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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Tohoku University method of fasting therapy was performed on 380 patients. The clinical results revealed an efficacy rate of 87%. With regard to psychosomatic diseases, irritable colon syndrome, neurocirculatory asthenia, mild diabetes mellitus, obesity and borderline hypertension were good indications for this therapy. In order to clarify the therapeutic mechanism, several clinical examinations were administered before, during and after therapy. EEG data was analysed according to the power spectral method. The peak frequency decreased as fasting progressed, while it increased as re-fed continued. Percent energy of alpha waves after fasting therapy was significantly higher than that of the pre-fasting stage. The dexamethasone suppression rate of urine 17-OHCS after fasting therapy was significantly lower than that of the pre-fasting stage. It seems that ketone nutrition may work as a strong stressor in the brain cell, temporarily placing all biological mechanisms in a stress state and then activating the natural healing power inherent to the human body, thereby bringing about homeostasis.
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PMID:Psychophysiological study on fasting therapy. 55 Jan 77

It has been well known that the fasting therapy which was invented in Medical School of Tohoku University reveals an excellent effect upon various kinds of psychosomatic diseases, but its therapeutic mechanism and suitable indication are not yet explained completely. In order to corroborate these problems, this study was undertaken on 262 cases of psychosomatic diseases in the field of internal medicine. It is a complete fasting for 10 days with nothing by mouth except for drinking water, and 500 ml of parenteral fluid containing vitamins are administered intravenously every day. Absolute bed rest and self meditation are required in a closed individual room, and patients are not allowed to meet anyone but physicians and nurse in charge. The return to normal ordinary diet follows the order of fluid diet, soft diet and semiordinary diet during 5 days. In the period of the therapy, various clinical and laboratory examinations were carried out. Significance of these examinations consists in prediction of possible danger during the fasting period and elucidation of its therapeutic mechanism. Consequently, an outstanding efficacy rate of 87% with excellent prognosis was attained, and the following diseases were determined as suitable indication of this therapy; irritable colon, dysorexia nervosa, borderline hypertension, neurocirculatory asthenia, bronchial asthma, mild diabetes mellitus, obesity, lumbago without organic findings, conversion hysteria, various neurosis with somatic symptoms and masked depression. Possible mechanism of action of the therapy is that fasting acts as an extreme stress on the function of the autonomic nervous and endocrine systems, then it regulates the function of whole body including the brain, also it acts as one of the behaviour therapy for abnormal conditioning.
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PMID:Fasting therapy for psychosomatic diseases with special reference to its indication and therapeutic mechanism. 96 29

Twenty-nine IDDM patients with borderline hypertension were randomly allocated to placebo or nitrendipine treatment. Nitrendipine was given orally at a dosage of 20 mg once daily over 4 weeks. Stimulated platelet thromboxane formation at rest and after standardized, non exhausting exercise was measured by standard methods. In addition, plasma levels of platelet factor 4 and aggregation responses to collagen and ADP were determined. In the treatment group thromboxane formation after stimulation with collagen (0.3 and 1.0 micrograms/ml) and 1 mM arachidonic acid (AA) was reduced in the resting state. Exercise induced change of thromboxane synthesis in response to 1.0 micrograms/ml collagen was significantly lower as compared to placebo (p < 0.05). In parallel, PF4 plasma levels were significantly lowered (p < 0.05). Whole blood aggregation after collagen stimulation (1.0 micrograms/ml) was reduced after 4 weeks of nitrendipine treatment, but ADP (5 microM) induced aggregation was not. These effects of nitrendipine were not seen in platelet rich plasma. In conclusion long-term nitrendipine treatment may inhibit collagen dependent platelet activation in the blood of diabetic patients with borderline hypertension.
Diabetes Res 1992 Mar
PMID:Reduced platelet thromboxane formation after long-term administration of a dihydropyridine calcium channel blocker: a prospective, double-blind, placebo-controlled study with nitrendipine in borderline hypertensive patients with IDDM-type diabetes mellitus. 128 47

