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Estrogen Hypoglycemia

15. Blood Sugar, Estrogen And Hormonal Balance

15. Blood Sugar, Estrogen And Hormonal Balance

The thyroid and hormonal balance Hormones are chemical messengers produced by one part of the body to tell some other part what to do. Thyroid hormone, is just one of many others including insulin, cortisol, estrogen, progesterone and testosterone. There are many other hormones, but these are amongst the most important. Usually, we only think of one hormone at a time. Thyroid symptoms indicate a thyroid problem. Blood sugar symptoms means there is an insulin problem. Symptoms around sexual function indicate a sex hormone problem. And high stress means a cortisol problem. This simple model may help medical students learn about hormones, and is good for books that convince you that if just your thyroid hormone, or if just your testosterone was normalized, you would feel fine, but the hormonal system really does not work like this. In real life each these four systems affects the other three in a complex balance game. Basically, when one hormone goes up, another goes down to compensate. This continues until a patient becomes so sick, that almost all of these hormones go down. Junk food, or foods high in sugar stimulate the pancreas to release insulin. Insulin's job is to lower blood sugar, by moving it into cells to be used for energy, or stored for later use. We store sugar for energy in two ways. Sugar can be converted to fat, or in the liver as glycogen. Fat is a long term energy reserve. Glycogen is more easily used, and is the first place we our body goes for energy when we have not eaten for a few hours. [84] Cortisol is insulin's counterpart. Among many other functions, cortisol takes sugar stored in the liver (glycogen) and puts it into the blood stream. To keep things simple, insulin lowers blood sugar, and cortisol raises blood sugar. This is what may sound confu Continue reading >>

5,575 Possible Causes For Hypoglycemia + Ptosis + Vitiligo + Estrogen Decreased In Usa

5,575 Possible Causes For Hypoglycemia + Ptosis + Vitiligo + Estrogen Decreased In Usa

Turner Syndrome Vitiligo Ptosis Estrogen Decreased Hypoglycemia Noonan Syndrome Definition: A multifaceted disorder characterized by short stature, webbed neck, ptosis, skeletal malformations, hypertelorism, hormonal imbalance, CRYPTORCHIDISM[hon.ch] Eye: Ptosis , strabismus, amblyopia , and cataract s are more common in girls with Turner syndrome.[emedicine.medscape.com] Madelung deformities of the wrist Short fourth and fifth metacarpals and metatarsals Shield chest: The chest appears to be broad with widely spaced nipples Lymphedema Eyes: Ptosis[emedicine.medscape.com] List represents a sample of symptoms, diseases, and other queries. Updated weekly. Hungry Bones Syndrome Altitude Sickness Cavernous Sinus Thrombosis Posterior Subcapsular Cataract Cellulitis Splenic Infarction Megaloblastic Anemia Islet Cell Tumor Chronic Phase of Chronic Myeloid Leukemia Penile Fracture Tuberous Sclerosis Primary Sclerosing Cholangitis Odynophagia, unilateral throat pain Costovertebral Angle Tenderness Dyspepsia Tenesmus Oliguria Scrotal Ulcer Choledochal Cyst Anal Fistula Essential Hypertension Enthesitis-Related Arthritis Glioblastoma Multiforme Leiomyosarcoma Brain Neoplasm Hyperventilation Wolff-Parkinson-White Syndrome Ethmoid Sinusitis Dementia with Lewy Bodies Infarction vaginal discharge, weight loss hemoglobin decreased, typhoid fever Fever, Polyserositis Hyponatremia, Ileus Burning Sensation Autoamputation of Digits Bradycardia Reduced Fetal Movement Calcaneal Spur Arteriovenous Malformation Berry Aneurysm Arachnoiditis Lateral Medullary Syndrome Myiasis Cryptogenic Organizing Pneumonia Hereditary Motor and Sensory Neuropathies Cheilitis Clonus, Hyperreflexia, muscle hypotonia Absent Triceps Reflex Cul De Sac Mass Delayed Bone Age Nystagmus Facial Grimacing Brushfield Spots Continue reading >>

Modulation Of Hypoglycemia-induced Increases In Plasma Epinephrine By Estrogen In The Female Rat

Modulation Of Hypoglycemia-induced Increases In Plasma Epinephrine By Estrogen In The Female Rat

