Good Calories, Bad Calories, by Gary Taubes

Carboyhydrates cause heart disease, type II diabetes, cancer, Alzheimers.
5:30
http://www.blogtalkradio.com/StopSugarShock/2007/...

Q: Let's go into one of the conclusions you make ... You were saying that refined carbs and sugars could give you cancer and heart disease and Alzheimers disease and Type II diabetes.A: Yeah. The basis of these ideas -- the concept of diseases of civilization -- and diseases of civilization, Western diseases, diseases that people get when they start eating the diets that we've all grown up eating. And these observations made by -- used to be physicians working in missionary hospitals or colonial hospitals around the world -- populations that eat their traditional diet -- whether they're African or Southeast Asian or Polynesian Islanders or the American Indian -- they don't get the diseases we get. They don't get heart disease, they don't get cancer, they don't get demented, they don't get diabetes, they don't get obese.

The defense of body weight has been well demonstrated in numerous human and animal studies. These data have led to the suggestion of a “set-point” for weight, similar to that for body temperature, so that the body maintains compensatory mechanisms designed either to restore or to protect weight in the event of change, or a buffering mechanism designed to oppose and minimize any imposed weight change, similar to the action of a chemical buffer.Caloric restriction, as in low-calorie (800-1500 kcal/d) and very low-calorie (800 kcal/d) diets, results in semi-starvation, a condition in which the individual experiences sustained negative nitrogen balance. Semistarvation is associated with changes in body composition and energy expenditure that mediate weight loss, in addition to compensatory changes designed to prevent it. It is these adaptive responses that make it so difficult to lose weight on diets and maintain the weight loss.

A 70-million-year-old dinosaur bone from Transylvania in the British Museum contains a periosteal osteogenic sarcoma.

A number of case reports, small series, and large autopsy series describe cancer in nonhuman primates, including chimpanzees, cynomolgus monkeys, marmosets, baboons, rhesus monkeys, African green monkeys, and a variety of other macaques.The malignancies described include non-Hodgkin's lymphoma, nasopharyngeal carcinoma, nephroblastoma (Wilms' tumor), plasmocytoma, pituitary adenoma, ovarian carcinoma, large bowel adenocarcinoma, and mammary carcinoma (Amyx et al. 1982; Baskerville et al. 1984; Baskin et al. 1982; Bennett, Beluhan, and Welsh 1982; Betton 1984; Blanchard and Watson 1988; Crews, Kerber, and Feinman 1967; Gleiser et al. 1984; Hubbard et al. 1984, 1985; Seibold and Wolf 1973).

Perhaps the earliest example of malignant tumor in a hominid is the Kanam mandibular fragment from East Africa, which was recovered by Louis Leakey in 1932 and probably belongs to a hominid that lived in the Lower/Middle Pleistocene era, 500,000 to one million years ago (Aufderheide and Rodriguez-Martin 1998; Strathapoulos 1975).

One such description is that by Herodotus who mentions that Queen Atossa (Persian) "had a tumor on her breast that burst open and was slowly spreading". In addition, the Greek Hippocratic school physician described "a woman had a karkinoma (cancer) developed in the breast"

Other examples of possible osteogenic sarcomas in antiquity include a Fifth Dynasty Egyptian femur and humeri, a Neolithic skeleton from Italy, a Swiss Iron Age skeleton with a humeral tumor, a femur from a Saxon grave, a fifth-century CE femur from a Visigoth in Spain, and an extensive tumor of a pre-Columbian Peruvian skull (Aufderheide and Rodriguez-Martin 1998; Brothwell 1967; Micozzi 1991).

Cases of multiple myeloma have been described in both a Pyrenees and a Danish late Neolithic skull, a Hungarian 10th- to 11th-century grave site, a British medieval skull, and in New World pre-Columbian specimens (Brothwell 1967; Deeley 1983). A few ancient cases of Ewing's sarcoma have also been reported (Aufderheide and Rodriguez-Martin 1998).

Gerszten and Allison (1988) reported a cheek rhabdomyosarcoma in a 12- to 18-month-old male mummy from northern Chile (300-600 CE). Several Peruvian Incan mummies, some estimated to be 2,400 years old, show cutaneous malignant melanoma with widespread bony metastases (Urteaga and Pack 1966).

One of the arguments against the hypothesis I am going to present to you is that it is too simple therefore it must be wrong and my counter argument is why is obesity research exempt from Occam’s razor - if you have a simple hypothesis that explains your observations why not go for it? So here’s the pseudoscience of obesity as I see it.

