Home Remedies for Hyperglycemia

Blood Sugar Miracle

If you are one of the many people suffering from high blood sugar or diabetes, this is the solution that you have been looking for. This ebook from Duke Anderson can teach you how to reverse the symptoms that you are facing in less than 3 weeks from your OWN home! It doesn't have to be hard to help your blood sugar get to where it needs to be Don't make it any harder! This is the solution that you need to get your blood sugar under control. You don't have to undergo dangerous, expensive surgery, leave scars from needles, or spend huge amounts of money on pharm drugs that end up doing nothing for you. The blood sugar problems that you have are reversible and curable, if you know the methods to use! And you can learn those methods inside this book. This book will mean a lifestyle change for you! Read more here...

Blood Sugar Miracle Summary


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Contents: Ebook
Author: Duke Anderson
Official Website: blood-sugar-miracle.com
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My Blood Sugar Miracle Review

Highly Recommended

The author presents a well detailed summery of the major headings. As a professional in this field, I must say that the points shared in this book are precise.

When compared to other e-books and paper publications I have read, I consider this to be the bible for this topic. Get this and you will never regret the decision.

Inhibition Of Parp Activity For Beta Cell Protection

The injection of a single dose of 160 to 200 mg streptozocin kg body weight (BW) to mice or 50 to 80 mg streptozocin kg BW to rats causes acute beta cell toxicity and results in persisting hyperglycemia about 2 days after application.21 Therefore, the administration of a single high dose of streptozocin represents a useful experimental approach to target a toxic attack, involving primary nuclear DNA damage, to the pancreatic beta cells in vivo. The application of multiple subdiabetogenic doses of streptozocin in mice (5 x 35 to 40 mg streptozocin kg BW on 5 consecutive days) elicits an immune response against autologous pancreatic islet structures, resulting in insulitis, beta cell destruction, and the development of hyperglycemia.64 The intraperitoneal application of nicotinamide at a dose of 500 mg kg BW preserved beta cell function and protected from diabetes development in mice treated with streptozocin at a single high dose of 200 mg kg BW. The animals were protected from...

Monitoring Glycemic Control In Diabetic Patients

Diabetes causes chronic high blood glucose leading to 1) hyperglycosylation of proteins and cellular structures, and 2) accumulation of toxic metabolites because of abnormal glucose metabolism (12). These metabolic disruptions lead to retinopathy, neuropathy, nephropathy, and other complications of the disease such that diabetes is the leading cause of blindness, end-stage renal disease, and lower-extremity amputations. Treatment of these disorders in the 16 million people in the United States with diabetes costs at least 100 billion annually, accounting for approx 15 of the national health care budget and 25 of Medicare costs (13). The Diabetes Control and Complications Trial (DCCT) (14) showed conclusively that intensive management of blood glucose, through frequent administration of insulin, markedly decreases the long-term complications of diabetes. The DCCT also concluded that glycohemoglobin is a good long-term indicator of average blood glucose and is therefore a good...

Diabetic Retinopathy

Diabetic retinopathy is a progressive dysfunction of the retinal vasculature caused by chronic hyperglycemia. The effects of advanced glycation end products (AGEs), which are increased in the vitreous of diabetic patients, on the photolysis of hyaluronan have been examined. Exposure to light decreased the molecular weight of hyaluronan, and the addition of AGEs promoted this change (48). The photosensitizer activities of AGEs may be associated with accelerated depolymer-ization of hyaluronan in diabetic patients. Microvascular leakage in diabetic reti-nopathy in association with the expression of heparan sulfate proteoglycans in retinal microvessels has been investigated (49). The results revealed that the increased microvascular permeability in human diabetic retinopathy was not associated with changes in the expression of heparan sulfate proteoglycans, suggesting that the mechanism underlying retinal leakage is different from that of diabetic glomerular capillary leakage, in which...

