Obesity
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Topics:
Other factors that affect obesity
Obesity involves lots of stories and theories. The most common theory is:"Eat fat, get fat". Another belief states that if one takes in more energy than one consumes, energy will be stored as body fat. In addition, it is often said that it is because of the "lack of will power of the obese or overweight person that they do not lose weight".
Fact or fiction?
So, seemingly we can identify 3 common, widespread statements concerning the etiology of obesity:
Next, I will elaborate on why I think these assumptions are based on dated arguments and have surprisingly less to do with the real cause of obesity and overweightness than many people are claiming.
Introduction
The western diet consists mainly of carbohydrates.
In the US there is a clear obesity epidemic: here, between 1971 and 2000 the intake of total fat dropped with 3.7%, the intake of saturated fat dropped with 2.3%, the intake of carbohydrates increased with 6.4% and the prevalence of obesity climbed from 15 to 31%.
In the Netherlands the obesity rate also grew: a doubling to 10% among adults. For ages 2 to 20 the prevalence of obesity was 11,5% in 1997. The number of six-year-old girls with obesity ws doubled compared to the situation in 1980 and for boys this number had tripled. These figures are expected to again double by the year 2020 (3).
Elaboration
Increasing intakes of carbs and lowered intakes of (saturated) fats in diet have apparently not been able to reduce the overall prevalence of obesity in the United States as well in the Netherlands a.o..
Physically this can quite simply be explained by a physiological system that gains in consensus:
The hormone insulin is released whenever carbohydrates enter the bloodstream. Without insulin, glucose will impossibly enter the cells and remains unable to be digested. Insulin also impairs fat burning, because it inhibits the release of its adversary hormone: glucagon. Moreover, insulin actually stimulates fat synthesis. (Why this is a central issue in obesity will be elaborated under 3))
Glucagon mobilizes body fat and the formation of ketones - an alternative fuel in case of low glucose levels. In a high glycemic index or glycemic load diet, blood levels of insuline remain high during prolonged periods, and fat metabolism is by definition not or hardly possible (4). The more carbs or proteins in the "fuel mix", the less the fats will contribute to this mix. Instead of being burned, the fats are stored as bodily fat (5).
Despite lower intakes of fat and energy and higher intakes of (high GI/GL) carbohydrates, the prevalence of obesity has been rising ever since. This should at least frown one's forehead, and be an invitation of nature to deeper investigate the widely spread statements concerning the physiological etiology of obesity and overweightness (5,6,7).
Moreover, results often favour the highfat lowcarb approach much more than the conventional one, like in this trial, where obese individuals were given a HFLC diet or a conventional one (8). Also with atherogenicity and glycemic control, a HFLC scores better than the conventional diet. This trial is just one among many trial consequently finding the exact same results...
Coconut oil
Coconut oil is surprisingly effective when it comes to losing weight. Coconut oil is one of the few plant based saturated fat rich oils. Most saturated fats are animal of origin. In cold climates, coconut oil turns solid, so it's called coconut fat; in warmer climates it's called coconut oil because it will turn liquid. But it's all the same fat.
In more primitive cultures this fat / oil has been used since ages and everywhere this fat is used, cardiovascular disease occurs significantly less! Coconut oil has proven antiviral, antibacteria, antifungal properties and in most cases lowers the virus load in HIV-/AIDS patients so much as to leave no trace of the virus at all...Yes, you heard right: The viral load in AIDS patients was obliterated and undetectable when given 50 grams of pure coconut oil daily.
Read more on coconut oil and its availability here.
At first sight, this seems to be a very logical and plausible explanation for causing obesity. However in the Dutch 2004 RIVM report "Ons eten gemeten" ("Our food measured"), dealing with Dutch food habits and obesity prevalence, it is claimed that there are no hard data on the supposed decrease in physical exercise as compared to energy intakes, while it is very clear indeed that the energy intake has dropped with 5 per cent in the last 25 years (2) (In the Netherlands, not the US).
So based on available data, this claim of "when using less energy than taken in one would gain weight", this argument cannot be held. The increase in obesity also cannot be ascribed to a higher energy intake, because the data indicate that the mean intake of energy has actually dropped.