Clinical studies have demonstrated that estrogen replacement therapy suppresses stress-induced increases in plasma catecholamines. The present study determined whether normal circulating levels of estrogen can modulate hypoglycemia-induced increases in plasma epinephrine (EPI). In anesthetized female rats, insulin-induced hypoglycemia (0.25 U/kg) increased plasma EPI concentration to a significantly greater extent in 14-day ovariectomized (OVEX) rats compared to that in sham-operated controls. In 17β-estradiol (E2)-replaced OVEX rats, the hypoglycemia-induced rise in plasma EPI was reduced significantly when compared to that in vehicle-replaced OVEX rats. OVEX and E2 replacement had no effect on tyrosine hydroxylase or phenylethanolamine N-methyltransferase mRNA levels in the adrenal medulla. In isolated adrenal medullary chromaffin cells, agonist-induced increases in intracellular Ca2+ were unaffected by 48-hr exposure to 10 nM E2. In contrast, acute (3-min) exposure to micromolar concentrations of E2 dose-dependently and reversibly inhibited agonist-induced Ca2+ transients. In addition, in OVEX rats, a constant infusion of E2 significantly reduced the insulin-induced increase in plasma EPI concentration compared to that in vehicle-infused controls. These data demonstrate that physiologic levels of circulating E2 can modulate hypoglycemia-induced increases in plasma EPI. This effect seems independent of steroid influence on adrenal medullary secretion or biosynthesis. In contrast, acute exposure to high levels of E2 can also suppress hypoglycemia-induced increases in plasma epinephrine, due at least in part to inhibition of stimulus-secretion coupling. © 2004 Wiley-Liss, Inc. Continue reading >>

Effect Of Estrogen Or Insulin-induced Hypoglycemia On Plasma Oxytocin Levels In Bulimia And Anorexia Nervosa☆

Effect Of Estrogen Or Insulin-induced Hypoglycemia On Plasma Oxytocin Levels In Bulimia And Anorexia Nervosa☆

Plasma oxytocin (OT) levels were measured before and after stimulation with estrogens (1 mg ethynylestradiol orally) or with insulin (0.15 IU/kg)-induced hypoglycemia in seven underweight women with anorexia nervosa, eight normal weight bulimic women, and nine normal controls. Anorectic patients were amenorrhoic; they were tested at their first hospitalization (first tests) and again 8 to 9 weeks later (second tests) when they were eating normally, but were still at a low weight. In addition, anorectic women were tested 16 to 17 weeks after the first test (third tests), when their weight was restored to normal. Normal and bulimic women were tested on the fourth days of normal menstrual cycles. Insulin induced similar hypoglycemic responses in all groups. At each time point of the estrogen tests, plasma estrogen levels were similar in bulimic and normal women, whereas they were significantly lower in anorectic subjects. There were no differences in the basal levels of OT among groups. Both insulin-induced hypoglycemia and estrogen treatment produced striking OT increments in bulimic and control women, without significant differences between groups. During the first tests, no significant increase in plasma OT levels was observed in underweight anorectic women in response to both releasing stimuli. After partial weight recovery, the anorectic women showed a slight, but significant, increase in the OT responses to both insulin-induced hypoglycemia and estrogen administration. Both hypoglycemia- and estrogen-induced OT increases observed during the second tests were significantly lower in underweight anorectic patients than in normal controls. Anorectic subjects regained normal OT responsiveness to both stimuli after complete weight recovery. When percent values of average b Continue reading >>

Site-specific Effects Of Intracranial Estradiol Administration On Recurrent Insulin-induced Hypoglycemia In The Ovariectomized Female Rat

Site-specific Effects Of Intracranial Estradiol Administration On Recurrent Insulin-induced Hypoglycemia In The Ovariectomized Female Rat

Abstract Clinical and experimental studies reveal gender differences in susceptibility to dampening effects of precedent hypoglycemia on recurrent insulin-induced hypoglycemia (RIIH). Recent studies implicate the ovarian steroid, estradiol, in the regulation of RIIH, since systemic replacement of this hormone at basal estrous cycle levels maintains glucose profiles during serial insulin dosing and prevents RIIH-associated reductions in neuronal activation in key metabolic structures in the ovariectomized female rat brain. The present study investigated the hypothesis that these effects are achieved, in part, by estrogenic action within the central nervous system, including glucoregulatory structures characterized by high estrogen receptor (ER) expression. Initial experiments evaluated the impact of global intracranial administration of estradiol on RIIH. Ovariectomized rats were treated by continuous infusion of graded doses of 17β-estradiol-3-benzoate (EB) or vehicle into the lateral ventricle (LV), and injected subcutaneously with 1 or 4 doses of the intermediate-release insulin, Humulin N (HN), 1 dose per day. Animals infused with 5 or 10 µg EB/day exhibited uniform glycemic responses to 1 versus 4 doses of insulin, whereas rescue from hypoglycemia was delayed during repetitive HN injection of rats infused with either vehicle or 1 µg EB/day. Recovery from both single and multiple bouts of hypoglycemia was more rapid in rats infused with the higher EB doses, compared to other groups. Mapping of ERα immunoreactivity in animals treated by LV infusion of EB revealed variable nuclear staining in ER-expressing metabolic loci typified by estrogen-dependent sustenance of neuronal reactivity to hypoglycemia, with highest levels of ERα immunoreactivity observed in the arc Continue reading >>

