New Hypoglycemia Cure

Guide To Beating Hypoglycemia

Here's Just A Tiny Glimpse Of The Topics Covered: The 3 main types of hypoglycemia and which type you're most likely suffering from. How snacking on chocolate bars can actually make you Fat and worsen your condition! (If you thought those delicious dark brown bars were great energy- boosters.think again!) The No. 1 question most folks have when it comes to hypoglycemia and hyperglycemia. Why you should insist on a 6-hour Gtt and not a 5-hour one. ( Why it might not be a good idea to consult a doctor to confirm your hypoglycemia. Aside from taking a Gtt, what other methods can you use to determine whether or not you're suffering from this condition? Well, refer Chapter 4, Pgs. 23-26 to take a revealing 67-question test especially designed to find out if you've got the symptoms. An inspiring motivational exercise that will help you effectively banish all of your negative thoughts that prevent you from having peace of mind. 2 good reasons why you should keep a food journal. 3 powerful nutrients that limit the effect of glucose on your blood sugar level. This is vital to a hypoglycemic as it helps slow down the absorption of sugar in the food. The secret impulse that literally forces you to say 'yes' to a candy bar or chocolate whenever you feel the hunger pangs gnawing at you. 2 ingredients that are lethal to a hypoglycemic. 'Hidden sugars' you must know to avoid buying products that can easily worsen your condition. 8 essential rules of food planning that are crucial to your speedy recovery from hypoglycemia. Leave out one of them and it could hurt your chances of recovering. How to create a healthy food plan that's suitable for both vegetarian and non- vegetarian hypoglycemics. Most food plans only focus on non-vegetarians, but this one works great for everybody! Read more here...

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Hypoglycemic Awareness

Awareness of hypoglycemic changes has been examined using the EEG state measures (Howorka et al, 1996 Tribl et al, 1996). Patients with impaired hypoglycemic awareness may be more likely to progress into severe hypo-glycemia because their inability to detect a state in which blood glucose is low will prevent them from taking appropriate measures. Furthermore, recurrent neuroglycopenia may result in reduced hypoglycemic awareness (Frier, 2001). Tribl and colleagues (1996) used a hypoglycemia protocol to examine patients varying in reported awareness. EEG was recorded as a function of decreasing glucose levels (normoglycemia, mild hypoglycemia, moderate hypoglycemia, and severe hypoglycemia). During the normo-glycemic stage, those with poor hypoglycemia awareness showed less theta power and more alpha power. During mild hypoglycemia, these effects were the reversed, however higher theta power and lower alpha power in those with poor hypoglycemia awareness. In the lowest hypoglycemic...

Diabetes Mellitus and Hypoglycemia

Inadequate secretion of insulin, or defects in the action of insulin, produce metabolic disturbances that are characteristic of diabetes mellitus. A person with type 1 diabetes requires injections of insulin a person with type 2 diabetes can control this condition by other methods. In both types, hyperglycemia and glycosuria result from a deficiency and or inadequate action of insulin. A person with reactive hypoglycemia, by contrast, secretes excessive amounts of insulin and thus experiences hypoglycemia in response to the stimulus of a carbohydrate meal. Figure 19.13 Reactive hypoglycemia. An idealized oral glucose tolerance test on a person with reactive hypoglycemia. The blood glucose concentration falls below the normal range within 5 hours of glucose ingestion as a result of excessive insulin secretion. performed. In the oral glucose tolerance test, for example, reactive hypoglycemia is shown when the initial rise in blood glucose produced by the ingestion of a glucose solution...


