Total Cholesterol

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    Historically, total cholesterol concentration was used to assess an individual’s risk of CAD (Bowden & Kingery, 2004). Because cholesterol contributes to the buildup of atherosclerotic plaques, an individual’s blood cholesterol concentration could be a way to measure risk for heart disease. Clinical studies are consistent in supporting the projection that for serum cholesterol levels in the 250-300 mg/dl range, each 1% reduction in serum cholesterol level reduces CAD rates by approximately 2% (NIH, 1989a). However, the degree of stenosis and CAD varies between individuals with the same total cholesterol and other lipid levels (Bowden, Kingery, Rust, 2004, Kmietowicz, 1998; Telenko & Sumner, 2002).

    Total cholesterol tends to reflect average dietary habits that affect LDL, and can reasonably provide an assessment of CVD risk between participants. Yet, the differences in risk between individuals can be strongly influenced by many additional factors. Therefore the measurement of total cholesterol alone cannot adequately reflect individual risk of CAD (NIH, 2002) and should rarely be used as the sole lipid measure in cholesterol screenings. Other studies have also demonstrated the process of heart disease to consist of many factors that are independent of total cholesterol (Katerndahl & Lawler, 1999). These other risk factors fall into two three broad categories, consisting of blood markers, behavior, and biology. New blood tests that identify increased cardiovascular risk include various subfractions of cholesterol. Many of these new markers relate to the physiological functions of cholesterol and the interaction between these markers and the cholesterol in the periphery.

    The generally accepted ranges for total cholesterol levels (NIH, 2002) consist of desirable (<200mg/dL), borderline high (200-239mg/dL), and high (≥240mg/dL). If a patient’s cholesterol level is in the high category, a LDL cholesterol measure should be performed. If the patient is in the borderline high range, another total cholesterol measurement should be taken within eight weeks and the average of the two readings used to guide future decisions (NIH, 2002).

    Cholesterol Subfractions
    LDL cholesterol accounts for 60-75% of the total serum cholesterol and is the terminal end of in the pathway of lipoprotein metabolism called cholesterol transport. Numerous epidemio-logical, physiological, and animal models have linked high LDL levels to CAD (American Heart Association, 2004; Assman, Cullen & Schulte, 1998; NIH, 1989a; Smith et al., 2004; Stone, 2005). High levels of LDL cholesterol are able to penetrate the porous endothelium of arteries and begin to accumulate if plasma concentrations are abnormal. This natural plaque is eventually converted to unstable plaque increasing the likelihood of rupture and possible thrombosis (NIH, 2002). Accordingly, the greatest absolute diminution of risk can be achieved by the reduction of LDL which may directly lower platelet aggregation, vascular reactivity, and lower cytokine release leading to a further reduction in risk for myocardial infarction (Sullivan, 2002). In fact, when elevated LDL levels are combined with comorbidity factors of smoking and hypertension, this complex explains over 90% of myocardial infarction cases occurring in middle age (Wilhelmsen, 1997). The landmark INTERHEART data suggests that 90% of risk comes from combination of abnormal levels of apolipoproteins found in LDL and smoking. LDL contains ApoB-100 which has been linked to atherogenesis (Yusef, Hawken, Ounpuu, Dans, Avesum, Lanas et al., 2004).

    Finally, it should be noted that although LDL lowering therapy is believe to offer the greatest benefit for CAD risk reduction, LDL alone is insufficient to predict CAD incidence and risk stratification. The best risk prediction strategy requires measurement of other cholesterol components and particle size and concentration (Wald, Law, Watt, Wu et al., 1994).

    According to the American Heart Association [AHA] (2002), more Americans die from CAD every year than the next five leading causes of death combined. One in every 2.5 deaths in the year 2000 was from heart disease (Kohlman-Trigoboff, 2005). Though there has been a decrease in mortality rate in the US, CAD has become a leading cause of global mortality, accounting for almost 17 million deaths annually with nearly 80% of mortality and disease burden occurring in developing countries (Smith, Jackson, Pearson, Fuster, Yusuf, & Faergeman, et al., 2004).