Benefits of Glycemic Control

Glycemic control is critical to the prevention of diabetic complications. The duration and severity of hyperglycemia correlates with both the development and rate of progression of diabetic retinopathy, nephropathy, and neuropathy. The DCCT and the UKPDS established the effectiveness of glycemic control in the prevention of diabetic complications in T1DM and T2DM, respectively, during the 1990s. The UKPDS, conducted from 1977 to 1997 in 23 centers throughout England, Northern Ireland, and Scotland, verified that optimal glycemic control has similar benefits in T2DM. This prospective, randomized intervention trial of 5102 newly diagnosed individuals with T2DM examined the effects of glucose control on cardiovascular and diabetic complications via diet therapy or pharmacologic intervention with sulfonylureas, metformin, or insulin therapy.54 After a 3-month dietary run-in period, subjects with persistent hyperglycemia were randomized to conventional therapy with diet alone (goal FPG

General principles of insulin therapy

Insulin has been used in combination with every other type of pharmacological therapy for glycemic control in T2DM. Combination therapy with a sulfonylurea has been extensively studied, with overall improved glycemic control in individuals on a bedtime dose of intermediate or long-acting insulin.79,80 The concurrent use of insulin and metformin can modestly decrease HbA1C values and may also decrease the amount of weight gain associated with insulin alone. Thiazolidinediones maintain or slightly lower HbA1C levels when used with insulin, and further decrease the required insulin dose, but may result in additional weight gain. A clinical study investigating the use of acarbose with insulin therapy showed a 0.5 decrease in HbA1C values, which is likely due to an improvement in postprandial hyperglycemia.

Type 2 diabetes mellitus

Although the diagnosis of T2DM is straightforward, it is extremely difficult to monitor and to treat successfully long-term. Therapy and the monitoring of its effectiveness are complex, invasive, and expensive. Lack of patient education and resources compounds the problem and contributes to non-compliance and suboptimal glycemic control. The asymptomatic nature of chronic hyperglycemia does not allow the patient to truly understand the risk of diabetic complications until irreversible damage has developed. Therapies that have been added to available options in recent years have new and different mechanisms of action. However, when used as monotherapy, none of them (save insulin and its analogs) sustain optimal control for long intervals of time in the majority of patients.

Incretin Augmentation of Insulin Secretion

Dipeptidyl peptidase-IV (DPP-IV) is a membrane-associated peptidase that is widely distributed in tissues and also exists as a soluble circulating form. Several DPP-IV inhibitors have been characterized and shown to lower blood glucose via prolongation of circulating GLP-1 and GIP action.87 Animal studies with DPP-IV inhibitors show promising results. Progressive improvement in glycemic control, enhanced insulin secretory response, increased

Antisense Oligonucleotide Therapy

Two phase I trials were conducted to evaluate the safety and activity of oblimersen as a single agent in patients with NHL.51,52 The larger included 21 patients with Bcl-2-positive relapsed NHL who received a 14-day subcutaneous infusion.52 The median age was 54 years, nine had follicular NHL, eight had small lymphocytic NHL, three had large cell lymphoma, and one had mantle cell lymphoma. All patients had received multiple chemotherapy regimens and four patients had received high-dose chemotherapy and autologous stem cell transplantation. Oblimersen was delivered by a continuous subcutaneous infusion for 14 days at doses of 4.6-195. 8 mg m2 day. All patients experienced local skin inflammation at the sites of subcutaneous infusion. Dose limiting toxicities were observed at doses greater than 147.2 mg m2 day and consisted of thrombocy-topenia, fevers, and hypotension. Non-dose-limiting toxicities included hyperglycemia during the infusion, fatigue, and transient increases in liver...

LMF as a Pleiotropic Mediator

Glucose metabolism is also affected by LMF. Treatment of ex-breeder male NMRI mice with LMF isolated from the urine of cachectic cancer patients caused a significant increase in glucose oxidation to CO2, compared with control mice receiving phosphate-buffered saline 25 . Glucose utilisation was elevated in brain, heart, BAT, and gastrocnemius muscle. The tissue glucose metabolic rate was increased almost threefold in brain, accounting for the ability of LMF to decrease blood glucose levels. LMF also increased overall lipid oxidation. There was a significant increase in lipid accumulation in plasma, liver, and white and brown adipose tissue after administration of LMF. These results provide further evidence that changes in carbohydrate metabolism and loss of adipose tissue, together with increased whole-body fatty acid oxidation in cachectic cancer patients, may arise from tumour production of LMF.