Sondike et al (9) put obese mail adolescents on two different weight loss programs. One was a low fat program yielding 1100 calories a day and the other was an Atkins program yielding between 1500 and 2500 calories. The men on the Atkins program lost significantly more weight than did the others and also abided by the rules better than the others did. Of the nine patients that completed the program after a year, eight were in the Atkins group, and the otherone was in the low fat group.
A second trial, conducted by Walter Willet (MD, PhD) et al (10) also showed remarkable results: a group of men and women wers assigned to either one of the following programs:
a low fat program of 1500 calories (women) or 1800 calories (men)
a low carb program of 1500 calories (women) or 1800 calories (men), or:
a low carb program of 1800 calories (women) or 2100 calories (men)
Can you guess where this story goes?
Right: the men and women on the low carb program with the most calories (1800-2100) lost more weight than the men and women on the low fat diet with less calories (1500-1800). The reason for this is that with a low carb program it's simply easier to stick to the program because there are less hunger signals and there is a better glycemic control, that is: a control of the blood sugar.
In many trials where low fat diets are compared with low carb diets, dropout is usually higer in the low fat group. Besides, the lowering of carbs and the addtion of fats stimulates the body to use it's own fat resources, leading to it's gradual decline.
The party goes on...
Recently (in 2004), Feinman and Fine elaborated on even more profound explanations concerning the fact that people seem to lose more weight on low carb diets rather than on low fat diets (11,12).
Since ages in nutrition it's been thought that "a calorie is a calorie", in other words, it's apparently unimportant which macronutrient delivers the calories, as long as it isn't too much. Lots of weight loss programs, such as Weight Watchers, but any conventional weight loss program that works with counting calories, are based on this "rule". By dramatically lowering your caloric intake, weight loss would be achieved. By now, you'll probably already know that this is not as simple as it seems...
Feinman and Fine show, revising the Laws of Thermodynamics, that one calorie is definitely not the other.
The catch is hidden in the following: when a person consumes a 2000 calorie diet (theoretical nutritional value) the efective usable energy will be < 2000 calories. In their dissertations Feinman and Fine show, for example, that the effective net energy of a 2000 cal diet based on 55 energy% carbs, 30% fat and 15% protein, is 1848 calories. This is attributed to the thermic effect of food, or TEF, which is an index of the thermogenetic effect food has in our body system. Generally, literature shows a TEF for carbs of 7%, fats 2.5% and proteins 27.5%.
Furthermore, Feinman and Fine show that when the calories from carbohydrates are equally redistributed to proteins and fats, the effective energy of the original 2000 calorie diet decreases even more. This means more energy "dissappears" as heat and less remains to be digested. When a diet consists of only 8 energy% carbs, the effective energy of this diet (originally 2000 cal) is only 1710 calories.
This is what Feinman and Fine call the 'metabolic advantage' of lowcarb diets.
As theoretical support of conventional weight loss diets based on a reduced caloric intake, the First Law of thermodynamics (FLT) was the only law that was consulted. However, as Feinman and Fine point out, this Law does not cover it at all, because 1) in a real biological system there is no conservation of energy (loss of energy occurs als heat, as price for recombining atoms) and 2) key aspects from te Second Law of Thermodynamics (SLT) dictate that entropy plays an important role and predicts that the theoretical energy is not the same as the real energy of a biological system. In a biological system, entropy increases by definition, leading to less available energy. (Read a chemist's view on this topic here).
This model points out, that you don't neceserriry have to grow thick when you consume more - theoretical - energy than you consume and why one calorie isn't at all per se the other.
May Sondike's and Greene's trials serve as a couple of practical examples of the theoretical dissertations of Feinman and Fine. Less recent practical examples go back to even the beginning of the twentieth century.