    The etiology of CAD is multi-factorial, involving numerous factors including genetics, diet, and environment with several risk factors significantly increasing an individual’s susceptibility to the disease. These risk factors include cigarette smoking, obesity, sedentary lifestyle, dietary habits, homocysteine, high blood pressure, high blood cholesterol and others. However, much of the research into CAD, which has being quite extensive and spanning a number of decades, has focused on the general relationship between plasma lipids and CAD (Gotto, 1997; Kannel, Castelli, Gordon, & McNamara, 1971; McGee, Reed, Stemmerman, Rhoads, Yano, & Feinlab, 1985; NCEP, 2002; NIH, 1989a;). Researchers have suggested that approximately twenty-five percent of the adult population ages twenty and older has blood cholesterol levels that are considered high (National Institutes of Health [NIH], 1989b). In addition, researchers have demonstrated that a total cholesterol level in the “high” category (>200 mg/dL) accompanied with high blood pressure (>130/85) increases an individual’s risk of coronary heart disease by a factor of six (NIH, 1989b). Therefore, establishing specific guidelines for cholesterol levels is both important and necessary to enhance the health of individuals.

    Lipoprotein metabolism is a process that is not completely understood with fragmentary findings (Tulenka & Sumner, 2002). Attempting to have a clearer understanding of the relationship between cholesterol levels and CAD, individuals who have abnormal lipid levels can make the lifestyle changes necessary to reduce the risk of CAD and its associated complications. Similarly, adequately informed health professionals are better able to educate the public about cholesterol and heart disease and more equipped to implement effective health intervention programs.

    Understanding the pathophysiology of CAD in population studies underlie the vital role of cholesterol metabolism. Protective mechanisms of the endothelium are evident in reverse cholesterol transport performed by high-density lipoprotein (HDL) and conversely low-density lipoprotein (LDL), specifically small, dense LDL, may penetrate the subendothelial space if concentrations are high in the plasma. Penetration of the endothelial space can cause acute and chronic endothelial damage, leading to CAD. Because movement into the arterial wall is likely driven by diffusion, hyper-cholesterolemia increases the infiltration of cholesterol into the endothelial space (Bowden, 2001; Wada & Karino, 1999). In response to this accumulation of cholesterol, macrophages respond to inflammatory markers from inflammatory cells, cytokines, growth factors and cellular responses (Sullivan, 2002) and absorb the cholesterol resulting in the formation of foam cells. Formations of foam cells are critical in the development of plaque in the endothelium (Ockene & Ockene, 1992). As the CAD progresses, lesions may begin to cause chronic injury to the endothelium. This process results in a positive-feedback cycle due to cytokine release that sends even more macrophages to the area, resulting in more foam cells, and eventually results in stenosis and occlusion of blood flow. Fatty streaks are first evident in this disease process followed by fibrous plaques that can develop necrotic cores which develop fissures leading to plague rupture. Hyperlipidemic concentrations also increase platelet aggregability, which attenuate the severity of the thrombotic process (Sullivan, 2002). Therefore, cholesterol metabolism plays a significant role in the development of plaque, stenosis, and eventually, myocardial infarction.