In vitro studies indicate that the intact endothelium prevents the access of circulating endothelin to vascular smooth muscle cells. Disease states like diabetes, that are associated with endothelium dysfunction, might facilitate the access of endothelin to vascular smooth muscle, causing increased vasoconstriction. To investigate whether differences between diabetic and nondiabetic subjects could be detected on superficial veins, venous diameter changes in response to local infusions of endothelin (1.53, 3.11 and 6.22 pmol/min) were compared in type 2-diabetics with albuminuria (greater than 300 mg/day) and borderline hypertension (diastolic blood pressure 90-95 mmHg), and in healthy volunteers. In addition, we studied the effect of histamine on the endothelin-induced venoconstriction. The dorsal hand vein compliance technique was employed. Endothelin caused a dose-dependent, slow-onset constriction of the hand vein in all subjects, without any difference in endothelin responsiveness between diabetic and control subjects. The maximal venoconstriction at 6.22 pmol endothelin/min was 29 +/- 26% (% of venous diameter at base line) in diabetics and 23 +/- 22% in controls (p greater than 0.02). Co-infusion of endothelin and a dose of histamine with minimal venodilatory effect ("ED5-ED20") had no influence on the endothelin responsiveness of the hand veins, in that the maximal venoconstriction after 6.22 pmol endothelin/min was 25 +/- 23% without, and 23 +/- 16% with added histamine. Submaximally venodilating histamine doses ("ED60-ED90") markedly attenuated the endothelin-induced venoconstriction (maximal venoconstriction: 63 +/- 43%). These data, obtained in veins, argue against a generalized defect in vascular responsiveness to endothelin associated with diabetes.
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PMID:Endothelin-induced venoconstriction is unaffected by type 2-diabetes: in vivo effect of histamine on the endothelin action on veins. 153 Mar 76

A health risk appraisal function has been developed for the prediction of stroke using the Framingham Study cohort. The stroke risk factors included in the profile are age, systolic blood pressure, the use of antihypertensive therapy, diabetes mellitus, cigarette smoking, prior cardiovascular disease (coronary heart disease, cardiac failure, or intermittent claudication), atrial fibrillation, and left ventricular hypertrophy by electrocardiogram. Based on 472 stroke events occurring during 10 years' follow-up from biennial examinations 9 and 14, stroke probabilities were computed using the Cox proportional hazards model for each sex based on a point system. On the basis of the risk factors in the profile, which can be readily determined on routine physical examination in a physician's office, stroke risk can be estimated. An individual's risk can be related to the average risk of stroke for persons of the same age and sex. The information that one's risk of stroke is several times higher than average may provide the impetus for risk factor modification. It may also help to identify persons at substantially increased stroke risk resulting from borderline levels of multiple risk factors such as those with mild or borderline hypertension and facilitate multifactorial risk factor modification.
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PMID:Probability of stroke: a risk profile from the Framingham Study. 200 1

Borderline hypertension, a condition in which the blood pressure oscillates between normal and high values, is a predictor of future more severe hypertension. Pathophysiologically, borderline hypertension is different from established hypertension. A large proportion of such patients have elevated cardiac output and a normal vascular resistance. In established hypertension, the output is normal and resistance is elevated. The elevation of cardiac output in borderline hypertension is neurogenic; it can be abolished by an autonomic blockade of the heart. In addition to an increased cardiac sympathetic drive, increased sympathetic tone to the kidney, arterioles, and veins has also been found. In parallel with the hypersympathetic state, patients with borderline hypertension also show decreased parasympathetic tone. The enhanced sympathetic tone leads to a decreased cardiac responsiveness, and eventually, the cardiac output returns to the normal range. High blood pressure causes vascular hypertrophy, and hypertrophic vessels are hyperresponsive to vasoconstriction. These secondary changes in the responsiveness of the heart and blood vessels are the basis of transition from a high cardiac output to high-resistance hypertension. These hemodynamic changes are associated with a downregulation of the sympathetic tone. A picture of an apparently nonneurogenic high-resistance hypertension emerges. Nevertheless, when assessed in regard to the enhanced pressor responsiveness, the sympathetic drive in such patients is still excessive. Despite the apparently normal tone, the sympathetic nervous system continues to play an important pathophysiological role in established hypertension. Borderline hypertension is associated with numerous metabolic abnormalities including obesity and insulin resistance. It is tempting to view all these abnormalities as a common expression of the increased sympathetic drive in hypertension. Explanation of the basis of the association of hypertension and metabolic abnormalities promises to bring new insights into the pathophysiology of two common diseases of civilization: hypertension and diabetes mellitus.
Diabetes Care 1991 Mar
PMID:Autonomic nervous dysfunction in essential hypertension. 204 40

Serum creatinine levels were determined prospectively every 2 to 3 months in 40 patients with diabetic nephropathy for a global observation period of 864 months. The monthly creatinine increasing rate was significantly lower in normotensive periods, mean arterial pressure (MAP) less than 115 mmHg, when compared with hypertensive periods, MAP greater than 125 mmHg. No significant difference was shown in periods with borderline hypertension (MAP between 115-124 mmHg). The mean creatinine increases were of 0.036 mg/dl/month, 0.3 mg/dl/month and 0.046 mg/dl/month respectively. Normotension was associated with a slowing down of the rate of decline in renal function in this group of moderate kidney failure with an initial mean serum creatinine of 2.26 mg/dl. The exposure of patients to nephrotoxics (aminoglycosides, and possibly anesthesia) significantly accelerated the decline in renal function: 0.39 mg/dl/month and 0.17 mg/dl/month respectively according to the concomitance or not of toxics and hypertension. The reported protective effect of diabetes against aminoglycosides nephrotoxicity in experimental conditions was not reflected in our clinical results. On the contrary, we suggest a possible enhanced sensibility of the diabetic patient with diabetic nephropathy to aminoglycosides leading to an acceleration of the progression of renal failure.
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PMID:Hypertension and nephrotoxicity in the rate of decline in kidney function in diabetic nephropathy. 381 4