Montignac
Many years ago, Michel Montignac, the founder of the Montignac Method, also had a plausible explanation for the fact that the conventional weight loss diets sadly don't offer any improvement:
"Given, that the human needs 2500 calories a day, and this amount of nutrition has been provided for a prolonged period in time. If the amount of calories suddenly drops back to 2000, indeed the equivalent of body fat will be used and weight loss is a fact. If, however, the caloric intake then keeps at the newly acquired level of 2000 calories as opposed to 2500, the body, inspired by its surviving instincts, will quickly tune its energy needs to this new supply of energy. If, as of now, it only gets 2000 calories, it will therefore only USE 2000 calories. Thus, the weight loss is quickly ending. But it goes even further. The body's surviving instincts will push it to an even greater prudence, in that it will grow "stock". If from now on, the body will only get 2000 calories, well, it'll simply diminish its energy needs to, let's say 1700 calories and it will store the remaining 300 calories as body fat."
"The torturing way of the undernourished dieter
(J.P Ruasse MD)"
This graph shows, how successive low calorie diets eventually lead to creating resistance to slimming. From the graph it can be seen that the effect of the diet lessens, as the amount of calories is reduced. The body not only seeks to retrieve its original weight, but also to make more fat reserves.
Excerpt from: 'Ik ben slank want ik eet - of De geheimen van onze voeding', Montignac, M., Artulen, Valkenswaard (1996) (Translation: 'I'm slim cause I eat - or the dsecrets of our nutrition', Montignac, M., Artulen, Valkenswaard (1996)
The trend that is nowadays seen as well in small scale as in large scale trials, is a reevaluation of the assumptions that were made with the introduction of the lipid hypothesis ("cholesterol blocks your arteries and saturated fat is bad or you"). It is thanks to the abundance of carbohydrates that the obesity epidemic has been able to take place.
Tht's why maybe it lies inherently within low fat high carb diets that such a diet simply cannot be maintained for longer periods.
How is this possible?
Lots of scientific trials have studied the dysbalance in metabolism, called hyperinsulinemia.
On their website, www.carbohydrateaddicts.com the American doctor couple Heller describe how the state of hyperinsulinemia is often undiagnosed in obese peopple who obviously are suffering from this metabolic dysfunction and how this can lead to a true carb addiction. Hyperinsulinemia is getting a lot of attention from current investigations and is often implied in obesity and prediabetic periods.
The etiology of the "jojo-effect" (losing and gaining weight over and over again) can very adequately be explained by this model, in which the newest insights on insulin and glucose metabolism have been integrated.
How does it work then?
Whenever a carbohydrate rich meal is eaten, the body first releases a set dosis of insulin in the blood stream, irrespective of the amount of carbs eaten. If, after an hour, the body feels that it had released too less insulin before, a second dose is secreted, but now according to physiological needs.
When, over prolonged periods, too many carbohydrate rich diets with a high glycemic index and/ or glycemic load are eaten (cola, other sugared beverages, candies, pastas, bread, sugar in your tea/ coffee etc), the body gets to deal with an abundance of insulin: the body develops hyperinsulinemia. This means, the body is chronically stuck with far too much insulin. Paradoxically, the sensitivity of the insulin receptors in your body cells grows weaker with prolonged, too high presence of insulin. Insuline subsequently inhibits the release of the hormone serotonin, leading to the hindering of a feeling of satiety. This results in the enduring wish to fulfill this lack of satiety and thus overeating.
This is exactly where the vicious cycle begins: too much of an insulin level demands more feeding, leaving your blood with far too high levels of glucose and insulin, because the insulin receptors by now don't function properly as they should. The carb addiction has actually begun...
Besides, insulin stimulates fat synthesis, and abundant carbohydrates are stored as FAT. Serum values for insulin in obese persons are way higher than that in non-obese persons.
What are characteristics of a carb addiction?
a compelling need for carbohydrate rich foods
an escalating or extraordinary craving for starch rich products, snacks, junkfood and/ or sugar rich products
It is a scientific probability that obese people, who are blamed for "holding it in their own hands, because they eat too much" are not at all holding it in their own hands, because their disturbed metabolism and carb addiction physically forces them to crave more carbs than they need.
In many studies that observe people in either a low carb or a low fat group, dropout is usually higher in the latter. People in low carb groups stick to the program better due to factors like satiety and glycemic control.
Evaluation
Fiction.