    As research continues in the field of coronary artery disease, more information is revealed about various etiological factors. Emerging lipoprotein risk factors have been identified and are now starting to surface as instrumental in the cause and prevention of coronary artery disease. In order to conduct comprehensive cholesterol screening programs and counseling sessions a health professional must have a thorough understanding of lipid metabolism. Recent changes in cholesterol guidelines make it necessary to have a review that addresses the specifics of lipid management. A health professional needs an appropriate knowledge base to be able to understand a major coronary artery disease risk factor and thereby more effectively educate the public about lipid management and coronary artery disease risk reduction. Therefore, the purpose of this article is to review the role of cholesterol in both normal physiological functioning and disease causation and to examine the research concerning new emerging cholesterol risk factors.
    Cholesterol Screening and the Health Professional
    Recommendations by the National Cholesterol Education Program (NCEP) suggest that all Americans over the age of twenty should have their cholesterol concentrations measured (National Heart, Lung, and Blood Institute [NHLBI], 2003). An estimated 70.8% of the US population twenty years and older had participated in cholesterol screening at least once by the year 2000. This is a substantial increase from the mid-1980s when 35% had been screened at least once (Brown, Giles, Greenlund, & Croft, 2001). A number of health education programs have an emphasis on cholesterol screening followed by counseling with a health professional. Through these screenings health professionals can have a significant impact on cardiovascular disease outcomes by being involved in primary and secondary prevention, raising awareness, and successfully referring participants to physicians for further testing (Bowden, Kingery, & Brizzolara, 1999; Muratova, Islam, Demerath, Minor, & Neal 2001). In order to conduct comprehensive cholesterol screening programs and counseling sessions, health professionals must have a thorough understanding of coronary artery disease (CAD) risk factors which includes lipid metabolism (Ostwald, Weiss-Farnan, & Monson, 1990). Since the most important aspect of cholesterol screening is the action the participants take after receiving their screening results (Garber & Browner, 1997), having accurate and up-to-date information on the role of cholesterol in CAD enables health professionals to effectively develop and implement prevention programs, educate the public, and make referrals (Sullivan, 2002). Recent changes in cholesterol guidelines make it necessary to have a review that addresses the specifics of lipid management and CAD prevention. Therefore, the purpose of this paper is to review the role of cholesterol in both normal physiological functioning and disease causation and to examine the latest research concerning the new emerging cholesterol risk factors of CAD.

    Immune system development in infants is closely tied to gastrointestinal maturation. The immunological factors found in breast milk are key instigators in the maturation of the gastrointestinal tract, as well as the gut-associated and systemic immune systems. Microflora such as Bifidobacterium have been identified in studies of infant fecal composition in association with maternal breast milk composition. Maternal breast milk Bifidobacterial counts dramatically impacted the infants’ fecal Bifidobacterium levels, demonstrating that breast milk is a powerful modifier of infantile gastrointestinal microflora and thus immune status. Breast milk–fed infants showed high levels of fecal calprotectin, indicating a low level of gastrointestinal inflammation. The excessive inflammation seen in NEC is less severe with a lower incidence when infants are given their mothers breast milk, in part due to the influence breast milk has on the intestinal flora. Recent research shows that the mucosal microflora acquired in early infancy determines the production of mucosal inflammation and the consequent development of mucosal disease, autoimmunity, and allergic disorders later in life. The non-absorbed milk oligosaccharides found in breast milk block attachment of microbes to the infant’s gastrointestinal mucosal membranes, thus preventing infections.Although oligosaccharides are major components of breast milk, the milk is also rich in other glycans, including glycoproteins, mucins, glycosaminoglycans, and glycolipids. Glycans protect the infant primarily by inhibiting pathogens’ binding to their host cell’s target ligands. At the same time, human milk oligosaccharides strongly attenuate inflammatory processes in the intestinal mucosa. Undigested glycans stimulate colonization by probiotic organisms through a prebiotic effect, modulating mucosal immunity and protecting against pathogens. Interactions between breast milk glycans, intestinal microflora, and intestinal mucosal surface glycans assist in the development of the innate mucosal immunity, protecting infants from infection and autoimmune inflammatory bowel diseases.

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    There is a need for more extensive research into the development of the immune system in infants so that we have a more complete understanding of how to target and prevent immune disorders. Our current understanding points to 4 main areas in the ontogeny of the infant’s immune system as potential early intervention points for the prevention of immune disorders. First, nutritional support that aids in the prevention of immune disorders must be provided for infants. Second, the infant requires Th1 support so that he has protection from infections and the inflammatory damage they can incite. Third, immune tolerance and anti-inflammatory measures must be encouraged so inflammatory reactions and the corresponding immune disorders can be prevented. Fourth, the gastrointestinal health of the infant plays such a foundational role in immune status that it must be supported as well. The research demonstrates how breast milk targets all 4 of these areas and has the potential to be a powerful tool in the prevention of immune disorders. More research is necessary to confirm breast milk as a preventative treatment for asthma, allergies, and autoimmune disorders, but the current evidence is promising.

