Significance of the renin-angiotensin-aldosterone system for pathogenesis and early diagnosis of pregnancy-induced hypertension with special reference to mineralocorticoid receptors.
High sensitivity test for the early diagnosis of gestational hypertension and preeclampsia. IV. Early detection of gestational hypertension and preeclampsia by the computation of a hyperbaric index.
Diagnosis of early hypertension with continuous ambulatory blood pressure monitoring.
Early diagnosis and management of renovascular hypertension.
Early diagnosis of renal ischemia in arterial hypertension by means of urine N-acetyl-beta-D-glucosaminidase.
Zentralbl Gynakol. 1999;121(12):596-602.
Significance of the renin-angiotensin-aldosterone system for pathogenesis and early diagnosis of pregnancy-induced hypertension with special reference to mineralocorticoid receptors.
Gerding C, Lorenzen A, Wacker J, Rehberger I, Werner P, Schwabe U, Bastert G.
Universitats-Frauenklinik Heidelberg.

OBJECTIVE: In women with pregnancy-induced hypertension (PIH) the density of mineralocorticoid receptors (MR) in human mononuclear leukocytes (HML) is reduced compared with healthy pregnant women. The same applies to plasma levels of aldosterone and 18-hydroxycorticosterone. In this study, we investigated whether alterations of these parameters preceded the development of clinical symptoms and, therefore, might be potential predictors of PIH involved in the pathogenesis. PATIENTS AND METHODS: In eighty-four women belonging to the risk-group for PIH but not showing any symptoms neither of PIH nor preeclampsia (PE) we characterized prospectively before the onset of disease in the second trimester of pregnancy mineralocorticoid receptor status in HML and steroid plasma levels of aldosterone and its precursors as well as cortisol through radioimmunoassay. RESULTS: 15 women developed PIH, three of which developed PE. Neither in the density of MR nor in the affinity the women that developed PIH showed any difference from healthy women. Steroid plasma levels were identical as well. CONCLUSION: We conclude that a reduction of mineralocorticoid receptors does not precede PIH within the peripheral blood. But still one can assume that the RAAS may be involved in the pathogenesis of PIH, possibly on a local level within the placenta or as a secondary change, initiated by still unknown factors.


J Perinat Med. 1997;25(3):254-73.
High sensitivity test for the early diagnosis of gestational hypertension and preeclampsia. IV. Early detection of gestational hypertension and preeclampsia by the computation of a hyperbaric index.
Hermida RC, Ayala DE, Mojon A, Fernandez JR, Silva I, Ucieda R, Iglesias M.
Bioengineering & Chronobiology Laboratories, E.T.S.I. Telecomunicacion, Universidad de Vigo, Spain.

The aims of this study were to examine whether the combined approach of 1) establishing tolerance intervals for the circadian variability of blood pressure as a function of gestational age, and 2) computing the hyperbaric index by comparison of any patient's blood pressure profile (obtained by ambulatory monitoring) with the tolerance limits, provides a new highly sensitive test for the early detection of gestational hypertension and preeclampsia. We analyzed a total of 745 blood pressure series sampled by ambulatory monitoring for about 48 hours in each of several occasions in 189 women with uncomplicated pregnancies, 71 with gestational hypertension, and 29 with preeclampsia. After synchronization of all data by expressing times of sampling in hours from bed-time, circadian tolerance limits were first computed from the normotensive subjects as a function of trimester of pregnancy. The hyperbaric index and the percentage time of excess were then computed for each individual blood pressure series. The maximum hyperbaric index was below 15 mmHg X hour for normotensive pregnant women in all trimesters of pregnancy, and mostly above that value for women who subsequently developed gestational hypertension or preeclampsia. Sensitivity of the test based on the maximum hyperbaric index was 97% for women sampled during the first trimester of gestation, and increased up to 100% in the third trimester. The positive predictive value was 100% in all trimesters. Moreover, the computation of the hyperbaric index provided, on the average, an early identification of gestational hypertension or preeclampsia 20 weeks prior to the clinical confirmation of the disease. CONCLUSIONS: Ambulatory monitoring of blood pressure during gestation provides sensitive endpoints for use in early risk assessment and as a guide for establishing preventive interventions. The approach presented here represents a simple, reproducible, non-invasive, and highly sensitive test for the very early identification of gestational hypertension and preeclampsia.


Pol Tyg Lek. 1994 Mar 7-14;49(10-11):257-60.
Diagnosis of early hypertension with continuous ambulatory blood pressure monitoring
Kawecka-Jaszcz K.
I Kliniki Kardiologii Instytutu Kardiologii AM, Krakowie.

