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Diabetes Mellitus Publications

 

JOURNALS

Bays H, Weiter K, Anderson J. A randomized study of raisins versus alternative snacks on glycemic control and other cardiovascular risk factors in patients with type 2 diabetes mellitus. Phys Sportsmed. 2015 Feb;43(1):37-43.

Bays HE, Brinton EA, Triscari J, Chen E, Maccubbin D, MacLean AA, Gibson KL, Ruck RA, Johnson-Levonas AO, O'Neill EA, Mitchel YB. Extended-release niacin/laropiprant significantly improves lipid levels in type 2 diabetes mellitus irrespective of baseline glycemic control. Vasc Health Risk Manag. 2015 Feb 24;11:165-72. doi: 10.2147/VHRM.S70907. eCollection 2015. PubMed PMID: 25750540; PubMed Central PMCID: PMC4348131.

Bays H. Sodium Glucose Co-transporter Type 2 (SGLT2) Inhibitors: Targeting the Kidney to Improve Glycemic Control in Diabetes Mellitus. Diabetes Ther. 2013 Oct 19. [Epub ahead of print] PubMed PMID: 24142577.

Hollander P, Gupta AK, Plodkowski R, Greenway F, Bays H, Burns C, Klassen P, Fujioka K; for the COR-Diabetes Study Group. Effects of Naltrexone Sustained- Release/Bupropion Sustained Release Combination Therapy on Body Weight and Glycemic Parameters in Overweight and Obese Patients With Type 2 Diabetes. Diabetes Care. 2013 Oct 21. [Epub ahead of print] PubMed PMID: 24144653.

Brinton EA, Ballantyne CM, Bays HE, Kastelein JJ, Braeckman RA, Soni PN. Effects of icosapent ethyl on lipid and inflammatory parameters in patients with diabetes mellitus-2, residual elevated triglycerides (200--500 mg/dL), and on statin therapy at LDL-C goal: the ANCHOR study. Cardiovasc Diabetol. 2013 Jul 9;12(1):100. [Epub ahead of print]

Bays HE. Adiposopathy, diabetes mellitus, and primary prevention of atherosclerotic coronary heart disease: treating "sick fat" through improving fat function with antidiabetes therapies. Am J Cardiol 2012;110:4B-12B.

Bays HE. Long-term (52-78 weeks) treatment with colesevelam HCl added to metformin therapy in type 2 diabetes mellitus patients. Diabetes Metab Syndr Obes 2012;5:125-34.

Rodbard HW, Bays HE, Gavin JR 3rd, Green AJ, Bazata DD, Lewis SJ, Fox KM, Reed ML, Grandy S. Rate and risk predictors for development of self-reported type-2 diabetes mellitus over a 5 year period: the SHIELD study. Int J Clin Pract. 2012;66:684-691.

Bays H, Giezek H, McKenney JM, O'Neil EA, Tershakovec AM. Extended-Release Niacin/Laropiprant Effects on Lipoprotein Subfractions in Patients with Type 2 Diabetes Mellitus. Metab Syndr Relat Disord. 2012 Epub ahead of print.

Bays H, Frestedt JL, Bell M, Williams C, Kolberg L, Schmelzer W, Anderson JW. Reduced viscosity Barley Beta-Glucan versus placebo: A randomized controlled trial of the effects on insulin sensitivity for individuals at risk for Diabetes Mellitus. Nutr Metab 2011 Epub ahead of print

Bays HE. Adiposopathy: Is "Sick Fat" a Cardiovascular Disease? Journal of the American College of Cardiology. 2011;57:2461-2473. (CLICK HERE FOR ONLINE MEDSCAPE REPRINT OF THIS ARTICLE)

Bays HE. Colesevelam HCl added to background metformin therapy in patients with type 2 diabetes mellitus: A pooled analysis from three clinical studies. Endocrine Practice. Endocr Pract. 2011;17:933-938.

Stalenhoef AF, Davidson MH, Robinson JG, Burgess T, Duttlinger-Maddux R, Kallend D, Goldberg AC, Bays H. Efficacy and safety of dalcetrapib in type 2 diabetes mellitus and/or metabolic syndrome patients, at high cardiovascular disease risk. Diabetes Obes Metab 2011 Epub ahead of print.

Bays HE, Roth EM, McKenney JM, Kelly MT, Thakker KM, Setze CM, Obermeyer K, Sleep DJ. The effects of fenofibric acid alone and with statins on the prevalence of metabolic syndrome and its diagnostic components in patients with mixed dyslipidemia. Diabetes Care. 2010 Sep;33(9):2113-6

Bays H. Bromocryptine Mesylate (Cyclocet): A new oral drug treatment for type 2 diabetes mellitus. Kentucky Diabetes Connection. 2010 (4th quarter), page 3.

Bays HE, Gonzalez-Campoy JM, Schorr AB. What men should know about metabolic syndrome, adiposopathy, and "sick fat." Int J Clin Pract. 2010;64:1735-1739.

Bays H. Phentermine, topiramate, and their combination for the treatment of adiposopathy ("sick fat") and metabolic disease. Expert Rev. Cardiovasc. Ther. 2010; 8(12):1777-801.