    Breast milk provides optimal nutrition to the developing infant, and that has prompted both the American Academy of Pediatrics and the World Health Organization to increase the recommendation for exclusive breastfeeding to age 6 months. As a part of the diet, the AAP recommends breast milk for at least 1 year, while the WHO advises continuing for 2 years or more. Breast milk provides nutrition with polyunsaturated fatty acids that have also been shown to help prevent allergies. In susceptible infants, the development of allergic symptoms was modified by the intake of n-3 long-chain polyunsaturated fatty acids through breast milk. Another study demonstrated the substantial reduction in risk of childhood asthma as assessed at age 6 years, if exclusive breastfeeding is continued for at least the first 4 months of life. Breast milk protects against the infant’s susceptibility to infections as well as against future development of allergic diseases, in part due to its fatty acid content. Breast milk not only provides nutrition that helps to balance immunity in infants, it also directly impacts the development of the Th1 response.
    Evidence points toward the importance of breast milk in the maturation of the infant’s immune system, helping with immature Th1 function. During the education of the immune system in infancy, maternal milk provides signals to the immune system that generate appropriate response and memory. Although infants’ Th1 response is somewhat inefficient, breast milk compensates for this relative inefficiency by providing considerable amounts of secretory IgA antibodies and lactoferrin. These secretory IgA antibodies bind the microbes at the infant’s mucosal membranes, preventing activation of the pro-inflammatory defenses while lactoferrin both destroys microbes and reduces inflammatory responses. Breast milk also contains various cytokines, including IL-1, IL-6, IL-12, TNF-alpha, IFN-gamma, and IL-8, that help defend against gastrointestinal and respiratory infections. A recent study found high levels of immune-related miRNAs that were stable under acidic environments in breast milk for the first 6 months of lactation. The dietary intake of miRNAs by infants can have a profound impact on the development of the infant’s immune system. Breast milk clearly imparts important factors for the proper maturation of the infant’s immune system.
    Breast milk also provides a significant amount of Th3 tolerance factors and anti-inflammatory compounds that help regulate immune responses and inflammation. Breast milk is rich in TGF-beta, IL-10, erythropoietin, and lactoferrin, which can help reduce the excessive inflammatory response to stimuli in the infant’s intestine. In research conducted with mice, the presence of TGF-beta and an allergen conveyed protection from allergic asthma. Some studies suggest that breast milk may even protect against type 1 diabetes, multiple sclerosis, and rheumatoid arthritis.