Characteristics of a 24-hour blood pressure monitoring and its usefulness in the diagnosis of early hypertension have been discussed. Measurements of ambulatory blood pressure in normotensive individuals are lower than those achieved with continuous monitoring at daytime whereas the situation in hypertensive subjects is reverse. Office blood pressure measurements produce higher values already in borderline hypertension and may use as differentiating diagnostic parameter. Continuous blood pressure monitoring enables to detect "white coat hypertension" estimated to occur in 7% of the general population and in 21% of patients with mild hypertension. Even a few hours of the continuous blood pressure monitoring identifies subjects with "white coat hypertension" and office hypertension and consequently avoidance of the unnecessary pharmacologic treatment. Ambulatory blood pressure monitoring is also useful in the diagnosis of early hypertension in adolescents provided that the tests will be carried out during school hours. Some investigators believe that the proportion of abnormal measurements (over 140/90 mm Hg), i.e. so-called blood pressure load, is more important at early stages of the disease because there closer correlation between blood pressure and organ damage than mean values of blood pressure. However, it was not established yet what is a percentage of abnormal blood pressure measurements in normotensive and hypertensive subjects. Blood pressure circadian rhythm in various groups but the highest changes are found in borderline hypertension. Blood pressure variability expressed as standard deviations from the mean values calculated from the ambulatory blood pressure monitoring is an individual feature considered also as a predictor of hypertension development with all its sequelae.


Am J Surg. 1987 May;153(5):495-500.
Early diagnosis and management of renovascular hypertension.
Tapper D, Brand T, Hickman R.

Renovascular hypertension is more common in hypertensive children than in hypertensive adults, and renal artery stenosis is second only to coarctation of the thoracic aorta as a cause of surgically correctable hypertension. Three infants presented with uncontrollable hypertension secondary to renal artery thrombosis due to umbilical artery catheterization for respiratory distress in the neonatal period. They all responded to nephrectomy. A fourth infant had stenosis of a polar vessel secondary to umbilical artery catheterization and was cured by partial nephrectomy. Two infants with renal artery stenosis secondary to fibromuscular dysplasia benefited from revascularization and, at last follow-up, were normotensive and off all blood pressure medication. Ultrasonography, isotope scanning, angiography and selective renal vein renin assays should be used to identify patients with surgically correctable lesions. The use of fine suture material and microvascular surgical techniques, including ex vivo revascularization and autotransplantation, can salvage renal parenchyma and relieve hypertension. Infants with less than 10 percent renal function on the involved side should have a nephrectomy. The infant with an umbilical arterial catheterization line needs blood pressure monitoring and aggressive evaluation and treatment of persistent hypertension.


Med Clin (Barc). 1981 Sep 25;77(5):200-4.
Early diagnosis of renal ischemia in arterial hypertension by means of urine N-acetyl-beta-D-glucosaminidase
Garcia M, Mendez X, Botey A, Pons JM, Revert L.

Essential arterial hypertension, malignant hypertension and renovascular hypertension were studied in 64 patients, divided into 5 groups according to creatinine clearance (Ccreat) and ophthalmic fundus. Urine N-Acetyl-b-d-glucosaminidase (NAG) was expressed in units/mg creatinine in urine. Results were; Group A: Ccreat greater than 60, ophthalmic fundus less than II (n=33), NAG 13.5 + 4.5; Group B: CCreat. greater than 60, ophthalmic fundus III-IV (n=4) NAG 42.4 +/- 12.5; Group C: Ccreat. less than 60, ophthalmic fundus less than II (n = 14) NAG 31.2 +/- 10,5; Group D: (clinically malignant arterial hypertension) Ccreat. less than 60, ophthalmic fundus III--IV (n = 8), NAG 91.1 +/- 55.7 and Group E: (renovascular hypertension) Ccreat. greater than 60, ophthalmic fundus less than II (n = 5), NAG 35.5 +/- 12.9. Only the patients in Group A had NAG within normal limits. Differences were found between groups: A-B (p less than 0.001), A-D (p less than 0.001), A-E (p less than 0.001) and C-D (p less than 0.001). Urine NAG is considered to be an early sign of renal involvement in arterial hypertension, an indication of the severity and a sign of ischemia even when the involvement is unilateral only, and helpful in the management of renovascular hypertension.