The three common statements on obesity are not so water tight as they seem and neither do they explain the true etiology of obesity. New and rapidly developing insights in dysfunctions like diabetes and hyperinsulinemia are casting a new light on the true origins of these dysfunctions. Being overweight isn't simply a case of 'energy in equals energy out'.
It seems that we must indeed discriminate between the origins of calories from different macronutrients.
Besides, low carb diets in "99 out of 100 cases" do better on all fronts than do conventional calorie restricted and/ or low fat diets.
"Modern" solutions, like Optimal Nutrition or Atkins, - or alike low carb / high fat / high protein lifestyles, rigorously exclude the problem that is called fluctuating blood sugar levels. This isn't really modern..."we" always used to eat high fat high protein!!
In my opinion, switching to a food lifestyle where abundant and empty carbs make place for tasteful fat and protein rich products with high nutritional values is a practical way to honour all these new insights, but most of all: to honour yourself!!
Other factors that affect overweightness.
Of course, the simplistic old "diet and exercise" dogma cannot account for just all obesity cases. This would be an arrogant and far too easy way to explain the etiology of obesity. Other factors have in fact been identified to explain that there's more to obesity than diet and exercise. This material was taken from http://www.myhealthyguide.com/Articles.aspx?m=49&amid=326 .
1. Too little sleep
Inadequate sleep (less than 7-9 hours) increases hunger and appetite and interferes with the hormonal regulation of fat metabolism. Research shows that less sleep leads to increased body weight. Sleep deprivation results in reduced levels of leptin, a protein that regulates body fat, and increases in ghrelin, which stimulates food intake. Sleep restriction increases hunger and appetite. Over the past 50 years the average daily time spent in bed has dropped from more than nine hours to about seven. “The changes are consistent with chronic sleep deprivation leading to increased risk of obesity,” say the scientists, writing in the International Journal of Obesity this month.
2. Pollutants
Endocrine disruptors — synthetic chemicals found in pesticides and some plastics — can enter the body through the food chain, and interfere with the work of hormones. When levels go up, so, too, does body mass index. Some of the chemicals are thought to work against male hormones, leading to higher levels of fat. Levels of these man-made chemicals in the environment have increased. The amount of polybrominated biphenyl ether concentration in women’s breast milk, for example, has almost doubled every five years from 1972. “By disturbing hormonal regulation, endocrine disruptors may fatten in a number of ways,” the scientists say.
3. Comfortable temperatures
Homes are on average warmer than they were 30 years ago. The average temperature in UK homes has increased from 13C to 18C (55F to 64F) since 1970. In hotter climates, we’re also keeping cooler. In the southern United States, which has some of the highest obesity rates, the percentage of homes with air-conditioning increased from 37 to 70 per cent. There is some evidence that living in homes and working in offices where the temperature is “comfortable” can contribute to weight gain. This is because the body doesn’t need to use energy to keep warm or cool, meaning that calories are not used up. “Exposure to temperatures above or below the thermoneutral zone increases energy expenditure which decreases fat,” say the scientists.
4. Not smoking
Research indicates that smokers tend to weigh less than non-smokers and that they put on weight when they give up. Nicotine works as an appetite-suppressant. Rates of cigarette smoking have declined steadily as obesity rates have gone up over the past few decades. Between 1993 and 2004 the number of men who smoked dropped from 28 per cent to 22 per cent. The scientists say: “Centers for Disease Control and Prevention scientists estimate that between 1978 and 1990, smoking cessation was responsible for about one quarter of the increase in the prevalence in overweight in men and for about one sixth of the increase in women.”
5. Use of medicines
Antidepressants, anticonvulsants, antidiabetics, antihypertensives, contraceptives and antihistamines have all been linked to weight gain.Beta-blockers can result in weight gain of about 3lb (1.4kg). One study of oral contraceptives estimated an average weight gain of 11lb. “Most (of these) pharmaceuticals were introduced or had their use dramatically increased in the past three decades,” say the scientists. Over the past 30 years there has been a particularly dramatic increase in the use of antidepressants.