Hypoglycemia's impact on neural processing has been documented reasonably well using EEG, EP, and ERP. The application of these measures to this aspect of diabetes was among the most thorough in the literature. Lingenfelser et al (1993) examined auditory EP's. Diabetic patients were exposed to three hypoglycemic episodes whereas in patients in the control group, glucose levels were strictly controlled around a set point. As glucose levels fell in the experimental group, the expected increased awareness of hypoglycemia was observed as well as expected counter regulatory blunting of adrenaline and cortisol responses. Mid latency components of the auditory EP were delayed, reflecting slowed auditory processing. Auditory ERPs, e.g., the P300, during hypo-glycemia were examined to document cognitive and neural processing deficits (Strachan et al, 2003). Diabetic patients were exposed to euglycemic (a control condition during which glucose levels were normal) or induced hypo-glycemia...

Drugdisease Interactions

Oral beta blockers can mask symptoms of thyrotoxicosis. Similarly, abrupt withdrawal of OBBs can exacerbate symptoms of hyperthyroidism. In a labile diabetic patient with known history of hypoglycemic unawareness, OBBs could theoretically mask the symptoms of hypoglycemia, which are mediated by catechol-amines. Patients with non-insulin-dependent diabetes mellitus receiving systemic beta blockers do not appear to be at increased risk of hypoglycemic unawareness, nor have beta blockers been shown to be associated with prolonged hypoglyce-mia due to blockade of catecholamine-mediated recovery. However, patients with insulin-dependent diabetes or labile diabetes may be potentially at greater risk for prolonged hypoglycemia when receiving systemic doses of beta blockers.97-99

Clinical Presentation Of Ghad

Sometimes, GHAD will first be suspected when there is severe neonatal hypoglycemia or other signs of hypopituitarism (hypothyroidism, small phallus in male babies, or neonatal hepatitis). During early childhood, children with GHAD are detected when they demonstrate short stature and subnormal rates of growth. Often these children will have proportionally small limbs, increased body fat, and a cherubic appearance.

Signal Transduction

G protein that activates the adenylate cyclase.52 This mechanism is common in this class of receptors and it involves a two-step process that starts with receptor phosphorylation by a G protein-coupled receptor kinase (GRK). The phosphorylation marks the receptor for beta arrestin binding, which leads to receptor silencing.53 Accordingly, in vitro studies showed that human GHRHR lacking intracellular phosphorylation sites (similarly to the ovine GHRHR) is more sensitive to GHRH stimulation if compared to the full-length receptor.54 However, desensitized somatotroph cells can still release GH in response to other secretagogues stress, arginine, GH-releasing peptide (GHRP), TRH, and hypoglycemia 21 by using signal-specific GH pools.55,56 GHRH desensitization can be prevented by SRIF, which restores GH response in GHRH-desensitized cells.57 In addition, desensitization is not complete, as demonstrated by the fact that patients with GHRH-secreting tumors present persistently elevated...

End Organ Targets and Receptors

Patients with GHI from GHR defects often do not respond well to exogenous GH therapy. Some patients have been treated with IGF-1 (133-135). In 1992, a 7-day trial of IGF-1 therapy in six adults with GHR defects revealed no adverse effects (136). A subsequent recent collaborative study examined IGF-1 therapy over 2 years in five patients with GHI and high basal GH levels and in three patients with complete GHD and growth hormone antibodies (133). The investigators found that with twice-daily subcutaneous IGF-1 treatment, these children initially had a greatly increased growth velocity (from 4.0 cm yr pre-treatment to 9.3 cm yr). After the first year, growth rate slowed (to 6.2 cm yr), but was still significantly greater than pre-IGF-1 treatment. Some patients on high dose (120 g IGF-1 kg twice daily) treatment developed hypoglycemia others had selective acceleration of lymphoid and renal tissue growth. It remains to be seen if IGF-1 will cause sustained gain of height velocity without...

Diagnosis Of Gh Deficiency Classical Evaluation

In most pediatric endocrine centers, provocative testing procedures for GH adequacy incorporate two of the following GH stimuli l-dopa, clonidine, arginine, propranolol, glucagon, insulin induced hypoglycemia, and or exercise. An inadequate response (currently defined in most centers as peak GH levels of < 10 ng mL) suggests GHD. Unfortunately, even provocative GH testing is not a reliable gold standard age and sex-specific norms are inadequately determined, GH assays in use are not well-standardized, and the specificity and result reproducibility of GH tests are poor (145). A consensus statement published by 16 endocrinologists at 14 centers in 1994 concluded that careful auxological evaluation, supplemented by assessment of appropriate elements of the GH-IGF axis, provides the best foundation for a rational diagnosis of GHD (146).

