Report of the Japan Atherosclerosis Society (JAS) Guideline for Diagnosis and Treatment of Hyperlipidemia in Japanese adults.
Hyperlipidemia in children and adolescents: diagnosis and therapy.
Progress in the diagnosis of endocrine and metabolic disorders: hyperlipidemia.
Diagnosis of chyliferous blockage by the hyperlipidemia test.
Report of the Japan Atherosclerosis Society (JAS) Guideline for Diagnosis and Treatment of Hyperlipidemia in Japanese adults.
Hata Y, Mabuchi H, Saito Y, Itakura H, Egusa G, Ito H, Teramoto T, Tsushima M, Tada N, Oikawa S, Yamada N, Yamashita S, Sakuma N, Sasaki J;
Working Committee on JAS Guideline for Diagnosis and Treatment of Hyperlipidemias.

This paper described the Guideline for Diagnosis and Management of Hyperlipidemias for Prevention of Atherosclerosis proposed by The Japan Atherosclerosis Society (JAS) Guideline Investigating Committee (1,995-2,000) under the auspices of the JAS Board of Directors. 1) The guideline defines the diagnostic criteria for serum total cholesterol (Table 1), LDL-cholesterol (Table 1), triglycerides (Table 4) and HDL-cholesterol (Table 7). It also indicates the desirable range (Table 1), the initiation levels of management (Table 2) and the target levels of treatment (Table 2) for total and LDL-cholesterol. 2) Though both total and LDL-cholesterol are shown as atherogenic parameter in the guideline, the use of LDL-cholesterol, rather than total cholesterol, is encouraged in daily medical practice and lipid-related studies, because LDL-cholesterol is more closely related to atherosclerosis. 3) Elevated triglycerides and low HDL-cholesterol are included in the risk factors, since no sufficient data have been accumulated to formulate the guideline for these two lipid disorders. 4) Emphasis is laid on evaluation of risk factors of each subject before starting any kind of treatment (Table 2). 5) This guideline is applied solely for adults (age 20-64). Lipid abnormalities in children or the youth under age 19, and the elderly with an age over 65 have to be evaluated by their own standard. 6) This part of the guideline gives only the diagnostic aspects of hyperlipidemias. The part of management and treatment will follow in the second section of the guideline that will be published in future.


Schweiz Med Wochenschr. 1998 Mar 28;128(13):477-85.
Hyperlipidemia in children and adolescents: diagnosis and therapy
Koletzko B, Herzog M.
Kinderpoliklinik, Klinikum Innenstadt der Ludwig-Maximilians-Universitat Munchen.

Severe hyperlipidemias should be diagnosed and treated even in childhood and adolescence, because vascular lipid deposition in the form of fatty streaks and progressive atherosclerotic lesions start to develop early in life. The heterozygous form of familial hypercholesterolemia found in about 1 of 500 newborn infants, and polygenic forms of hypercholesterolemia, are the most frequent forms of primary genetic hypercholesterolemia found in children. Secondary hyperlipidemias, e.g. in diabetes mellitus, hypothyroidism and renal disease, are relatively frequent in children and adolescents and need to be searched for in the diagnostic evaluation, because they can be influenced by treatment of the underlying disorder. Children and adolescents with severe forms of hyperlipidemias should be diagnosed and treated early in life. Dietary modification is the basis of treatment of affected children and can lower LDL cholesterol by about 15-20%. In patients with severe hypercholesterolemia, dietary cholesterol intake should not exceed 150 mg/day in children or 250-300 mg/day in adolescents. Even more important is a reduction of the intake of saturated fats and trans fatty acids and their replacement by polyunsaturated and particularly monounsaturated fats. Some additional lowering of LDL cholesterol may be achieved by the preferential use of vegetable over animal proteins and of complex carbohydrates over sugars. Repeated motivation, counseling and intensive practical training of the patient and family, supported by appropriate teaching materials, are essential for effective dietary treatment. Additional drug treatment is considered in children from the age of 8-9 years of age onwards if, in spite of adequate dietary modification, LDL cholesterol remains above 190 mg/dl (4.9 mmol/l), or above 160 mg/dl (3.9 mmol/l) in the presence of additional risk factors. The drugs of first choice are anion exchange resins (colestyramine or colestipol) because of their well documented efficacy and safety. More convenient to take but often somewhat less effective is beta-sitosterol. If efficacy or compliance with resins or sitosterin is unsatisfactory, fibrates (e.g. bezafibrate, fenofibrate) may be considered as a drug of second choice. Cholesterol synthesis inhibitors are not recommended for general use in children at this time.


Rinsho Byori. 1995 Nov;43(11):1120-7.
Progress in the diagnosis of endocrine and metabolic disorders: hyperlipidemia.
Yamashita S.
2nd Department of Internal Medicine, Osaka University Medical School, Suita.

Hyperlipidemia is one of the risk factors for coronary atherosclerosis and the establishment of its simple etiological diagnosis is crucial. Hyperlipidemia can be classified into primary and secondary hyperlipidemia. Primary hyperlipidemia includes familial lipoprotein lipase (LPL) deficiency, familial hypercholesterolemia (FH), familial type III hyperlipidemia, and familial combined hyperlipidemia. Many genetic mutations have been identified in patients with familial LPL deficiency and FH. An ELISA kit has been established to determine LPL mass levels, using monoclonal antibodies against LPL. FH is a deficiency of LDL receptor and is characterized by marked hypercholesterolemia and Achilles tendon xanthomas. It can be diagnosed by an LDL receptor assay, using 125I-LDL in skin fibroblasts. However, the diagnosis can be made easily by measuring the uptake of DiI-LDL by peripheral lymphocytes. Familial type III hyperlipidemia is a genetic disorder characterized by the presence of a broad beta pattern in lipoprotein electrophoresis and is based upon the abnormality of apo E isoform (apo E2/2). Apo E4 has been shown to be associated with late-onset Alzheimer's disease. Cholesteryl ester transfer protein (CETP) deficiency is characterized by a marked hyperalphalipoproteinemia and various abnormalities in the size and composition of LDL and HDL. Two common mutations in the CETP deficiency have been identified; an intron 14 splicing defect and D442: G missense mutation. These mutations account for at least one half of hyper-HDL-cholesterolemia in the Japanese. We have recently identified an area (Omagari City, Akita) where the frequency of heterozygotes for the intron 14 splicing defect is approximately 28% of the general population.


Sem Hop. 1980 Feb 8-15;56(5-6):224-30.
Diagnosis of chyliferous blockage by the hyperlipidemia test
Servelle M, Soulie J, Pourrias B, Coupier J, Nogues C, Andrieux JB, Terhedebrugge R.

In our hyperlipidemia test, the total lipids curve, a plateau without a postprandial peak, allows an easy diagnosis of the chyliferous blockage. The malformation of chyliferous vessels produces the congenital forms: exsudative enteropathy, chyloperitoneum, spontaneous chylothorax, chylous cyst of the mediastinum, reflux of chyle in the pulmonary lymphatics, lymphoedema with chyle reflux in the lymphatics of the leg and chyluria. The acquired forms comprise the post-infectious sclerosis of the intestinal lymphatics and the neoplastic invasions of the mesenteric lymph nodes. The optical density curve brings some informations for a better understanding of lipid's absorption.

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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