on the Adriatic Coast
The Anti-Aging Fasting Program consists of a 7-28 days program (including 3 - 14 fasting days). 7-28-day low-calorie diet program is also available .
More information
    The anti-aging story (summary)
Introduction. Statistical review. Your personal aging curve
  Aging and Anti-aging. Why do we age?
    2.1  Aging forces (forces that cause aging
Internal (free radicals, glycosylation, chelation etc.) 
External (Unhealthy diet, lifestyle, wrong habits, environmental pollution, stress, poverty-change "poverty zones", or take it easy. etc.) 
    2.2 Anti-aging forces
Internal (apoptosis, boosting your immune system, DNA repair, longevity genes) 
External (wellness, changing your environment; achieving comfortable social atmosphere in your life, regular intake of anti-aging drugs, use of replacement organs, high-tech medicine, exercise)
    2.3 Aging versus anti-aging: how to tip the balance in your favour!
    3.1 Caloric restriction and fasting extend lifespan and decrease all-cause mortality (Evidence)
      Human studies
Monkey studies
Mouse and rat studies
Other animal studies
    3.2 Fasting and caloric restriction prevent and cure diseases (Evidence)
Hypertension and Stroke
Skin disorders
Mental disorders
Neurogical disorders
Asthmatic bronchitis, Bronchial asthma
Bones (osteoporosis) and fasting
Arteriosclerosis and Heart Disease
Cancer and caloric restriction
Cancer and fasting - a matter of controversy
Eye diseases
Chronic fatigue syndrome
Sleeping disorders
Rheumatoid arthritis
Gastrointestinal diseases
    3.3 Fasting and caloric restriction produce various
      biological effects. Effects on:
        Energy metabolism
Lipids metabolism
Protein metabolism and protein quality
Neuroendocrine and hormonal system
Immune system
Physiological functions
Reproductive function
Cognitive and behavioral functions
Biomarkers of aging
    3.4 Mechanisms: how does calorie restriction retard aging and boost health?
        Diminishing of aging forces
  Lowering of the rate of gene damage
  Reduction of free-radical production
  Reduction of metabolic rate (i.e. rate of aging)
  Lowering of body temperature
  Lowering of protein glycation
Increase of anti-aging forces
  Enhancement of gene reparation
  Enhancement of free radical neutralisation
  Enhancement of protein turnover (protein regeneration)
  Enhancement of immune response
  Activation of mono-oxygenase systems
  Enhance elimination of damaged cells
  Optimisation of neuroendocrine functions
    3.5 Practical implementation: your anti-aging dieting
        Fasting period.
Re-feeding period.
Safety of fasting and low-calorie dieting. Precautions.
      3.6 What can help you make the transition to the low-calorie life style?
        Social, psychological and religious support - crucial factors for a successful transition.
Drugs to ease the transition to caloric restriction and to overcome food cravings (use of adaptogenic herbs)
Food composition
Finding the right physician
    3.7Fasting centers and fasting programs.
  Food to eat. Dishes and menus.
    What to eat on non-fasting days. Dishes and menus. Healthy nutrition. Relation between foodstuffs and diseases. Functional foods. Glycemic index. Diet plan: practical summary. "Dr. Atkins", "Hollywood" and other fad diets versus medical science

Bread, cereals, pasta, fiber
Glycemic index
Meat and poultry
Sugar and sweet
Fats and oils
Dairy and eggs
Nuts and seeds
Food composition

  Anti-aging drugs and supplements
    5.1 Drugs that are highly recommended
      (for inclusion in your supplementation anti-aging program)
        Vitamin E
Vitamin C
Co-enzyme Q10
Lipoic acid
Folic acid
Flavonoids, carotenes
Vitamin B
Vinpocetine (Cavinton)
Deprenyl (Eldepryl)
    5.2 Drugs with controversial or unproven anti-aging effect, or awaiting other evaluation (side-effects)
        Phyto-medicines, Herbs
      5.3 Drugs for treatment and prevention of specific diseases of aging. High-tech modern pharmacology.
        Alzheimer's disease and Dementia
Immune decline
Infections, bacterial
Infections, fungal
Memory loss
Muscle weakness
Parkinson's disease
Prostate hyperplasia
Sexual disorders
Stroke risk
Weight gaining
    5.4 The place of anti-aging drugs in the whole
      program - a realistic evaluation
    6.1 Early diagnosis of disease - key factor to successful treatment.
      Alzheimer's disease and Dementia
Cataracts and Glaucoma
Genetic disorders
Heart attacks
Immune decline
Infectious diseases
Memory loss
Muscle weakness
Parkinson's disease
Prostate hyperplasia
Stroke risk
Weight gaining
    6.2 Biomarkers of aging and specific diseases
    6.3 Stem cell therapy and therapeutic cloning
    6.4 Gene manipulation
    6.5 Prosthetic body-parts, artificial organs
Bones, limbs, joints etc.
Heart & heart devices
    6.6 Obesity reduction by ultrasonic treatment
  Physical activity and aging. Experimental and clinical data.
        Aerobic exercises
Weight-lifting - body-building
Professional sport: negative aspects
  Conclusion: the whole anti-aging program
    9.1 Modifying your personal aging curve
      Average life span increment. Expert evaluation.
Periodic fasting and caloric restriction can add 40 - 50 years to your lifespan
Regular intake of anti-aging drugs can add 20-30 years to your lifespan
Good nutrition (well balanced, healthy food, individually tailord diet) can add 15-25 years to your lifespan
High-tech bio-medicine service can add 15-25 years to your lifespan
Quality of life (prosperity, relaxation, regular vocations) can add 15-25 years to your lifespan
Regular exercise and moderate physical activity can add 10-20 years to your lifespan
These approaches taken together can add 60-80 years to your lifespan, if you start young (say at age 20). But even if you only start later (say at 45-50), you can still gain 30-40 years

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    9.2 The whole anti-aging life style - brief summary 
    References eXTReMe Tracker
        The whole anti-aging program: overview

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