Vitamin D Levels And Liver Disease: Type I Vs Type Ii Diabetes
In the American epidemic of diabetes and obesity, doctors diagnose an additional 3,700 American children with type-2 diabetes every year. In addition, the most common form of liver disease in children, potentially severe, non-alcoholic fatty liver disease, is also increasing. If your child has diabetes, his or her chances of getting non-alcoholic fatty liver disease increase significantly. What is not known is how the two are connected; nor is it known if the liver disease impairs the liver’s ability to make 25(OH)D in these children, thus rendering them even more D deficient than sun avoidance would otherwise leave them. In a brilliantly designed experiment, Dr. Benjamin Nwosu and colleagues from the University of Massachusetts Medical School compared young teenagers with the autoimmune disease, type I diabetes, with children suffering from the obesity-driven type II diabetes, measuring 25(OH)D, liver function, and diabetic severity in all the children. Nwosu BU, Stavre ZG, Maranda L, Cullen K, Lee MM. Hepatic dysfunction is associated with vitamin D deficiency and poor glycemic control in diabetes mellitus. J Pediatr Endocrinol Metab. 2012;25(1-2):181-6. They discovered that the type II kids had much lower vitamin D levels than the type I kids. In fact, almost three times as many type II children were very deficient (<15 ng/ml) compared to type I, and the type II kids were more likely to have liver disease. Furthermore, in type II diabetes, low 25(OH)D was linearly related to both an elevated liver function test (ALT) and with elevated hemoglobin A1C (a measure of long-term blood glucose). The higher the 25(OH)D, the better both those tests; neither test showed evidence of a threshold or upper limit cutoff for the effectiveness of vitamin D. The authors conclud Continue reading >>
Why Do I Always Feel Hungry When I Am So Overweight? I Try To Eat Small Portions, But I Still Feel Hungry, And Thus I Eat More.
I had the same problem. It was so frustrating. To answer this question, I will have to teach you first about insulin, HGH, and water. When breaking down what insulin is, it is like a double-edged sword, and when used incorrectly it will cut us instead of the fat. Insulin is anabolic and will spur muscle growth and cell reproduction. Pretty f***ing awesome right? Well, only if it is timed correctly. The other side of this blade is it also spurs the growth of any kind, including fat while blunting the production of “HGH” (the magic fat burning, muscle building anti-ager). The body can not burn fat while insulin levels are high. Fat is an emergency fuel, only used when it is absolute needed. What we see as ugly superficial excess skin, the body see’s as life-saving fuel that is needed to survive. The Trick Outsmarting our bodies is not the easiest thing to do. The trick here is to make the body believe that it needs to burn this precious fuel (fat) because it is under stress. Insulin levels lower approximately 2-4 hours after ingesting, so don't take carbs 4 hours before going to bed if you can. People who underestimate the first HGH spike of the night when we sleep do not realize this is the biggest HGH release of the night, as the second one is second best and third is third best and so on. If we spike our insulin dramatically right before sleeping, we’re preventing the biggest release of the night. If we do this every day, this will result in so much HGH loss over time. Worst of all are the people who compound this with spiking the insulin at night and wake up and spike their insulin again first thing in the morning with breakfast. These people are never giving their bodies the adequate HGH that it needs to function optimally. When we were hunter gathers, carbs Continue reading >>
Horm Res Paediatr 2014;82:283–289 Doi: 10.1159/000365192
E-Mail [email protected] Mini Review Horm Res Paediatr 2014;82:283–289 DOI: 10.1159/000365192 Non-Alcoholic Fatty Liver and Metabolic Syndrome in Children: A Vicious Circle Arianna Alterio Anna Alisi Daniela Liccardo Valerio Nobili Hepato-Metabolic Disease Unit and Liver Research Unit, ‘Bambino Gesù’ Children’s Hospital, IRCCS, Rome , Italy Introduction Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in Western countries and its worldwide prevalence in adults and children is increasing and becoming an obesity epidem- ic [1, 2] . Particularly, there is an alarming increase of number of children affected by NAFLD supported by high prevalence data ranging from 3 to 12% in the gen- eral paediatric population up to 70–90% in young obese [3] . Paediatric NAFLD is associated with several factors of metabolic syndrome (MS), like abdominal (central) obesity, dyslipidaemia (hypertriglyceridaemia and/or hy- percholesterolaemia) and insulin resistance. Therefore, NAFLD can be considered as the hepatic manifestation of MS, even if there is no agreement that NAFLD contrib- utes to MS and vice versa [4] . In fact, the aetiology and pathogenesis of both diseases are multifaceted and close- ly related to genetic predisposing factors, intrauterine environment and unhealthy lifestyle [5] . Bad eating hab- its and sedentarity may favour the onset of childhood obesity strongly contributing to make a child more prone to develop NAFLD and MS during adolescence [6] . Fur- thermore, as a large part of children with NAFLD and traits of MS remain undiagnosed, it is plausible that, in the coming years, adolescents with NAFLD characteris- tics may present a rapid course of disease towards more severe forms of Continue reading >>
