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Everything posted by trs

  1. Haven't been around much just stopped by to see the new boards. Wow what a change. It will take me a while to learn to navigate them but, the site looks good Mary. Thanks for taking your time to update it.

  2. My first thought was at least he isn't from Transylvania. LOL. Good for your family.
  3. Maybe we are all just body builders in disquise. We should start a contest to see who is strongest with all of our "big muscles" showing off. I agree with the moron assessment you should've ask him which ways more a pound of feathers or a pound of lead. I betcha he would say the lead. A pound is a pound. I really doubt that medical school is as hard as they say.
  4. http://www.springerlink.com/content/u8361471j4484302/ Hypercoagulability in Cushing?s syndrome: the role of specific haemostatic and fibrinolytic markers Journal Endocrine Publisher Humana Press Inc. ISSN 0969-711X (Print) 1559-0100 (Online) Category Original Article DOI 10.1007/s12020-009-9186-y Subject Collection Medicine SpringerLink Date Tuesday, April 21, 2009 Add to marked items Add to shopping cart Add to saved items Permissions & Reprints Recommend this article PDF (194.0 KB)HTMLFree Preview Original Article Hypercoagulability in Cushing?s syndrome: the role of specific haemostatic and fibrinolytic markers Darko Kastelan1 , Tina Dusek1, Ivana Kraljevic1, Ozren Polasek2, Zlatko Giljevic1, Mirsala Solak3, Silva Zupancic Salek4, Jozo Jelcic1, Izet Aganovic1 and Mirko Korsic1 (1) Division of Endocrinology, Department of Internal Medicine, University Hospital Zagreb, Kispaticeva 12, 10000 Zagreb, Croatia (2) Department of Medical Statistics, Epidemiology and Medical Informatics, Andrija Stampar School of Public Health, Zagreb University School of Medicine, Zagreb, Croatia (3) University Hospital for Pulmonary Diseases, Zagreb, Croatia (4) Division of Haematology, Department of Internal Medicine, University Hospital Zagreb, Zagreb, Croatia Received: 14 January 2009 Accepted: 26 March 2009 Published online: 21 April 2009 Abstract Objective Hypercoagulability is a commonly described complication in patients with Cushing?s syndrome. Recent clinical studies have indicated various abnormalities of coagulation and fibrinolysis parameters which may be related to that phenomenon. The aim of this study was to investigate the mechanisms underlying the hypercoagulable state in patients with Cushing?s syndrome. Research methods and procedures A wide range of serum markers involved in the processes of blood coagulation and fibrinolysis was measured in a group of 33 patients with Cushing?s syndrome and 31 healthy controls. No participant was taking medication which could influence the result or had known diseases, except hypertension and diabetes, which could affect blood coagulation or fibrinolysis parameters. Results Patients with Cushing?s syndrome had higher levels of clotting factors II (P = 0.003), V (P < 0.001), VIII (P < 0.001), IX (P < 0.001), XI (P < 0.001) and XII (P = 0.019), protein C (P < 0.001), protein S (P < 0.001), C1-inhibitor (P < 0.001) and plasminogen activator inhibitor-1 (PAI-1) (P = 0.004). The activity of fibrinolytic markers, plasminogen (P < 0.001), antithrombin (P < 0.001) and antithrombin antigen (P = 0.001) was also increased in the patient group. Conclusion The study has demonstrated hypercoagulability in patients with Cushing?s syndrome manifest as increased prothrombotic activity and compensatory activation of the fibrinolytic system. We propose the introduction of thromboprophylaxis in the preoperative and early postoperative periods, combined with a close follow-up in order to prevent possible thromboembolic events in patients with Cushing?s syndrome.