Neelima V Chu MD and Robert R Henry MD

Polyuria, Weight Loss, and Hyperglycemia Case 2 52-Yr-Old Man with Lipid Abnormalities CASE 1 40-YR-OLD OBESE MAN WITH PROGRESSIVE POLYDIPSIA, POLYURIA, WEIGHT LOSS, AND HYPERGLYCEMIA Diabetic ketoacidosis (DKA) is defined as a metabolic acidosis caused by significant insulin deficiency. The physiologic abnormalities present with DKA include 1) Chronic hyperglycemia and glucose toxicity (glucose of 300-800 mg dL) 2) acidosis caused by catabolism of fat and buildup of ketone bodies (pH 6.8-7.3 and HCO3

Highdose Dexamethasone Monotherapy

Dexamethasone, 20 mg m2 day on days 1-4, 9-12, and 17-20, induces responses in previously untreated patients with MM 40-50 of the time,55, 56 suggesting that dexamethasone accounts for most of the benefit derived from VAD and TD (described below). Dexamethasone monotherapy may be preferred for frail patients, since the toxicity is generally less than that seen with VAD or TD. Still, primary pulse dexam-ethasone treatment is somewhat more toxic than MP,57 and patients should be monitored closely for specific side effects, including hyperglycemia, gastrointestinal bleeding, mood disorder, insomnia, weight gain, increased susceptibility to infections, and rarely pancreatitis.58

Mechanisms Of Diabetic Peripheral Neuropathy

Hyperglycemia and the polyol pathway Hyperglycemia is the primary reason for the development of DN as has been demonstrated by the DCCT (20). This group also showed that with excellent control of hyperglycemia there is a significant reduction of autonomic dysfunction (53 ), neuropathy (64 ), and motor conduction velocity changes (44 ) in type 1 diabetics (24,59). Activation of protein kinase C (PKC) occurs secondary to hyperglycemia, which leads to increased diacylglycerol synthesis and PKC activation. PKC may also be activated by oxidative stress. It increases vascular permeability, blood flow changes, and impairment of nitric oxide synthesis (70-72). Regardless of the pathophysiologic mechanism, or combination of mechanisms that coalesce to induce the production of DN, chronic hyperglycemia appears to have a significant if not pivotal role in its pathoetiology.

Arsenic trioxideassociated toxicities

The most prominent adverse events with ATO in APL have included weight gain and fluid retention, leukocytosis, the APL differentiation syndrome, and prolongation of the QTc interval on the electrocardiogram (Table 3). Peripheral neuropathy, hyperglycemia, and cutaneous reactions have also been described (37,63).

Corroborative Results From Genetic And Pharmacological Inactivation Of Parp

The PARP knockout mice also have been used extensively either to confirm or to explore the role of PARP activation in various animal models of human diseases. One of the early implications for its role in pathogenesis came from the finding that PARP activation was the culprit of streptozotocin-induced diabetes, an animal model to study type 1 diabetes.97 In P-islet cells, free radicals derived from streptozotocin catabolism damaged DNA and activated PARP. Consequently, depletion of NAD due to PARP activation prohibited the release of insulin and led to cell death, as PARP inhibitors such as nicotinamide and 3-aminobenzamide prevented stretptozo-tocin toxicity.98 Three groups have now independently replicated the studies in PARP knockout mice, and all demonstrated that PARP gene deletion renders mice resistant to P-islet cell destruction and hyperglycemia after streptozotocin treatment.36,45,46 In the nervous system, PARP activation was found to mediate glutamate excitotoxicity and...

Using E coli to make insulin

It helps move sugars and starches from the bloodstream into the cells, where they can be used for energy. People who have a disease called diabetes either do not make enough insulin or do not use it properly. They need to take insulin every day to keep their blood sugar levels under control. In the past, people with diabetes were often given insulin that was taken from

Type 1 Diabetes Mellitus

Age at onset of 11 to 12 years, and the incidence is increasing. The disease is characterized by hyperglycemia and ketoacidosis. Chronic complications of type 1 diabetes include progressive atherosclerosis of arteries, which can lead to ischemic necrosis of limbs and internal organs, and microvascular obstruction causing damage to the retina, renal glomeruli, and peripheral nerves. These patients have a deficiency of insulin resulting from immune-mediated destruction of the insulin-producing P cells of the islets of Langerhans in the pancreas, and continuous hormone replacement therapy is needed.