Clinical Characteristics Of Patients With Diabetes Mellitus And Fatty Liver Diagnosed By Liver/spleen Hounsfield Units On Ct Scan
Of 970 patients (717 male and 253 female; mean age 64.4 years), 175 males (24.4%) and 60 females (23.7%) had fatty liver. None of the 28 patients with type 1 diabetes had fatty liver. In male patients with type 2 diabetes, age, visceral adipose tissue (VAT), albumin, alanine amino-transferase (ALT), and triglycerides were independently associated with fatty liver. In females, age and bilirubin were associated with fatty liver. Continue reading >>
Diet And Diabetes: Why Saturated Fats Are The Real Enemy
This is the seventh article in our “Controversies” series and the third piece focusing on the subject of fats. Today, we are going to explore the very important relationship between saturated fat intake and the onset of diabetes. As we mentioned in The Ultimate Guide to Saturated Fats, “Once we control for weight, alcohol, smoking, exercise and family history, the incidence of diabetes is significantly associated with the proportion of saturated fat in our blood.” Today we will take a deep dive to fully understand why there is such a strong link between diabetes and saturated fat consumption. We will also discuss how a plant-based diet may protect you from (or even reverse!) the disease. What Is Insulin Resistance? Insulin resistance is a hallmark of both prediabetes and type 2 diabetes. So what is insulin resistance exactly (and why is it important)? Let me explain. Insulin is what permits glucose (sugar) in the blood to enter our (muscle) cells. In essence, insulin ‘unlocks’ the door, allowing the glucose to come in. If there is no insulin at all (the case of type 1 diabetes), the blood sugar ‘hangs out’ in the bloodstream because it cannot get inside. That causes the blood sugar levels to rise. But what happens if the insulin is there but is simply not working properly? In that case, the lock to the cell door is ‘blocked.’ This is what is called insulin resistance. So what causes insulin resistance in the first place? Insulin resistance is caused by fat. Fat build-up inside (muscle) cells creates toxic fatty breakdown products and free radicals that ‘block’ the insulin-signaling process, close the ‘glucose gate,’ and make blood sugar levels rise. And this cycle can happen really fast. In fact, insulin resistance can occur in 180 short minu Continue reading >>
Insulin And Fatty Liver Disease
Dr. Alfred Frohlich from the University of Vienna first began to unravel the neuro-hormonal basis of obesity in 1890. He described a young boy with the sudden onset of obesity who was eventually diagnosed with a lesion in the hypothalamus area of the brain. It would be later confirmed that hypothalamic damage resulted in intractable weight gain in humans, establishing this region as a key regulator of energy balance. In rats and other animals, hypothalamic injury could experimentally produce insatiable appetites and induce obesity. But, researchers quickly noticed something else, too. All these obese animals shared characteristic liver damage, which was occasionally severe enough progress to complete destruction. Looking back at hereditarily obese strains of mice, they noted the same liver changes. Strange, they thought. What does the liver have to do with obesity? Dr. Samuel Zelman first made the connection between liver disease and obesity in 1952. He observed fatty liver disease in a hospital aide who drank in excess of twenty bottles of Coca-Cola daily. This was already a well-known complication of alcoholism, but this patient did not drink alcohol. That obesity could cause similar liver damage by itself was completely unknown at that time. Zelman, aware of the animal data, spent the next few years tracking down twenty other obese, non-alcoholic patients with evidence of liver disease. One oddity he noted was that they unanimously preferred carbohydrate rich diets. Fatty liver in patients that are not alcoholics It would be almost thirty years later, in 1980, that Dr. Ludwig and colleagues at the Mayo Clinic described their own experience. Twenty patients had developed fatty liver disease, similar to what is found in alcoholics but they did not drink alcohol. This Continue reading >>
Diabetes – Is It Causing Your Sleep Problems?