So this implies a corollary to the overeating hypothesis. Prosperity makes us fat. One way this is phrased is by Kelly Brown (?) who is the director of the Rudd Center for Food Policy and Obesity - he calls it the toxic environment theory that encourages overeating and physical inactivity. Basically we are so wealthy and there is so much junk food around that we don’t have to hunt down wooly mammoths anymore. You know, we don’t have to work for our food so we don’t have to expend enough energy.

These people are saying it’s (overeating and sedentary lifestyle + obesity) happening simultaneously so it must be cause and effect - and no it musn’t be cause and effect. So let’s see what’s really happening. One of the things I did in my research and one of the things you do in science is you look for observations, you look for phenomena that the hypothesis can’t explain . and this is what I call the Fat Louisa Paradox.

Aside from the biochemistry arguments (which Molbiogirl disputed - and she likely knows better than either of us) the arguments seem to be very poor, and even inconsistent.

A ketogenic diet is low in carbohydrates and high in fat. It has been known since the 1920s that such a diet can significantly reduce the incidence rate of epileptic seizures in children.

We know about good and bad fats. Now suspicion is growing that not all sugars are created equal either. Overweight adults who consume large amounts of fructose have been found to experience alarming changes in body fat and insulin sensitivity that do not occur after eating glucose.Pure fructose is found in fresh fruit, fruit juice and preserves. But much of it sneaks into our diets though high-fructose corn syrup (HFCS) in soft drinks - which gets broken down into 55 per cent fructose and 45 per cent glucose in the body - or via sucrose (ordinary sugar), which is broken down into the same two sugars.Fears that fructose and are fuelling the obesity epidemic and triggering insulin resistance and diabetes have been circulating for years (New Scientist , 1 September 2001, p 26), but there have been few direct investigations in humans.So Peter Havel at the University of California, Davis, persuaded 33 overweight and obese adults to go on a diet that was 30 per cent fat, 55 per cent complex carbohydrates and 15 per cent protein for two weeks. For a further 10 weeks, they switched to a diet in which 25 per cent of their energy came from either fructose or glucose.In those given fructose there was an increase in the amount of intra-abdominal fat, which wraps around internal organs, causes a pot belly and has been linked to an increased risk of diabetes and cardiovascular disease. This did not happen with the group who consumed glucose instead, even though both gained an average 1.5 kilograms in weight.Those who consumed fructose also had raised levels of fatty triglycerides, which get deposited as intra-abdominal fat, and cholesterol. Their insulin sensitivity also fell by 20 per cent. Glucose appeared to have no effect on these measures. Havel presented the results at a meeting of the Endocrine Society in San Francisco last week.Because Havel's test looked only at pure fructose, not HFCS or sucrose, it is not yet clear whether these substances are to blame for obesity and diabetes. "The question is, what is the amount of HFCS or normal sugar you need to consume to get these effects?" says Havel, who is planning a long-term study to find out. But he says it's not too soon for people with metabolic syndrome - the blend of conditions including belly fat and insulin resistance that raise the risk of diabetes and cardiovascular disease - to avoid drinking too many fructose-containing beverages.PepsiCo, which sponsored Havel's research, disagrees. "This is a very interesting and important study," says a spokeswoman. "But it does not reflect a real-world situation nor is it applicable to PepsiCo since pure fructose is not an ingredient in any of our food and beverage products."In a separate study, Havel's team compared the immediate effects of consuming a meal in which 25 per cent of the energy came from one of HFCS, sucrose, fructose or glucose. Blood triglyceride levels were all elevated to a similar level 24 hours after consuming fructose, sucrose or HFCS, but not glucose (The American Journal of Clinical Nutrition , vol 87, p 1194), suggesting that all three substances may have similar, negative health impacts. Longer-term studies are needed to confirm whether the triglycerides produced by sucrose or HFCS have similar effects to fructose on abdominal fat and insulin resistance."It adds to what we have known for a long time," says Francine Kaufman at the Keck School of Medicine in Los Angeles. "It's probably not a good idea to consume too much sugar."

This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome.

Along with an increase in total energy consumption over the past few decades (19), there has been a shift in the types of nutrients consumed in the American diet. The consumption of fructose has increased, largely because of an increased consumption of soft drinks and many other beverages that are high in fructose and because of the consumption of foods such as breakfast cereals, baked goods, condiments, and prepared desserts sweetened with sucrose and high-fructose corn syrup (HFCS).

The commercial use of HFCS began to increase in the 1970s and, by 1985, HFCS accounted for {approx}35% of the total amount of sweeteners by dry weight in the food supply (21).

Calculated on a daily basis, the per capita use of added fructose, obtained by combining the disappearance data for the fructose contained in sucrose and in HFCS, increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. This represents an average daily energy intake from added fructose of {approx}1356 kJ (324 kcal).