Abstract: Positive caloric balance often causes pathologic adipocyte and adipose tissue anatomical and functional changes (termed adiposopathy or 'sick fat'), which may lead to pathogenic adipocyte and adipose tissue responses and metabolic disease. Fat weight loss may improve adiposopathy, and thus improve metabolic disease in overweight patients. Unfortunately, the efficacy of nonsurgical weight loss therapies is often limited due to redundant physiological systems that help 'protect' against starvation and/or negative caloric balance. One strategy to overcome these limitations is to combine weight loss drug therapies having complementary mechanisms of action, thereby affecting more than one physiologic process influencing body fat accumulation. Phentermine is a noradrenergic sympathomimetic amine approved for short-term treatment of obesity. Topiramate is a sulfamate-substituted monosaccharide derivative of the naturally occurring sugar monosaccharide d-fructose approved as treatment for migraine headaches and seizure disorders. Although known to facilitate weight loss since its approval, topiramate monotherapy does not have a regulatory indication as an anti-obesity agent. Phentermine HCl / topiramate controlled-release (PHEN/TPM CR) is a combination agent containing immediaterelease phentermine and controlled-release topiramate. Clinical trials involving thousands of patients demonstrate PHEN/TPM CR to be effective in improving the weight of patients, and also effective in improving adiposopathy-associated metabolic diseases. This review examines the pathophysiology of adiposopathy as a contributor to metabolic disease, the data supporting phentermine monotherapy, topiramate monotherapy and their combination as anti-obesity and anti-adiposopathy agents, and the preliminary evidence supporting PHEN/TPM CR as a generally well-tolerated and effective agent to improve metabolic disease.[CLICK HERE FOR A FREE DOWNLOAD OF THIS ARTICLE]

Bays HE. Lorcaserin and adiposopathy: 5-HT2c agonism as a treatment for ‘sick fat’ and metabolic disease. Expert Rev. Cardiovasc. Ther. 7(11), 1429–1445 (2009)

Abstract: Agonists of 5-hydroxytryptamine (5-HT; serotonin) receptors promote loss of excessive body fat (adiposity) and improve metabolic parameters associated with adiposity-induced adipose tissue dysfunction (adiposopathy or ‘sick fat’). By improving adipose tissue pathogenic endocrine and immune responses in overweight patients, 5-HT receptor agonists may improve metabolic disease. Lorcaserin (APD-356) is a selective 5-HT2c receptor agonist that promotes weight loss. Probably owing to its selectivity for the 5-HT2c receptor, clinical trial evidence supports that lorcaserin does not adversely affect heart valves or pulmonary artery pressure. This review examines: the mechanisms by which serotonergic pathways improve adiposity and adiposopathy; historical data and perspective regarding the efficacy and safety of prior 5-HT agonists; speculation regarding future paradigms in treating adiposopathy; and why lorcaserin may prove to be a safe and generally well-tolerated agent that not only improves the weight of patients, but also improves the health of patients. [CLICK HERE FOR A FREE DOWNLOAD OF THIS ARTICLE]

Bays HE, Bazata DD, Fox KM, Grandy G, Gavin JR, SHIELD Study Group. Perceived body image in men and women with type 2 diabetes mellitus: correlation of body mass index with the figure rating scale. Nutr J 2009 16;5:57

Bays HE, Laferrere B, Dixon J, Arrone L, Gonzalez-Campoy JM, Apovian C, Wolfe BM. "Adiposopathy and bariatric surgery: is 'sick fat' a surgical disease?" Consensus. Int J Clin Pract Sept. 2009 63(9) 1285-1300

Objective: To review how bariatric surgery in obese patients may effectively treatadiposopathy (pathogenic adipose tissue or ‘sick fat’), and to provide clinicians arationale as to why bariatric surgery is a potential treatment option for overweightpatients with type 2 diabetes, hypertension, and dyslipidaemia. Methods: A groupof clinicians, researchers, and surgeons, all with a background in treating obesityand the adverse metabolic consequences of excessive body fat, reviewed the medicalliterature regarding the improvement in metabolic disease with bariatric surgery. Results: Bariatric surgery improves metabolic disease through multiple, likelyinterrelated mechanisms including: (i) initial acute fasting and diminished caloricintake inherent with many gastrointestinal surgical procedures; (ii) favourable alterationsin gastrointestinal endocrine and immune responses, especially with bariatricsurgeries that reroute nutrient gastrointestinal delivery such as gastric bypass procedures;and (iii) a decrease in adipose tissue mass. Regarding adipose tissuemass, during positive caloric balance, impaired adipogenesis (resulting in limitationsin adipocyte number or size) and visceral adiposity are anatomic manifestationsof pathogenic adipose tissue (adiposopathy). This may cause adverse adiposetissue endocrine and immune responses that lead to metabolic disease. A decreasein adipocyte size and decrease in visceral adiposity, as often occurs with bariatricsurgery, may effectively improve adiposopathy, and thus effectively treat metabolicdisease. It is the relationship between bariatric surgery and its effects upon pathogenicadipose tissue that is the focus of this discussion. Conclusions: In selectiveobese patients with metabolic disease who are refractory to medical management,adiposopathy is a surgical disease. [CLICK HERE FOR A FREE DOWNLOAD OF THIS ARTICLE]

Bays H. From victim to ally: the kidney as an emerging target for the treatment of diabetes mellitus. Curr Med Res Opin. 2009;25:671-81.