Candidate Gene Studies

The PPARG (peroxisome proliferatoracti-vated receptor-y) gene has been widely studied because of its importance in adipocyte and lipid metabolism (Tontonoz and Spiegelman, 2008). In addition, it is a target for hypoglycemic drugs known as thiazolidinediones. A proline-to-alanine (Pro12Ala) change in codon 12 of PPARG was the first genetic variant to be definitively implicated in the common form of type 2 diabetes. The rare Ala allele is present in 15 of white Europeans and was shown to be associated with increased insulin sensitivity. A study that combined data on a Finnish and a second generation Japanese cohort (Deeb et al, 1998) found that Pro allele homozygotes had 4.35 times higher risk for developing type 2 diabetes compared to those who do not carry the allele (p 0.028). Although a number of subsequent small studies were not able to replicate this initial finding, a meta-analysis combining the results from 16 studies published before 2000 confirmed the association with type 2...

GHD in the Newborn Period

In general, newborns with congenital hypopituitarism have normal birth weights and body proportions. Micropenis, with or without hypoglycemia, may be owing to hypopi-tuitarism. GH deficiency must be considered when there are midline lesions including septo-optic dysplasia (optic nerve hypoplasia and absence of the septum pellucidum).

GHD Presenting During Childhood

GHD insufficiency and hypopituitarism can present in infancy and childhood in the following clinical settings hypoglycemia growth failure (< 7 cm yr prior to age 3 yr, < 4.5-5.0 cm yr from age 3 yr to puberty, < 5.5-6.0 cm yr during pubertal yr) diabetes insipidus disorders of pubertal development including micropenis and pubertal delay children with visual, neurological abnormalities and developmental defects characteristic truncal obesity. GHD insufficiency should be considered in children with abnormal linear growth for age, subnormal height (> 2 SD below mean for age), delayed bone age, absence of organic disease that could cause growth failure, and normal body proportions. The diagnostic protocols used to detect (GHD) can be classified as either pharmacologic (use of provocative agents) or physiologic (measurement of spontaneous endogenous GH secretion). Standard provocative stimuli include insulin-induced hypoglycemia, arginine, clonidine, levodopa, propranolol, levodopa...

Growth Hormone and Age Related Osteoporosis

Because both GHD and normal aging are associated with decreases in bone density, it has been hypothesized that reduced GH secretion may account in part for age-related loss of bone mass (24). However, a causal relationship between GHD and osteoporosis has not been established. Nocturnal serum GH peaks average 20 ng mL in 30-yr-old men, but this value declines steadily to 3 ng mL by age 80 (24). These values are reflected in the fall of IGF-1 levels, which also occurs with aging (24). Because aging is associated with numerous physiological and hormonal changes, it has been difficult to determine definitively the degree to which the age-related decline in GH levels is responsible for bone loss. Bone density peaks at age 30, then declines progressively. In men, 25 of trabecular bone is lost by age 75 (25). One study of women with osteoporosis and vertebral compression fractures showed no difference in the GH response to insulin-induced hypoglycemia in these patients compared to...

Methodological Aspects When to Measure Neuroendocrine Markers

Basal hormone assessments do not necessarily reveal information on the integrity and reactivity of neuroendocrine axes. Therefore, a variety of challenge tests have been developed, using either pharmacological agents or real-life stimuli. Pharmacological challenge tests either stimulate or suppress an endocrine axis. For stimulating hormone secretion, hypothalamic releasing hormones and pituitary hormones have been used. The feedback sensitivity of an axis may be estimated by the degree of axis suppression after administering a synthetic version of the natural hormone exerting inhibitory feedback actions (see also Section 2.2). Other physiological stimuli activating endocrine axes may be mimicked by the administration of pharmacological agents. For example, hypoglycemia, which stimulates the HPA axis, the hypothalamic-pituitary-gonadal axis and the prolactinergic system, can be induced by insulin administration (insulin tolerance test). Other pharmacological tests target brain...