The objectives of this research were to determine the prevalence of essential and borderline hypertension in a population of blood donors and their families and to determine if there is a correlation between blood pressure and lifestyle and/or other cardiovascular risk factors. The study was comprised of 1976 individuals, of whom 1290 were men and 686 were women, aged 18-65 years. The prevalence of essential hypertension was 15.1% for males and 12.5% for females: the prevalence of borderline hypertension was 22.3% for males and 15.7% for females. The population was divided into two groups: the first group included only subjects (1170 men, 543 women) who did not regularly use drugs that could modify the blood pressure and the heart rate, the second group included the entire population. In the first group, the multiple regression analysis indicated, in order of importance: age, BMI (body mass index), and heart rate. These variables were important in determining the systolic blood pressure in both sexes, uricemia for males and glycemia for females. The diastolic blood pressure was dependent on BMI, heart rate, and alcohol in both sexes, and glycemia, LDL cholesterol, and uricemia in the men. In the second group, primary and borderline hypertension are significantly correlated with age, BMI, and uricemia in both sexes and glycemia in females. A program of health and nutritional education could modify some factors related to blood pressure, such as obesity and alcohol consumption. The result would be a reduction of the prevalence not only of essential and borderline hypertension, but also of metabolic diseases such as dyslipidaemias, diabetes and hyperuricemia, with a global reduction of the cardiovascular risk.
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PMID:[Arterial hypertension in relation to life style and other cardiovascular risk factors. Epidemiologic study of a population of blood donors. Project AVIS]. 802 51

Alterations in the renal dopamine [DA] system have been suggested to contribute to the development of hypertension and diabetic nephropathy. To identify early abnormalities in renal handling of DA and sodium we challenged 16 normotensive patients with uncomplicated insulin-dependent diabetes (IDDM), 18 normotensive nondiabetic subjects with familial borderline hypertension, and 16 healthy controls, 14-29 years old, with a high-sodium diet (HSD). Systolic blood pressure was slightly higher in subjects with familial borderline hypertension than in the other groups on a normal sodium diet (NSD) (P < 0.05). Blood pressure and 24-h urinary measurements were performed on a NSD and after 3 days on a HSD. Twenty-four-hour urinary DA excretion was similar in all groups on NSD. A significant rise in DA excretion was noted after HSD in control subjects (P < 0.01), but not in subjects with a family history of hypertension or with IDDM. Urinary sodium excretion increased in all groups. A correlation between the change in DA and sodium/creatinine ratio after HSD was seen in healthy controls (r = 0.57, P = 0.02) but not in those with familial borderline hypertension (r = 0.18, P = 0.47) or with IDDM (r = 0.40, P = 0.15). A rise in systolic (but not diastolic) pressure was noted only in the IDDM group after HSD (P = 0.02). In conclusion, an impairment in the renal DA and sodium system can be detected early in IDDM and in individuals with familial hypertension. We speculate that this impairment may contribute to the development of hypertension and microvascular disease in both conditions.
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PMID:The dopaminuric response to high salt diet in insulin-dependent diabetes mellitus and in family history of hypertension. 909 Jun 56

The present report describes the relationship between the glucose tolerance and hypertension surveyed in a ten-year longitudinal epidemiological study in two rural communities in Hokkaido, Japan. The 1972 subjects (928 men and 1044 women, aged 40-64, mean 51.1 +/- 7.0 years) were randomly selected in 1977 and 1978, underwent a 50-g oral glucose tolerance test (GTT) at the first year. The prevalences of borderline hypertension (BHT) and of hypertension (HT) were highest in those with diabetes mellitus (DM), followed by those with borderline diabetes (BDM) and those normal glucose tolerance (NGT). Systolic and diastolic blood pressure were significantly and positively correlated with plasma glucose levels during fasting (FPG), 60 min. after GTT (60G), and 120 min. after GTT (120G), and were ordered as follows: NGT < BDM < DM. The FPG, 60G and 120G plasma glucose levels were all significantly higher in BHT and HT than in NT. The prevalences of the progression to hypertension from non-hypertension over the ten-year follow-up period were ordered as follows: NGT < BDM < DM. Glucose levels in progression group were higher than those in non-progression group. Multiple logistic regression analysis indicated that age, glucose intolerance, systolic blood pressure, and obesity index were significant predictors of the progression to hypertension. These results indicate that impaired glucose tolerance may be associated with hypertension, and might play a role in the development of hypertension.
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PMID:[Role of impaired glucose tolerance in the progression of hypertension]. 1006 70


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