    We must first look at the immune system of an infant and the necessity of its proper development in the prevention of immune disorders. The infant’s immune system differs from that of an adult. During gestation, the immune system of the fetus is actively down-regulated to avoid immunological reactions that would end in termination of the pregnancy. This adaptation is demonstrated by high levels of Treg cells, by the down-regulation of antigen-specific T-cell proliferation, and by removal of activated T cells via FasL-induced apoptosis. The immune system remains in this state through birth and doesn’t fully develop until several years after birth.17,18 Th1 cytokines, such as interleukin-2 (IL-2), interferon-g (IFN-gamma) and Th2 cytokines, mainly interleukin-4 (IL-4), are seen at different levels in infants versus adults. Infants have more IL-2 and IL-4, with less IFN-gamma than seen in adults, giving them a predominately Th2-driven immune system.19 Infants have less Th1 memory effector function compared to adults.20 Even though infants produce ample amounts of IL-2, it does not induce the increase in IFN-gamma necessary to incite a Th1 response.21 When looking at the immunological cytokine response in infants, we see the production of Th1 cytokines tumor necrosis factoralpha (TNF-alpha), IFN-gamma, IL-12, and IL-1 are downregulated, whereas the cytokines IL-6, IL-8, IL-10, and IL-23 that are associated with inflammation and autoimmunity are up-regulated.
    All of these contribute to a down-regulation of the Th1 immune response in infants. The immune response of tolerance, which modulates rampant Th1 or Th2 reactions, is vital to the immune development and health of the infant. A study that examined children with no clinical or pathological diagnosis, children with multiple food allergies, children with celiac disease, and children with inflammatory enteropathies showed that the deciding factor in the allergic group was the reduction of a Th3 response with a corresponding reduction in TGF-beta.23 The celiac and inflammatory enteropathies groups showed a dominance of the Th1 response, typical of inflammatory autoimmune diseases in which the control of the Th3 Treg cells is a necessity.
    The production of IL-10, a cytokine released by Treg cells, was lower in infants of atopic mothers compared with non-atopic mothers. Oral TGF-beta has demonstrated a preventive role for allergic diseases in infants, again highlighting the importance of immune tolerance in the prevention of immune disorders. Research into the etiology of necrotizing enterocolitis (NEC) has found another difference in the immunological state of adults and infants. The immature enterocytes that line the infant’s intestine react with an excessive pro-inflammatory cytokine production after inflammatory stimulation. This reaction leaves infants vulnerable to the influence of excessive inflammation. Another difference in the infants’ mucosa is the variety of glycoproteins as compared to adults. Lining the gastrointestinal and respiratory tracts are glycoproteins, such as mucins, which cover the entire epithelial layer with protective mucus. These glycoproteins play an important role in inflammatory and antigen control in these mucosal tracts. The composition and glycosylation of the mucus layer differs significantly between infants and adults. An infant’s gastrointestinal tract not only has low levels of mucus, but it also has increased permeability and low levels of secretory immunoglobulin A.Although much is known, more studies are needed to complete our understanding of the immunological workings of infants. Research highlights the infant’s need for Th1 support to protect against infection and the damage that can ensue, a refined and effective Th3 response that can control rampant immune responses, and a healthy mucosal lining to ensure proper immune development and potentially prevent allergy, asthma, and autoimmune disorders.

    Allergies, asthma, and autoimmunity are the most prevalent immune disorders and affect millions
    of people worldwide.
    The role of prevention of these immune disorders at the level of infancy and early childhood has become an important emphasis of recent research.
    The proper development of the growing infant’s immune system provides a promising avenue into prevention of these disorders. Breast milk has long been acknowledged as the optimal source of nutrition for infants, and emerging research points to its profound effect on the immune development of infants.
    Immune disorders like asthma, allergies, and autoimmunity have become predominant issues in both pediatric and adult healthcare. An estimated 300 million people worldwide suffer from asthma, with 250,000 annual deaths attributed to the disease.Allergic diseases affect as many as 40 to 50 million Americans.Autoimmune diseases include more than 70 different disorders and affect approximately 5 percent of the U.S. population, or an estimated 23.5 million Americans.3 Early intervention as a means of preventing immune disorders later in life has become the subject of abundant research in recent years. Special attention must be paid to the infant’s developing immune system in order for this type of prevention to be a success. The infant is born with an immature immune system that doesn’t fully develop until several years after birth.
    Mounting evidence shows that breast milk is not only an excellent source of nutrition, but it also has a profound influence on the development of the immune system and thus, the pathogenesis of asthma, allergies, and autoimmunity. This paper will focus on immune development in infants and the use of breast milk as a potential prevention of immune disorders. We will briefly review the workings of a healthy, mature immune system before discussing the developing immune system of an infant and how breast milk best promotes its proper development. Although our knowledge of the system is always advancing, the immune system in healthy adults has several distinct arms: Th0, Th1, Th2, Th3, and Th17. The T helper cells 0 (Th0) refer to mature T cells that have yet to encounter an antigen. When these naпve Th0 cells encounter an antigen, they differentiate into Th1 or Th2 cells depending on the cytokine environment. The T helper cells 1 (Th1) are recruited in response to infection and are the predominant cells used against bacterial and viral infections. T helper cells 2 (Th2) are responsible for allergic responses and responses to parasites.
    Cytokines are secreted proteins that stimulate most of the biological effects in the immune system, such as the cell-mediated immunity seen in infections, predominately driven by Th1, and allergictype responses, predominately driven by Th2. These cytokines inhibit the opposing immune reaction, so a robust Th1 response to an infection inhibits a Th2 response and vice versa. Immune tolerance is characterized by a Th3 response, which involves T regulatory cells (Treg cells) and the cytokine, transforming growth factor-beta (TGF-beta). Treg cells play a major part in the regulation of immune responses, sustaining immunological self-tolerance and immune homeostasis.6 They also play a crucial role in the control of auto-reactive T-cells, making them a necessary combatant against autoimmune reactions. A Th17 immune response is associated with autoimmune conditions and the cytokine secretion of various interleukins: IL-17, IL-12 and IL-23 IL-17 is produced by Th17, which comes from a different lineage than Th1 and Th2 cells but can also stimulate the secretion of TNF-alpha and IL-1.Th17 and Treg cells have taken center stage in the discussion of autoimmune conditions.
    A new category of cells named Th22 was recently discovered. Th22 enables innate epithelial immune responses.Allergies, asthma, and autoimmune conditions are associated with unresolved inflammation that contributes to the pathogenesis of these conditions. The immune system contains this system of checks and balances with responses like Th3 so that the immune system stays plastic without ever becoming stuck in one particular immune response.