Bays HE. "Sick Fat," metabolic disease, and atherosclerosis. Am J Med. 2009;122(1Suppl):S26-37.

Abstract: Atherosclerotic coronary heart disease (CHD) is the most common cause of morbidity and mortality among men and women in developed nations. The obesity epidemic contributes to the increasing prevalence of high blood sugar (as may be found in patients with diabetes mellitus and metabolic syndrome), high blood pressure, and dyslipidemia--all CHD risk factors. Metabolic syndrome describes the common clinical finding wherein component CHD risk factors cluster within a single patient, but this term does not identify any unified pathophysiologic process. However, a component of the metabolic syndrome is abdominal obesity, which does reflect an anatomic manifestation of a "common-soil" pathophysiologic process that promotes the onset of CHD risk factors, and thus increases CHD risk. Adiposopathy ("sick fat") is anatomically characterized by visceral adiposity and adipocyte hypertrophy; it is manifested physiologically by a net increase in release of free fatty acids and by pathogenic adipose tissue metabolic/immune responses that promote metabolic disease and increase CHD risk. Understanding the relation of adiposopathy to CHD risk factors and recognizing the importance of treating both the "cause and effect" of metabolic diseases are critical toward a comprehensive approach in reducing CHD risk. Regarding the "cause," clinicians and their patients should be diligent regarding appropriate nutritional and lifestyle interventions that may favorably affect health. Regarding the "effect," clinicians and their patients should be equally diligent toward appropriate pharmaceutical interventions that reduce CHD risk factors when nutritional and lifestyle interventions do not sufficiently achieve desired metabolic treatment goals. [CLICK HERE FOR A FREE DOWNLOAD OF THIS ARTICLE]

Bays HE, Gonzalez-Campoy JM, Henry RR, Bergman DA, Schorr AB, Rodbard. Is adiposopathy ("sick fat") an endocrine disease? Int J Clin Pract. 2008:10:1474-83.

Abstract: OBJECTIVE: To review current consensus and controversy regarding whether obesity is a 'disease', examine the pathogenic potential of adipose tissue to promote metabolic disease and explore the merits of 'adiposopathy' and 'sick fat' as scientifically and clinically useful terms in defining when excessive body fat may represent a 'disease'. METHODS: A group of clinicians and researchers, all with a background in endocrinology, assembled to evaluate the medical literature, as it pertains to the pathologic and pathogenic potential of adipose tissue, with an emphasis on metabolic diseases that are often promoted by excessive body weight. RESULTS: The data support pathogenic adipose tissue as a disease. Challenges exist to convince many clinicians, patients, healthcare entities and the public that excessive body fat is often no less a 'disease' than the pathophysiological consequences related to anatomical abnormalities of other body tissues. 'Adiposopathy' has the potential to scientifically define adipose tissue anatomic and physiologic abnormalities, and their adverse consequences to patient health. Adiposopathy acknowledges that when positive caloric balance leads to adipocyte hypertrophy and visceral adiposity, then this may lead to pathogenic adipose tissue metabolic and immune responses that promote metabolic disease. From a patient perspective, explaining how excessive caloric intake might cause fat to become 'sick' also helps provide a rationale for patients to avoid weight gain. Adiposopathy also better justifies recommendations of weight loss as an effective therapeutic modality to improve metabolic disease in overweight and obese patients. CONCLUSION: Adiposopathy (sick fat) is an endocrine disease.[CLICK HERE FOR A FREE DOWNLOAD OF THIS ARTICLE]

Bays HE, Goldberg RB, Truitt KE, Jones MR. Colesevelam Hydrochloride Therapy in Patients With Type 2 Diabetes Mellitus Treated With Metformin: Glucose and Lipid Effects Arch Intern Med. 2008;168(18):1975-1983.

Bays HE, Gonzalez-Campoy JM, Henry RR, Bergman DA, Schorr AB, Rodbard. Is adiposopathy ("sick fat") an endocrine disease? Int J Clin Pract. 2008:10:1474-83.

Bays HE, Goldberg RB.  The Forgotten Bile Acid Sequestrants: Is Now a Good Time to Remember?  American Journal of Therapeutics 14, 567–580 (2007)

Bays H, Jones PH. Colesevelam hydrochloride:  reducing atherosclerotic coronary heart disease risk factors. Vascular Health and Risk Management 2007;3(5):1-10.

Bays HE, Gonzalez-Campoy JM, Bray GA, Kitabchi AE, Bergman DA, Schorr AB, Rodbard HW, Henry RR.  Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hypertrophy and increased visceral adiposity.  Expert Rev Cardiovasc Ther. 2008;3:343-368.