The Hypothalamic PituitaryGrowth Hormone Axis

Acute psychosocial stress, severe injury, hypoglycemia, pain or hemorrhage, increases plasma GH levels in humans, probably due to stimulating actions of glucocorticoids binding to a GH gene promoter. On the other hand, chronic stress or chronically increased glucocorticoid levels decrease GH secretion in humans and induce a state of IGF-1 resistance in peripheral tissues. This may occur because of CRH-induced increases in somatostatin secretion (Pacak and McCarthy, 2007). Severe psychosocial stress

Gh Treatment Of Patients With Abdominal Obesity

GH exerts direct insulin-antagonistic effects even after the administration of physiologic doses of GH. GH has been considered to be the principal factor in the decrease in insulin sensitivity observed in the early morning, the so-called dawn phenomenon (109) and the insulin resistance following hypoglycemia (110). Thus, our observation of increased insulin sensitivity during prolonged GH treatment is unexpected although not inexplicable. This improvement could be explained by the decrease in visceral adipose tissue mass induced by GH, followed by a decrease in FFA exposure to the liver counteracting the insulin-antagonistic effects of GH. Alternatively, as the major site of glucose disposal is in the skeletal muscle (111), the possibility has to be considered that the improvement in GDR in response to the more prolonged GH treatment might also be an effect of increased glucose transport in the skeletal muscle, possibly mediated through the IGF-1 receptor (71) and an increased...

Diabetes and Neuroendocrine Disorder

Research using EEG ERP directed at diabetes has been characterized by use of both EEG as a measure of state and EP's ERP's as a probe of cognitive or sensory function. Both measures are largely directed at the impact of glucose dys-regulation on neural function. Hypoglycemia is a fall in blood glucose levels that can occur as a complication of insulin treatment in diabetes mellitus. Hypoglycemia, if uncontrolled, can spiral through autonomic, cognitive, and affective disruption down to coma. Early awareness of hypoglycemia is important, as is the long-term effect of glucose dysregulation in general.

Long Term Effects of Diabetes

Obtained a significant correlation between blood glucose levels and P300 latencies as blood glucose levels increased, P300 latencies were less delayed - an effect not examined by Pozzessere et al (1991). This particular finding suggests that hypoglycemia plays a role in the obtained differences between patients and controls. In order to examine the long-term detrimental effects of diabetes the alternative explanation needs to be ruled out that the observed differences between patients and healthy controls could be due to the short-term effects of hypoglycemia.

Phenotypic Presentation of BWS with Mosaic Paternal Isodisomy UPD11p15

In this latter study (Slatter et al., 1994), comparison of the nine cases with paternal UPD11p to those 23 BWS without paternal UPD11p indicated that the UPD cases were more likely to have hemihypertrophy (6 9 versus 1 23) and less likely to have exomphalos (0 0 versus 13 23), whereas no differences were seen with respect to other features such as neoplasia, developmental delay, hypoglycemia, and nephro-

Imprinted Genes In The Bws 11p155 Critical Segment Igf2 and H19 in BWS

The methylation status on INS and IGF2, distal to the breakpoint of a BWS patient with a t(4 11)(p15.2 15.4)mat, was found to be diminished at the insulin locus relative to various controls (Mannens et al., 1994). At birth, both alleles were hypomethylated, but remarkably after the first three years only, the maternal allele remained as such. BWS patients have elevated levels of insulin and IGF2 so that hypomethylation of these genes could link their involvement in some features of the syndrome such as hypoglycemia, growth abnormalities, and neoplasia.

