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A Personal Message From Dr. Dominguez


Time For A Change

I know you want to lose weight because you clicked on this NEW Diet button. Let me ask you why are you interested in losing weight. Is it because you want to look better? Is it because you don’t want to increase your risk of Diabetes, Heart Attack, High Blood Pressure, LDL, Triglycerides, and Inflammatory Joint Disease? Is it because you already have these diseases and want to improve your health? Is it because you have no energy, get tired easily, or have no gusto for life? OK, I can help you.

Remember that looking better is easy, but it's a quick fix that won't last. Becoming and STAYING healthy requires a life-long changes in your Core Behaviors: eating habits and exercise levels. I can help you with these life-long changes. But first I want you to understand why I believe you should improve your overall medical and physical health, IT'S FOR YOUR LIFE, not your looks.

Many of you have asked me to provide you with my lecture slides and materials. So, here it is (the mini-version).

Let’s look at the facts. Throughout much of recorded history, people struggled to get enough food to eat. Today, many people in the world, and even in the United States, remain undernourished. However, the majority of Americans face the opposite situation: they are overweight and find it difficult to lose the unwanted pounds. This is a major public health issue because being overweight can lead to serious health problems and death.


Every year in the United States, about 300,000 adults die from causes related to excess body weight. Look at the slide on the right and focus on the orange bars. Since before 1998 we have shown that if you have diabetes, your risk of a first heart attack is 20%; and if you had a heart attack and are diabetic then your risk of a second MI is 50%. That’s flipping your lucky coin every morning to see if you live or die.

Why do I need to lose weight if I am overweight?

Being overweight increases your risk for high blood pressure, heart disease, stroke, diabetes, and some forms of cancer. If you are overweight, losing just 5 to 10% of your weight and keeping it off lowers your risk for developing most of these diseases.


How can I know if I am overweight?

The number you see on the scale doesn't necessarily tell you whether you need to lose weight. That's because 2 people of the same height and weight can have different bone structures. They may carry different amounts of muscle and body fat. For most adults, determining your body mass index (BMI) and waist size are reliable ways to tell whether you are overweight and to estimate your risk for health problems.

Your BMI uses your height and weight to estimate how much fat is on your body. A BMI of at least 25 indicates overweight. A BMI of 30 or more indicates you are obese. Generally, the higher your BMI, the higher your weight risk. Your waist size indicates whether you have an apple shape and tend to carry fat around your midsection. Your health risks increase even further with increasing waist size. A waist measurement greater than 40 inches for men or 35 inches for women indicates a significant increase in health risk.

To tell whether your weight is a health risk, you can determine your BMI and health risk with the Body Mass Index chart.

What is Metabolic Syndrome?

You might have heard me speak on Metabolic Syndrome either one on one in my office, or during a formal lecture. If you haven't, let me tell you about my passion for this disease complex. In the late 1970's as an undergraduate at the UCLA School of Public Health studying Health Education and Disease Prevention, I researched the incidence of Diabetes, High Blood Pressure, Nutrition, and Weight related problems in multi-cultural Los Angeles. In medical school at the University of Iowa, I learned the specifics of each medical disease and how one disease leads to another. At the Cleveland Clinic Department of Head & Neck Cancer - Facial Plastic Surgery, I dealt first hand with Diabetes, Obesity, Malnutrition, High Cholesterol, Heart and Vascular disease, and their resulting increased Cancer risks and post-surgery poor wound healing. At the UCLA Department of Emergency Medicine, I treated thousands of patients with preventable Acute Heart Attack, Stroke, Diabetes Out of Control, Renal Failure, Sepsis, Congestive Heart Failure....most of these patients had a significant weight problem. At the UCLA School of Public Health Masters Program in Health Services Organization Management, I learned how to build organizations that can affect the health and welfare of not "one" through direct patient care, but "many" through the application of science and technology. This is the same philosophy that drives my cosmetic "surgery" and "medicine" practice.

Today, my "medicine" practice allows me to identify, treat, and prevent Obesity induced Metabolic Syndrome and its' destructive effect on the heart, blood vessels, kidneys, lungs, brain, and endocrine system of the "one" before me and their "many" family and friends through education and my "inventions".

