyle.

2.5.3.1 Dietary fiber

The Standard American Diet is fiber deficient, typically including less than 7 g day−1. Low dietary fiber intake requires the body to work harder to push waste along. One of the best ways to support an optimal transit time of 12–18 h is to increase fiber content in the diet. Good fiber intake also provides considerable benefit to gut health and contributes to a healthy microflora population. Additional benefits of fiber include

• prevention of the development of pathogens in the intestine and their adherence to the gut wall;

• improved blood cholesterol levels;

• improved vitamin activation;

• better absorption and elimination of toxins such as heavy metals;

• enhanced mental clarity and reduced brain fog;

• lower carbohydrate content and therefore healthier induction of glucose into the bloodstream;

• reduced body weight and lower body mass index (Murakami et al., 2007).

Fiber provides a cleansing function to sweep pathogens away from the intestinal tract – fewer pathogens means that fewer immune defenses are required, resulting in lower levels of inflammation in the body.

On the most basic level, fiber promotes good elimination. The ideal goal is intake of 40–100 g of total soluble and insoluble fiber throughout the day, with a balance of 80% soluble fiber and 20% insoluble fiber to support healthy digestion. For example, on a diet that provides about 30 g fiber daily, 7–14 g of additional fiber is indicated. Supplementation with 15–30 g from multiple forms of unprocessed fiber is recommended, selecting a source that contains no stimulants, artificial sweeteners, or flavors.

2.5.3.2 Exercise and physical activity

Core body strength is a function of breath and stretch. With the practice of abdominal breathing, stress is reduced and core body strength is enhanced. Twenty minutes a day of gentle stretching complements the breath in maintaining visceral, core connective tissue, and musculoskeletal health. Walking as a source of spontaneous, pleasant irregular movement can be enhanced by the practice of Trager movement education, Feldenkrais technique, Alexander work, or such classic approaches as hatha yoga. In the system preferred by the individual, a gentle appreciation for improved flexibility, resilience, comfort, and tolerance is suggested.

3 Systemic Influences on GI Health

Seventy percent of the body’s immune system lies along the digestive tract (the Peyers patches housed here are also known as Gut Associated Lymphoid Tissue (GALT)). In a healthy person, the food is broken down completely and is never immunogenic. However, malabsorption, takes a toll on the immune system. A poorly functioning digestive system has lost ability to turn food that is consumed into a form the body can use. Poor digestion creates the same predicament as poor nutrition – a lack of nutrients to support immune response and physiologic function.

Today, loss of tolerance and homeostasis accounts for an estimated one third of all chronic disease. Yet, research and clinical experience have shown that healing can be stimulated and repair induced with the protocol described here: identifying and then avoiding offending substances, following an alkalinizing diet, and individualizing supplementation. This concept has been extensively tested in controlled outcome studies on insulin resistance and diabetes, in cases of IBS and chronic fatigue syndrome. Clinical outcome studies suggest that autoimmune conditions respond to this comprehensive clinical approach over 80% of the time through application of lower risk, lower cost, safer, and yet more effective personalized integrative therapies known as The Alkaline Way.

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Relevant Websites

1. http://www.Healthstudiescollegium.org.

2. http://www.ELISAACT.com.

3. http://www.PERQUE.com.

4. http://www.PERQUEWheyGuard.com.

5. http://www.ncbi.nlm.nih.gov/pubmed.

Chapter 3

Antioxidants in Inflammatory Bowel Disease, Ulcerative Colitis, and Crohn Disease

H. Asakura* and T. Kitahora†

*Koukann Clinics, Kawasaki, Kanagawa, Japan

†International University of Health and Welfare, Atami, Shizuoka, Japan

1 The Pathogenesis of Ulcerative Colitis and Crohn Disease

Intestinal mucosa has a single cell layer of epithelial cells that separates the gut lumen harboring the commensal flora and foodborne pathogenic antigens from the body. Normal intestinal mucosa has no hypersensitivity against the commensal flora because of oral tolerance. Gut-associated lymphoid tissue protects the intestinal mucosa from the intestinal