Use of GHRH in Diagnosis

In contrast to its use in adult-onset GHD, the variability in GH responses to GHRH alone, and the alteration of baseline responses by the use of somatostatin inhibitors both make GHRH a relatively poor tool for gaging the endogenous activity of the GH axis. Other tests, such as insulin-induced hypoglycemia, have so far proven to be better

Pharmacology Mechanism of Action

Several lines of evidence indirectly support an interaction of growth hormone secretagogues and somatostatin. Stimulation of GH by the secretagogues is synergistic with GHRH (29-32). Coadministration of atropine with GHRP-6 completely inhibits the stimulation of GH secretion, whereas coadministration with pyridostigmine increases GH secretion, as does insulin-induced hypoglycemia (33). To explain these data, these authors propose that somatostatin tone was increased by atropine, a cholinergic receptor antagonist, and decreased by pyridostigmine and hypoglycemia. They conclude that GHRP-6 induced GH secretion is dependent upon somatostatin tone, but does not act through mediating somatostatin release. In explaining the results of GHRP-6 infusion in healthy male volunteers, Huhn et al. (34) have suggested that growth hormone secretagogues act as functional somatostatin antagonists. Several other investigators have provided indirect data to support this hypothesis. Maccario et al. (35)...

Ivutility Of This Enzyme In Foods

Diallylthiosulfinate (allicin) is the antibacterial compound which has been used (as garlic extract) for thousands of years by many cultures (1). This and other medicinal properties attributed to garlic and onion are due to sulfurous compounds produced through enzymatic and nonenzymatic reactions following the reaction of alliinase on S-alk(en)yl-L-cysteine sulfox-ides (10). Current research is focused on the specific compounds which give extracts from alliaceous plants their properties as antimicrobial, anticancer, anti-blood clotting, and hypoglycemic agents, as well as

Insulinlike Growth Factor1 Igf1

Preliminary studies have also been performed to identify the optimal subcutaneous dosing regimen for rhIGF-1 (53). First, an HIV-negative subject was treated with increasing doses of rhIGF-1 for a total of 23 d. Because a tendency to hypoglycemia occurred at doses greater than 90 g kg d, that dose was chosen for subsequent studies. In one HIV-negative and one HIV-positive subject who received a constant dose of 90 g kg d, given as a single subcutaneous injection for 14 d, decreases in urine urea nitrogen excretion averaging +1.6 and +3.4 g d in the HIV-negative and HIV-positive patient, respectively, were observed during the entire treatment period. Thus, there was no evidence of the tachyphylaxis reported to occur during IV infusion of rhIGF-1 in a study in HIV-positive subjects (39). Interestingly, increases in REE also occurred in a dose-dependent manner, and increases in lipid oxidation rates were observed in all three patients given rhIGF-1 (53). Overall, the nitrogen-retaining...

Beckwith Wiedemann Syndrome

Transient neonatal hypoglycemia, which may cause mental retardation if untreated, is a common feature of BWS (Engstrom et al., 1988). In approximately 6 of BWS patients, there is an increased risk of developing tumors and hemihyperplasia (Hoyme et al., 1998). Other variable defects, including visceromegaly, earlobe creases, nevus flammeus, and mid-face hypoplasia, are often observed (Pettenati et al., 1986). one study (Slatter et al., 1994), nine cases of BWS with UPD11 were compared to 23 without UPD. The UPD11 cases appeared more likely to have hemihypertrophy (6 9 versus 1 23) and less likely to have exomphalos (0 9 versus 13 23). No differences were seen with respect to other features such as neoplasia, developmental delay, hypoglycemia, and nephromegaly. In another comparison between UPD11 and non-UPD cases of BWS, the incidence of tumors was higher in UPD11 cases (50 versus 8 ), although the sample size was small (Henry et al., 1993). It would be tempting to speculate that...