  5. My mom has been struggling with her weight for years. She has been seeing this heart doctor that is one of the best in our state for over a decade. She just had two heart stints put in last week for a 80% blocked main artery and a 70% blocked secondary. She sees this doctor at least once a year. The first time I met him almost 8 or 9 years ago I told her to find a new doctor he was only focused on her weight being her only problem. If she had had heart problems during a colonoscopy and lucked out by her doctor being out of town who knows when the blockage would have been found. My guess would be have been on autopsy. I totally agree weight is a symptom. It takes 3,500 calories to make on pound of fat. 3,500 calories x 30 days=105,000 calories divided by 20lbs =5,250 calories a day. If I did the math right. I am not mathematician. That is how many calories you would need to consume (on top of any other calories need to just maintain your everyday physcial needs) to gain 20 lbs in one month. That means for the average woman who needs 1,500 calories a day for normal every day existience would have to be eating 6,750 calories a day to gain that much weight. How many of us have gained that kind of weight in a month and how many of us have eaten that many calories every day. There were many weeks that I wouldn't consume 5,250 calories all week while going to the gym working out hard. I didn't loose I gained. The math just doesn't add up does it. To consume 6,750 calories a day you would need to eat: 16 c (gal) 2%milk @120 calories/c=1,920 12 large eggs x 78 calories/egg=936 16 oz bacon (1 lb) x 145 calories/oz=2,320 16 oz bread(loaf)x74 calories/oz=1,184 3.5 choco. chip cookies 128/ea =320 35 cups of coffee x 2 calories/c=70 total 6,750 Please feel free to check my math I won't be offended.LOL. As long as you get the point. We should all make a chart like that to keep handy and give it to every doctor that tells us the standard crapola of eat less and exercise more. It breakfast time my fat butt better get cookin.
  6. LoriJane, the trip to Torrance is worth every single cent. I wish I had gone there on my first trip to LA. Hindsight is 20/20 as they say.
  7. Saw him on the news this morning. First thought endocrine.
  8. Ok this is what I have so far. What do you guys think. I just cut and pasted it so try to ignore the highlights etc. I fix those before I print. I am trying to make it easy on the attorney so they can get a quick overview of Cushings. I didn't know to use hypercortisolism to late now. Cushing?s disease Definition Cushing?s disease is a pituitary tumor that releases excessive amounts of cortisol (a steriod). Cortisol is a hormone that controls the sleep/wake cycle, metabolism, immunity, and the relative composition of body between fat/bone and muscle. Cortisol is the hormone that the body produces in response to stress. Cortisol, a very potent glucocorticoid?a group of adrenocortical hormones that protects the body from stress and affect protein and carbohydrate metabolism? is involved in regulating the functioning of nearly every type of organ and tissue in the body, and is considered to be one of the few hormones absolutely necessary for life. Cortisol is normally released during stressful situations. It controls the body's use of carbohydrates, fats, and proteins and also helps reduce the immune system's response to swelling (inflammation). Cortisol is involved in:  complex processing and utilization of many nutrients, including sugars (carbohydrates), fats, and proteins  normal functioning of the circulatory system and the heart  functioning of muscles  normal kidney function  production of blood cells  normal processes involved in maintaining the skeletal system  proper functioning of the brain and nerves  normal responses of the immune system Causes Cushing's disease is caused by a tumor or excess growth ( hyperplasia) of the pituitary gland. This gland is located at the base of the brain. People with Cushing's disease have too much ACTH. ACTH stimulates the production and release of cortisol, a stress hormone. Too much ACTH means too much cortisol. The adrenal glands are located on top of each kidney, and are responsible for releasing cortisol. The site of cortisol production is in the outer layer of the adrenal gland called the adrenal cortex. Release of cortisol is stimulated by ACTH, which is produced by the pituitary gland. The pituitary is juxtaposed to the base of the brain and serves as a type of control center for many other glands in the body. ACTH production occurs only when there is a low concentration of cortisol in the blood. Therefore, cortisol production can be abnormal due to abnormalities in the function of the adrenal gland or the pituitary gland. It can also be overproduced by abnormal regulation of ACTH Symptoms  Abdomen that sticks out and thin arms and legs (central obesity)  Acne or skin infections  Collection of fat on the back of the neck (buffalo hump)  Depression  Diabetes  Easy bruising  Excessive facial hair growth in females  Headache  Impotence  Increased urination  Moon face (round, red, and full)  Osteoporosis  Purple stretch marks on the abdomen, thighs, and breasts  Stopping of menstruation  Weakness  Weight gain Other clinical manifestations resulting from excessive cortisol production can be quite serious. Myopathy, or