I firmly believe that obesity is the root cause of many of our societal medical problems. We can work together at preventing obesity early, allowing all of us and our children to live happier, longer, and without the aweful consequences of Metabolic Syndrome.

Metabolic Syndrome was first defined by an endocrinologist, Dr. Raven, who associated obesity with insulin resistance. This defining association led other physician researchers in the field of cardiology to recognize the significantly increased risk in cardiac disease in diabetic patients. Hence, Metabolic Syndrome was revealed formally in 2001 as a constellation of risk factors that accelerate atherosclerotic cardiovascular disease (ASCVD).

Cardiac Risk in Metabolic Syndrome is Greater than the Sum of its Parts

The question is constantly raised as to whether the risk for heart disease associated with the metabolic syndrome is greater than the sum of its risk factors. The answer is the YES!!

Epidemiological studies strongly show that multiple risk factors raise risk more than the sum of accompanying single risk factors; risk rises geometrically instead of linearly. This phenomenon is called multiplicative risk.

This does not include several metabolic risk factors in standard risk algorithms; which continue to increase your risk. These are a prothrombotic state, a proinflammatory state, and elevated triglyceride. This additional risk exceeds that which can be explained by standard risk factors.

Remember that because metabolic syndrome often progresses and culminates in type 2 diabetes, the syndrome's long-term risk is underestimated at any one time. Thus several lines of evidence indicate that the risk accompanying the metabolic syndrome is greater than the sum of its measured components.

In 2002, the National Health and Nutrition Examination Survey (NHANES) data published a prevalence rate of 20% to 24% for metabolic syndrome in the US adult population. The range of Metabolic Syndrome is 5% for the age group 20-29 years old to a high of 45% for both males and females age 60 – 69 years old. The graph clearly illustrates the increase in Metabolic Syndrome with age.

Metabolic Syndrome accelerates and worsens abnormal cholesterol levels or ratios, elevated blood pressure, elevated fasting blood sugars, the prothrombotic state (clotting), and the proinflammatory state. For instance:

Cholesterol: abnormal cholesterol levels or ratios consists of elevated triglycerides, low levels of high-density lipoproteins (HDL), and increased levels of low density lipoproteins (LDL).

Glucose: Elevated fasting glucose falling in the range of either pre-diabetes or diabetes.

Clotting: A prothrombotic (clotting) state signifies anomalies in procoagulant (clot forming) factors (i.e., increases in fibrinogen and factor VII), anti-fibrinolytic (clot dissolving) factors (i.e., increases in plasminogen activator inhibitor-1), platelet aberrations, and endothelial (blood vessel)dysfunction.

Inflammation: A proinflammatory state is characterized by elevations of circulating acute and chronic phase reactant proteins (e.g., HS-CRP, ESR, etc).

This age adjusted graph demonstrates the metabolic diseases found as a percentage in the diagnosis of Metabolic Syndrome (Diabetes, Hypertension, Cholesterol abnormalities: HDL/TG, and increased abdominal girth).

The major underlying risk factors are obesity and insulin resistance. The risk associated with obesity is best identified by increased waist circumference (visceral obesity). Insulin resistance can be secondary to obesity. The increasing prevalence of metabolic syndrome in the U.S. and worldwide, seems to be driven largely by more obesity exacerbated by sedentary lifestyles. Losing 10% of your body weight significantly IMPROVES your Metabolic Syndrome risk profile.

Obesity and Metabolic Syndrome

Obesity as defined by a BMI of greater than 30 when accompanied by an abdominal girth of greater than 35 for a woman or greater than 40 for a man. Visceral (abdominal) fat is an endocrine organ that secretes various proteins.

Cytokine proteins are produced by fat cell and are associated with inflammation of the heart, arteries, kidneys, muscles, and joints. Fat cell cytokines are interleukin 1 and 6, C-Reactive Protein, tumor necrosis factor alpha, adiponectin, and plasminogen activator inhibitor 1.

Losing Weight vs. Not Gaining Weight

The average American gains 40 pounds between the ages of 20 and 40. Ever ask WHY. Because as you age, your neuro-endocrine system begins to slow down. This in plain english means that your thyroid, adrenal, pancreas, and testicles/ovaries glands don't work as well so you begin to feel sluggish and constantly tired, leading to decreased physical activity and weight gain. As you gain weight, your body begins to store the energy that you used to burn through exercise into FAT. Now the fat becomes another endocrine organ, releasing enzymes to make you fatter, more tired, and achy.

