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Physician formulated to RESULT in:
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Boosting your ENERGY
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Increasing your alertness
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Rejuvenating your metabolism
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Losing Weight
These days, it seems as though most people are trying to lose weight, and for good reason: about 97 million Americans are overweight or obese.
Being over-weight causes an increased risk of all-cause mortality, as well as increased morbidity from hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, stroke, gallbladder disease, osteoarthritis, sleep apnea, and other respiratory problems. In addition to certain malignancies, such as cancers of the endometrium, prostate, and breast.
The National Heart, Lung, and Blood Institute and the National Institute of Diabetes and Digestive and Kidney Disease published guidelines for the treatment of overweight and obese adults. These recommendations are intended for patients with a body mass index (BMI) ≥ 30, or ≥ 27 with obesity-related risk factors or diseases present. The guidelines recommend initial lifestyle modifications, including a reduced-calorie diet of 500-1000 calories per day, increased physical activity, and behavioral therapy. If these changes fail to produce a result in 6 months, pharmacotherapy is recommended.
These are the prescription medications approved by the US Food and Drug Administration (FDA) for weight loss: sibutramine (Meridia, by Abbott Laboratories), which inhibits the reuptake of serotonin, norepinephrine, and dopamine; orlistat (Xenical and Alli) a reversible inhibitor of gastric and pancreatic lipase which makes you expel “wet gas and floating diarrhea”; phentermine, an adrenergic medication, diethylpropion, benzphetamine, and phendimetrazine. Off-label medications for weight loss include carbohydrate and fat binders, thyroid supplements, metformin, and newer antidepressants (fluoxetine, sertraline, bupropion) and novel anticonvulsants (topiramate, zonisamide). And if all else failed, bariatric surgery is recommended in cases of extreme obesity.
Sympathomimetic amines have been used as over-the-counter diet aids, including phenylpropanolamine, Ma Huang (ephedra), and ephedrine. These products are notorious for causing dose-related increases in blood pressure that can be hazardous. When the use of phenylpropanolamine (Acutrim, by Amerifit Brands) was correlated with hypertension and stroke, the FDA banned it from the market in November 2000. Likewise, Ma Huang and ephedrine-containing supplements have been removed from the US market.
Improve your overall medical and physical health, IT'S FOR YOUR LIFE, not your looks that matter.
Remember that looking better is easy, but it's a quick fix that won't last. Becoming and STAYING healthy requires life-long changes in your Core Behaviors: eating habits and exercise levels.
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. Before 1998 if you had 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%.
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?
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.
DHEA: Dehydroepiandrosterone
DHEA and DHEAS output is maximal between the ages of 20 and 30 years and then starts a decline of approximately 2% per year, leaving a residual of 10-20% of the peak production by the eighth or ninth decade of life.
DHEA and DHEAS are interconvertible by sulfohydrolases in peripheral and adrenal tissues. Some 64-74% of the DHEAS produced each day is converted to DHEA, but only 13% of the DHEA produced is metabolized to DHEAS. In humans, the brain-to-plasma ratios for DHEA and DHEAS are 4-6.5 and 8.5, respectively, indicating a neuroendocrine role for these hormones.
DHEA and DHEAS serve as the precursors of approximately 50% of androgens in men, 75% of active estrogens in premenopausal women, and 100% of active estrogens after menopause. There appears to be a sex-specific response to DHEA replacement therapy in humans. In postmenopausal women (ages 50-65), supraphysiological doses of DHEA have predominantly androgenic effects, increasing testosterone levels approximately 300% over baseline levels.
Several mechanisms of action of DHEA and DHEAS other than their role as precursors of the sex hormones have been proposed. In the central nervous system, both DHEA and DHEAS appear to affect neurotransmitter receptors. DHEAS binds to the GABA-RC and acts as a negative noncompetitive modulator of GABA-RC. DHEA, on the other hand, has GABA-agonist effects on the GABA-RC. Also, DHEA and DHEAS have neurotrophic effects, increasing the number of neurofilament-positive neurons and regulating the motility and growth of corticothalamic projections in cultured mouse embryo brain cells.
Supraphysiological oral doses of DHEA in humans have been found to inhibit the synthesis of thromboxane A 2 in activated platelets, reduce plasma plasminogen activator inhibitor type 1 and tissue plasminogen activator antigen, increase serum levels of insulin-like growth factor 1 (IGF-1), and increase cyclic guanosine monophosphate (GMP) and nitric oxide synthesis (either directly or via increased levels of IGF-1).
