Most people think of epidemics in terms of acute disease, such as the rapid spread of a virus to a large part of the population. The likelihood of epidemics of acute disease continues to grow, so people are justified in being concerned about epidemics of this kind. However, people are also justified in being even more concerned about the current epidemics of chronic disease.
Widespread chronic disease and increased susceptibility to disease have already reached pandemic proportions in the U.S. and other industrialized nations. Potential trouble can be detected even within newborn infants, children, and adults who appear healthy. These epidemics of chronic disease and increased susceptibility to disease are the basis for future epidemics of acute disease.
The nature and cause of chronic disease are topics of major concern in the scientific literature. Cancer, heart disease, obesity, hypertension, dementia, diabetes, osteoporosis, arthritis, liver and kidney disease, autoimmune disease, and many others are perpetually treated medically but rarely resolved. These chronic conditions are not occurring independently. They are all related, in two ways:
The major reason for the continuing rise in chronic disease and disease susceptibility is the ongoing spread and growing intensity of disease inducers that disrupt health by interfering with health's requirements. Many life-supporting functions are required to sustain health, as discussed in Health's Requirements, and these functions can be impaired by an increasingly hostile environment. Exposures to infectious agents, economic and natural disasters, hunger, toxic chemicals, disease-inducing foods and drugs, electromagnetic fog, and less-recognized inducers of disease continue to spread worldwide.
Effective preparations to minimize the personal and national impact of future epidemics should include educational material on the causes of disease susceptibility and specific inducers of disease. Although health concerns and corrective measures vary with local conditions, fundamental principles of health care for the protection, restoration, and maintenance of health are the same for everyone, everywhere.
Some facts and findings quoted from biomedical journal abstracts include the following:
Essential fatty acid (EFA)-deficient animals develop severe osteoporosis coupled with increased renal and arterial calcification. This picture is similar to that seen in osteoporosis in the elderly, where the loss of bone calcium is associated with ectopic calcification of other tissues, particularly the arteries and the kidneys. (Kruger, Horrobin, et al. 1997)
The purpose of this review is to put into perspective the many health benefits of vitamin D and the role of vitamin D deficiency in increasing the risk of many common and serious diseases, including some common cancers, type 1 diabetes, cardiovascular disease, and osteoporosis. (Holick 2004)
Experimental evidence suggests that chlorination products promote allergic sensitization by compromising the permeability or the immunoregulatory function of epithelial barriers. These findings led to the chlorine hypothesis proposing that the rise of allergic diseases could result less from the declining exposure to microbial agents (the hygiene hypothesis) than from the increasing and largely uncontrolled exposure to products of chlorination, the most widely used method to achieve hygiene in the developed world. (Bernard 2007)
Exposure to organophosphate (OP) pesticides is virtually ubiquitous. These inevitable agents are neurotoxicants, but recent evidence also points to lasting effects on carbohydrate metabolism. ... Thus, results of the present study suggest that Malathion can be considered as an important risk factor in the development of diabetes type 2, which prevalence increased substantially in our country and around the world. (Rezg, Mornagui, et al. 2010)
Currently, we are experiencing an epidemic of cardiorenal disease characterized by increasing rates of obesity, hypertension, the metabolic syndrome, type 2 diabetes, and kidney disease. Whereas excessive caloric intake and physical inactivity are likely important factors driving the obesity epidemic, it is important to consider additional mechanisms. We revisit an old hypothesis that sugar, particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease. (Johnson, Summer, et al. 2007)
The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). (Nakagawa, Hu, et al. 2006)
Most recently, obesity and diabetes join the growing list of adverse consequences that have been associated with developmental exposure to environmental estrogens during critical stages of differentiation. These diseases are quickly becoming significant public health issues and are fast reaching epidemic proportions worldwide. (Newbold, Padilla-Banks, and Jefferson 2009)