The more fatter, tired, and achy you become, the more gratification you receive from eating unhealthy foods. This occurs through stimulation of our “feel good” neuro-endocrine EC system. The EC system gives you a strong sense of well-being and satisfaction through eating. The more you eat, the better and more satisfied you feel. The better and more satisfied you feel, the more you want to eat.

This cycle continues until you are out of control. Your intestines start to slow down and have decreased secretion of proteins to absorb essential nutrients (B12, Folate, etc) and micronutrients (zinc, chromium, etc,). Your sleep-wake cycle falters. Overall, your neuro-endocrine system becomes markedly depressed and your weight gain accelerates. It's a vicious cycle.

At the end you notice your weight is profound, your liver is fatty and enlarged, your heart is weak, your lipid levels are extremely abnormal, and your joints achy when you move.

Modest Increases of Thyroid-Stimulating Hormone (TSH) Linked With Weight Gain

Caroline S. Fox, MD, MPH, from the National Heart, Lung, and Blood Institute's Framingham Heart Study in Framingham, Massachusetts, and colleagues. "We assessed whether variations in thyroid function within the reference (physiologic) range are associated with body weight." This study included 2407 participants in the Framingham Offspring Study who attended 2 consecutive routine examinations, were not receiving thyroid hormone therapy, and had baseline serum thyrotropin (TSH) concentrations of 0.5 to 5.0 mIU/L and follow-up concentrations of 0.5 to 10.0 mIU/L. During 3.5 years of follow-up, the relationship of baseline TSH concentrations with body weight and body weight change was determined.

"Thyroid function (as assessed by serum TSH concentration) within the reference range is associated with body weight in both sexes," the study authors write. "Our findings raise the possibility that modest increases in serum TSH concentrations within the reference range (Clinical Hypothyroidism) may be associated with weight gain."

"The identification of change in thyroid function as a risk factor for weight gain might help guide research into the identification, prevention, and treatment of individuals at risk for the development of excess adiposity," the study authors write.

The National Heart, Lung, and Blood Institute's Framingham Heart Study supported this study. The Archives of Internal Medicine authors have been supported by the National Heart, Lung, and Blood Institute and the National Institute of Diabetes and Digestive and Kidney Diseases.

Starting Therapy With High-Dose Levothyroxine Is Safe in Asymptomatic Cardiac Patients by Laurie Barclay, MD

June 23, 2003 — Starting therapy with high-dose levothyroxine (L-T4) is safe in asymptomatic cardiac patients, according to the results of a prospective, double-blind, randomized trial presented on June 21 at the 85th annual meeting of The Endocrine Society (Endo 2003) held in Philadelphia, Pennsylvania. Previous studies addressing the safety of high-dose L-T4 in cardiac disease have usually started with a low dose and have gradually increased the dose. These studies have been "anecdotal, retrospective, biased," according to senior author Arie Berghout, FRCP, an endocrinologist and head of the Department of Medicine at Medical Center Rotterdam in South Netherlands. "This is the first randomized, double-blinded trial," he told Medscape. "The implication is that you don't have to treat your patients with primary hypothyroidism with a low starting dose of l-thyroxine but can give the full replacement dose from the start, given that there is no history of angina pectoris."

In this study, 51 consecutive hypothyroid patients with normal dobutamine stress echocardiography were randomized to L-T4 treatment at a dose of either 1.6 µg/kg body weight or 25 µg daily, in stratified blocks according to thyroid-stimulating hormone (TSH) level. Mean starting dose was 128 vs. 25 µg L-T4, given in liquid form at bedtime. The dose of L-T4 was adjusted every four weeks.

Biochemical measurements, bicycle ergometry (XECG) and symptoms scores were obtained at baseline and at four- to 12-week intervals until 48 weeks. At baseline, both groups were similar in age, sex distribution, TSH, FT4, TT3, total cholesterol, body mass index, heart rate, blood pressure, and symptoms score.