Medical Implications of the AMPK System

Type 2 diabetes, which affects over 100 million people worldwide, is a hyperglycemic condition caused by reduced glucose uptake by muscle and increased glucose production by liver. Physical exercise is known to provide protection against its development, and because AMPK is activated by exercise it regulates the activity and expression of the insulin-sensitive glucose transporter GLUT4 and inhibits expression of enzymes of gluconeogenesis 30 , this suggesting that AMPK could be a promising target for therapy of Type 2 diabetes 26 . This idea has been supported by recent findings that metformin, an important oral hypoglycemic agent used to treat Type 2 diabetes, activates AMPK in vivo 29 .

Pharmacological Toxicological Effects 51 Endocrine Effects

P. ginseng may exert hypoglycemic effects possibly by accelerating hepatic lipogenesis and increasing glycogen storage (16-18). In a study of 36 newly diagnosed patients with type II diabetes, ginseng at a dose of 200 mg daily exerted a statistically significant benefit on glycosylated hemoglobin (HbA1c) compared to 100 mg of ginseng daily or placebo after 8 weeks of therapy, and patients receiving 100 mg of ginseng had smaller mean fasting blood glucose levels than patients taking 200 mg of ginseng or placebo (18). The actual difference among the mean HbA1c in the three groups was small the 200-mg ginseng group had a mean glycosylated hemoglobin of 6 vs 6.5 for the 100-mg ginseng and placebo groups. Likewise, the actual difference among mean fasting blood glucose in the three groups was small the mean fasting blood glucose was 7.7 mmol L for the 100-mg ginseng group, 7.4 mmol L for the 200-mg ginseng group, and 8.3 mmol L for the placebo group at the end of the study. The observed...


All alternatives to co-trimoxazole are less effective. In cases of intolerability or history of sulfonamide allergy, intravenous pentamidine is recommended as the drug of second choice. An induction therapy is administered over the first few days (200-300 mg in 500 ml 5 glucose or 0.9 NaCl), and half the dose can then be given from day 6. This treatment is very toxic, which is why we have not used it for many years. Severe decompensations of electrolyte and blood glucose levels (both hyper- and hypoglycemia) are possible, as well as pancreatitis, arrhythmia and renal failure. Initially, blood glucose, electrolytes and renal parameters should be monitored daily.

Cranial Irradiation

The deleterious effects of cranial irradiation on GH secretion are an unfortunate and common morbidity for individuals with a variety of neoplastic and hematologic diseases. The initial studies detailing the hypothalamic-pituitary effects of cranial irradiation exposure were performed with male rhesus monkeys (40 Gray), demonstrating a blunted GH secretory response to insulin hypoglycemia and a decrease in GH pulse frequency and amplitude. Doubling the dose of insulin (0.1-0.2 units kg) normalized the GH response, suggesting an intact, but altered or reset hypothalamic sensitivity for influencing GH secretion (Figs. 1 and 2) (46).


The GH response to a variety of provocative stimuli (insulin-hypoglycemia, arginine, opiates, glucagon, levodopa and GHRH), is diminished in obese subjects (52). One study evaluating spontaneous GH secretory dynamics in obese men (body mass index BMI > 42) demonstrated a reduction in endogenous GH half-life relative to control subjects (BMI < 31), a daily production rate of GH 4.1-fold less compared with controls and a threefold decrease in GH secretory burst frequency despite preservation of the GH ultradian rhythm (52). This principle applies to children as well.

Case Example

A 51-year-old woman was transferred from a small community emergency department for subspecialty evaluation. The patient had presented to that facility the previous night complaining of headache and fever for three days with a sudden loss of vision in her left eye. During our evaluation, the patient reported that one week earlier, she fell, striking the left side of her face and sustaining several small abrasions. She denied other facial trauma. Further history revealed a general malaise and gradual weight loss for about one month's duration. She also admitted to falling occasionally in the past. Her past medical history included non-insulin-dependent diabetes mellitus for several years. She was non-compliant with her oral hypoglycemic medication. She denied other past medical history.

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