Abstract:  When caloric intake exceeds caloric expenditure, the positive caloric balance and storage of energy in adipose tissue often causes adipocyte hypertrophy and visceral adipose tissue accumulation. These pathogenic anatomic abnormalities may incite metabolic and immune responses that promote Type 2 diabetes mellitus, hypertension and dyslipidemia. These are the most common metabolic diseases managed by clinicians and are all major cardiovascular disease risk factors. 'Disease' is traditionally characterized as anatomic and physiologic abnormalities of an organ or organ system that contributes to adverse health consequences.  Using this definition, pathogenic adipose tissue is no less a disease than diseases of other body organs. This review describes the consequences of pathogenic fat cell hypertrophy and visceral adiposity, emphasizing the mechanistic contributions of genetic and environmental predispositions, adipogenesis, fat storage, free fatty acid metabolism, adipocyte factors and inflammation. Appreciating the full pathogenic potential of adipose tissue requires an integrated perspective, recognizing the importance of 'cross-talk' and interactions between adipose tissue and other body systems. Thus, the adverse metabolic consequences that accompany fat cell hypertrophy and visceral adiposity are best viewed as a pathologic partnership between the pathogenic potential adipose tissue and the inherited or acquired limitations and/or impairments of other body organs. A better understanding of the physiological and pathological interplay of pathogenic adipose tissue with other organs and organ systems may assist in developing better strategies in treating metabolic disease and reducing cardiovascular disease risk.  [CLICK HERE FOR A FREE DOWNLOAD OF THIS ARTICLE]

Bays HE, Rodbard RW, Schorr AB, González-Campoy JM. Treating Pathogenic Adipose Tissue (Adiposopathy) to Reduce Cardiovascular Disease Risk. Current Treatment Options in Cardiovascular Medicine 2007 9;259-271

Abstract:  Excessive adipose tissue is potentially pathogenic due to its mass effects and through adverse metabolic/immune responses, which may lead to cardiovascular disease risk factors (eg, type 2 diabetes mellitus, hypertension, dyslipidemia, and possibly atherosclerosis itself). Positive caloric balance in genetically/environmentally susceptible patients may result in adipocyte hypertrophy, visceral adipose tissue accumulation, and ectopic fat deposition, all causally associated with metabolic disease, and all anatomic manifestations of “adiposopathy” (a term used to describe adipose tissue pathology). Weight loss through improved nutrition, increased physical activity, and weight loss agents (ie, orlistat and sibutramine) improves adiposopathy and improves many metabolic diseases whose prevalence are directly associated with an increase in body fat and sedentary lifestyle. Cannabinoid receptor antagonists improve adiposopathy through weight reduction and favorable metabolic effects upon multiple body organs (including adipocytes). Peroxisome proliferator-activated receptor-γ agonists may improve adiposopathy through recruitment of functional fat cells and apoptosis of dysfunctional fat cells.

Bays H, McElhattan J, Bryzinski BS; On Behalf of the Gallant 6 Study Group.  A double-blind, randomised trial of tesaglitazar versus pioglitazone in patients with type 2 diabetes mellitus.  Diab Vasc Dis Res 2007, 4(3):181-93

Bays HE, Bazata DD, Clark NG, Gavin JR 3rd, Green AJ, Lweis SJ, Reed ML, Stewart W, Chapman RH, Fox KM, Grandy S.  Prevalence of self-reported diagnosis of diabetes mellitus and associated risk factors in a national survey in the US population:  SHIELD (Study to Help Improve Early evaluation and management of risk factors Leading to Diabetes.  BMC Public Health 2007;7(1):277

Fox KM, Gandhi SK, Ohsfeldt RL, JW Blasetto, Bays HE.  Effectiveness of rosuvastatin in low-density lipoprotein cholesterol lowering and National Cholesterol Education Program Adult Treatment Panel guideline III LDL‑C goal attainment compared to other statins among diabetes mellitus patients: a retrospective study using an electronic medical records dataset in the United States.  Current Medical Research and Opinion 23;9:2007, 2125–2133

Bays HE, Chapman RH, Grandy S.  The relationship of body mass index to diabetes mellitus, hypertension and dyslipidaemia: comparison of data from two national surveys.  Int J Clin Pract, May 2007, 61, 5, 737–747

Bays H, Blonde L, Rosenson R.  Adiposopathy:  how do diet, exercise, and weight loss drug therapies improve metabolic disease in overweight patients.  Expert Rev. Cardiovasc. Ther. 4(6), 871–895 (2006)  [Click here for a free download of this article]