The basis for the current obesity epidemic remains controversial. However, the simplistic idea that obesity can be explained by two factors: energy intake and energy expenditure, is now being challenged ... In this article we propose an emerging hypothesis that the recent dramatic increase in obesity could be due to developmental nutrition, developmental exposure to environmental chemicals or the interaction of nutrition and environmental chemical exposures during development. Indeed, developmental exposure to environmental chemicals in animal studies has been shown to increase the susceptibility to a number of diseases including obesity. (Heindel, vom Saal, et al. 2009)
Asthma is an increasingly common disorder responsible for considerable morbidity and mortality. Although obesity is a risk factor for asthma and weight loss can improve symptoms, many patients do not adhere to low calorie diets and the impact of dietary restriction on the disease process is unknown. A study was designed to determine if overweight asthma patients would adhere to an alternate day calorie restriction (ADCR) dietary regimen, and to establish the effects of the diet on their symptoms, pulmonary function and markers of oxidative stress, and inflammation. Ten subjects with BMI>30 were maintained for 8 weeks on a dietary regimen in which they ate ad libitum every other day, while consuming less than 20% of their normal calorie intake on the intervening days. At baseline, and at designated time points during the 8-week study, asthma control, symptoms, and Quality of Life questionnaires (ACQ, ASUI, mini-AQLQ) were assessed and blood was collected for analyses of markers of general health, oxidative stress, and inflammation. Peak expiratory flow (PEF) was measured daily on awakening. Pre- and postbronchodilator spirometry was obtained at baseline and 8 weeks. Nine of the subjects adhered to the diet and lost an average of 8% of their initial weight during the study. Their asthma-related symptoms, control, and QOL improved significantly, and PEF increased significantly, within 2 weeks of diet initiation; these changes persisted for the duration of the study. Spirometry was unaffected by ADCR. Levels of serum beta-hydroxybutyrate were increased and levels of leptin were decreased on CR days, indicating a shift in energy metabolism toward utilization of fatty acids and confirming compliance with the diet. The improved clinical findings were associated with decreased levels of serum cholesterol and triglycerides, striking reductions in markers of oxidative stress (8-isoprostane, nitrotyrosine, protein carbonyls, and 4-hydroxynonenal adducts), and increased levels of the antioxidant uric acid. Indicators of inflammation, including serum tumor necrosis factor-alpha and brain-derived neurotrophic factor, were also significantly decreased by ADCR. Compliance with the ADCR diet was high, symptoms and pulmonary function improved, and oxidative stress and inflammation declined in response to the dietary intervention. These findings demonstrate rapid and sustained beneficial effects of ADCR on the underlying disease process in subjects with asthma, suggesting a novel approach for therapeutic intervention in this disorder.
Free Radical Biology & Medicine. 2007 Mar; 42(5):665-74.
James B. Johnson, Warren Summer, Roy G. Cutler, Bronwen Martin, Dong-Hoon Hyun, Vishwa D. Dixit, Michelle Pearson, Matthew Nassar, Richard Telljohann, Stuart Maudsley, Olga Carlson, Sujit John, Donald R. Laub, and Mark P. Mattson
Department of Surgery, Louisiana State University Medical Center, New Orleans, LA 70006, USA. jim@jbjmd.com
PubMed ID # 17291990
Essential fatty acid (EFA)-deficient animals develop severe osteoporosis coupled with increased renal and arterial calcification. This picture is similar to that seen in osteoporosis in the elderly, where the loss of bone calcium is associated with ectopic calcification of other tissues, particularly the arteries and the kidneys. Recent mortality studies indicate that the ectopic calcification may be considerably more dangerous than the osteoporosis itself, since the great majority of excess deaths in women with osteoporosis are vascular and unrelated to fractures or other bone abnormalities. EFAs have now been shown to increase calcium absorption from the gut, in part by enhancing the effects of vitamin D, to reduce urinary excretion of calcium, to increase calcium deposition in bone and improve bone strength and to enhance the synthesis of bone collagen. These desirable actions are associated with reduced ectopic calcification. The interaction between EFA and calcium metabolism deserves further investigation since it may offer novel approaches to osteoporosis and also to the ectopic calcification associated with osteoporosis which seems to be responsible for so many deaths.
Progress in Lipid Research. 1997 Sep; 36(2-3):131-51.
M. C. Kruger and D. F. Horrobin
Department of Physiology, University of Pretoria, South Africa.