Diabetes – Is it causing your sleep problems? Adequate sleep and quality sleep are critically important for good health. You can be eating healthy food and exercising regularly, but if you don’t sleep well you are at high risk of developing health problems. For diabetics, good sleep is even more important. If you do not sleep well, your blood sugar tends to rise. Lack of sleep is known to worsen insulin resistance. That means it causes insulin to be less effective in your body. If insulin doesn’t work as well, it has poor control over your blood sugar, and it is likely to rise. Unfortunately, having diabetes can create its own set of sleeping troubles. For various reasons, diabetics are often more prone to insomnia. Sometimes sleeping problems are what prompts an undiagnosed diabetic to visit their GP in the first place. A blood test for glucose then leads to a diagnosis of diabetes. Here are some common sleep problems in diabetics and ways to overcome them: Sleep apnea This is one of the most prevalent problems in type 2 diabetics who are overweight. Sleep apnea is an extremely common cause of waking up feeling unrefreshed, and being tired all day. It is quite a common cause of motor vehicle accidents as people may fall asleep at the wheel. People who get sleep anpea are more likely to carry excess weight on their upper body – torso and neck area. When adipose tissue (fat) encroaches the upper respiratory tract and throat, it impedes the flow of air, particularly when a person is laying down. Sleep apnea is also more common in people who drink alcohol (particularly in the evening) and people with a blocked nose or sinuses. Sleep apnea significantly raises the risk of high blood pressure and dementia. If you are overweight and suffering with significant fatigue, Continue reading >>
Diabetes As A Disease Of Fat Toxicity
The reason people get results with low-carb high fat diet is because of the minimal effects on insulin fat provides. There is no 2 ways around it. The camp that is lying is the camp that promotes starchy and moderate to high carb as either a cure or a mean to prevent diabetes. It’s all completely just wrong. Put it this way, you ever heard of the term “if it ain’t broke don’t fix it”? Well there is a reason the primary and go-to cure from nearly every doctor (including the mainstream western doctors) is low-carb & high fat. The other issue is, there was a person here who wrote up a decent little spiel on how insulin and diabetes go hand in hand. It got tons of likes, and consequently the mods of this forum pulled it, because I guess it “didn’t agree” with their views. Therein lies the problem, they don’t want people to know the truth for some odd reason. I’ll break it down in a nutshell: Type 1 Diabetes: Insulin dependent. People are usually born with this or acquire it at a very young age. These people are usually paper thin. They need to take insulin so they can in fact store their nutrients, otherwise they starve and die. Type 2 Diabetes: Insulin Resistant – People acquire this through bad diet and partly (possibly) pre-disposed to it at birth making them a little more likely to get it if they aren’t careful. Insulin resistant is at it sounds, the body (or cells in this case) are resistant to the insulin the body produces. So the question is, why? Well when you think of insulin as some annoying dude who continually knocks at the door, and your insulin receptors attached to cells are the guy inside who opens the door.. well eventually that guy inside gets sick of hearing the door knock so he ignores it. The more he ignores it, the louder the kn Continue reading >>
Liver And Fat In Type 2 Diabetes: New Insights And Clinical Relevance
Abstract Among various organs such as the pancreas, kidney, liver, skeletal muscle, and adipose tissue responsible for control of blood glucose levels, the liver is emerging as one of the principal organs involved in insulin resistance associated with type 2 diabetes mellitus. The liver is involved both short- as well as long-term maintenance of glucose concentrations in the blood. In type 2 diabetes, impaired insulin-mediated suppression of glucose production and diminished glucose uptake ultimately causes an increase in postabsorptive glucose production. Type 2 diabetes associated with liver dysfunction and the vicious circle between liver, adipose tissue, and pancreas leads to various other diseases including nonalcoholic fatty liver disease, cardiovascular complications, and cancer. Despite current advances in pharmacotherapy for diabetes, attaining optimal glycemic control and preventing micro- and macrovascular diabetic complications has remained intangible and daunting. Novel therapeutic targets and their modulators, which include protein tyrosine phosphatase 1B inhibitors, glycogen phosphorylase inhibitors, glucokinase activators, diacylglycerol acyltransferase inhibitors, acetyl-CoA carboxylases inhibitors, and sirtuin activators, show promising results in preclinical and clinical studies. Adding new options with new mechanisms of action to the treatment armamentarium may eventually help to improve outcomes and reduce the burden of type 2 diabetes, which is only possible if we explore and understand the involvement of liver and fats in the pathogenesis of type 2 diabetes. Continue reading >>
Breaking The Vicious Circle Of Dementia And Hypoglycemia In Type 2 Diabetes: New Niches And New Opportunities
1Division of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Hospital, Ministry of Health and Welfare, No. 199 Section 1, Sanmin Road, Taichung 403, Taiwan 2Division of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, No. 1650, Section 4, Taiwan Boulevard, Taichung 40705, Taiwan 3School of Medicine, National Defense Medical Center, Taipei, Taiwan 4School of Medicine, National Yang-Ming University, Taipei, Taiwan 5Institute of Medical Technology, National Chung-Hsing University, Taichung, Taiwan Citation: Sheen YJ, Sheu WHH (2016) Breaking the Vicious Circle of Dementia and Hypoglycemia in Type 2 Diabetes: New Niches and New Opportunities. J Alzheimers Dis Parkinsonism 6:266. doi: 10.4172/2161-0460.1000266 Copyright: © 2016 Sheen YJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Alzheimers Disease & Parkinsonism Abbreviations TZD: Thiazolidinedione, DPP4I: Dipeptidyl Peptidase-4 Inhibitors, GLP-1R: Glucagon-like Peptide 1 Receptor Agonist, SGLT2i: Sodium Glucose Co-transporter 2 Inhibitors, SMBG: Self-Monitoring of Blood Glucose Dementia is a major cause of disability in elderly populations. As the prevalence of dementia still continues to increase globally, the World Health Organization has recognized dementia as a top public health priority [1]. Poor glycemic control is well known to lead to both macrovascular and microvascular complications. Recent studies have also confirmed that diabetes subjects may develop central nervous system disorders, presenting a Continue reading >>
Hypomagnesemia In Type 2 Diabetes: A Vicious Circle?