Abstract:  An increase in bodyweight is generally associated with an increased risk of excessive fat-related metabolic diseases (EFRMD), including Type 2 diabetes mellitus, hypertension and dyslipidemia. However, not all patients who are overweight have EFRMD, and not all patients with EFRMD are significantly overweight. The adipocentric paradigm provides the basis for a unifying, pathophysiological process whereby fat gain in susceptible patients leads to fat dysfunction (‘sick fat’), and wherein pathological abnormalities in fat function (adiposopathy) are more directly related to the onset of EFRMD than increases in fat mass (adiposity) alone. But just as worsening fat function worsens EFRMD, improved fat function improves EFRMD. Peroxisome proliferator-activated receptor-γ agonists increase the recruitment, proliferation and differentiation of preadipocytes (‘healthy fat’) and cause apoptosis of hypertrophic and dysfunctional (including visceral) adipocytes resulting in improved fat function and improved metabolic parameters associated with EFRMD. Weight loss interventions, such as a hypocaloric diet and physical exercise, in addition to agents such as orlistat, sibutramine and cannabinoid receptor antagonists, may have favorable effects upon fat storage (lipogenesis and fat distribution), nutrient metabolism (such as free fatty acids), favorable effects upon adipose tissue factors involved in metabolic processes and inflammation, and enhanced ‘cross-talk’ with other major organ systems. In some cases, weight loss therapeutic agents may even affect metabolic parameters and adipocyte function independently of weight loss alone, suggesting that the benefit of these agents in improving EFRMD may go beyond their efficacy in weight reduction. This review describes how adiposopathy interventions may affect fat function, and thus improve EFRMD.

Bays H, Ballantyne C.  Adiposopathy:  why do adiposity and obesity cause metabolic disease?  Future Lipidol. 2006 1(4), 389-420

Abstract: In the adipocentric paradigm, fat health affects patient health. Adiposopathy (‘pathos’ of adipose tissue or fat dysfunction) is more directly associated with excessive fat-related metabolic disease (EFRMD) than adiposity (increased fat mass) alone. Examples of adipocyte factors whose dysmetabolism may contribute to Type 2 diabetes mellitus include: 11 β-hydroxysteroid dehydrogenase type 1, acylation-stimulating protein, adiponectin, adipsin, angiotensinogen, autotaxin, ceramide, free fatty acids, hormone-sensitive lipase, interleukin-6, insulin-like growth factor-1, leptin, lipin, lysophospholipids, perilipin, phosphoenolpyrovate carboxykinase, plasminogen activator inhibitor-1, resistin, retinol-binding protein, tumor necrosis factor-α, visceral adipose tissue-derived serpin and visfatin. Excessive body fat may lead to hypertension due to physical compression of kidneys, sleep apnea, and other mechanisms. Examples of adipocyte factors whose dysmetabolism may contribute to hypertension include: 11 β-hydroxysteroid dehydrogenase type 1, adiponectin, angiotensinogen, angiotensin I and II, angiotensin-converting enzyme, renin, cathepsin, chymase, free fatty acids, interleukin-6 and leptin. Examples of adipocyte factors whose dysmetabolism may contribute to dyslipidemia include: 11 β-hydroxysteroid dehydrogenase type 1, acylation-stimulating protein, adipophilin, adiponectin, adipsin, cholesteryl ester-transfer protein, free fatty acids, hormone-sensitive lipase, leptin, lipoprotein lipase, perilipin, phospholipid transfer protein, sex hormones and tumor necrosis factor-α. Numerous other adipocyte factors may directly affect atherosclerosis and cardiomyopathy. A better understanding and recognition of how fat weight gain contributes to EFRMD will substantially affect the research and development of therapeutic interventions that may treat or prevent adiposopathy, and dramatically influence which patients with EFRMD are best treated and how.

Bays HE, Dujovne CA.  Adiposopathy is a More Rational Treatment Target for Metabolic Disease Than Obesity Alone.  Current Atherosclerosis Reports 2006, 8:144–156

Abstract:  Current guidelines recommend that weight-loss therapy should be primarily based upon specific body mass index (BMI) cut-off limits. However, in the adipocentric paradigm, it is acknowledged that co-morbidities, such as type 2 diabetes mellitus, hypertension, and dyslipidemia, occur at all levels of BMI.  Excessive fat mass (adiposity) in genetically susceptible individuals results in fat dysfunction (adiposopathy), which then contributes to metabolic disorders that increase the risk of atherosclerotic cardiovascular disease. In this paradigm, the term “anti-obesity” treatment might best be replaced by “anti-adiposopathy” treatment, wherein the focus is not based solely on BMI, but instead directed towards physiologically improving fat cell function and clinically improving the metabolic health of patients. This may occur through appropriate diet, physical exercise, and other lifestyle changes, and/or from drug therapies. Cannabinoid receptor antagonists and peroxisome proliferator activated receptor agonists are examples of agents that physiologically improve fat function and clinically improve metabolic disease.

Bays HE.  I was wrong #2:  Inhaled Insulin.  Louisville Medicine.  2006;53:395

Bays H.  Adiposopathy:  role of adipocyte factors in a new paradigm.  Expert Rev Cardiovasc Ther. 2005;3:187-9

Bays HE.  Adiposopathy, metabolic syndrome, quantum physics, general relativity, chaos and the Theory of Everything.  Expert Rev. Cardiovasc. Ther. 3(3), 393–404 (2005)

