Beta Endorphins & Wellness
Our bodies produce thousands of chemicals that control impulses necessary for everyday function and sensory navigation. Endorphins, a multi-functional chemical, are emitted to counteract and deal with sensations by transmitting electrical impulses through the body to the nervous system. One of their duties is to help combat pain, much in the same way as morphine or codeine does. Endorphins are also responsible for producing the euphoric feeling one usually experiences after sex, or after an intense work out (often referred to as runners-high). Rigorous work outs not only keep us in shape, but also decrease our stress level due to the endorphins released into the body during the exercise. Other ways to trigger the release of these hormones is through the practice of meditation, acupuncture, and massage therapy.
The common obesity of middle age presents as a set of features that strongly resembles the cardinal symptoms of Cushing’s syndrome: obesity of the face (moon face), upper back (buffalo hump) and trunk (pot belly) accompanied by signs of protein-wasting. In non-obese individuals who remain at a constant weight throughout life, the proportion of adipose tissue increases with age at the expense of lean tissue loss. Thus, a mild version of Cushing’s syndrome may be part of the normal aging process. A more intense version of this process may occur in overweight adults. Excess and chronic activity of two pituitary hormones may contribute to this adiposity. Both hormones are produced in the same pituitary cell by cleavage from a common large precursor known as pro-opiocortin. One hormone is adrenocorticotrophin (ACTH), which stimulates the release of the glucocorticoid hormones. These hormones promote the conversion of bodily proteins to glucose (gluconeogenesis). The other pituitary hormone is beta-endorphin, a stimulant of appetite that causes the release of insulin. This pancreatic hormone promotes the conversion of glucose and fatty acids to triglycerides (lipogenesis). Three different etiologies are suggested for the excessive and chronic action of these two pituitary hormones: tumors that increase the number of cells that synthesize pro-opiocortin: mutant strains such as the genetically obese mouse (ob/ob) and rat (fa/fa) that produce excessive amounts of ACTH and beta-endorphin: and an age-determined shift in the type of cleavage enzymes present in the pro-opiocortin cell that favors ACTH and beta-endorphin production. Lean body weight loss may be an important contributor to the increased medical problems and mortality of the obese.
Administration of human B-endorphin (2.5 mg IV bolus) to three subjects with non-insulin-dependent diabetes mellitus (type II) induced prompt and simultaneous increments in the plasma concentrations of insulin and glucagon lasting up to 90 minutes. In contrast to the hyperglycemic response previously observed in normal subjects following β-endorphin, these diabetics showed a progressive decline in plasma glucose throughout the study period. This disparity may be related to a relatively greater release of insulin and lesser rise in glucagon observed in diabetic subjects than in non diabetic subjects. These preliminary findings suggest that further studies to elucidate the role of pancreatic β-endorphin on glucose regulation may be rewarding.
Naltrexone, an opiate antagonist, was administered to young obese (ob/ob) and lean mice for five weeks. Animals had continuous access to food and received 10 mg/kg SC twice daily with equivalent volumes of saline given to controls. The effects on body weight, and pituitary and plasma levels of β-endorphin-like material were measured. Naltrexone-injected obese animals gained weight more slowly over the first three weeks while the weight gain of lean animals was not affected by naltrexone. Plasma levels of B endorphin were shown to be significantly higher in untreated ob/ob mice and this difference increased with age four to twenty weeks. With naltrexone treatment, plasma levels in +/? mice rose and exceeded those in ob/ob. The infusion of synthetic human β-endorphin (4.5 ng/kg/min) produced the following:
(1) in normal-weight subjects, no significant change of plasma glucose and pancreatic hormones (insulin, C- peptide, and glucagon), a significant plasma free fatty acids (FFA) increase, and a suppression of glycerol plasma levels;
(2) in obese subjects, significant increases of glucose, insulin, C-peptide, and glucagon, a progressive decline of circulating FFA, and no change in glycerol plasma levels. In obese subjects, the intravenous administration of naloxone, given as a bolus (5 mg injected in 5 minutes) before the start of β-endorphin infusion, reduced the plasma glucose response to the opioid by approximately half, annulled the pancreatic hormonal responses, and also reduced the FFA, but not glycerol, response. In normal-weight subjects, naloxone pre treatment did not induce any change of the flat glucose and hormonal responses to β-endorphin, but reversed its effects on circulating FFA and glycerol. These data suggest that physiological elevations of plasma β-endorphin concentrations produce metabolic and hormonal effects in obese subjects significantly different from those occurring in normal-weight subjects; these effects are partially naloxone-sensitive, suggesting the mediation of endogenous opioid receptors.