Over the past decades, hypomagnesemia (serum Mg2+ <0.7 mmol/L) has been strongly associated with type 2 diabetes mellitus (T2DM). Patients with hypomagnesemia show a more rapid disease progression and have an increased risk for diabetes complications. Clinical studies demonstrate that T2DM patients with hypomagnesemia have reduced pancreatic β-cell activity and are more insulin resistant. Moreover, dietary Mg2+ supplementation for patients with T2DM improves glucose metabolism and insulin sensitivity. Intracellular Mg2+ regulates glucokinase, KATP channels, and L-type Ca2+ channels in pancreatic β-cells, preceding insulin secretion. Moreover, insulin receptor autophosphorylation is dependent on intracellular Mg2+ concentrations, making Mg2+ a direct factor in the development of insulin resistance. Conversely, insulin is an important regulator of Mg2+ homeostasis. In the kidney, insulin activates the renal Mg2+ channel transient receptor potential melastatin type 6 that determines the final urinary Mg2+ excretion. Consequently, patients with T2DM and hypomagnesemia enter a vicious circle in which hypomagnesemia causes insulin resistance and insulin resistance reduces serum Mg2+ concentrations. This Perspective provides a systematic overview of the molecular mechanisms underlying the effects of Mg2+ on insulin secretion and insulin signaling. In addition to providing a review of current knowledge, we provide novel directions for future research and identify previously neglected contributors to hypomagnesemia in T2DM. Introduction Globally, over 300 million people suffer from type 2 diabetes mellitus (T2DM), and the prevalence is predicted to rise to over 600 million over the next decades (1). T2DM is characterized by a combination of insulin deficiency and insulin resis Continue reading >>
Insulin Resistance: A Vicious Circle Of Excess Fat
Every day I see patients I talk about insulin resistance and how it leads to diabetes. I have based my conversations, on what I thought was the best data. Now that I read Insulin Resistance: A Vicious Circle Of Excess Fat, by Phil Wood DVM, MS, PhD I realize that I am going to have to change a few of my statements as there are some facts you won’t want to miss. Insulin Resistance: A Vicious Circle Of Excess Fat Phillip Wood DVM, MS, PhD Insulin resistance is a common feature in patients who are obese or who have metabolic syndrome or type 2 diabetes. Insulin-resistant patients require higher than normal amounts of insulin to maintain normal blood glucose concentrations. The development of insulin resistance is complex, and many of its mechanisms are poorly understood. However, a common denominator in insulin-resistant patients is excess fatty acids (1), and insulin sensitivity is increased by any activity that reduces fatty acids in the tissues of the body. Such activities include increasing exercise with or without weight loss, reducing visceral adiposity with weight loss, or taking drugs that reduce fatty acids (thiazolidinediones, commonly known as “glitazones,” fibrates or metformin). The bottom line is that clearing the body of excess fat increases insulin sensitivity and, thus, decreases symptoms associated with insulin resistance. Often, insulin resistance is thought of as a focal process restricting the uptake of glucose as accomplished by muscle and mediated by insulin. It is true that muscle is a major location for insulin-mediated glucose uptake; however, uptake of glucose by muscle is only one of many metabolic processes that are disrupted by insulin resistance. I want to focus on three of those processes to demonstrate the vicious circle of insulin re Continue reading >>
Dispatch Diabetes: The Importance Of The Liver
The predominant form of diabetes mellitus, non-insulin dependent diabetes mellitus (NIDDM) or type 2 diabetes, afflicts approximately 4% of the population of the Western world, and its treatment consumes more than 10% of the total National Health Service budget in Britain. The disease is characterised by the failure of sensitive tissues to respond normally to insulin — ‘insulin resistance’. These tissues therefore fail to take up and store glucose, leading to chronically elevated blood glucose (‘hyperglycaemia’). In mild cases, increased insulin production by β cells in the pancreatic islets of Langerhans — leading to ‘hyperinsulinaemia’ — can compensate for the decreased responsiveness to the hormone, but diabetes results when the islets fail [1]. The causes of the disease remain poorly understood, but its predominance amongst overweight individuals — 80% of type 2 diabetics are obese — suggests that dysregulated lipid metabolism may be an important factor. The three major tissues largely responsible for clearing glucose from the blood in healthy individuals — liver, muscle and adipose tissue — all become insulin resistant in NIDDM, but the relative importance of each has been unclear. Two new studies [2,3] shed light on this question. Michael et al.