Postprandial hyperglycemia in patients with type 2 diabetes mellitus,diabetes tipo 1 curacion,natural diabetes treatment system cost - Plans On 2016


DIFFERENCE BETWEEN HYPERGLYCEMIA AND TYPE 2 DIABETESH hyperglycemic nonketotic syndrome or hhns occurs most commonly occurs most. Presentation on theme: "Glycemic Targets in Clinical Practice: Postprandial vs Preprandial and Fasting? The question is not whether to target postprandial, preprandial or fasting glycemia, but when, how, and to what goals. UKPDS Epidemiologic Data in Type 2 Diabetes No A1C Threshold 0% 10% 20% 30% 40% 50% 60% 70% 80% 567891011 Adjusted incidence per 1000 person- years Myocardial infarction Microvascular endpoints Updated mean A1C (%) Stratton IM, et al. To achieve a normal or near normal HbA 1c, both FPG and PPG levels must be normal or near normal. Patients With Type 2 Diabetes May Spend More Than 12 Hours per Day in the Postprandial State Adapted from Monnier L.
Correlation between plasma glucose levels after OGTT and standard mixed meal Wolever TMS et al. As Patients Get Closer to A1C Goal, the Need to Successfully Manage PPG Significantly Increases Adapted from Monnier L, Lapinski H, Collette C. Fasting Plasma Glucose Reflects Endogenous Glucose Production Dinneen S, Gerich J, Rizza R. Effect of Glyburide or NPH Insulin on Glycemia in Type 2 Diabetes Time of day From: Shapiro ET et al. Among the sleep disorders obstructive sleep apnea (OSA),insomnia, sleep deprivation, excessive sleepiness and restless legs syndrome have an impact on the glucose metabolism.
Sleep is a metabolic regulator and sleep debt has harmful effects on carbohydrate metabolism. Subjects deprived of sleep for several days or more become irritable, fatigued, unable to concentrate and usually disoriented. Chronically reduced sleep times are associated with obesity.8 SD induced stress has a role to play in the development of obesity.
Sleep deprivation induces or aggravates snoring by increasing muscular hypotonia and delaying contractions of the dilator muscles of the pharynx.9 Chronic partial sleep deprivation is seen in many important groups including doctors, soldiers, shift workers, mothers particularly nursing mothers, cross country truck drivers and taxi drivers. I have observed rebound sleep deprivation in elderly subjects who wait for their children and loved ones to return from place of work.
Sleep disordered breathing (SDB) is a spectrum of disorders consisting of snoring, upper airway resistance syndrome and sleep apnea. Snoring is a common symptom and is evident when a group of subjects sleep together for eg in sleeper coaches of railway trains.
In 1985 Mondini and Guillemenault24 reported an increased frequency of abnormal breathing in lean and obese individuals. Insulin resistance denotes the inability of insulin to produce usual biological effects at circulating concentrations that are effective in normal subjects. Recent studies indicate that visceral fat is more important than generalised obesity that predisposes obese subjects to sleep apnea. Obstructive sleep apnea (OSA) is a common disorder which is usually not suspected in clinical practice. Nocturia results in arousals.Nocturia is often due to (a) secretion of atrial natriuretic peptide from right atrium in patients with OSA and (b) hyperglycemia (c) Urinary tract infection. The prevalence of SDB increases with age.32,33 In elderly subjects polysomnography shows predominance of obstructive events over central or mixed events. Fatty liver is a seat of insulin resistance.37 Its role in the pathogenesis of diabetes and metabolic syndrome is well recognized. Recent reports suggest that hepatic dysfunction has also been associated with irregular breathing during sleep. Evidence suggests that testosterone promotes upper airway collapsibility in patients with sleep apnea.
I had suggested in 2003 (possibly for the first time) that since retina is the highest oxygen consuming part of the body, it is likely that cyclical hypoxemia in sleep in subjects suffering from OSA will have deleterious effects on the retina.3 This should be considered especially in patients of diabetic retinopathy since type 2 diabetes mellitus and OSA are usually associated. It is known that cortisol can cause moderate degree of fatty acid mobilization from adipose tissue. The unique neuroendocrine aspects of REM sleep coupled with sleep disruption in OSA patients is conducive for the development of insulin resistance and diabetes.
Evidence points to a possible role of sleep disorders as risk factors for metabolic abnormalities. In a given patient of type 2 diabetes though the question remains whether these associations are causal, it would be worthwhile to rule out the presence of sleep disorders viz SDB, clinically and polysomnographically. Gottlieb DJ, Punjabi NM ,Newmann AB et al.Association of sleep time with diabetes mellitus and impaired glucose tolerance.
