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.
SLIM - voorkomen is beter dan genezen
- Evolutionary Medicine
Collecting work from leaders in the field, this volume describes an array of new and innovative approaches to human health that are based on an appreciation of our long evolutionary history. For example, it shows how evolution helps to explain the complex relationship between our immune systems and the virulence and transmission of human viruses. It also shows how comparisons between how we live today and how our hunter-gatherer ancestors lived thousands of years ago illuminate a variety of contemporary ills, including obesity, lower-back pain, and insomnia - Evolutionary medicine: update on the relevance to family practice
Evolutionary medicine deals with the interplay of biology and the environment in the understanding of human disease. Evolutionary medicine should be studied further and incorporated into medical training and practice. Its practical utility will be proven through the generation of testable hypotheses and their application in relation to disease causation and possible prevention - Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective
From a genetic standpoint, humans living today are Stone Age hunter-gatherers displaced through time to a world that differs from that for which our genetic constitution was selected. Although our genes have hardly changed, our culture has been transformed almost beyond recognition during the past 10,000 years, especially since the Industrial Revolution. There is increasing evidence that the resulting mismatch fosters "diseases of civilization" that together cause 75 percent of all deaths in Western nations - Eating, exercise, and "thrifty" genotypes: connecting the dots toward an evolutionary understanding of modern chronic diseases
Thus it is contended that the ancient hunter-gatherer had cycles of feast and famine, punctuated with obligate periods of physical activity and rest. Hence, gene selection in the Late-Paleolithic era was probably influenced by physical activity and rest. To ensure survival during periods of famine, certain genes evolved to regulate efficient intake and utilization of fuel stores. Such genes were termed "thrifty genes" in 1962. Furthermore, convincing evidence shows that this ancient genome has remained essentially unchanged over the past 10,000 years and certainly not changed in the past 40-100 years. Although the absolute caloric intake of modern-day humans is likely lower compared with our hunter-gatherer ancestors, it is nevertheless in positive caloric balance in the majority of the US adult population mainly due to the increased sedentary lifestyle in present society - Control of food intake in the obese
In general, humans display a system of weight regulation that is asymmetrical--a reduction in body weight is strongly defended but weight gain is not. The body seems to tolerate a positive energy balance. There is no mechanism that can detect a positive energy balance per se or that can implement a sufficiently strong correction to behavior to maintain body weight in an environment that promotes consumption. The evolutionary process has favored biological traits associated with preferences for high energy density (sweet and/or fatty) energy-yielding foods - Interactions between the "cognitive" and "metabolic" brain in the control of food intake
It is hypothesized that this naturally occurring leptin resistance allowed temporary neutralization of satiety mechanisms and evolved as a response to survive subsequent periods of famine - The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic
In this review we have analyzed the 13 known quantitative dietary studies of HG and demonstrate that animal food actually provided the dominant (65%) energy source, while gathered plant foods comprised the remainder (35%). This data is consistent with a more recent, comprehensive review of the entire ethnographic data (n=229 HG societies) that showed the mean subsistence dependence upon gathered plant foods was 32%, whereas it was 68% for animal foods. Although fat intake (28-58% energy) would have been similar to or higher than that found in Western diets, it is likely that important qualitative differences in fat intake, including relatively high levels of MUFA and PUFA and a lower omega-6/omega-3 fatty acid ratio, would have served to inhibit the development of CVD. Other dietary characteristics including high intakes of antioxidants, fiber, vitamins and phytochemicals along with a low salt intake may have operated synergistically with lifestyle characteristics (more exercise, less stress and no smoking) to further deter the development of CVD - The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition?
