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The current results of this trial indicate that medical therapy as delivered in this trial is superior to PTAS with the Wingspan stent system, which is associated with a high risk of periprocedural stroke or death in this population. Although not all the components of the aggressive medical regimen used in this trial may be easy to duplicate in clinical practice, essential elements can readily be adopted, including adding clopidogrel to aspirin for the first 90 days and following the trial’s protocol with respect to lowering blood pressure and LDL cholesterol in order to achieve target levels that are based on national guidelines. cheap canadian cialis

Supported by a research grant (U01 NS058728) from the National Institute of Neurological Disorders and Stroke (NINDS). In addition, the following institutions received Clinical and Translational Science Awards, funded by the National Institutes of Health, that provided local support for the evaluation of patients in the trial: Medical University of South Carolina (UL1RR029882), University of Florida (UL1RR029889), University of Cincinnati (UL1RR029890), and University of California, San Francisco (UL1RR024131). This research is also supported by the Investigator-Sponsored Study Program of AstraZeneca, which donates rosuvastatin (Crestor) to study patients. Stryker Neurovascular (formerly Boston Scientific Neurovascular) provided study devices and supplemental funding for third-party distribution of devices and continues to provide funding for site monitoring and study auditing, and Nationwide Better Health–INTERVENT provides the lifestyle modification program to the study at a discounted rate. The Regulatory and Clinical Research Institute (Minneapolis) provided assistance in designing the site monitoring processes and performs the site monitoring visits. The Cooperative Studies Program Clinical Research Pharmacy Coordinating Center of the Department of Veterans Affairs (Albuquerque, NM) handles the procurement, labeling, distribution, and inventory management of the study devices and rosuvastatin. Walgreens pharmacies provide study medications, except rosuvastatin, to patients at a discounted price (paid for by the study). The Physician-based Assessment and Counseling for Exercise (PACE) self-assessment forms for physical activity and smoking cessation were provided by the San Diego Center for Health Interventions.

The rate of stroke in the medical-management group was much lower than expected. Patients in the WASID trial with the same entry criteria who were treated with aspirin or warfarin and standard management of risk factors had a 30-day rate of stroke or death of 10.7% and a 1-year rate of the primary end point of 25%. In contrast, the corresponding rates in the medical-management group in this trial were 5.8% and 12.2%. Although we expected the rate of stroke to be reduced with intensive management of risk factors — on the basis of post hoc analyses from the WASID trial that suggested that lowering LDL cholesterol and systolic blood pressure could reduce the risk of stroke — we were surprised at the extent and rapidity of the reduction. It is also possible that the combination of aspirin and clopidogrel played an important role in lowering the early risk of stroke. This is supported by the results of a study of transcranial Doppler ultrasonography involving patients with recently symptomatic intracranial stenosis, which showed that aspirin and clopidogrel, as compared with aspirin alone, reduced the frequency of ipsilateral distal microemboli. The effect of the lifestyle modification program on the outcome can be determined only at the end of the follow-up period, but it is unlikely that it contributed to a reduction in the risk of stroke in the medical-management group within 30 days after enrollment.

The difference between the treatment groups in the rate of the primary end point is driven by the early events, since the rates of the primary end point beyond 30 days are currently similar in the two groups. However, fewer than half the patients have been followed for longer than 1 year. Therefore, continued follow-up of the patients who are currently enrolled will be important to determine the long-term outcome in the two groups. Among patients who are receiving medical management only, progression of stenosis may occur over time that could result in a stroke from a distal embolism or hypoperfusion. Among patients in whom a stent has been placed, restenosis occurs in 25 to 30% within 6 months after intracranial PTAS and could also lead to later stroke.

Patients with symptoms that occurred more than 30 days before enrollment or with stenosis of 50 to 69% of an intracranial artery were excluded from this trial because their risk of stroke while receiving standard medical care is relatively low (approximately 3 to 9% at 1 year8,21), making it unlikely that they would benefit from PTAS. These patients could have an even lower risk of stroke if they received aggressive medical therapy. This trial did not evaluate angioplasty alone or other devices (e.g., balloon-mounted stents) that are used off-label to treat patients with intracranial stenosis. Although these devices may have benefits over the Wingspan system (e.g., single-step delivery and deployment of the stent and less residual stenosis after the procedure), none have been compared with medical management.