Adenosine A Receptor Agonists

An example of how such tools have been used to develop novel, mechanism-based PK PD models is a project exploring the potential of a series of deoxribose and 8-alkylamino analogs of N6-cyclopentyladenosine (CPA), which were identified as adenosine A1 receptor agonists with reduced intrinsic efficacy54,55 as antilipolytic agents for the treatment of non insulin-dependent diabetes mellitus. Increased levels of non-esterified fatty acids (NEFAs) are a characteristic of non insulin-dependent diabetes and are believed to exacerbate insulin resistance and hyperglycemia. Therefore, selective A1 receptor agonists may provide a novel therapeutic strategy for the treatment of diabetes, since stimulation of adenosine A1 receptors in adipose tissue has been shown to decrease NEFA levels in rat and human.51 A key first step in this project was the development of an efficient and quality animal model and sensitive analytical assays for simultaneous and detailed characterization of the...

Acute vs Chronic Amphetamine Toxicity

Labs Hyperglycemia, leukocytosis, elevated liver function tests (LFTs), elevated creatine phosphokinase (CPK) from rhabdomyolysis with myoglobinuria. False-positive urine drug screens may result from ephedrine, pseudoephedrine, or phenylpropanolamine (PPA), often found in over-the-counter (OTC) cold medications.

Inulin and Diabetes Mellitus

Of sucrose or glucose prompts blood sugar and insulin changes, but no corresponding effects are noted when equivalent amounts of inulin or fructooligosaccharides are ingested (Roch-Norlund et al., 1972). Therefore, consuming inulin-rich foods helps to restore normal levels of blood sugar, whereas foods containing starch and sucrose further raise blood sugar levels. Experiments during the 1980s and 1990s confirmed the beneficial role of inulin-rich foods in diabetic diets. Daily intake of fructooligosaccharides has been shown to reduce blood sugar levels in both diabetic and healthy subjects (Luo et al., 1996 Yamashita et al., 1984), for instance, while inulin reduced insulin peaks compared to diets containing other carbohydrates (Rumessen et al., 1990). An intake of around 16 to 23 g of inulin per meal has been recommended in diabetic diets (Van Loo et al., 1995). There is a long history of inulin-containing plants being used to treat diabetes. The Greek physician Theophrastus used...

PI3KPKB Pathway Modulators with Unknown Mechanism of Action

Of PKB (IC50 0.5 M) and induces apoptosis in human tumor cells with elevated levels of PKB, it does not inhibit the kinase activity of recombinant myr-PKB , PI3K, or PDK1. In vivo antitumor activity (tumor growth inhibition 80 ) against a panel of s.c. human tumors xenografts (e.g., OV-CAR3, OVAR8, and PANC1) with aberrant PKB activation was observed when triciribine was administered i.p at 1 mg kg day. Ex vivo analyses of tumor samples showed that the compound blocks PKB phosphorylation at Thr308 and Ser473 without affecting protein content. At the therapeutic dose, the compound did not affect body weight and glucose levels in plasma. The compound fulfilled the preclinical requirements and entered Phase I clinical trials a few years ago. Hepatotoxicity, hypertriglyceridimia, thrombocytopenia, hypocalcemia, and hyperglycemia have been reported as the most common side effects, and, due to its side effects at high doses, the compound has been limited in the clinic. Phase II clinical...

The Assessment of Care Quiz

If you do have protein or glucose in your urine that was not previously recognized, you may need to consult your doctor. But note that the transient appearance of protein in the urine can also be caused by vigorous exercise, infection, fever, or very high blood sugar. You may want to check it again before you consult your doctor.