PubMed ID # 9624425
The worldwide epidemic of metabolic syndrome correlates with an elevation in serum uric acid as well as a marked increase in total fructose intake (in the form of table sugar and high-fructose corn syrup). Fructose raises uric acid, and the latter inhibits nitric oxide bioavailability. Because insulin requires nitric oxide to stimulate glucose uptake, we hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome. Four sets of experiments were performed. First, pair-feeding studies showed that fructose, and not dextrose, induced features (hyperinsulinemia, hypertriglyceridemia, and hyperuricemia) of metabolic syndrome. Second, in rats receiving a high-fructose diet, the lowering of uric acid with either allopurinol (a xanthine oxidase inhibitor) or benzbromarone (a uricosuric agent) was able to prevent or reverse features of metabolic syndrome. In particular, the administration of allopurinol prophylactically prevented fructose-induced hyperinsulinemia (272.3 vs.160.8 pmol/l, P < 0.05), systolic hypertension (142 vs. 133 mmHg, P < 0.05), hypertriglyceridemia (233.7 vs. 65.4 mg/dl, P < 0.01), and weight gain (455 vs. 425 g, P < 0.05) at 8 wk. Neither allopurinol nor benzbromarone affected dietary intake of control diet in rats. Finally, uric acid dose dependently inhibited endothelial function as manifested by a reduced vasodilatory response of aortic artery rings to acetylcholine. These data provide the first evidence that uric acid may be a cause of metabolic syndrome, possibly due to its ability to inhibit endothelial function. Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid.
American Journal of Physiology. Renal Physiology. 2006 Mar; 290(3):F625-31.
Takahiko Nakagawa, Hanbo Hu, Sergey Zharikov, Katherine R. Tuttle, Robert A. Short, Olena Glushakova, Xiaosen Ouyang, Daniel I. Feig, Edward R. Block, Jaime Herrera-Acosta, Jawaharlal M. Patel, and Richard J. Johnson
Division of Nephrology, Hypertension, and Transplantation, PO Box 100224, University of Florida, Gainesville, FL 32610, USA. nakagt@medicine.ufl.edu
PubMed ID # 16234313
The basis for the current obesity epidemic remains controversial. However, the simplistic idea that obesity can be explained by two factors: energy intake and energy expenditure, is now being challenged due to the lack of success in decreasing obesity based on a focus on only these two factors. In this article we propose an emerging hypothesis that the recent dramatic increase in obesity could be due to developmental nutrition, developmental exposure to environmental chemicals or the interaction of nutrition and environmental chemical exposures during development. Indeed, developmental exposure to environmental chemicals in animal studies has been shown to increase the susceptibility to a number of diseases including obesity. Obesity is thus one of many diseases shown to have a developmental origin. We show that factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, as well as components of the maternal and infant diets, can influence weight gain later in life. In addition, we show that developmental exposure to endocrine disrupting chemicals can create abnormalities in homeostatic control systems required to maintain a normal body weight throughout life. Eliminating exposures to these chemicals and improving nutrition during development offer the potential for reducing obesity and associated diseases.
Molecular and Cellular Endocrinology. 2009 May; 304(1-2):90-6.
Jerrold J. Heindel and Frederick S. vom Saal
Division of Extramural Research and Training, National Institute of Environmental Health Sciences, NIH/DHHS, Cellular, Organs and Systems Pathobiology Branch, Research Triangle Park, NC 27709, USA. heindelj@niehs.nih.gov
PubMed ID # 19433253
Exposure of the human population to chlorination products has considerably increased during the 20(th) century especially after the 1960s with the development of public and leisure pools. The present article summarizes current knowledge regarding the human exposure to chlorination products and reviews studies suggesting that these chemicals might be involved in the development or exacerbation of allergic diseases. Populations regularly in contact with chlorination products such as swimmers, lifeguards or workers using chlorine as cleaning or bleaching agent show increased risks of allergic diseases or of respiratory disorders frequently associated with allergy. Experimental evidence suggests that chlorination products promote allergic sensitization by compromising the permeability or the immunoregulatory function of epithelial barriers. These findings led to the chlorine hypothesis proposing that the rise of allergic diseases could result less from the declining exposure to microbial agents (the hygiene hypothesis) than from the increasing and largely uncontrolled exposure to products of chlorination, the most widely used method to achieve hygiene in the developed world. Giving the increasing popularity of water recreational areas, there is an obvious need to assess the effects of chlorine-based oxidants on human health and their possible implication in the epidemic of allergic diseases.
Current Medicinal Chemistry. 2007; 14(16):1771-82.