More recently, a low-dose infusion of fructose has been shown to increase carbon flux through glycogen synthase (EC 2.4.1.11) and thereby stimulate glycogen synthesis in humans (25).

Fructose has also been found to restore the ability of hyperglycemia to regulate hepatic glucose production (26), and the addition of 7.5 g fructose to the standard 75 g glucose reduced the glycemic response to oral-glucose-tolerance tests in adults with type 2 diabetes (27). Thus catalytic amounts of oral fructose may be beneficial in improving glycemic control in type 2 diabetes. In addition, fructose ingestion results in smaller postprandial glycemic excursions (28).

De novo lipogenesis does not increase in response to eucaloric glucose ingestion (31).

The effects of dietary fructose on weight gain have been reported in 3 studies in human subjects.

(In one of the 3 studies) body weight increased in a group of 14 middle-aged men, 11 with type 2 diabetes mellitus and 3 with type 1 diabetes mellitus, who incorporated 50-60 g fructose/d into their diets for 24 wk (38).

Fructose, unlike glucose, does not stimulate insulin secretion from pancreatic cells (40, 41). ... Although high-carbohydrate meals stimulate leptin production in humans relative to high-fat meals (80), if the carbohydrate provided in this study had been fructose rather than glucose, the results would probably have been different because of the dissimilar effects of the 2 sugars on insulin secretion. To compare the effects of glucose and fructose on leptin production, plasma leptin concentrations were measured in rhesus monkeys after intravenous infusion with saline, glucose, or fructose. Glucose infusion markedly increased plasma glucose and insulin concentrations and progressively increased plasma leptin 4-8 h into the infusions. In contrast, an intravenous infusion of the same amount of fructose only modestly increased plasma glucose and did not stimulate insulin secretion or increase circulating leptin concentrations over an 8-h period (65).

Although fructose does not stimulate insulin secretion (41), the insulin resistance and obesity induced by long-term fructose feeding in experimental animals induces compensatory hyperinsulinemia.

The classic relation between insulin resistance, increased fasting plasma insulin concentrations, and glucose intolerance has been hypothesized to be mediated by changes in ambient nonesterified fatty acid concentrations (see review in reference 96). The exposure to increased concentrations of nonesterified fatty acids may reduce insulin sensitivity by increasing the intramyocellular lipid content (98). Increased portal delivery of nonesterified fatty acids, particularly from visceral adipose tissue, could also lead to impaired carbohydrate metabolism, because elevated portal nonesterified fatty acid concentrations increase hepatic glucose production (99, 100). In addition, over time, increased nonesterified fatty acid concentrations may have a deleterious effect on cell function (101).

An increased supply of nonesterified fatty acids in the liver also leads to an increase in the production of VLDL triacylglycerol (102).

The combination of the high-fat diet with fructose resulted in increased circulating triacylglycerol, and fructose with copper deficiency resulted in significant increases in blood cholesterol.

Hyperlipidemia did not develop when starch was combined with a high-fat diet (110).

Hellerstein (111) showed that there is little de novo lipogenesis from glucose under eucaloric conditions in humans.

Stephan Guyenet, a neurobiologist who studies the neurobiology of body fat regulation, wrote a long, detailed critique of Gary Taubes' book, Good Calories, Bad Calories on his terrific blog, Whole Health Source.

Guyenet writes:Carbohydrate consumption per se is not behind the obesity epidemic. However, once overweight or obesity is established, carbohydrate restriction can aid fat loss in some people. The mechanism by which this occurs is not totally clear, but it has nothing to do with removing the supposed suppressive effect of insulin on fat release from fat cells.

Mayo Clinic writes:Top 5 lifestyle changes to reduce cholesterol1. Lose weightCarrying some extra pounds even just a few contributes to high cholesterol. So losing as little as 5 to 10 pounds (about 2 to 5 kilograms) can help reduce cholesterol levels.

Mayo Clinic writes:What's the best way to lower triglycerides?Lose weight. If you're overweight, losing 5 to 10 pounds can help lower your triglycerides. Motivate yourself by focusing on the benefits of losing weight, such as more energy and improved health.

Guyenet writes:I hope you can see by now that the carbohydrate hypothesis of obesity is not only incorrect on a number of levels, but may even be backward.

Guyenet writes:The reason why obesity and metabolism researchers don't take Taubes's idea seriously is that it is contradicted by a large body of evidence from multiple fields.

Those opposed to low carb diets need to start saying things that actually turn out to be true before their recommendations can be taken seriously.

A greater percent lowering of LDL occurs in older people than in younger people.716216. Wilcosky T, Hyde J, Anderson JJB, Bangdiwala S, Duncan B. Obesity and mortality in the Lipid Research Clinics Program Follow-Up Study. J Clin Epidemiol1990 ;43:743 -52.