Awareness of the ancestral human diet might advance traditional nutrition science. The human genome has hardly changed since the emergence of behaviourally-modern humans in East Africa 100-50 x 10(3) years ago; genetically, man remains adapted for the foods consumed then. The best available estimates suggest that those ancestors obtained about 35% of their dietary energy from fats, 35% from carbohydrates and 30% from protein. Saturated fats contributed approximately 7.5% total energy and harmful trans-fatty acids contributed negligible amounts. Polyunsaturated fat intake was high, with n-6:n-3 approaching 2:1 (v. 10:1 today). Cholesterol consumption was substantial, perhaps 480 mg/d. Carbohydrate came from uncultivated fruits and vegetables, approximately 50% energy intake as compared with the present level of 16% energy intake for Americans. High fruit and vegetable intake and minimal grain and dairy consumption made ancestral diets base-yielding, unlike today's acid-producing pattern. Honey comprised 2-3% energy intake as compared with the 15% added sugars contribute currently. Fibre consumption was high, perhaps 100 g/d, but phytate content was minimal. Vitamin, mineral and (probably) phytochemical intake was typically 1.5 to eight times that of today except for that of Na, generally <1000 mg/d, i.e. much less than that of K. The field of nutrition science suffers from the absence of a unifying hypothesis on which to build a dietary strategy for prevention; there is no Kuhnian paradigm, which some researchers believe to be a prerequisite for progress in any scientific discipline. An understanding of human evolutionary experience and its relevance to contemporary nutritional requirements may address this critical deficiency - Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: nutritional implications for chronic diseases
Anthropological and epidemiological studies and studies at the molecular level indicate that human beings evolved on a diet with a ratio of omega-6 to omega-3 essential fatty acids (EFA) of approximately 1 whereas in Western diets the ratio is 15/1 to 16.7/1 - The importance of the ratio of omega-6/omega-3 essential fatty acids
Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today's Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases - Margarine's trans-fatty acid composition: modifications during the last decades and new trends
Trans fatty acids isomers are formed during the hydrogenation process used in the food industry to harden oils. In the last decades there has been a great controversy about the consumption of margarine due to the levels of trans fatty acids they contain - Enkele belangrijke ontwikkelingen in de voedselconsumpti
Ook de samenstelling van de vetzuren in de voeding vertoonde een gunstige ontwikkeling: het percentage verzadigde vetzuren en transvetzuren nam af tot respectievelijk ongeveer 14% en 1,7%. Toch is de inname nog steeds hoger dan de 10% en 0,8% die vanuit gezondheidskundig oogpunt aanvaardbaar wordt geacht. De veranderingen in consumptie hebben van 1987 tot 1997 geleid tot een verminderde inname van vitamines (vooral A, E, D en foliumzuur) en mineralen (zoals ijzer). - Trans fatty acids and insulin resistance
Since trans fatty acids (TFA) might interfere with cell membrane functions, there are reasons to believe that high TFA intakes could affect insulin sensitivity and consequently diabetes risk - Dietary fat intake and risk of type 2 diabetes in women
These data suggest that total fat and saturated and monounsaturated fatty acid intakes are not associated with risk of type 2 diabetes in women, but that trans fatty acids increase and polyunsaturated fatty acids reduce risk - Trans fatty acids - effects on systemic inflammation and endothelial function
Consumption of trans fatty acids (TFA) predicts higher risk of coronary heart disease, sudden death, and possibly diabetes mellitus. These associations are greater than would be predicted by effects of TFA on serum lipoproteins alone
Prospective observational studies demonstrate strong positive associations between TFA consumption and risk of myocardial infarction, coronary heart disease death, and sudden death- Association between serum trans-monounsaturated fatty acids and breast cancer risk in the E3N-EPIC Study
A high serum level of trans-monounsaturated fatty acids, presumably reflecting a high intake of industrially processed foods, is probably one factor contributing to increased risk of invasive breast cancer in women - Dietary trans fatty acid intake is associated with increased fetal loss
Since PPAR-gamma plays a pivotal role in placental biology and is down-regulated by TFAs, TFAs may be a reversible risk factor for fetal loss - Trans fatty acids in maternal milk lead to cardiac insulin resistance in adult offspring
Our data suggest that the consumption of hydrogenated fat, rich in TFAs, by the mothers during the lactation period caused cardiac insulin resistance in the adult progeny, thus reinforcing the hypothesis that early adaptations may cause deleterious consequences later in life - Smeersels met weinig vet zijn de beste keus