Abstract:  Excessive fat (adiposity) and dysfunctional fat (adiposopathy) constitute the most common worldwide epidemics of our time – and perhaps of all time. Ongoing efforts to explain how the micro (adipocyte) and macro (body organ) biologic systems interact through function and dysfunction in promoting Type 2 diabetes mellitus, hypertension and dyslipidemia are not unlike the mechanistic and philosophical thinking processes involved in reconciling the micro (quantum physics) and macro (general relativity) theories in physics. Currently, the term metabolic syndrome refers to a constellation of consequences often associated with excess body fat and is an attempt to unify the associations known to exist between the four fundamental metabolic diseases of obesity, hyperglycemia (including Type 2 diabetes mellitus), hypertension and dyslipidemia. However, the association of adiposity with these metabolic disorders is not absolute and the metabolic syndrome does not describe underlying causality, nor does the metabolic syndrome necessarily reflect any reasonably related pathophysiologic process. Just as with quantum physics, general relativity and the four fundamental forces of the universe, the lack of an adequate unifying theory of micro causality and macro consequence is unsatisfying, and in medicine, impairs the development of agents that may globally improve both obesity and obesity-related metabolic disease. Emerging scientific and clinical evidence strongly supports the novel concept that it is not adiposity alone, but rather it is adiposopathy that is the underlying cause of most cases of Type 2 diabetes mellitus, hypertension and dyslipidemia. Adiposopathy is a plausible Theory of Everything for mankind’s greatest metabolic epidemics.

Bays H, Abate N, Chandalia M.  Adiposopathy:  Sick Fat Causes High Blood Sugar, High Blood Pressure, and Dyslipidemia.  Future Cardiology (2005) 1(1), 39-59.

Abstract:  Adiposopathy is defined as pathological adipose tissue function that may be promoted and exacerbated by fat accumulation (adiposity) and sedentary lifestyle in genetically susceptible patients. Adiposopathy is a root cause of some of the most common metabolic diseases observed in clinical practice, including Type 2 diabetes mellitus, hypertension and dyslipidemia. The most common term for the metabolic consequences of adiposopathy is currently ‘the metabolic syndrome’. Drug usage to treat the metabolic syndrome has focused on the safety and efficacy of treatments directed towards individual components of the metabolic syndrome, and not so much upon adiposopathy itself. However, enough is known about the pathophysiology of adiposopathy to propose diagnostic criteria. Regulatory issues are important obstacles to the research and development of new drug treatments for the metabolic syndrome. It is hoped that these obstacles can, to some extent, be addressed and overcome by clearly defining and increasing our understanding of adiposopathy.  (NOTE:  This above article is copyrighted.  All reprints should be obtained through Future Medicine.)

Bays H, Shepherd J.  Diabetes, Metabolic Syndrome and Dyslipidemia.  Management Strategies in Diabetes.  Cambridge Medical Publications.  ISBN 0 904052 88 5.  (2004) 1 - 28.

Deedwania PC, Hunninghake DB, Bays HE,  Jones PH, Cain VA, Blasetto JW, for the STELLAR Study Group.  Effects of Rosuvastatin, Atorvastatin, Simvastatin, and Pravastatin on the Atherogenic Dyslipidemia of Patients with Characteristics of the Metabolic Syndrome.  Am J Cardiology  2005 95(3)360-6 

Bays HE.  Metabolic Syndrome:  What might be occurring?  Managed Care Supplement.  October 2004 Vol. 13 No 10.  Pages 13-16.

Deedwania PC, Hunninghake DB, Bays HE  Effects of lipid-altering treatment in diabetes mellitus and the metabolic syndrome.  Am J Cardiol - 3-JUN-2004; 93(11A): 18C-26C

Bays H, Mandarino L, DeFronzo RA.  Role of the Adipocyte, FFA, and Ectopic Fat in Pathogenesis of Type 2 Diabetes Mellitus.  Journal of Clinical Endocrinology and Metabolism 2004 89: 463-478.

Bays HE, McGovern ME.  Once-Daily Niacin Extended-Release/Lovastatin Combination Tablet has More Favorable Effects on Lipoprotein Particle Size and Subclass Distribution Compared to Atorvastatin and Simvastatin.  Preventive Cardiology. 2003;6:179-188  (Discusses the therapeutic effects of lipid-altering drugs in a patient population consistent with metabolic syndrome.)

Bays HE.  Atherogenic Dyslipidaemia in Type 2 Diabetes and Metabolic Syndrome: Current and Possible Future Treatment OptionsBr. J Diabetes Vasc Dis 2003;3(5)356-360

Brier ME, Bays HE, et. al. Pharmacokinetics of Oral Glyburide in Subjects with Non-Insulin Dependent Diabetes Mellitus and Renal Failure. American Journal of Kidney Diseases 1997: Vol 29, No 6 (June): 907-911.

Bays HE, Dujovne CA. Management of Multiple Cardiovascular Risk Factors in Primary Care. Resident and Staff Physician 1994;40:1-28

Bays HE, Pfeifer MA; Peripheral Diabetic Neuropathy. Medical Clinics of North America Nov. 1988;72:1439-1464

 

ABSTRACTS

Harold E. Bays, Kathleen M. Fox, Susan Grandy, for the SHIELD Study GroupValidated Functional Scales Among Adults with and without Type 2 Diabetes Mellitus: Study to Help Improve Early Evaluation and Management of Risk Factors Leading to Diabetes (SHIELD) Poster presentation. American Diabetes Association 73 Scientific Session Chicago Ilinois USA June 21-25 2013