We tested the primary hypothesis by comparing the rate of the primary end point between the two treatment groups using a two-sided log-rank test. Data from patients who were lost to follow-up or who withdrew consent were censored at the last contact date. Secondary end points were analyzed with the use of the same techniques. The probability of a primary end point by 30 days after enrollment was compared between the two treatment groups with the use of a z test. All analyses were performed in the intention-to-treat population unless otherwise specified. All reported P values are two-sided and have not been adjusted for multiple testing.

Contrary to what we hypothesized, the results of this trial showed that aggressive medical therapy was superior to PTAS with the use of the Wingspan system in high-risk patients with intracranial stenosis, because the rate of periprocedural stroke after PTAS was higher than expected and the rate of stroke in the medical-management group was lower than estimated. The 30-day rate of stroke or death in the PTAS group (14.7%) is substantially higher than the rates previously reported with the use of the Wingspan stent in the phase I trial and in two registries (rates ranging from 4.4% to 9.6%).10,20,25 The higher rate in the current study does not reflect inexperience of the operators, because most of the interventionists who participated in the registries also participated in this trial, and all the interventionists in this trial were credentialed to participate on the basis of evidence of their experience. In addition, the rates of periprocedural stroke did not decline over the course of the enrollment period and did not differ significantly between high-enrolling sites and low-enrolling sites in this trial.
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One possible explanation for the higher rate of periprocedural stroke in this trial as compared with the registries is that all the patients in this study had stenosis of 70 to 99% and recent symptoms, whereas the registries included patients with stenosis of 50 to 99% and symptoms that had occurred more than 30 days before enrollment. Recent symptoms may be a marker for unstable plaque, which could increase the risk of distal embolism during stenting, as has been reported with extracranial carotid stenting. Another explanation for the higher rate of periprocedural stroke in this trial is that the rigorous protocol for evaluating events (i.e., evaluation of all potential end points by neurologists, the adjudication process, and site-monitoring visits) could have resulted in the detection of some milder strokes that may not have been detected in the registries. However, the percentage of primary end-point strokes in the PTAS group that were disabling or fatal (35%; 16 of 46 patients) is higher than the percentage of primary end-point strokes that were categorized as major in the stenting group (21%) or the endarterectomy group (28%) in a recent randomized trial involving patients with extracranial carotid stenosis.

Patients were evaluated at the time of study entry, at 4 days, and at 30 days and have continued to be evaluated every 4 months; patients undergo assessments until 90 days after a primary end point occurs, the patient dies, 3 years of follow-up have been completed, or the close-out visit for the trial is held, which will occur when the last patient enrolled has been followed for 1 year. At follow-up visits, patients are examined by study neurologists who also manage the patients’ vascular risk factors. If a stroke is suspected during the follow-up period, the patient is examined by the study neurologist, and magnetic resonance imaging (MRI) or computed tomography (CT) of the brain is typically performed. Because the treatment assignment is known to the study neurologist, we require that a second site neurologist, who is not aware of the treatment assignments, evaluate any patient who has had a prolonged TIA (lasting more than 1 hour) or mild ischemic stroke (an increase in the patient’s score on the National Institutes of Health Stroke Scale [NIHSS] of <4 points from the score at study entry), since these events may be difficult to classify. (The NIHSS is a 42-point scale that quantifies neurologic deficits in 11 categories, with higher scores indicating more severe deficits.) The assessments of both neurologists are sent for central adjudication.