Investigation has been carried out on 50 samples of fetal pancreata from the 10th to the 32nd week of gestation using the PAP technique. (3-Endorphin-reactive cells were morphometrically recorded by means of the point-counting method.
β-Endorphin reactivity occurred for the first time during the 15th week. During further development, β-endorphin cells were found inside and outside the islets. From the 18th to the 23rd week, these cells were primarily localized in the islet periphery. From the 24th week, they rearranged and occurred in irregular positions mixed with other islet cells. This rearrangement took place with a 4 week delay compared with the basic cell types of the islet organ.
The extrainsular portion of these cells in the exocrine parenchyma varied between 0.3 % in the 27th week and up to 10% in the 22nd week. Concerning the adult human pancreas, it has been suggested whether (3-endorphin cells may be a 6th basic cell type of the islet organ. Previous studies on the coexistence of somatostatin, glucagon and (3-endorphin in the same islet cell and the morphometric analysis would support this assumption.
Endogenous opioids have a tonic inhibitory effect on sympathetic tone and have been implicated in the pathophysiology of vasodepressor syncope. Plasma beta endorphin concentrations increase after vasodepressor syncope induced by exercise or by fasting. AIMS–To take frequent samples for plasma beta endorphin estimation during tilt testing, and to determine whether plasma beta endorphin increased before the start of syncope. PATIENTS–24 patients undergoing tilt testing for investigation of unexplained syncope. SETTING–Tertiary referral center. Blood samples were obtained during 70 degrees head up tilt testing. Plasma beta endorphin concentrations were estimated by radioimmunoassay (mean(SD) pmol/l). RESULTS–Patients with a positive test showed a rise in beta endorphin concentrations before syncope baseline 4.4(1.5) v start of syncope 8.5(3.1), p < 0.002). In contrast, patients with a negative test showed no change in beta endorphin concentrations (baseline 3.4(1.0) v end of test 4.5(2.3), NS). After syncope all patients showed a large secondary increase in beta endorphins (32.3(18.6)). An increase in plasma beta endorphins precedes vasodepressor syncope. This finding supports a pathophysiological role for endogenous opioids in diabetes, obesity and other related disorders.
Contrary to popular belief, obesity is not simply the result of eating too many calories and not exercising enough. The following factors can contribute to obesity and your waist line:
Antibiotics in Food and Medicine
Enhancing Drugs & Hormones used in Livestock
Endocrine Disrupting Chemicals, Including Pesticides
Artificial Sweeteners
Aggressive Stealth Marketing of Junk Food
Eating Organic Foods and avoiding the above hidden factors is the most effective in reversing Obesity & Diabesity.
when insulin is high, the body cannot burn fat. And most of what you eat gets stored as fat instead of being used for energy. Weight loss becomes next to impossible. That is why type 2 diabetics gain so much weight after starting insulin shots. For 70% of my clients, simply reducing insulin by means of controlling carbohydrates is just what the doctor ordered.
Your Fat Cells Will Actually Shrink When IGF-1 [Insulin Like Growth Factor]Hormone Turns On Your Metabolically Active Tissue (M.A.T.). IGF-1 is the single most important factor in sustainable weight loss and in creating a metabolic response that rejuvenates the body.
Low IGF-1 & HGH [Human Growth Hormone], Beta Endorpins can result in obesity & diabesity.