At four weeks, mean values for the 1.6 µg/kg group vs. the 25 µg group, respectively, were TSH, 15.5 vs. 53.1 mU/L (P = .01); FT4, 18.7 vs. 10.4 pmol/L (P < .001); TT3, 2.3 vs. 1.8 nmol/L (P = .01); heart rate, 70 vs. 64 bpm (P <.05). Cholesterol levels and symptoms score were similar in both groups, and blood pressure and body mass index did not change. None of the patients had angina pectoris or serious arrhythmias during treatment. One patient receiving 1.6 µg/kg had a nonsignificant ST depression on XECG at 12 and 24 weeks. At 12 weeks, exercise performance improved by 14% in the 1.6 µg/kg group vs. 0% in the 25 µg group, but at 24 weeks and thereafter, both groups were comparable in all respects, including exercise performance and quality of life.

"No patient in our study [had] any signs of silent cardiac ischemia either by bicycle ergometry or by dobutamine stress test, in contrast for instance to patients with type 2 diabetes mellitus," Dr. Berghout said. "This raises the question whether primary hypothyroidism is indeed a risk factor for coronary ischemia. It could be that a far more important effect of hypothyroidism on the heart is diastolic dysfunction, which has been demonstrated in several studies. In that case, more rapid restoration of cardiac function could be more important."

There was no external funding for this study, and the authors report no pertinent financial disclosures. Endo 2003: Abstract P3-674. Presented June 21, 2003. Reviewed by Gary D. Vogin, MD

L-Thyroxine Beneficial in Subclinical Hypothyroidism

NEW YORK (Reuters Health) Jun 08 - Treatment of adults with subclinical hypothyroidism with L-thyroxine has beneficial effects on cardiovascular risk factors, endothelial function and quality of life, clinicians from the UK report.

In a randomized crossover study, they treated 100 individuals with subclinical hypothyroidism without previously treated thyroid or vascular disease with 100 g L-thyroxine or placebo daily for 12 weeks each. The subjects, whose average age was 53.8 years, had mean TSH levels of 6.6 (1.3 mIU/liter).

In the June Journal of Clinical Endocrinology and Metabolism, Dr. Salman Razvi from Queen Elizabeth Hospital, Gateshead and colleagues report that L-thyroxine therapy was associated with "significant, although modest, improvement across a wide spectrum of cardiovascular risk factors." Compared to placebo, L-thyroxine treatment reduced total cholesterol from 231.6 to 220 mg/dL (p < 0.001 and LDL cholesterol from 142.9 to 131.3 mg/dL (p < 0.05). If sustained long term, this reduction in LDL-C, the researchers estimate, "would result in a relative reduction in 10-year cardiovascular mortality of about 10%."

"Rather surprisingly, when considering the short treatment period," L-thyroxine was also associated with a reduction in waist to hip ratio from 0.83 to 0.81 (p < 0.006). Active treatment also improved brachial artery flow-mediated dilatation (FMD), a validated surrogate marker for coronary artery endothelial function, from 4.2 to 5.9% (p < 0.001).

In a multivariate analysis, an increase in serum free T4 level was the most significant predictor of a reduction in total cholesterol or improvement in FMD, the authors report.

Fewer subjects reported tiredness while on L-thyroxine and there was a trend toward improvement in the perceived negative impact of hypothyroidism on sex life, "which is interesting and warrants further research into the underlying mechanism," Dr. Razvi and colleagues write.

"However, this is not an isolated finding, as L-thyroxine has been shown to improve impaired sexual function and performance in men with overt hypothyroidism," they note. "This may be due to the effect of thyroid hormones on psychological aspects (e.g. reducing tiredness)."

Dr. Razvi and colleagues write that long term studies are needed to determine whether the apparent short term benefits of L-thyroxine therapy in subclinical hypothyroidism will translate into reduction in cardiovascular illness and death.

J Clin Endocrinol Metab 2007;92:1715-1723.

Effects of Low Testosterone on Future Development of Type 2 Diabetes and/or Metabolic Syndrome

A recent meta-analysis reported that men in the upper vs lower dichotomy of testosterone values had a 42% lower risk of developing type 2 diabetes. Included in this analysis was a large prospective Finnish study that also looked at future development of metabolic syndrome. In their report they compared men with testosterone levels in the lower quartile vs those in the upper quartile; the average follow-up was 11 years. They found that:

• 35% of men in the lowest quartile had developed metabolic syndrome alone
• 45% had developed metabolic syndrome and type 2 diabetes
• 33% had developed type 2 diabetes alone
• 20% failed to develop either metabolic syndrome or type 2 diabetes.