Basic theoretical concepts

In this concept, the initial step is considered dysfunction of the endothelium, the innermost layer of the vasculature, by local disturbances of blood flow, along with metabolic and humoral risk factors (e.g. hyperglycemia, dyslipidemia, cigarette smoking, inflammation). These alterations of the endothelium perpetuate a series of events that culminate in the development of an atherosclerotic plaque.

Mechanisms of Renal Dysfunction

Endothelial dysfunction commonly occurs in obesity, type 2 diabetes, and hypertension. The endothelium acts to regulate vascular homeostasis by maintaining a balance between vasodilation and vasoconstriction, inhibition and stimulation of smooth muscle cell proliferation and migration, and inhibition of platelet activation, adhesion, and aggregation.24 Essential hypertension was first recognized to cause endothelial dysfunction early in the last decade where the increase in blood pressure has a direct influence on vascular function independent of other cardiovascular risk factors. Dysfunction of the endothelium could be due to decreased vasodilatory mediators and or increased vasoconstrictor mediators. Factors that lead to reduction of vasodilation and endothelial dysfunction include a reduction in nitric oxide (NO) production, increased oxidative stress, a decrease in NO bioavailability decreased prostacyclin levels, and a reduction of hyperpolarizing factors. Inflammatory responses...

Annexins And Diabetes

Diabetes is a chronic condition that can present in two different ways type-1 insulin-dependent diabetes or the more common type-2 insulin non-dependent diabetes. In both instances it is the resulting hyperglycemia that is thought to be primarily responsible for the disease facies. Although diabetes is a systemic condition that affects all parts of the body, for the purposes of this discussion the endothelium will be the main point of focus, since the most complete data regarding the role of annexins in diabetes have come from studies examining their actions in endothelial cells. There are thought to be four major effects of hyperglycemia on endothelial cells an increase in flux through the polyol pathway which leads to a depletion of NADPH and ultimately diminishes the cell's ability to produce protective anti-oxidants, an increase in conversion of glucosamine-6-phosphate to N-acetylglucosamine which leads to the formation of transcription factor-sugar adducts (which can affect...

Reduced Side Effect Liability

Current pharmacological approaches to the treatment of schizophrenia suffer from two major issues side effects and limited efficacy. The first major unmet medical need is improved side effect liability. Even the best of the modern atypical antipsychotics produce significant side effects with a low therapeutic index. Individuals with schizophrenia have an increased risk of death and, in general a 20 shorter life span84'85 that, in part, may be attributable to the use of current antipsychotic medications. As discussed above, atypical antipsychotics have a clear lower risk of inducing EPS and hyperprolactinemia (with the exception of risperidone) when compared to typical antipsychotics, but the risk still exists. Furthermore, several atypicals, particularly clozapine and olanzapine, increase the risk of sedation, obesity, high blood sugar and diabetes, and dyslipidemia. Very rare cases of neuroleptic malignant syndrome, a rare but potentially fatal reaction characterized by fever,...

Other Dietary Considerations in MS

Constipation is a frequent complaint in people with MS. One way to improve constipation is to increase the amount of fiber in the diet. Good sources of fiber include whole grain breads and cereals, as well as fruits and vegetables. An increased intake of water and other fluids also may be beneficial for constipation six to eight 8-oz. glasses of fluid daily generally are recommended. Some people with MS may have frequent urinary tract infections, and increased fluid intake also may be helpful for this problem. Finally, for some people with MS-associated fatigue, it may be beneficial to avoid large increases or decreases in the blood sugar level. This may be accomplished by eating small meals and snacks throughout the day.

Diagnostic Tests

Labs Hyperglycemia, hypokalemia, increased CPK, and increased CPK-MB. Electrocardiogram (ECG) All tachydysrhyth-mias increased, ischemia, MI. Head CT All CVAs increased subarach-noid hemorrhage (SAH), intracranial (ICH), interventricular hemorrhage (IVH), ischemic cerebral infarcts, septic cerebral emboli, brain abscesses.