Premenstrual Syndrome

Premenstrual Syndrome

Premenstrual Syndrome or PMS has only come to be an accepted medical condition in the past several decades. Before that the cyclic monthly symptoms that presented themselves were regarded by the medical profession as psychosis, hypochondria, an attention-getting device, or simply (with derision) a woman's unstable personality. However, it is now widely documented and recognized that the symptoms of PMS are real and are the result of the action of hormones. The Cycle It is important to understand how the hormones normally fluctuate in a woman's monthly cycle. We use the first day of menstrual bleeding as the starting point. The hypothalamus (part of the brain) sends a message to the pituitary gland to begin to secrete a substance, the follicle stimulating hormone (FSH). This, in turn, stimulates the ovaries to begin production of estrogen, a hormone. In one of the ovaries, a follicle containing an egg will begin to enlarge with this stimulation of estrogen. At the peak of estrogen production the ripened egg will erupt from the follicle and pass into the fallopian tube and proceed on its way to the uterus. Meanwhile, the follicle turns into a hormone factory and begins to produce progesterone and some estrogen. This causes the lining of the uterus to quickly thicken and enrich in preparation for nourishing a fertilized egg. When conception does not take place the follicle begins to slow production of progesterone/estrogen and finally to cease. The egg by now is dead (it can only live a few days without conception) and the lining of the uterus is sloughed off. The levels of estrogen at this time are so low that the hypothalamus again sends the signal to the pituitary to secrete FSH to stimulate estrogen production and we have the whole cycle again. Enter PMS So what goes w Continue reading >>

Article: Balancing Hormones From A Natural

Article: Balancing Hormones From A Natural

Balancing Hormones from a Natural Perspective The following article contains helpful education regarding natural health. It is to be viewed as a guide, and not as a prescription or a method of diagnosing medical conditions and/or treatments. Part I: Many women are uninformed about what their bodies need nutritionally in order to maintain hormone balance. Unless we have been avoiding the news, we have all heard about the potential dangers of chemical hormone replacement therapy. So where does this place women who need help with female issues and do not want to take chemical therapies? The intention of this article is to enlighten women about their choices. Initially, let’s become acquainted with hormone activity during the monthly cycle. With day 1 of the cycle being the first day of menstrual bleeding, days 1 - 3 have very little hormone activity. Days 3 - 13 are estrogen dominant. Days 15 – 28 are progesterone dominant. If the body does not detect pregnancy around day 22, hormone levels drop and bleeding begins the cycle at day 1 again. If a pregnancy is determined, progesterone levels remain high until labor begins. One of the amazing qualities of progesterone is that it selectively recognizes and eliminates foreigners in the body. This despite the fact that ½ of the DNA of a fetus is foreign to the mother’s body. Progesterone is also a precursor to cortisone, estrogen, and testosterone. When hormonal balance is disturbed we will often see constipation and a weakened liver. The liver is then unable to eliminate excess hormones. Estrogen – Estrogen is not a single hormone but is the name of a family of hormones. Estradiol is the strongest and therefore hardest to process and eliminate excesses, estrone is the second in terms of strength, and estriol is the wea Continue reading >>