The estimated frequency of the allele leading to the phenotype characterised by predominance of small, dense LDL subclasses was about 15%. Expression of this phenotype appears to be age dependent, in that most affected subjects in this population were older than 40 years.

Although plasma lipid levels were normal in most subjects with this trait, levels of plasma apoprotein B and triglyceride were higher and levels of apoprotein AI and HDL2 lower than in unaffected family members.

Guyenet writes:That is, Taubes is not disagreeing with the first law of thermodynamics: he understands that fat accumulation depends on how much energy is entering the body vs. leaving it.

Guyenet writes:I've already demonstrated that Taubes's conception of the effects of insulin are badly misguided, therefore it makes no sense to invoke insulin as a mechanism between carbohydrate consumption and body fatness, unless your hypothesis is that carbohydrate lowers body fatness by increasing insulin secretion.

Guyenet writes:Therefore, the insulin hypothesis is not consistent with basic thermodynamics, and it's not consistent with research on the biological functions of insulin.

Guyenet writes:Weight stable obese people have a higher energy flux out of fat cells, and a higher metabolic rate, but it is not enough to overcome the higher calorie intake that is also observed (26, 27). That has been repeatedly confirmed and it is simply a fact at this point.

PD writes:When a theory doesn't ring true for an individual, that individual has to go with what works whether it is a scientific truth or not.

I did and I disagree with your quote.

That is not the way I read what Taubes wrote.

And from the abstract #26

Abstract writes:Although generally now accepted, one of the major surprises from the early applications of DLW was that obese individuals have higher energy expenditures than lean controls. Moreover, weight gain, even in the already obese, is associated with an increase in energy expenditure as weight is one of the strongest predictors of total energy expenditure.

[This does] not account for the common cessation of weight loss observed after 12-26 weeks of restriction.

A series of studies demonstrated good agreement between mean energy intake and mean energy expenditure when food intake was recorded by observers or when it was self-reported by normal-weight, self-selected, highly motivated volunteer subjects using weighed records. However, in randomly recruited men and women, energy intake by weighed records was 82% and 81%, of energy expenditure, respectively, indicating underestimation of habitual intake.

Reported intake of obese and previously obese women was only 73% and 64% of expenditure, whether measured by weighed record or by diet history, confirming suspicions that these subjects misrepresented their intake.

Guyenet writes:DLW studies have shown that after controlling for confounding factors, obese people almost invariably expend more, and consume more calories than lean people (24, 25).

PD writes:Show me how Taubes mangled the papers.

Guyenet writes:Leptin is the system that Drs. Jules Hirsch and Rudy Leibel have shown in carefully controlled human studies is responsible for the metabolic defect he's getting at (1). It's also the system that is mutated in the genetically obese rodents he discusses (2, 3). Yet it receives no mention in the book.

Guyenet writes:Taubes states here that the typical diet is "primarily milk", therefore by inference, low in carbohydrate. ... The typical diet is 81% carbohydrate, and primarily based on millet, according to Taubes's own reference.

Guyenet writes:The Pima of New Mexico currently have one of the highest obesity rates in the world, on par with Nauru. It is rather ironic that Taubes uses them as an example in GCBC, when they are at odds with his hypothesis.

Guyenet writes:Insulin infused into the brains of baboons causes a suppression of appetite and fat loss, which is consistent with the well-established fact that insulin and leptin have overlapping functions in the brain (10, 11). Knocking out insulin receptors in the brain leads to increased fat mass in rodents, suggesting that its normal function involves constraining fat mass (12). Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13). This is why insulin is viewed by most obesity researchers as an anti-obesity hormone, not an obesity hormone.

Guyenet writes:Therefore, the insulin hypothesis is not consistent with basic thermodynamics, and it's not consistent with research on the biological functions of insulin. Obese people do not have a defect in the ability to release fat from fat cells and burn it, to the contrary. They release more fat from fat cells than lean people, and burn more of it.

Guyenet writes:The fat cells of obese people do not suffer from excessive insulin signaling, to the contrary, the evidence suggests that their fat cells are insulin resistant and therefore insulin signaling is reduced. This shows that insulin does not cause obesity by acting directly on fat cells to cause fat storage. To understand obesity, we have to understand what causes increased food intake, and that factor is not insulin.

Guyenet writes:New Guinea highland tribe at Tukisenta 1960s and 70s. West Nile district, Uganda, 1940s. Northern Cameroon, 1980s. Most of Asia, 20th century. Kitava, 1990s. Pima, 20th century.

It was very much about what type of energy enters the body. All calories are not equal.

Resorting to creo rudeness doesn't make your point either.