If you have More than 3 YES, probably you have low IGF-1:
1. Have more than an inch of body fat stored on your right love handle? Simply pinch there now. If you can pinch more than the length of your index finger then answer YES.
2. Feel sleepy after eating a rich meal, especially one hour after eating a carb-heavy lunch? If so, then answer YES.
3. Currently carry more than 30 pounds of extra weight that you have tried to lose at least 3 times with no success? If so, answer YES.
4. Have cellulite or other areas of pocket obesity, such as a lower belly pooch, or saddle bags on the hips and thighs? If so, then answer YES.
5. Struggle with losing weight and keeping it off, even when restricting calories or going on an exercise plan? If so, then answer YES.
The primary IGF-1 vampires are…
AGING
Currently, there is nothing we can do about aging. That is too bad because your IGF-1 levels fall by 14% when you hit your 30s. Fall 25% in your 40s. And plummet a full 56% in your 60s.
However, you can make your body look as if it is aging slower by increasing your IGF-1 levels naturally with what I am about to show you.
OUR TOXIC ENVIRONMENT
Toxins in our air, water, food and homes can block IGF-1 fat burning signals, rendering it useless.
For example, high blood levels of the common heavy metal lead have been associated with lower IGF-1 expression.
CARB-RICH DIETS
Our carb-heavy diet culture has put a massive dent into your IGF-1 production.
Eliminating junk carbs is a start, but it is not the complete answer.
Low IGF-1 levels have been directly connected to memory-related disease states like Alzheimers and dementia. This is known as Type 3 Diabetes.
Low levels of IGF-1 may accelerate the formation of these bone diseases.
A 2011 study in the Journal of Bone and Mineral Research showed that those with lower levels of IGF-1 had a 23% higher risk of bone fractures, especially for the two most debilitating kind: hip and spine fractures.
A 2010 study in the Journal of Clinical Endocrinology & Metabolism found that the risk of dying from heart disease jumped 38% for every 40 ng/ml decrease in IGF-1 levels.
Elevated IGF-1 combined with low insulin keeps you feeling full, which means you never have to count a single calorie.
Your body will do it for you automatically. Your body hunger signals will automatically adjust, allowing you to eat freely without feeling hungry.
A 2003 study in the Journal of the American Geriatrics Society showed that higher IGF-1 levels predicted lower loss of lean muscle mass in aging men.
A 2013 study in the British Journal of Dermatology showed higher levels of the biologically active form of IGF-1 lead to people looking younger, by way of reduced skin wrinkling and facial aging.
Fortunately, increasing your levels of IGF-1 can reboot an aging brain through a process called hippocampal neurogenesis. This grows new brain cells in the hippocampus, a part of the brain heavily involved in short- and long-term memory.
From our research we found that consuming 7 vegetable and only 2 fruits, restricting the intake of sugar, flour and gluetin and using the patented access bar to turn Fat to Fuel along with using the Bio Mat increases IGF-1, HGH and Beta Endorphins and achieve optimal weight management. See our published research on Thermotherapy using the Bio mat on this website. www.academyofwellness.com
Studies show that gluten contains certain proteins called opioid peptides or “exorphins.” And just like opium, these peptides can interfere with brain function. Also, in sensitive people, gluten causes inflammation, which also can irritate the brain and cause it to malfunction. But as the results of this study show, the brain fog that gluten causes does not actually damage the brain. All you have to do is to stop eating gluten and you’re good as gold.
As one of the authors of the study put it, “People who promote an anti-grain or anti-gluten agenda sometimes cite our work in celiac disease, drawing far-ranging conclusions that extend well beyond evidence-based medicine. We know brain fog’ is a serious symptom commonly reported by our patients, and it’s understandable that people have been worried about a possible connection to dementia. Fortunately, our work with Dr. Ludvigsson provides concrete evidence that this particular worry can be laid to rest.”
