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Estrogen Hypoglycemia

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 >>

Blood Sugar Imbalances Can Alter Estrogen And Testosterone Levels

Blood Sugar Imbalances Can Alter Estrogen And Testosterone Levels

If you’ve been reading my website even modestly, you know that I speak about blood sugar regulation as one of the most important aspects of health and wellness. The reason for this is because the deleterious, systemic effects that ensue from unbalanced blood sugar, both directly and indirectly, are enormous. If you’re interested in reading my articles on the topic, click here. This article will focus on the basics of blood sugar imbalances and “male” and “female” hormones. There is certainly a difference between hypo- and hyperglycemia. But regardless of which end of the spectrum a person lies, surges of insulin can accompany both. Insulin is the hormone that helps transport sugar (or glucose) out of the bloodstream and into the cells of the body. Because of insulin’s action, it is generally more elevated in those with chronically high blood sugar, but can also surge if a person is hypoglycemic and experiences wide fluctuations in blood sugar. The complications regarding insulin and the sex hormones estrogen and testosterone can be seen very straightforward. As you know, both males and females have estrogen and testosterone although women have higher levels of the former, whereas men have high higher levels of the latter. It’s important for this hormonal balance to be maintained for a number of reasons beyond the scope of this article. Essentially, when females experience elevated insulin levels, there is an enzyme known as 17,20 lyase that gets up-regulated and then converts (some of) their estrogen into testosterone. In males, elevated insulin levels will increase the enzyme aromatase which will cause (some of) their testosterone to be converted into estrogen. This scenario may not sound terrible, but it’s important to realize that it’s a serious p 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 >>

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 >>

Hypoglycemia

Hypoglycemia

Both stress and adrenal fatigue can contribute to hypoglycemia (low blood sugar) because of the key roles the adrenal hormones epinephrine, norepinephrine and cortisol play in blood sugar regulation. Stress (and the anticipation of stress) signals the body to raise blood sugar (glucose) levels in order to generate energy to respond to the stress. If the body cannot meet this higher demand for blood glucose, hypoglycemia can result. Stress may also provoke blood sugar swings that can have a cumulative effect on the body’s ability to maintain blood sugar balance, and aggravate hypoglycemic symptoms. In fact, some of the symptoms of hypoglycemia, such as irritability and nervousness, may sometimes be the effects of high levels of stress hormones rather than of the low blood sugar itself. During adrenal fatigue, when adrenal hormone levels are lower, it becomes harder to maintain blood sugar balance, especially in response the increased demand from stress. It has been known for almost a century that people who are chronically hypoglycemic are often also experiencing adrenal fatigue, and that people going through adrenal fatigue almost always have some form of irregular blood sugar pattern. Hypoglycemia is the most common of these. Hypoglycemia commonly occurs during adrenal fatigue when low epinephrine, norepinephrine and cortisol are combined with the high insulin levels of stress. The low levels of adrenal hormones that can occur during adrenal fatigue may fail to raise blood glucose enough to meet the increased demand. As a result, the cells do not get the glucose and other nutrients they require, and the person may crave sugar as well as feel tired, shaky and weak. Circulating epinephrine, norepinephrine and cortisol help the liver convert glycogen (stored glucose) in 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 >>

Doctor Detective With Bryan Walsh

Doctor Detective With Bryan Walsh

In this week’s case study, Doctor Detective meets a woman suffering from adult acne. But he quickly discovers that acne is the least of her problems. With sex hormone, cortisol, and blood sugar imbalances, can Doctor Detective help get her back on the right track? Find out below. Eat less and exercise more. It’s generally a great prescription for improving health and improving body composition. However, it doesn’t always work. Even with an awesome exercise plan and a rock-solid diet, some people suffer from mysterious symptoms and complaints that seem puzzling, given how much effort they put into their fitness and health. When we meet clients who have problems that exercise and nutrition — not to mention their own doctors — can’t seem to solve, we know there are only a few experts on the planet to turn to. One of them is Bryan Walsh. Dr. Walsh has a sharp mind, a fitness background, a degree in naturopathic medicine, and extensive additional training and certifications. His wife is a naturopath too. (We bet his kids are the healthiest on the planet.) So, when clients have nowhere else to turn, Dr. Walsh turns from mild-mannered dad and husband into forensic physiologist. He pulls out his microscope, analyzes blood, saliva, urine, lifestyle – whatever he has to. And he frees up the physiological jam. That’s why, when Dr. Walsh volunteered to work on a monthly case study feature with us, we jumped at the chance. By following along with these fascinating cases, you’ll see exactly how a talented practitioner thinks; and you’ll also learn how to improve your own health. In today’s case, we’ll meet a client who came to Dr. Walsh with a single complaint: adult acne. However, upon further investigation, Dr. Walsh discovered that she was suffering from pr Continue reading >>

