The Harvard-educated physician and New York Times best-selling author of The Hormone Cure shows you how to grow new receptors for your seven metabolic hormones, making you lose weight and feel great fast! When it comes to weight loss, most people don't think about hormones. But when you develop resistance to your seven major metabolic hormones--cortisol, thyroid, testosterone, growth hormone, leptin, insulin, and estrogen--your body adjusts by increasingly raising your hormone levels and ultimately slowing down your metabolism. And a slower metabolism leads to weight gain and difficulty losing weight. The solution, Dr. Sara Gottfried contends, is to reset the efficiency of your hormones by repairing and growing new hormone receptors. Based on leading scientific research, The Hormone Reset Diet is her proven weight-loss and energy program to reverse hormone resistance in just three weeks. It will help you: Boost your metabolism and calorie burning by growing new and fresh thyroid receptors Increase your weight loss by rebalancing estrogen and progesterone receptors Reverse your aging by resetting glucocorticoid receptors (for better processing of cortisol) For the last 20 years, this Harvard-MIT educated physician has helped thousands of women address the root hormonal causes of what bothers them most: excess weight, lack of energy, aging, and illness. Going beyond her best-selling The Hormone Cure, this program is the next generation of her deep understanding of hormonal optimization for rapid weight loss. PLEASE NOTE: When you purchase this title, the accompanying reference material will be available in your My Library section along with the audio. 1. Language: English. Narrator: Tanya Eby. Audio sample: http://samples.audible.de/bk/harp/004366/bk_harp_004366_sample.mp3. Digital audiobook in aax.
Prolonged stress has long been shown to have major effects on the development of both type of diabetes mellitus, Type 1 and Type 2. Type 1 diabetes is an autoimmune disease that is characterized by the immune system attacking self-antigens. There is a failure or breakdown in immunological tolerance to allow this to happen. Prolonged physical or emotional stress can activate the hypothalamus-pituitary-adrenal (HPA) axis to induce production of the stress hormone glucocorticoid, causing abrupt thymus involution and result in escape of autoreactive T- cells. Though regulatory T-cells (Treg) are present in the circulation, they are unable to suppress the autoreative T-cells from initiating the destruction of -cells and the subsequent development of Type 1 diabetes. Stress also causes metabolic disturbances, including altered hepatic glucose metabolism, increased peripheral insulin resistance and hyperglycemia. Glucocorticoid is the potential contributor to the chronic hyperglycemia that results in insulin resistance and -cell dysfunction via the generation of oxidative stress which ultimately leads to the development of Type 2 diabetes.
Background and aimAdrenarche [the increase in adrenal androgen (AA) secretion] and puberty are two importantevents in human’s growth and maturation. Children with premature adrenarche or precociouspuberty are at a risk for the development of hormone-related cancers or chronic disease later inlife. Childhood nutritional status has been suggested to be associated with pubertal timing,whether it is also relevant for adrenarche is not clear. Therefore, the first aim of this thesis wasto examine whether body composition and certain dietary intakes may influence AA productionin children.Excess adrenal steroid hormone [especially AA and glucocorticoid (GC)] exposures caninfluence somatic growth and sexual maturation - two important physiological signs of pubertaldevelopment. The evidence for the role of them in the physiological range in pubertal timing islimited. Accordingly, the second and the third aims were to examine the association ofprepubertal AA and GC status respectively with early and late pubertal markers, independent ofnutritional status.Evidence of growth promoting properties of low circulating concentration of estrogens duringchildhood also exists, however, further elucidation of the role of estrogens in the pubertal timinghas been hampered so far by the lack of a sensitive measurement method. The last aim was toinvestigate prepubertal urinary estrogen (E) excretion level (using a recently developed isotopicdilution/gas chromatography-mass spectrometry method) and its association with pubertalmarkers. Data came from the prospective DOrtmund Nutritional and AnthropometricLongitudinally Designed (DONALD) Study, which observes diet, growth, and metabolism inhealthy children from birth until young adulthood.ResultsFour consecutive analyses (Studies I-IV) were performed. In Study I (n=137), among all theexamined anthropometric (fat mass and fat free mass) and dietary (protein, fat and fiber intake,glycemic index and load) factors, only fat mass and animal protein intake were positivelyassociated with AA-secretion and explained 6% of total AA variation even after accounting forthe indices of major steroidogenic enzyme activities. Although animal protein intake and AAsecretion were associated with each other, Study II (n=109) showed that the negativeassociations of AA secretion with ages at Tanner stage 2 for breast (B2, girls), genital (G2,boys) and pubic hair (PH2, boys and girls) development were independent of animal proteinintake and the negative associations of animal protein intake with the start of pubertal growthspurt (ATO) and age at peak height velocity (APHV) were independent of AA. Children with ahigher AA secretion had a 1.5 yrs earlier begin of PH2, a 0.8 yrs earlier begin of B2_G2, and0.2 yr shorter duration of pubertal growth acceleration than those with a lower one. In contrastto AA, GC secretion [Study III (n=110)] was positively associated with pubertal timing and thisassociation seemed to be sex specific, i.e. only in girls. Girls with higher prepubertal GCsecretion reached ATO 0.7 yrs later and menarche 0.9 yrs later, age at B2, PH2 and PHVtended also to occur later. In Study IV (n=120), urinary E excretions were not associated withATO, APHV, or age at PH2, but with duration of pubertal growth acceleration in both sexes.Girls with higher E levels reached B2 0.9 yr and menarche 0.3 yrs earlier than girls with lowerone. Prepubertal E production was not associated with age at G2 in boys.ConclusionsBody fat mass may relevantly influence prepubertal adrenarchal androgen status and animalprotein intake may also make a small contribution to children’s AA-secretion levels. Prepubertalvariations of steroid hormones (AA, GC, and E) in physiological range appear to be differentlyinvolved in the modulation of pubertal timing in healthy children. Higher AA and E secretion maynot be critical for the earlier onset of pubertal growth spurt and APHV, but precipitate a shorterpubertal growth spurt in boys and girls. In girls, higher AA or E production predicts a notablyearlier onset of breast development, however age at menarche appears to be only determinedby E. In boys, AA but not E is relevant for genital development. GC may influence pubertaltiming of girls but not of boys. Higher GC secretion, as a marker of higher stress activity,predicts notably later onset of pubertal growth spurt and menarche. Breast and pubic hairdevelopment as well as APHV may also tend to occur later.