wasting away of the muscles often occurs. Due to the abnormal blood cell development that results from cortisol overproduction, the skin bruises more frequently and wounds do not heal as quickly. Skin tends to be fragile and thin. People with Cushing syndrome are susceptible to developing fractures, especially in the pelvic and spinal regions. Women are at a higher risk for developing osteoporosis or brittle bones. For all affected individuals, difficulty with activities such as lifting objects or getting up from a sitting position can lead to back pain and fractures. Because cortisol is also important for regulating insulin, patients with Cushing syndrome are at risk for developing diabetes. The function of cortisol is to regulate blood pressure, act as an anti-inflammatory mediator, and to regulate insulin metabolism. Cortisol plays a role during the metabolic activities associated with fat, protein, and carbohydrate metabolism. High levels of cortisol can cause sodium and water retention. Therefore, overproduction of cortisol can have medically important health-related implications that affect muscle contractions, heartbeat, and blood cell function. Possible Complications  Compression fractures  Diabetes  High blood pressure  Infections  Kidney stones  Anxiety, cognitive dysfunction, psychosis Most people have severe fatigue, weak muscles, high blood pressure and high blood sugar. Irritability, anxiety and depression are common. An individual with HPA-axis suppression cannot increase steroid production appropriately during a medical illness or other stress and would need to receive stress doses of steroids to avoid adrenal crisis. Thus, in an emergency, the potential for relative adrenal insufficiency should be considered in any patient with Cushing syndrome. Morbidity and Mortality Morbidity and mortality associated with Cushing syndrome are related primarily to the effects of excess glucocorticoids. However, a large primary pituitary tumor may cause panhypopituitarism and visual loss.  Two catastrophic medical crises that occur in glucocorticoid excess states are perforated viscera and opportunistic fungal infections.  Exposure to excess glucocorticoids results in multiple medical problems, including hypertension, obesity, osteoporosis, fractures, impaired immune function, impaired wound healing, glucose intolerance, and depression, emotional lability psychosis. The higher mortality rate observed in CS seems to be mainly caused by cardiovascular complications. Chronic hypercortisolism is associated with an increased incidence of cardiovascular risk factors such as systemic arterial hypertension, impaired glucose tolerance or diabetes, central obesity, hyperlipidemia, and hypercoagulability. Hypercortisolism promotes the development of hyperglycemia and decreased carbohydrate tolerance by increasing hepatic glycogen and glucose production and decreasing glucose uptake and utilization by peripheral tissues Increased body weight is one of the earliest signs of CS, with a characteristic redistribution of fat from peripheral to central parts of the body, mainly in the abdominal region. Glucocorticoids play a central role in the abdominal accumulation of body fat. An increased local generation of cortisol may take place in visceral adipose tissue because of high activity of 11?-hydroxysteroid dehydrogenase type I, resulting in high local concentrations of cortisol, by converting inactive cortisone into active cortisol. Visceral obesity is an independent risk factor for reduced life expectancy and also correlates with increased risk for disorders such as insulin resistance and diabetes, hyperlipidemia, hypertension, and atherosclerosis of coronary, cerebral, and peripheral vessels In hypercortisolism, there is an increase in circulating very low-density lipoprotein and low-density lipoprotein, but not high-density lipoprotein, with consequent elevation of total triglycerides and cholesterol levels. The insulin resistance state induced by glucocorticoid excess is likely to play a key role in the determination of lipid abnormalities. A complex derangement of the hemostatic system, characterized by both hypercoagulability and impaired fibrinolysis, is responsible for the thrombophilic state observed in patients with CS. Increased cortisol levels stimulate the synthesis of several clotting factors, such as fibrinogen by the liver, and von Willebrand factor by endothelial cells. Glucocorticoids also up-regulate the synthesis of plasminogen activator inhibitor type 1, the main inhibitor of the fibrinolytic system. This hypercoagulability state is a crucial factor predisposing CS patients to thromboembolic events, mostly after surgery and during IPS sampling. Therefore, patients with active CS should be treated as having a prothrombotic disorder, and antithrombotic prophylaxis should be considered. Glucocorticoids affect behavior, mood, neural activity, and a number of specific biochemical processes in the central nervous system. A number of psychiatric and psychological disturbances may be associated with CS, regardless of its etiology. Depending on the series, 50?80% of patients with CS meet Diagnostic and Statistical Manual of Mental Disorders IV criteria for major depression. A minority of patients have other psychopathological manifestations including mania, anxiety, and