All the end points are adjudicated by independent panels of neurologists and cardiologists who are not informed of the treatment assignments. The primary end point is stroke or death within 30 days after enrollment or after a revascularization procedure for the qualifying lesion during the follow-up period (i.e., angioplasty for symptomatic restenosis in a patient in the PTAS group or placement of a stent in a patient in the medical-management group) or ischemic stroke in the territory of the qualifying artery between day 31 and the end of the follow-up period. Ischemic stroke is defined as a new focal neurologic deficit of sudden onset, lasting at least 24 hours, that is not associated with a hemorrhage on CT or MRI of the brain. Ischemic strokes are further classified by the neurologic adjudicators as being either in the territory or out of the territory of the qualifying artery. Symptomatic brain hemorrhage is defined as a parenchymal, subarachnoid, or intraventricular hemorrhage detected on CT or MRI that is associated with a seizure or with new neurologic signs or symptoms lasting at least 24 hours; it is included as a primary end point only if it occurs within 30 days after enrollment or within 30 days after a revascularization procedure for the qualifying lesion during the follow-up period.

Statistical Analysis

The mean length of follow-up was designed to be 2 years. In the Warfarin–Aspirin Symptomatic Intracranial Disease trial (WASID; ClinicalTrials.gov number, NCT00004728),7 the rate of the same primary end point among patients with symptoms within 30 days before enrollment and 70 to 99% stenosis was 29% at 2 years. With adjustment of that rate to account for an estimated 15% relative reduction in risk with aggressive medical management, the projected rate of the primary end point in the medical-management group was 24.7% at 2 years. We estimated that we would need to enroll 382 patients in each group for the study to have 80% power to show a relative reduction of 35% with PTAS in the risk of the primary end point, assuming a 5% crossover rate from the medical-management group to the PTAS group and a 2% loss to follow-up, with the use of a two-sided log-rank test, at a type I error rate of 0.05.

The data and safety monitoring board met every 6 months and reviewed monthly reports to monitor the study’s progress and the accumulated data. Two interim efficacy analyses were planned when approximately 33% and 66% of the required primary end points had occurred. There were no prespecified stopping rules for safety.

Study Patients

Eligible patients had a TIA or nondisabling stroke within 30 days before enrollment, attributed to angiographically verified stenosis of 70 to 99% of the diameter of a major intracranial artery. The other eligibility criteria are provided in the study protocol. All the patients gave written informed consent to participate, and patients who did not undergo diagnostic angiography as part of routine care gave consent for angiography as part of the study protocol.

Treatments

Aggressive Medical Management

The rationale for the medical-management regimen and details on the management of risk factors in the study patients have been published previously.21-23 Medical management is identical in the two groups and consists of aspirin, at a dose of 325 mg per day; clopidogrel, at a dose of 75 mg per day for 90 days after enrollment; management of the primary risk factors (elevated systolic blood pressure and elevated low-density lipoprotein [LDL] cholesterol levels); and management of secondary risk factors (diabetes, elevated non–high-density lipoprotein [non-HDL] cholesterol levels, smoking, excess weight, and insufficient exercise) with the help of a lifestyle modification program. With respect to the primary risk factors, we targeted a systolic blood pressure of less than 140 mm Hg (<130 mm Hg in the case of patients with diabetes) and an LDL cholesterol level of less than 70 mg per deciliter (1.81 mmol per liter). We provide the aspirin, clopidogrel, one drug from each major class of antihypertensive agents, rosuvastatin, and the lifestyle program to the study patients. PTAS Procedure PTAS was performed by neurointerventionists who were selected by a committee of experienced neurointerventionists on the basis of their review of procedure notes and outcomes for the 20 most recent consecutive cases of intracranial stenting or angioplasty (if angioplasty had been performed to treat atherosclerosis) performed by the neurointerventionists under consideration. Further details regarding the credentialing process and the monitoring of the interventionists’ performance of PTAS during the trial have been published previously. Patients who were randomly assigned to PTAS were required to undergo the procedure within 3 business days after randomization. Patients who were not taking clopidogrel at a dose of 75 mg each day for at least 5 days before PTAS were given a 600-mg loading dose of clopidogrel between 6 and 24 hours before PTAS. Details of the procedure, which was performed under general anesthesia with the use of the Gateway PTA Balloon Catheter and Wingspan Stent System (both manufactured by Boston Scientific Corporation), and of the care of the patients after the procedure are provided in the protocol.