So if you’re suffering from the symptoms of brain fog, it’s not a bad idea to stop eating gluten for a month to see if the symptoms get better
Author’s Bio:
Dr. George Grant is considered by his peers as Wellness Ambassador & Champion. He is the founder & CEO of Academy of Wellness in 1983. Dr Grant enjoys a stellar academic background as well as a fascinating career in research. He is a scientist, professor, analytical chemist, toxicologist, pharmacologist, microbiologist, nutritionist, biofeedback, stress management & pain specialist, and indoor air quality specialist. Dr Grant is the author of 7 best selling books, former Scientist at University of Saskatchewan Faculty of Pharmacy and Nutrition, Professor at Seneca College in Toronto, and Senior Consultant for Health Canada as well as in private practice.
Prof. Dr. Grant is among International Who is Who of Professionals. He has 100 published articles, conference presentations, book reviews and 7 bestselling books, including a chapter in 100 ways to improve your life with Mark Victor Hanson, the author of Chicken Soup for the Soul. Dr Grant helped 7 Olympic athletes to remain competitive. Dr. Grant helped thousands of his clients, corporations and non profit organizations worldwide through his passion for wellness and compassion for his clients. He pioneered the research of Beta Endorphins on SIDS at the Faculty of Pharmacy, University of Sask., Saskatoon, Sask. Canada in 1981.
There is an epidemic of blood sugar problems in America and scientists now believe they have found out the reason why.
Scientists tested 2,016 Americans for the presence of six toxins known as POPs (persistent organic pollutants). The scientists then compared the levels of these 6 toxins in the participants bodies to their history of blood sugar problems.
And here is what they discovered. The people with the highest levels of these 6 toxins were 38 times more likely to have blood sugar problems compared to the people with the lowest levels!
That is because these toxins can destroy the beta cells in your pancreas that produce insulin, the hormone that regulates your blood sugar levels. These toxins can also interfere with the cell receptors that carry glucose (sugar) to your muscle and fat cells. And they can limit your cell receptors ability to use insulin. When your cells have a hard time accepting and using insulin, then your blood sugar rises.
In the October 2014 IHN a novel dietary approach was discussed which successfully reversed
type 2 diabetes in 8 weeks. The research group headed by Dr. Roy Taylor of the University of
Newcastle in the UK has just published a second clinical trial.17 This trial addresses the question
of the efficacy of the diet for individuals with long-term duration of diabetes (> 8 years) as
compared to those with short-term duration < 4 years), the latter group being similar to those the
original study published in 2011.18 The report was prefaced by the statement: The inevitably
progressive nature of type 2 diabetes has been widely accepted since the UK Prospective
Diabetes Study was carried out, which showed that glucose control steadily worsened towards
requirement for insulin treatment despite best possible therapy.
There were 15 subjects in the short-duration and 14 in the long-duration groups. The protocol
was similar to the earlier study with subjects taken off anti-diabetic medications prior to the start
and then all put on a diet of approximately 700 calories for 8 weeks. The diet consisted of 600
calories from a meal replacement product and the balance from vegetables. Using fasting blood
glucose (FBG) as the criterion, all the subjects in the short-duration group regressed to normal
glycemia and could be considered at least temporarily cured. As is indicated in the table
presented below, those with > 8 years with a diagnosis of type 2 diabetes did not do as well.
www.freiburgstudy.com
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Jul 30, 2015 – Citation: Grant G (2015) Beta Endorphins & Wellness. … different endorphins with possible benefits and uses that researchers are investigating.