cognitive dysfunction. If psychotic symptoms occur, they are likely to be a complication of mania or severe depression. Suicidal tendency also has been reported in patients with CS. The somatotropic axis is negatively affected by exogenous or endogenous hypercortisolism, which reduces spontaneous GH secretion as well as the GH response to various stimuli, although with apparently minor changes in circulating IGF-I. Patients with CS develop the manifestations of the metabolic syndrome or syndrome X, including insulin resistance, visceral adiposity, dyslipidemia, carbohydrate intolerance, and/or diabetes mellitus type 2, coagulopathy, and hypertension as a direct or indirect consequence of concurrent and chronic cortisol excess. The abnormalities enhance the global cardiovascular risk that is responsible for the increased mortality of these patients. Prognosis The prognosis for individuals who receive treatment for Cushing syndrome is good with a high likelihood of being cured. However, in affected individuals that are not treated, the prognosis can be poor, with death eventually resulting from complications from hypertension, diabetes, or heart disease Despite cure of hypercortisolism, many patients exhibit residual symptoms in the first postoperative year or even longer, including problems with social and interpersonal relationships, anxiety, irritability, and demoralization. Adults with hypercortisolism have also impaired cognitive function associated with reversible apparent loss of brain volume. Cognitive deficits are often specific to the medial temporal lobe declarative memory system. Adult patients studied 1 yr after surgical cure show improvement in mood but no change in cognitive function, with a concomitant increased, but not normalization, of brain volume. Treatment Treatment depends on the specific reason for cortisol excess and may include surgery, radiation, chemotherapy or the use of cortisol-inhibiting drugs. If the cause is long-term use of glucocorticoid hormones to treat another disorder, the doctor will gradually reduce the dosage to the lowest dose adequate for control of that disorder. Once control is established, the daily dose of glucocorticoid hormones may be doubled and given on alternate days to lessen side effects. Pituitary Adenomas Several therapies are available to treat the ACTH-secreting pituitary adenomas of Cushing's disease. The most widely used treatment is surgical removal of the tumor, known as transsphenoidal adenomectomy. Using a special microscope and very fine instruments, the surgeon approaches the pituitary gland through a nostril or an opening made below the upper lip. Because this is an extremely delicate procedure, patients are often referred to centers specializing in this type of surgery. The success, or cure, rate of this procedure is over 80 percent when performed by a surgeon with extensive experience. If surgery fails, or only produces a temporary cure, surgery can be repeated, often with good results. After curative pituitary surgery, the production of ACTH drops two levels below normal. This is a natural, but temporary, drop in ACTH production, and patients are given a synthetic form of cortisol (such as hydrocortisone or prednisone). Most patients can stop this replacement therapy in less than a year. For patients in whom transsphenoidal surgery has failed or who are not suitable candidates for surgery, radiotherapy is another possible treatment. Radiation to the pituitary gland is given over a 6-week period, with improvement occurring in 40 to 50 percent of adults and up to 80 percent of children. It may take several months or years before patients feel better from radiation treatment alone. However, the combination of radiation and the drug mitotane (Lysodren?) can help speed recovery. Mitotane suppresses cortisol production and lowers plasma and urine hormone levels. Treatment with mitotane alone can be successful in 30 to 40 percent of patients. Other drugs used alone or in combination to control the production of excess cortisol are aminoglutethimide, metyrapone, trilostane and ketoconazole. Each has its own side effects that doctors consider when prescribing therapy for individual patients. Surgical Care  Cushing disease  Treatment of choice for classic Cushing disease is transsphenoidal surgery by an experienced neurosurgeon. The goal of surgery is to remove the adenoma, preserving as much pituitary function as possible.  The more extensive the mass and the resulting resection, the greater the risk for loss of pituitary function. Successful amelioration of hypercortisolism occurs in 60-80% of cases. Both open and laparoscopic techniques are possible. If unsuccessful, MRI-guided pituitary surgery, a new procedure, may be indicated. Lateralization of ACTH secretion via IPS catheterization and sampling is sometimes helpful in difficult cases.  Pituitary irradiation is employed when transsphenoidal surgery is not successful or not possible. The procedure is less successful than surgery in adults, with a 45% cure rate in adults and 85% cure rate in children. Late-onset adverse effects include hypopituitarism.  Bilateral adrenalectomy is an option if transsphenoidal surgery, pituitary irradiation, and medical therapy fail or if rapid normalization of cortisol levels is required. The patient then requires lifelong glucocorticoid and mineralocorticoid therapy.  