Alle artikelen en behandelingsprotocollen zijn volgens het zelfzorg principe geschreven. Bij zelfzorg is niet de arts of specialist maar de patiënt verantwoordelijk voor het correct uitvoeren van de behandeling. Toch adviseer ik patiënten om bij gezondheidsklachten eerst een arts te raadplegen. Een juiste diagnose is ook bij een zelfzorgtraject van onschatbare waarde. Als u reeds onder behandeling bent van een arts overleg dan met uw arts voordat u voedingssupplementen gaat gebruiken.

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Wetenschappelijke artikelen gebruikt in het boek

Alle claims in dit boek zijn gebaseerd op wetenschappelijke studies. Bij elke claim is dan ook een verwijzing geplaatst naar het corresponderende wetenschappelijke artikel. Deze “verwijzingen” worden aangegeven met kleine cijfertjes in de tekst in mijn boek. Om het eenvoudiger te maken om deze verwijzingen terug te vinden wordt in dit referentie hoofdstuk dezelfde hoofdstukstructuur als in het boek aangehouden.

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Als u meer wetenschappelijk onderzoek wilt lezen over een bepaald onderwerp dan kunt nadat u een PubMed artikel heeft opgevraagd ook kijken naar de "Related Articles" rechts in de pagina.
 
  1. Gastrointestinal hormones and regulation of food intake
    Several peptides synthesised in the gastrointestinal tract which affect food intake have been identified including ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (7-36) amide (GLP-1), oxyntomodulin, peptide YY (PYY) and pancreatic polypeptide (PP).
  2. Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance
    Leptin, the long-sought factor of adipocytes origin, has emerged as one of the major signals that relay the status of fat stores to the hypothalamus and plays a significant role in energy homeostasis. It is now established that central leptin resistance contributes to the development of diet-induced obesity and ageing associated obesity
  3. Appetite regulation and energy bala
    Thirty minutes after the start of eating, satiety signals arise from the intestinal tract and, in between meals, from the adipose tissue and liver. Satiety signals are sedative and arrest the processing of food in the intestine, hence leading to termination of eating
  4. Elevated leptin: consequence or cause of obesity?
    Once leptin resistance takes hold, each subsequent exposure to high-density food faces diminished counter-regulatory responses, leading to exacerbated weight gain
  5. The hypothalamus, hormones, and hunger: alterations in human obesity and ill
    While obese subjects have appropriate reductions in orexigenic ghrelin, other gut-hormone disturbances may contribute to obesity such as reduced anorexigenic PYY and PP
  6. Gut hormones as peripheral anti obesity targets
    Obese subjects have lower basal fasting PYY levels and have a smaller post prandial rise.
  7. Basal and postprandial plasma levels of PYY, ghrelin, cholecystokinin, gastrin and insulin in women with moderate and morbid obesity and metabolic synd
    In MOB-MS women the fasting PYY(3-36) levels were lower compared to lean controls and OB-MS, whilst postprandially in both OB-MS and MOB-MS, it was much lower than in lean women
  8. Low resting metabolic rate as a risk factor for weight gain: role of the sympathetic nervous system
    RMR is believed to be genetically determined. Individuals with a low RMR for a given body size are at higher risk of significant weight gain, relative to those with a high RMR
  9. Adaptation to low energy intakes: the responses and limits to low intakes in infants, children and adults
    Reduction in energy intake below the acceptable level of requirement for an individual results in a series of physiological and behavioural responses, which are considered as an adaptation to the low energy intake. This ability of the human body to adapt to a lowering of the energy intake is without doubt beneficial to the survival of the individual
  10. Fasting--wrong in obesity
    Fasting has been advocated as an effective way to reduce body weight. However, few data support any long-term effect of this therapy. On the contrary, evidence is accumulating that the repeated weight loss and concomitant weight gain, typical of fasting in many individuals, will lead to a subsequently higher body weight. Each weight cycle seems to increase the risk of a higher waist/hip ratio, greater metabolic efficiency and a food preference towards fat. All these trends result in further problems associated with weight loss and a vicious circle is established
  11. Carbohydrate cravings: a disorder of food intake and mood
    Obese individuals who crave carbohydrates, exhibit positive changes in mood after carbohydrate intake
  12. Brain serotonin, carbohydrate-craving, obesity and depression
    Hence many patients learn to overeat carbohydrates (particularly snack foods, like potato chips or pastries, which are rich in carbohydrates and fats) to make themselves feel better. This tendency to use certain foods as though they were drugs is a frequent cause of weight gain
  13. Carbohydrate craving. Relationship between carbohydrate intake and disorders of mood
    The brain neurotransmitter, serotonin, seems to be involved in the abnormal regulation of mood and food intake that underlies diet failures or weight gain in individuals who suffer from carbohydrate craving obesity (CCO), premenstrual syndrome (PMS) and seasonal affective disorder (SAD).
  14. Does carbohydrate-rich, protein-poor food prevent a deterioration of mood and cognitive performance of stress-prone subjects when subjected to a stressful task?
    It is suggested that CR/PP food in HS subjects may increase personal control, probably under the influence of higher levels of brain tryptophan and serotonin.
  15. Hyperinsulinism. Causes and mechanisms