Progesterone

Progesterone

Hormones and the Menstrual Cycle The ovary and the adrenals are the source of two types of “female” hormones, estrogens and progesterone. At least six different estrogens have been identified, but only estrone, estradiol (E2), and estriol are circulate in significant quantities in the blood. Estrogen levels begin to increase during the first part of the menstrual cycle, (follicular phase) peak just before ovulation, and then decline slowly until they reach their lowest point at the onset of menses. The principal function of the estrogens is to cause cellular proliferation and growth of the tissues of the sexual organs and tissues related to reproduction. Progesterone is a hormone that prepares the lining of the uterus for the fertilized egg and maintains pregnancy. The name tells the story, promotes gestation hormone. Progesterone is derived primarily from the corpus luteum in the ovary after ovulation. When the follicle ruptures, it is transformed into the corpus luteum. Progesterone is also produced by the placenta during pregnancy and in small amounts by the adrenal cortex. Progesterone is a “precursor” hormone that is converted into other steroid hormones like testosterone, estrogens, cortisol and aldosterone. During the follicular phase (before ovulation), the concentration of progesterone in the bloodstream is less than 1 ng/ml, although still present in much higher amounts than estrogen. Ovulation initiates the second half (luteal phase) of the cycle, and at this time progesterone levels in the blood increase up to 20 ng/ml and may be 140 times as high as estrogen. As its levels increase, progesterone acts as a powerful antagonist to the action of estrogens. A sharp decline in progesterone initiates the onset of the menses. Pre-Menstrual Syndrome Pre-mens 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 >>

Chakraborty's Laboratory

Chakraborty's Laboratory

Home Research Projects Teachings Current students/ AlumniPublications Meetings and Presentation Animal Facility Project 1: ‘Hypoglycemia And Estrogen’ Model: Hypothalamic cell line Hypoglycemia is a condition when the blood glucose level falls below normal levels. Glucose is the main metabolic fuel of the brain. Recurrent episodes of hypoglycemia can lead to seizures, coma, and even death. There is evidence that estrogen, a steroid hormone, mainly produced by ovaries, is required for the maintenance of glucose homeostasis.It has been suggested that estrogen affects cell viability, survival and proliferation and regulates genes positively and negatively through intracellular signaling of membrane receptors (e.g. G- protein, Ca++, cAMP, PKC, etc) where the receptors are outside the nucleus in the cytoplasm or the plasma membrane; the nongenomic pathway or membrane initiated steroid signaling.. However, the molecular mechanism involving the event is a subject of debate. We propose that estrogen exerts its neuroprotective effect through the AKT-GSK3b signaling pathway since our DNA microarray data suggest that AKT is downregulated in the absence of glucose and in the presence of estrogen thre is an upregulation promoting cell survival. 1. Does hypoglycemic injury trigger apoptosis in subpopulations of hypothalamic neurons through specific death pathways? Is estrogen able to provide protection against injury? 2. Is the neuroprotection of estrogen mediated through ERalpha or plasma membrane receptor? 3. Are there caspase induced neuronal cell death? Project 2: ‘Atrazine as an Endocrine Disrupting Chemical’ Model: Hypothalamic cell line/ Animals Atrazine is a widely used herbicide. It has been shown to exhibit endocrine disrupting properties. A few studies demonstrate Continue reading >>

Insulin Resistance & Estrogen

Insulin Resistance & Estrogen

Estrogen has many beneficial effects in the body, including helping optimize the action of insulin, the hormone that prevents high blood sugar levels. Consequently, low estrogen levels may lead to insulin resistance, or impaired insulin action. Insulin resistance is linked to metabolic syndrome, a group of traits and medical conditions that increase the risk of health problems such as diabetes, heart attack and stroke. Low estrogen levels and insulin resistance can have negative health consequences, and your doctor can best guide you on how to manage and treat these health concerns. Insulin resistance is a distinguishing feature of metabolic syndrome, a cluster of conditions including the elevated blood sugar levels found in prediabetes and type 2 diabetes (T2DM); central or abdominal obesity; high blood pressure; and abnormal blood lipids -- specifically elevated levels of triglycerides, a blood fat, and low levels of HDL, a protective cholesterol made by the body. Metabolic syndrome affects about 35 percent of U.S. adults, according to a study published in the May 2015 issue of "The Journal of the American Medical Association." The relationship between metabolic syndrome, insulin resistance and estrogen is complex, and more research is needed to clarify the interplay of these hormones in health and disease. A review of animal and human studies published in the March 2016 "Journal of Diabetes Research" discussed the known association between estrogen and insulin action. In addition to impairing insulin action, low estrogen levels may hinder the secretion of insulin from the pancreas, suggest the study authors. Insufficient insulin causes the liver to produce excess glucose and send this surplus into the blood. Estrogen deficiency may also cause inflammation, which can 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 >>

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 >>

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