Estrogen And Blood Sugar

Estrogen And Blood Sugar

As I mentioned in my previous posts, I went off my long-term Estrogen Replacement Therapy about three weeks ago. I did this after reading an excellent book, Hot flashes, hormones, & your health, by Joann E. Manson and Shari Bassuk. Dr. Manson heads the Woman's Health Initiative (WHI) which studied the long term effects of HRT and ERT. This book made an excellent case for using the kind of estrogen I was taking (Menest) for about five years, and then stopping, because that is the point where the potential to stimulate cancers outweighs the benefit. The author also explained that most of the side effects associated with menopause, like hot flashes, are caused by sputtering hormone levels, and that once these levels flatten out, the side effects stop for most women. With that in mind, I figured it was time to stop my estrogen, as I've been on it for six years. When I tried to stop it 3 1/2 years ago, I had a miserable time with interrupted sleep, hot flashes, and terrible moods. But so far, I am feeling fine and have not had any hot flashes yet. I have, however, seen my blood pressure and blood sugar creep up. This is exactly what happened the last time I stopped the estrogen, so I thought it would be worth discussing both these effects here for any of you who might be going through something similar. Estrogen lowers blood pressure by increasing the elasticity of blood vessels. This is one reason why it was expected to help prevent heart disease, which it turned out not to do. Over the past weeks my blood pressure which had stabilized over the past year at a high of 120/80, which is normal, even when stressed at the doctors office, to 130/80 at home when not stressed. Unfortunately, while this doesn't seem like a big change, it pushes me back into the range that is not hea Continue reading >>

Effect Of Estrogen Or Insulin-induced Hypoglycemia On Plasma Oxytocin Levels In Bulimia And Anorexia Nervosa.

Effect Of Estrogen Or Insulin-induced Hypoglycemia On Plasma Oxytocin Levels In Bulimia And Anorexia Nervosa.

Abstract Plasma oxytocin (OT) levels were measured before and after stimulation with estrogens (1 mg ethynylestradiol orally) or with insulin (0.15 IU/kg)-induced hypoglycemia in seven underweight women with anorexia nervosa, eight normal weight bulimic women, and nine normal controls. Anorectic patients were amenorrhoic; they were tested at their first hospitalization (first tests) and again 8 to 9 weeks later (second tests) when they were eating normally, but were still at a low weight. In addition, anorectic women were tested 16 to 17 weeks after the first test (third tests), when their weight was restored to normal. Normal and bulimic women were tested on the fourth days of normal menstrual cycles. Insulin induced similar hypoglycemic responses in all groups. At each time point of the estrogen tests, plasma estrogen levels were similar in bulimic and normal women, whereas they were significantly lower in anorectic subjects. There were no differences in the basal levels of OT among groups. Both insulin-induced hypoglycemia and estrogen treatment produced striking OT increments in bulimic and control women, without significant differences between groups. During the first tests, no significant increase in plasma OT levels was observed in underweight anorectic women in response to both releasing stimuli. After partial weight recovery, the anorectic women showed a slight, but significant, increase in the OT responses to both insulin-induced hypoglycemia and estrogen administration. Both hypoglycemia- and estrogen-induced OT increases observed during the second tests were significantly lower in underweight anorectic patients than in normal controls. Anorectic subjects regained normal OT responsiveness to both stimuli after complete weight recovery.(ABSTRACT TRUNCATED AT 2 Continue reading >>

Role Of Estrogen In Hypoglycemia- And

Role Of Estrogen In Hypoglycemia- And

glucoprivation-induced food intake Akira Takamata, Kana Miyake, and Keiko Morimoto Department of Environmental Health, Nara Women's University, Nara, 630-8506, Japan Maintenance of a desirable weight is important to reduce risks for lifestyle-related diseases, such as cerebro- and cardiovascular diseases and diabetics. Incidence of obesity and lifestyle-related diseases reportedly increase in postmenopausal women with aging, suggesting that female gonadal hormones play an important role in energy balance. Body weight is regulated by both energy intake and expenditure, and estrogen has an anorexic action. Thus, to elucidate the mechanism for estrogen-induced anorexia, we examined the effect of estrogen (E2) replacement in ovariectomized rats on food intake and lateral hypothalamic orexinergic neuron’s activity during glucoprivation induced by i.v. 2-deoxy-D-glucose (2DG) administration and hypoglycemia induced by s.c. insulin administration. Rats were ovariectomized and implanted a silicon capsule containing E2 or vehicle (cholesterol) subcutaneously. Two weeks after the replacement, rats were injected with either 2DG (400 mg/kg) or insulin (5 units/kg), and food intake was measured for 3-4 hours. The same experiment was performed for immunohistochemical examination of c-Fos and orexin A expressions in the lateral hypothalamic area (LH) and c-Fos at the arcuate nucleus (Arc). Both 2DG and insulin administration induced c-Fos expression in the orexin A neurons locating at the perifornical region of LH, and significantly induced food intake. Both 2DG- and insulin-induced food intakes were significantly lower in E2-replaced group than E2-deficit group. The fraction of c-Fos expressed orexinergic neurons, induced by both 2DG and insulin injections, were significantly less Continue reading >>