Ashely R Waters, Harold Bays, James Anderson, James E. Painter. The Effect of Raisins on Blood Glucose. Food & Nutrition Conference & Expo (FNCE). October 19 - 22 2013 Houston Texas USA

Eliot A. Brinton, Christie M.. Ballantyne, Harold E. Bays, John J. Kastelein, Rene A. Braeckman, Paresh N. Soni.  629-P - Effects of Icosapent Ethyl on Lipid and Inflammatory Parameters in Patients with Diabetes Mellitus-2 and Residual Elevated Triglycerides (200-500 mg/dL) on Statin Therapy at LDL-C Goal: The ANCHOR Study. European Society of Cardiology Congress. August 25 - 29, 2012. Munich Germany

Harold E. Bays, Kathy Schmitz, Amber Christian, Michelle Ritchey, James W. Anderson.  2301-Po - Raisins And Glucose: A Randomized, Controlled Trial.  American Diabetes Association Scientific Session.  June 8 – 12, 2012.  Philadelphia PA USA

Eliot A. Brinton, Christie M.. Ballantyne, Harold E. Bays, John J. Kastelein, Rene A. Braeckman, Paresh N. Soni.  629-P - Effects of AMR101 on Lipid and Inflammatory Parameters in Patients with Diabetes Mellitus-2 and Residual Elevated Triglycerides (200-500 mg/dL) on Statin Therapy at LDL-C Goal: The ANCHOR Study  American Diabetes Association Scientific Session.  June 8 – 12, 2012.  Philadelphia PA USA

Bays H. Prevalence of Metabolic Risk Among Individuals with Defined Metabolic Risk Factors and Type 2 Diabetes Mellitus. Final Results of the SHIELD Study - Epidemiologic and Public Policy Considerations from a 5-Year Prospective Diabetes Mellitus Study. Podium/Oral Presentation. American Diabetes Association 71 nd Scientific Session June 24-28, 2011 San Diego California USA

Bays H, Schwartz S, Greenway F, Clapper B, Wang W, Kim D, Dunayevich E. Naltrexone SR/Bupropion SR Therapy in Overweight/Obese Subjects with Type 2 Diabetes Mellitus: Effects on Glycemic Control after Accounting for the Influence of Rescue Medications for Hyperglycemia. Abstract 1866 Guided Audio Poster Presentation. American Diabetes Association 71 nd Scientific Session June 24-28, 2011 San Diego California USA

Bays H, Kolberg L, Bell M, Frestedt J, Anderson J. Barley ²Glucan Beverage Improves Insulin Sensitivity in Individuals at High Risk for Diabetes Mellitus. Abstract 2355−PO American Diabetes Association 71 nd Scientific Session June 24-28, 2011 San Diego California USA

Bays HE, Davidson M, Schwartz SL, Price C, Sasiela WJ, Parris M, Meagher E, Rader D. Body Weight Reducitons with Low Dose AEGR-733, a Microsomal Triglyceride Transfer Protein Inhibitor: Results from Three Phase 2 Trials. Abstract Poster Presentation #471. American Diabetes Association 69th Scientific Session June 5-9, 2009 New Orleans LA USA

Conard S, Bays H, Leiter L, Bird S, Lin J, Hanson M, Shah A, Tershakovec AM. Ezetimibe Added to Atorvastatin Compared with Titration of Atorvastatin in Patients at High Risk of Coronary Heart Disease with Diabetes Mellitus or Metabolic Syndrome. Abstract Poster Presentation #669. American Diabetes Association 69th Scientific Session June 5-9, 2009 New Orleans LA USA

Bazata DD, Bays HE, Fox KM, Grandy S. Self-Reported Nutritional Habits among Adults with and without Type 2 Diabetes Mellitus. Abstract Poster Presentation #1736. American Diabetes Association 69th Scientific Session June 5-9, 2009 New Orleans LA USA

Gavin JR, Rodbard HW, Fox KM, Grandy S, Bays HE. Abstract Poster Publication #2275. Waht Does "Ethnicity" Really Mean in Demographics of Diabetes Mellitus? American Diabetes Association 69th Scientific Session June 5-9, 2009 New Orleans LA USA

Bays HE, Maki KC, Carter RN, Doyle RT, Stein E. Effect of Prescription Omega-3 Fatty Acids on Body Weight in Patients with Very High Triglyceride Levels. Abstract Poster Publication #2444. American Diabetes Association 69th Scientific Session June 5-9, 2009 New Orleans LA USA

Bays H, Goldfine AB, Jones MR, Abby SL, Misir S, Nagendran S. Long-term Use of Colesevelam HCl in Subjects with Type 2 Diabetes Mellitus on Metformin Therapy. Poster Presentation American Association of Clinical Endocrinologists 18th Annual Meeting May 15 & 16, 2009. Houston Texas USA

Bays HE, Setze CM, Kelly MT, Sun H, Sleep DJ, Stolzenbach JC. ABT-335 Effects upon Glucose Levels in Patients with Mixed (Atherogenic) Dyslipidemia and "Pre-Diabetes." The Endocrine Society 90th Annual Meeting Podium/Oral Presentation June 18th 2008 San Francisco USA