These effects suggest that DHEA are beneficial in improving circulation in the microvasculature and regulating some of the risk factors of cardiovascular disease, such as platelet aggregation and ischemia. The majority of clinical studies in this area have shown an inverse relationship between DHEA or DHEAS levels and cardiovascular morbidity and mortality.
DHEA may play a positive role in modulation of the immune response. Clinical studies in elderly persons have demonstrated that oral DHEA doses of 50 mg/day increase IGF-1 levels (p < 0.01) and cause functional activation of T cells (increases in CD8+ and CD56+ cells [natural killer cells] and enhanced cytotoxic activity). Serum levels of interleukin- 6 (a proinflammatory cytokine involved in the pathogenesis of osteoporosis, rheumatoid arthritis, atherosclerosis, Alzheimer's disease, Parkinson's disease, and beta-cell malignancies) increase significantly with age and are inversely correlated with serum DHEA and DHEAS levels (p < 0.001). In addition, DHEA, DHEAS, and androstenedione inhibit the production of interleukin-6 by peripheral blood mononuclear cells in a concentration-dependent manner (p < 0.001).
Serum Dehydroepiandrosterone Sulfate Levels Predict Longevity in Men: 27-Year Follow-Up Study in a Community-Based Cohort
Objectives: To determine whether serum dehydroepiandrosterone sulfate (DHEAS) levels could predict longevity in residents.
Results: Baseline DHEAS levels were higher in men than in women and decreased with age in both sexes. In a Cox proportional hazards model, age, DHEAS (inversely), blood pressure, and fasting plasma glucose were significantly associated with shorter longevity in men but not in women. Of these variables, high DHEAS levels in men were the strongest predictor of longevity (β = -2.032, hazard ratio = 0.131, 95% confidence interval = 0.029–0.584 in the Cox proportional hazards model after adjustment for age). The Kaplan-Meier survival curve, stratified according to tertiles of DHEAS levels, in men after adjustments for age, systolic blood pressure, and fasting plasma glucose showed significantly (log-rank stat = 10.6; P <.001) greater longevity in the highest group (200 μg/dL) than in the moderate (130–199 μg/dL) or lowest groups (129 μg/dL).
Conclusion: This 27-year study in a community-based cohort indicated that DHEAS level may be a predictor of longevity in men, independent of age, blood pressure, and plasma glucose.
Effects of Low Testosterone on Future evelopment 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:
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35% of men in the lowest quartile had developed metabolic syndrome alone
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45% had developed metabolic syndrome and type 2 diabetes
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33% had developed type 2 diabetes alone
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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:
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Testosterone levels < 300 ng/dL were found in 836 of 2165 men (38.6%).
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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.
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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.
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· Increased bone density
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· Increased skeletal muscle mass and perhaps strength
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· Decreased fat mass
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· Improved libido and perhaps erectile function
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· Increased red blood cell mass
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· Improved mood
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· Improved cognition
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· 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.
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.
Stress and Exercise: Getting the Balance Right for Aging Immunity
The immune response is negatively modified by both aging and chronic stress. The effects extend to both the innate and adaptive immune systems and have clinical significance in that they combine to result in reduced vaccination responses and an increased incidence and severity of infections and mortality. An altered stress reaction, as a result of adrenopause, may be a significant component of immune suppression at times of chronic stress. Several interventions have been proposed to improve immunity, and we hypothesize that regular moderate aerobic exercise may have real benefits for immunity. At times of physical stress, such as after a hip fracture or surgery, short-term pharmacological intervention with DHEA to counteract elevated stress hormones is likely to be more appropriate. We conclude that maintaining a healthy balance of stress hormones is essential to optimizing immunity.
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.
May God Bless You and Your Family.
Steven Dominguez, M.D., M.P.H.
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UCLA School of Public Health; B.S. and M.P.H.
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University of Iowa College of Medicine, M.D.
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Cleveland Clinic Foundation Head and Neck, Facial Plastic Surgery Program
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UCLA Emergency Medicine Program
Now the legal stuff: The statements herein have not been evaluated by the FDA and are not intended to advise, diagnose, treat, cure, prevent, or infer medical care. Seek medical advice from your physician prior to purchasing or using any products represented in this website.
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