    A high plasma insulin concentration in the presence of a normal or high plasma glucose level appears to be a common feature of glucose intolerance, obesity, and hypertension
  16. Basal and postprandial plasma levels of PYY, ghrelin, cholecystokinin, gastrin and insulin in women with moderate and morbid obesity and metabolic syndrome
    Metabolic syndrome (MS), defined as central obesity, hyperinsulinemia, insulin resistance, hypertension, dyslipidemia and glucose intolerance, has been associated with inflammatory biomarkers and cardiovascular disea
  17. Obesity and the metabolic syndrome
    The metabolic syndrome associated with abdominal obesity, which includes insulin resistance, dyslipidemia, and elevated CRP levels, identifies subjects who have an increase in cardiovascular morbidity and mortality. Twenty to 25% of the adult population in the United States have the metabolic syndrome, and in some older groups this prevalence approaches 50%.
  18. Hyperinsulinism syndromes caused by insulin resistance
    Resistance to insulin consists in a decrease in insulin's biologic action and is manifested mainly by hyperinsulinism
  19. Dietary carbohydrate's effects on lipogenesis and the relationship of lipogenesis to blood insulin and glucose concentrations
    The process by which dietary carbohydrate is transformed into fat in the human body is termed de novo lipogenesis
  20. Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men
    De novo lipogenesis was significantly higher before and after meal intake in the overweight men and was positively associated with fasting serum glucose and insulin concentrat
  21. The insulin resistance syndrome: physiological considerations
    The combination of insulin resistance and subsequent hyperinsulinaemia causes a number of metabolic and cardiovascular changes that result in a syndrome typically characterised by type 2 diabetes, obesity, dyslipidaemia, coronary artery disease and hypertension
  22. Visceral and subcutaneous adiposity: are both potential therapeutic targets for tackling the metabolic syndrome?
    The metabolic syndrome represents a constellation of co-morbidities that include central adiposity, insulin resistance, dyslipidemia and hypertension, which results from an elevated prevalence of obesity
  23. Laboratorial evaluation and diagnosis of insulin resistance
    HOMA is a mathematical model that predicts IS simply by measuring insulinemia and fasting blood glucose and shows good correlation with hyperinsulinemic-euglycemic clamp method, considered a gold standard in the measurement of IS
  24. Fasting serum insulin and the homeostasis model of insulin resistance (HOMA-IR) in the monitoring of lifestyle interventions in obese persons
    HOMA-IR index (homeostasis model of insulin resistance) was calculated as [fasting serum glucose*fasting serum insulin/22.5], with lower values indicating a higher degree of insulin sensitivity. Individual changes in the carbohydrate metabolism achieved by a lifestyle intervention program were displayed by fasting serum insulin concentrations and the HOMA-IR but not by fasting glucose measurement alone
  25. Global Prevalence of Diabetes
    The prevalence of diabetes for all age-groups worldwide was estimated to be 2.8% in 2000 and 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. Given the increasing prevalence of obesity, it is likely that these figures provide an underestimate of future diabetes prev
  26. Overgewicht, definitie, ernst en omvang
    In de periode 1980-2004 is het percentage mensen met (ernstig) overgewicht in Nederland sterk toegenomen (De Hollander et al., 2006). Een stijging in het vóórkomen van (ernstig) overgewicht is te zien bij alle leeftijdscategorieën. Ook bij kinderen vanaf 4 jaar is een sterke toename van overgewicht en obesitas te zien (Van Leest, 2004).
  27. Obesity: the emerging cost of economic prosperity
    Western countries are experiencing an epidemic of obesity and face increasing rates of related complications, including diabetes mellitus, elevated lipid levels and hypertension
  28. Physical activity and resting metabolic rate
    Resting metabolic rate (RMR) is the largest component of the daily energy budget in most human societies and, therefore, any increases in RMR in response to exercise interventions are potentially of great importance. Long-term effects of training include increases in RMR due to increases in lean muscle mass. Many studies of human subjects indicate a short-term elevation in RMR in response to single exercise events (generally termed the excess post-exercise O2 consumption; EPOC). This EPOC appears to have two phases, one lasting < 2 h and a smaller much more prolonged effect lasting up to 48 h
  29. The prevalence of the metabolic syndrome in the Netherlands: increased risk of cardiovascular diseases and diabetes mellitus type 2 in one quarter of persons under 60
    Approximately 1 million Dutch adults below 60 years of age had the metabolic syndrome in the 1990's. Based on the total prevalence of the metabolic syndrome and hypercholesterolaemia, one quarter of the Dutch population younger then 60 runs an increased risk of cardiovascular disease and type 2 diabetes mellitus
  30. The metabolic syndrome in women
    The metabolic syndrome is estimated to be present in 47 million US residents with a similar age-adjusted prevalence in men (24%) and women (23%
  31. Impaired cholecystokinin secretion and disturbed appetite regulation in women with polycystic ovary syndrome
    We conclude that women with PCOS have reduced postprandial CCK secretion and deranged appetite regulation associated with increased levels of testosterone. Impaired CCK secretion may play a role in the greater frequency of binge eating and overweight in women with PCOS.
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