Atherosclerotic intracranial arterial stenosis is one of the most common causes of stroke worldwide and is associated with a high risk of recurrent stroke. Patients with a recent transient ischemic attack (TIA) or stroke and severe stenosis (70 to 99% of the diameter of a major intracranial artery) are at particularly high risk for recurrent stroke in the territory of the stenotic artery (approximately 23% at 1 year) despite treatment with aspirin and standard management of vascular risk factors. Therefore, alternative therapies are urgently needed for these patients.

Two strategies have emerged for the treatment of high-risk patients: aggressive medical therapy (combination antiplatelet therapy and intensive management of risk factors) and percutaneous transluminal angioplasty and stenting (PTAS). Over the past decade, intracranial PTAS has increasingly been used in clinical practice in the United States and other countries. Currently, the self-expanding Wingspan stent (Boston Scientific) is the only device approved by the Food and Drug Administration (FDA) for use in patients with atherosclerotic intracranial arterial stenosis; it has been available since 2005 for the treatment of patients with 50 to 99% stenosis who have had a TIA or stroke while receiving antithrombotic therapy.

Because of uncertainty regarding the safety and efficacy of aggressive medical management alone as compared with aggressive medical management plus PTAS with the use of the Wingspan stent system, we began a randomized trial in November 2008 to compare these two treatments in high-risk patients with intracranial arterial stenosis. On April 5, 2011, the trial’s independent data and safety monitoring board recommended that enrollment be stopped because of safety concerns regarding the risk of periprocedural stroke or death in the PTAS group and because futility analyses indicated that there was virtually no chance that a benefit from PTAS would be shown by the end of the follow-up period if enrollment continued. Although follow-up of patients is ongoing, the clinical importance of these findings mandated the reporting of the current results.

Study Design and Oversight
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Details of the trial design have been published previously. This study is an investigator-initiated, randomized, clinical trial funded by the National Institute of Neurological Disorders and Stroke and conducted at 50 sites in the United States. Stryker Neurovascular (formerly Boston Scientific Neurovascular) provided the study devices and supplemental funding for third-party distribution of devices and continues to provide funding for site monitoring and auditing of the study. The Investigator-Sponsored Study Program of AstraZeneca donates rosuvastatin (Crestor) to study patients. Other industry partners are listed at the end of the article. None of the industry partners participated in the design of the trial or in the analysis or reporting of the results.

Primarily, the toxic amines could overwhelm the liver’s detoxification function, in turn decreasing perfusion of the kidneys’ juxtaglomerular apparatus resulting in an increased release of the enzyme renin. Once renin is released, it converts angiotensinogen to angiotensin I that is then converted to angiotensin II by angiotensinconverting enzyme (ACE), found in the lung capillaries, and causes vasoconstriction and eventually increases blood pressure. Thus as kidney perfusion decreases and renin is increased, a rise in BP would follow. When the harmful metabolites are in the bloodstream, the kidneys become the only real route of elimination and detoxification. As the interference of the kidneys’ normal function occurs, such as regulation of fluids and minerals, fluid retention may result. This may also explain why our patient has woken up with swollen ankles and pitting edema on her legs in the past. We hypothesize that the Eubiotic diet provides optimal conditions for the growth of beneficial intestinal flora and at the same time reduces toxic amines produced by bacterial putrefaction of food. The Eubiotic diet may then help to keep the liver, stomach, kidneys and other body systems from becoming overwhelmed. When organ systems work more efficiently, energy and immunity are improved. Blood pressure may thus be reduced by decreased arteriolar resistance (especially renal) and through increased cardiac output. One provocative hypothetical possibility is that ‘essential’ hypertension, of generally unknown cause, may in fact be due in part to dysbiosis and imbalances within the intestinal flora. Although intestinal flora could contribute to PB’s high blood pressure, her family history of renal disease plays an important role as well. It is interesting to note that the Eubiotic diet may also have improved her kidney function. In the past, her urinalysis results often showed hematuria, but her recent urinalysis results were normal. These changes correlated with the changed diet as well as other naturopathic recommendations. Unfortunately her urinary pH was not measured at each visit; otherwise urinary pH may have been a good method of monitoring her progress on the Eubiotic diet since it is believed that the reduction in amine production would correct to a shift in urinary pH.