Neuroprotection Of Estrogen Of Hypothalamic Cell Line Due To Hypoglycemic Injury

Neuroprotection Of Estrogen Of Hypothalamic Cell Line Due To Hypoglycemic Injury

Abstract Glucose is the main metabolic fuel of the brain. Recurrent episodes of hypoglycemia can lead to seizures, coma, and even death. Hypothalamus involved in feeding and energy balance is most vulnerable to this injury. In the present study we report neuroprotection of estrogen on hypoglycemic injury in hypothalamic cell line. The cell viability, toxicity and proliferation were determined using different bioassays like cell count, MTT and LDH assay. There was a marked decrease in the cell count when exposed to hypoglycemia and the cell count increased in the presence of estrogen (p<0.0001). Under hypoglycemic conditions within 24 hours there was a significant loss in mitochondrial function with about 80% of retrieval in the presence of estrogen. The attenuation of the death pathways was only seen within the first 24 hours and gradually decreased with time. Cell damage and cellular toxicity was further analyzed by LDH. LDH increased in the absence of glucose and decreased in the presence of estrogen. In order to determine whether estrogen exerted its action through the AKT pathway, AKT activity was determined using PRAS40. There was reduction of PRAS40 when cells were exposed to hypoglycemic shock which dissipated in the presence of estrogen. Taking together the biochemical and molecular data it seems that estrogen shows neuroprotection against hypoglycemic shock and maybe via the activation of Akt pathway. Continue reading >>

Low Blood Sugar: A Common Cause Of Hormone Imbalance

Low Blood Sugar: A Common Cause Of Hormone Imbalance

Did you know that blood sugar imbalance could be the underlying cause of various unpleasant symptoms you experience throughout your menstrual cycle? And you don’t have to be diabetic or pre-diabetic with an elevated blood sugar level to be affected either. In fact, low blood sugar is a fairly common, but often overlooked, cause of hormonal imbalance among women. How Low Blood Sugar Creates Hormone Imbalance Our brain, along with every cell in the body, needs a constant and even flow of glucose (sugar) for energy – and to function properly. When the supply of blood sugar is unstable, either too high or too low, it puts stress on various organs, among them the brain. At this point the adrenal glands are called in to rescue the situation. They release the stress hormone cortisol to normalize the blood sugar level with emergency stores of a special sugar called glycogen. Our brain and cells get the sugar they need and all is good. However, if this stressful scenario repeats itself too often, the adrenal glands will become overwhelmed, fatigued, and eventually exhausted. And a burned-out adrenal system is a sure way to disrupt the natural balance of reproductive hormones such as estrogen, progesterone and testosterone. If you're interested in learning more, check out my article on adrenal fatigue. Common Symptoms of Low Blood Sugar When there's an insufficient supply of sugar to our brain and various parts of the body, we're likely to feel less than optimal. Below are some common symptoms of low blood sugar: Sugar cravings Fatigue, exhaustion Constant worrying, nervousness, anxiety, depression Headache, blurred vision, fainting, dizziness, drowsiness Forgetfulness, poor concentration, confusion, indecisiveness Digestive problems Insomnia Heart palpitation, rapid pulse, t Continue reading >>

Estrogen Blunts Neuroendocrine And Metabolic Responses To Hypoglycemia

Estrogen Blunts Neuroendocrine And Metabolic Responses To Hypoglycemia

This study tested the hypothesis that estrogen is the mechanism responsible for the sexual dimorphism present in the neuroendocrine and metabolic responses to hypoglycemia. Postmenopausal women receiving (E2; n = 8) or not receiving (NO E2; n = 9) estrogen replacement were compared with age- and BMI-matched male subjects (n = 8) during a single-step 2-h hyperinsulinemic-hypoglycemic clamp. Plasma insulin (599 ± 28 pmol/l) and glucose (2.9 ± 0.03 mmol/l) levels were similar among all groups during the glucose clamp. In response to hypoglycemia, epinephrine (2.8 ± 0.6 vs. 5.8 ± 0.8 and 4.4 ± 0.5 nmol/l), glucagon (57 ± 8 vs. 77 ± 8 and 126 ± 18 ng/l), and endogenous glucose production (2 ± 2 vs. 10 ± 2 and 6 ± 3 μmol · kg−1 · min−1) were significantly lower in E2 vs. both NO E2 and male subjects (P < 0.05). These reduced counterregulatory responses resulted in significantly greater glucose infusion rates (16 ± 2 vs. 6 ± 2 and 6 ± 3 μmol · kg−1 · min−1; P < 0.01) in E2 vs. both NO E2 and male subjects. Pancreatic polypeptide was significantly lower (P < 0.05) in both the E2 and NO E2 groups compared with the male subjects (136 ± 20 and 136 ± 23 vs. 194 ± 16 pmol/l). Last, glycerol (36 ± 3 vs. 47 ± 5 μmol/l; P < 0.05), lactate (1.4 ± 0.1 vs. 1.8 ± 0.2 mmol/l; P < 0.05), and muscle sympathetic nerve activity (19 ± 4 to 27 ± 4 vs. 27 ± 5 to 42 ± 6 bursts/min; P < 0.05) responses to hypoglycemia were all significantly lower in E2 vs. NO E2 subjects. We conclude that estrogen appears to play a major role in the sexual dimorphism present in counterregulatory responses to hypoglycemia in healthy humans. Men and women respond differently to an acute bout of hypoglycemia. We have previously shown that healthy and type 1 diabetic women, compar Continue reading >>