Bixler EO, Vgontzas AN, Lin H-M et al.Association of hypertension and sleep disordered breathing. Sleep in Tabers Cyclopedic Medical Dictionary Page1772.Ed Thomas Clatton L Pub Jaypee Brothers Medical Publishers (P) Ltd. Young T, Palta DM, Dempsey J et al The occurrence of sleep disordered breathing among middle aged adults. Tanne F, Gagnadoux F, Chazouilleres O, Fleury B,Wendum D,Lasnier F, Lebeau B, Poupon R and Serfaty L.
It used a crossover design so subjects were randomized to one diet for 7 days then switched to the other diet for 7 days.
From the chart below… Glucose was higher after breakfast in the big-breakfast (Bdiet) group, but was considerably lower after lunch and dinner, such that the total glucose roaming the bloodstream during the day, shown by the total area under the curve (AUC), was significantly lower in the Bdiet group. Despite the diets being isoenergetic, lunch resulted in lower glucose (by 21–25%) and higher insulin (by 23%) with the Bdiet vs Ddiet.
This is achieved in part by the circadian secretion and activity of enzymes and hormones involved in the regulation of postprandial glycaemia [9–13]. The omission of breakfast was also associated with increased risk of type 2 diabetes, poor glycaemic control, higher HbA1c, increased lipogenesis, visceral adiposity and high blood pressure and increased cardiovascular risk despite the same daily energy intake in individuals with type 2 diabetes [20,21].
This study, since it focuses more on when to eat instead of what to eat, reminds me of the study in this post: Limiting Eating To 8-12 Hour Period Causes Weight Loss, Diabetes Reversal In Mice. Bix Saturated fat is one of our best sources for environmental pollutants, a confounder not adjusted for here. Fanatic Cook by Bix is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.


Contributions of fasting and postprandial plasnma glucose increments to the overall diurnal hyper glycemia of Type 2 diabetic patients: variations with increasing levels of HBA(1c). Lowering FPG first will lower all PG values throughout the day and thus will also reduce PPG and may be sufficient. Modern life style has generated several diseases of which type 2 diabetes mellitus, cardiovascular disorders and sleep disorders occupy prime positions. OSA appears to have the strongest association with these metabolic disorders.1 In clinical practice detailed sleep history is often not recorded. Van Helder4 and colleagues showed that the insulin response to an oral glucose challenge was higher when comparing the total sleep deprivation condition i.e 60 hours of continuous waking) to the normal sleep condition, suggesting an insulin resistant state that is induced by acute sleep deprivation. Sleep deprived subjects have daytime sleepiness and have a tendency to overeat and eat fast.
Subjects travelling long distances for work are plagued with late night sleeps and early awakenings.
Grimble21 has reported that chronic inflammation is known to act as a trigger for chronic insulin insensitivity. The sleep complaints are often related to the presence of underlying SDB, nocturia, physical complications of disease and underlying depression. Vgontzas et al28 in a well controlled study included 3 groups of subjects (i) obese patients with sleep apnea (ii)obese patients without sleep apnea (iii) normal weight controls. There is repetitive pharyngeal collapse in sleep resulting in cyclical hypoxemia, cyclical hypertension and release of stress hormones and catecholamines.
There are multiple etiologic factors and the exact cause of non alcoholic fatty liver disease still unknown. Non-alcohol drinking subjects with apnea and hypopneas during sleep were found to raised liver enzymes and more steatosis and fibrosis on liver biopsy, independent of body weight.38 Cyclical hypoxemia, sympathetic stimulation, cyclical release of stress hormones in patients of OSA can pave the path for liver insults and injury. However testosterone levels appear to be low in men with sleep apnea, possibly because of hypoxia and sleep fragmentation. There is increased blood flow to erectile tissues which possibly prevents excessive collagen formation in these tissues. In a well designed study improvement in insulin sensitivity by CPAP therapy in patients with OSA has been demonstrated by Harsch et al.42 Forty patients of OSA were taken up in this study. Cuellar and Ratcliffe 47 showed that in type 2 diabetes with and without RLS, poor glycemic control (determined by haemoglobin A1c levels) was directly correlated with sleepiness regardless of underlying RLS. A peculiar moon facies and buffalo like torso occurs in patients who have excessive cortisol secretions.