In individuals who undergo bilateral adrenalectomy, Nelson syndrome, that is symptomatic enlargement of the pituitary gland and adenoma, may occur in one quarter to one half of adults not treated with pituitary irradiation and in as many as one quarter of patients pretreated with radiation therapy. Outlook (Prognosis) If the tumor can be surgically removed, the outlook is fair to good, depending upon whether the entire tumor is removed. Possible Complications The most serious complication is blindness, which can occur if the optic nerve is seriously damaged. Permanent hormonal imbalances may be caused by the tumor or its removal. This may require replacement of the affected hormones. (I have diagrams for this part but they would not paste) The pituitary gland is one of the body?s endocrine glands. It is sometimes called the ?master gland,? because it controls the functions of other endocrine glands. Endocrine glands release chemical messengers (hormones) into the bloodstream to be carried to organs and tissues throughout the body. The pituitary is located at the base of the brain. It is small and is divided into three parts: anterior lobe, intermediate lobe and posterior lobe. The anterior lobe is largest, making up about 80 percent of the gland. The anterior lobe produces the following hormones:  Growth hormone, which affects many other glands  Prolactin, which stimulates milk production in women after giving birth  Adrenocorticotropic hormone, which stimulates the adrenal glands  Thyroid-stimulating hormone, which stimulates the thyroid gland  Luteinizing hormone , which stimulates the ovaries or testes  Follicle-stimulating hormone, which stimulates ovaries or testes The intermediate lobe produces melanocyte, a hormone that controls skin pigmentation. The posterior lobe of the pituitary stores and releases an antidiuretic hormone that increases the absorption of water by the kidneys. This lobe also stores and releases oxytocin, a hormone that causes the uterus to contract , helps to slow blood flow during the birthing process and causes milk to flow when a woman breast-feeds. The pituitary is intimately involved in growth, development, maintenance and reproduction. The pituitary supplies growth hormone, which is responsible for growth from before birth to the end of growth at the end of puberty. The pituitary determines the timing for the onset of puberty and the cycling of the female menstrual cycle. It regulates the production of thyroid hormones that govern the overall metabolism of the body. It also controls the production of corticosteroids, which help govern such functions as electrolyte maintenance, blood pressure, inflammatory response and response to stress. Sources NIH Medline Plus The Hormone Foundation The Pituitary Society Mayo Clinic The Journal of Clinical Endocrinology and Metabolism Thanks everyone for your help.
  9. Well I kept telling the man filling out the intial form that I thought Cushings was my trouble but, there is not a category or whatever it is they call that. So he listed obesity and heart problems. I didn't have the Cushings diagnosis then I do now. Since obesity is a major symptom of Cushings along with cognitive problems (short term memory loss per their psychologist) and heart problems I would think a good lawyer could put that together. I hope anyway.
  10. I am trying to compile a few short to the point Cushings articles for a disability appeal. I have decided to use an attorney and would like to take some information on Cushings with me to the appt. I have Vs. article and some others for what Cushings is I really need some that tell the damage it causes in more detail than the basic heart problems, diabetes and infection. I have some that are really long and detailed with various aspects of symptoms but, I think these would be a little to long for the intial appeal. The attorney won't have much time to file the appeal.
  11. Were were you a few days ago when I was trying to find simple articles like that for disability attorney. Thanks for the find.
  12. Excellent interview you did a really good job.
  13. I took it a few years back. I didn't loose any weight with it. I am sure it was Cushings gain looking back now. I joined the class action lawsuit a few years ago and was reimbursed my cost of prescreptions all of about $400. or so. I couldn't find all of my reciepts and my doc didn't keep good notes (or he wouldn't give them to me). I do have heart trouble now and I often wonder if the Fen-Phen made it worse.
  14. Y'all now I will testify to the miraculous benefits of vitamin D3. Shelley I have seen them advertise for it helping seasonal affective disorder which, IMO, is a vitamin D3 deficiency.
  15. Thats the way I read it, also. Both rat groups with cortisol gained but, the sed. rats gained the most. The cortisol exercising rats didn't gain any more fat than the control group. It is saying that we should exercise to keep the high cortisol from turning to fat. I will sign up for there human control group because I know that the opposite is true in me. The more I exercised the fatter I got. Didn't need any lab rat to tell me so either.
  16. Very cool. Hope they get your like fixed you got Cushies to meet you know. I don't know about SusanM's story. Where can I find it?