Conclusion

Given other recommendations for care, the holistic treatment approach used with PB does not allow a perfectly clear picture of exactly what treatment produced what results. This, in addition to the fact that ours is an observational report without comparator or means for replication, imposes some strict limitations with respect to the conclusions that can be drawn. That said, the clinicians in charge of the patient’s care, BK and SL, are confident that the Eubiotic diet was responsible for the improvements exhibited by PB. Although the patient’s hypertension was partially controlled by medications, her blood pressure often exceeded the normal range. We believe that the Eubiotic diet was the core component of our naturopathic treatment, and was most responsible for helping control this patient’s high blood pressure. We also believe that dysbiosis was the root cause of the condition and treated accordingly. This unique case helps elucidate potential connections between systemic dysbiosis, kidney damage, and high blood pressure. The case highlights a generally unrecognized treatment approach for hypertension and emphasizes the need for scientific and clinical exploration. Further research should include an appropriate comparator group and be conducted to explore the benefits of this diet for high blood pressure specifically.

Discussion
The result of most importance with respect to this report is the control achieved in the patient’s blood pressure. The absolute changes in the diastolic and systolic blood pressure numbers are not of great clinical significance. What is most relevant, however, is that the drug previously used to control the blood pressure was dramatically reduced over the course of treatment. This, of course, is of clinical and personal significance to the patient. The goal of the treatment plan was to use the Eubiotic diet to repair her intestinal flora, reduce toxic amines produced by bacterial putrefaction of food, lower her blood pressure, increase immunity, improve energy levels and enhance overall health. We hypothesize that her high blood pressure was partially caused by dysbiosis. Based on the data and outcomes realized, we hypothesize that the Eubiotic diet not only improved the patient’s overall health, but lowered her blood pressure as well. According to clinical studies, diets high in protein and sulfates (primarily derived from food additives) have been shown to play a role in the production of potentially toxic products in the gut. The production and absorption of toxic metabolites, referred to as bowel toxemia,21 may have contributed to the patient’s pathology. The patient’s previous diet was high in animal protein, animal fat, simple carbohydrates, sugar, and low in insoluble fiber. The patient’s typical diet may have resulted in bowel toxemia and the production of irritant toxic amines. As a result, chronic exposure to these metabolites may have made her digestive system hypersensitive and caused it to react to antigens it normally would not react to, such as carbohydrates, animal proteins, sweets, fruits, juices, and even spices. In the case of dysbiosis, vasoactive and neurotoxic amines, such as histamine, octopamine, tryptamine, and many others are produced by bacterial putrefaction of food, or more specifically by bacterial decarboxylation of amino acids. These toxic amines are absorbed through the portal circulation and deaminated in the liver. The symptoms of hypochondriac pain, stomach irritation, food intolerance, bitter taste, and intestinal activity are believed to be closely associated with the patient’s dysbiosis and ‘bowel toxemia’.

Regarding the cause of hypertension, it is believed that the production of potentially harmful bacterial metabolites could be an important etiologic agent. The accumulation of ammonia, amines, phenols, sulfide, and indoles could lead to a reduction in metabolic efficiency and an increased production of reactive metabolites, such as increased production of histamine, octopamine, or tryptamine. It is hypothesized that this harmful accumulation could lead to hypertension through the following process.