Mediation of β‐endorphin in exercise‐induced improvement in insulin resistance in obese Zucker rats
CF Su, YY Chang, HH Pai, IM Liu… – … research and reviews, 2005 – Wiley Online LibraryBackground Aerobic exercise including treadmill running has long been used to
successfully treat and/or prevent insulin resistance and type‐2 diabetes. Increase of plasma
β‐endorphin is observed with exercise. The present study was designed to clarify the role of …Cited by 47Related articlesAll 8 versions
Infusion of β–endorphin improves insulin resistance in fructose-fed rats
CF Su, YY Chang, HH Pai, IM Liu… – Hormone and …, 2004 – thieme-connect.comIn an attempt to probe the effect of β–endorphin on insulin resistance, we used Wistar rats
that were fed fructose-rich chow to induce insulin resistance. Insulin action on glucose
disposal rate (GDR) was measured using the hyperinsulinemic euglycemic clamp …Cited by 31Related articlesAll 4 versions[PDF] hindawi.com
Myricetin ameliorates defective post-receptor insulin signaling via β–endorphin signaling in the skeletal muscles of fructose-fed rats
TF Tzeng, SS Liou, IM Liu – Evidence-Based Complementary and …, 2011 – hindawi.com… View at PubMed · View at Scopus; CF Su, YY Chang, HH Pai, IM Liu, CY Lo, and JT Cheng,
“Mediation of beta–endorphin in exercise … C.-F. Su, Y.-Y. Chang, H.-H. Pai, I.-M. Liu, C.-Y. Lo, and
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Metformin increases insulin sensitivity and plasma β–endorphin in human subjects
HY Ou, JT Cheng, EH Yu, TJ Wu – Hormone and metabolic …, 2006 – thieme-connect.com… Y Y, Pai H H, Liu I M, Lo C Y, Cheng J T. Infusion of β–endorphin improves insulin … Y Y, Pai H H,
Liu I M, Lo C Y, Cheng J T. Mediation of beta–endorphin in exercise … Rudenski A S, Naylor B A,
Treacher D F, Turner R C. Homeostasis model assessment: insulinresistance and betaCited by 36Related articlesAll 6 versions
Insulin, C-peptide, androgens, and beta–endorphin response to oral glucose in patients with polycystic ovary syndrome
G Tropeano, A Lucisano, I Liberale… – The Journal of …, 1994 – academic.oup.com… based on the observation of elevated fasting and glucose-stimulated P-endorphin (PEP) levels …
a glucose challenge would allow us to document and quantitate insulinresistance and that …
associated with an increase in androgens and PEP levels in insulin–resistant women with …Cited by 39Related articlesAll 7 versions
Reduction of hyperinsulinemia and insulin resistance by opiate receptor blockade in the polycystic ovary syndrome with acanthosis nigricans
JR GIVENS, BR KURTZ, AE KITABCHI… – The Journal of …, 1987 – academic.oup.com… (8) sug- gested that the hyperglycemic action of endorphins is mediated at … J Clin Endocrinol Metab
52:592 8. Feldman M, Riser RS, Unger RH, Li CH 1983 Beta–endorphin and the … Aleem FA,
Mclntosh T 1984 Elevated plasma levels of/8-endorphin in a group of women with …Cited by 48Related articlesAll 5 versions[HTML] fertstert.org
Insulin resistance influences central opioid activity in polycystic ovary syndrome
A Berent-Spillson, T Love, R Pop-Busui, MF Sowers… – Fertility and sterility, 2011 – Elsevier… emission tomography. glucose regulation. μ-opioid receptors. neuroimaging. β–endorphins. PCOS.
insulin … are expressed in proopiomelanocortin-containing neurons, the precursor of β–endorphin
RC TurnerHomeostasis model assessment: insulinresistance and beta-cell function …Cited by 13Related articlesAll 16 versions
Opioid μ-receptors as new target for insulin resistance
KC Cheng, A Asakawa, YX Li, IM Liu, H Amitani… – Pharmacology & …, 2013 – Elsevier… of insulinresistance was associated with an elevation of circulating β–endorphin to ameliorate
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phosphatidylinositol 3-kinase (PI3-kinase) signaling pathway. In insulinresistant rats, Loperamide …Cited by 17Related articlesAll 8 versions
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Body fat distribution, insulin resistance, and metabolic diseases
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J Boyer, MC CloixAnthropometry of obesity, diabetes, adrenal and beta-cell functions … R Pasquali,
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