  17. I was born weighing around 6 lbs. How about you guys? Interesting articles. http://jcem.endojournals.org/cgi/content/abstract/83/3/757 Original Studies Elevated Plasma Cortisol Concentrations: A Link between Low Birth Weight and the Insulin Resistance Syndrome?1 D. I. W. Phillips, D. J. P. Barker, C. H. D. Fall, J. R. Seckl, C. B. Whorwood, P. J. Wood and B. R. Walker Medical Research Council Environmental Epidemiology Unit, University of Southampton (D.I.W.P., D.J.P.B., C.H.D.F, C.B.W.), and the Regional Endocrine Unit, Southampton General Hospital (P.W.), Southampton, United Kingdom; and the Department of Medicine, University of Edinburgh, Western General Hospital (J.R.S., B.R.W.), Edinburgh, Scotland Address all correspondence and requests for reprints to: Dr. D. I. W. Phillips, Medical Research Council Unit, Southampton General Hospital, Tremona Road, Southampton, United Kingdom SO16 6YD. E-mail: diwp@mrc.soton.ac.uk. Recent studies have shown that reduced fetal growth is associated with the development of the insulin resistance syndrome in adult life. The mechanisms are not known. However increased activity of the hypothalamic-pituitary-adrenal axis (HPAA) may underlie this association; the axis is known to be reset by fetal growth retardation in animals, and there is evidence in humans of an association between raised HPAA activity and the insulin resistance syndrome. We have, therefore, examined the relations among size at birth, plasma cortisol concentrations, and components of the insulin resistance syndrome in a sample of healthy men. We measured 0900 h fasting plasma cortisol and corticosteroid-binding globulin levels in 370 men who were born in Hertfordshire, UK, between 1920?1930 and whose birth weights were recorded. Fasting plasma cortisol concentrations varied from 112?702 nmol/L and were related to systolic blood pressure (P = 0.02), fasting and 2-h plasma glucose concentrations after an oral glucose tolerance test (P = 0.0002 and P = 0.04), plasma triglyceride levels (P = 0.009), and insulin resistance (P = 0.006). Plasma cortisol concentrations fell progressively (P = 0.007) from 408 nmol/L in men whose birth weights were 5.5 lb (2.50 kg) or less to 309 nmol/L among those who weighed 9.5 lb (4.31 kg) or more at birth, a trend independent of age and body mass index. These findings suggest that plasma concentrations of cortisol within the normal range could have an important effect on blood pressure and glucose tolerance. Moreover, this study provides the first evidence that intrauterine programming of the HPAA may be a mechanism underlying the association between low birth weight and the insulin resistance syndrome in adult life. http://jcem.endojournals.org/cgi/content/abstract/92/11/4094 Body Size at Birth Predicts Hypothalamic-Pituitary-Adrenal Axis Response to Psychosocial Stress at Age 60 to 70 Years Eero Kajantie, Kimmo Feldt, Katri R?ikk?nen, David I. W. Phillips, Clive Osmond, Kati Heinonen, Anu-Katriina Pesonen, Sture Andersson, David J. P. Barker and Johan G. Eriksson Department of Health Promotion and Chronic Disease Prevention (E.K., J.G.E.), National Public Health Institute, 00300 Helsinki, Finland; Hospital for Children and Adolescents (E.K., S.A.), Helsinki University Central Hospital, 00029 HUS, Helsinki, Finland; Departments of Psychology (K.F., K.R., K.H., A.-K.P.) and Public Health (J.G.E.), University of Helsinki, 00014 Helsinki, Finland; Medical Research Council Epidemiology Resource Centre and Developmental Origins of Health and Disease Division (D.I.W.P., C.O., D.J.P.B.), University of Southampton, Southampton SO16 6YD, United Kingdom; and Department of Medicine (D.J.P.B.), Heart Research Center, Oregon Health and Sciences University, Portland, Oregon 97201-3098 Address all correspondence and requests for reprints to: Eero Kajantie, M.D., Ph.D., National Public Health Institute, Department of Health Promotion and Chronic Disease Prevention, Mannerheimintie 166, 00300 Helsinki, Finland. E-mail: eero.kajantie@helsinki.fi. Background: Studies in humans and animals have suggested intrauterine programming of hypothalamic-pituitary-adrenal axis (HPAA) function as an important mechanism in linking fetal life conditions with adult disease. Objective: Our aim was to assess how body size at birth, a marker of intrauterine conditions, is associated with hypothalamic-pituitary-adrenal axis response to psychosocial stress in late adulthood. Design and Setting: We conducted a clinical study in the Helsinki Birth Cohort. Participants: Two hundred eighty-seven men and women born between 1934 and 1944 whose birth measurements and gestational age came from hospital records participated in the study. Measurements: We measured salivary cortisol and, for 215 individuals, plasma cortisol and ACTH concentrations in conjunction with a standardized psychosocial stressor (Trier Social Stress Test). Results: There was a linear relationship between low birth weight and low plasma ACTH but no linear relationship with cortisol. There were, however, quadratic relationships between birth weight and salivary (mixed model P = 0.001) and plasma cortisol (P = 0.005) but not with plasma ACTH (P = 0.1). The lowest peak salivary cortisol concentrations were seen in the lowest third of birth weights (adjusted for gestational age and sex): 12.9 nmol/liter (95% confidence interval of mean 11.2?15.0), compared with 17.1 nmol/liter (14.8?19.8) in the middle and 14.1 nmol/liter (12.6?15.7) in the highest third of birth weights. Corresponding figures for plasma cortisol were 418 nmol/liter (380?459), 498 nmol/liter (455?545), and 454 nmol/liter (428?482), and for plasma ACTH 8.17 pmol/liter (6.98?9.57), 12.42 pmol/liter (10.64?14.51), and 11.50 (10.06?13.14), respectively. Results for areas under the curve were similar. Conclusions: We found an inverse U-shaped relationship between birth weight and cortisol concentrations during psychosocial stress. The lowest cortisol and ACTH concentrations were seen in subjects with the lowest birth weights. These results support the hypothesis that both hyper- and hypocortisolism may be programmed during the fetal period.