Het Voorlichtingsbureau Margarine, Vetten en Oliën (MVO) is een campagne gestart om het besmeren van brood te promoten. Onder het motto ‘Een boterham is gezond, maar een boterham met margarine is gezonder’ wordt aangegeven dat het besmeren van brood een belangrijke bijdrage levert aan een gezond eetpatroon. Het Voedingscentrum is het daarmee eens, maar geeft daarbij de voorkeur aan smeersels met zo min mogelijk vet. Die bevatten weinig verzadigd vet én leveren minder calorieë - Cardiovascular disease resulting from a diet and lifestyle at odds with our Paleolithic genome: how to become a 21st-century hunter-gatherer
Our genetic make-up, shaped through millions of years of evolution, determines our nutritional and activity needs. Although the human genome has remained primarily unchanged since the agricultural revolution 10,000 years ago, our diet and lifestyle have become progressively more divergent from those of our ancient ancestors. Accumulating evidence suggests that this mismatch between our modern diet and lifestyle and our Paleolithic genome is playing a substantial role in the ongoing epidemics of obesity, hypertension, diabetes, and atherosclerotic cardiovascular disease. - Paleolithic vs. modern diets--selected pathophysiological implications
Our Our genome can have changed little since the beginnings of agriculture, so, genetically, humans remain Stone Agers--adapted for a Paleolithic dietary regimen. Such diets were based chiefly on wild game, fish and uncultivated plant foods. They provided abundant protein; a fat profile much different from that of affluent Western nations; high fibre; carbohydrate from fruits and vegetables (and some honey) but not from cereals, refined sugars and dairy products; high levels of micronutrients and probably of phytochemicals as well - The 'carnivore connection'--evolutionary aspects of insulin resistance
Following the end of the last Ice Age and the advent of agriculture, dietary carbohydrate increased. Although this resulted in a sharp increase in the quantity of carbohydrate consumed, these traditional carbohydrate foods had a low glycaemic index and produced only modest increases in plasma insulin. The industrial revolution changed the quality of dietary carbohydrate. The milling of cereals made starch more digestible and postprandial glycaemic and insulin responses increased 2-3 fold compared with coarsely ground flour or whole grains - Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic asse
Increasing intakes of refined carbohydrate (corn syrup) concomitant with decreasing intakes of fiber paralleled the upward trend in the prevalence of type 2 diabetes observed in the United States during the 20th century - Position of the American Dietetic Association: health implications of dietary fiber
Dietary fiber consists of the structural and storage polysaccharides and lignin in plants that are not digested in the human stomach and small intestine. A wealth of information supports the American Dietetic Association position that the public should consume adequate amounts of dietary fiber from a variety of plant foods. Recommended intakes, 20-35 g/day for healthy adults and age plus 5 g/day for children, are not being met, because intakes of good sources of dietary fiber, fruits, vegetables, whole and high-fiber grain products, and legumes are low - Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity
The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity - Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance
we have reported that consumption of a high-fructose diet, but not a high-glucose diet, promotes the development of three of the pathological characteristics associated with metabolic syndrome: visceral adiposity, dyslipidemia, and insulin resistance - Fructose, weight gain, and the insulin resistance syndrome
Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae - Dietary fructose and the metabolic syndrome
There is much evidence from both animal models and human studies supporting the notion that fructose is a highly lipogenic nutrient that, when consumed in high quantities, contributes to tissue insulin insensitivity, metabolic defects, and the development of a prediabetic state. Recently evidence has helped to decipher the mechanisms involved in these metabolic changes - Fructose and the metabolic syndrome: pathophysiology and molecular mechanisms
Emerging evidence suggests that increased dietary consumption of fructose in Western society may be a potentially important factor in the growing rates of obesity and the metabolic syndrome - Fructose consumption as a risk factor for non-alcoholic fatty liver diseas
The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption - Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study
High fructose and sucrose intakes may play a role in pancreatic cancer etiology. Conditions such as overweight or obesity in which a degree of insulin resistance may be present may also be important - Fructose consumption and the risk of kidney stones