    Patients who forgo medications for both diabetes and chronic pain appear to be influenced primarily by economic pressures, whereas patients who cut back selectively on their diabetes treatments are influenced by their mood and medication beliefs. Our findings point toward more targeted strategies to assist diabetic patients who experience CRN.

    Prescription drug spending in 2007 was >750 USD per capita in the U.S., of which patients must pay a growing share through medication copayments. Nine of 10 older adults use prescription medications, and those with Medicare Part D take five prescriptions per month on average. Even among low-income patients, most take their medications despite copayments; however, one-fifth or more of all patients may cut back because of cost concerns. Cost-related nonadherence to medications (CRN) has been associated with increased rates of serious adverse events, emergency department visits, hospitalizations, and poorer health.

    Empirical studies have implicated financial, attitudinal, mood, and provider influences in CRN, although their relative effects are not well understood. Most of the variance in patients’ reports of CRN remains unexplained by financial measures. Although economic pressures drive these decisions, noncost factors appear to modify the effect of medication cost at a given level of ability to pay.

    Most survey-based studies of CRN have used a single global question to ascertain adherence and, therefore, could not discern whether patients cut back uniformly across their medications or selectively. Studies using administrative data indicate that patients vary in their adherence across medications, but these studies could not explore fully the influences of factors such as patients’ mood and medication-related beliefs.

    Building on our theoretical model of factors that influence patients’ elasticity of demand for prescription drugs, in the present study we explored further how cost and noncost factors influence patients’ adherence to prescription medications for two chronic conditions: type 2 diabetes and chronic pain. We hypothesized that although some patients would cut back on medications for both conditions, others would cut back selectively, and sought to understand the factors associated with these behaviors.

    These analyses are important for clinical care because most efforts to address CRN have targeted patients’ ability to pay exclusively, for example, through government assistance (e.g., Medicare Part D), pharmaceutical industry programs, and prescribing of less expensive therapeutic alternatives. Physicians are now called upon to incorporate discussions of medication cost pressures into their routine patient interactions. Because insufficient time may be the greatest barrier to such provider-initiated discussions, it is essential that we distinguish patients for whom ability to pay, as opposed to other factors, constitutes the dominant challenge to adherence.