Case Description
PB is a 69-year-old Caribbean female who presented with hypertension, post-nasal drip, sinus congestion, a bitter taste in her mouth, hypochondriac pain, dry throat and mouth, and increased thirst. PB’s past medical history includes chronic stomach pain, gastritis, hematuria, gingivitis, atherosclerosis, and prior appendectomy and cholecystectomy. Her hypertension was controlled with enalapril (5mg bid) and aspirin (81mg qd). Table 1 details the medication and supplements the patient was taking at the time of her first visit. Recent medical history included dysbiotic syndrome, such as sinus congestion, bitter taste in the mouth, hypochondriac pain, gassy and bloated feeling, hypertension, and atherosclerosis. Naturopathic treatment commenced with the addition of the Eubiotic diet, nutritional supplementation, nebulized glutathione, exercise, constitutional hydrotherapy, homeopathic treatment, and lifestyle counselling. The Eubiotic diet in combination with nutritional supplementation was designed to improve the gastrointestinal flora, whereas the exercise, hydrotherapy, nebulized glutathione, and lifestyle counselling were initiated to improve the overall health and well-being of the patient. The patient began the Eubiotic diet on Aug 31 2006. She continued to experience her negative dysbiotic symptoms mentioned above after four weeks, and a constitutional homeopathic remedy, Dioscorea villosa 200C (one dose, 3 pellets), was prescribed to address the symptoms of hypochondriac pain, bitter taste in the mouth, and ear-nosethroat problems. The remedy was taken on day 29 of the diet (Sept 28 ‘06) and a week later the patient reported resolution of her hypochondriac pain. By day 36, Oct 5 ‘06, PB had regained some of her energy and was carrying out daily living activities without difficulty (determined by using energy scales during the regular visits). It was noted that her blood pressure (BP) was lower by a 10 point drop in systolic pressure and an 18 point drop in diastolic pressure when compared to Aug 4 ’06, even though her medication use had not changed.

The patient began to report frequent dizziness at the same time, especially when her BP fell below 120/60mmHg. The patient was referred to her family doctor to discuss the possibility of adjusting the dosage of enalapril. Data for these outcomes is not included as there was no significant change over time in any of these endpoints. Based on the linear regression lines in Figures 2 and 3, the patient’s average BP over the past 217 days was about 121/69mmHg. If we are to assume that the regression line provides an effective measure of change over time, then based on this assumption the patient’s starting BP is calculated to be 124/70mmHg and her final BP 118/68mmHg. This change corresponds to a 6 point drop in systolic BP and nearly a 2 point drop in diastolic BP. These changes are further magnified if we assume that the initial blood pressure value of 134/83mmHg is a more accurate reflection of the patient’s hypertensive status to begin with. Although there is a trend towards decrease being witnessed, no test for statistical significance was conducted on the changes observed. On day 106 (Dec 14 ‘06), PB decreased her blood pressure medication from 10mg of enalapril daily to 7.5mg. She continued to feel dizzy and weak upon waking and on her own volition decided to stop taking daily aspirin (81mg). PB began to take greater responsibility for her own health and would titrate her medication based on self-monitoring her blood pressure three times per day. From January until April 2007, she had not taken any aspirin, but would occasionally take hawthorn (as needed) or enalapril (averaging 2.5mg/ wk). Her decision to take enalapril or hawthorn depended mostly on her level of anxiety. At this point, her current working diagnoses continued to be dysbiosis, controlled hypertension, and atherosclerosis.

Based on available research and clinical data, it is believed there are four common causes of intestinal dysbiosis: putrefaction, fermentation, deficiency, and sensitization.

1) Putrefaction dysbiosis is the result of diets high in fat and animal flesh and with a low intake of insoluble fiber. It often occurs when one consumes animal proteins without enough chewing, or with achlorhydria. When animal proteins are not decomposed, fermentation occurs and amines may be produced, resulting in putrid odor.

2) Fermentation dysbiosis results from inefficient host digestion of dietary starch or sugar leading to an accumulation of short-chain fatty acids (i.e. acetate, propionate, butyrate and valerate),9 lactic acids, and ethanol. This form of dysbiosis usually causes carbohydrate intolerance and fatigue due to an overgrowth of bacteria or fungi in the stomach, small intestine and the ascending colon.

3) Deficiency dysbiosis is often caused by antibiotic exposure or a low soluble-fiber diet, which leads to a deficiency of normal intestinal flora.

4) Sensitization dysbiosis is the result of abnormal immune responses caused by an alteration of the normal intestinal flora.