We documented 4902 incident kidney stones during a combined 48 years of follow-up. The multivariate relative risks of kidney stones significantly increased for participants in the highest compared to the lowest quintile of total-fructose intake for all three study groups - From instinct to intellect: the challenge of maintaining healthy weight in the modern world
We propose that the modern environment has taken body weight control from an instinctual (unconscious) process to one that requires substantial cognitive effort. In the current environment, people who are not devoting substantial conscious effort to managing body weight are probably gaining weight. It is unlikely that we would be able to build the political will to undo our modern lifestyle, to change the environment back to one in which body weight control again becomes instinctual. In order to combat the growing epidemic we should focus our efforts on providing the knowledge, cognitive skills and incentives for controlling body weight and at the same time begin creating a supportive environment to allow better management of body weight. - The Dutch Famine of 1944-1945: a pathophysiological model of long-term consequences of wasting disease
Exposure to famine during gestation resulted in increases in impaired glucose tolerance, obesity, coronary heart disease, atherogenic lipid profile, hypertension, microalbuminuria, schizophrenia, antisocial personality and affective disorders - The Dutch famine and its long-term consequences for adult health
These findings show that maternal undernutrition during gestation has important effects on health in later life, but that the effects on health depend on its timing during gestation. Especially early gestation seems to be a vulnerable period. Adequate dietary advice to women before and during pregnancy seems a promising strategy in preventing chronic diseases in future generations - Fetal and neonatal pathways to obesity
One pathway to obesity represents the maladaptive consequences of an evolutionarily preserved mechanism by which the developing mammal monitors nutritional cues from its mother and adjusts its developmental trajectory accordingly. Prediction of a nutritionally sparse environment leads to a phenotype that promotes metabolic parsimony by favouring fat deposition, insulin resistance, sarcopenia and low energy expenditure - Consequences of fetal exposure to maternal diabetes in offspring
Thus, fetal exposure to maternal diabetes may contribute to the worldwide diabetes epidemic. Public health interventions targeting high-risk populations should focus on long-term follow-up of subjects who have been exposed in utero to a diabetic environment and on a better glycemic control during pregnancy. - Effect of a diabetic environment in utero on predisposition to type 2 diabetes
Exposure to a diabetic environment in utero is associated with increased occurrence of impaired glucose tolerance and a defective insulin secretory response in adult offspring, independent of genetic predisposition to type 2 diabetes - Role of leptin during perinatal metabolic programming and obesity
The incidence of obesity is rapidly increasing all over the world in epidemic proportions.The epidemia now affects young children and accumulative evidences suggest that the origin of the disease may occur during foetal development and early life. This has introduced the concept of "developmental programming" supported by experimental studies in animal models and numerous epidemiological data - Scientific American, You have to eat everything on your plate (Movie)
- Scientific American, Food restrictions for Children (Movie)
- The 'skinny' on childhood obesity: how our western environment starves kids' brains
In this review, the mechanism of our "toxic environment's" effects on insulin and weight gain in the genesis of obesity is elaborated. The composition of our diet is highly insulinogenic. The insulin drives energy into fat, and interferes with leptin signaling in the VMH. This results in weight gain and the sense of starvation, which results in decreased SNS activity, reducing energy expenditure and physical activity; and increased vagal activity, which promotes yet further insulin release and energy storage. Thus, hyperinsulinemia turns the leptin negative feedback system into a "vicious cycle" of obesity (see Figure 3, page 905). Externally, this appears as "gluttony and sloth" but it is biochemically driven. How does this work? A thin, insulin-sensitive, 13-year-old boy might consume a daily allotment of 2,000 kcal, and burn 2,000 kcal daily (or 50 kcal/kg fat-free mass) in order to remain weight-stable, with a stable leptin level. However, if that same 13-year-old became hyperinsulinemic and/or insulin resistant, perhaps as many as 250 kcal of the daily allotment would be shunted to storage in adipose tissue, promoting a persistent obligate weight gain. Due to the obligate energy storage, he now only has 1,750 kcal per day to burn. The hyperinsulinemia also results in a lower level of leptin signal transduction, conveying