Hormonal dysfunction can have a major and often complex impact on all key components of the metabolic syndrome. This book comprises state-of-the-art reviews on the subject written by recognized experts in the field of endocrinology. Each chapter covers specific manifestations associated with the metabolic syndrome in classic endocrine diseases. Compelling questions are highlighted and future directions presented. The topics covered include hypopituitarism, adrenal insufficiency, acromegaly, glucocorticoid excess, androgen excess, hypogonadism, prolactin, and thyroid and parathyroid hormone abnormalities. This book is meant to inspire subsequent research related to metabolic complications in endocrine diseases, thus enabling early detection as well as prompt and appropriate management.
Over recent years, impressive advances in genetic/epigenetic technology have greatly improved the understanding of the pathogenesis of pediatric endocrine diseases due to hormone resistance and hypersensitivity. This book presents reviews of thyroid hormone and thyroid hormone receptor resistance, and genetics and epigenetics of parathyroid hormone resistance. Abnormalities of the pituitary-gonadal axis affecting puberty as well as androgen receptor are covered. Novel insights into the diseases affecting ACTH, glucocorticoid and aldosterone receptors are discussed. Further chapters address new aspects of the physiology of the GH and IGF-1 axis as well as the diseases related to GH-IGF-1 receptor and post-receptor signaling defects. A key chapter on metabolic insights into insulin resistance is also included. Covering clinical and genetic aspects of hormone resistance and hypersensitivity, this book will be a useful tool in the hands of scientists, physicians and other healthcare professionals who wish to be up to date with novel research findings in this area.
Chronic Psychological stress has several adverse effects both on HIV- people and on HIV+ patient. When the HIV- people are concerned, stress makes them more susceptible to HIV infection. T-cells have CXCR4 receptor and Macrophage have CCR5 receptor which can bind with both glucocorticoid and catecholamine hormone. HIV has GP120 protein which has to bind with both CD4 and CXCR4/CCR5 receptor for its entry into the host cells. Mental stress increases glucocorticoid and catecholamine concentration in blood. When these stress hormones, glucocorticoid and catecholamine, bind with the CXCR4/CCR5 receptors, cAMP signaling pathway gets activated. This signal transduction pathway leads to the synthesis of more CXCR4 and CCR5 receptors by those cells, which in turn become more susceptible to HIV infection. Stress inhibits Th2 when the cell produces INF- as a response to viral attacks. So that other cells remain vulnerable to viral infection. When T-cell count is decreased in the blood, the body cannot protect itself from other opportunistic infectious pathogens. As a result progression of AIDS is increased.
Cortisol is a corticosteroid hormone or glucocorticoid produced by zona fasciculata of the adrenal cortex, which is a part of the adrenal gland. It is usually referred to as the "stress hormone" as it is involved in response to stress and anxiety, controlled by CRH. It increases blood pressure and blood sugar, and reduces immune responses. Various synthetic forms of cortisol are used to treat a variety of different illnesses. The most well-known of these is a natural metabolic intermediary of cortisol called hydrocortisone. When first introduced as a treatment for rheumatoid arthritis, hydrocortisone was referred to as Compound E.
Nuclear Receptors and Genetic Disease provides the first compilation of the role of nuclear hormones in health and disease and incorporates the latest breakthroughs in the field. It provides comprehensive reviews of the major receptors prepared by the acknowledged experts in each area. Each chapter provides information on the history, physiology, structure, mechanism of action, genetics, pathophysiology, disease diagnosis, and disease treatment for a particular nuclear receptor. Each chapter also includes a table showing all the known mutations of the respective nuclear receptor with the corresponding clinical disorder. Receptors included in this book are: * The Nuclear Receptor Superfamily * Thyroid Hormone Receptors * Estrogen and Progesterone Receptors * The Androgen Receptor * DAX-1 and Related Orphan Receptors * The Vitamin D Receptor * Retinoid Receptors * Mineralocorticoid and Glucocorticoid Receptors * Hepatocyte Nuclear Factor 4 a * Peroxisome Proliferator Activated Receptors * Coactivators and Corepressors