  18. I can go along with altered genes but, I still don't think it is even related to overeating. Metabolic syndrome was my first dx and back then it wasn't from over eating or underexercising. I was gaining weight not matter how little I eat or how much I exercised. I think it is a problem with the genes. Hope more research is done on it.
  19. http://www.biologynews.net/archives/2007/1...r_bacteria.html Long denigrated as vestigial or useless, the appendix now appears to have a reason to be ? as a ?safe house? for the beneficial bacteria living in the human gut. Drawing upon a series of observations and experiments, Duke University Medical Center investigators postulate that the beneficial bacteria in the appendix that aid digestion can ride out a bout of diarrhea that completely evacuates the intestines and emerge afterwards to repopulate the gut. Their theory appears online in the Journal of Theoretical Biology. ?While there is no smoking gun, the abundance of circumstantial evidence makes a strong case for the role of the appendix as a place where the good bacteria can live safe and undisturbed until they are needed,? said William Parker, Ph.D., assistant professor of experimental surgery, who conducted the analysis in collaboration with R. Randal Bollinger, M.D., Ph.D., Duke professor emeritus in general surgery. The appendix is a slender two- to four-inch pouch located near the juncture of the large and small intestines. While its exact function in humans has been debated by physicians, it is known that there is immune system tissue in the appendix. The gut is populated with different microbes that help the digestive system break down the foods we eat. In return, the gut provides nourishment and safety to the bacteria. Parker now believes that the immune system cells found in the appendix are there to protect, rather than harm, the good bacteria. For the past ten years, Parker has been studying the interplay of these bacteria in the bowels, and in the process has documented the existence in the bowel of what is known as a biofilm. This thin and delicate layer is an amalgamation of microbes, mucous and immune system molecules living together atop of the lining the intestines. ?Our studies have indicated that the immune system protects and nourishes the colonies of microbes living in the biofilm,? Parkers explained. ?By protecting these good microbes, the harmful microbes have no place to locate. We have also shown that biofilms are most pronounced in the appendix and their prevalence decreases moving away from it.? This new function of the appendix might be envisioned if conditions in the absence of modern health care and sanitation are considered, Parker said. ?Diseases causing severe diarrhea are endemic in countries without modern health and sanitation practices, which often results in the entire contents of the bowels, including the biofilms, being flushed from the body,? Parker said. He added that the appendix?s location and position is such that it is expected to be relatively difficult for anything to enter it as the contents of the bowels are emptied. ?Once the bowel contents have left the body, the good bacteria hidden away in the appendix can emerge and repopulate the lining of the intestine before more harmful bacteria can take up residence,? Parker continued. ?In industrialized societies with modern medical care and sanitation practices, the maintenance of a reserve of beneficial bacteria may not be necessary. This is consistent with the observation that removing the appendix in modern societies has no discernable negative effects.? Several decades ago, scientists suggested that people in industrialized societies might have such a high rate of appendicitis because of the so-called ?hygiene hypothesis,? Parker said. This hypothesis posits that people in "hygienic" societies have higher rates of allergy and perhaps autoimmune disease because they -- and hence their immune systems -- have not been as challenged during everyday life by the host of parasites or other disease-causing organisms commonly found in the environment. So when these immune systems are challenged, they can over-react. ?This over-reactive immune system may lead to the inflammation associated with appendicitis and could lead to the obstruction of the intestines that causes acute appendicitis,? Parker said. ?Thus, our modern health care and sanitation practices may account not only for the lack of a need for an appendix in our society, but also for much of the problems caused by the appendix in our society.? Parker conducted a deductive study because direct examination the appendix?s function would be difficult. Other than humans, the only mammals known to have appendices are rabbits, opossums and wombats, and their appendices are markedly different than the human appendix. Parker?s overall research into the existence and function of biofilms is supported by the National Institutes of Health. Other Duke members of the team were Andrew Barbas, Errol Bush, and Shu Lin. Source : Duke University Medical Center