a CNS signal of energy insufficiency. The remaining calories available are lower than his energy expenditure; the CNS would sense starvation. Through decreased SNS tone, he would reduce his physical activity, resulting in decreased quality of life; and through increased vagal tone, he would increase caloric intake and insulin secretion, but now at a much higher level. Thus, the vicious cycle of gluttony, sloth, and obesity is promulgated. Is this personal responsibility, when a kid's brain thinks it's starving? Is it personal responsibility when the American Academy of Pediatrics still recommends juice for toddlers? Is it personal responsibility when the Women, Infant and Children program subsidizes fruit juice but not fruit? Is it personal responsibility when the first ingredient in the barbecue sauce is high-fructose corn syrup? Is it personal responsibility when high-fiber fresh produce is unavailable in poor neighborhoods? Is it personal responsibility when the local fast food restaurant is the only neighborhood venue that is clean and air-conditioned? Is it personal responsibility when in order to meet the criteria for No Child Left Behind, the school does away with physical education class? Is it personal responsibility when children are not allowed out of the house to play for fear of crime? We must get the insulin down. Fixing the "toxic environment" by altering the food supply and promoting physical activity for all children can't be done by government, and won't be done by Big Food. This will require a grassroots, bottom-up effort on the part of parents and community leaders. We as pediatricians must lead the way - Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics
Childhood obesity has become epidemic over the past 30 years. The First Law of Thermodynamics is routinely interpreted to imply that weight gain is secondary to increased caloric intake and/or decreased energy expenditure, two behaviors that have been documented during this interval; nonetheless, lifestyle interventions are notoriously ineffective at promoting weight loss. Obesity is characterized by hyperinsulinemia. Although hyperinsulinemia is usually thought to be secondary to obesity, it can instead be primary, due to autonomic dysfunction. Obesity is also a state of leptin resistance, in which defective leptin signal transduction promotes excess energy intake, to maintain normal energy expenditure. Insulin and leptin share a common central signaling pathway, and it seems that insulin functions as an endogenous leptin antagonist. Suppressing insulin ameliorates leptin resistance, with ensuing reduction of caloric intake, increased spontaneous activity, and improved quality of life. Hyperinsulinemia also interferes with dopamine clearance in the ventral tegmental area and nucleus accumbens, promoting increased food reward. Accordingly, the First Law of Thermodynamics can be reinterpreted, such that the behaviors of increased caloric intake and decreased energy expenditure are secondary to obligate weight gain. This weight gain is driven by the hyperinsulinemic state, through three mechanisms: energy partitioning into adipose tissue; interference with leptin signal transduction; and interference with extinction of the hedonic response to food - On Hendrikje van Andel-Schipper and other remarkable developments in the life expectancy of the Dutch population
Experts are deeply divided about the prospects for further increases in life expectancy. Some have argued that such estimates are too optimistic because, for example, the obesity epidemic might even reduce average life expectancy in the future - The consequences of childhood overweight and obesity
Daniels notes that the possibility has even been raised that the increasing prevalence and severity of childhood obesity may reverse the modern era's steady increase in life expectancy, with today's youth on average living less healthy and ultimately shorter lives than their parents-the first such reversal in lifespan in modern history. Such a possibility, he concludes, makes obesity in children an issue of utmost public health concern
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- Candida: Candida infectie - CVS/ME: Chronische vermoeidheid Syndroom - Diabetische complicaties: Behandeling diabetische complicaties - Neuropathie - Retinopathie - Nefropathie - Bloeduiker stabilisatie - Hart en vaatziekten: Cardiomyopathie en Hartfalen - Cardiomyopathy and Heart Failure - Hoge bloeddruk - Cholesterol verlaging - Aderverkalking (atherosclerose) - Levensverlenging: Levensverlenging - DHEA - Melatonine - 65+ - Kanker: - Ondersteuningstherapie bij kanker - Artrose en artritis: - Artrose - Artritis - Fibromyalgie: - Fibromyalgie - Urinewegen: - Prostaatklachten - Blaasontsteking - Voeding: Voeding wat is er mis mee - Melk - Suiker - Aanvulling onvolwaardige voeding - Vitamine supplementen: Voedingssupplementen - Overgewicht: - Overgewicht - SLIM - Andere artikelen: - HPU - Astma - Multiple Sclerose - Psoriasis - Staar - Depressie - Behandelingsforum - Orthomoleculaire Geneeskunde