[2] have shown that targeted inactivation of the insulin receptor gene specifically in the liver leads to diabetes-like symptoms in mice. This is an important result, as it demonstrates that insulin has a direct role in regulating liver metabolism. Using two further animal models, Shimomura et al.[3] found that the development of insulin resistance in the liver involves selective inactivation of the capacity of insulin to block hepatic glucose production. On the other hand, the ability of the horm Continue reading >>
Hypothyroidism And Diabetes: How To Reverse It And Why Sugar Is Not The Problem
Hypothyroidism and diabetes tend to go hand-in-hand. Anyone who is diabetic will functionally become hypothyroid because their cells become blocked from using thyroid hormone efficiently. And anyone who is hypothyroid will have a tendency toward becoming pre-diabetic and eventually diabetic because of how their body compensates for their thyroid condition. In this article, which is based largely on the work of Dr. Raymond Peat, I’m going to show you how you can prevent this from happening, but in order for this to all make sense… …you first have to understand the truth about diabetes and the vicious cycle that causes it. Today, diabetes (along with a list of other health conditions) is blamed directly on the over-consumption of sugar. It’s oftentimes referred to as the “Sugar Disease”. And for those without a proper understanding of how the body works, this might make sense. When a diabetic consumes large amounts of glucose, their blood sugar rises. And a chronic rise in blood sugar can lead to various health complications. But, let me ask you this… Imagine you have a clogged sink drain while your water is running. As the water level continues to get higher and higher do you curse the water and blame it for clogging your sink? No, that wouldn’t make any sense. Would turning off the water and letting the water sit there solve your problem? Of course not. We all know the underlying problem that you have to fix is the clog itself. Then why are so many people guilty of taking this very approach with diabetes today? Diabetes is NOT a Sugar Disease Let’s get one thing straight… Diabetes is not a disease “caused” by sugar. You require insulin to deliver glucose to your cells. This is why in type 2 diabetes, insulin injections are prescribed to treat the Continue reading >>
Diabetes: How Do I Help Protect My Liver?
If I have diabetes, is there anything special I need to do to take care of my liver? Answers from M. Regina Castro, M.D. You're wise to wonder about steps to protect your liver. Diabetes raises your risk of nonalcoholic fatty liver disease, a condition in which excess fat builds up in your liver even if you drink little or no alcohol. This condition occurs in at least half of those with type 2 diabetes. It isn't clear whether the condition appears more often in people with type 1 diabetes than in the general population because obesity, which is a risk factor, occurs with similar frequency in both groups. Other medical conditions, such as high cholesterol and high blood pressure, also raise your risk of nonalcoholic fatty liver disease. Fatty liver disease itself usually causes no symptoms. But it raises your risk of developing liver inflammation or scarring (cirrhosis). It's also linked to an increased risk of liver cancer, heart disease and kidney disease. Fatty liver disease may even play a role in the development of type 2 diabetes. Once you have both conditions, poorly managed type 2 diabetes can make fatty liver disease worse. Your best defense against fatty liver disease includes these strategies: Work with your health care team to achieve good control of your blood sugar. Lose weight if you need to, and try to maintain a healthy weight. Take steps to reduce high blood pressure. Keep your low-density lipoprotein (LDL, or "bad") cholesterol and triglycerides — a type of blood fat — within recommended limits. Don't drink too much alcohol. If you have diabetes, your doctor may recommend an ultrasound examination of your liver when you're first diagnosed and regular follow-up blood tests to monitor your liver function. Continue reading >>