  20. http://ajpendo.physiology.org/cgi/content/full/292/3/E654 This is a long article but good. First paragraph: "Insulin resistance is viewed as an insufficiency in insulin action, with glucocorticoids being recognized to play a key role in its pathogenesis. With insulin resistance, metabolism in multiple organ systems such as skeletal muscle, liver, and adipose tissue is altered. These metabolic alterations are widely believed to be important factors in the morbidity and mortality of cardiovascular disease. More importantly, clinical and experimental studies have established that metabolic abnormalities in the heart per se also play a crucial role in the development of heart failure. Following glucocorticoids, glucose utilization is compromised in the heart. This attenuated glucose metabolism is associated with altered fatty acid supply, composition, and utilization. In the heart, elevated fatty acid use has been implicated in a number of metabolic, morphological, and mechanical changes and, more recently, in "lipotoxicity". In the present article, we review the action of glucocorticoids, their role in insulin resistance, and their influence in modulating peripheral and cardiac metabolism and heart disease..........
  21. Makes sense. I would be willing to try it. Thanks for the article Robin.
  22. Ok, if the ghost post shows up please ignore it. I can't figure out what is happening to my replies. Sorry. I just sent the email thank you. I would like everyone who has been involved in making this happen know that I appreciate your work. Thank You. Hopefully making more people aware will mean that more people get involeved in treatment, diagnosis and research. Good job. Here is the link to Senator Inofe office. http://inhofe.senate.gov/public/index.cfm?...act.ContactForm
  23. I spent last summer in the sun most of the time. I worked outside for many hours admittedly, without sunblock and had a very deep dark tan. I was dx with low vitamin D during this time. I think our bodies stop making it from sunlight at some point. I was also taking about 1,000 iu a day of vitamin D3 to help with fibromyalgia, it didn't help at that dose. The higher dose of 50,000 iu made a huge difference. The cortisol or its effects must damage the bodies ability convert the vitamin D3.
  24. I found it interesting that this article says 40% of patients with CD will have a normal MRI. This is a long article, I just copied the last paragraph and posted it here. http://jcem.endojournals.org/cgi/content/full/87/4/1640 Optimal Response Criteria for the Human CRH Test in the Differential Diagnosis of ACTH-Dependent Cushing?s Syndrome ("By themselves, none of the noninvasive or dynamic tests used for the differential diagnosis of ACTH-dependent CS are completely reliable, and several tests may need to be used. If the hCRH test shows a rise above 20% in serum cortisol at 15 and 30 min, EC is very unlikely. However, the sensitivity of the test, in either its oCRH or hCRH form, for CD is still significantly less than 100%. What then are the recommendations for the use of the test in clinical practice? Bilateral inferior petrosal sinus sampling (BIPSS) remains the gold standard for establishing whether there is a central to peripheral gradient of plasma ACTH consistent with CD, with a sensitivity of 95?100% with a specificity of virtually 100% in major centers (1). This is, however, an invasive test requiring considerable expertise in specialist centers, and some clinicians will only option for it in cases of doubt. Forty percent of patients with CD will have a normal pituitary magnetic resonance image, whereas conversely there is a 10% prevalence of pituitary incidentalomas in the age range in which CD typically presents (1). It is, therefore, clear that magnetic resonance imaging of the pituitary cannot be relied on and weight should be given to the biochemical evaluation of a given patient. With a clear response to hCRH and an obvious pituitary lesion with stalk deviation, BIPSS may not be needed. An additional advantage of the hCRH test is that if plasma ACTH is also measured a persistently undetectable ACTH will confirm ACTH independence and the primacy of adrenal pathology (1). However, given the problems in interpreting any dynamic test in isolation, we currently consider that BIPSS or cavernous sinus sampling will continue to be necessary in the great majority of patients.")
  25. I was found deficient in DHEAS but, my doctor told me not to take them while testing for Cushings. Does anyone know why/how it affects testing? I didn't think to ask at the time.
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