With the four types of dysbiosis in mind, we describe the following diet that has been called the Eubiotic diet. Eu- is a prefix meaning “good”, —biotic is a suffix meaning “life”,10 Thus, Eubiotic = ‘good life’. The purpose of the Eubiotic diet is to achieve an ideal terrain in the GI that will limit the overgrowth of pathogenic microbes and optimize conditions for the beneficial bacteria. Following the Eubiotic diet is intended to minimize the occurrence of putrefaction, fermentation, deficiency, and sensitization. Although many clinical studies have associated intestinal dysbiosis with inflammatory bowel disease, irritable bowel syndrome, eczema, asthma, arthritis, and ankylosing spondylitis, no studies have investigated its possible relationship to hypertension.

The Eubiotic diet is a specific dietary program initiated to achieve microfloral balance through an increase of insoluble fiber and a decrease of saturated fat, animal flesh, starchy vegetables, and sugar consumption. Following this kind of diet has been shown to lead to a lowering of GI Bacteroides levels and a concomitant increase in the levels of lactic acidproducing bacteria like Bifidobacteria, Lactobacillus, and beneficial lactic acid Streptococcus. In addition, fruits and starchy vegetables are not recommended due to their high sugar content. The basic premise behind the diet is to stop feeding harmful bacteria and instead feed the beneficial intestinal flora.

This report describes how following a specific diet, the Eubiotic diet, was associated with a clinically significant reduction in blood pressure. We hypothesize that this benefit is a result of adherence to the Eubiotic diet and a concomitant improvement in the patient’s gastrointestinal flora and associated dysbiosis.

A 69-year-old female patient presented with chief concerns of hypertension, hypercholesterolemia, low immunity, and osteoarthritis in June 2006. It was hypothesized that the patient was suffering from dysbiosis based on her presenting symptoms and past medical history. The patient was treated with dietary interventions — specifically, the Eubiotic diet — in order to repair her gut tissues and function, and restore beneficial intestinal flora. After approximately six months on the diet, her symptoms of dysbiosis such as sinus congestion, bitter taste in the mouth, hypochondriac pain, and feeling gassy and bloated, all disappeared and her blood pressure stabilized, resulting in a dramatic reduction in prescription blood pressure medication use. The following report discusses how a naturopathic approach employing the Eubiotic diet is hypothesized to be the major intervention responsible for improving the patient’s hypertension. In this report, the potential physiological mechanisms and rationale are discussed with respect to this novel approach of care with an emphasis given to issues of gastrointestinal health and terrain.

The term “dysbiosis” was first introduced by Dr. Elie Metchnikoff, a Russian scientist, to describe altered pathogenic bacteria in the gut. Intestinal flora consists of the microorganisms normally living in the digestive tract, which serve many necessary functions, such as providing energy, synthesis of vitamins (B group and K), enhancement of gastrointestinal (GI) tract motility and function, stimulation of the immune system, digestion and absorption of food, metabolism of plant compounds and drugs, production of short-chain fatty acids and polyamines, and inhibition of growth of exogenous and harmful bacteria within the host. The GI tract contains approximately 100 trillion viable bacteria. About 99% of the bacteria come from 30 to 40 species. Concentrated in the mucosa are 60-90% of all measured immune parameters, such as mast cells, dendritic cells and macrophages. When the host is healthy and the intestinal microbial population is in a state of balance there is a symbiotic relationship established between the intestinal flora and the host to optimize intestinal and immune function. However, when there is an overgrowth of harmful pathogens, such as Clostridium perfringens and E. coli in the intestines, and decreased concentrations of Bifidobacteria species, ratios activities of the bowel flora can be altered, resulting in dysbiosis. This is often the result of poor diet and lifestyle, antibiotic use, psychological, physical, environmental and emotional stressors, radiation, change in GI peristalsis, surgical trauma, hypochlorhydria, and decreased mucosal immunity. It is believed that the growth of these harmful bacteria in the intestine can produce harmful substances that may play a role in chronic diseases, such as hypertension in this case.