A. Bernard
Department of Public Health, Unit of Toxicology, Catholic University of Louvain, Brussels, Belgium. alfred.bernard@uclouvain.be
PubMed ID # 17627515
Many chemicals in the environment, in particular those with estrogenic activity, can disrupt the programming of endocrine signaling pathways that are established during development and result in adverse consequences that may not be apparent until much later in life. Most recently, obesity and diabetes join the growing list of adverse consequences that have been associated with developmental exposure to environmental estrogens during critical stages of differentiation. These diseases are quickly becoming significant public health issues and are fast reaching epidemic proportions worldwide. In this review, we summarize the literature from experimental animal studies documenting an association of environmental estrogens and the development of obesity, and further describe an animal model of exposure to diethylstilbestrol (DES) that has proven useful in studying mechanisms involved in abnormal programming of various differentiating estrogen-target tissues. Other examples of environmental estrogens including the phytoestrogen genistein and the environmental contaminant Bisphenol A are also discussed. Together, these data suggest new targets (i.e., adipocyte differentiation and molecular mechanisms involved in weight homeostasis) for abnormal programming by estrogenic chemicals, and provide evidence that support the scientific hypothesis termed "the developmental origins of adult disease". The proposal of an association of environmental estrogens with obesity and diabetes expands the focus on the diseases from intervention/treatment to include prevention/avoidance of chemical modifiers especially during critical windows of development.
Molecular and Cellular Endocrinology. 2009 May; 304(1-2):84-9.
Retha R. Newbold, Elizabeth Padilla-Banks, and Wendy N. Jefferson
Developmental Endocrinology and Endocrine Disruptor Section, Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC 27709, United States. newbold1@niehs.nih.gov
PubMed ID # 19433252
The basis for the current obesity epidemic remains controversial. However, the simplistic idea that obesity can be explained by two factors: energy intake and energy expenditure, is now being challenged due to the lack of success in decreasing obesity based on a focus on only these two factors. In this article we propose an emerging hypothesis that the recent dramatic increase in obesity could be due to developmental nutrition, developmental exposure to environmental chemicals or the interaction of nutrition and environmental chemical exposures during development. Indeed, developmental exposure to environmental chemicals in animal studies has been shown to increase the susceptibility to a number of diseases including obesity. Obesity is thus one of many diseases shown to have a developmental origin. We show that factors that impact growth during fetal and neonatal life, such as placental blood flow and nutrient transport to fetuses, as well as components of the maternal and infant diets, can influence weight gain later in life. In addition, we show that developmental exposure to endocrine disrupting chemicals can create abnormalities in homeostatic control systems required to maintain a normal body weight throughout life. Eliminating exposures to these chemicals and improving nutrition during development offer the potential for reducing obesity and associated diseases.
Molecular and Cellular Endocrinology. 2009 May; 304(1-2):90-6.
Jerrold J. Heindel and Frederick S. vom Saal
Division of Extramural Research and Training, National Institute of Environmental Health Sciences, NIH/DHHS, Cellular, Organs and Systems Pathobiology Branch, Research Triangle Park, NC 27709, USA. heindelj@niehs.nih.gov
PubMed ID # 19433253
The purpose of this review is to put into perspective the many health benefits of vitamin D and the role of vitamin D deficiency in increasing the risk of many common and serious diseases, including some common cancers, type 1 diabetes, cardiovascular disease, and osteoporosis. Numerous epidemiologic studies suggest that exposure to sunlight, which enhances the production of vitamin D(3) in the skin, is important in preventing many chronic diseases. Because very few foods naturally contain vitamin D, sunlight supplies most of our vitamin D requirement. 25-Hydroxyvitamin D [25(OH)D] is the metabolite that should be measured in the blood to determine vitamin D status. Vitamin D deficiency is prevalent in infants who are solely breastfed and who do not receive vitamin D supplementation and in adults of all ages who have increased skin pigmentation or who always wear sun protection or limit their outdoor activities. Vitamin D deficiency is often misdiagnosed as fibromyalgia. A new dietary source of vitamin D is orange juice fortified with vitamin D. Studies in both human and animal models add strength to the hypothesis that the unrecognized epidemic of vitamin D deficiency worldwide is a contributing factor of many chronic debilitating diseases. Greater awareness of the insidious consequences of vitamin D deficiency is needed. Annual measurement of serum 25(OH)D is a reasonable approach to monitoring for vitamin D deficiency. The recommended adequate intakes for vitamin D are inadequate, and, in the absence of exposure to sunlight, a minimum of 1000 IU vitamin D/d is required to maintain a healthy concentration of 25(OH)D in the blood.
The American Journal of Clinical Nutrition. 2004 Mar; 79(3):362-71.
Michael F. Holick
Vitamin D, Skin, and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, MA 02118-2394, USA.
PubMed ID # 14985208