6. Getting older
As men and women age, weight increases. Women tend to put on weight after 35 and after the menopause because of hormonal and metabolic changes. In men, extra weight is often the result of increased abdominal fat linked to conditions such as diabetes. Developed countries such as the UK and America, which have the higher rates of obesity, now have an older population. Between 1970 to 2000, the proportion of the adult population aged 35 to 44 has increased by 43 per cent.
“It is likely that these demographic changes are contributing to the increased prevalence of obesity in at least a small way,” say the scientists.
7. The age of your mother
Studies of children in Britain have found that the risk of obesity increases with the age of mother. In nine-year-olds, the odds of being obese increased by 14.4 per cent for every five-year increase in maternal age. One theory is that as women age, their offspring get lower levels of the proteins they need to regulate fat. The age at which women have children is increasing globally. In the UK, it has increased by 1.4 years in a decade. “
Increases in maternal age might produce a 7 per cent increase in the odds of obesity,” say the scientists.
8. Low birth weight
Research suggests that low birth weight, and the rapid catch-up in growth that often follows, may increase the risk of obesity. Mothers who were themselves of low birth weight are at increased risk of gestational diabetes which, in turn, increases the risk of obesity in their child. Overfed babies are also at risk of obesity and the effects can be inherited over several generations. Incidence of low birth weight in the United States increased to 7.8 per cent in 2002, the highest for more than 30 years.
9. Your genes
Research with animals and human beings suggests that body-mass index (BMI) may be inherited. There is also some evidence that men and women with a genetic predisposition toward greater fatty tissue are reproducing at a higher rate. The higher the parents’ body-mass index, the greater the number of offspring. If men and women with a larger BMI are more likely to reproduce, it will result in more children with genes that predispose them to obesity.
10. Your parents’ choice of mating partner
Men and women with a predisposition to a greater BMI are more likely to pair with each other. This phenomenon is known as “assortative mating”. As BMI is partly inherited, this increases the number of children being born who are predisposed to obesity. Because the number of very thin people has stayed about the same, assortative mating seems to increase the average population weight. The scientists say: “Combined evidence strongly suggests that assortative mating has contributed to the epidemic.”
Sources
1. Voedselconsumptiepeiling 1998, Voedingscentrum (1998), Delft Drukkers
2. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm, Trends of intake of energy and macronutrients - United States, 1971--2000, Centre for Disease Control and Prevention, 2004
3. http://www.rivm.nl/bibliotheek/rapporten/270555007.pdf "Ons eten gemeten" (2004), Bohn en Stafleu van Loghum, Houten
4. http://www.jpands.org/vol9no4/ottoboni.pdf
5. "Understanding normal and clinical nutrition", Whitney, E.N. et al, 6e editie 2002, Wadsworth.
6. Bell SJ, Sears B, "Low-glycemic-load diets: impact on obesity and chronic diseases", Crit Rev Food Sci Nutr. 2003;43(4):357-77
7. Nielsen JV, Jonsson E, Nilsson AK, "Lasting improvement of hyperglycaemia and bodyweight: low-carbohydrate diet in type 2 diabetes--a brief report", Ups J Med Sci. 2005;110(1):69-73
8. Stern L et al, "The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial", Ann Intern Med. 2004 May 18;140(10):778-85
9. Sondike, S.B., et al., "Effects of a Low-Carbohydrate Diet on Weight Loss and Cardiovascular Risk Factor in Overweight Adolescents," The Journal of Pediatrics, 142(3), 2003, pag. 253-258
10. Greene, P., Willett, W., Devecis, J., et al., "Pilot 12-Week Feeding Weight-Loss Comparison: Low-Fat vs Low-Carbohydrate (Ketogenic) Diets," Abstract Presented at The North American Association for the Study of Obesity Annual Meeting 2003, Obesity Research, 11S, 2003, page 95OR.
11. Feinman RD, Fine EJ, "A calorie is a calorie" violates the second law of thermodynamics", Nutrition Journal, juli 2004, 3:9 (Full text, PDF)
12. Fine EJ, Feinman RD, "Thermodynamics of weight loss diets", Nutrition & Metabolism, december 2004, 1:15 (Full text, PDF)
13. Ege SN, 'Organic chemistry', D.C. Heath and Company, 3d edition, 1994, p.98-101