Hypoestrogenism

Hypoestrogenism

Hypoestrogenism, or estrogen deficiency, refers to a lower than normal level of estrogen, the primary sex hormone in women. In general, lower levels of estrogen may cause differences in the breasts, genitals, urinary tract, and skin. Hypoestrogenism is most commonly found in women who are postmenopausal, have premature ovarian failure, or are suffering from amenorrhea; however, it is also associated with hyperprolactinemia and the use of gonadotropin-releasing hormone (GnRH) analogues in treatment of endometriosis. It has also been linked to scoliosis and young women with type 1 diabetes mellitus. Symptoms[edit] Presentations of low estrogen levels include hot flashes, headaches, lowered libido, and breast atrophy. Reduced bone density leading to secondary osteoporosis and atrophic changes such as pH change in the vagina[1] is also linked to hypoestrogenism. Low levels of estrogen can lead to dyspareunia and limited genital arousal because of changes in the four layers of the vaginal wall.[2] Hypoestrogenism is also considered one of the major risk factors for developing uncomplicated urinary tract infections (UTIs) in postmenopausal women who do not take hormone replacement therapy. Causes[edit] Hypogonadotropic hypogonadism such as due to hyperandrogenism, lactation, certain medications (e.g., androgens/anabolic steroids, progestogens, prolactin releasers, GnRH analogues), pituitary gland/hypothalamus damage, or isolated hypogonadotropic hypogonadism (e.g., Kallmann syndrome, CHARGE syndrome, GnRH insensitivity) Hypergonadotropic hypogonadism such as due to menopause, premature ovarian failure, certain medications (e.g., aromatase inhibitors, CYP17A1 inhibitors), gonadotropin insensitivity, or inborn errors of steroid metabolism (e.g., aromatase deficiency, 17α-hydro Continue reading >>

Hypoglycemia

Hypoglycemia

What Is It? Hypoglycemia is an abnormally low level of blood sugar (blood glucose). Because the brain depends on blood sugar as its primary source of energy, hypoglycemia interferes with the brain's ability to function properly. This can cause dizziness, headache, blurred vision, difficulty concentrating and other neurological symptoms. Hypoglycemia also triggers the release of body hormones, such as epinephrine and norepinephrine. Your brain relies on these hormones to raise blood sugar levels. The release of these hormones causes additional symptoms of tremor, sweating, rapid heartbeat, anxiety and hunger. Hypoglycemia is most common in people with diabetes. For a person with diabetes, hypoglycemia occurs because of too high a dose of diabetic medication, especially insulin, or a change in diet or exercise. Insulin and exercise both lower blood sugar and food raises it. Hypoglycemia is common in people who are taking insulin or oral medications that lower blood glucose, especially drugs in the sulfonylurea group (Glyburide and others). True hypoglycemia with laboratory reports of low blood sugar rarely occurs in people who do not have diabetes. When it does occur outside of diabetes, hypoglycemia can be caused by many different medical problems. A partial list includes: Gastrointestinal surgery, usually involving removal of some part of the stomach. Surgery that removes part of the stomach can alter the normal relationships between digestion and insulin release The antibiotics gatifloxacin (Tequin, which was recently removed from the market in the U.S.), levofloxacin (Levoquin), and related drugs A pancreatic tumor, called an insulinoma, that secretes insulin A deficiency of growth hormone from the pituitary gland or of cortisol from the adrenal glands. Both of these Continue reading >>

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