The possibility that low testosterone levels predict future development of the metabolic syndrome also is supported by a report from the Massachusetts Male Aging Study.

The Hypogonadism in Males (HIM) study is an industry-sponsored study that measured testosterone levels in men 45 years of age and older who presented to 130 offices of primary care clinicians over a 2-week period and who consented to participate in the study:

• Testosterone levels < 300 ng/dL were found in 836 of 2165 men (38.6%).
• The prevalence increased from 34% in the 45- to 54-year-old age group to 39.9% in the 65-74,
45.5% in the 75-84, and 50% in the 80+ age groups.
• The prevalence of low total testosterone levels were found in men with obesity (52.4%), diabetes (50%), hypertension (42.4%), hyperlipidemia (40.4%), osteoporosis (44.4%).

Testosterone replacement in men with low testosterone levels can bring about a number of beneficial effects.

  • Increased bone density
  • Increased skeletal muscle mass and perhaps strength
  • Decreased fat mass
  • Improved libido and perhaps erectile function
  • Increased red blood cell mass
  • Improved mood
  • Improved cognition
  • Reduced cardiovascular events
  • Because men under 50 have more cardiovascular events than women in the same age group, it has been thought that testosterone may be causative, but other epidemiologic data suggest that normal testosterone levels may in fact decrease cardiovascular disease. As yet, no studies have been undertaken to evaluate the effects of testosterone replacement on cardiovascular events.

    It is important to measure serum testosterone in patients receiving replacement therapy to determine whether treatment is raising the level to the desired range. The serum level required to treat organ systems varies, but in general I strive to get the levels in the 400-600 range. Some studies recommend a range of 350-500 in older men.

    In the older man it is very important to monitor for potential adverse effects of testosterone treatment and for delivery system-specific adverse effects. The most common adverse effect is an excessive rise in the hematocrit (> 54%). When this occurs, I stop treatment to allow the hematocrit to normalize, after which treatment may be resumed at a lower dose.

    The most serious safety concern is the potential for stimulating an occult prostate cancer to become a clinical prostate cancer. We can use the prostate cancer risk calculator (http://www.compass.fhcrc.org/edrnnci/bin/calculator/main.asp) to evaluate risk prior to initiating treatment. Should my patient develop a significant rise in hematocrit or PSA, or an abnormal DRE, it would be easier to stop treatment while further evaluation is being conducted. This usually is of less concern after a patient has been on testosterone replacement therapy for 3 months.

    A Systematic Review of Metformin Treatment in Persons at Risk for Diabetes Mellitus

    Shelley R. Salpeter, MD; Santa Clara Valley Medical Center, San Jose, and Stanford University School of Medicine, Stanford, CA. Significant improvements in weight, lipid profiles, fasting glucose levels, and insulin resistance, as well as a 40% decrease in the progression to new-onset diabetes over time, have been shown with metformin treatment among individuals at risk for diabetes. Studies have shown that the most successful strategy to decrease weight and the incidence of diabetes is to implement intensive lifestyle modifications in persons at risk for diabetes, although long-term sustained effects are difficult to achieve. The available evidence indicates that metformin now can be added to lifestyle interventions as an approach to the prevention of diabetes. The results of new long-term studies will show whether the metabolic improvements achieved with metformin treatment will ultimately result in a decrease in cardiovascular morbidity and mortality. http://www.cardiologyreviewonline.com/issues/articles/2008-07_01.asp

    As many of you know, I am a strong believer in the benefits of metformin in weight management. This meta-analysis confirms the use of metformin and advances its' use in weight management despite the "old school fear of lactic acidosis" as demonstrated by the article below.

    Should metformin be used to prevent diabetes in high-risk patients?

    Byron Hoogwerf, MD, Cleveland Clinic Staff Physician, Department of Endocrinology and the Preventive Cardiology Clinic, Cleveland Clinic Foundation, Cleveland, OH.