Glutamine is broken down to produce energy in many tissues in the body. It is especially important as an energy source for the cells lining the digestive tract and the white blood cells. Glutamine can be taken up by the liver and converted to glucose to maintain blood sugar levels.2

Ischemic Myocardium

The reperfusate composition was modified to allow incorporation of the following principles 1) oxygenation with blood to provide substrate (O2) to generate energy for repair of cellular processes 3 2) cardioplegia (K+) to keep the heart from resuming electromechanical activity and raising O2 demand 3) replenishing of amino acid precursors of Krebs' cycle intermediates, i.e., glutamate aspartate and needed to ensure more effective oxidative metabolism to produce energy for cell repair and subsequent mechanical function65,95 because it has been shown that both hypoxia106 and ischemia14 reduce the tissue concentrations of precursors and some intermediates of the Krebs' cycle, 4) limitation of calcium influx by reperfusate hypo-calcemia (150 to 250 micromol L) with citrate-phosphate-dextrose to reduce calcium load and addition of a calcium channel-blocking drug, i.e., diltiazem, that could continue to retard calcium cell entry after normocalcemic reperfusion is started 2,38 5) reversal of...

Vorinostat SAHA

The most common drug related Grade 3 4 toxicities are fatigue, nausea, vomiting, diarrhea, anorexia, anemia, thrombocytopenia, hyperglycemia and hypocalcemia. No clinically significant electrocardiograph (EKG) changes or cardiac toxicities, including arrhythmias attributable to the drug, were seen. In fact, SAHA is probably the only HDACi that has not resulted in EKG changes. Toxicities including myelosuppression were rapidly reversible upon discontinuation of drug. It has been postulated that the thrombocytopenia is due to impairment of megakaryocyte differentiation 104 .

Micronutrients CHD

Lowers LDL cholesterol and raises HDLs, thereby reducing risk of heart attack.13 Side effects (flushing) can be minimized by raising the dose gradually and taking the niacin with meals. Should betaken only under medical supervision at doses 1 g day because of rare but potentially serious side effects, including liver inflammation and hyperglycemia


Diabetes is a chronic disease caused by inadequate secretion of, or peripheral resistance to, insulin. It is characterized by hyperglycemia and hyperlipidemia. Diabetes, when poorly controlled, causes widespread damage to blood vessels and nerves, which can result in blindness, kidney failure, or heart attack.

Diet Insomnia

The more caffeine consumed during the day, the higher the risk of insomnia. Consumption of coffee, tea, or cola drinks should be avoided within 6 hours of bedtime and minimized during the day. Some individuals are sensitive to small amounts of natural stimulants found in aged cheeses, bacon, ham, sausages, sauerkraut, eggplant, spinach, and tomatoes, and these foods may contribute to insomnia if eaten in the evening. Low nighttime blood-sugar levels can cause frequent or early awakening and may be a sign of reactive hy-poglycemia (see pp. 185.)2

Diet Alcohol

Further lowers nutrient absorption from foods. The liver is particularly vulnerable to alcohol - more than three drinks a day causes inflammation and accumulation of fat in the liver. This impairs liver function, reducing the ability to detoxify chemicals and drugs. Because the liver is important for blood sugar control, alcohol-induced liver damage can produce hypoglycemia, leading to fatigue, irritability, and concentration difficulties. Alcohol increases urinary losses of many minerals, including zinc, calcium, and magne-sium.5 Because of these effects, a diet rich in fresh fruits and vegetables, whole grains, lean meats, and low-fat milk products should be carefully chosen.


The antihypertensive activity of diuretics was discovered in the clinic. Diuretics do not lower arterial pressure in acute experiments on normotensive animals. Only in chronic experiments on DSS or SH rats can the mild antihypertensive effect of diuretics be detected. The first diuretic found to lower arterial pressure in hypertensive patients was chlorothiazide, discovered by Beyer and his colleagues at Merck. Its discovery was soon followed by the introduction of hydrochlorothiazide, a closely related derivative with much higher relative potency that was discovered at Merck as well as at Ciba-Geigy. Many similar thiazides have been subsequently developed and marketed, but only a few are still available on the American market. The major side effect of thiazides is hypokalemia, due to the excessive excretion of K+ ions. Other side effects include hyperuricemia and hyperglycemia. The search for diuretics with longer duration of action and fewer side effects led to the discovery of...

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