There is a close relation between sleep, circadian rhythm, obesity, insulin resistance, hypertension and cardiovascular disorders which needs to be dissected and managed.
The treatment of SDB particularly OSA by CPAP will help the patient in varying degrees by reducing insulin resistance and preserving beta cell function. Obstructive sleep apnea is independently associated with an increased prevalence of metabolic syndrome. The role of habitual snoring and obesity in the development of diabetes: A 10-year follow-up study in a male population. Habitual snoring is associated with elevated hemoglobin A1c levels in non-obese middle-aged adults.
Sleep Apnea in Harrisona€™s Prinicples of Internal Medicine 17th Edn McGraw Hill,1665-1667.
Continuous positive airway pressure treatment rapidly improves insulin sensitivity in patients with obstructive sleep apnea syndrome.
CPAP treatment of a population based sample-what are the benefits and the treatment compliance? A comparison of glycemic control,sleep, fatigue and depression in type 2 diabetes with and without restless legs syndrome. This dietary adjustment may have a therapeutic advantage for the achievement of optimal metabolic control and may have the potential for being preventive for cardiovascular and other complications of type 2 diabetes. Indeed, there was animal food at least 7 times a day (tuna, egg, yogurt, milk, chicken, cheese, turkey). Thus both FPG and PPG must be targets for therapy Thus both FPG and PPG must be targets for therapy Nevertheless, might there be situations in which it is preferable to treat one or the other first ???
Defects in sleep quality and quantity can result in metabolic errors and cardiovascular dysfunction. Detection and treatment of sleep disorders in diabetes is essential since their treatment is highly rewarding.
The secretory rate of ACTH and cortisol are all high in early morning and low in the late evening.
Intake of food in various forms help the sleep deprived subject to overcome daytime sleepiness. Also late night television viewing exposes the retina to bright light which can inhibit the release of melatonin and delay the sleep onset further. The first 2 groups were matched for weight whereas all 3 groups were matched for age and sex.
Habitual snoring and excessive daytime sleepiness are two prominent symptoms of obstructive sleep apnea. REM sleep deprivation may cause anxiety, increased appetite and hypersexuality.31 Patients who are sleep deprived often exhibit fast eating and binge eating which adversely affects glycemic status and digestion.
I would like to coin the term Lean metabolic syndrome to these subset of patients who are metabolically non obese.
Insulin resistance and obesity occupy the center stage but the factors responsible for the progress and transformation from one stage to another is matter of research and debate. Increased fibre formation in the erectile tissues could lead to tissue cell death and eventual loss of erectile function. Vgontzas et al41 have demonstrated that premenopausal women with diagnoses of PCOS are at much higher risk for development of sleep apnea and daytime sleepiness. We have also reported beneficial effects of CPAP in 4 patients with type 2 diabetes.43 Lindberg et al44 demonstrated reductions in fasting insulin levels and insulin resistance(estimated by HOMA) after 3 weeks of CPAP treatment in 28 men with OSA compared with matched controls. In OSA there is excessive release of stress hormones viz catecholamines, cortisol in sleep causing a Cushings like disease. Administration of thyroxine without treating OSA can precipitate cardiovascular events in sleep due to cyclical hypoxemia particularly in REM sleep.


There is evidence to show sleep disorders such as OSA, insomnia, short or long-term sleep duration and restless legs syndrome are potential risk factors for insulin resistance, glucose intolerance, type 2 diabetes mellitus and metabolic syndrome. Obstructive sleep apnea (OSA) is one of the most important disorder identified in the last 50 years which has systemic effects including glucose metabolism. Sleep is an emotional issue and all diseases particularly chronic diseases like diabetes invites emotional reactions which can also affect sleep adversely.
These effects result from a 24 hour cyclic alteration in the signals from the hypothalamus that cause cortisol secretion. Chewing tobacco, smoking also drive away sleep but are risk factors for type 2 diabetes.3 Chronic sleep restriction coupled with eating contributes separately to the development of obesity. Shift work can have deleterious effects on metabolic equilibrium and can precipitate diabetes particularly in genetically prone subjects due to chronic SD.
In lean subjects anatomical features which promote SDB include macroglossia, short neck, retruded chin, retruded maxilla and neck circumference of more than (17 inches) 43 cms. Daytime sleepiness is usually overcome by consuming tea, coffee and tobacco singly or in combination.