Bays HE, Maccubbin D, Shah A, Lin J, Sisk CM, Paolini JF. Lipid-Altering Efficacy of ER Niacin/Laropiprant in Dyslipidemic Patients with Metabolic Syndrome American Diabetes Association 68th Scientific Session Podium/Oral Presentation June 7, 2008 San Francisco USA

Bays HE, Abby SL, Jones MR. Dual Efficacy: A1c and LDL-C Lowering With Colesevelam HCl in Patients with Type 2 Diabetes Mellitus. Poster and Podium/Oral Presentation. National Lipid Association Scientific Session. May 31, 2008. Seattle Washington USA

Bays HE, Rodbard HW, Fox KM, Fox KM, Grandy S.  Impact of Type 2 Diabetes Mellitus on Prescription Medication Burden and Out-of-Pocket Expenses.   Poster presentation.  American Diabetes Association Annual Meeting. San Francisco California USA. June 8, 2008

Bays HE, Rodbard HW, Fox KM, Grandy S.  Changes in Weight, BMI, and Waist Circumference after 2 Years in Respondents with or at Risk for Metabolic Disease: Study to Help Improve Early evaluation and management of risk factors Leading to Diabetes (SHIELD)  World Congress on Insulin Resistance Syndrome.  Poster presentation.  Boston Massachusetts October 11, 2007

Bays HE, Abby S, Truitt K, Jones MR.  Colesevelam HCl Reduces Cholesterol and Glucose Levels When Added to Metformin-Based Therapy in Patients with Type 2 Diabetes Mellitus.  Journal of Clinical Lipidology.  Vol 1, No 5, October 2007 Abstract #401 DALM October 4-7 New York, New York. USA

Bays HE, Goldberg RB, Truitt K, Dmuchowski C, Jones MR.  Effect of Colesevelam HCl on Glycemic Control in Subjects with Type 2 Diabetes Mellitus Receiving Metformin Monotherapy   485-P abstract. American Diabetes Association 67th Scientific Sessions.  Chicago Illinois June 24 2007

Goldberg RB, Bays HE, Truitt K, Dmuchowski C. Jones MR. Colesevelam HCl Improves the Lipid Profile in Subjects with Type 2 with Inadequate Glycemic Control on Metformin American Diabetes Association.  484-P abstract.  67th Scientific Sessions.  Chicago Illinois June 24 2007

Bays HE, Goldberg RB.  Truitt K, Dmuchowski C, Jones MR.  Addition of Colesevelam HCl to Patients with Type 2 Diabetes Mellitus Inadequately Controlled on a Metformin-Based Therapy Improves Glycemic Control.  Poster Presentation Abstract #204.  AACE 16th Annual Meeting and Clinical Congress, Seattle Washington USA.  Friday, April 14th, 2007

Fox KM, Gandhi SK, Ohsfeldt RL, Blasetto J, Bays HE.  Effectiveness of Rosuvastatin in LDL-C Lowering and National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III Goal Attainment compared to other Statins among Diabetes Patients.  2448-PO  Diabetes - June Supplement.  67th Scientific Sessions Chicago Illinois USA (June 22 - 26) Abstract Book 2007

Bays HE, Davies MJ, Shah A, Macdonell G, Gumbiner B.  Effects of Coadministered Ezetimibe and Fenofibrate in Mixed Dyslipidemic Patients with Metabolic Syndrome (Published abstract only) Diabetes 55(Suppl. 1): A519 (#2245-PO), June 2006

Bays, H. E., Davies, M., Shah, A., Macdonell, G., Gumbiner, B.  Effects of co-administered ezetimibe (EZE) and fenofibrate(FENO) in mixed dyslipidemic patients with metabolic syndrome (METS). Diabetes 2006; 55 (Suppl. 1):A519

Weinstein SP, Tardiff BE, Bays HE, Guler HP, Aronne LJ.  Weight Loss with Recombinant Human Variant Ciliary Neurotrophic Factor (CNTF [AXOKINE]) Improves Glycemic Control in Overweight/Obese Subjects, Especially in Those with Abnormal Glycemic Parameters at Baseline  Diabetes 2004.  Supplement.  Abstract Publication Number:  2523-PO  64th Scientific Sessions
 

Glicklich A, Bays H, Russell T, Weinstein S, Hollander P.  AXOKINE Ò Promotes Weight Loss in Overweight and Obese Patients with Type 2 Diabetes Mellitus.  Poster Abstract 471-P.  NAASO's 2003 Annual Meeting.  October 11-15, 2003  Ft. Lauderdale Florida

Bays-Harold; Mitchel-Yale; Mercuri-Michele. Effect of simvastatin on high-density lipoprotein cholesterol and apolipoprotein A-I in patients with elevated triglyceride blood levels. Presented at the 61st Scientific Sessions of the American Diabetes Association, Philadelphia, Pennsylvania, USA, June 22-26, 2001. Diabetes 2001;50(Suppl 2):A141.

 

BOOKS

Bays HE, Self MA. "Insulin Therapy in Pregnancy" in Danakas GT, Pietrantoni M. "Practical Guide to The Care of the Gynecologic/Obstetric Patient" 1997: Mosby-Year Book Inc.

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