    Helfgott employs experienced faculty in the fields of nutrition, psychology, immunology, whole systems research, and acupuncture, among other natural medicine research faculty, to carry out natural medicine clinical trials. Further, Helfgott faculty work with conventional biomedical researchers, using groundbreaking technology to study ancient traditions. A donation from Don Helfgott has helped fund the state-of-the-art basic science laboratory, as well as the resources to carry out clinical research.
    Dedicated to the advancement of natural medicine, Helfgott was founded with the goals of training students and faculty interested in conducting research, collaborating with other research institutes and organizations, and conducting research specifically on naturopathic and Chinese medicine. At Helfgott, scientists from the fields of naturopathic medicine, Chinese medicine, acupuncture, immunology, and nutrition work together to apply their expertise to the study of natural medicine. “Our philosophy is that every study is a collaboration,” notes Zwickey, emphasizing the importance of collaborative research at Helfgott. Studies at Helfgott almost always involve external organizations, which “not only strengthens the study, but those relationships are what ultimately get natural medicine accepted in some of these more mainstream places.” Current faculty research projects at Helfgott include grants directly funded by the National Institutes of Health’s National Center for Complementary and Alternative Medicine.
    In addition, Helfgott participates in several collaborative grants with Oregon Health & Sciences University as well as with other Western biomedical and naturopathic schools. In addition to working with external health organizations nationwide, Helfgott is largely involved in the local community as well. “One of the things that we’ve been doing is being the conduit for people in Portland to learn about who’s in their community and what type of research they’re doing,” says Zwickey. Helfgott is active not only at the local level, but at national and international levels as well.
    “We envision Helfgott as the premier natural medicine research institute. Our vision includes a consortium of researchers from naturopathic medicine, Chinese medicine, Ayurvedic medicine, physical medicine, energy medicine, and other natural medicine disciplines. We envision an institute based on health rather than disease. We see a think tank that develops new innovative approaches to healthcare, and clinical floors where these approaches can be piloted. We see the development of research moving away from treating symptoms, and moving toward promoting health.” —From Helfgott Research Institute’s vision

    Chronic diseases like heart disease, stroke, cancer,respiratory disease, and diabetes are the leading cause of mortality in the world, causing 60% of all deaths, according to the World Health Organization. Of the 35 million people who died worldwide from chronic disease in 2005, half were under age 70. These numbers emphasize the intense need for research related to chronic disease. In America, chronic disease is replacing infectious disease as the primary health concern, further highlighting the need for research related to its complex nature. At the Helfgott Research Institute in Portland, Ore., healing chronic disease is one of the manygoals of researchers. Established in 2003 at the National College of Natural Medicine (NCNM), Helfgott is a professionally independent, nonprofit research institute whose mission is to conduct rigorous, high-quality research on the art and science of healing, specifically working to understand natural forms of medicine. Although chronic illness can sometimes be effectively treated by pharmaceutical medicine alone, it often requires a more comprehensive approach due to its complex nature.

    Lifestyle, nutrition, and behavioral changes all affect chronic disease, so Helfgott employs traditional approaches combined with natural medicine such as herbs, homeopathy, hydrotherapy, and acupuncture in order to prevention and treatment. One of the unique aspects of Helfgott’s research is the way clinical trials are conducted. “We are committed to studying natural medicine the way that it’s practiced,” says Heather Zwickey, PhD, director of research at Helfgott and dean of research at NCNM. “When a naturopath sees a patient, they don’t ever give just one thing. They always address the diet, and the lifestyle, and may provide some herbs, and maybe a homeopathic; it’s never one thing. If that’s what naturopaths are doing in practice, then that’s what we ought to be studying.” Instead of studying medicines individually or in a manner that would reduce an herb to its constituent components, Helfgott researchers look at a combination of herbs being administered. Zwickey continues, “Part of our mission is to study whole systems of medicine; we try to do as little with isolated components as possible.” The need for evidence-based research and clinical studies to evaluate and confirm the safety and effectiveness of natural medicine continues to grow.

    Just as pharmaceutical medicine undergoes clinical trials, natural medicine is researched and studied through clinical trials. Helfgott employs experienced faculty in the fields of nutrition, psychology, immunology, whole systems research, and acupuncture, among other natural medicine research faculty, to carry out natural medicine clinical trials. Further, Helfgott faculty work with conventional biomedical researchers, using groundbreaking technology to study ancient traditions. A donation from Don Helfgott has helped fund the state-of-the-art basic science laboratory, as well as the resources to carry out clinical research.