Figure 1 flow chart shows the close association of sleep deprivation, obstructive sleep apnea and type 2 diabetes mellitus and also the path taken by nocturnal events in a patient of obstructive sleep apnea leading to the development of type 2 diabetes mellitus. However OSA patients may exhibit hypersexual behavior due to REM sleep deprivation.(REM sleep deprivation is common in OSA). In situations of chronic sleep deprivation particularly REM sleep deprivation as occurs in OSA these nocturnal mechanisms may be affected causing erectile dysfunction(ED). This has important implications since patients with impaired glucose tolerance and mild diabetes can look forward to reversal of diabetes with treatment of associated OSA. The nocturnal excessive cortisol and catecholamine secretion can also spill over in the day (spill over effect) resulting in fasting hyperglycemia.
Also the correction of hypoxemia in sleep will have beneficial effects in various system dysfunctions like cardiovascular, neurological and the eye.
It has been demonstrated that glucose tolerance is markedly better in the morning than in the evening.5 Spigel et al6 have shown that sleep debt results in impaired glucose tolerance. It is not uncommon to find nap pod in commercial organizations where employees can take a power nap to boost their performances. This raises an important issue whether sleep disordered breathing which occurs in normal weight or low body weight subjects poses a risk for the development of type 2 diabetes mellitus?
Those with sleep apnea had significantly higher levels of fasting plasma insulin and glucose levels than their obese controls.
The other nocturnal symptoms include witnessed apneas, choking, dyspnea, restlessness, diaphoresis, acid reflux, drooling, somniloquy, frequent change of posture in sleep, unable to sleep supine and bruxism. Experimental evidence suggests OSA impairs lipid homeostasis and could therefore worsen non-alcoholic fatty liver disease. Patients of sleep apnea with sexual dysfunction may be advised to take testosterone injections which can aggravate OSA.
As reported insulin resistance in OSA can be treated with Continuous Positive Airway Pressure (CPAP) (see below.) Therefore it is desirable to screen patients of PCOS for SDB. However fast eating may not occur in subjects who have dentures or in patients with associated hypothyroidism.
Also the group with sleep apnea demonstrated a higher degree of visceral but not subcutaneous fat compared to their obese controls.
The daytime symptoms apart from sleepiness include fatigue, morning headache, poor concentration, decrease libido or impotence, decreased attention, depression, decreased dexterity and personality changes. In a recent prospective series of adults presenting to a sleep clinic, a threefold increase in the likelihood of elevated liver enzymes was found in subjects with newly diagnosed severe OSA39.
It is wise to open the pharynx in sleep and close the gates which lead to systemic diseases.
Based on these observations Vgontzas et al29 in an extensive review commented that there is pernicious association between sleep apnea and insulin resistance primarily in obese patients.
Mood swings and angry behavior is often present which may force the subject to seek psychiatric advice. Liver biopsy, performed only on subjects with abnormal liver enzymes in this same study identified NASH in the vast majority of subjects with severe OSA whereas a minority of subjects with mild or no OSA had biopsy proven NASH.
The daytime sleepinessin OSA is reflected in development of obesity due to lack of exercise and physical activity. There is mounting evidence to show a close association between sleep deprivation, sleep disordered breathing-OSA, excessive sleepiness, insomnia, restless legs syndrome and Type 2 DM.
In diabetic subjects there is often postprandial drowsiness, poor concentration, fatigue and depression. It must be appreciated that children with Type 1 diabetes run the risk of developing OSA with advancing age which can worsen the metabolic status. The role of sleep deprivation, particularly REM sleep deprivation, in the genesis of obesity needs to be recognized. Exercise against a background of hypoxemia and elevated catecholamines can precipitate cardiovascular events. The close association of OSA with insulin resistance demands the recognition of OSA in fatty liver and polycystic ovary syndrome. In OSA there is intermittent hypoxia, recurrent arousals from sleep and sleep fragmentation causing sympathetic stimulation. Treatment of OSA by continuous positive airway pressure has been shown to increase insulin sensitivity.
It is important for primary care physicians to have a high degree of suspicion of an underlying sleep disorder in patients with diabetes. Also altered corticotrotropic and somatotropic function increase circulating adipocytokines which alter glucose metabolism.30 There is strong possibility that changes in sympathetic nervous system activity, corticotropic function and systemic inflammation are associated with subjects with short sleep duration and insomnia, thereby causing metabolic dysfunctions. Hiranandani Hospital, Powai, Mumbai and Asian Institute of Medical Sciences, Dombivli (Dist.



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