    Lifestyle and pharmacologic efforts to reduce the risk of new-onset diabetes mellitus have been the subject of multiple investigations. Retrospective and prospective studies have suggested benefits with use of glucose-lowering agents, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers. The article by Salpeter and colleagues is a meta-analysis of the metformin studies. As outlined by the authors' use of metformin is an appealing option because it is safe, produces few side effects, and is a cost-effective way to target some of the defects known to contribute to the metabolic defects associated with diabetes. I think there may be a role for the use of metformin in patients at risk of developing diabetes, but widespread use of this drug has not yet become the clinical norm. http://www.cardiologyreviewonline.com/issues/articles/2008-07_03.asp

    Eating better

    Trends in eating habits may help explain why so many people in the United States are overweight and obese today. Americans currently consume 23% more sugar than we did in 1970, and soft drinks are the major source of the added sugar in our diets. On average, the foods we ate had 24% more total fat in 2000 than in 1970. And we eat meals away from home roughly twice as much as we used to.

    DROP THE CARBS!! DROP THE FATS!!! INCREASE PROTEIN!!

    Being more active

    Regular physical activity has been shown to help prevent heart disease, type 2 diabetes and osteoporosis, as well as other chronic conditions. It is important for maintaining your good health, regardless of whether your weight is a problem or not.

    The Bella Milagros™ Executive Rejuvenation Medicine Program

    This unique Executive Rejuvenation Medicine Program thoroughly evaluates your current health status. This is a commitment from both of us to Achieve Optimal Health. In this Concierge program, you will undergo a complete history and physical examination, colon cancer screening test, urinalysis, VIP blood panel identifying your:complete blood count, electrolytes panel, Hg-A1C, kidney panel, liver panel, 5 protein thyroid function panel, inflammatory markers of the joints and heart, 4 different cholesterol values, triglycerides, DHEA, testosteron, PSA (men), micro-nutrients; ECG, Resting Cardiac ECHO, Carotid Ultrasounds, and Thyroid Ultrasound. Optional studies include a chest x-ray and Cardiac Stress Treadmill with Stress ECHO, Abdominal Aorta Ultrasound, Lower Extremity Arterial Ultrasound, and Nerve Conduction Velocities.

    Your initial visit will take between 3 and 4 hours. Once monthly, we will meet and discuss your progress in detail (45-60 minutes). Some of these tests may be repeated monthly to assess your response to our mutually agreed upon health care program.

    As you can imagine, your health insurance (PacifiCare, Blue Cross/Shield, Aetna, Cigna) won't pay for "screening" tests or for prevention of illness. If you have one of the disease states above, we may be able to get some of the tests and/or treatments paid by your PPO insurance company. We work under the assumption that they will deny your requested tests and services, and we provide you with the costs before any tests or services are rendered. If you chose to have tests or services provided, we will provide you with a detailed receipt so you can submit it to your accountant, insurance company, etc, for any future reimbursements that may be due to you by your insurance company. I'll put in the time and effort it takes to improve your health, if you are willing to do the same!

    Thank you. I hope I have provided you with enough academic information to motivate you changing your life and the lives of those you love. I look forward to seeing you at my lectures or in my office.

    May God Bless You and Your Family.

    Steven Dominguez, M.D., M.P.H.

  • UCLA School of Public Health; B.S. and M.P.H.
  • University of Iowa College of Medicine; M.D.
  • Cleveland Clinic Foundation Head and Neck, Facial Plastic Surgery Program
  • UCLA Emergency Medicine Program


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    28. 28. UK Prospective Diabetes Study (UKPDS) Group. UK prospective diabetes study 16. Overview of 6 years' therapy of type 2 diabetes: a progressive disease. Diabetes. 1995; 44(11):1249-1258.
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    30. 30. Viberti G, Kahn SE, Greene DA, et al. A diabetes outcome progression trial (ADOPT): an international multicenter study of the comparative efficacy of rosiglitazone, glyburide, and metformin in recently diagnosed type 2 diabetes. Diabetes Care. 2002; 25(10):1737-1743.
    31. 31. Nissen SE, Wolski K. Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes. N Engl J Med. 2007; 356(24):2457-2471.
    32. 32. Action to Control Cardiovascular Risk in Diabetes Study Group, Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes. N Engl J Med. 2008;358(24):2545-2559.


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    © 2004-2014 Steven Dominguez, MD, MPH All Rights Reserved.

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